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1320
CHAPTER
Colon and Rectum 
Susan Galandiuk, Uri Netz, Emilio Morpurgo, Sara Maria Tosato, 
Naim Abu-Freha, C. Tyler Ellis
52
O U T L I N E
Embryology of the Colon and Rectum
Anatomy of the Colon, Rectum, and Pelvic Floor
Colon Anatomy
Rectal Anatomy
Physiology of the Colon
Absorption of Fluid and Electrolytes
Secretion
Urea Recycling
Recycling Bile Salts
Colonic Flora, Fermentation, and Short-Chain Fatty Acids
Probiotics and Prebiotics
Colonic Motility
Defecation
Preoperative Evaluation
Nutritional and Risk Assessment
Preoperative Bowel Preparation
Planning Intestinal Stomas
Colostomy
Ileostomy
Enhanced Recovery Protocols
Preoperative Interventions
Preadmission Nutrition and Bowel Preparation
Perioperative Interventions
Postoperative Interventions
Diverticular Disease
Background
Pathophysiology and Epidemiology
Clinical Evaluation
Management
Special Populations
Large Bowel Obstruction
Diagnosis and Assessment
Treatment
Colonic Pseudo-Obstruction
Diagnosis
Management
Inflammatory Bowel Disease
Epidemiology and Etiology
Disease Distribution and Classification
Clinical Presentation and Disease Diagnosis
Biologics in the Treatment of Inflammatory Bowel Disease
Assessment of Symptom Severity
Indications for Surgery for Ulcerative Colitis
Indications for Surgery for Crohn Disease
Surgical Options for Ulcerative Colitis
Surgery for Crohn Disease
Cancer Risk
Postoperative Complications
Postoperative Recurrence
Infectious Colitis
Clostridium difficile Infection
Epidemiology
Microbiology and Transmission
Risk Factors
Clinical Presentation
Diagnosis
Treatment
Other Colonic Infections
Ischemic Colitis
Anatomic Considerations
Risk Factors
Presentation and Diagnosis
Treatment
Neoplasia
Colorectal Cancer Genetics
Epithelial-Mesenchymal Transition
Consensus Molecular Subtypes
Colorectal Polyps
Nonneoplastic Polyps
Serrated Polyps
Neoplastic Polyps
Malignant Polyps
Postpolypectomy Surveillance
Hereditary Cancer Syndromes
Familial Adenomatous Polyposis
MUTYH-Associated Polyposis
Peutz-Jeghers Syndrome
Juvenile Polyposis Syndrome
Lynch Syndrome
Staging
Rules for Classification
Clinical Staging
Pathologic Staging
Additional Prognostic Factors
Surgical Treatment of Colorectal Cancer
General Rules and Principles
Surgical Technique
Obstructing Colon Cancers
Management of Left-Sided Obstructions
Management of Right-Sided Obstructions
Rectal Cancer
Preoperative Evaluation of Patients With Rectal Cancer
Local Excision
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1321CHAPTER 52 Colon and Rectum 
Colon and Rectum 
Susan Galandiuk, Uri Netz, Emilio Morpurgo, Sara Maria Tosato, 
Naim Abu-Freha, C. Tyler Ellis
Please access Elsevier eBooks for Practicing Clinicians to view 
the videos for this chapter https://expertconsult.inkling.com/.
Acknowledgments: Josè Adolfo Navarro, MD; Silvia Neri, MD; 
and Alberto Morabito, MD.
EMBRYOLOGY OF THE COLON AND RECTUM
A sound knowledge base of the gastrointestinal (GI) tract em-
bryologic development is important in understanding colon and 
rectal anatomy and pathophysiology. The primitive gut tube is 
formed from the endodermal roof of the yolk sac. Early in the 
development process, beginning in the third week of gestation, 
the gut tube divides into three sections: the foregut, midgut, and 
hindgut (Fig. 52.1).
The foregut forms the oral (buccopharyngeal) membrane, 
esophagus, stomach, and proximal duodenum (to the duodenal 
ampulla) and is supplied by the celiac artery. The midgut, includ-
ing the distal part of the duodenum, small intestine, right colon, 
and the proximal two thirds of the transverse colon, receives it 
blood supply from the superior mesenteric artery (SMA). The 
midgut temporarily herniates ventrally out of the abdomen, a key 
step in the physiologic development progress for acquiring length 
and correct positioning of its structures (Fig. 52.2). The hindgut 
develops into the distal third of the transverse colon, descending 
colon, sigmoid, and rectum all the way to the upper anal canal. 
It is supplied by the inferior mesenteric artery (IMA). The venous 
and lymphatic networks develop parallel to their corresponding 
sectional arteries.
The embryologic development of the rectum is complex and 
prone to developmental complications (see Chapter 67, Pediatric 
Surgery). The proximal rectum develops similar to the colon. The 
distal regions develop from the terminal hindgut that enters into 
the cloaca (an endoderm-lined cavity in contact with the surface 
ectoderm at the cloacal membrane). Prior to 5 weeks, the intestinal 
and urogenital tracts terminate at a common cavity in the cloaca. 
During the next few weeks, the urorectal septum migrates caudally 
and divides the cloaca into an anterior urogenital sinus and poste-
rior distal rectum and anal sinus (Fig. 52.3). The urorectal septum 
fusion with the cloacal membrane is represented in the adult by the 
perineal body. The external anal sphincter is formed by the posteri-
or part of the cloacal sphincter, whereas the internal anal sphincter 
is formed from enlarging circular fibers of the rectum. The upper 
two thirds of the anal canal are derived from the hindgut and the 
lower third from the proctodeum. The dentate line marks the fu-
sion of endodermal (hindgut) and ectodermal depression (procto-
deum). The anal transition zone is formed from the cloacal part of 
the anal canal. The hindgut part of the anal canal is supplied by 
the IMA, while the lower third, by the internal pudendal artery. 
ANATOMY OF THE COLON, RECTUM, AND PELVIC 
FLOOR
The large bowel including the colon and rectum is a tube of vari-
able diameter, approximately 150 cm in length (Fig. 52.4).
Colon Anatomy
The cecum is the saccular beginning of the colon, with an aver-
age diameter of 7.5 cm and a length of 10 cm. It has no mesen-
tery and is completely covered with peritoneum and is therefore 
considered an intraperitoneal structure. The cecum is variably 
connected to the posterior abdominal wall by a peritoneal reflec-
tion. Patients with an abnormally mobile cecum and ascending 
colon, found in a small proportion of patients, can be predis-
posed to volvulus (torsion) or cecal bascule (intermittent ante-
rior and superior folding of the cecum associated with obstruc-
tive symptoms). The cecum has a thin wall compared to the rest 
of the colon, and considering its large diameter, in accordance 
with the law of Laplace, it is the site most likely to perforate in 
the presence of large bowel obstructions. Although it is disten-
sible, acute dilation of the cecum to a diameter of more than 12 
cm, which can be measured on a plain abdominal radiograph, 
is associated with risk of ischemic necrosis and perforation of 
the bowel wall and should be treated promptly, usually with sur-
gery. The terminal ileum empties into the cecum along its medial 
border through the ileocecal valve, a thickened, nipple-shaped 
invagination containing circular muscle. In cases of large bowel 
obstruction, the ileocecal valve is clinically important. An ileo-
cecal valve that does not allow reflux of colonic contents into 
the ileum (competent ileocecal valve) can result in a closed-loop 
Septum 
transversum
Omphaloenteric
duct and
vitelline artery
Allantois
Anal pit
Cloacal 
membrane
Cloaca Hindgut
Inferior mesenteric
artery
Superior
mesenteric
artery to midgut
Primordium 
of liver
Celiac trunk
Gastric and
duodenal regions
Esophageal region
Aorta
Heart Pharynx
Stomodeum
FIG. 52.1 Median section of the embryo showing the early alimentary 
system and its blood supply (week 4). (From Moore KL, Persaud TVN, 
Torchia MG. Alimentary system. In: The Developing Human. 11th ed. 
Philadelphia: Elsevier; 2020:193–221.)
Resections for Rectal Cancers
Low Anterior Resection
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1337CHAPTER 52 Colon and Rectum 
The use of goal-directed fluid therapy in the intraoperative and 
postoperative phases of care is associated with a reduction in time 
to return of bowel function and length of stay. Lastly, minimally 
invasive surgical (MIS) approaches should be used, when possible, 
with avoidance of routine use of intraabdominal drains and naso-
gastric tubes. 
Postoperative Interventions
Early patient mobilization with early feeding has good evidence 
to support its role in an ERP. Alvimopan use has been shown to 
hasten return of bowel function after open surgery, but not with 
MIS. In addition, intravenous (IV) fluids and urinary catheters 
should be discontinued early in the postoperative period.
In summary, ERPs are evidence-based protocols that benefit 
colorectal surgery patients. Local implementation involves buy-in 
for a range of stakeholders that may be in opposition to the pref-
erences of individual healthcare professionals. Adherence to the 
constellation of ERP components and the outcomes of interest 
should be continually monitored and evaluated. 
DIVERTICULAR DISEASE
Background
Diverticular disease is used to describe a spectrum of manifes-
tations associated with colonic diverticulosis. Diverticula are 
saccular outpouchings of the bowel wall. They are described as 
“true” diverticula when they contain all layers of the bowel wall; 
these are rare and usually congenital. The vast majority of di-
verticula in the colon are “false” diverticula (pulsion, pseudodi-
verticula), containing only the mucosa and muscularis mucosa. 
Diverticulitis is thought to be mainly a disease of the modern 
world, coinciding with dietary changes following the industrial 
revolution. 
Pathophysiology and Epidemiology
Hypertrophy of the muscular layers of the colon wall, com-
bined with a narrowed lumen and disordered colonic motility, 
causes localized high-pressure zones in which the mucosa herni-
ates through areas of relative weakness. Diverticula are classically 
formed on the mesenteric side of the colonic wall in regions where 
vasa recta traverse through the muscular layer to provide blood 
to the mucosa (Fig. 52.20). The sigmoid and descending colon 
are typically affected, whereas the rectum, having an extra layer 
of muscle, is generally not affected (Fig. 52.21). This has impli-
cations for surgery and is why the distal anastomosis margin in 
operations for diverticulitis should always be within the rectum. 
Diverticulosis increases with age and is relatively rare in young 
adults. Colonic diverticula are noted in approximately 40% of in-
dividuals between the ages of 50 and 60 years and in over 60% of 
individuals over the age of 80 years (Fig. 52.22). The mechanism 
for developing diverticulitis is thought to be a result of obstruc-
tion of the orifice of a diverticulum, with stasis leading to bacterial 
overgrowth, inflammation, and increased pressure within the di-
verticulum, causing ischemia and microperforation. Interestingly, 
only a small proportion of patients with diverticulosis develop di-
verticulitis. Modern estimates indicate that fewer than 5% of pa-
tients with diverticulosis will develop diverticulitis; however, due 
to the high prevalence of diverticulosis, it has become a significant 
clinical and financial burden, accounting for more than 2.7 mil-
lion outpatient visits in the United States annually and more than 
200,000 inpatient admissions for diverticulitis at an estimated 
cost of more than $2 billion.
Diet and lifestyle factors play an important role in diverticular 
disease. Western dietary patterns high in red meat, fat, and refined 
grains are associated with an increased risk of the disease, whereas 
increased fiber intake, with abundant fruit, vegetables, and whole 
grains, reduces the risk of diverticulitis. Intake of nuts, seeds, and 
popcorn does not appear to increase the risk. Central obesity and 
smoking increase the risk, whereas physical activity such as run-
ning has been correlated with a decreased risk. A study examining 
the joint contribution of multiple lifestyle risk factors, defined as 
fewer than four servings of red meat per week, at least 23 g of fiber 
per day, 2 hours of vigorous activity per week, a body mass index 
18.5 to 24.9 kg/m2, and no history of smoking on the risk of 
incident diverticulitis, found that adherence to a low-risk lifestyle 
could prevent 50% of incident diverticulitis.5 
Clinical Evaluation
Diverticular disease can manifest as diverticulitis, but it is also 
the most common reason for severe lower GI bleeding (discussed 
Peritoneum
Circular
muscle
Mucosa
Taenia coli
Epiploic
appendix
Diverticulum
Concentration
in diverticulum
Blood vessel
piercing
musculature
FIG. 52.20 Pathogenesis of diverticulosis. (From Netter FH. Netter 
Collection of Medical Illustrations. Vol 9. Philadelphia: Elsevier Saunders; 
2016:145.)
FIG. 52.21 Computed tomography scan of the pelvis showing exten-
sive sigmoid diverticulosis.
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1338 SECTION X Abdomen
elsewhere). Since diverticulitis is caused by inflammation and 
perforation of a colonic diverticulum, signs and symptoms will 
generally result from the pericolonic inflammation. Patients will 
commonly present with abdominal pain localized to the left lower 
quadrant (following the location of the inflamed sigmoid colon). 
Additionally, fever, change in bowel habits, anorexia, and urinary 
urgency (in cases where the bladder is secondarily inflamed) are 
frequent. On physical examination, localized tenderness is noted, 
commonly with moderate abdominal distension. A tender mass 
can be palpable if there is a significant phlegmon. Rectal bleeding 
is rare in the presentation of acute diverticulitis and should raise 
suspicion of another diagnosis such as ischemic colitis or IBD. 
Leukocytosis is a common laboratory finding.
Several imaging modalities have been used to evaluate patients 
with suspected diverticular disease. Flat and upright plain films 
can be used to diagnose obstruction or free intraperitoneal air 
but are generally nonspecific. Contrast studies, ultrasound, and 
magnetic resonance imaging (MRI) have also been used, but cur-
rently, computed tomography (CT) has become the most useful 
examination to confirm the diagnosis, exclude other diagnoses, 
and classify the severity of the disease. Signs of diverticulitis on 
CT include the presence of diverticula, colonic wall thickening, 
pericolic fat stranding, and abscess formation. CT studies have 
the capacity to localize abscesses and fistulas and define the ex-
tent of the disease. The modified Hinchey classification6 is the 
most commonly used tool to describe the severity of diverticulitis 
(Table 52.1).
Grade 0, not included in the original publication, is commonly 
used to describe mild clinical diverticulitis. If CT is performed, 
colonic wall thickening without pericolonic fat stranding can be 
seen. Grade 1a presents with a phlegmon with colonic wall thick-
ening and pericolonic fat stranding, while grade 1b also includes a 
pericolonic or mesocolic abscess (Fig. 52.23). Patients with grade 
2 disease have distant intraabdominal or pelvic abscesses. Patients 
with grade 3 disease have generalized purulent peritonitis, and 
grade 4 disease, fecal peritonitis. The ability of a CT scan to dis-
tinguish between grade 3 and grade 4 is limited, and in these cases, 
accurate diagnosis is usually made in the operating room.
Flexible endoscopy during the acute setting should be ap-
proached with caution because distentionof the colon may result 
in worsening perforation. 
Management
Complicated Diverticulitis
Patients with complicated diverticulitis are characterized by the 
presence of an abscess, fistula, obstruction, or free perforation.
Abscess. Signs and symptoms will depend on the size and lo-
cation of the abscess, with diagnosis usually provided on imag-
ing. Smaller abscesses can often be treated successfully with an-
tibiotics alone. Larger abscesses will require drainage. Following 
recovery, elective surgery is generally recommended; however, 
some of these patients, especially those with smaller abscesses 
that were treated without drainage, can probably be managed 
nonoperatively. Patients with abscesses not amenable to percu-
taneous drainage and unresponsive to treatment require urgent 
surgery. 
Fistula. Fistulas are abnormal connections to surrounding 
epithelial lined organs and are a relatively common complication 
of diverticulitis. They are a result of the local inflammation and 
development of an abscess that decompresses into a neighboring 
organ. The most common type, especially in men, is a colovesi-
cal fistula to the dome of the bladder. Patients will present with 
recurrent urinary tract infections, which are in many cases poly-
microbial. Pneumaturia and fecaluria may also be present. CT 
FIG. 52.22 Endoscopic view of diverticulosis.
TABLE 52.1 Modified Hinchey 
classification system.
Stage 0 Mild clinical diverticulitis
Stage Ia Confined pericolic inflammation—phlegmon
Stage Ib Confined pericolic abscess (within sigmoid mesocolon)
Stage II Pelvic, distant intraabdominal or intraperitoneal abscess
Stage III Generalized purulent peritonitis
Stage IV Fecal peritonitis
From Klarenbeek BR, de Korte N, van der Peet DL, et al. Review of 
current classifications for diverticular disease and a translation into 
clinical practice. Int J Colorectal Dis. 2012;27:207–214.
FIG. 52.23 Computed tomography of the pelvis demonstrating sigmoid 
diverticulitis with a thickened bowel wall, fat stranding a pericolonic ab-
scess (arrow), modified Hinchey grade 1b. 333
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1339CHAPTER 52 Colon and Rectum 
can reveal air or contrast in the bladder in the absence of prior 
instrumentation. Cystoscopy will usually disclose inflammation 
at the site of the fistula. Colovaginal fistulas occur almost exclu-
sively in women who have undergone previous hysterectomy and 
present with vaginal discharge and passing of air per vagina. Co-
locutaneous fistulas usually present at a previous drain site in pa-
tients who have undergone percutaneous drainage. Patients with 
fistulas usually do not need emergency surgery as the abscess has 
usually decompressed. Initial management includes broad spec-
trum antibiotics to decrease the inflammation. Patients are then 
investigated with colonoscopy and appropriate imaging (i.e., 
cystoscopy) to exclude malignancy and Crohn disease. Surgi-
cal principles then encompass resection of the involved colon 
and fistula tract with primary anastomosis. If possible, the fistula 
opening into the secondarily involved organ is primarily suture 
repaired; however, in many cases, the opening is small and dif-
ficult to recognize. In the case of the bladder, with small fistula 
openings, drainage of the bladder with a Foley catheter for 7 to 
10 days will usually allow for healing. A cystogram can be done 
to confirm fistula healing prior to Foley removal. Fistulas to the 
small bowel will characteristically require resection and primary 
anastomosis. 
Obstruction. Patients with recurrent and chronic diverticulitis 
can develop fibrosis of the colonic wall, leading to stricture for-
mation. In most cases, these patients will present with insidious 
symptoms and a partial obstruction. Small bowel obstruction may 
also be seen as a result of a small bowel loop adhering to an area 
of inflamed colonic tissue or abscess. Management depends on 
the degree and type of obstruction. Patients with a partial obstruc-
tion can usually be initially treated with a nasogastric tube for 
decompression, antibiotics, fluids, and bowel rest. If the obstruc-
tion resolves, elective resection can be planned. It is usually im-
portant, prior to resection, to perform a colonoscopy to rule out 
malignancy. In cases where the stricture is impossible to pass using 
a colonoscope, virtual colonoscopy or a retrograde contrast study 
can be helpful to visualize the remainder of the bowel. Patients 
with a complete obstruction unresponsive to therapy will require 
emergency surgery. 
Perforation. Patients with a free intraabdominal perforation 
with widespread contamination will present with diffuse peritoni-
tis with rebound tenderness and guarding. Signs of sepsis includ-
ing fever, tachycardia, and hemodynamic instability are frequently 
seen. Imaging can demonstrate free abdominal fluid, signs of 
peritonitis, and free intraabdominal air. The ability to distinguish 
between purulent and fecal diverticulitis prior to surgery is lim-
ited. Hinchey grades 3 and 4 are considered a surgical emergency. 
Following initial resuscitation, patients are taken to the operating 
room with a goal of controlling the source of infection by resec-
tion and washing out the abdominal contamination.
The mainstay of treatment in these cases has traditionally been 
the Hartmann procedure, which removes the involved colon and 
exteriorizes an end colostomy. Reversing the colostomy, however, 
requires a second major surgical procedure with its own signifi-
cant morbidity and mortality. Practically, up to 50% of patients 
will never be reversed, with even higher rates in the elderly. Given 
these implications, several studies have investigated alternatives 
to the Hartmann procedure. One option has been laparoscopic 
lavage, which entails laparoscopic irrigation of the abdominal 
cavity to reduce the abdominal contamination and placement of 
drains without resection (mainly for Hinchey grade 3 diverticu-
litis). Although this approach results in lower stoma rates, it has 
been associated with significantly higher rates of ongoing and re-
current sepsis and emergency reoperations.7 This approach is still 
controversial and should probably only be used in highly selected 
individuals. Another option is performing a resection with a pri-
mary anastomosis and diverting ileostomy. Although lengthening 
the initial surgery, this technique has been found to be safe and 
significantly simplifies and shortens the second operation. Over-
all morbidity and mortality are similar; however, a much higher 
proportion of patients will have their stomas reversed (94%–96% 
for primary anastomosis vs. 65%–72% for Hartmann).8 This has 
become an attractive option for patients who are stable enough to 
withstand the additional time of the initial surgery. 
Uncomplicated Diverticulitis
The treatment for uncomplicated diverticulitis depends on the 
severity of symptoms, and the approach is subsequently indi-
vidualized. The majority of these patients can be managed as 
outpatients. The mainstay of treatment is based on pain medi-
cations, short-term alteration of diet, and antibiotics. Com-
monly, patients are initially prescribed clear liquids, followed by 
a low-residue diet until the inflammation subsides. Antibiotics 
have traditionally been prescribed to cover colonic bacteria. A 
systematic review and metaanalysis assessing the effect of antibi-
otic administration in patients with uncomplicated diverticulitis 
has not shown the usage of antibiotics to accelerate recovery or 
prevent complications or subsequent surgery.9 As a result, some 
physicians have stopped prescribing antibiotics for uncompli-
cated diverticulitis.
A small proportion of patients diagnosed with diverticulitiswill actually have a colonic neoplasm mimicking diverticulitis. 
Overall, this is currently estimated at around 1% to 3%, with sig-
nificantly higher rates observed in complicated disease.10 Upon 
recovery, it is recommended that patients undergo a colonoscopy 
after 4 to 8 weeks to exclude malignancy.
Following the initial episode of acute, uncomplicated diver-
ticulitis, only 10% to 35% of individuals will have another epi-
sode.11 After more episodes, the chances of recurrence increase 
significantly. In an attempt to avoid severe complicated diverticu-
litis, elective surgery was previously suggested following uncom-
plicated diverticulitis, depending on the number of episodes, with 
the thought that more episodes would lead to more chances of 
recurrence and a higher chance of severe complicated diverticuli-
tis. However, recurrences in general tend to follow the severity of 
the initial episode. As a result, the number of attacks of uncom-
plicated diverticulitis has fallen out of favor as an indication for 
surgery. Currently, an individual assessment is performed on the 
frequency of attacks, ongoing symptoms, and their effect on qual-
ity of life versus the age and medical condition of the patient and 
their surgical risk.
The aim of elective surgery is to remove the affected segment 
of the colon (usually the sigmoid colon) and to perform a primary 
anastomosis of the healthy remaining bowel. When removing the 
sigmoid colon, the proximal margin should be in soft pliable bow-
el, but it is not necessary to include all proximal diverticula. The 
distal anastomosis, however, should be to the upper rectum, since 
leaving a section of distal sigmoid colon is associated with a higher 
risk of recurrent diverticulitis. Surgery can be performed by either 
an open, laparoscopic, hand-assisted, or robotic approach. MIS 
for diverticular disease has been shown to be safe, with advantages 
of more rapid recovery of bowel function, less pain, and shorter 
hospitalization. 
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1340 SECTION X Abdomen
Special Populations
Right-Sided Diverticulitis
This is common in Asian countries but rare in the west. This 
typically affects younger patients and may be challenging to 
diagnose as signs and symptoms are very similar to those of 
acute appendicitis. Other differential diagnoses to be consid-
ered include Meckel’s diverticulitis, cholecystitis, ischemic coli-
tis, mesenteric adenitis, pyelonephritis, and pelvic inflamma-
tory disease. The recommended approach should generally be 
similar to that for diverticulitis in other sites. Patients who have 
recurrent episodes or complicated disease and patients with an 
uncertain diagnosis should be considered for resection with a 
right hemicolectomy. 
Immunocompromised Patients
Immunocompromised patients include transplant patients; patients 
with diabetes mellitus, renal failure, or cirrhosis; and patients be-
ing treated with systemic steroids and/or chemotherapy. While 
the prevalence of diverticulitis in these patients is similar to the 
general population, they are more likely to present with free per-
foration and complicated disease because of their impaired ability 
to mount an inflammatory response. Because of this risk, there 
should be a lower threshold for resection after a single attack of 
diverticulitis. Immunocompromised patients who require emer-
gency surgery and resection should probably not undergo primary 
anastomosis at the initial surgery because of their impaired im-
mune system and healing. 
Young Patients
Historically, patients younger than 50 were considered to have a 
more virulent form of diverticulitis and were recommended to 
undergo resection after one episode of uncomplicated disease. 
Although current evidence does demonstrate higher rates of re-
currence, young patients do not have a higher rate of emergency 
surgical intervention. Current guidelines do not support treating 
young patients differently than others. 
LARGE BOWEL OBSTRUCTION
Large bowel obstruction, defined as bowel obstruction distal to 
the ileocecal valve, can occur as a result of a variety of etiologies. 
Broadly, it is classified into mechanical (dynamic) obstruction and 
functional (adynamic or pseudoobstruction). Mechanical obstruc-
tion can be further characterized into endoluminal, mural, and 
extraluminal causes (Box 52.1).
The most common etiology of mechanical obstruction in the 
United States is colorectal cancer (CRC), whereas colonic vol-
vulus is more common in Russia, Eastern Europe, Africa, the 
Middle East, and India. Presentation and symptoms depend on 
whether it is an acute obstruction or a more chronic progressive 
change, as well as partial, in which some gas/fecal contents are 
able to pass versus complete obstruction in which nothing passes 
distally. It is thought that worldwide, volvulus is responsible for 
roughly one third of the cases of large bowel obstruction. The 
most common site of volvulus is the sigmoid colon; however, ce-
cal volvulus can also occur. Any portion of the colon that is not 
fixed to the retroperitoneum and that has an elongated mesentery 
has the potential for volvulus. In these cases, there is an axial 
twisting of the colon around the mesentery resulting in an ob-
struction.
Mechanical obstruction will generally present with increased 
peristalsis and low-grade colicky pain, but late, long-lasting obstruc-
tion may have decreased bowel sounds. In addition, patients will fail 
to pass stool and flatus and demonstrate increasing abdominal dis-
tention. Acute obstructions tend to present more dramatically with 
rapid onset of pain, distension, and abdominal tenderness, whereas 
patients with progressive obstruction may present with increasing 
constipation, pencil-thin stools, and intermittent abdominal pain. 
Functional obstruction usually presents with distension, vague ab-
dominal pain, and weak or absent bowel sounds.
Patients with a closed-loop obstruction in which both the 
proximal and distal parts of a segment of bowel are blocked must 
be promptly recognized and treated, as they have the potential for 
ischemia and perforation with rapid deterioration. Closed-loop 
obstruction is commonly encountered in cases such as volvulus 
and strangulated hernias. Fig. 52.24 shows a plain film of a patient 
with a sigmoid volvulus. Note the bent, inner-tube appearance of 
the colon. The volvulus has resulted in a closed-loop obstruction. 
In these situations, the colon becomes progressively distended 
with pressure increasing to the point of ischemic necrosis and per-
foration. Fig. 52.25 shows a CT scan illustrating the characteristic 
mesenteric whorl seen in patients with a volvulus.
Another common circumstance of closed-loop obstruction is 
patients with obstructing colon cancers that have a competent 
ileocecal valve, which does not allow backflow of intestinal con-
tents. Obstructing cancers with an incompetent ileocecal valve 
will usually present less acutely, with a much lower chance of 
Mechanical
Intraluminal
Intrinsic mass—neoplasm
Foreign body
Bezoar
Fecal impaction 
Mural
Diverticular stricture
Crohn disease stricture
Ischemic stricture
Radiation stricture
Infectious (i.e., lymphogranuloma venereum, tuberculosis, schistosomiasis)
Hirschsprung disease 
Extraluminal
Sigmoid volvulus
Cecal volvulus
Hernia (inguinal, ventral, internal)
Metastatic/intraabdominal tumor
Abdominal abscess
Retroperitoneal fibrosis
Adhesions (rare in large bowel) 
Functional
Colonic pseudo-obstruction (Ogilvie)
Toxic megacolon
Paralytic ileus
BOX 52.1 Large bowel obstruction 
common etiologies.
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1341CHAPTER 52 Colon and Rectum 
perforation as the valve allows backflow of intestinal contents into 
the small bowel, resulting in a progressively distended abdomen 
with nausea and vomiting of a feculent nature.
Distention of the colon occurs as a result of gas and stool that 
gather proximal to the obstruction. The gas originates both from 
swallowed air (around two thirds) and bacterial fermentation. In 
segments that undergo increasing distension, the pressure within 
the bowel wall can rise above the capillary pressure, diminishing 
adequate oxygenation, leading to ischemic necrosis and perfora-
tion. Although most malignant obstructions occur in the distal 
parts of the colon, the necrosis and perforation usually occur in 
the cecum as it has the largest diameter, and in accordance with 
the law of Laplace will distend more under lower pressures and 
develop higher wall stress.
In cases such as incarcerated hernias and volvulus, pressure on 
the mesentery can compromise the blood supply initially obstruct-
ing venous return, and with increasing edema and inflammation, 
eventually occluding the arterial blood supply. The resultant isch-
emia can also lead to early necrosis and perforation. In closed-loop 
obstructions, distention initially involves the trapped or incarcer-
ated segment, but with time, the proximal bowel will also distend 
as a result of ongoing accumulation of gas and stool.
Diagnosis and Assessment
A good history and physical examination are critical in the di-
agnosis of large bowel obstruction. The onset and progression of 
symptoms, background illnesses, and medications can provide 
important clues. The abdomen should be palpated for masses, 
tenderness, and previous incisions; the groins should be examined 
for hernias; and a digital rectal examination should be performed 
to inspect for neoplasms and for the presence of fecal impaction 
(Fig. 52.26).
Plain films of the abdomen can help in localizing the obstruc-
tion, demonstrating the degree of distension as well as the status of 
the ileocecal valve (competent vs. incompetent), and, in some cases, 
provide the diagnosis. Water-soluble and IV contrast-enhanced CT 
scans provide significant information revealing the location and eti-
ology of the obstruction such as diverticulitis, IBD, and extralu-
minal causes (e.g., abscesses and inflammation) (Fig. 52.27). CT 
can also provide clues regarding tissue ischemia and impending 
perforation. Flexible endoscopy can assist in the diagnosis of the 
obstruction and permit biopsies to be collected for further investiga-
tion. Endoscopy can also allow for treatment such as detorsion of 
a sigmoid volvulus and insertion of stents in cases of malignant or 
benign obstruction. Basic blood analyses are also important in the 
initial workup. Electrolyte abnormalities can be diagnosed, which 
are important both as a cause for adynamic nonfunction and being 
in the operative and perioperative care. Increased white blood cell 
counts and CRP, as well as increased lactate, base excess, and de-
creased pH, are all generally associated with a more severe state and 
can help guide the aggressiveness of treatment. 
Treatment
The treatment of large bowel obstruction is tailored to the etiology 
of the obstruction, several of which are discussed in detail later in 
the chapter. Treatment options vary considerably depending on the 
cause of obstruction, suspicion of bowel ischemia, and impending 
perforation, as well as the patient’s general condition and comor-
bidities. Patients who present with peritonitis, signs of perforation, 
or ischemic bowel should be taken immediately to surgery.
It is imperative to promptly relieve mechanical obstructions, par-
ticularly those with complete and closed-loop obstructions before 
compromise of the blood supply results in necrosis and perforation. 
Patients who do not present with immediate, ominous signs can be 
managed according to the cause of obstruction. In patients with sig-
moid volvulus, endoscopic decompression is often successful using 
either a rigid or flexible sigmoidoscope with placement of a rectal 
tube proximal to the point of torsion. If this is unsuccessful, patients 
require surgery with resection, colostomy, and a Hartmann proce-
dure. If decompression is successful, elective sigmoid resection with 
primary anastomosis should be performed due to the high rate of 
recurrence. With cecal volvulus, primary resection and anastomosis 
FIG. 52.24 Plain film of sigmoid volvulus. Note bent inner tube appear-
ance.
FIG. 52.25 Computed tomography scan of the abdomen in a patient 
with sigmoid volvulus. Note characteristic whorl in mesentery.
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1342 SECTION X Abdomen
can typically be performed unless the patient is at increased risk of 
anastomotic leak (e.g., nonviable bowel, sepsis, hypotension, etc.). 
Patients with obstruction as a result of active IBD will commonly 
respond initially to steroids. Paracolic abscesses can be drained per-
cutaneously. Foreign bodies can usually be removed endoscopically. 
Fecal impaction is commonly relieved with a combination of stool 
softeners and laxatives from above and manual disimpaction at the 
bedside or in the operating room under anesthesia. Hernias causing 
mechanical large bowel obstruction usually require surgery. Adult 
colonic intussusceptions, in contrast to pediatric intussusceptions, 
are almost always associated with a pathologic lead point, such as 
a polyp, cancer, Meckel, or colonic diverticulum. A recent meta-
analysis found malignancy as the causative factor in 36.9% of il-
eocolonic and 46.5% of colonic intussusceptions.12 Most authors 
recommend surgical resection adhering to oncologic principles 
without reduction.
Patients with malignant obstruction of the low and mid rectum 
usually require an initial diverting stoma to allow for neoadjuvant 
chemoradiation prior to definitive surgery. Malignant obstructions 
of the sigmoid and left colon without signs of impending perfora-
tion can be treated with initial endoscopic stenting as a bridge to 
surgery, or initial surgery. Surgical options include segmental resec-
tion with Hartmann operation (end colostomy with internal clo-
sure of the rectal stump) or primary anastomosis with or without a 
diverting stoma. If the cecum is ischemic or nonviable, a subtotal 
colectomy is performed. In cases of right-sided obstruction, a right 
hemicolectomy is typically performed with primary anastomosis. 
Patients who are unstable with a high risk for anastomotic failure 
should undergo creation of a temporary diverting stoma or exterior-
ization of the anastomosis as a loop ileostomy. 
COLONIC PSEUDO-OBSTRUCTION
Acute colonic pseudo-obstruction, also termed Ogilvie syndrome, 
was initially described by Sir William Heneage Ogilvie in 1948. 
It is characterized by acute colonic dilatation in the absence of a 
mechanical obstruction. Ogilvie syndrome is rare, with an esti-
mated incidence of 100/100,000 admissions.13 Dysregulation of 
the colonic autonomic innervation is hypothesized to play an im-
portant part. Several mechanisms have been implicated including 
autonomic imbalance with a relative excess of sympathetic over 
100 mm
Lossy
P
FIG. 52.26 Computed tomography scan of the pelvis showing a sizable 
barium impaction following a barium enema resulting in a large bowel 
obstruction. This patient required disimpaction in the operating room.
A B
120 mm
Loosy
FIG. 52.27 (A) Gastrografin enema in a patient presenting with obstructing symptoms revealing an “apple-
core” type lesion in the vicinity of the hepatic flexure (arrow). (B) Computedtomography scan of the abdomen 
and pelvis in the same patient showing a large hepatic flexure carcinoma with perforation into the mesentery 
and associated mesenteric abscess (arrow). Computed tomography–guided abscess drainage was not possible. 
This patient underwent extended right hemicolectomy with exteriorization of his ileocolic anastomosis as a loop 
ileostomy.
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1343CHAPTER 52 Colon and Rectum 
parasympathetic activity, disrupted colonic reflex arcs, chronic 
disease, and medications.13
It is most commonly encountered among elderly and comor-
bid patients, classically following an acute illness on a background 
of neurologic, cardiac, or respiratory diseases. Common associated 
conditions are depicted in Table 52.2.
Diagnosis
The typical patient is elderly with multiple comorbidities who is 
hospitalized for an acute medical event or has undergone surgery 
(abdominal or nonabdominal). The presenting symptoms of the 
condition commonly include abdominal distension, pain, nausea, 
and vomiting. Obstipation is common, but some patients will 
have diarrhea due to hypersecretion of water. Lack of intestinal 
contractility is often associated with decreased or absent bowel 
sounds, but high-pitched, tinkling bowel sounds may also be en-
countered. Systemic toxicity and peritoneal signs are uncommon 
and should raise suspicion of ischemia and perforation. Initial 
evaluation should include a complete blood count, serum elec-
trolytes, renal function assessment, and diagnostic imaging. Plain 
abdominal radiographs typically demonstrate a distended colon, 
with the largest diameter usually encountered in the cecum and 
right colon, which can reach 10 to 12 cm in diameter (Fig. 52.28). 
Dilation and gas continuing all the way down to the distal rec-
tum support the suspicion of pseudo-obstruction in contrast to 
a mechanical obstruction in which a paucity of gas is commonly 
encountered distal to the obstruction. A water-soluble contrast 
enema can reliably distinguish between a mechanical obstruction 
and pseudo-obstruction. Currently, however, abdominal CT is 
typically utilized as the standard confirmatory test with the abil-
ity to commonly distinguish the type of obstruction as well as 
to assess for signs of ischemia and impending perforation (Fig. 
52.29). Abdominal tenderness, leukocytosis, fever, and cecal dila-
tion more than 12 cm are signs that may be indicative of colon 
ischemia, perforation, or impending perforation.
The differential diagnosis includes mechanical obstruction, 
toxic megacolon due to C. difficile, or toxic megacolon due to 
other causes. 
Management
The treatment of colonic pseudo-obstruction comprises a series of 
escalating interventions contingent on the degree of distension, 
risk for perforation, and the patient’s response. Treatment options 
include supportive care, pharmacologic therapy (neostigmine), 
endoscopic decompression (colonoscopy), and surgery. Readers 
are referred to the American Society of Colon & Rectal Surgeons’ 
Clinical Practice Guidelines.
Nonoperative, supportive care is initiated for patients with a 
cecal diameter that is less than 12 cm without evidence of ischemia 
TABLE 52.2 Conditions associated with 
pseudo-obstruction.
CATEGORY RISK FACTORS
Postsurgical Following major orthopedic and/or spinal 
surgery, solid organ transplants, cardiac 
procedures
Neurologic disease Parkinson disease, Alzheimer disease, stroke, 
spinal cord injury
Cardiac Congestive heart failure, myocardial infarction
Pulmonary Chronic obstructive pulmonary disease
Trauma Major trauma, shock, burns
Metabolic Diabetes mellitus, renal failure, electrolyte 
disturbances
Infectious Cytomegalovirus, varicella-zoster virus
Obstetric/gynecologic Caesarean section, normal and instrumental 
delivery
Miscellaneous Lupus, scleroderma
Drugs Opiates, chemotherapy, anti-Parkinson drugs, 
anticholinergics, antipsychotic drugs, 
clonidine
100 mm
AP SUPINE PORTABLE
S
Lossy
I
FIG. 52.28 Massive transverse colon distension due to Ogilvie 
 syndrome in a woman with multiple comorbidities including a body mass 
index of 69, severe pulmonary hypertension, and cardiac disease.
160 mm
A
Lossy
P
FIG. 52.29 Computed tomography scan showing massively distended 
colon without sign of ischemic change.
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1344 SECTION X Abdomen
or perforation. This includes nothing by mouth (NPO), correction 
of electrolyte disturbances, and discontinuation of medications that 
may be contributing such as opiates, anticholinergics, anti- Parkinson 
agents, antidepressants, neuroleptics, clonidine, atropines, and an-
tihypertensives. Insertion of a nasogastric tube and rectal tube for 
decompression may be of help. Osmotic and stimulant laxatives 
should be avoided as they can worsen colonic dilation. Ambulation, 
prone positioning, and knee-chest position to encourage passage of 
flatus can assist. Patients should be monitored with serial physical 
exams and abdominal x-rays to assess for response or deterioration. 
Ischemia or perforation of the colon is the most feared complication 
and has been reported in the range of 3% to 15% of cases, leading 
to an associated mortality rate of close to 50%. In cases that do not 
improve with supportive care or with a cecal diameter of more than 
12 cm, but without systemic toxicity and abdominal tenderness, 
colonic decompression is indicated.
Neostigmine is the keystone of pharmacologic decompression 
therapy. It is an acetylcholinesterase inhibitor that stimulates the 
muscarinic receptors and enhances colonic motor activity. Neo-
stigmine is given as a 2 to 2.5 mg IV bolus injected over 3 to 5 
minutes and results in significant parasympathetic stimulation 
causing strong colonic peristalsis that usually leads to subsequent 
flatus and bowel movements. It has been found to be a safe and 
effective option for patients with acute colonic pseudo-obstruc-
tion who have failed conservative management. Success rates for 
neostigmine treatment range from 60% to 94%, with recurrences 
observed in up to 31% of patients, with some patients requiring 
multiple drug administrations. Neostigmine is contraindicated 
in mechanical bowel obstruction and in patients with signs of 
ischemia or perforation. It should be used with caution among 
patients with asthma, chronic obstructive lung disease, bradycar-
dia, and recent acute coronary syndrome and in those with re-
nal failure. Neostigmine should be given in a monitored setting 
with atropine immediately available. Common side effects include 
vomiting, crampy abdominal pain, excessive salivation, and bra-
dycardia. Colonoscopic decompression should be considered in 
patients with contraindications to neostigmine or for those who 
are unresponsive to it. The aim of endoscopic decompression is 
to advance the scope to the right colon with minimal insuffla-
tion and use of narcotics and place a colonic decompression tube 
while removing as much gas as possible from the colon. Endo-
scopic decompression has a high success rate of 61% to 95% for 
initial decompression and 70% to 90% for sustained decompres-
sion. Colonoscopic perforation rates following decompression for 
pseudo-obstruction are in the range of 1% to 3%.
Patients who do not respond to other lines of treatment or 
those who demonstrate signs of systemic toxicity, ischemia, or per-
foration require surgery. Surgical options are determined accord-
ing to the condition of the colon and the patient. If the colonis 
viable, tube cecostomy or cecostomy can be performed, with high 
rates of success. For patients with signs of ischemia or perforation, 
a resection, usually with a diverting stoma, is recommended. 
INFLAMMATORY BOWEL DISEASE
Epidemiology and Etiology
IBD, which includes both UC and Crohn disease, are largely dis-
eases of the Western world. As Asian countries are adopting a more 
Western diet, the incidence of these disorders is increasing in these 
countries as well. The prevalence of IBD in Western countries is 
approximately 0.5% of the general population.14 In the United 
States, over 1 million individuals are estimated to have IBD, with 
over 200,000 Canadians affected, and 2.5 to 3 million individu-
als in Europe having these disorders.14 The highest incidence of 
UC has been reported in Europe, followed by the United States, 
whereas for Crohn disease, the highest incidence was observed in 
the United States, followed by Europe. Europe was noted to have 
the highest prevalence of IBD. Over time, the incidence of both 
disorders appears to be increasing. Both disorders appear to have a 
genetic predisposition with many contributing environmental fac-
tors. Over 10% of patients with IBD have a family history of IBD. 
To date, genome-wide association studies have linked to over 230 
IBD susceptibility loci.15 Cigarette smoking is the most studied 
environmental factor, having opposite effects in UC and Crohn 
disease. In UC, smoking tends to suppress symptoms, whereas in 
Crohn disease, smoking tends to exacerbate symptoms. Antibiotic 
use in early life has also been thought to predispose to IBD, as has 
NSAID use. 
Disease Distribution and Classification
The extent of UC can also be graded with respect to the extent of 
inflammation within the colon. It can be limited only to the rec-
tum and sigmoid colon (proctitis or proctosigmoiditis), restricted 
to the left side of the colon, or extended to involve the entire colon 
(pancolitis).
There are many classification schemes of Crohn disease. How-
ever, one of the most popular was initially the Vienna Classifica-
tion, which was later updated to the Montreal Classification. With 
these classification schemes, patients are classified according to age 
of onset of disease, bowel location of their Crohn disease, as well 
as type of disease behavior. In addition to the different ages of on-
set, the Vienna Classification divided patients into whether or not 
they develop inflammatory Crohn disease at age of 40 or later. The 
Montreal Classification subdivides this into less than 20 or greater 
than 20 years old. In addition, the Montreal Classification adds a 
further subdivision of whether the patients have perianal Crohn dis-
ease. The three different types of behavior classifications for Crohn 
disease that are possible include inflammatory Crohn disease, fibro-
stenotic Crohn disease, and fistulizing Crohn disease. Many people 
feel that these three types of disease behaviors represent different 
time points in the progression of disease. In other words, a patient 
is initially diagnosed with inflammatory Crohn disease, which over 
time progresses to fibrostenotic Crohn disease. This, in turn, will 
frequently progress to an obstruction, with perforation proximal to 
the obstruction and abscess formation. When this abscess spontane-
ously drains into an adjacent structure or organ, fistula formation 
ensues. In this manner, there is a progression from inflammatory to 
fibrostenosing to fistulizing Crohn disease. It is with this thought 
in mind that the progression to “top-down” medical therapy has 
evolved (see later discussion on medical therapy). The goal is to 
interrupt this natural progression or cycle in the course of Crohn 
disease to prevent the progressive fibrosis that results in many of the 
complications leading to surgery. 
Clinical Presentation and Disease Diagnosis
Clinical Presentation
Clinical presentation of both diseases can be similar. Diarrhea can 
be a presenting symptom in both diseases; however, this is typi-
cally more prevalent and severe in UC, where the diarrhea is char-
acteristically bloody. Significant hemorrhage is much more com-
mon with UC than with Crohn disease. Typical UC symptoms 
also include tenesmus and urgency as well as associated anemia. In 
Crohn disease, symptoms of abdominal pain may predominate. 
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1345CHAPTER 52 Colon and Rectum 
In any patient initially presenting with diarrhea, stool cultures 
should first be obtained to exclude the presence of infectious 
causes of diarrhea, such as Salmonella, Giardia, or community-
acquired C. difficile that is now increasingly seen. Patients with 
Crohn disease may present with a palpable abdominal mass due 
to an intraabdominal abscess or have an external fistula. Roughly 
25% of patients with Crohn disease will have associated perianal 
disease. This can include a variety of problems, including anal fis-
sure, which in contrast to patients without Crohn, is often not 
painful and may be multiple. In addition, these patients can pres-
ent with large anal skin tags (Fig. 52.30), which are not true ex-
ternal hemorrhoids. As a rule, these should not be excised, as they 
may lead to very delayed wound healing. These patients may also 
present with anorectal abscesses, fistula(s) (Fig. 52.31), and anal 
stenosis. Digital rectal examination should always be performed.
Extraintestinal manifestations. Extraintestinal manifestations 
can occur in many IBD patients, and it is estimated that up to 
half of IBD patients will have one or more extraintestinal mani-
festations. There is a slightly higher prevalence of extraintestinal 
manifestations in patients with Crohn disease as compared with 
those with UC and can be divided into those affecting the joints, 
eyes, and skin. Arthritis is by far the most common extraintes-
tinal manifestation. One of the most common manifestations is 
sacroiliitis. One of the most serious joint manifestations is anky-
losing spondylitis which runs a course independent of the bowel 
disease. These patients are HLA-B27 positive and may present in 
advanced cases with decreased cervical flexion, which has impor-
tant anesthetic implications for intubation. These patients may 
require fiber optic intubation and will require specific preoperative 
anesthesia evaluation.
Cutaneous extraintestinal manifestations include erythema 
nodosum and pyoderma gangrenosum. From long experience of 
treating surgical patients with IBD, pyoderma is much more fre-
quent than erythema nodosum. Erythema nodosum (Fig. 52.32) 
is characterized by red painful swollen nodules that can occur and 
usually will respond to systemic steroid administration, whereas 
pyoderma gangrenosum is characterized by typically extremely 
painful ulcerating lesions that frequently occur at sites of repeat-
ed trauma such as in the vicinity of surgical incisions or more 
frequently around intestinal stomas (Fig. 52.33). There is a phe-
nomenon called “pathergy,” which refers to a worsening of the 
FIG. 52.30 Large anal Crohn tags. Note the bluish coloring and waxy 
appearance of the perianal skin
FIG. 52.31 A woman with significant fistulizing perianal Crohn disease. 
Note the multiple external fistula openings shown by the white arrows. 
These all had a common internal opening in the anterior midline, which 
was also associated with a rectovaginal fistula. This patient ultimately 
elected to undergo ileostomy diversion.
FIG. 52.32 A patient with a Crohn disease flare and active erythema 
nodosum. Note the red purplish nodule on the dorsum of the foot.
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1346 SECTION X Abdomen
pyoderma with any type of surgical manipulation or debridement. 
These lesions are therefore best treated by nonoperative means and 
can include intralesional steroid injections (i.e., triamcinalone), 
topical (tacrolimus 0.1%), or systemic biologic therapy (anti-
tumor necrosis factor [TNF] antibodies or similar agents). Such 
treatment will typically result in symptom resolution.
Ocular manifestations of UC can include uveitis, iritis, and 
episcleritis. Some of these can lead to significant irritation and 
require referral to an ophthalmologist.
Sclerosing cholangitis is estimated to affect approximately 5% 
of patients with IBD. It has a course that is curiously indepen-
dent of the IBD. At its worst, it can progress to cirrhosis, result 
in liver failure, and require hepatic transplantation. Patients with 
sclerosing cholangitis are at higher risk for developing colorectal 
neoplasia, as will be discussed later, and are also at higher risk of 
developing pouchitis, as will be discussed in the section on IPAA 
and surgical treatment. 
Disease Diagnosis
Endoscopy. The diagnosis of IBD is frequently made by endos-
copy. This can be accomplished by either rigid proctoscopy, flex-
ible sigmoidoscopy, or colonoscopy. Generally, a complete evalua-
tion of the colon with colonoscopy is performed both to evaluate 
the extent of the disease as well as to examine the terminal ileum.
With UC, inflammation begins at the level of the dentate line 
and extends proximally, whereas in Crohn disease, in many cases, 
the inflammation is more patchy and there can be discontinuous 
inflammation (i.e., skip areas), with areas of intervening normal-
appearing mucosa. In some cases, differentiation between the two 
diseases can be difficult, both endoscopically as well as histologi-
cally. A typical endoscopic view of UC is shown in Fig. 52.34. Note 
the more roughened or granular appearance of the colonic mucosa. 
One of the most common scoring systems for endoscopic assess-
ment of UC is the Mayo Clinic Scoring System, which grades the 
endoscopic findings based upon the severity of the mucosal ulcer-
ation or the absence thereof. Grade 1 refers to a normal endoscopic 
appearance, grade 2 refers to slightly more erythematous, grade 3 re-
fers to even more erythematous area with touch bleeding, and grade 
4 refers to significant bleeding and friability. As the disease becomes 
more severe, there is an increasingly erythematous appearance of the 
mucosa with progressive mucosal ulceration.
With respect to endoscopy, Crohn disease is more characterized 
by deeper punched-out appearing ulcerations. In these cases, there 
are often longer serpiginous ulcerations covered with fibrin. These 
can oftentimes extend longitudinally along the lumen of the bowel, 
in which case they are sometimes referred to as “bear claw” ulcer-
ations (Fig. 52.35). In many cases, Crohn disease ulcers are worse 
on the mesenteric side of the bowel. Regarding the distribution of 
Crohn disease, the most common site of involvement in nearly half 
of patients is ileocolic, followed by colonic involvement. Crohn dis-
ease can also affect the small bowel or upper GI tract. 
Histologic evaluation. In UC, colonic mucosal biopsies will 
typically show significant inflammation with the presence of mul-
tiple polymorphonuclear leukocytes within the lamina propria. 
There may be depletion of mucin in goblet cells. One can also 
identify crypt abscesses, although this is somewhat of a nonspecif-
ic finding. As a rule, inflammation in UC is restricted to the sur-
face epithelium (Fig. 52.36). The disease process is limited to the 
large intestine. Proximal colonic disease occurs in continuity with 
an involved rectum (i.e., no gross or histologic skip lesions). The 
inflammation is characterized by the absence of mural sinus tracts, 
deep fissural ulcers, and granulomas, as well as by the absence of 
transmural lymphoid aggregates in an area not deeply ulcerated.
In contrast, in patients with Crohn disease, there is often 
transmural inflammation, which is seen in histologic evalu-
ation of resected specimens. In approximately one third of 
patients, there are noncaseating granulomas (Fig. 52.37). In 
biopsy specimens, the diagnosis of Crohn disease is made in 
the presence of non-necrotizing granulomas or the presence 
of transmural lymphoid aggregates in an area not deeply ul-
cerated. In patients with Crohn disease, just as one can mac-
roscopically see “skip” disease with patchy inflammation, the 
same is true on microscopic evaluation. The term “focal active 
enteritis” is used. The differential diagnosis frequently includes 
infectious colitis or drug-induced colitis, and pathology re-
ports often include this differential diagnosis when areas are 
biopsied during GI endoscopy. In patients who are suspected 
of having Crohn disease, it is important to make an effort to 
intubate the terminal ileum, as this is a common site of disease 
involvement.
IBD undetermined refers to a subset of patients who have 
overlapping characteristics of both Crohn disease as well as UC 
on endoscopic biopsy. It is thought that up to 10% to 15% of 
patients fall into this category. The diagnosis of indeterminate 
colitis is made in patients in whom there is uncertainty of the 
diagnosis on evaluation of the colectomy specimen, since his-
tologic features of both Crohn and UC are seen. Overall, this 
diagnosis is more likely in patients with fulminant disease where 
the significant amount of inflammation interferes with precise 
disease diagnosis. 
Medical Treatment
Changing medical treatment philosophy. The last two decades 
has seen a tremendous change in medical treatment for IBD. 
There has been a gradual evolution from a “bottom-up” approach 
to what is termed “top-down” approach. These terms refer to the 
FIG. 52.33 Pyoderma gangrenosum adjacent to an end ileostomy in a 
patient with Crohn disease. Here, the lesions have started to heal with 
granulation tissue.
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1347CHAPTER 52 Colon and Rectum 
A B
FIG. 52.34 (A) Endoscopic view of moderately severe ulcerative colitis. Note the bleeding and ulceration. (B) 
Macroscopic view of right colon following total proctocolectomy for fulminant ulcerative colitis.
A B
FIG. 52.35 Bear claw ulcers in Crohn colitis. (A) Endoscopic view. (B) Macroscopic view.
FIG. 52.36 Histologic section of active ulcerative colitis. There is gland-
ular architectural distortion manifested by irregular branching and orienta-
tion of glands relative to the surface. The lamina propria is expanded with 
inflammatory cells, and intraepithelial neutrophils are present. A crypt 
abscess is noted (lower left). (Courtesy Dr. Jeffrey P. Baliff, Thomas Jef-
ferson University, Philadelphia.)
FIG. 52.37 Crohn colitis with noncaseating granuloma.
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1348 SECTION X Abdomen
“bottom-up approach,” beginning with the safest, least expensive 
medications first and only proceeding to the more potent, more 
expensive medications with a higher side effect profile once these 
have failed. This treatment approach has been largely replaced by 
the top-down approach, whereby patients are initially treated with 
the stronger, more potent medications which may, in turn, have 
a greater side effect profile and are associated with higher costs. 
Many of these drugs have been implicatedwith a higher rate of 
postoperative complications in patients undergoing surgery, and 
their use also has been associated with reactivation of certain re-
mote infections. It is important for the surgeon to be aware of 
these medications and knowledgeable about their mechanism 
of action. Table 52.3 lists some of the more commonly utilized 
medications used in the treatment of IBD. The surgeon will find 
that these medications are being used increasingly not only in pa-
tients with IBD but also in patients with rheumatoid arthritis and 
psoriasis. Medical therapy formerly was based largely on medica-
tions such as sulfasalazine and steroids. However, the last 25 years 
has seen a revolution with the introduction of “biologic therapy,” 
based largely on treatment with antibodies directed against TNF-α 
(anti-TNF-α). This began with the Food and Drug Administration 
(FDA) approval for infliximab (chimeric anti-TNF antibody) for 
Crohn disease in 1998, followed by adalimumab (humanized anti-
TNF antibody) in 2007, certolizumab pegol (a PEGylated Fab’ 
fragment of a humanized TNF antibody) and natalizumab (hu-
manized monoclonal antibody to α4-integrin) both in 2008, goli-
mumab (human monoclonal anti-TNF) approval for UC in 2013, 
vedolizumab (monoclonal antibody to integrin α4β7) in 2014, 
ustekinumab (human monoclonal antibody to p40 protein sub-
unit used by interleukin [IL]-12 and IL-23) in 2016, and tofaci-
tinib (janus kinase inhibitor) approval for UC in 2018. Currently, 
there is a wide assortment of drugs to choose from. There has also 
been a change in the philosophy of treatment with respect to IBD. 
Medications for treatment of IBD
Aminosalicylates. Sulfasalazine has long been used for the 
treatment of colonic IBD. Originally used as a treatment for 
arthritis, it was noted that many arthritis patients with coexisting 
IBD noted an improvement in the latter when taking this medica-
tion. Use of this drug was limited by its sulfapyridine ring, which 
excludes use in patients with sulfa allergies. When this medication 
is used, patients require folic acid supplementation. Eventually, the 
sulfapyridine ring is cleaved, leaving the active 5-aminosalicylate 
(5-ASA) moiety. Pharmacologists rapidly realized that, depend-
ing upon how this drug was formulated, its delivery could be tar-
geted to different portions of the GI tract. For example, mesal-
mine (Pentasa) begins to dissolve in the stomach and releases drug 
throughout the GI tract, whereas Asacol begins to be released in 
the terminal ileum by means of a pH-dependent mechanism and 
coats the entire colon. Drugs manufactured with an “MMX tech-
nology” are designed as once-a-day preparations and formulated 
so that they slowly dissolve, thus releasing medication throughout 
the colon. For this reason, they are thought to have greater patient 
compliance. There are also topical formulations of these medica-
tions for distal disease. Suppository formulations are administered 
at bedtime. While the patient sleeps, the suppositories melt and 
coat the rectum with mesalamine, which has a very potent an-
tiinflammatory effect. The most popular brand of suppository is 
Canasa. The same medication in small-volume enema form (Row-
asa enemas) can be administered also at bedtime. The patient is 
advised to lie on their left side, allowing the small volume of fluid 
to be delivered not only to the rectum but also sigmoid and, in 
some cases, the left colon. These medications are most effective for 
mild to moderate disease. 
Corticosteroids. If the patient has severe disease, steroids still 
play a prominent role in the treatment of IBD. Although they 
have numerous side effects, they are inexpensive, act quickly, 
and are readily available, not requiring lengthy insurance pre-
authorizations as with the more expensive biologic medication 
alternatives. The recognized side effects of steroids include the 
following:
	•	 	Cushingoid	 appearance	 that	 is	 very	 unpopular,	 particularly	
among young patients
	•	 	Feared	complication	of	aseptic	necrosis	of	the	hips
TABLE 52.3 Different types of medical treatment used for inflammatory bowel disease.
DRUG CLASS EXAMPLES INDICATION ADMINISTRATION
Biologics Infliximab UC, CD IV
Adalimumab UC, CD SC
Golimumab UC IV
Natalizumab CD IV
Vedolizumab UC, CD IV
Ustekinumab UC, CD IV, SC
Antiinflammatory Sulfasalazine
Mesalamine
UC, CD
UC, CD
PO
PO, enema, suppository
Immunosuppressives Conventional steroids
Budesonide
Antimetabolites
Tofacitinib
UC, CD
UC, CD
UC, CD
UC
PO, IV, suppository
PO, rectal foam
PO
PO
Probiotics Lactobacillus
Bifidobacterium
UC, CD Food, tablets, capsules, powders
Antibiotics Ciprofloxacin
Metronidazole
Rifaximin
UC, CD
UC, CD
Off-label
PO, IV
PO, IV
PO
CD, Crohn disease; IV, intravenous; PO, per os; SC, subcutaneous; UC, ulcerative colitis.
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1349CHAPTER 52 Colon and Rectum 
	•	 	Hypertension
	•	 	Mood	changes	that	can	escalate	up	to	actual	psychiatric	condi-
tions
	•	 	Hyperglycemia
	•	 	Increased	risk	of	infectious	complications	after	surgery
	•	 	Cataract	formation
	•	 	Striae	and	others
Because of these complications, as well as the growth retarda-
tion seen when these drugs are used for prolonged periods in chil-
dren, these medications should be used sparingly for as short a 
period as possible. Steroids are usually started at a high dose and 
then tapered quickly. Their main uses are either in the outpatient 
setting in the form of pulse therapy, as high doses that are ta-
pered quickly, or intravenously in patients who are hospitalized 
with flares of their disease. In the outpatient setting, pulse therapy 
is usually given in the form of prednisone at doses starting at 40 
to 60 mg/day, tapering by 5 to 10 mg at 2-week intervals until 
10 mg/day is reached and then tapering by 5 mg every 2 weeks, 
at which time the drug is discontinued. In the hospital setting, 
100 mg of hydrocortisone can be given intravenously every 6 to 8 
hours depending on disease severity. 
Immunomodulators
Thiopurines. Thiopurines are a “steroid-sparing” class of medi-
cation that are usually begun once patients are placed on steroids 
and perhaps have been unsuccessful in weaning off steroids af-
ter one or two attempts at pulse therapy. Thiopurines have been 
used for many decades in the treatment of Crohn disease and have 
long been used in the organ transplant population. Two drugs fall 
into this category: azathioprine and its metabolite 6-mercapto-
purine. The side effects of this therapy include leukopenia and 
pancreatitis. These side effects are largely seen in individuals who 
are homozygous for a variant of the enzyme thiopurine methyl-
transferase responsible for metabolizing these drugs poorly. For 
this reason, many physicians now routinely perform thiopurine 
methyltransferase genotyping of patients to see whether they will 
be able to metabolize these drugs properly prior to initiating thio-
purine treatment. These drugs have several advantages in that they 
are readily available and are an oral medication taken once a day, 
and dosing is based on body weight. On the downside, once a 
patient begins therapy, there is usually a 3- to 4-month lag time 
until these medications exert their therapeutic effect. For this rea-
son, these medications cannot be used to treat a flare. Long-term 
thiopurine use is also associated with a higher risk of developing 
non-Hodgkin lymphoma than the general population. 
Methotrexate. Methotrexate is another commonly used im-
munosuppressive for the treatment of IBD. This medication, 
which has long been used particularly in the treatment of pa-
tients with arthritis, can be dosed either orally or intramuscu-
larly. Intramuscular dosing is particularly convenientin patients 
who have problems with significant diarrhea or absorption issues 
(e.g., short bowel syndrome). The side effects of methotrexate 
include elevations in liver function tests, as well as pulmonary 
fibrosis. When methotrexate is given, patients require folic acid 
supplementation. 
Biologics in the Treatment of Inflammatory 
Bowel Disease
The term “biologics” as it pertains to drugs used for IBD initially 
referred to monoclonal antibodies directed against TNF-α. The 
first such agent, infliximab, was approved by the FDA for use in 
1998. Since then, there has been a continued increase in both the 
number and type (based upon mechanism of action) of medica-
tions that have been approved (see Table 52.3). The side effects of 
these drugs include reactivation of infections including tuberculo-
sis, histoplasmosis, actinomycosis, and hepatitis. For this reason, a 
careful patient history regarding these infections should be taken 
prior to consideration of treatment. In addition, before starting 
these drugs, the patient should have either a tuberculin skin test 
or undergo testing with QuantiFERON gold assay as well as ob-
tain a hepatitis profile. There is currently no accurate test for past 
exposure for histoplasmosis. In addition, these types of agents, 
similar to the thiopurines, can be associated with a higher risk 
of developing non-Hodgkin lymphoma compared to the general 
population. In addition, anti-TNF-α antibody has been associat-
ed with a low risk of hepatosplenic T-cell lymphomas, particularly 
in young men who have been taking anti-TNF antibody therapy 
in combination with other immunosuppressive therapy such as a 
thiopurine. 
Assessment of Symptom Severity
Truelove and Witts is a popular classification scheme that char-
acterizes patients by the severity of their diarrhea, the presence of 
blood in stool, the presence of fever, tachycardia, anemia, or an el-
evated erythrocyte sedimentation rate. Many similar classification 
schemes are used, in addition to analyzing stool samples for either 
fecal calprotectin or lactoferrin that can be used as an inflamma-
tory marker to assess disease activity. With Crohn disease, both 
the Crohn disease activity index (CDAI) and the Harvey Brad-
shaw index have been used to quantitate symptoms.16 The CDAI 
is made up of eight clinical and laboratory variables, including 
the number of bowel movements/day, the presence of abdominal 
pain, hematocrit, and weight loss. A score of less than 150 indi-
cates clinical remission, and a score of more than 450 denotes 
severe disease. Since the CDAI requires a 7-day patient symptom 
diary, the Harvey-Bradshaw Index was proposed as a modification 
of this scheme that only used clinical data. 
Indications for Surgery for Ulcerative Colitis
There are several indications for surgery for UC, the foremost of 
which is failure to respond to maximum medical therapy. The 
frequency of surgery for UC has actually decreased over the last 
several decades with the improvement in efficacy and the num-
ber of new and more effective medical options such as the entire 
class of biologic therapies. However, despite these new therapies, 
patients still present with a failure to respond. Patients falling 
into this category range from those patients who have severe 
disease, namely, those patients with multiple bowel movements, 
poor nutritional status, “failure to thrive,” and a need for sur-
gery in order to regain their good physical health. These patients 
have a very poor quality of life with urgency, tenesmus, and low 
body weight; surgery represents a significant improvement in the 
quality of life. The second group of patients failing to respond 
to maximum medical therapy refers to patients with fulminant 
colitis. These patients have such severe disease that they need to 
be hospitalized and placed on IV steroids. In some cases, they 
have received in-hospital biologic therapy; in rare cases, these 
patients may be receiving intravenous cyclosporine as an attempt 
to avert colectomy. In these patients with fulminant colitis, tox-
ic megacolon may be present (Fig. 52.38). This has arbitrarily 
been defined as having three or more of the following criteria 
present: tachycardia greater than 100, leukocytosis greater than 
12,000/dL3, hypoalbuminemia less than 3 g/dL3, a temperature 
greater than 38°C, or a diameter of the transverse colon on a 
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1350 SECTION X Abdomen
plain abdominal radiograph greater than 5 cm. Three or more of 
these criteria meet the definition of toxic megacolon; note that 
a “megacolon” does not need to be present in order to meet this 
definition. Thus, the definition of toxic megacolon merely refers 
to a patient who is septic due to very severe colitis. Toxic mega-
colon can be present not only from severe UC but also due to se-
vere Crohn colitis or severe infectious or ischemic colitis. When 
the colitis is severe enough, it is associated with a significant 
colonic ileus, and, in these cases, the colon becomes dilated and 
there is a significant risk of colonic perforation. The next cat-
egory of indication for surgery occurs in patients in whom there 
is significant GI bleeding. Recalling basic anatomy, the vessels 
located underneath the colonic vessels are located underneath 
the mucosa. If the mucosa sloughs, this will, in effect, expose the 
underlying blood vessels of the colon and can result in massive 
GI hemorrhage if an ulcer erodes into these vessels. Significant 
hemorrhage can be one of the reasons for urgent surgery with 
UC, although the frequency of this complication has decreased 
over time. Another indication for surgery in children with UC is 
failure to grow, which is also an indication for surgery in patients 
with Crohn disease. The presence of a dysplasia or cancer is an 
indication for surgery, as well. Patients with longstanding UC 
(>8 years) have a high risk of developing dysplasia or cancer, as 
do those who have sclerosing cholangitis. Once the disease has 
been present longer than 8 years, patients are advised to undergo 
regular (yearly) colonoscopic surveillance with or without chro-
moendoscopy. If multiple areas of low-grade dysplasia or areas 
of high-grade dysplasia (Fig. 52.39) are found, a colectomy is 
recommended to prevent the development of invasive adeno-
carcinoma. The finding of colonic dysplasia in patients with 
longstanding UC is an indication for surgery that has undergone 
significant change over the last 20 years. There is currently some-
what of a controversy as to exactly who requires surgery and who 
requires continued observation with close surveillance. Much of 
this has arisen due to the development of high-definition colo-
noscopy, as well as the development of techniques of surveil-
lance such as chromoendoscopy. Chromoendoscopy involves the 
performance of colonoscopy with the spraying of dyes such as 
methylene blue or indigo carmine onto the colonic mucosa at 
the time of colonoscopy to highlight areas suspicious for dyspla-
sia to permit targeted biopsies rather than just performing the 
random biopsies that were previously standard of care. In addi-
tion to this, there has been recognition that there are different 
types of dysplasia. The flat dysplasia that is difficult to detect and 
blends in with the surrounding mucosa is very different from the 
“polypoid” dysplasia that is apparent and can be treated in many 
cases like a polyp and removed using techniques similar to that 
used for removal of a conventional polyp during colonoscopy. In 
some studies, patients with UC have undergone “polypectomy” 
removal of dysplastic lesions and have been followed long-term 
without interval development of cancer.17 What is important to 
stressis that patients must have very close follow-up colonosco-
py and that meticulous colonoscopy and pathology expertise are 
vital to this process, as is excellent patient compliance. If any one 
of these three factors is lacking, this is clearly not a viable treat-
ment alternative. There is, however, still agreement that if there 
are multiple areas of flat dysplasia within the colon, colectomy is 
indicated. There is still much to be learned regarding the actual 
risk of cancer in patients with IBD. Overall, it is felt that ap-
proximately one fifth of the world’s cancers arise in the setting 
of chronic inflammation. This mirrors t nhe problem with hep-
atitis, anal cancer, gastric cancer, and many others. With the 
advent of better medications and interruption in this chronic 
cycle of inflammation, it will be interesting to see whether the 
incidence of cancer and IBD begins to decline compared to 
historical data. The same is true regarding the indication for 
failure to grow in children. As more effective medications are 
identified and are able to be instituted at earlier ages, it is an-
ticipated that there will be less of an indication to operate in 
these young patients.
Similarly, if an adenocarcinoma is identified, colectomy is indi-
cated. In certain patients, the presence of severe extraintestinal dis-
ease is also an indication for surgery. In some cases, severe extrain-
testinal disease will respond to surgery; however, there are some 
cases in which the extraintestinal disease has a course relatively 
independent of the colon. 
Indications for Surgery for Crohn Disease
Unlike indications for surgery for UC, indications for surgery for 
Crohn disease are generally reserved for complications of the dis-
ease. Similar to UC, surgery is also performed in children with 
Crohn disease when they show failure to grow. In addition, surgery 
is frequently performed for symptoms of obstruction secondary to 
fibrostenosing Crohn disease (Fig. 52.40). Also, if patients have a 
perforating Crohn disease associated with abscess or fistula, surgery 
may be indicated. The presence of many types of fistulas is also a 
relative indication for surgery. For example, the presence of a symp-
tomatic ileal sigmoid fistula resulting in significant diarrhea bypass-
ing the entire colon can be an indication for surgery. The occurrence 
of enterocutaneous fistulas is an indication for surgery. Enteroen-
teric fistulae are not an indication for surgery unless they are associ-
ated with significant symptoms of obstruction or discomfort. The 
73 mm
120 mm
FIG. 52.38 Toxic megacolon. Abdominal film shows significant disten-
sion of the transverse colon in a 20-year-old man with toxic megacolon. 
(From Rojas-Khalil Y, Galandiuk S. Management of chronic ulcerative coli-
tis. In: Cameron JL, Cameron A, eds. Current Surgical Therapy. 13th ed. 
Philadelphia: Elsevier; in press.)
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1351CHAPTER 52 Colon and Rectum 
presence of significant abdominal pain associated with obstruction 
is considered an indication for surgery. Patients with Crohn disease 
who have associated cancer or dysplasia, as with patients with UC, 
are an indication for surgery. In patients with Crohn disease, as with 
UC, areas of dysplasia in the colon can be multifocal, and for this 
reason, if this occurs in the colon, a total proctocolectomy is consid-
ered preferable to a segmental resection. 
Surgical Options for Ulcerative Colitis
There are several operations that are currently performed for UC. 
These include subtotal colectomy, ileostomy, and Hartmann pro-
cedure, frequently performed for fulminant disease. Total procto-
colectomy with end ileostomy and proctocolectomy with either 
stapled or hand-sewn IPAA are commonly performed in the elec-
tive setting. Subtotal colectomy and ileal rectal anastomosis and 
total proctocolectomy with continent ileostomy are less common-
ly performed procedures. We discuss these in order next.
Total Proctocolectomy With End Ileostomy
Subtotal colectomy and ileostomy and Hartmann procedure is the 
treatment for patients with fulminant colitis not responding to 
maximal medical therapy. The term “toxic megacolon” has long 
been used to refer to a condition arising when patients become 
toxic from colitis irrespective of its etiology (e.g., whether this be 
UC, Crohn colitis, infectious, or ischemic). In any of these con-
ditions, as the mucosa sloughs, the endotoxins within the bowel 
A B
FIG. 52.39 (A) A dysplasia-associated lesion or mass (DALM) in a patient with long-standing ulcerative colitis 
and sclerosing cholangitis. (B) High-grade dysplasia within a DALM in a patient with long-standing ulcerative 
colitis and sclerosing cholangitis.
A B
FIG. 52.40 (A) Gastrografin enema showing significant stricture (arrow) of sigmoid colon secondary to Crohn 
disease. (B) Segmental colonic resection for fibrostenotic disease. Note the significant wall thickening and nar-
rowed lumen (arrow) and its size compared to the tip of the scissors.
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1352 SECTION X Abdomen
lumen are absorbed leading to a septic state characterized by leu-
kocytosis, tachycardia, fever, and in severe cases, hemodynamic 
instability. Many of these patients have protein-losing enteropa-
thy and have associated hypoalbuminemia. If the colitis is severe 
enough to have an associated colonic ileus, this is apparent on 
an abdominal film with an increased diameter of the transverse 
colon (>5 cm). The definition of toxic megacolon is made when 
any three of these five factors are present. It is important to realize 
that a patient can have toxic megacolon without having a “mega-
colon” (i.e., they can just be “toxic” or septic from their colitis). 
When patients begin exhibiting symptoms of toxic megacolon, 
prompt surgery is indicated in order to prevent colonic perfora-
tion. With the improved medical therapy, this clinical scenario is 
becoming less common. In performing this operation, whether 
performed open or in a minimally invasive fashion, it is important 
to be gentle with the colon, as ordinary manipulation can result in 
perforation. If the colon is very dilated and there is loss of domain, 
the procedure may not be able to be safely performed in a mini-
mally invasive fashion. One of the common complications of this 
procedure postoperatively is a “blow out” of the Hartmann stump, 
resulting in a pelvic abscess. This complication many times can be 
avoided simply by leaving a very long Hartmann stump and in-
corporating this into the fascial closure of the midline abdominal 
laparotomy wound or the specimen extraction site, depending on 
whether it is an open or minimally invasive procedure, and clos-
ing the incision over this. In this manner, if the stump dehisces 
and a wound infection develops, the wound is opened and there 
is a controlled mucous fistula rather than a deep pelvic infection. 
Once the patient has stabilized and weaned off immunosuppres-
sant medications, usually after a period of 3 months, another pro-
cedure for restoration of intestinal continuity can be performed. 
Subtotal Colectomy and Ileorectal Anastomosis
The option of ileal rectal anastomosis for the treatment of UC 
avoids complications of pelvic dissection such as disturbances of 
sexual function in men and reduced fertility seen in women, since 
there is no pelvic dissection. The key to good function following 
this operation is proper patient selection. Patients with limited 
rectal involvement do best,for Low Rectal Cancers
Transanal Total Mesorectal Excision
Abdominoperineal Resection
Special Circumstances
Complications
Postoperative Treatment and Follow-up
Pelvic Floor Disorders and Constipation
Diagnosis: Testing and Evaluation
Rectal Prolapse (Procidentia)
Solitary Rectal Ulcer
Rectocele
Constipation
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http://ExpertConsult.com
1322 SECTION X Abdomen
obstruction, a surgical emergency, whereas a valve that allows 
retrograde flow into the ileum (incompetent ileocecal valve) will 
result in less colonic distension and a less acute clinical scenario.
The vermiform appendix extends from the cecum approxi-
mately 3 cm below the ileocecal valve as a blind-ending elongated 
tube, 8 to 10 cm in length (Fig. 52.5). It is most commonly found 
in a retrocecal position (65%), followed by pelvic (31%), subcecal 
(2.3%), preileal (1.0%), and retroileal (0.4%) locations. In the 
setting of inflammation and adhesions, locating the appendix can 
be difficult. One can reliably reach its base by following the an-
terior taenia of the cecum to the convergence with the other two 
taeniae. The bloodless fold of Treves extends from the antimesen-
teric border of the terminal ileum to the base of the appendix or 
the anterior surface of the mesoappendix, or to both areas. This 
fold contains no sizable blood vessels. Since it is the only part of 
the ileum that has a fold on the antimesenteric side of the bowel, 
it can help in the recognition of the ileocecal region and the base 
of the appendix.
Amniotic
cavity Proctodeum
Body stalk
Allantois
B
A
C D
F
M H
FIG. 52.2 At the third week of development, the primitive tube can be divided into three regions (A): the fore-
gut (F) in the head fold, the hindgut (H) with its ventral allantoic outgrowth in the smaller tail fold, and the midgut 
(M) between these two portions. Stages of development of the midgut are physiologic herniation (B), return 
to the abdomen (C), and fixation (D). (From Corman ML, ed. Colon and Rectal Surgery. 4th ed. Philadelphia: 
Lippincott-Raven; 1998:2.)
Urorectal
septum
Cloacal
membrane
A
B C
D
Cloacal membrane Coronal fold of
forming urorectal
septum
Rupturing cloacal
membrane
Anorectal
canal
Urorectal septum
Urogenital
sinus
Urogenital
sinus
Genital
tubercle
Perineum
Cloaca
Allantois
Urorectal septum
FIG. 52.3 Development of the distal rectum and anus. Progressive steps between 4 and 6 weeks in subdivision of 
the cloaca into a ventral primitive urogenital sinus and a dorsal anorectal canal (A–D). The urorectal septum is formed 
by the fusion of yolk sac extraembryonic mesoderm and allantois mesoderm, which produces a tissue wedge be-
tween the hindgut and urogenital sinus during craniocaudal folding of the embryo. As the tip of the urorectal septum 
approaches the cloacal membrane dividing the cloaca into the urogenital sinus and anorectal canal, the cloacal mem-
brane ruptures, thereby opening the urogenital sinus and dorsal anorectal canal to the exterior. The tip of urorectal 
septum forms the perineum. A, B, and D, Sections through the cloacal and related endoderm-derived structures. 
C, Surface view of the caudal endoderm to better depict its three-dimensional shape. Curved arrows indicate the 
direction of growth of the developing urorectal septum. (From Schoenwolf GC, Bleyl SB, Brauer PR, et al. Larsen’s 
Human Embryology. 5th ed. Philadelphia, PA: Churchill Livingstone, an imprint of Elsevier; 2015.)
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1323CHAPTER 52 Colon and Rectum 
The ascending colon begins at the ileocecal junction and extends 
upward toward the hepatic flexure on the right side and is approxi-
mately 15 cm in length. The anterior and lateral surfaces are covered 
with peritoneum and are considered intraperitoneal, whereas the 
posterior surface is fixed against the retroperitoneum by the fascia 
of Toldt. The ascending colon is best mobilized along the lateral 
peritoneal reflection by incising the “white line of Toldt,” which rep-
resents the fusion of the peritoneum with the posterior fascia of the 
same name. When releasing the hepatic flexure and lifting the colon 
medially, one must be aware of the proximity of the second part of 
the duodenum, which can be inadvertently injured.
The transverse colon, which is approximately 45 cm in length, 
is suspended between the hepatic and splenic flexures, which are 
fixed structures. It is completely covered by visceral peritoneum 
and connected to the posterior abdominal wall by the transverse 
mesocolon. It has a “U”-shaped curve, which can even reach down 
to the pelvis in some patients. Recognizing its variability in posi-
tion is very important when attempting to exteriorize a loop of co-
lon with a “target incision” for a transverse or sigmoid colostomy.
The greater omentum is attached to the superior aspect of the 
transverse colon. It has two parts, the superior gastrocolic liga-
ment composed of two serous layers, and the inferior portion, 
which is composed of four serous layers draping over the anterior 
abdominal cavity like an apron. Its size and volume are highly 
variable, although in most cases correlated with body weight. Lift-
ing the greater omentum upward with downward traction of the 
transverse colon will reveal an avascular plane adjacent to the co-
lon most easily identified close to the midline. This plane is use-
ful when separating these two structures. The greater omentum 
is commonly used to cover the intraperitoneal contents when 
closing abdominal incisions and also used to fill cavities after sur-
gery helping to control infection. It also provides a good patch, 
or reinforcement, in cases when closure of inflamed and friable 
tissues is not possible or likely to fail, such as in the treatment 
of perforated duodenal ulcer. The omentum can be mobilized to 
create an omental pedicle that reaches the pelvis, by ligating and 
detaching either the right- or left-sided omental vessels, achieving 
extra omental length while the blood supply is adequately main-
tained by the distal arcade from the other side. Such an omental 
pedicle can be positioned between the rectum and vagina to but-
tress a colo- or rectovaginal fistula repair or used to fill the pelvic 
and perineal spaces after rectal excision.
The splenic flexure, where the transverse colon flexes down-
ward, is found adjacent and inferior to the spleen. It is usually situ-
ated higher and deeper than the right colic or hepatic flexure. The 
splenic flexure is suspended by four mainly avascular ligaments: by 
the phrenicocolic ligament to the diaphragm, by the splenocolic 
ligament to the lower pole of the spleen, by the renocolic ligament 
to the Gerota fascia, which surrounds the left kidney, and by the 
pancreaticocolic ligament to the tail of the pancreas. The splenic 
flexure can be released or mobilized without dividing any major 
blood vessels if one is separating the correct plane (Fig. 52.6). Sur-
geons commonly dissect the descending colon along the line of 
Toldt from below and then enter the lesser sac by lifting the omen-
tum above the transverse colon. This maneuver allows mobiliza-
tion of the flexure to be achieved, with minimal traction. Bleeding 
is most commonly encountered from excessive downward traction 
resulting in avulsion of a portion of the splenic capsule.
Spleen
Right lobe of the liver
Hepatic flexure
Third part of the duodenum
Right kidney
Ascending colon
Anterior taenia (libera)
Caecum
Vermiform appendix
First part of the duodenumhowever, that is uncommon in UC, 
where the worst disease is usually located distally. In addition, 
since the patient retains the rectum with this procedure, these 
patients need to undergo continued surveillance for dysplasia be-
cause they are at in an increased risk of cancer in the retained 
rectum over time. 
Ileal Pouch–Anal Anastomosis
IPAA has become the most popular procedure for UC not re-
sponding to medical therapy as well as for patients requiring col-
ectomy for the presence of dysplasia. It has several advantages over 
ileal-rectal anastomosis in that it removes the entire colon as well 
as the majority of the at-risk mucosa, depending on how the oper-
ation is performed (i.e., stapled or hand-sewn anastomosis). IPAA 
was described in the mid to late 1970s and involves removing the 
entire colon and the majority of the rectum. It has two essential 
components: proctocolectomy and creation of a small bowel reser-
voir using the terminal ileum. This reservoir is then either sewn or 
sutured to the anal canal or lower rectum. There have been many 
different configurations of pouches or reservoirs that have been 
proposed in the past, including S Pouches, W Pouches, and H 
Pouches, all with relative advantages and disadvantages. However, 
by far, the simplest and easiest pouch and the one with the least 
complications is the J Pouch, which has withstood the test of time. 
This is created using 15-cm limbs of terminal ileum and two fir-
ings of a GIA stapler (Fig. 52.41). The apex of this J Pouch is then 
either stapled to the distal rectum, leaving a very short rectal cuff 
(Fig. 52.42), or hand-sewn to the distal rectum after a 2-cm mu-
cosectomy is performed (Fig. 52.43). Currently, the stapled ap-
proach is preferred simply because it provides superior continence 
and it is much quicker to perform. However, in cases of dysplasia 
or cancer, hand-sewn approaches still may be warranted.
IPAA generally yields good functional results in patients with 
UC. Since many patients who are undergoing this operation are 
on immunosuppressives at the time of surgery or in poor nutri-
tional state, this operation is commonly performed with tempo-
rary fecal diversion (temporary loop ileostomy). This is in place for 
2 to 3 months, during which these immunosuppressant medica-
tions are weaned and the patient regains their normal nutritional 
state. The temporary ileostomy can then be closed, typically with-
out requiring a laparotomy. In patients who are not on immune 
suppression and in good nutritional state (this usually refers to 
patients undergoing surgery for the findings of colonic dyspla-
sia), the operation can safely be done in one stage without fecal 
diversion provided that there is no tension on the IPAA. Several 
technical maneuvers can be performed to lessen the tension on the 
IPAA. These include mobilization of the small bowel mesentery 
to the level of the pancreas (Fig. 52.44). When dividing the right 
colon mesentery, the ileocolic vessels should be preserved in their 
entirety. If distal traction is placed on the apex of the J pouch, it 
should easily reach just below the symphysis pubis (Fig. 52.45). 
When this maneuver is performed, one can either feel or visualize 
which small bowel mesenteric vessel is under more tension, the 
superior mesentery vessels or the ileocolic vessels. The vessel with 
the greater amount of tension can be divided, allowing greater 
length on the small bowel mesentery. “Peritoneal windowing” can 
FIG. 52.41 Creation of an ileal J pouch using a cutting linear stapler. For 
replacement of the rectum, a reservoir is created from the distal ileum. 
The stapler joins two limbs of intestine with staples while dividing the 
intervening wall. The diameter of the pouch is created twice as large 
as the original diameter of the ileum. The limbs of the J pouch should be 
15 cm in length. Two fires of a linear stapler are required; either a 75- or 
100-mm stapler can be used.
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1353CHAPTER 52 Colon and Rectum 
also provide mesenteric length. This is a maneuver whereby small 
slits are created in the anterior and posterior peritoneum covering 
the mesenteric vessels. These horizontal slits in the peritoneum, in 
most cases, provide for one or two extra centimeters of mesenteric 
length (Fig. 52.46). Needless to say, the more obese an individu-
al is, the more difficult it can be to obtain sufficient mesenteric 
length for the small bowel to reach tension-free to the pelvis. In 
addition to this, with very tall individuals and those with a long 
torso, tension can be an issue as well.
Common early complications of IPAA include those as-
sociated with nonhealing of the IPAA: pelvic sepsis, ileal 
pouch–anal anastomotic fistulae, ileal pouch–vaginal fistulae, 
ileal pouch–anal anastomotic sinuses, and ileal pouch–anal 
FIG. 52.42 Fashioning of stapled ileal pouch–anal anastomosis. A circular stapler is used; typically a 29-mm 
stapler is selected. A common error is to leave too long a segment of rectum, resulting in the persistent symp-
toms due to this retained segment of mucosa affected with inflammatory bowel disease (cuffitis).
FIG. 52.43 Hand-sewn ileal pouch–anal anastomosis after anorectal 
mucosectomy.
FIG. 52.44 Mobilization of the small bowel mesentery to the third por-
tion of the duodenum. Here the small bowel mesentery has been re-
tracted cephalad exposing the third portion of the duodenum (arrow).
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1354 SECTION X Abdomen
anastomotic strictures (often a reflection of anastomotic ten-
sion). Late complications include the diagnosis of Crohn dis-
ease, which is more common in patients who undergo emer-
gent colectomy and in those patients who have a diagnosis of 
indeterminate colitis.
With a “good” result, patients with IPAA will have up to six 
bowel movements within a 24-hour period, usually including one 
nocturnal bowel movement. In the majority of patients, at about 
6 months, there will be significant enlargement of the ileal pouch, 
allowing patients to reduce the amount of antidiarrheal medica-
tion they take to control their output. 
Continent Ileostomy
Continent ileostomy was first described in the late 1960s and re-
mained very popular until IPAA surpassed it as the procedure of 
choice for young patients with UC. This operation involved con-
struction of a reservoir, similar to that used with the IPAA. Here, 
instead of continence being maintained by the anal sphincter, 
continence was maintained by an intussuscepted segment of il-
eum positioned between this reservoir and the end ileostomy. A 
continent ileostomy is air and water tight; however, the intus-
suscepted segment is very prone to dessusception, rendering the 
stoma incontinent and requiring revisional surgery. This proce-
dure works best in individuals with a thin body habitus as with 
heavier individuals the thicker mesentery also predisposes to des-
susception. 
Surgery for Crohn Disease
Ileocolic Resection
Ileocolic resection is one of the most common operations per-
formed for patients with Crohn disease as it is estimated that the 
ileocecal area is the site of involvement in nearly half of patients. 
Indications for surgery in these patients are usually either due to 
fibrostenosing disease with obstruction or associated fistulizing 
disease/mass/abscess or phlegmon. As the terminal ileum lies in 
the pelvis in close proximity to a number of pelvic structures, if 
there is a significant obstruction and a proximal perforationoc-
curs, the resulting abscess can perforate into the sigmoid colon or 
bladder. The sigmoid colon is by far the more common, and the 
resulting ileosigmoid fistula fairly frequently occurs in these pa-
tients. When performing an ileocolic resection, one must always 
be alert to any “adhesions” and make sure these are not entero-
enteric fistulas. Ileocolic resection lends itself well to the laparo-
scopic approach. Exceptions are cases in which there is extensive 
fistulizing disease or a significant phlegmon in which there is dif-
ficulty separating the right colon mesentery/terminal ileum away 
from the retroperitoneal structures. In deciding margins of resec-
tion, one should select areas of bowel that feel normal and are not 
thickened and have a normal thickness of the bowel-mesenteric 
junction. The ability to palpate a discrete small bowel-mesenteric 
junction is usually a good indicator that the lumen is free of sig-
nificant Crohn inflammation. While there are many ways to con-
struct the ileocolic anastomosis, the authors prefer a hand-sewn 
FIG. 52.45 Estimation of J-pouch length. The apex of the J pouch 
should be able to be brought down below the level of the symphysis 
pubis. This is a good estimate of a tension-free reach to the anal canal.
A B
FIG. 52.46 Peritoneal windowing. (A) The mesenteric peritoneum is lifted away from the superior mesenteric 
artery by lifting it up with a hemostat and then divided using the electrocautery. (B) The mesenteric peritoneum 
has been divided perpendicular to the axis of the superior mesenteric artery. Note that at each area where the 
peritoneum has been divided, an additional 1 cm of mesenteric length has been obtained.
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1355CHAPTER 52 Colon and Rectum 
end-to-end anastomosis. Postoperatively, these anastomoses are 
very easy to evaluate endoscopically and to dilate in the event of 
recurrent disease, which is not true of side-to-side stapled anas-
tomoses. It is paramount that however the anastomosis is con-
structed, it is made very wide. 
Segmental Colon Resection
Segmental colonic resection has increasingly been used in the 
treatment of Crohn disease over the last two decades. This has 
been performed for two reasons: (1) recognition of the impor-
tant role of water absorption (see section on colonic physiology) 
performed by the colon, and recognition that many of these pa-
tients will undergo repeated operations, and (2) availability of 
newer and more potent medications for Crohn disease allow-
ing more effective suppression of recurrent disease. The idea of 
segmental resection for colonic Crohn disease can be performed 
in patients who have isolated areas of colonic stricture with rela-
tively normal areas of “skipped” normal-appearing colon with 
normal colonic distensibility. In these patients, performing a 
segmental resection is associated with a much higher risk of re-
currence, so this should always be accompanied by some type of 
postoperative chemoprophylaxis to reduce the risk of recurrence 
of the disease. 
Subtotal Colectomy and Ileorectal Anastomosis
This is an operation that is well suited to patients with Crohn 
disease if they have a relative rectal-sparing and an otherwise 
diseased colon. Segmental resection is preferable if there are ar-
eas of normal intervening colon. However, this operation also, 
as with segmental colectomy, is associated with a much higher 
rate of recurrence. Options for this, if there is a smaller amount 
of retained rectum, are to perform an ileal pouch–rectal anasto-
mosis in order to lessen the number of bowel movements that 
the patient has after surgery. Depending on the height of the 
anastomosis and the circumstances of the surgery (redo, associ-
ated immunosuppression, patients’ nutritional state), this may 
require temporary fecal diversion (temporary loop ileostomy) to 
facilitate healing. 
Proctocolectomy and Ileal-Pouch–Anal Anastomosis
In previous editions of the Sabiston textbook, there perhaps was 
only a passing mention of this procedure; however, every year, 
this is more frequently considered a possibility for patients with 
Crohn disease, providing that they do not have obvious perianal 
disease. With the advent of newer and more potent immuno-
suppressive drugs, this procedure is considered an option in an 
educated patient who is aware of the increased risk of morbidity 
and the less favorable functional results (i.e., greater number of 
bowel movements) as compared to when this operation is per-
formed for patients with UC. In addition, there is, of course, a 
higher risk of fistulizing disease and the need to convert to an 
end ileostomy. However, in the motivated patient who recog-
nizes and accepts these risks, this procedure can be performed. 
See the section on IPAA for UC for technical details regarding 
this procedure. 
Cancer Risk
As with UC, there is an increased risk of colon cancer in patients 
with longstanding Crohn disease, although it is thought to be 
somewhat less than with UC. However, in patients in whom there 
has been a cancer identified, total colectomy should be performed, 
as there have been studies showing colonic procarcinogenic muta-
tions tracking along the colon and the risk of a subsequent cancer 
in other areas of the colon is high.18 
Postoperative Complications
Many patients with IBD who undergo surgery are on immu-
nosuppressive medications, and in addition, many of these 
patients are hypoalbuminemic, since they have protein-los-
ing enteropathy from their disease. Because of this, they are 
at increased risk for infectious postoperative complications. 
There are differing opinions as to the relative risk of complica-
tions with these different medications. However, overall, it is 
thought that steroids pose an increased risk for infectious com-
plications, as do the administration of biologic medications, 
within several months before surgery.19 Because of this, there 
should be a discussion with patients regarding the possibility 
of a temporary fecal diversion if an operation is undertaken in 
which an anastomosis is considered so that, if in the clinical 
judgment of the surgeon a temporary ileostomy is considered 
prudent, this can be performed. 
Postoperative Recurrence
Recurrence rate following surgery for Crohn disease varies de-
pending on the site of surgery as well as other factors such as en-
vironmental factors. It has been reported that Crohn patients who 
smoke are at higher risk of early disease recurrence, as are patients 
younger than 30 years old and those who have already had two 
or more operations for fistulizing disease.20 There has been an in-
creasing recognition that early intensive medical treatment begin-
ning very soon postoperatively may successfully reduce the risk of 
recurrence. Regular endoscopic monitoring of the lower GI tract 
for signs of recurrent disease is important to allow therapeutic in-
tervention prior to the development of therapy-resistant fibrosis. 
INFECTIOUS COLITIS
Infectious colitis may be diagnosed among patients with acute 
diarrhea and colonic inflammation. Their importance for the sur-
geon arises in their capacity to mimic surgical conditions such as 
an acute abdomen or IBD and in some cases to deteriorate to the 
point where they require surgical treatment.
Clostridium difficile Infection
C. difficile is a common inhabitant of the GI tract that can mani-
fest in a spectrum of symptoms ranging from that of an asymp-
tomatic carrier to fulminant colitis. 
Epidemiology
C. difficile is the most common cause of healthcare-associated di-
arrhea and is considered to be a major source of healthcare-asso-
ciated morbidity occurring in 2% of all hospital discharges for all 
diseases. The prevalence of asymptomaticcolonization of C. dif-
ficile among adult hospitalized patients ranges from 3% to 26% in 
different studies. Around 453,000 new cases of CDI are diagnosed 
annually in the United States, of which 83,000 are recurrent cases, 
with 29,300 attributed deaths.21 Interestingly, after plateauing at 
historical high rates, some regions have begun to show a decline 
in incidence attributed to specific prevention and treatment pro-
grams. In participating Canadian hospitals, for example, the in-
cidence of CDI has decreased from 7.9/10,000 patient-days in 
2011 to 4.3/10,000 patient-days in 2015.22 
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1356 SECTION X Abdomen
Microbiology and Transmission
C. difficile is an anaerobic, spore-forming, gram-positive bacillus. 
Transmission routes include person-to-person spread through the 
fecal-oral route or through exposure to a contaminated environ-
ment by ingestion of spores from other patients and transmission 
via healthcare personnel’s hands. Toxicogenic C. difficile pathogens 
can produce A and B toxins, both of which have been associated 
with colitis. Binding of toxin A or B to colonocyte glycoprotein 
receptors leads to colonocyte death and release of inflammatory 
mediators. The emergence of the C. difficile Ribotype 027 strain in 
the mid-2000s resulted in significant outbreaks across the Western 
world associated with more severe disease outcomes and deaths. 
Risk Factors
The most important risk factor for the development of a clinical in-
fection is recent exposure to antibiotics. Antibiotics affect the natu-
ral bowel flora, decreasing the natural ability to suppress the growth 
and spread of C. difficile. Virtually all antibiotics have been associ-
ated with C. difficile, but particularly third and fourth generation 
cephalosporins, fluoroquinolones, clindamycin, and carbapenems 
have been linked to a higher risk of CDI. Other risk factors include 
immunodeficiency (including human immunodeficiency virus in-
fection), chemotherapy treatment, use of acid suppressing medica-
tions such as proton pump inhibitors, GI surgery or manipulation 
of GI tract including tube feeding, and prolonged hospitalization 
or lengthy stay in nursing homes or rehabilitation units. Patients 
with IBD have increased rates of CDI, along with worse outcomes 
[HIV] and higher rates of colectomy. These patients are more likely 
to receive immunosuppressants and antibiotics and have a different 
intestinal flora compared to healthy subjects. Differentiating be-
tween an IBD exacerbation and CDI can be difficult as the symp-
toms overlap, and a high index of suspicion must be maintained. 
Patients with an increased risk for death from CDI include those 
with advanced age, multiple comorbidities, hypoalbuminemia, leu-
kocytosis, acute renal failure, and those infected with Ribotype 027. 
Clinical Presentation
Symptoms of CDI commonly begin 4 to 9 days after initiation of 
antibiotics but can commence 10 weeks or more after antibiotic 
treatment. Patients presenting with new-onset, unexplained, watery 
diarrhea (with three or more unformed stools in 24 hours) should 
be suspected of having CDI. Patients may also have abdominal 
pain, fever, and an associated ileus. Patients with CDI can be cat-
egorized into asymptomatic colonization, nonsevere disease, severe 
disease, and fulminant disease. A variety of scores have been utilized 
to assess clinical severity and treatment response. Leukocytes of at 
least 15,000 cells/μL and/or serum creatinine of at least 1.5 cells/μL 
are predictors of severe disease according to the Infectious Disease 
Society of America. Fulminant or severe CDI is diagnosed in pa-
tients demonstrating hypotension or shock, ileus, or megacolon. The 
ATLAS criteria is a simple clinical bedside score, which includes age, 
temperature, leukocytosis, albumin, and systemic antibiotic treat-
ment and has been used to assess response to treatment.23 
Diagnosis
The diagnosis of CDI is based on typical symptoms in combina-
tion with stool testing. Laboratory testing is based on detection of 
C. difficile toxins, C. difficile antigen, or the bacteria itself. A vari-
ety of commercial tests are utilized, including enzyme-linked im-
munosorbent assay for toxin detection, glutamate dehydrogenase 
immunoassay for C. difficile antigen detection, nucleic acid ampli-
fication test, polymerase chain reaction testing, and stool cultures.
Flexible sigmoidoscopy may be helpful as a diagnostic modal-
ity for CDI. Although it is not a first-line modality for diagnosis, 
it can be helpful in cases of inconclusive stool testing or to help 
exclude other etiologies. Classically raised, yellowish-white small 
(2–10 mm) plaques (pseudomembranes) can be observed in ap-
proximately half of patients with CDI (Fig. 52.47). Nonspecific 
colitis can be found in an additional 25%. Histologic findings 
from the plaques reveal an inflammatory exudate with mucinous 
debris, fibrin, necrotic epithelial cells, and polymorphonuclear 
cells. In fulminant colitis, colonoscopy may increase the risk of 
perforation and should be considered only when the benefit is 
higher than the risk of complications.
Imaging is not very useful for diagnosis as it is not specific but can 
assist in assessing disease severity and response to treatment. Typical 
CT findings include significant colonic wall thickening, bowel dila-
tion, pericolonic fat stranding, high attenuation oral contrast in the 
colonic lumen alternating with low-attenuation inflamed mucosa 
(accordion sign), and ascites. Ultrasound may also be useful, espe-
cially among critically ill patients who cannot be transported to the 
CT scanner in radiology. Ultrasonography may show bowel wall 
thickening, narrowing of the lumen, as well as pseudomembranes, 
which are seen as hyperechoic lines covering the mucosa. 
Treatment
Initial treatment includes stopping or minimizing previous anti-
biotics, parenteral fluids, and correction of electrolytes. The use of 
antiperistaltic agents for the treatment of CDI should be avoided. 
Antibiotic treatment of CDI is determined according to the clini-
cal setting and can be divided into the initial episode, recurrent 
episode, severe, and fulminant disease. Table 52.4 summarizes 
current antibiotic treatment recommendations for initial episodes 
and for severe and fulminant disease.
Treatment options for recurrent episodes generally include 
changing antibiotics (from metronidazole to vancomycin or fidax-
omicin from vancomycin). In addition, tapered and pulsed regi-
mens are used.
Fecal Microbiota Transplant
Fecal microbiota transplant (FMT) for patients with recurrent 
episodes of CDI is a relatively new treatment. Patients with CDI 
lack protective colonic microbiota to resist replication and coloni-
zation of C. difficile. Reimplantation of normal gut bacteria, par-
ticularly bacteria resistant to C. difficile from healthy donors can 
help restore normal gut biodiversity and correct the imbalance. 
Different routes of administration have been described in the liter-
ature including nasogastric, oral (frozen fecal microbial capsules), 
rectal enema, and colonic per colonoscopy. A recent comparison 
between upper and lower methods of delivery demonstrated the 
lower approaches being more effective.24 The efficacy of FMT 
ranges from 77% to 100%, with multiple FMTs needed to achieve 
a good clinical response. Current guidelines recommend FMT for 
patients with multiple recurrences of CDI, in whom antibiotic 
treatment has failed. 
Monoclonal Antibodies
Bezlotoxumab and actoxumab are monoclonal antibodies directed 
against C. difficile toxins B and A, respectively. These antibodies 
limit colonic damage by neutralization of the toxin and block the 
binding to host cells.25 Theycan be used as coadjuvant treatment 
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1357CHAPTER 52 Colon and Rectum 
with antimicrobial therapy to help prevent recurrence, especially 
among patients infected by Ribotype 027, in severe CDI, and in 
immunocompromised patients. 
Surgery
Patients with fulminant CDI who develop signs of systemic tox-
icity, toxic megacolon, or perforation should be operated upon 
emergently. Emergency colectomy for patients with fulminant 
colitis provides a survival advantage compared with continuing 
antibiotics. Among severely ill patients, a total or subtotal abdom-
inal colectomy with preservation of the rectum has traditionally 
been performed. A newer option with similar results for patients 
without necrosis or perforation is exteriorization of a diverting 
loop ileostomy with on-table colonic lavage followed by antegrade 
vancomycin flushes.26 
OTHER COLONIC INFECTIONS
Diarrhea and colitis can be caused by other pathogens. Most of 
these will not require surgery. A careful history can discover the 
source in many cases, such as polluted drinking or recreational 
water, consumption of contaminated fruits and vegetables, 
unpasteurized milk, undercooked meat and fish, shellfish, and 
eggs. International travel, as well as contact with animals and 
their feces should also be queried. Table 52.5 summarizes the 
important characteristics of common bacteria causing diarrhea 
and colitis.
The initial approach includes a careful history, evaluation for 
dehydration and electrolyte disturbances, and stool testing for ova 
and parasites and for culture and sensitivity. Patients with signs of 
sepsis or those who have traveled from enteric fever–endemic re-
gions and immunocompromised patients should also have blood 
cultures obtained.
Initial treatment includes rehydration and correction of elec-
trolyte disturbances. Oral rehydration solution is recommended 
for mild to moderate disease. Nasogastric administration of oral 
rehydration solution may be considered for patients who do not 
tolerate oral intake. Patients with signs of severe dehydration or 
ileus should be treated with isotonic IV fluids (normal saline or 
lactated Ringer’s solution). The majority of patients who present 
with acute watery diarrhea and those without recent international 
travel do not require antimicrobial therapy. Immunocompromised 
A
1
B
FIG. 52.47 (A) Endoscopic view of pseudomembranes associated with Clostridium difficile. (B) Pseudomem-
branes overlying the colon mucosa at the time of colectomy. The patient had active Clostridium difficile colitis 
with coexisting Crohn colitis.
TABLE 52.4 Antibiotic treatment of Clostridium difficile infection.
CLINICAL CONDITIONS TREATMENT TREATMENT DURATION
First episode 1. Oral vancomycin 125 mg 4 times daily OR 
 2. Fidaxomicin 200t mg twice Daily
If vancomycin and fidaxomicin are not available: metronidazole 500 mg 3 
times daily can be given for nonsevere disease.
10 days
First episode—fulminant 
(hypotension, shock, ileus, 
megacolon)
Vancomycin, 500 mg 4 times daily (oral or by nasogastric tube).
In case of ileus:
 1. Consider adding rectal instillation of vancomycin.
 2. Intravenously administered metronidazole (500 mg every 8 hours) should 
be administered together with oral or rectal vancomycin.
At least 10 days, duration should be individualized
Adopted from McDonald LC, Gerding DN, Johnson S, et al, Clinical Practice Guidelines for Clostridium difficile infection in adults and children: 
2017 update by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA). Clin Infect Dis. 
2018;66:987–994.
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1358 SECTION X Abdomen
or septic patients, as well as those suspected of enteric fever, should 
be treated with empirical, broad-spectrum antimicrobial therapy, 
usually with fluoroquinolones, such as ciprofloxacin, or macro-
lides, such as azithromycin, depending on local susceptibility 
patterns. Surgical intervention is rarely required apart from those 
cases developing severe fulminant disease that lead to perforation 
or toxic megacolon.
Viruses can also cause acute diarrhea and colitis. Cytomega-
lovirus (CMV) is an important etiology to consider in immu-
nocompromised hosts, particularly in advanced HIV infection, 
transplant patients, patients with IBD, and in those receiving 
chemotherapy. CMV colitis commonly presents with watery or 
bloody diarrhea, fever, and abdominal pain. Diagnosis is estab-
lished by serology and by determining viral load in the blood. 
Endoscopy demonstrates patchy mucosal erythema in the colon. 
Inclusion bodies seen on biopsy are pathognomonic for CMV. 
CMV colitis can progress to sepsis, toxic megacolon and colon 
perforation. Treatment is usually supportive with the addition of 
ganciclovir. Patients with severe, complicated disease may require 
surgery. 
ISCHEMIC COLITIS
Ischemic colitis is a common disorder that develops when the ar-
terial blood supply to the colon is insufficient to support cellular 
metabolic demands. It is the most common form of GI ischemia, 
with rates of 7.1 to 22.9/100,000 person-years.27 Severity varies 
within a wide spectrum, from mild self-limiting disease to severe 
life-threatening colonic ischemia. Considering the wide range of 
clinical findings with most patients presenting with mild non-
specific symptoms, the true incidence is likely much higher. It 
is important to differentiate ischemic colitis from situations of 
acute mesenteric ischemia, in which a major vessel of the bowel is 
obstructed, wherein patients commonly present with severe pain 
out of proportion to physical findings and require immediate 
vascular intervention. Ischemic colitis is considered a disease of 
small blood vessels and typically presents less dramatically, seldom 
requiring vascular intervention. Most cases, when recognized and 
managed promptly, do not require surgery. Delays in diagnosis 
and treatment, however, can result in the need for emergency col-
ectomy with high morbidity and mortality.
Anatomic Considerations
The arterial blood supply to the colon is derived from the SMA 
and the IMA. The SMA gives off the ileocolic, right colic, and 
middle colic arteries. The IMA gives rise to the left colic and sig-
moid arteries and ends as the superior rectal (hemorrhoidal) ar-
tery (Fig. 52.8). There are two well-described collateral networks 
that aid in preventing colonic ischemia by providing “backup” 
both within the territories of the two major arteries and between 
them. The main collateral vessel is the marginal artery of Drum-
mond, which runs parallel and close to the mesenteric margin of 
the colon from the cecocolic junction to the rectosigmoid junc-
tion. The colon can receive collateral blood supply through this 
artery when one of the larger arteries is obstructed. It is important 
when resecting a section of colon to preserve this artery since only 
the vasa recta are located between it and the colon. When it is 
compromised, ischemia of that section of colon may result. The 
second collateral circulation can be found in the proximal region 
of the large arteries. The “arc of Riolan” (meandering mesenteric 
artery) is an infrequent finding, traversing close to the mesenteric 
root and connecting the SMA or middle colic artery to the IMA 
or left colic artery (Fig. 52.48). It can have a critical role in situ-
ations of SMA or IMA occlusion. The presence of a large arc of 
Riolan commonly indicates an obstruction ofone of the major 
mesenteric arteries.
Watershed areas of the colon are potentially found at the edge 
of the region supplied by the two main arteries, the SMA and the 
IMA, zones that are frequently dependent upon collateral circu-
lation (Fig. 52.49). There are two well-described watershed ar-
eas where the collateral circulation is classically inconsistent and 
vulnerable to ischemia. The first is the area of the splenic flexure 
(Griffiths point). In some studies, up to 50% of specimens were 
found to lack a marginal artery in the region where the SMA 
and IMA circulations meet. Commonly, surgeons avoid making 
anastomoses in this area for fear that the impaired blood sup-
ply will not be sufficient to permit anastomotic healing, leading 
to anastomotic leaks. A second potential watershed area is the 
TABLE 52.5 Clinical characteristics of common enteric infections.
PATHOGEN CHARACTERISTICS AND CLINCAL PRESENTATION
Campylobacter jejuni Spiral, microaerophilic gram-positive rod.
Exposure to improperly prepared chicken or beef.
Fever, watery diarrhea, and abdominal pain. Commonly involves the cecum and terminal ileum. May mimic appendicitis or 
Crohn disease.
Yersinia enterocolitica Gram-negative coccobacillus.
Exposure to contaminated water or food.
Abdominal pain and bloody diarrhea, may mimic appendicitis or Crohn disease.
Shigella Gram-negative, facultative anaerobe.
Common cause for dysentery in developing countries.
Often affects rectum and sigmoid colon.
Fever, abdominal pain, watery diarrhea that can progress to bloody diarrhea.
Salmonella typhi or Salmonella 
enterica serotypes 
Paratyphi
Gram-negative, facultatively anaerobic bacilli
Recent travel to an endemic area, consumption of foods prepared by a traveler to an endemic area.
Fever with or without diarrhea, abdominal pain, cramping and vomiting.
Adapted from Shane AL, Mody RK, Crump JA, et al. 2017 Infectious Diseases Society of America Clinical Practice Guidelines for the diagnosis and 
management of infectious diarrhea. Clin Infect Dis. 2017;65:1963–1973.
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1359CHAPTER 52 Colon and Rectum 
rectosigmoid junction (Sudeck’s point). This region receives it 
blood supply from the superior hemorrhoidal artery and distal 
sigmoid branches, both terminal branches of the IMA and prone 
to atherosclerotic changes. The right colon, although not classi-
cally considered a watershed area, it is also vulnerable to ischemia 
from embolic occlusion because the ileocolic artery is the termi-
nal branch of the SMA. For this reason, the right colon is also 
particularly prone to low-flow conditions such as heart failure, 
hemorrhage, and sepsis. The rectum, which has a good blood 
supply from both the IMA and the iliac circulation, as well as a 
strong collateral network, is rarely the victim of ischemic injury. 
Risk Factors
Ischemic colitis may occur in all ages but is significantly more 
common in elderly patients, in women, and in patients with mul-
tiple comorbidities. Several medical conditions and medications 
have been associated with ischemic colitis (Box 52.2)28
Patients with low-flow states, as a result of heart failure or 
sepsis, are especially prone to develop ischemic colitis. Dia-
betes mellitus, hypertension, chronic obstructive pulmonary 
disease, peripheral vascular disease, and renal disease have also 
been associated with this disorder. Patients undergoing aortic 
reconstructive surgery or abdominal surgery in which the IMA 
is ligated are also especially predisposed to colonic ischemia. 
In these patients, if the collateral circulation is not sufficient, 
acute occlusion of the IMA can result in sigmoid and left colon 
ischemia.
Several medications have been implicated in ischemic colitis. 
Constipation-inducing drugs can cause ischemic colitis, most 
likely as a result of reduced blood flow and increased intraluminal 
pressure. Immunomodulator drugs such as anti-TNF-α inhibitors 
can affect thrombogenesis, and illicit drugs such as cocaine and 
methamphetamines cause ischemia through vasoconstriction, hy-
percoagulation, and direct endothelial injury. 
Presentation and Diagnosis
The majority of patients with partial-thickness ischemia of a lo-
calized section of colon present with relatively nonspecific signs 
and symptoms. A high index of suspicion is needed to make an 
early diagnosis. Presenting symptoms usually include sudden ab-
dominal pain and cramping, tenesmus, and bloody diarrhea or 
hematochezia. The combination of these symptoms is present in 
close to 50% of the patients, with the pain usually beginning prior 
to the bleeding. Bleeding associated with ischemic colitis is usually 
minor and seldom requires blood transfusions. Patients may also 
experience nausea, vomiting, and a low-grade fever. On physical 
exam, abdominal distension may be noted, as well as tenderness 
overlying the involved region. A good medical history is impor-
tant in establishing the diagnosis, with a focus on associated dis-
eases and medications.
The most common affected region is the left colon (includ-
ing the splenic flexure), followed by the sigmoid colon based on 
the affected blood supply. Pancolitis due to ischemia is associated 
with a worse prognosis. About a quarter of the patients present 
with isolated right-sided ischemic colitis. These patients are more 
likely to present with abdominal pain without bleeding and more 
commonly have atrial fibrillation, coronary artery disease, and/or 
chronic renal failure. Patients with isolated right-sided ischemic 
colitis have a higher chance of requiring surgery and have a poorer 
prognosis. A minority of patients will present with full-thickness 
ischemia. These patients are sicker and commonly present with 
high fever, leukocytosis, acidosis, and peritonitis.
Basic laboratory testing is nonspecific but can assist in predict-
ing severity. Severe disease has been associated with an increased 
white blood cell count, blood urea nitrogen, lactate dehydroge-
nase, and decreased hemoglobin and albumin levels. Acidosis, de-
creased bicarbonate, and increased lactate levels are also associated 
with severe ischemic colitis. It is also recommended to test stool 
for C. difficile toxin, ova and parasites, and culture and sensitivity 
in order to exclude an infectious etiology.
Abdominal plain films may show bowel distension and 
“thumbprinting,” which are rounded densities along the sides of 
a gas-filled colon indicative of submucosal edema. These are non-
specific to ischemic colitis since thumbprinting can be found with 
other situations of colonic inflammation. Free intraperitoneal air 
suggests bowel perforation and should lead to immediate opera-
tive management. Water-soluble contrast enemas have generally 
become obsolete in the diagnosis of ischemic colitis but may still 
be used for the evaluation of chronic ischemic strictures. CT scans 
of the abdomen have become the primary noninvasive modality 
for the initial diagnosis of colonic pathology. CT scans, performed 
using both IV and oral contrast, can assist in determining the loca-
tion of involved areas, to assess the severity, identify complications, 
and exclude the presence of other diseases. Findings suggestive of 
ischemic colitis, although relatively nonspecific, include segmental 
bowel thickening, pericolonic fat stranding, and thumb printing. 
Pneumatosis intestinalis (the presence of gas in the colonic wall), 
portal venous gas, and the absence of large bowel enhancement on 
contrast-enhanced CT usually indicate severe transmural disease 
favoring immediate surgical intervention. Vascular imaging is usu-
ally not indicated in cases of ischemic colitis, as this is usually a 
disease of small vessels; however, in cases of pain of suddenonset 
Middle
colic artery
Superior
mesenteric
artery
Arc of Riolan
FIG. 52.48 The Arc of Riolan. (From Gordon PH, Nivatvongs S, ed. Prin-
ciples and Practice of Surgery for the Colon, Rectum and Anus. 2nd ed. 
St. Louis: Quality Medical Publishing; 1999:27.)
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1360 SECTION X Abdomen
that is out of proportion to physical and laboratory findings and 
in isolated right colon ischemic colitis, multiphasic CT angiogra-
phy should be performed to exclude acute proximal mesenteric 
ischemia.
The gold standard for the diagnosis of ischemic colitis is flexi-
ble endoscopy. Early colonoscopy should be performed (within 48 
hours), except in cases of acute peritonitis or in cases of suspected 
severe transmural ischemia. In contrast to the expected increased 
risk of perforation due to endoscopy in the evaluation of isch-
emic colitis, current published literature does not demonstrate a 
higher rate of perforation compared to other patients. It is recom-
mended, however, to refrain from overinsufflation and avoid ad-
vancing the scope beyond the most distal extent of disease. Com-
mon endoscopic findings characteristic of ischemic colitis include 
edematous and friable mucosa, erythema, petechial hemorrhage, 
and mucosal ulceration. The “single-stripe sign,” a single linear 
ulcer running along the longitudinal axis of the colon is rare but 
considered specific for ischemic colitis. Segmental distribution, 
with abrupt transition between injured and noninjured mucosa, 
and sparing of the rectum support ischemia over IBD. It is impor-
tant to note that diagnostic endoscopy usually cannot distinguish 
between partial-thickness and full-thickness ischemia. Fig. 52.50 
depicts a recommended algorithm for diagnosis and treatment of 
ischemic colitis. 
Treatment
The majority of patients, nearly 80%, will respond to conservative 
nonoperative treatment, with significant improvement within a 
few days. The mainstay of treatment includes bowel rest, IV flu-
ids, and broad-spectrum antibiotics. A nasogastric tube should be 
inserted if ileus is present.
Efforts should be made to correct low-flow states and hypo-
tension with aggressive fluid resuscitation and optimal treatment 
of associated conditions such as heart failure and sepsis. Colonic 
ischemia can result in failure of the intestinal epithelial barrier 
with bacterial translocation leading to overt sepsis. For this rea-
son, empiric broad-spectrum antibiotics against both anaerobic 
and aerobic coliform bacteria are prescribed in ischemic colitis to 
cover the normal colonic bacterial flora. Cathartics are not recom-
mended as they may lead to colon perforation. Glucocorticoids 
should be avoided unless treating a preexisting disorder such as 
lupus or rheumatoid arthritis.
Most episodes of ischemic colitis are mild and self-limiting. 
Patients who fail to improve or have worsening symptoms within 
a few days should raise the concern for the development of full-
thickness ischemia and should have repeat imaging or endoscopy 
to help guide treatment.
A small proportion of patients with mild to moderate symptoms 
will develop a chronic colitis, with ongoing or recurrent bouts of 
Middle
colic
artery
Right
colic
artery
Ileocolic
artery
Superior
hemorrhoidal
artery
Superior
mesenteric
artery
Inferior
mesenteric
artery
Arch of
Riolan
Left
colic
artery
Sigmoidal
arteries
Marginal
artery of
Drummond
FIG. 52.49 Lightly shaded colonic regions especially vulnerable to ischemia. (From Netz U, Galandiuk S. Man-
agement of ischemic colitis. In: Cameron JL, Cameron A, eds. Current Surgical Therapy. 12th ed. Philadelphia: 
Elsevier; 2017:171–176.)
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1361CHAPTER 52 Colon and Rectum 
symptoms of abdominal pain, bloody diarrhea, and sepsis. These 
patients have a higher rate of complications and commonly require 
surgical resection of the involved segment. Some patients who ini-
tially recover from partial-thickness ischemic colitis will eventually 
develop a chronic stricture at the involved segment. These patients 
may complain of constipation, narrowed stools, and abdominal 
pain. Diagnosis can be confirmed with a contrast enema, CT, or 
endoscopy. Symptomatic patients or those in which malignancy 
cannot be excluded should undergo elective resection.
Patients who present with, or develop signs of transmural isch-
emia and perforation, including peritonitis, hemodynamic insta-
bility, free peritoneal air, and ominous signs on CT as mentioned 
earlier, such as portal venous gas, require emergent surgical ex-
ploration. A recent large database study identified a 25% 30-day 
postoperative mortality rate for ischemic colitis29 with other stud-
ies ranging up to 47% mortality following acute surgical inter-
vention. Risk factors independently identified as associated with 
perioperative mortality after colectomy for ischemic colitis in-
clude the elderly, poor functional status, multiple comorbidities, 
preoperative septic shock, preoperative blood transfusions, pre-
operative acute renal failure, and delay from hospital admission 
to surgery.
During surgery, it is important to visualize and assess the en-
tire small and large intestine for signs of ischemia and gangrene. 
Ischemia commonly affects a recognizable segment of the colon, 
frequently in watershed areas. In these cases, an anatomic resec-
tion should be performed to allow sufficient blood supply to the 
remaining colon with minimal reliance on stressed collaterals. 
Deciding how much to resect or whether a specific segment is 
likely to survive can be difficult. Visual examination tends to be 
inaccurate, especially when the bowel is ischemic but still viable. 
Intraoperative infrared angiography is a relatively new technique 
that has been gaining popularity as an adjunct for determining 
bowel viability and for determining the integrity of intestinal 
anastomoses. In this technique, indocyanine green is injected 
intravenously and distributes throughout the circulation. Then, 
using a variety of commercially available imaging systems, the in-
docyanine green undergoes laser excitation, demonstrating real-
time tissue perfusion (Fig. 52.51). Creation of an anastomosis is 
usually not recommended in the acute setting, due to the concern 
for evolving ischemia and the existence of hemodynamic instabil-
ity and sepsis commonly encountered in these situations. A tem-
porary abdominal closure with a planned second-look after 24 
hours may be prudent to determine the need for further resection. 
Staple the ends and leave them in the abdomen, avoiding com-
plications of a stoma as in very obese patients. Pancolic ischemia 
is rare, but such cases require total colectomy with ileostomy. In 
contrast to mesenteric ischemia of the small intestine, there is 
usually no indication for revascularizing the large bowel in prima-
ry colonic ischemia, which is not generally related to large artery 
obstruction. 
NEOPLASIA
Colorectal Cancer Genetics
As CRC is one of the most common cancers worldwide, much re-
search has been directed into the genetics of CRC. It has long been 
appreciated that genetics play a role in the disorder and there has 
been an appreciation and recognition of specific inherited cancer 
syndromes that has greatly aided in our understanding of sporadic 
CRC. Before the reader passes on the next section, this section 
explains why some patients will develop a CRC very quickly and 
others, more slowly.
Chromosomal Instability Pathway
Much of our initialunderstanding of the genetic basis of CRC 
comes from the work of Vogelstein and colleagues, who evalu-
ated nearly 200 samples of colorectal neoplasia ranging from 
polyps to invasive cancers. By checking for alterations in spe-
cific genes, they were able to propose a step-wise model of CRC 
carcinogenesis, involving the activation of an oncogene (a gene 
Low Flow State
• Septic shock
• Congestive heart failure
• Hemorrhagic shock
• Hypotension 
Atherosclerosis
• Ischemic heart disease
• Cerebrovascular disease
• Peripheral vascular disease 
Gastrointestinal
• Constipation
• Diarrhea
• Irritable bowel syndrome 
Surgery and Invasive Interventions
• Abdominal surgery
• Aortic surgery (especially abdominal aortic aneurysm repair)
• Cardiovascular surgery
• Following endovascular abdominal manipulations (i.e., chemoembolization)
• Postcolonoscopy 
Cardiovascular/Pulmonary
• Chronic obstructive pulmonary disease
• Atrial fibrillation
• Hypertension 
Metabolic/Rheumatoid
• Diabetes mellitus
• Dyslipidemia
• Systemic lupus erythematosus
• Rheumatoid arthritis 
Miscellaneous
• Hypercoagulable states
• Sickle cell disease
• Long-distance running 
Drugs
• Constipation inducing drugs (opioids and nonopioids)
• Cocaine and methamphetamines
• Immunomodulatory drugs (anti-tumor necrosis factor-α, type 1 interferon-α, 
type 1 interferon-β)
• Chemotherapeutic drugs (i.e., taxanes)
• Female hormones and oral contraceptives
• Decongestants (pseudoephedrine)
• Serotoninergic (i.e., alosetron, sumatriptan)
BOX 52.2 Conditions and drugs 
associated with ischemic colitis.
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1362 SECTION X Abdomen
that can induce cancer formation) and loss of several genes that 
act as tumor suppressors. Currently, it is thought that the ma-
jority of sporadic CRC arise in this fashion over the course of 
approximately 10 years from a precursor dysplastic adenoma. 
The molecular events involved include early APC (adenomatous 
polyposis coli) gene mutations, subsequent activating muta-
tions in the oncogene KRAS, as well as mutations resulting in 
inactivation of the tumor suppressor gene TP53. Chromosomal 
instability refers to changes (gains or losses) in the numbers of 
chromosomes (aneuploidy) as well as subchromosomal genomic 
amplifications and loss of heterozygosity seen with this pathway 
of carcinogenesis. It is currently thought that this pathway ac-
counts for approximately 60% of patients with CRC. The second 
major pathway accounting for approximately 35% of patients 
is the CpG island methylator phenotype cancer, and then the 
mutator phenotype associated with Lynch syndrome, account-
ing for 5%. Fig. 52.52 shows the different genetic pathways or 
mechanisms for development of CRC and their overlap. This is 
a complex topic, and a detailed discussion is beyond the scope of 
this chapter. The surgeon does, however, need to know the basics 
Symptoms:
Abdominal pain, tenesmus, bright red blood per rectum, diarrhea
History: Comorbid conditions, surgical and recent procedural history, medications
Physical exam and initial laboratory evaluation: Complete blood count, blood chemistry,
arterial blood gases, serum lactate, coagulation studies
Initial treatment: Broad-spectrum antibiotics, hydration, analgesics
Peritonitis Localized tenderness
CT Oral and IV contrast
Pneumoperitoneum
pneumatosis, portal air
Apparent transmural
necrosis
Surgery
Consider resection, determine margins
using visual inspection, indocyanine
green, or fluoroscein; anastomosis vs.
Hartmann and diversion
Segmental colon thickening,
pericolonic inflammation
Endoscopy
Segmental edema, erythema
and petechial hemorrhages,
ulceration
Observation, IV fluids,
bowel rest, antibiotics
Continued symptomsRepear endoscopy/CT
Late complications
(e.g., stricture) Resolution
FIG. 52.50 Algorithm for investigation and treatment for ischemic colitis. (From Netz U, Galandiuk S. Man-
agement of ischemic colitis. In: Cameron JL, Cameron A, eds. Current Surgical Therapy. 12th ed. Philadelphia: 
Elsevier; 2017:171–176.) CT, Computed tomography; IV, intravenous.
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1363CHAPTER 52 Colon and Rectum 
A B
FIG. 52.51 Indocyanine green–based infrared angiography. (A) Colon before injection. (B) Colon after injection: 
ischemia of resection margin (blue arrow); normal perfusion of colon (yellow arrow). (From Netz U, Galandiuk S. 
Management of ischemic colitis. In: Cameron JL, Cameron A, eds. Current Surgical Therapy. 12th ed. Philadelphia: 
Elsevier; 2017:171–176.)
FAP-associated carcinoma
CIMP-MSS –1%
Suppressor (chromosomal
instability) pathway Familial
adenomatous
polyposis CIMP+MSS
pathway
CIMP+MSS
carcinoma –20%
Serrated
(CIMP+)
pathway
Mutator
(microsatellite
instability)
pathway
Lynch syndrome carcinoma
CIMP-MSI-H –5%
Sporadic CIMP-MSS
carcinoma –60%
Conventional adenoma-
carcinoma sequence
TSA
pathway
MYH pathway
Sporadic CIMP+MSI-H
carcinoma –13%
TSA-associated
carcinoma (?CIMP+
MSI-L) –1%
FIG. 52.52 Schematic represents several overlapping ways to describe the development of colorectal car-
cinoma. The red circles represent mechanisms based on suppressor and mutator pathways. The blue circles 
represent mechanisms based on the precursor lesion (the conventional adenoma-carcinoma sequence and ser-
rated pathways). The yellow circles represent poorly characterized pathways. (From Snover DC. Update on the 
serrated pathway to colorectal carcinoma. Hum Pathol. 2011;42:1–10.) CIMP-, CpG island methylator phenotype 
negative; CIMP+, CpG island methylator phenotype positive; FAP, familial adenomatous polyposis; MSI-H, high 
degree of microsatellite instability; MSI-L, low degree of microsatellite instability; MSS, microsatellite stable; 
TSA, traditional serrated adenoma. 
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1364 SECTION X Abdomen
regarding these pathways. Fig. 52.53 provides a summary of the 
different molecular subtypes of cancer, their frequency, and com-
mon genetic mutations. 
CpG Island Methylator Phenotype
The most common initiating mutation in this CpG island meth-
ylator phenotype pathway involves a mutation of the BRAF gene 
resulting in inhibition of normal colon cell apoptosis. This in turn 
leads to the development of hyperplastic or sessile serrated adeno-
mas or polyps, which are prone to epigenetic silencing of genes 
within “CpG islands” in promoter regions by hypermethylation. 
A CpG island merely refers to a short segment of DNA with a cy-
tosine and guanine content. The hMLH1 gene (one of the DNA 
repair genes involved in Lynch syndrome) is one of the best char-
acterized genes that undergoes this type of epigenetic silencing by 
CpG hypermethylation. This will, in turn, result in a microsatel-
lite instable-high (MSI-H) cancer if there is further gene muta-
tion or methylation. As a consequence of this, most cancers arising 
from sessile serrated adenomas will have a MSI-H phenotype and 
are often located in the right colon. 
Microsatellite Instability Mutator Pathway
The microsatellite instability (MSI) pathway is thought to be in-
volved in up to 15% of early-stage CRCs. This is due to a muta-
tion in genes that are responsible for repairing base mismatches in 
DNA. These genes include mutL homologue 1 (MLH1), MLH3,mutS homologue 2 (MSH2), MSH3, MSH6, or PMS1 homo-
logue 2 (PMS2).30 When mutations in these genes are present, 
mistakes that occur during DNA replication lead to mismatches 
between DNA base pairs that are not repaired and accumulate 
further, leading to a progressive accumulation of mutations (mi-
crosatellites). Microsatellites refer to normally occurring repeated 
sequences of one to six DNA base pairs. These associated cancers 
will be MSI-H and are often characterized by location in the prox-
imal colon, large local tumor, typical absence of metastatic disease, 
and poor tumor differentiation. When this occurs in patients with 
sporadic cancer, they are often elderly; when this occurs in the 
hereditary form (i.e., Lynch syndrome), patients are often younger 
(or-
ange box). These changes in gene expression result in cellular changes that include the disassembly of epithelial 
cell-cell junctions and the dissolution of apical-basal cell polarity via repression of crumbs, PALS1-associated 
tight junction protein (PATJ) and lethal giant larvae (LGL), which are proteins that specifically regulate tight junc-
tion formation and apical-basal polarity. This progressive loss of epithelial features is accompanied by acquisition 
of a partial set of mesenchymal features with retention of certain epithelial features; in certain circumstances, 
a complete set of mesenchymal features may be acquired. Mesenchymal cells display front-to-back polarity 
and an extensively reorganized cytoskeleton and express a distinct set of molecules and EMT-TFs that promote 
and maintain the mesenchymal state. During EMT, cells become motile and acquire invasive capacities. EMT 
is a reversible process, and mesenchymal cells can revert to the epithelial state by undergoing mesenchymal-
epithelial transition (MET). EMT and MET occur during normal development and during cancer progression. 
It should be noted, however, that carcinoma cells in spontaneously arising tumors only very rarely advance into 
a completely mesenchymal state. (From Dongre A, Weinberg RA. New insights into the mechanisms of epi-
thelial-mesenchymal transition and implications for cancer. Nat Rev Mol Cell Biol. 2019;20:69–84.) E-cadherin, 
Epithelial cadherin; MMP, matrix metalloproteinase; N-cadherin, neural cadherin.
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1366 SECTION X Abdomen
found in diseased colons otherwise at risk for cancer (e.g., in 
IBD) and must be differentiated from neoplastic lesions.
Hamartomas are uncommon polyps found in the GI tract. 
They can be sporadic, but are commonly related to a genetic 
syndrome such as Peutz-Jeghers syndrome (PJS), juvenile 
polyposis syndrome, and PTEN hamartoma syndrome. 
They do not have an intrinsic malignant potential. Removal 
is indicated for obstructive symptoms or bleeding. 
Serrated Polyps
Serrated polyps can be divided into three types: hyperplastic pol-
yps (which are not considered precancerous), sessile serrated pol-
yps, and traditional serrated adenomas. Sessile serrated polyps and 
traditional serrated adenomas are combinations of adenomatous 
and hyperplastic polyps, sharing features of both types including 
colonic crypts with a saw-tooth serrated configuration and nuclear 
atypia (Fig. 52.58). Patients with sessile serrated polyps and tra-
ditional serrated adenomas are recognized as having an increased 
Genomic
MSI CMS1 Highly
immunogenic
C
an
ce
r-
as
so
ci
at
ed
 fi
br
ob
la
st
sImmune activation
JAK-STAT activation
Caspases
DNA damage repair
Glutaminolysis
Lipidogenesis
Cell cycle
WNT targets
MYC activation
EGFR or SRC activation
VEGF or VEGFR activation
Integrins activation
TGFβ activation
Mesenchymal transition
Complement activation
Immunosuppression
CMS3
CMS2
CMS4
CIN
M
ut
at
io
n 
co
un
t
M
et
hy
la
tio
n
C
op
y 
nu
m
be
r
Epigenomic Transcriptomic pathways Stroma-immune microenvironment Driver genes Clinical
Poorly
immunogenic
(I
m
m
un
e 
re
sp
on
se
)
A
da
pt
iv
e
R
A
S
 a
nd
 B
R
A
F
 m
ut
at
io
ns
In
na
te
(T
um
ou
r 
lo
ca
tio
n)
P
ro
xi
m
al
D
is
ta
l
Inflamed
(immune-
tolerant)
FIG. 52.55 Schematic representation of colorectal cancer (CRC) subtypes. Microsatellite instability (MSI) is 
linked to hypermutation, hypermethylation, immune infiltration, activation of RAS, BRAF mutations, and loca-
tions in the proximal colon. Tumors with chromosomal instability (CIN) are more heterogeneous at the gene-
expression level, showing a spectrum of pathway activation ranging from epithelial canonical (consensus mo-
lecular subtype 2 [CMS2] ) to mesenchymal (CMS4). Tumors with CIN are mainly diagnosed in left colon or 
rectum, and their microenvironment is either poorly immunogenic or inflamed, with marked stromal infiltration. 
A subset of CRC tumors enriched for RAS mutations has strong metabolic adaptation (CMS3) and intermediate 
levels of mutation, methylation and copy number events. (From Dienstmann R, Vermeulen L, Guinney J, et al. 
Consensus molecular subtypes and the evolution of precision medicine in colorectal cancer. Nat Rev Cancer. 
2017;17:79–92.) EGFR, Epidermal growth factor receptor; JAK, Janus kinase; SRC, steroid receptor coactiva-
tor; STAT, signal transducer and activator of transcription; TGFβ, transforming growth factor-β; VEGF, vascular 
endothelial growth factor; VEGFR, VEGF receptor.
FIG. 52.56 Colonoscopic view of pedunculated polyp with a long nar-
row stalk (arrow showing stalk).
FIG. 52.57 Colonoscopic view of sessile polyp in colon.
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1367CHAPTER 52 Colon and Rectum 
risk of CRC.32 The development of CRC in these patients usually 
follows the serrated neoplasia pathway in contrast to the classic 
adenoma–carcinoma pathway seen in adenomatous polyps. These 
polyps should be removed, and patients should be followed with 
serial endoscopy. 
Neoplastic Polyps
All adenomas have a malignant potential. Tubular adenomas 
are characterized by branched tubular glands on histology (Fig. 
52.59). Villous adenomas have long fingerlike projections of the 
surface epithelium (Fig. 52.60). Tubulovillous adenomas have ele-
ments of both types. The most common type are tubular adeno-
mas, comprising 65% to 80% of polyps removed, and they are 
frequently pedunculated. Approximately 5% to 10% are villous 
adenomas and 10% to 25% are tubulovillous adenomas. Villous 
adenomas are commonly sessile. The risk of malignancy increases 
dependent on the size (large), gross shape (sessile), histologic type 
(villous), and grade of dysplasia. Patients with an advanced ad-
enoma defined as size at least 1 cm, high-grade dysplasia, or tubu-
lovillous or villous histology are at a significantly increased risk of 
developing CRC.33 For example, there is less than a 5% incidence 
of carcinoma in a tubular adenoma smaller than 1 cm, whereas 
there is a 50% chance that a villous adenoma larger than 2 cm will 
contain a cancer.
Adenomatous polyps that are discovered during colonoscopy 
should be excised. A variety of techniques are employed for endo-
scopic removal of polyps, such as forceps and snares. Pedunculated 
polyps are commonly removed using cold or hot snare polypec-
tomy. Sessile polyps are frequently elevated from the underlying 
muscularis by injection of saline and then excised using an as-
sortment of techniques. Sessile polyps with a central depression 
that do not elevate adequately with saline injection (nonlifting 
sign) are at increased risk for perforation with endoscopic remov-
al and at higher risk of harboring neoplasia and are commonly 
referred for surgical removal by segmental colectomy. Large pol-
yps that cannot be removed endoscopically are also referred for 
surgery. Larger polyps can also be removed endoscopically using 
techniques such as endoscopic mucosal resection and endoscopic 
submucosal resection. 
Malignant Polyps
Malignant polyps are those in which histologic examination 
following removal of a polyp reveals a focus of carcinoma that 
has invaded through the muscularis mucosa. The question that 
arises is whether complete endoscopic removal of these polyps 
is sufficient. Carcinomas that do not pass the muscularis mu-
cosa are considered “carcinoma in situ” and do not carry meta-
static risk. However, those that invade the muscularis mucosa 
harbor asignificant risk of local recurrence and lymph node 
metastasis. One of the important risk factors is the depth of 
penetration. This can be defined by the Haggitt classification 
(Fig. 52.61):
Level 0: Carcinoma limited to the mucosa, carcinoma in situ.
Level 1: Carcinoma invading into the submucosa, limited to the 
head of the polyp.
Level 2: Carcinoma invading to the level of the neck (junction of 
the head and stalk).
Level 3: Carcinoma invading any part of the stalk.
A
B
FIG. 52.58 (A) Histology of sessile serrated adenoma. (B) Histology of 
sessile serrated adenoma (high-power view). (Courtesy of Dr. Benzion 
Samueli, Department of Pathology, Soroka University Medical Center, 
Be’er Sheva, Israel.)
FIG. 52.59 Histology of tubular adenoma. (Courtesy of Dr. Benzion 
Samueli, Department of Pathology, Soroka University Medical Center, 
Be’er Sheva, Israel.)
FIG. 52.60 Histology of a villous adenoma. (Courtesy of Dr. Benzion 
Samueli, Department of Pathology, Soroka University Medical Center, 
Be’er Sheva, Israel.)
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1368 SECTION X Abdomen
Level 4: Carcinoma invading into the submucosa of the colon 
wall, below the level of the stalk, but above the muscularis 
propria.
Sessile polyps in which invasion of the muscularis mucosa is 
seen are by definition Haggit level 4. For these, the Kikuchi clas-
sification34 can be used, in which Sm1 describes invasion into the 
upper third of the submucosa; Sm2, into the middle third; and 
Sm3, penetration into the lower third.
Malignant polyps are commonly referred for completion colec-
tomy in cases of pedunculated Haggitt level 4, sessile Kikuchi level 
Sm2 and Sm3, histologic poor differentiation, lymphovascular 
invasion, and incomplete removal or close resection margins. In 
these cases, the risk of residual cancer and lymph node metastasis 
is higher than 10%. 
Postpolypectomy Surveillance
The finding of adenomas in colonoscopy is considered a risk factor 
for future development of additional polyps. Table 52.6 depicts 
current recommendations for repeat colonoscopy following endo-
scopic removal of polyps. 
Hereditary Cancer Syndromes
CRC is the third most common cancer in men and women in the 
United States. In approximately 20% to 30% of cases, these CRCs 
are associated with a family history of colorectal polyps or cancer, 
but only 3% to 5% of cases are associated with an identifiable in-
herited CRC syndrome such as Lynch syndrome, familial adeno-
matous polyposis (FAP), mutY Homolog (MUTYH)-associated 
polyposis (MAP), juvenile polyposis or PJS (Table 52.7). Timely 
identification of individuals at risk for hereditary CRC syndromes 
offers an opportunity to intervene to prevent the development 
of cancer. The reader is referred to the ASCRS Clinical Practice 
Guidelines for the Management of Inherited Polyposis Syndromes 
and for the Surgical Treatment of Patients with Lynch Syndrome. 
Familial Adenomatous Polyposis
FAP is an autosomal dominant inherited disease that occurs in 
approximately 1:10,000 live births and affects genders and races 
equally. FAP is a syndrome caused by germline mutation in the 
APC tumor suppressor gene which is responsible for regulation of 
β-catenin and located on chromosome 5q21. Depending on the 
location of the APC mutation, the affected individuals can have a 
range of disease severity. Severe FAP is characterized by thousands 
of colorectal adenomas. Classical polyposis is described as having 
between 100 and 1000 colorectal adenomas (Fig. 52.62). Patients 
with fewer than 100 adenomas are considered to have attenuated 
FAP (AFAP). Germline mutations in the APC gene are found in 
80% to 90% of patients with classic FAP and in 10% to 30% of 
patients with AFAP. About 25% of patients with FAP have a de 
novo mutation and thus have no family history. For individuals 
with the classic phenotype, the lifetime risk for CRC may exceed 
90%, nearly 100% in the absence of treatment. If left untreated, 
patients with FAP develop CRC at an average age of 39 years 
(range 35–43 years).35
Clinically, FAP is characterized by early development of a wide 
range of colorectal adenomatous polyps after the second decade of 
life and many extracolonic manifestations. Patients with FAP may 
be asymptomatic or may present with bleeding, diarrhea, abdomi-
nal pain, or mucous discharge per rectum. Other symptoms such 
as anemia, obstruction, or weight loss usually occur as polyps grow 
larger in size or number and may foreshadow the presence of cancer. 
A variety of benign and malignant extracolonic manifestations have 
been described in FAP. These include gastroduodenal adenomas and 
carcinoma, desmoids, osteomas, epidermoid cysts, papillary thyroid 
Adenocarcinoma
Adenomatous
epithelium
Normal colonic
mucosa
Muscularis
mucosae
Adenocarcinoma
Submucosa
Muscularis
Subserosal connective tissue
Submucosa
Muscularis
Subserosal connective tissue
Sessile adenoma
Level 0
Level 1
Level 2
Level 3
Level 4
Pedunculated adenoma
propriapropria
FIG. 52.61 Haggitt classification. Anatomic landmarks of pedunculated and sessile adenomas. (From Haggitt 
RC, Glotzbach RE, Soffer EE, et al. Prognostic factors in colorectal carcinoma arising in adenomas: implications 
for lesions removed by endoscopic polypectomy. Gastroenterology. 1985;89:328–336.)
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1369CHAPTER 52 Colon and Rectum 
carcinoma, small bowel polyps and carcinoma, congenital hyperpla-
sia of the retinal pigment epithelium (CHRPE), and dental anoma-
lies.
Nonneoplastic gastric fundic gland polyps are a common find-
ing in about 50% of patients. Gastric adenomas are present in 
about 10% of patients with FAP, usually in the antrum. The risk 
of gastric cancer is low. Duodenal adenomas occur in 30% to 70% 
of patients with FAP, and there is a predilection for the ampullary 
and periampullary regions. The lifetime risk for duodenal cancer is 
4% to 10%, constituting the second most common cause of death 
in FAP patients. The Spigelman classification is used to grade the 
severity of and guide the clinical management of duodenal pol-
yposis (Table 52.8). Adenomas can occur rarely in the gallblad-
der, bile duct, and the small bowel, particularly the distal ileum. 
Most patients are eligible for chemoprevention for adenomas with 
NSAIDs (e.g., sulindac or celecoxib) after surgery, but this seems 
less effective than in the colorectum.35
Desmoid tumors are histologically benign but locally invasive 
monoclonal proliferations of fibroblasts. They are only occasion-
ally seen in the general population but affect 10% to 15% of all 
patients with FAP. These tumors are associated with female gender 
and with a family history of desmoids. About half of FAP-asso-
ciated desmoid tumors arise intraabdominally in the bowel mes-
entery and 40% develop in the abdominal wall. The remainder 
present in the back, neck, and limbs. Desmoids can manifest as 
flat, fibrous, sheet-like lesions or as defined discrete masses. This 
may result in pain, bowel or ureteral obstruction, vascular compro-
mise, and perioperative complications. Desmoid tumors, together 
TABLE 52.6 Recommendations for repeat colonoscopy following endoscopic removal 
of polyps.
INDEX COLONOSCOPY FINDINGS REPEAT COLONOSCOPY
Small (Transverse colon Superior taenia
Tail of pancreas
Splenic flexure
Left kidney
Descending colon
Anterior taenia (libera)
Left iliac crest
Sigmoid colon
Rectum
FIG. 52.4 The large bowel includes the colon, consisting of ascending, transverse, descending, and sigmoid 
colon and the rectum, shown here in relation to neighboring anatomic structures. (From Standring S, Anand N, 
Rolfe B, et al. Gray’s Anatomy. 41st ed. Philadelphia: Elsevier; 2016.)
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1324 SECTION X Abdomen
Ileocolic artery
Colic branch
Ileal branch
Superior mesenteric artery
Posterior cecal artery
Appendicular artery
Anterior cecal artery
Vascular fold of cecum
Superior ileocecal recess
Ileocecal fold (bloodless fold of Treves) 
Terminal part of ileum
Inferior ileocecal recess
Mesoappendix
Appendicular artery
Freetaenia
(taenia libera) 
External iliac vessels
(retroperitoneal)
Retrocecal recess
Cecal folds
Right paracolic gutter Appendicular artery
Mesocolic taeniaOmental taenia
Posterior cecal artery
Cecal folds
Retrocecal recess
Attached
area
Lines of
posterior
peritoneal
reflection
Lines of
posterior
peritoneal
reflection
Lines of
posterior
peritoneal
reflection
Lines of
posterior
peritoneal
reflection
Attached
area
Attached
area
Attached
area 
Some variations in posterior peritoneal attachment of cecum
Cecum
Vermiform appendix
FIG. 52.5 The appendix and mesoappendix in relation to the cecum and surrounding structures. (From Netter 
FH. Atlas of Human Anatomy. Philadelphia: Elsevier; 2019.)
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1325CHAPTER 52 Colon and Rectum 
The descending colon begins at the splenic flexure where the 
intestine loses its mesentery and extends downward on the left 
side of the abdomen approximately 25 cm until it transitions into 
the sigmoid colon. It is smaller in diameter than the ascending 
colon. The descending colon is similar to the ascending colon with 
regard to its peritoneal coverage and approach to dissection.
The sigmoid colon begins at or below the level of the iliac 
crest, where the colon becomes completely intraperitoneal again, 
acquiring a mesentery covered on both sides with peritoneum. 
The sigmoid is thicker and more mobile compared to the de-
scending colon varying in length from 15 to 50 cm (average, 38 
cm). The mobile portion of the sigmoid colon is attached by the 
sigmoid mesocolon to the posterior abdominal wall and pelvis in 
the pattern of an inverted V creating the intersigmoid fossa (Fig. 
52.7). When mobilizing the sigmoid colon, this mesenteric fold 
is a surgical landmark for the underlying left ureter. The sigmoid 
colon ends at the rectosigmoid junction, which is recognized as 
the point where the colonic taeniae confluence to form a complete 
longitudinal muscle layer, and the colon loses its mesentery, usual-
ly between the level of the sacral promontory and the S3 vertebra.
Blood Supply, Lymphatic Drainage, and Innervation of the 
Colon
Arterial blood supply. The anatomy of the blood supply is in 
accordance with the embryologic development of the GI tract. 
The celiac artery supplies the foregut, the SMA the midgut, and 
the IMA the hindgut. The colon receives its blood supply from 
the SMA and the IMA, both anterior branches of the abdominal 
aorta (Fig. 52.8).
The SMA is the second unpaired anterior branch of the aorta, 
arising at the level of the lower border of the L1 vertebra, it de-
scends posterior to the pancreas and then crosses anteriorly to the 
uncinate process of the pancreas and the third part of the duode-
num and enters the mesentery of the bowel. On the left side, it 
provides up to 20 branches to the small intestine. On the right, 
it gives off three major branches to the colon. The first branch 
is the middle colic artery, arising near the inferior border of the 
pancreas, followed by the right colic and ileocolic arteries. The 
ileocolic artery is the most constant of these arteries. It runs to-
ward the ileocecal junction within the mesentery giving off the 
anterior and posterior cecal arteries and the appendicular artery, 
supplying the terminal ileum, cecum, and appendix. The avascular 
space between the SMA and the ileocolic artery is a safe region to 
begin vascular dissection in a minimally invasive right colectomy 
and can also be used as a space through which one can pull the 
transverse or right colon through in cases of “retroileal” colorectal 
anastomoses to gain bowel length. The right colic artery, absent 
in up to 20%, usually arises from the SMA but may be a branch 
of the ileocolic or left colic vessels. The middle colic artery enters 
the transverse mesocolon and divides into right and left branches, 
which supply the proximal and distal transverse colon, respective-
ly. When lifting the transverse colon, the middle colic artery can 
be tracked to the base of the mesentery just to the right of the 
ligament of Treitz, and into the proximal SMA. The middle colic 
artery is the main blood supply to the splenic flexure in about a 
third of the cases.
The IMA is the third unpaired anterior artery arising from 
the aorta at the level of the L2–3 vertebrae approximately 3 cm 
above the aortic bifurcation. The IMA descends inferiorly and to 
the left giving off the left colic artery, followed by several sigmoid 
branches, and culminating in the superior rectal (hemorrhoidal) 
artery. The left colic artery divides into an ascending branch to the 
splenic flexure and a descending branch to the descending colon.
The marginal artery of Drummond runs along the mes-
enteric margin of the colon from the cecocolic junction to the 
Greater
omentum
Descending
colon
Parietal
peritoneum
Splenocolic
ligament
Spleen
Kidney
Pancreas
Pancreaticocolic
ligament
Vertebra
FIG. 52.6 Ligaments of the splenic flexure; the arrow indicates poten-
tial plane of dissection. (From Netz U, Galandiuk S. Clinical anatomy for 
procedures involving the small bowel, colon, rectum and anus. In: Fischer 
JE, Ellison EC, Upchurgh Jr. GR, et al., eds. Fischer’s Mastery of Surgery. 
7th ed. Philadelphia: Wolter Kluwer; 2019.)
Sigmoid
colon
Descending
colon
Intersigmoid recess External iliac arteryUreter
FIG. 52.7 The intersigmoid recess, the sigmoid colon being retracted 
upward and to the right. (From Hollinshead WH. Anatomy for Surgeons. 
Vol 2, 2nd ed. New York: Harper and Row; 1971.)
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1326 SECTION X Abdomen
rectosigmoid junction. Vasa recta from this artery branch off at 
short intervals and supply the bowel wall directly. The marginal 
artery is important clinically for when one of the larger arteries 
is obstructed (emboli, atherosclerosis, surgical ligation, etc.). The 
colon can receive collateral blood supply through this artery.
The meandering mesenteric artery, or “arc of Riolan,” is an un-
common finding described as a thick tortuous collateral vessel that 
runs close to the base of the mesentery and connects the SMA 
or middle colic artery to the IMA or left colic artery. It can have 
an important role in blood delivery in cases of SMA or IMA oc-
clusion. Flow can be forward (IMA stenosis) or retrograde (SMA 
stenosis), depending on the site of obstruction. The presence of a 
large arc of Riolan suggests occlusion of one of the major mesen-size ≥10 mm or ≥3 polyps
3 years
Piecemeal removal of polyp 6 months
Sessile serrated polyp 10 mm or with dysplasia or traditional serrated adenoma 3 years
Adapted from Hassan C, Quintero E, Dumonceau JM, et al. Post-polypectomy colonoscopy surveillance: European Society of Gastrointestinal 
Endoscopy (ESGE) guideline. Endoscopy. 2013;45:842–851, and Lieberman DA, Rex DK, Winawer SJ, et al. Guidelines for colonoscopy 
surveillance after screening and polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer. Gastroenterology. 
2012;143:844–857.
AGA, American Gastroenterological Association; ESGE, European Society of Gastrointestinal Endoscopy.
TABLE 52.7 Inherited colorectal cancer syndromes.
SYNDROME GENES POLYP TYPE INHERITANCE CLINICAL FINDINGS CRC RISK
Classical FAP APC Adenoma AD 100–1000 adenomas; duodenal adenomas and 
carcinomas; gastric fundic gland polyps, desmoid 
tumors, epidermoid cysts, osteomas
100%
Severe FAP APC Adenoma AD >1000 adenomas 100%
Attenuated FAP APC Adenoma AD 20
Histology Tubular Tubulovillous Villous
Dysplasia Mild Moderate Severe
From Spigelman AD, Williams CB, Talbot IC, et al. Upper gastrointestinal cancer in patients with familial adenomatous polyposis. Lancet. 
1989;2:783–785.
Stage 0 = 0 points; stage I = 1–4 points; stage II = 5–6 points; stage III = 7–8 points; stage IV= 9–12 points. Stage 0. Repeat endoscopy in 5 
years. Stage I. Repeat endoscopy in 5 years. Stage II. Repeat endoscopy in 2–3 years. Stage III. Repeat endoscopy in 6–12 months and surgical 
evaluation. Stage IV. Repeat endoscopy in 6–12 months and surgical evaluation.
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1371CHAPTER 52 Colon and Rectum 
Patients withrectal cancer, a large polyp burden (>20 syn-
chronous adenomas, adenoma with high-grade dysplasia, 
large (>30 mm) adenomas), or a severe familial phenotype 
(>1000 synchronous adenomas) should undergo IPAA. 
This operation is also the treatment of choice for patients 
with a large number of rectal adenomas, but the optimal 
timing of surgery should be individualized. IPAA should 
be performed with removal of the anal transitional zone 
by mucosectomy and a handsewn anastomosis or retaining 
some of the anal transitional zone with a stapled anasto-
mosis. The choice of which is best to perform has been 
debated. The benefits of a stapled anastomosis include bet-
ter function (less risk of incontinence) and fewer compli-
cations. A stapled IPAA is also easier to survey, and anal 
transitional zone adenomas may possibly be treated endo-
scopically or transanally. The benefit of a handsewn IPAA 
is a reduced incidence of anal transitional zone adenomas, 
but this is achieved at a potential cost of worse function. 
This procedure can be performed with or without a divert-
ing ileostomy. A temporary diverting ileostomy proximal 
to the pouch has been classically performed in order to 
mitigate the effects of anastomotic leakage and to prevent 
pelvic sepsis (reported in as low as 6% and as high as 37%, 
respectively), fistulization, and thus compromised pouch 
function. Consequently, it should also prevent the need 
for relaparotomy. Ileostomy omission has been advocated 
in selected cases. The benefits of laparoscopy can be ap-
plied in this surgery, but in the literature, there is no evi-
dence that this approach is better than the open approach. 
IPAA should be performed only in specialized centers and 
by skilled and experienced surgical teams.
	•	 	Subtotal colectomy and IRA provide good surgical and func-
tional outcomes but require long-term follow-up of the re-
tained rectum. The risk of metachronous rectal cancer is on the 
order of 30%. IRA is generally recommended for patients with 
few rectal polyps, AFAP, and a family history of a mild pheno-
type and for those young women with desire to become preg-
nant after recommendations of genetic counseling. IRA should 
not be performed in patients with a severely diseased rectum 
(adenomas >3 cm diameter, adenomas with severe dysplasia, 
cancer, sphincter dysfunction, or a rectum containing more 
than 20 rectal adenomas) or in the presence of colon cancer. 
IRA may provide good results in AFAP, MAP, and mild FAP 
patients who agree to undergo close follow-up, and procto-
colectomy and IPAA should be reserved for those with profuse 
polyposis.
	•	 	Proctocolectomy with end ileostomy is currently rarely per-
formed as a permanent stoma and is usually unacceptable to 
young patients. However, this option still has a role in the treat-
ment of very low rectal cancer, when sphincter preservation is 
not possible, in cases of malignant transformation after IPAA or 
ileal pouch failure or in cases in which there is poor sphincter 
function.
Most patients are eligible for chemoprevention after surgery be-
cause proctocolectomy with IPAA or a colectomy with IRA can 
retain “at-risk” rectal mucosa, and the duodenal mucosa remains 
“at risk” in all these patients. Chemoprevention (i.e., taking medi-
cations that slow polyp growth such as sulindac or celecoxib) 
should not replace routine endoscopic surveillance.
Regular follow-up is mandatory after any procedure. Standard 
care includes perianal digital and flexible endoscopic examination 
at yearly intervals. 
MUTYH-Associated Polyposis
MAP is an autosomal recessively inherited syndrome caused by 
germline mutation of both alleles of the MUTYH gene, located 
on chromosome 1. Because the autosomal recessive inheritance 
pattern requires that affected individuals have a biallelic mu-
tation, both parents of affected individuals must be at least 
monoallelic carriers. If so, siblings of affected individuals have 
a 25% chance of biallelic mutations. Monoallelic MUTYH 
mutations are found in 0.7% to 1% of unselected individuals 
in population-based cohorts, with biallelic mutations identi-
fied in 1.7% of unselected individuals with CRC. CRC risk 
is increased twenty-eight fold for individuals with biallelic 
 MUTYH mutations, while the risk for monoallelic carriers 
 appears to be only moderately increased.36
The colonic phenotype mimics that of AFAP. The diagnosis of 
MAP should be considered in patients presenting with colorec-
tal polyposis (>20 lifetime adenomas). Although most polyps in 
MAP are adenomas, patients can present with serrated polyps or a 
mixture of adenomas and serrated polyps. Bleeding or obstruction 
may occur, but the disease is suspected on findings from a screen-
ing colonoscopy. The syndrome is primarily characterized by 
multiple colorectal adenomas and an increased risk for CRC at a 
younger age (40–50 years of age). The colorectal polyp phenotype 
TABLE 52.9 Timing of surgery in patients with familial polyposis.
REASONS TO INDICATE OR POSTPONE SURGERY TIMING FOR SURGERY
Presence of symptoms (> risk of CRC) As soon as possible
Asymptomatic patient with mild disease Discuss opportunity (before 20 years?)
CRC before the age of 20 is rare
Patients diagnosed in their third decade or beyond
Sized lesions or with high-grade dysplasia, not amenable to endoscopic resection
Immediately
Severe disease at colonoscopy or by family history/genotype As soon as practicable
Attenuated polyposis at colonoscopy or by family history/genotype Personal decision (16–20 years if mild or 21–25 years if attenuated polyposis)
Preoperative diagnosis, positive family history or genetically susceptible for 
desmoids
Delay surgery (after evaluating CRC risk)
Delaying surgery in women with a low polyp burden who wish to have children. Reasonable to delay surgery as long as the patient remains in a strict 
surveillance program
From Campos FG: Surgical treatment of familial adenomatous polyposis: Dilemmas and current recommendations. World J Gastroenterol. 
2014;20:16620–16629.
CRC, Colorectal cancer.
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1372 SECTION X Abdomen
is highly variable usually with moderate polyposis (most commonly 
in the small bowel, followed by the colon, stomach, and rectum 
in decreasing frequency. PJS patients have a 90% lifetime risk of 
cancer, including colorectal (most common), gastric, pancreatic, 
lung, breast, uterine, cervical, testicular, and ovarian.
PJS is caused by a mutation of the STK11/LKB1 gene located 
on chromosome 19p. Approximately half of PJS cases are inher-
ited from a parent; the remainder occur in patients with no family 
history and appear to result from a spontaneous mutation.
Polyps differ histologically from juvenile polyps in that they 
arise due to an overgrowth of the muscularis mucosa rather than 
the lamina propria.
PJS is a clinical diagnosis based on any one of the following 
World Health Organization criteria: (1) three or more histologi-
cally confirmed Peutz-Jeghers polyps; (2) any number of PJ polyps 
with a family history of PJS; (3) characteristic, prominent, muco-
cutaneous pigmentation with a family history of PJS; or (4) any 
number of Peutz-Jeghers polyps and characteristic prominent, 
mucocutaneous pigmentation.
PJS patients require special surveillance that includes multiple 
organs, as it is associated with an increased risk of cancer in many 
organs (small bowel, stomach, pancreas, colon, esophagus, ovary, 
lung, uterus, breast, testes, and others). Screening begins at 8 to 10 
years of age with an evaluation of the small bowel. If initial exam is 
normal, a repeat evaluation is recommended at the age of 18 and 
then at 2- to 3-year intervals. Males should undergo annual tes-
ticular physical examination starting at age 10 years, and females 
should undergo an annual pelvic examination and Papanicolaou 
stain starting at age 18 to 20 years. Women should have breast 
physical examinations every 6 months and yearly mammogram 
and breast MRI starting at age 25 years. Colonoscopy and upper 
endoscopy should start in the late teens and be repeated every 
2 to 3 years for both genders. Pancreatic cancer screening involves 
endoscopic ultrasound or magnetic resonance cholangiopancrea-
tography along with serum CA19-9 every 1 to 2 years starting at 
age 25 to 30 years.
Polypectomy plays a key role in the management of PJS. 
 Asymptomatic gastric or colonic polyps larger than 1 cm should be 
removed endoscopically. Small bowel polyps larger than 1 to 1.5 
cm or those that are have grown rapidly should be removed to de-
crease future complications such as bleeding and intussusception.
Surgery is most commonly reserved for symptoms, the most 
common being obstruction (caused by intussusception) and 
bleeding in the small bowel. The goal of surgery is to remove the 
affected segment, preserving as much bowel as possible. Interven-
tion may require push enteroscopy or combined laparoscopy/
laparotomy with endoscopy in the operating room as these small 
bowel polyps may not be visualized by other means.36 
Juvenile Polyposis Syndrome
Juvenile polyposis syndrome is an inherited autosomal-dominant 
pattern and is characterized by the development of hamartomatous 
intestinal polyps. Patients with JPS exhibit a 10% to 38% lifetime 
risk of colon cancer, and the average age at diagnosis is 34 years. 
JPS is clinically diagnosed when there are five or more juvenile 
polyps in the colorectum, multiple juvenile polyps throughout the 
GI tract, any number or juvenile polyps with a family history, or 
juvenile polyposis. Symptoms are related to the polyps and most 
commonly include acute or chronic GI bleeding, iron-deficiency 
anemia, prolapsed rectal polyps, abdominal pain, or diarrhea.
Two genes, SMAD4 (chromosome 18q) and BMPR1A (chro-
mosome 10q), have been linked to JPS. However, a pathogenic 
mutation in one of these two genes is detected in only 40%–50% 
of patients with JPS. There is an increased cancer risk in afflicted 
individuals, with a malignant potential of at least 10% in patients 
with multiple juvenile polyps.
Screening by colonoscopy should begin between the ages of 12 
to 15 years. The interval between colonoscopies depends on exam 
findings. If there are no polyps, colonoscopy should be repeated in 
2 to 3 years. When polyps are present and removed, colonoscopy 
should be done annually.
Surgical indications include the presence of high-grade dyspla-
sia or cancer or if the polyp burden cannot be effectively man-
aged endoscopically. Prophylactic colectomy may be considered 
for patients with poor surveillance compliance or in patients with 
family history of CRC. For colorectal disease, surgical options in-
clude subtotal colectomy and IRA, segmental colectomy or total 
colectomy, and IPAA.36 
Lynch Syndrome
Lynch syndrome was previously used as a synonym for heredi-
tary nonpolyposis CRC (HNPCC) but it was felt that the term 
“HNPCC” was a misnomer because patients can develop many 
non-CRCs, as well as one or more polyps or adenomas. This syn-
drome accounts for 3% to 5% of all CRCs and 10% to 19% of 
CRCs diagnosed before age 50. It is an autosomal dominantly in-
herited syndrome characterized by a mutation in one of the DNA 
mismatch repair (MMR) genes (MLH1, MSH2, MSH6, PMS2, 
EpCAM).These genes maintain fidelity of the DNA during repli-
cation by correction of nucleotide base mispairs and small inser-
tions or deletions generated by misincorporations or slippage of 
DNA polymerase during DNA replication. Mutations in MLH1 
and MSH2 account for up to 90% of patients with Lynch syn-
drome. Because of this genetic defect, Lynch syndrome tumors are 
characterized by MSI, in which ubiquitous mutations at simple 
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1373CHAPTER 52 Colon and Rectum 
repetitive sequences (microsatellites) are found in the tumor DNA 
(but not in the DNA of adjacent normal colorectal mucosa) of 
individuals with MMR gene defects. Microsatellites are noncod-
ing segments of DNA that contain repetitive sequences of one to 
six nucleotides. There are hundreds of thousands of microsatellites 
in the genome, and microsatellite patterns provide a unique DNA 
fingerprint. When these errors are not repaired due to MMR defi-
ciency, the length of the microsatellite regions are altered and the 
fingerprint changes. MSI is found in most (>90%) colon malig-
nancies in patients with Lynch syndrome. Immunohistochemistry 
test, using antibodies to the MMR gene proteins, evaluates for the 
loss of MMR protein expression and assists in the identification of 
patients with Lynch syndrome.
Somatic mutations in the BRAF gene are noted in 15% of spo-
radic CRCs but not in Lynch syndrome tumors. The presence of 
BRAF mutations in an MSI CRC is evidence against the presence 
of Lynch syndrome.
Lynch syndrome is characterized by an increased predisposi-
tion to the development of CRC and other tumors, which tend 
to develop at early ages. The estimated lifetime risk for CRC is 
70% for men and 40% for women. The mean age of diagnosis for 
Lynch syndrome–related CRC is 44 to 61 years, compared with 
69 years in patients with sporadic CRC. Lynch syndrome–associ-
ated CRCs show a predilection for the right colon as compared 
to sporadic CRC, but left-sided colon cancers, rectal cancers, and 
synchronous lesions at different sites of the colon and rectum are 
also common presentations. Among Lynch syndrome patients 
who have had an initial CRC treated by less than a total colectomy, 
the risk for a metachronous CRC is 16% at 10 years, 41% at 20 
years, and 62% at 30 years. Compared with patients with AFAP or 
MAP, patients with Lynch syndrome develop few colorectal ade-
nomas by the age of 50 years (usually fewer than three adenomas). 
Adenoma may progress to carcinoma within 2 to 3 years, com-
pared with from 4 to 10 years in the general population. Histolog-
ic features showing poor differentiation, mucinousor signet-ring 
cell histology, tumor-infiltrating lymphocytes, and lymphoid host 
response are common.
Endometrial adenocarcinoma is the most common extracolon-
ic cancer (lifetime risk of 32%–45%). Ovarian, gastric, small bow-
el, urinary tract, brain, and pancreas cancers are also frequently 
seen in these patients. Sebaceous adenomas and carcinomas of the 
skin, as well as keratoacanthomas, can be seen in the Muir-Torre 
variant of Lynch syndrome.36
Although germline sequencing of the MMR genes remains the 
“gold standard” for confirming the causative gene mutation for 
Lynch syndrome, patients with Lynch syndrome can be initially 
identified using Amsterdam (Box 52.3) or Bethesda (Box 52.4) 
criteria.
Screening for CRC by colonoscopy is recommended in per-
sons at risk (first-degree relatives of known MMR gene muta-
tion carriers who have not had genetic testing) or those affected 
with Lynch syndrome every 1 to 2 years, beginning at 20 to 25 
years of age or 2 to 5 years before the youngest age of diagnosis of 
CRC in the family if diagnosed before age 25 years. This may not 
be covered by insurance in all cases. For MMR germline muta-
tion–positive patients, consideration should be given to annual 
colonoscopy. For the endometrial cancer, the screening should be 
offered to women at risk for or affected with Lynch syndrome by 
pelvic examination and endometrial sampling annually starting at 
age 30 to 35 years. Similarly, screening of ovarian cancer should 
be offered beginning at the same age. Hysterectomy and bilateral 
salpingo-oophorectomy should be offered to women with Lynch 
syndrome undergoing colectomy, in all women over age 40 years 
or who have finished childbearing. Screening for gastric cancer 
should be considered in persons with Lynch syndrome by esopha-
gogastroduodenoscopy with gastric biopsy of the antrum at 30 
to 35 years, and subsequent surveillance every 2 to 3 years can 
be considered based on individual patient risk factors. Screening 
for cancer of the urinary tract should be considered for persons at 
risk for or affected with Lynch syndrome, with urinalysis annually 
starting at age 30 to 35 years.
In contrast to sporadic colon cancer, three issues must be eval-
uated when considering the appropriate surgical treatment for 
colon cancer in the setting of Lynch syndrome: (1) appropriate 
treatment of the primary tumor, (2) consideration of risk reduc-
tion with prophylactic removal of non-neoplastic colon, and (3) 
morbidity and quality of life after colectomy.
There is still no clear consensus on the surgical management 
of colon cancer. The options (partial or total colectomy) should 
be discussed with the patient, taking into account age, comor-
bidities, and cancer stage. There is no prospective randomized trial 
comparing extended resection with a limited resection. The cumu-
lative risk of metachronous CRC in patients with segmental col-
ectomy is 16% at 10 years, 41% at 20 years, and 62% at 30 years. 
However, based on currently available evidence, there is superior 
Three or more relatives with hereditary nonpolyposis colorectal cancer–asso-
ciated cancer (colorectal cancer or cancer of the endometrium, small bowel, 
ureter, or renal pelvis) plus all of the following:
 1. One affected patient is a first-degree relative of the other two.
 2. Two or more successive generations are affected.
 3. Cancer in one or more affected relatives is diagnosed before the age of 50 
years.
 4. Familial adenomatous polyposis is excluded.
 5. Pathologic diagnosis of cancer is verified.
BOX 52.3 Amsterdam II citeria.
Tumors from individuals in the following situations should be tested for MSI:
 1. Colorectal cancer diagnosed in a patient before age 50.
 2. Presence of synchronous/metachronous colorectal or other hereditary non-
polyposis colorectal cancer (HNPCC)–related tumors (including endome-
trial, stomach, ovarian, pancreas, ureter and renal pelvis, biliary tract, brain 
(usually glioblastoma), sebaceous gland adenomas and keratoacanthomas, 
and carcinoma of the small bowel), regardless of age.
 3. Colorectal cancer with the MSI histology (defined by the presence of tumor-
infiltrating lymphocytes, Crohn-like lymphocytic reaction, mucinous/signet-
ring differentiation, or medullary growth pattern) diagnosed in a patient 
before age 60.
 4. Colorectal cancer diagnosed in at least one first-degree relative with an 
HNPCC-related tumor in which one cancer was diagnosed before age 50.
 5. Colorectal cancer diagnosed in at least two first- or second-degree relatives 
with HNPCC-related tumors, regardless of age.
BOX 52.4 Bethesda criteria for testing 
colorectal tumors for microsatellite instability 
(MSI).
From Herzig DO, Buie WD, Weiser MR, et al. Clinical Practice 
Guidelines for the surgical treatment of patients with lynch syndrome. 
Dis Colon Rectum. 2017;60:137–143.
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1374 SECTION X Abdomen
cancer risk reduction with total colectomy for the treatment of co-
lon cancer in the setting of Lynch syndrome, and total abdominal 
colectomy with IRA is the preferred treatment for most patients. 
For patients with Lynch syndrome and rectal cancer, the rectal 
cancer should be treated based on standard oncologic principles, 
as in sporadic rectal cancer. The decision to remove the rest of 
the colon in patients with rectal cancer may be performed on an 
individual basis after discussion with the patient.
Consideration for less extensive surgery should be given in pa-
tients older than 60 to 65 years and those with underlying sphinc-
ter dysfunction. Annual colonoscopy should be performed after 
segmental resection of colon cancer. 
STAGING
Following a diagnosis of CRC, the local and distant spread of the 
disease is defined and the tumor’s stage is determined. Once an in-
dividual’s stage has been designated, it can be used as a framework 
for information regarding survival with or without treatment, 
chance of cure, likelihood of residual disease, and recurrence as 
well as a support tool for planning treatment type. Staging is gen-
erally performed once the diagnosis has been established.
Rules for Classification
Historical staging systems for CRC include the Dukes classifica-
tion and the modified Astler-Coller classification. Presently, the 
stage of the tumor is determined according to the tumor, node, 
metastasis (TNM) system, which assesses the depth of penetra-
tion of the tumor into the bowel wall (T stage), the extent of 
lymph node involvement (N stage), and the presence or absence 
of distant metastases (M stage). The TNM system was developed 
by the American Joint Committee on Cancer (AJCC) staging sys-
tem and approved by the International Union Against Cancer. 
This classification combines clinical information obtained pre-
operatively with data obtained during surgery and after histo-
logic examination of the specimen. There have been numerous 
and significant amendments in the classification system since its 
initial publication. The latest classification based on eighth edi-
tion of the AJCC Cancer Staging Manual is depicted in a table 
in Ref. 36a. 
Clinical Staging
Clinical staging, given the prescript c (cTNM) is based on evi-
dence obtained by medical history, physical examination, endos-
copy, and imaging. Assessment for metastatic disease is usually 
completed with CT (including pelvis, abdomen, and chest). Oth-
er modalities such as MRI, positron emission tomography (PET), 
or fused PET/CT scans are usually not used for initial staging 
but may be used in patients with contrast allergy/renal failure or 
in equivocal cases. For rectal cancer, an accurate preoperative as-
sessment of local spread is important in order to determine the 
need for preoperativeneoadjuvant therapy. Modalities to assess 
the local spread of rectal cancer usually consist of pelvic MRI or 
endorectal ultrasound for superficial tumors and when MRI is 
contraindicated or unavailable. 
Pathologic Staging
The pathologic examination of the resected specimen, given the 
prescript p (pTNM), provides additional information for progno-
sis and consideration of the need for additional (adjuvant) treat-
ment. Patients who were given neoadjuvant therapy prior to resec-
tion based on their clinical staging will have a modified pathologic 
staging indicated by the y prescript (ypTNM). Once the three 
components of the TNM have been defined, they can be grouped 
together into overall stage as shown in a table in Ref. 36a 
Additional Prognostic Factors
In addition to the classic TNM staging, the AJCC manual also 
recommends additional prognostic factors that should be deter-
mined and reported. Among these are the serum carcinoembry-
onic antigen (CEA) levels, the presence of tumor deposits within 
the lymph drainage area of a cancer, and their association with 
blood vessels and neural structures (lymphovascular and perineu-
ral invasion respectfully), all associated with a poorer prognosis. 
The histologic grade of the tumor (low grade vs. high grade) is 
determined by the pathologist, as well as specific histologic sub-
types such as mucinous and signet ring adenocarcinomas, which 
are usually more aggressive and carry a worse prognosis. The cir-
cumferential resection margin should be reported by the patholo-
gist, as well as the proximal and distal margin status and in rectal 
cancer, the completeness of the mesorectal excision. Pathologic 
response to neoadjuvant treatment is assessed on the primary tu-
mor and reported as the tumor regression grade, a four-point re-
gression grade scale from 0 (complete response) to 3 (poor or no 
response). In addition to the above, molecular markers for somatic 
and germline mutations are investigated, such as MSI, KRAS, 
BRAF, and NRAS mutations, which can help in both prognosis 
and treatment planning. 
SURGICAL TREATMENT OF COLORECTAL CANCER
The goal of curative surgical treatment of CRC is the resection of 
the primary tumor with adequate free margins, en bloc with loco 
regional lymphadenectomy. Regional lymph nodes are located in 
the mesocolon along the main vascular pedicles. Therefore, an on-
cologically adequate resection implies the removal of the portion 
of colon where the primary cancer is located with its vascular ped-
icles, which must be ligated and divided at their origin. The aim of 
lymphadenectomy is to ensure an adequate pathologic staging and 
to remove any possible residual lymph node metastasis. No less 
than 12 lymph nodes are required for an oncologically adequate 
resection and for proper staging, but, in most cases, more than 20 
nodes are retrieved from the specimen. The reader may wish to 
refer to the ASCRS Clinical Practice Guidelines for the Treatment 
of Colon Cancer and for the practice parameters for the manage-
ment of rectal cancer.
There are some anatomic vascular landmarks when performing 
a colorectal resection.
	•	 	The	 ileocolic	pedicle	originates	 from	 the	 superior	mesenteric	
vessels just caudal to the second portion of the duodenum 
(Fig. 52.63).
	•	 	The	middle	colic	vessels	originate	from	the	superior	mesenteric	
vessels at the level of the inferior margin of the pancreas.
	•	 	The	inferior	mesenteric	vein	can	be	easily	identified	at	the	level	
of the ligament of Treitz (Fig. 52.64).
	•	 	The	IMA	originates	from	the	aorta,	2	to	3	cm	caudal	from	the	
area where the IMV is identified; its origin is surrounded by 
the mesenteric and hypogastric nervous plexus (Fig. 52.65).
	•	 	The	left	colic	artery	originates	about	2	cm	distally	to	the	origin	
of the IMA.
General Rules and Principles
	•	 	Surgery	 should	 be	 gentle,	 and	 manipulation	 of	 the	 tumor	
should be avoided as much as possible (“no touch” technique).
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1375CHAPTER 52 Colon and Rectum 
	•	 	“Free”	margins	must	 be	 adequate:	 for	 colon	 cancer,	 a	 5-cm	
“free” margin is recommended in order to minimize the risk of 
recurrent cancer caused by distal spread and in order to avoid 
leaving behind perivisceral lymph nodes, which could be in-
volved with metastatic disease.
	•	 	For	 rectal	 cancer,	 a	 2-cm	 distal	 margin	 is	 sufficient:	 distal	
spread of the cancer occurs in 1% to 2% of cases when the 
distal margin is 2 cm. In ultradistal sphincter-sparing surgery 
resections, a cancer-free margin of 1 cm or, in selected cases, a 
free margin at frozen section examination can be accepted.
	•	 	In	order	to	restore	bowel	continuity,	the	anastomosis	must	be	
constructed without any tension, utilizing well-vascularized 
segments of bowel.
	•	 	The	vascular	supply	of	the	colon,	which	is	mobilized	and	uti-
lized for the anastomosis, relies on marginal vessels located in 
the mesocolon. Therefore, great care must be used during the 
manipulation of the mesocolon, as minimal injury of these ves-
sels can result in irreversible ischemic damage of the transposed 
colon. 
Surgical Technique
Colorectal resections can be approached by open access or with 
minimally invasive techniques. The latter have shown favorable 
short-term benefits when compared to standard open colecto-
mies: less postoperative pain, shorter postoperative hospital stay, 
faster recovery of bowel function, and a lower wound infection 
rate. Surgical resection quality was proven to be noninferior in 
laparoscopy also for rectal cancer resections, and local recurrence 
rate and disease-free survival (DFS) are similar after open or lapa-
roscopic resections.37 Therefore, the laparoscopic approach should 
be preferred given the availability of expertise and proven experi-
ence. During the last decade, the use of laparoscopy for colorec-
tal resections gradually increased to about 40%, with an overall 
conversion rate below 10%. The percentage varies greatly based 
on hospital setting (urban vs. rural, high volume vs. low volume) 
and the surgeon’s expertise and may be as high as 80% in high-
volume specialized institutions with a low conversion rate. Robot-
ics is the evolution of MIS: the surgeon operates while sitting at a 
Ileocolic
artery
Right colic artery
Mesenteric
artery
Duodenum
FIG. 52.63 Origin of the ileocolic pedicle from the mesenteric pedicle 
right below the duodenum.
Inferior
mesenteric
artery
Inferior mesenteric
vein
Ligament of Treitz
FIG. 52.64 In left-sided resections, the inferior mesenteric vein is iden-
tified at the ligament of Treitz and the mesocolon of the left colon is dis-
sected away from the retroperitoneum along the fascia of Toldt. (From 
D’Annibale A, Morpurgo E, Menin N. Laparoscopic and robotic surgery 
in rectal cancer. In: Delaini GG, ed. Rectal Cancer. New Frontiers in Diag-
nosis, Treatment and Rehabilitation. New York: Springer; 2005:167–176.)
Inferior
mesenteric
artery
Hypogastric plexus
Left colon
Gonadal
vessels
Ureter
FIG. 52.65 The inferior mesenteric artery originates from the aorta, 2 
to 3 cm caudal from the area where the inferior mesenteric vein is identi-
fied; its origin is surrounded by the mesenteric and hypogastric nervous 
plexus. (From D’Annibale A, Morpurgo E, Menin N. Laparoscopic and 
robotic surgery in rectal cancer. In: Delaini GG, ed. Rectal Cancer. New 
Frontiers in Diagnosis, Treatment and Rehabilitation. New York: Springer; 
2005:167–176.)
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1376SECTION X Abdomen
console and maneuvers the robotic instruments using joy sticks. 
The robot gives a deep three-dimensional vision and adds the ca-
pability of intracorporeal hand wristed movements to laparoscopic 
instruments. Randomized trials and results of metaanalysis do not 
show yet clear advantages in conversion rate and short-term on-
cologic results for robotic low anterior resections as compared to 
conventional laparoscopy, but this technology overcomes some of 
the intrinsic difficulties of laparoscopy: the rigidity of the instru-
ments and the two-dimensional vision. It allows the instruments 
to move in the three dimensions of space and therefore gives the 
possibility to easily perform intracorporeal sutures and anastomo-
sis. The technology is under fast evolution, and new developments 
of single arms and single access devices with wristed movements 
designed for intrarectal and deep pelvic space use are in progress.
Right-Sided Tumors
For cancers located in the cecum and ascending colon, the pro-
cedure of choice is right hemicolectomy. The procedure includes 
division of the ileocecal pedicle at its origin from the superior mes-
enteric vessels and division of the right colic vessels (Fig. 52.66A); 
the lymphatic tissue that surrounds the superior mesenteric vein 
can be removed en bloc in order to perform a complete lymph 
node dissection (Fig. 52.66B). The right branch of the middle 
colic vessels is divided. The terminal ileum is divided with a sta-
pler 5 to 6 cm from the ileocecal valve and the transverse colon at 
the junction between its mid and proximal third. The omentum 
has to be removed en bloc, together with the gastrocolic ligament 
that is divided along the gastroepiploic arcade. Bowel continuity 
is restored with an ileotransverse anastomosis, in most cases lat-
erolateral. When approached in laparotomy, the first maneuver is 
the detachment of the right abdominal side-wall attachment; the 
vascular pedicles are ligated once the right colon has been fully 
mobilized from the retroperitoneum and from the duodenum. In 
laparoscopy or robotics, the colectomy is usually performed with 
a medial to lateral approach with initial vascular control and then 
detachment from the abdominal side wall. If approached lapa-
roscopically, the anastomosis can be extracorporeal (through an 
umbilical mini laparotomy, which is also utilized for specimen ex-
traction) or intracorporeal. An intracorporeal anastomosis seems 
to bring advantages in terms of fewer anastomotic complications 
(leaks and twists) and faster recovery of bowel function and dis-
charge when compared to extracorporeal anastomosis, but it is 
technically challenging in laparoscopy. The robot facilitates the 
anastomosis that can be done with the articulated robotic linear 
stapler and the enterotomies can be hand sewn with robotic in-
struments. Reported leak rates are about 1% and the specimen in 
these cases can be extracted through a Pfannenstiel incision that 
has fewer short- and long-term complications as compared to a 
midline mini-laparotomy. 
Tumors of the Transverse Colon
The standard procedure for the majority of these cancers is right 
extended colectomy that differs from right colectomy because, 
here, the middle colic vessels are divided at their origin at the level 
of the inferior margin of the pancreatic neck (Fig. 52.67A). The 
ileocolic anastomosis is made at the distal third of the transverse 
colon. Indocyanine green angiography can allow one to assess the 
vascular supply of the residual colon and to identify the area of 
vascular demarcation. The transection with the stapler must be 
done in a well vascularized area (Fig. 52.67B). This test is cru-
cial when multiple vascular pedicles are resected—as is the case 
in extended right hemicolectomy—or when the viability of the 
mobilized colon relies on small marginal vessels, especially in el-
derly atherosclerotic patients. 
Tumors of the Splenic Flexure
This has been debated as to the ideal procedure for splenic flexure 
lesions—ranging from extended right-sided resection, to encom-
pass the splenic flexure, to resection of the splenic flexure alone 
(Fig. 52.68). The inferior mesenteric vein is ligated at the level 
A
Middle
colic
vessels
Right
colic
vessels
Pancreas
Duodenum
Ileocolic
pedicle
B
B
A
C
FIG. 52.66 (A) Resection for a right-sided cancer: ileocolic, right colic, 
and right branch of the middle colic vessels are ligated. The terminal 
ileum and the transverse colon are divided as shown. (B) Robotic dis-
section in right colectomy. The lymph nodes are peeled off the superior 
mesenteric vein, and the ileocolic vein is isolated at its origin. A, Superior 
mesenteric vein; B, ileocolic vein at its origin; C, duodenum.
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1377CHAPTER 52 Colon and Rectum 
of the ligament of Treitz and the left colic artery is divided at its 
origin from the IMA and the specimen is taken en bloc with the 
omentum. In the majority of cases, bowel continuity is restored 
with an anastomosis between the transverse and the descending 
colon. In selected cases, where the mesentery of the colon is thick 
and the colon is short, this colocolic anastomosis can compress 
and obstruct the duodenum at the ligament of Treitz. In these 
cases, extended right hemicolectomy with ileo-descending anas-
tomosis is preferable. 
Left-Sided Tumors
Left hemicolectomy includes the high ligation of the IMA 
at its origin (Fig. 52.69A). The IMA can also be ligated 2 
to 3 cm more distally without compromising the oncologic 
outcome but lowering the risk of injuring the mesenteric 
and hypogastric nervous plexus. A damage of the nervous 
plexus carries the risk of genitourinary complications, in-
cluding retrograde ejaculation in males, bladder dysfunction, 
and vaginal dryness in women. The inferior mesenteric vein 
is divided at the level of the ligament of Treitz. The splenic 
flexure must be fully mobilized with coloepiploic detach-
ment, detachment of the mesocolon of the splenic flexure 
and distal transverse from the pancreas, and left abdominal 
gutter detachment. The detachment of the splenic flexure 
is necessary in order to guarantee an anastomosis without 
tension between the left colon and the proximal rectum be-
low the rectosigmoid junction. Also, for left colectomies, 
in laparoscopy, the preferred approach is mediolateral with 
initial vascular control and then subsequent colon mobi-
lization. Restoration of bowel continuity is made with a 
transanal circular stapler that should have a caliber of about 
3 cm (Fig. 52.69B). 
OBSTRUCTING COLON CANCERS
Patients with obstructing tumors of the colon may present in-
dolently with pencil-thin stools, increasing constipation, and 
an increasingly distended abdomen, or acutely with obstipa-
tion, complete obstruction, abdominal pain, and vomiting, 
which may be feculent. Diagnosis is commonly confirmed with 
imaging such as plain films, contrast enemas, abdominal CT, 
and lower endoscopy. Treatment objectives entail relief of the 
obstruction, resection of ischemic or nonviable bowel, and re-
section of the tumor.
A
Middle
colic
vessels
Right
colic
vessels
Pancreas
Duodenum
Ileocolic
pedicle
B
FIG. 52.67 (A) Resection for cancers of the transverse colon. The il-
eocolic, right, and middle colic vessels are ligated. The terminal ileum 
and the transverse colon are transected as shown. (B) Indocyanine green 
angiography. After transection of the middle colic vessels, the line of vas-
cular demarcation is clearly visible (arrow).
Middle
colic
vessels
Right
colic
vessels
Pancreas
Duodenum
Ileocolic
pedicle
Left colic
vessels
Inferior
mesenteric
arteries
FIG. 52.68 Resection for cancers of the splenic flexure. Theleft colic 
artery and the left branch of the middle colic artery are ligated as shown.
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1378 SECTION X Abdomen
Management of Left-Sided Obstructions
The approach to left-sided obstructions is tailored according to 
the location of obstruction, viability of the proximal bowel, and 
general stability of the patient. In sigmoid and left colon obstruc-
tions, patients are commonly referred for urgent surgery. A seg-
mental resection of the primary tumor is typically performed. If 
the proximal large bowel has perforated or is showing signs of 
ischemia, a subtotal colectomy is completed. Historically, primary 
anastomosis has been avoided, with the distal stump closed and 
a proximal stoma exteriorized (Hartmann operation). However, 
reestablishing intestinal continuity then entails a major operation, 
and a large proportion of patients will never be reversed. Current 
evidence supports the option of a primary anastomosis in appro-
priate patients who are hemodynamically stable, and a tension-free 
anastomosis with a good blood supply can be achieved, usually by 
specialized surgeons. In these cases, leak rates are in the range of 
2% to 12%, which are almost comparable to the 2% to 8% leak 
rate in elective surgery.38 Intraoperative colonic lavage or manual 
decompression prior to anastomosis can be performed with simi-
lar results between them, but evidence is lacking supporting either 
with regard to anastomotic leaks or infectious complications. A 
proximal diverting stoma may also be exteriorized combined with 
a primary anastomosis. This does not reduce the anastomotic leak 
rate but may decrease the quantity of leaks requiring reoperation.
Endoscopic stenting as a bridge for surgery has also emerged 
as an attractive technique to relieve obstructions and permit elec-
tive surgery under more favorable conditions. Stenting has been 
shown to permit higher rates of primary anastomosis, decreased 
wound infections, and a higher rate of completion of surgery lapa-
roscopically. Stenting is contraindicated in suspected ischemic or 
perforated bowel. Clinical success is in the 70% to 80% range, 
with the main immediate risk being stent-related perforation. 
Concerns about inferior long-term oncologic outcomes have lim-
ited usage in patients with average risk curable disease. Although 
recent evidence has suggested that long-term oncologic outcomes 
may be acceptable,39 current guidelines recommend stenting as 
a bridge for surgery on an individual basis, mainly in high-risk 
patients to allow optimization with interval colectomy. 
Management of Right-Sided Obstructions
Treatment of right-sided obstructions generally includes an onco-
logic segmental resection. In most cases, a primary ileocolic anas-
tomosis can be performed safely, but for patients with a high risk 
of anastomotic failure, a diverting stoma can be exteriorized. 
RECTAL CANCER
Preoperative Evaluation of Patients With Rectal Cancer
Every year, there are approximately 44,000 new diagnoses of pa-
tients with rectal cancer in the United States. The main chang-
ing trend in the United States is the increasing number of young 
patients being diagnosed with rectal cancer. This is a significantly 
changing demographic that is projected to increase over the next 
10 to 15 years. Similar to colon cancer, patients with rectal cancer 
are staged upon presentation to determine the extent of disease. 
Unlike colon cancers, rectal cancers have a much higher risk of 
A B
Middle
colic
vessels
Right
colic
vessels
Pancreas
Duodenum
Ileocolic
pedicle
Left colic
vessels
Inferior
mesenteric
arteries
1
2
FIG. 52.69 (A) Left hemicolectomy. The inferior mesenteric artery is ligated and the marginal artery is ligated 
just distal to level of transection of the colon. The hemorrhoidal vessels are ligated within the proximal meso-
rectum. (B) Colorectal anastomosis with circular stapler. 1, Anvil in the proximal colon; 2, Shaft of the transanally 
placed circular stapler.
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1379CHAPTER 52 Colon and Rectum 
local recurrence; therefore, there has been an evolution in their 
treatment and preoperative assessment. Because of the boney con-
fines of the pelvis, obtaining a clear “circumferential margin of 
resection” is less straightforward than within the true confines of 
the abdomen. As noted in the section on anatomy earlier in this 
chapter, the lower half of the rectum is either entirely or partly 
an extraperitoneal structure. Also, based on its blood supply, the 
lower half of the rectum drains into the systemic circulation and 
therefore can also metastasize through the systemic circulation to 
the lungs, whereas upper rectal cancers tend to metastasize, just 
as colon cancers do, to the liver. In assessing a patient with rectal 
cancer, the first thing would be to, on physical examination, as-
sess if it is within reach of the examining finger of the surgeon. 
If it is palpable at the tip of the finger, one can ascertain whether 
there is good anal sphincter tone, in which case, in the majority 
of patients, the cancer will be amenable to treatment by a sphinc-
ter-sparing approach. Initial assessment of the patient with rectal 
cancer should include a physical examination, including digital 
exam. In evaluating patients with rectal cancer, one should always 
document any pathology as anterior, posterior, left, or right. Doc-
umentation of lesion location as at “six o’clock” or “twelve o’clock” 
is always confusing, as one does not know whether the patient is 
lying supine or prone. In women, it is always crucial to document 
whether or not there is invasion of the rectovaginal septum, as this 
will be a prime consideration of whether or not a vaginal resection 
will need to be performed at the time of surgery. In addition to 
this, assessment of sphincter involvement is critical.
A proctoscopic examination assessing for tumor height should 
be performed if possible as height assessments with flexible en-
doscopy are notoriously inaccurate. What is judged to be at 
15 cm during a flexible endoscopic examination can be much 
closer or farther away on rigid endoscopy. Treating rectal cancers 
in men with a narrow pelvis, particularly obese males, is par-
ticularly challenging, as is the peritoneal reflection. Examining a 
patient on a tilt table in knee-chest position is particularly benefi-
cial, especially in the extremely obese patients, as even in the very 
large patient this permits a fairly good digital examination and 
examination of the lower rectum.
Staging of the rectal cancer can be performed either with 
endorectal ultrasound or with MRI. The quality of MRI, as 
well as endorectal ultrasound, varies by center. Endorectal ul-
trasound is performed by a surgeon, gastroenterologist, or ra-
diologist, whereas the MRI is performed by a radiologist. Both 
have advantages and disadvantages. Endorectal ultrasound is a 
much less expensive test, can be performed without sedation, 
and provides an accurate assessment of the T stage of a rectal 
cancer. Not all facilities have the equipment for performing en-
dorectal ultrasonography. Some facilities may have endoscopic 
ultrasonography capability. Fig. 52.70 shows a representative 
endorectal ultrasound in a patient with rectal cancer. The rectal 
wall is indicated by three white lines and two hypoechoic lines. 
The innermost line represents the interface between the water-
filled balloon and the transducer. The transducer rotates 360 
degrees to givean image of the rectum. In most studies, the ac-
curacy of lymph node detection is much less than the accuracy 
of detecting T stage.
With respect to MRI, in order to obtain a meaningful study 
for rectal cancer staging, the MRI has to be performed according 
to a specific rectal cancer protocol in which the MRI is accessed 
in the same axis as the rectum. In addition, it is very helpful to 
fill the rectum with ultrasound gel mixed with gadolinium. MRI 
interpretation is dependent upon the experience of the radiolo-
gist reading the MRI. A pelvic MRI will, however, permit assess-
ment of lymph node involvement and circumferential resection 
margin status as well as assessment of extrarectal disease, which 
is not possible with endorectal ultrasound. Currently, clinically 
T3 and node positive rectal cancers and those with cancers in 
close proximity of the sphincter in whom sphincter sparing is 
B
CA
PR
PR
CA
1.5 CM/DIV 3.1 cmA
FIG. 52.70 (A) Endorectal ultrasound showing hypoechoic lymph node (arrow) between cancer and prostate. 
(B) Endorectal ultrasound showing irregular anterior border where cancer has grown through rectal wall (arrow) 
(T3). CA, Cancer; PR, prostrate.
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1380 SECTION X Abdomen
desired are recommended to undergo preoperative neoadjuvant 
chemoradiation.
There has been an evolution in the overall treatment of rec-
tal cancer with the recognition that patients’ rectal cancers can 
be “downstaged,” facilitating the surgery, increasing the chance 
of a sphincter-sparing operation, and also providing improved 
functional results (lesser number of bowel movements and im-
proved control) as compared to when these treatments are given 
after surgery. These observations are derived from several studies. 
A major study was the German Rectal Cancer Study, whose re-
sults were published in 2004.40 T3 and T4 rectal cancer patients 
were randomized to receive either preoperative or postoperative 
chemoradiation. There was no overall difference in morbidity or 
mortality; however, lower rates of local recurrence and both acute 
and long-term toxicity were seen with preoperative treatment. 
Importantly, significantly more patients in the preoperative treat-
ment group were able to undergo sphincter-sparing procedures. 
Beginning in the 1980s, Richard Heald began to popularize a 
technique that many surgeons were already performing, namely, 
complete excision of the mesorectum. This involves removing the 
entire mesorectum intact using sharp dissection. This technique 
was associated with a much lower risk of local recurrence and im-
proved survival rates. Publications from Quirke and colleagues 
emphasized the role of the circumferential margin in reducing 
recurrence. A combination of these techniques (i.e., performing 
preoperative chemoradiation) and TME and recognition of the 
importance of the circumferential margin have led to improved 
outcomes for rectal cancer surgery. In fact, much as has been 
done for anal squamous cell cancer; there have been variations 
in protocols, waiting different amounts of time from completion 
of chemoradiation until surgery. Professor Habr-Gama has been 
the lead of a new treatment philosophy entitled “watch and wait.” 
The concept of “complete pathologic response” has been exten-
sively studied. Initially reported in a small group of patients with 
rectal cancer undergoing preoperative neoadjuvant therapy, it was 
noted that 27% of patients had no clinically detectable evidence 
of cancer following this treatment.41 When these patients were 
compared to those undergoing surgery with the finding of a com-
plete response in their specimen, there was no difference in lo-
cal or systemic recurrence between groups. Among rectal cancer 
patients undergoing neoadjuvant chemoradiation, approximately 
20% will achieve a “complete response.” Typically, a restaging is 
performed following treatment. In high-risk patients, or in select 
patients after an in-depth discussion, a watch and wait strategy 
may be chosen. This is currently not standard of care. The absence 
of luminal disease does not imply the absence of disease, and such 
patients must be followed longitudinally, not only with physical 
and endoscopic examination but also with cross-sectional imag-
ing, preferably MRI. With respect to response to neoadjuvant 
therapy in patients undergoing resection for rectal cancer, there 
have been different staging systems proposed to grade the degree 
of tumor regression. One common scale ranges from 1 to 3, with 
respect to how many viable tumor cells remain, with 1 referring 
to a complete response and 3 referring to a minimal response.42 
As stated previously under Colon Cancer Staging, any staging that 
has a “y” prefix refers to an AJCC stage that is obtained following 
neoadjuvant treatment. 
Local Excision
Local excision of rectal neoplasms can be accomplished through 
both endoscopic and transanal techniques. Endoscopic techniques 
include routine polypectomy, endoscopic mucosal resection, and 
endoscopic submucosal resection. Surgical excision can be per-
formed via standard transanal excision, transanal MIS (TAMIS), 
as well as by transanal endoscopic microsurgery.
Endoscopy for the transanal removal of large rectal lesions has 
expanded with the availability of improved staging techniques, in-
cluding endorectal and endoscopic ultrasound and MRI described 
elsewhere in this chapter. Careful digital examination is also ac-
curate at staging lesions within reach of the examining finger, as 
a lesion that is soft to the touch typically is benign. This goes 
particularly for villous adenomas of the rectum. Villous adenomas 
of the lower rectum are commonly amenable to a transanal exci-
sion or endoscopic excision. The key here is, however, excision of 
a lesion with a free margin to reduce the risk of local recurrence.
Partial- or full-thickness (for cancers) excision of lesions can 
be performed. With partial-thickness excision, such as is done for 
benign lesions, these techniques are made easier by submucosal 
injection of a solution to elevate the lesion off of the underlying 
muscularis mucosa. Some of these solutions used for endoscopy 
are colored, making visualization even easier. Endoscopic submu-
cosal dissection is used for lesions that are superficial. In doing 
this, a hollow cap is placed over the tip of the endoscope. After 
submucosal injection has been performed to lift the lesion away 
from the underlying muscularis, suction is applied to the colo-
noscope when the cap is positioned over the lesion. The lesion is 
drawn into the cap by suction, the snare that fits around the cap 
then is tightened, cutting off the area of mucosa that has been 
aspirated into the cap, much like a routine polypectomy. In us-
ing this technique, fairly large areas of mucosa can be safely re-
moved. When lesions go somewhat deeper through the muscle 
wall, a technique called endoscopic submucosal resection can be 
performed. In this technique, submucosal injection is performed 
to facilitate dissection of a lesion off the underlying colon wall 
after the margin has been scored.
Surgical transanal resection of rectal lesions has long been pop-
ular as a form of sphincter-sparing surgery but has become less so 
with the advent of circular staplers and especially with minimally 
invasive techniques for resectional rectal surgery. Traditional cri-
teria for performing a local excision for a rectal cancer have been 
small lesions (group of patients has been unacceptable. If a traditional lo-
cal excision is performed, cautery is used to score a 1-cm margin 
around the lesion. Traction is used, and a full-thickness incision 
is performed down to perirectal fat (Fig. 52.71). Local excision 
is safe when performed for lesions that are located lateral to or 
posterior to the rectum due to the presence of the mesorectum. If 
these lesions are located in the anterior rectum in women, there is 
risk of iatrogenic rectovaginal fistula or, in the case of men, injury 
to the prostate. In addition, as one goes higher above 6 or 7 cm, 
there is concern that one may be intraperitoneal. These procedures 
are most safely performed in the lower rectum.
The development in the early 1990s of transanal endoscopic 
microsurgery made possible the excision of larger lesions and le-
sions higher than could be safely performed using conventional 
transanal surgery. This required a specialized set of instruments 
and demanded a very special set of skills working with rigid in-
struments with a high learning curve. This technique has now 
largely been supplanted with the technique of TAMIS, whereby 
standard laparoscopic instruments and an access port similar to 
that used for single-port laparoscopy is used in the anal canal to 
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1381CHAPTER 52 Colon and Rectum 
allow for safe excision of lesions above the level of the very dis-
tal rectum (Fig. 52.72, Video 52.1). Due to the anchoring of the 
laparoscopic access device itself, this technique is not suitable for 
lesions in the very lower rectum. 
Resections for Rectal Cancers
The rectum is the distal portion of the large intestine. It is divided 
into three parts: proximal rectum (approximately from 15–10 cm 
from the anal verge), mid rectum (from 10–5 cm from anal verge), 
and distal rectum (5 cm and less). The upper portion of the mid 
rectum and distal rectum are extraperitoneal. The rectum is locat-
ed in the narrow space of the pelvis. It has close anatomic relations 
with the genitourinary organs (bladder, seminal vesicles, prostate, 
vagina, uterus) and with the endopelvic nerves. It has an impor-
tant role as a fecal reservoir. The rectum plays an active role in def-
ecation and is in continuity with the sphincter apparatus. Its distal 
mucosa is fundamental to discriminate between stool and gas. An 
oncologically radical resection of the rectum must be performed 
along a very precise anatomic plane en bloc with its mesorectum 
where the lymphatics and the rectal lymph nodes are located. The 
mesorectum, in turn, is enveloped by the mesorectal fascia that 
has to be kept intact during the dissection because its integrity has 
been shown to be crucial to reduce the risk of local recurrence. For 
all these reasons, surgical resection of the rectum and the meso-
rectum—the so-called “total mesorectal excision” or TME—poses 
some specific challenges with respect to surgical technique. 
Low Anterior Resection
After vascular division similar to left colectomies, the peritoneal 
reflection of the rectum is divided at the level of the sacral promon-
tory and the rectum with its proximal mesorectum is gently pulled 
anteriorly entering the avascular “cotton candy” plane between the 
fascia of the mesorectum and the presacral fascia. Extra care must 
be taken in order to avoid any injury to the hypogastric nerves 
that must be visualized. Anteriorly, the cul-de-sac is divided, and 
the rectum is dissected from the anteriorly located seminal vesicles 
in males and the vagina in females. The dissection is continued 
distally and the rectum and the mesorectum are divided 5 cm be-
low the cancer (Fig. 52.73), thus indicating a subtotal mesorectal 
excision. For cancers located in the distal two thirds of the rectum, 
the dissection must be continued more distally, dissecting the rec-
tum away from the prostate along the fascia of Denonvilliers. Pos-
teriorly, the rectum has to be dissected distally, up to the level of 
the levator muscles en bloc with the entire mesorectum, keeping 
the mesorectal fascia intact. The most distal part of the rectum 
is “naked” (i.e., not surrounded by the mesorectum that ends a 
few cm proximally) (Fig. 52.74). At this level, the rectum can be 
divided with a stapler. In laparoscopy, several reloads may be nec-
essary to complete the transection of the rectum in the distal pel-
vis. This operation is called TME because it removes the rectum 
en bloc with its entire mesorectum. The integrity of the visceral 
B CA
FIG. 52.71 (A) Transanal excision of a small rectal cancer. A 1-cm lesion has been scored around the lesion 
to be excised using electrocautery. Using careful traction, full-thickness excision is performed. (B) Transanal 
excision of a small rectal cancer. Electrocautery is used to perform a full-thickness excision extending into the 
mesorectum. (C) Transanal excision of a small rectal cancer. The defect can be sutured closed or left open to 
heal by secondary intention.
FIG. 52.72 Rectal cancer patient undergoing transanal minimally inva-
sive surgical removal of residual scar following apparent complete clinical 
response following neoadjuvant chemoradiation. The arrow points to fat 
of rectal mesentery seen with full-thickness excision.
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1382 SECTION X Abdomen
fascia is a crucial point that defines the quality of a TME and is 
directly related to the DFS interval. The proper excision along the 
anatomic plane is essential in order to obtain free circumferential 
radial margins, thus reducing the local recurrence rate below 5%; 
it also results in a significant decrease in the frequency of urinary 
and sexual dysfunction (retrograde ejaculation and impotence). 
Recent evidence demonstrates that the laparoscopic approach has 
similar results with regard to the quality of resection, clear cir-
cumferential margins, and recurrence rate when compared to the 
open approach. The DFS for stages II–III cancer is about 75% 
regardless of the surgical approach utilized (i.e., laparoscopy or 
open surgery). The colorectal anastomosis is eventually made with 
a circular stapler inserted transanally. Air is then insufflated into 
the rectum through the anastomosis while the proximal colon is 
occluded, and the pelvis is filled with water in order to exclude the 
presence of leaks. In order to avoid the passage of stool through 
the anastomosis until complete healing, a loop diverting ileostomy 
is performed to protect the distal colorectal anastomosis, especially 
in patients who have received preoperative chemoradiation. The 
diverting stoma is usually maintained for at least 8 weeks after sur-
gery and is closed only after the perfect healing of the anastomosis 
has been confirmed with a gastrografin enema or with endoscopy 
Sphincter-Sparing Surgery Procedures for Low Rectal 
Cancers
Tumors located in the ultradistal portion of the rectum (i.e., at the 
level of the dentate line or just above it) are a specific entity due to 
their proximity to the anal sphincter and the implications that the 
resection may have upon sphincter function. In young and fit pa-
tients with good preoperative sphincter function, if the sphincters 
are not infiltrated with cancer and do not need to be sacrificed for 
oncologic reasons, an anastomosis between the colon and the anal 
A B
Middle
colic
vessels
Right
colic
vessels
Pancreas
Duodenum
Ileocolic
pedicle
Left colic
vessels
Inferior
mesenteric
arteries
Meso-
rectum
Line of dissectionBladder
FIG. 52.73 (A) Low anterior resection for cancer of the upper rectum. The inferior mesenteric artery is ligated. 
The marginal artery is ligated just distal to level of colon transection; the hemorrhoidal vessels are ligated in the 
mesorectum. (B) Low anterior resection for cancer of the upper rectum. (Dotted line) A line of dissection of the 
rectum en bloc with the mesorectum.
Meso-
rectum
Line of
dissection
Bladder
FIG. 52.74 Low anterior resection for cancer of the upper rectum. 
 Dotted line of dissection of the rectum en bloc with the mesorectum.
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1383CHAPTER 52 Colon and Rectum 
canal is feasible. The ultradistal rectum cannot be stapled from the 
abdomen, and therefore, the dissection and reconstruction has to 
be performed transanally. Different instruments can be used: the 
sphincter is denuded starting just distally from the tumor with 
scissors or with a harmonic scalpel. Different types of dissection 
can be done and may have different functional results based on 
the structures that are excised with the dissection. With a standard 
mucosectomy, the distal mucosa is peeled off from the internal 
sphincter. Ideally, 1 to 2 cm of mucosa above the dentate line 
should be saved because this portion of distal mucosa has a critical 
importance in rectal sensibility and consequently for postopera-
tive functional outcomes (Fig. 52.75). With this dissection, the 
internal sphincter that lies underneath the mucosa is spared. If the 
cancer is lower but small in size and involving only a small portion 
of the mucosa, an asymmetrical mucosectomy can be performed 
en bloc with the underlying internal sphincter on one side of the 
anal canal, sparing part of the distal mucosa and sphincter (Fig. 
52.76). If the cancer involves a larger part of the anal canal, an 
intersphincteric dissection must be done (Fig. 52.77). With this 
dissection, the internal sphincter—responsible for resting pressure 
of the anal sphincter—is removed circumferentially: functional 
results are poor due to the loss of part of the sensation and the 
decrease of resting anal pressure. 
Transanal Total Mesorectal Excision
Recently, a new emerging technique has been proposed when ap-
proaching sphincter-preserving procedures in order to facilitate 
the detachment of the rectum and to improve the vision in the 
narrow pelvic space.43 This approach utilizes transanal platforms 
also used for TAMIS (Fig. 52.78). The distal rectum is closed with 
a purse string and is divided with a harmonic scalpel. At this point, 
the port platform for transanal surgery is positioned through 
the anus and the dissection of the rectum is continued from the 
bottom upward, thus gradually going from a narrow space to a 
wider space. Retropneumoperitoneum inflated through the port 
facilitates the blunt atraumatic dissection of the rectum with its 
External
sphincter
Internal
sphincter
Levator
ani
A
B
FIG. 52.75 Both external and internal sphincters and 1 to 2 cm of mucosa above the dentate line are left un-
touched. Sphincter-sparing surgery procedure. (B) Completed coloanal anastomosis. The anastomosis is hand-
sewn with interrupted sutures between the colon and the distal rectum. About 1 cm of rectal mucosa is left 
intact above the dentate line.
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1384 SECTION X Abdomen
External
sphincter
Internal
sphincter
Levator
ani
A
B
FIG. 52.76 (A) Sphincter-sparing surgery procedure. The cancer is ultradistal and located on the right side. In 
this case, the right side of the mucosa and the internal sphincter are dissected; on the patient’s left side, 1 to 2 
cm of mucosa are left untouched, together with part of the internal sphincter. (B) Resection of the distal mucosa 
of the rectum. A self-retaining retractor displays the dentate line; the mucosa of the distal rectum is indicated 
by the white arrow, while the black arrow indicates the underlying external anal sphincter in the area where the 
mucosa has already been dissected off using the harmonic scalpel.
External
sphincter
Internal
sphincter
Levator
ani
FIG. 52.77 Sphincter-sparing surgery procedure: intersphincteric dissection.
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1385CHAPTER 52 Colon and Rectum 
mesorectum along avascular planes under clear laparoscopic vi-
sion. The detachment of the rectum is first done posteriorly and 
then anteriorly from the prostate plane and can be continued until 
the cul-de-sac is entered. At this point, the procedure is continued 
within the abdomen with standard laparoscopic or robotic instru-
ments. After the colon has been mobilized, when the pelvis is ap-
proached transabdominally, the distal rectum appears already fully 
detached and can be easily exteriorized (Video 52.2). The trans-
anal TME technique has been shown to be oncologically safe with 
a low rate of involved circumferential margins and good quality 
of mesorectal excision. After the operation, all patients show a de-
crease of resting sphincter pressures, but the squeeze pressures are 
unchanged and functional results are acceptable.44 
Abdominoperineal Resection
If the sphincters are infiltrated by tumor, complete excision of 
both the rectum and the anus, along with the sphincter apparatus, 
must be performed along with creation of a permanent colostomy. 
This procedure (abdominoperineal resection [APR], known as the 
Miles procedure) is also an option for elderly patients with distal 
rectal cancer with poor sphincter function because an end colos-
tomy offers a better quality of life if compared with an ultradistal 
coloanal anastomosis that could further compromise continence. 
The IMA is divided, the descending colon is mobilized and di-
vided above the rectosigmoid junction, and the rectum is dissected 
according to the TME principles to the level of the levator ani. 
The colostomy aperture is created. At this point, the perineal part 
of the operation begins (Fig. 52.79A). A purse-string suture is 
placed around the anus, and an elliptical incision is made around 
the anus that is then excised en bloc with the sphincter. Dissec-
tion continues cephalad until the abdominal plane of dissection 
is reached. The specimen is removed through the pelvic incision 
and the perineum is closed in layers (Fig. 52.79BC). The empty 
space of the pelvis can often be filled with an omental pedicle. If 
wider perineal resections are needed, especially in irradiated pel-
vises that may have healing difficulties, the perineal defect can be 
closed using a rectus abdominis flap or gracilis muscle flap. The 
specimen includes the origin of the IMA, the mesorectum with 
hemorrhoidal vessels and the “naked” portion of the ultradistal 
rectum and the anal sphincters.
APR carries intrinsic risk of higher recurrence rates (up to 
33%) compared to low anterior resection. This is in part explained 
by the fact that APR is done in more aggressive cancers, but an-
other explanation is the fact that there is an intrinsic higher risk of 
specimen perforation and a higher rate of positive circumferential 
margins (up to 40%) in patients undergoing APR.
For this reason, a wider excision has been proposed that allows 
a more cylindrical resection avoiding the risk of “coning” toward 
the rectum (Fig. 52.80). After the abdominalteric arteries. 
Venous drainage. Venous drainage somewhat follows the arte-
rial supply through the superior mesenteric and inferior mesenter-
ic veins (IMVs), which contribute to the formation of the portal 
vein. It is important to note that the IMV continues beyond the 
IMA along the base of the mesentery to the left of the ligament 
of Treitz and into the portal vein (Fig. 52.9). The IMV can be 
divided to achieve extra colonic length for low pelvic anastomoses. 
Lymphatic system. Lymphatic drainage generally follows the 
vascular supply. The wall of the large bowel is supplied with a rich 
network of lymphatic capillaries that drain to groups of lymph 
nodes paralleling the arterial supply. Most of the lymphatic drain-
age goes in this direction, but communications are found between 
groups of lymph nodes, especially at the level of the paracolic 
groups at the level of the marginal arteries. There is also some dual 
drainage from the distal transverse and splenic flexure into both 
the superior and inferior mesenteric lymph nodes. 
Innervation. The innervation of the large intestine has both 
sympathetic and parasympathetic components, which generally 
follow the blood supply. 
Rectal Anatomy
The rectum begins at the rectosigmoid junction and ends at the 
level of the anus. Anatomists define the distal border as the dentate 
(pectinate) line based on the mucosal surface, whereas surgeons 
Middle colic artery
Superior
mesenteric artery
Right colic artery
Ileocolic artery
Ileal branch
Anterior cecal branch
Median sacral artery
Posterior cecal branch
Appendicular artery
Internal iliac artery
Accessory middle rectal artery
Middle rectal artery
Inferior rectal artery
Ascending branch
of left colic artery
Marginal artery
Inferior
mesenteric artery
Left colic 
artery
Left common iliac
artery
Sigmoid arteries
Bifurcation of superior
rectal artery
FIG. 52.8 The arterial blood supply to the colon is from the superior and inferior mesenteric arteries. (From 
Gordon PH, Nivatvongs S, eds. Principles and Practice of Surgery for the Colon, Rectum and Anus. 2nd ed. St. 
Louis: Quality Medical Publishing; 1999:23.)
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1327CHAPTER 52 Colon and Rectum 
define it as the proximal border of the anal sphincter complex at 
the level of the levator ani (about 2 cm above the dentate line). 
The rectum with a total length of around 15 to 20 cm is divided 
into thirds based on its peritoneal relationships. The upper rec-
tum is covered by peritoneum anteriorly and laterally and its lower 
limit extends to approximately 10 cm above the dentate line. The 
middle third is covered by peritoneum only anteriorly and extends 
from 5 to 10 cm above the dentate line. The lower third of the 
rectum is totally extraperitoneal, extending from 1 to 5 cm above 
the dentate line. The rectum has three lateral curves or valves of 
Houston, the proximal and distal valves fold to the right and the 
middle to the left. They are lost after full surgical mobilization of 
the rectum, providing approximately 5 cm of additional length as-
sisting the surgeon’s ability to fashion an anastomosis deep in the 
pelvis. Structurally, the rectum lacks taeniae coli, epiploic appen-
dices, and haustra. The anterior peritoneal reflection between the 
rectum and anterior structures, the rectovesicular pouch in males 
and rectouterine or Douglas pouch in females, is 7 to 9 cm from 
the anal verge in men and 5 to 7.5 cm in women (Fig. 52.10). The 
anterior peritoneal reflection is the lowest dependent part of the 
peritoneal cavity. It is clinically important as a common location 
of fluid and pus accumulation and may serve as a site of peritoneal 
metastases from visceral tumors. These “drop” metastases can form 
a mass in the cul-de-sac (Blumer shelf ) that can be recognized 
on digital rectal examination. “Mesorectum” refers to the visceral 
mesentery of the rectum. Recognition of mesorectal planes during 
rectal surgery is extremely important as it allows for a relatively 
bloodless dissection with consistent excision of relevant lymphatic 
tissues, adhering to the basic surgical oncologic principle of re-
moving the cancer in continuity with its blood and lymphatic 
supply. Total mesorectal excision (TME), based on a detailed un-
derstanding of anatomy, has been shown to reduce the incidence 
of local recurrence of rectal cancer and increase the preservation 
of urinary and sexual function. The mesorectum is relatively thick 
posteriorly, thinner along the sides, and very thin anteriorly.
Anatomic structures adjacent to the rectum are clinically im-
portant with regard to dissection planes and to direct extension of 
tumors and/or fistulas. In males, the rectum is adjacent anteriorly 
and extraperitoneally to the urinary bladder, ureters, vas deferens, 
seminal vesicles, and prostate. In women, intraperitoneally, it is 
Superior pancreaticoduodenal vein
Portal vein
Superior mesenteric vein
Right colic vein
Ileocolic vein
Superior
mesenteric vein
Inferior vena cava
Right common
iliac vein
Right internal
iliac vein
Right external
iliac vein
Middle rectal vein
Internal pudendal vein
Inferior rectal vein
Inferior
mesenteric vein
Left colic vein
Testicular/ovarian
veins
Sigmoid veins
Middle
sacral vein
Superior
rectal vein
Internal hemorrhoidal plexus
External hemorrhoidal plexus
Splenic vein
FIG. 52.9 Venous anatomy of the colon and rectum. (From Gordon PH, Nivatvongs S, ed. Principles and 
Practice of Surgery for the Colon, Rectum and Anus. 2nd ed. St. Louis: Quality Medical Publishing; 1999:30.)
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1328 SECTION X Abdomen
adjacent to the uterus, tubes, ovaries, and to the upper part of the 
posterior vaginal wall. Extraperitoneally, the rectum is adjacent 
to the uterine cervix and posterior vaginal wall. In both genders, 
the intraperitoneal cul-de-sac is commonly filled with small bowel 
and colon. The sacrum, sacral vessels, and sacral nerve roots are 
located posterior to the rectum.
The posterior aspect of the rectum is invested with a thick, 
closely applied mesorectum (Fig. 52.11). A thin layer of invest-
ing fascia (fascia propria) coats the mesorectum and represents a 
distinct layer from the presacral fascia against which it lies. Dur-
ing proctectomy for rectal cancer, mobilization and dissection of 
the rectum proceed between the presacral fascia and fascia pro-
pria. The presacral fascia covers the anterior sacrum and coccyx. 
A group of veins, on the presacral periosteum, the presacral veins, 
drain into the sacral foramina. Dissection deep to the presacral fas-
cia can cause severe bleeding from the underlying presacral venous 
plexus. Such bleeding can be very difficult to control, as the torn 
vessels tend to withdraw into the sacral foramina. The rectosacral 
fascia, or Waldeyer fascia, is a thick condensation of endopelvic 
fascia connecting the presacral fascia to the fascia propria at the 
level of S4 that extends to the posterior-inferior rectum. Dividing 
Waldeyer fascia during dissection from an abdominal approach 
provides access to the deep retrorectal pelvis. Laterally, the rec-
tum is connected to the pelvic sidewall by the “lateral stalks” or 
ligaments. These are found in the low pelvis at the level of the 
prostate or mid-vagina. It is important to remember that in about 
a quarter of the cases, a branch of the middle rectal artery tra-
verses them and may cause bleeding when cutting through them. 
Denonvilliers fascia, located anterior topart of the operation 
is completed, the patient is rotated in a prone jackknife position. 
A wider elliptical incision is made up to tip of the coccyx (that 
can be removed with the specimen) and the sphincter apparatus is 
removed en bloc with the levator ani in a cylindrical manner. The 
wide perineal defect, if needed, can be closed with a biologic mesh 
or with a muscle flap. 
Special Circumstances
Synchronous Cancers
In patients with synchronous cancers, depending on the site of the 
tumors, more extended resections are indicated. For synchronous 
cancers of the right and left colon, an abdominal colectomy with 
FIG. 52.78 Transanal total mesorectal excision (Ta TME). Transanal lapa-
roscopy for the dissection of the rectum from below.
A B
V
L
C
FIG. 52.79 (A) Perineal incision in Miles procedure. A purse-string suture is placed around the anal canal 
and the entire anal sphincter excised. (B) Photo of operative field after specimen has been removed. Perineal 
incision shows large defect in the pelvis (white arrow denotes posterior vaginal wall). L, Levator; V, vagina. (C) 
Perineal incision following skin closure following Miles procedure.
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1386 SECTION X Abdomen
IRA is indicated. If the second cancer is located in the rectum, a 
total proctocolectomy with an IPAA may be necessary. 
Short Residual Colon
In cases of re-resections for recurrent or metachronous cancers, the 
residual colon may be too short to reach the pelvis for a tension-
free anastomosis, despite a complete mobilization of the splenic 
flexure. In such cases, the colon can be transposed through a “ret-
roileal” transmesenteric route. Using this path, which is especially 
feasible in nonobese patients, the colon is pulled toward the pelvis 
more medially and led to the pelvis through the avascular space in 
the mesentery of the ileum just adjacent to the ileocolic resection. 
This gives the surgeon 4 to 5 cm of additional length that may be 
sufficient to reach for the tension-free anastomosis. If the colon is 
still under tension, another possibility is to rotate the right colon. 
In these cases, the middle colic and the right colic vessels, which 
are short and prevent the colon to be fully mobilized to the pelvis, 
are divided. The colon is transected at the site of ischemic demar-
cation (generally the hepatic flexure) and the residual right colon, 
whose blood supply now relies on the ileocolic pedicle, is rotated 
counterclockwise and mobilized to reach the rectal stump in the 
pelvis (Fig. 52.81) 
Complications
Patients undergoing colorectal resection can experience general 
complications just as those undergoing any major abdominal sur-
gery, but complications related to the anastomosis are specific to 
these patients and include leaks, bleeding, twisting, strictures, and 
low anterior resection syndrome (LARS).
Anastomotic Leaks or Dehiscences
An anastomotic dehiscence is a leak of bowel content through 
an anastomosis. The incidence of anastomotic leaks varies widely 
from 1% to 3% in ileocolic anastomoses to up to 20% in co-
loanal anastomoses. Risk factors associated with postoperative 
dehiscence are male gender, obesity, low extraperitoneal anasto-
moses, ASA score III to V, emergency operations, intraoperative 
complications, use of oral anticoagulants, nutrition status, and 
hospital size and volume.45 Anastomotic leak increases postopera-
tive mortality and the length of postoperative hospital stay. The 
presence of a diverting stoma does not decrease the risk of a leak, 
but it reduces its severity and lowers the risk of reoperation. Di-
agnosis of a postoperative anastomotic leak is established when 
enteric, fecal, or purulent material, even if minimal, is detected 
in perianastomotic drains. Clinical signs of anastomotic leak are 
usually present including fever, signs of sepsis, abdominal pain, 
prolonged ileus, leukocytosis, increased CRP, and increased pro-
calcitonin. The diagnosis can be confirmed by radiologic studies: 
CT scan demonstrates intraabdominal or perianastomotic fluid 
collections and gas (Fig. 52.82) or when gastrografin enema dem-
onstrates leak of contrast. The majority of leaks become apparent 
between the second and seventh postoperative days with median 
time of 5.5 days, but up to 12% can appear 1 month after surgery, 
making the diagnosis more challenging.
Treatment. If the leak is subclinical with minimal discharge 
from the drains and no systemic signs, it can be managed conserva-
tively with close clinical observation, broad spectrum antibiotics, 
A B
Line of
dissection
FIG. 52.80 (A) Conventional abdominoperineal resection. The line of the dissection tends to cone toward the 
rectum. (B) Cylindrical abdominoperineal resection with en bloc removal of the levator ani.
Middle
colic
vessels
Right
colic
vessels
Ileocolic
pedicle
Inferior
mesenteric
arteries
FIG. 52.81 Rotation of the right colon to reach the pelvis. The vascular-
ization of the right colon is based on the ileocolic pedicle.
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1387CHAPTER 52 Colon and Rectum 
bowel rest, and parenteral nutrition. If a small perianastomotic 
abscess is demonstrated with no abdominal collections or free 
air and without systemic symptoms, an attempt of percutaneous 
drainage should be made with close clinical observation. In pa-
tients with signs of peritonitis or signs of sepsis, even if minimal, 
reoperation is required and should not be delayed. Abdominal ex-
ploration allows peritoneal lavage and reposition of new drains if 
needed. If possible, a laparoscopic approach may be preferred in 
order to minimize septic contamination of the abdominal wall. 
In left-sided colectomies, intraoperative endoscopic exploration of 
the anastomosis is helpful to determine the extent of the leak, and 
it also allows colonic lavage. If the leak involves less than one third 
of the anastomosis and the abdominal contamination is minimal, 
a diverting stoma may be sufficient. If the leak is larger or the 
anastomosis is disrupted, it has to be dismantled with the creation 
of a terminal stoma. An ileocolic anastomosis in right-sided resec-
tions can be managed ideally by redo of the anastomosis, but if the 
patient is unstable, the anastomosis has to be dismantled and an 
end ileostomy constructed. 
Necrosis of the Transposed Colon
This is a rare and serious complication that has a subtle presen-
tation characterized by malaise, early leukocytosis, and initially 
low-grade fever with foul-smelling material in the perianastomotic 
drains. It is a manifestation of ischemic injury of the transposed 
colon. Its presentation may mimic an anastomotic leak, but it 
must be immediately differentiated from a simple dehiscence be-
cause the treatment must be more aggressive. The diagnosis is of-
ten made with abdominal exploration or intraoperative endoscopy 
(Fig. 52.83) that shows a clear demarcation line. Its treatment re-
quires immediate dismantling of the anastomosis with creation of 
a terminal stoma. 
Bleeding
Minor bleeding—self-limited and not requiring blood transfusion 
or active treatment—is very common after colorectal resections 
and is observed with the first bowel movements. Major bleeding, 
with hemodynamic instability requiring active resuscitation, need 
of blood transfusion, and active treatment, can occur in up to 4% 
of cases. This may happen in the early postoperative period and 
in these cases is generally caused by small arterioles at the staple 
lining. Treatment is usuallyendoscopic with positioning of clips 
at the suture line, epinephrine injection, or electrocoagulation. If 
endoscopy fails, angiographic treatment is possible, but it might 
lead to ischemia of the anastomotic rim and subsequent possible 
further leaks. 
Twisting
Twist is another very rare but serious complication. It is described 
almost exclusively in extracorporeal ileocolic anastomosis after 
laparoscopic hybrid right colectomies, and it is caused by the lack 
of optimal visualization of the mesentery and mesocolon through 
the mini-laparotomy. When the anastomosis is twisted, there is 
an immediate swelling and edema of the small bowel that, if over-
looked and if left untreated, can lead to ischemia and gangrene 
of the intestine. Immediate redo of the anastomosis is necessary. 
Strictures
Clinically significant strictures are those that present with obstruc-
tive symptoms and occur in 4% to 10% of circular anastomoses 
(Fig. 52.84). Risk factors are the use of a small-diameter stapler 
(25-mm circular staplers should never be used in colorectal anas-
tomosis in adults), anastomotic leaks, ischemia, and radiation. 
A B
B
A A
V
[L]
[R]
[L]
FIG. 52.82 (A) Leak at a colorectal anastomosis. A, Air around the anastomosis; B, a fluid collection behind the 
anastomosis. (B) Leak at a colorectal anastomosis. A, Air along the perianastomotic drains.
FIG. 52.83 A nonviable anastomosis with a visible leak (white arrow). 
The necrotic appearance of one half of the anastomosed bowel is appar-
ent with a clear line of demarcation (black arrow).
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1388 SECTION X Abdomen
Treatment is usually endoscopic with balloon dilation or place-
ment of radial incisions or positioning of endoluminal stents. 
Redo of the anastomosis may be necessary in strictures not re-
sponding to the endoscopic treatment. 
Low Anterior Resection Syndrome
Rather than a true complication, this is a consequence of low 
anterior resection and coloanal anastomosis and may be present 
in up to 80% of patients undergoing a low anterior resection. It 
is a syndrome characterized by a mixture of multiple symptoms 
that include frequency, multiple fragmented bowel movements, 
a sensation of incomplete emptying, incontinence, constipation, 
and diarrhea. Most of the symptoms improve 1 year or more after 
the resection, but long-term dysfunction is described in the ma-
jority of patients. The cause of LARS is multifactorial. It may be 
due to an injury of the internal sphincter, loss of sensitivity in the 
anorectal mucosa, loss or impairment of the rectoanal-inhibitory 
reflex, reduction of the capacity of the rectal reservoir, and/or loss 
of compliance of the transposed colon. The incidence is higher 
in patients undergoing TME, in those with coloanal anastomo-
sis, in those who received neoadjuvant chemoradiation, and in 
those who had an anastomotic leak. Preventive technical mecha-
nisms are currently used to improve LARS symptoms that aim to 
increase the capacity of the neorectum: anastomosis with a 5 to 
6-cm colonic J-pouch or with a transverse coloplasty or side-to-
end colorectal anastomosis (Fig. 52.85). The coloplasty is a pos-
sible alternative in obese patients in which the J pouch does not 
fit into the narrow pelvis. A longitudinal 10-cm colotomy is made 
about 5 cm from the distal end of the transposed colon and is 
then sutured transversely in order to widen the colon and increase 
it compliance. The treatment of LARS is often empirical, based 
on diet control, balanced use of loperamide associated with fiber 
products, physical therapy including biofeedback, and transanal 
irrigation. In a minority of highly symptomatic patients with low 
quality of life, after failure of conservative treatment, the construc-
tion of a stoma can be necessary as a definitive treatment.46 
Postoperative Treatment and Follow-up
Five-year survival rate for patients with stage I cancer is approxi-
mately 90%; for stage II, 75%; and for stage III (with positive 
lymph nodes), 50%. Patients with distant nonresectable metas-
tases have a 5-year survival rate of about 5%. Patients with re-
sectable liver metastases amenable to curative liver resection with FIG. 52.84 Endoscopic view of a tight anastomotic stricture (arrow).
B CA
10 cm
5 cm
10 cm
FIG. 52.85 Coloplasty. (A) A 10-cm longitudinal colotomy is made approximately 5 cm proximal to the end 
of the colon and the anvil of a circular stapler placed into the bowel lumen and pierced through adjacent to the 
distal staple line or secured using a purse-string suture (B). The colotomy is then closed transversely in one or 
two layers. (C) A circular stapled colorectal anastomosis is then performed.
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1389CHAPTER 52 Colon and Rectum 
free margins and favorable clinical risk factors may have a 5-year 
survival rate up to 60%. The majority of recurrences occur within 
the first 2 years after resection of the primary tumor. Close follow-
up is therefore necessary especially within this interval in order 
to allow for early detection of any recurrence or metachronous 
tumor that could be amenable to curative treatment. The reader 
is referred to the ASCRS Practice Guideline for the Surveillance 
of Patients After Curative Treatment of Colon and Rectal Cancer.
Follow-up includes office visits with CEA levels obtained every 
6 months for 5 years after surgery, then annually. Rising levels 
of CEA require additional tests in order to identify recurrent or 
metastatic disease. Colonoscopy should be scheduled 1 year after 
surgery (or 3–6 months after surgery if the entire colon was not 
completely investigated at the time of diagnosis); further colo-
noscopies should be repeated every 3 years if no adenomas were 
detected and every year if adenomatous polyps are found until 
the colon is found clean. Chest and abdominal CT scans are per-
formed annually.
Postoperative Treatment
Adjuvant chemotherapy may be indicated in certain subsets of 
 patients based on postoperative pathologic status.
Stage I: tumor invades muscularis propria, negative lymph nodes. 
Follow-up alone is the appropriate choice. 
Stage II tumors: tumor penetrates into pericolic fat, negative lymph 
nodes. In general, in the absence of risk factors, there is limited 
evidence of any benefit from adjuvant chemotherapy: the absolute 
survival advantage with 5-fluorouracil (5-FU)/leucovorin (folinic 
acid [FA]) is about 3% to 4% (P borderline significant). In a 
 recent metaanalysis by Bockelman et al., the 5-year DFS with or 
without chemotherapy is 81.4% versus 79.3%, respectively.
In stage II colon cancer patients, the following potential risk 
factors can be considered as relative indications for chemotherapy: 
poorly differentiated cancer (G3–4), vascular and perineural inva-
sion, obstruction, perforation, adjacent organ invasion (pT4), and 
an inadequate number of examined number lymph nodes (is 
due to the effect of other regulatory genes.
MSI-H condition (deficient expression of MMR genes) is 
more frequent in stage II disease (22%) than in stages III (12%) 
and IV (3%) and does appear to have a favorable prognostic 
 significance in stage II. Moreover, adjuvant 5-FU treatment seems 
to have a detrimental effect on survival in stage II but not stage III 
colon cancer patients. All these elements are to be considered with 
 respect to uncertain effectiveness. 
Stage III disease: positive lymph nodes. Adjuvant chemotherapy 
is indicated in stage III patients. 5-FU and FA are combined with 
oxaliplatin in the FOLFOX protocol. In the CAPOX (or Xelox) 
regimen, oral capecitabine is used instead of 5-f luorouracil fo-
linic acid (5-FUFA). Recently, a preplanned pooled analysis of 
data from six randomized phase III trials of adjuvant therapy in 
stage III colon cancer patients, was carried out48: a shorter treat-
ment duration may reduce side effects, particularly neurotoxic-
ity that is dose dependent and related to oxaliplatin. This analysis 
evaluated the noninferiority of 3 months versus 6 months of ad-
juvant FOLFOX/CAPOX therapy. The primary end point, the 
rate of DFS at 3 years, was not confirmed: 3 months is inferior 
to 6 months of adjuvant chemotherapy. However, in an analysis 
that had not been planned prior to starting the study, there was a 
difference between FOLFOX and CAPOX related to the risk class 
of patients. Low-risk patients were defined as pT3pN1, and high-
risk patients, pT4 (any N) or N2.
In low-risk patients, 3 months (four cycles) of CAPOX was not 
inferior to 6 months of the same regimen (3 years DFS: 85.0% vs. 
83.1%, 3 months vs. 6 months). In high-risk patients, 3 months 
of the CAPOX regimen was sufficient (3 years DFS: 64.1% vs. 
64.0%, 3 months vs. 6 months).
With regard to the FOLFOX regimen, 6 months seems su-
perior to 3 months, regardless of the risk group (3 years DFS in 
high-risk: 61.5% vs. 64.7%, 3 months vs. 6 months). One has to 
remember, however, that these are unexpected findings because 
a comparison between treatments was not preplanned: patients 
were not randomized to receive CAPOX or FOLFOX treatment. 
Metastatic disease. There are several issues that have to be con-
sidered when choosing a treatment for metastatic disease: tumor 
burden, goal of the treatments chronicity, induction of resect-
ability in borderline resectable disease, primary resection, age and 
comorbidities, patient’s preferences, site of primary tumor, and 
molecular biology: N-Ras, K-Ras (i.e., pan-Ras), and BRAF mu-
tation status.
Possible chemotherapy regimens are as follows:
 1. Anti-EGFR antibodies (panitumumab, cetuximab) can be 
used in pan-Ras wild-type and BRAF wild-type neoplasia. The 
mutational analysis can be performed on the primary tumor 
but also preferably on the metastatic tumor
 2. The standard treatment in BRAF-mutated metastatic disease is 
the administration of FOLFOXIRI (oxaliplatin + irinotecan + 
5-FUFA) and bevacizumab. BRAF mutated patients have the 
worst prognosis.
 3. If the primary tumor is right sided, anti-EGFR antibodies 
given in addition to chemotherapy (FOLFOX [oxaliplatin + 
5-FUFA] or FOLFIRI [irinotecan + 5-FUFA]) are not superior 
to chemotherapy alone in first-line treatment: therefore, they 
are usually not administered in this phase. Doublets (FOLF-
OX or FOLFIRI) or the triplet FOLFOXIRI in fit patients, 
in combination with anti–vascular endothelial growth factor 
antibody (bevacizumab), could be the best choice.
 4. In left-sided primary tumors, the addition of cetuximab or pa-
nitumumab to FOLFOX/FOLFIRI could be the first line of 
treatment. However, also in this case, the use of FOLFOXIRI 
can be considered.
 5. In older or unfit patients, unable to tolerate doublets, 
capecitabine with bevacizumab is an appropriate treatment.
If the goal of treatment is the resection of hepatic disease, no 
more than six cycles of chemotherapy should be administered be-
fore surgery, in order to avoid hepatic toxicity (steatohepatitis with 
irinotecan and sinusoidal damage with oxaliplatin). In addition, 
bevacizumab needs to be stopped 6 weeks before hepatic resec-
tion because of its detrimental effects on wound healing. Beva-
cizumab can be started 4 weeks after surgery or once the wounds 
have healed. 
PELVIC FLOOR DISORDERS AND CONSTIPATION
Disorders of the pelvic floor include multiple conditions, of-
ten involving colorectal, urologic, and gynecologic specialists. 
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1390 SECTION X Abdomen
Constipation is a dysfunction of colonic motility and of the 
defecation process. It can be present with several medical and 
colorectal conditions, including colon obstruction and pelvic 
floor diseases. Functional constipation is an entity that must be 
differentiated from distinct anatomic problems during patient 
evaluation and may be considered for surgical treatment if un-
responsive to active medical therapy. The reader is again referred 
to the ASCRS Consensus Statement of Definitions for Anorectal 
Physiology Testing and Pelvic Floor Terminology, Clinical Prac-
tice Guidelines for the Treatment of Rectal Prolapse, and Clini-
cal Practice Guideline for the Evaluation and Management of 
Constipation.
The pelvic floor disorders that present to the surgeon include:
	•	 	rectal	prolapse	or	procidentia:	a	circumferential,	full-thickness	
intussusception of the rectum
	•	 	rectocele:	a	bulging	of	the	rectum	into	the	posterior	wall	of	the	
vagina
	•	 	cul-de-sac	hernia:	a	protrusion	of	the	peritoneum	between	the	
rectum and the vagina, referred to as “enterocele” if it contains 
the small bowel, and as “sigmoidocele” if it contains the sig-
moid colon.
	•	 	anismus:	the	failure	of	the	puborectalis	and	the	external	anal	
sphincter to relax during defecation (simple nonrelaxation or 
paradoxical contraction).
Even if functional disorders do not always require surgical op-
eration, the surgeon is almost always involved in the evaluation of 
these patients and in establishing a treatment plan.
Diagnosis: Testing and Evaluation
Anorectal Physiology Laboratory Tests
Anorectal physiology tests are performed to evaluate anal canal 
pressures to determine the presence of anal reflexes, anal sensation, 
and electromyography recruitment.
Anorectal manometry evaluates the high-pressure zone (i.e., the 
length of the anal canal), the resting pressure, mostly due to 
the internal sphincter, the maximum voluntary pressure, and 
the squeeze pressure, due to the external anal sphincter (Fig. 
52.86). The test is performed by placing a manometry catheter 
with a water-filled balloon at its tip in the anal canal, so that 
the balloon at the tip lies within the rectal lumen. Normal rest-
ing pressure values are 40 to 80 mm Hg. Anorectal manometry 
also provides information on intrarectal pressures, reflexes, rec-
tal sensation, and rectal compliance. High-resolution manom-
etry can provide greater physiologic resolution and minimizes 
motion artifacts.
The balloon expulsion test evaluates the ability of the patient to 
expel a balloon inflated with 50 to 60 cc of water/gas/air that 
simulates stool.
Pudendal nerve terminal motor latency measures the conduction 
of the pudendal nerve from its emergence at the level of the 
ischial spines to the internal anal sphincter, by the use of a trans-
ducer. Normal pudendal nerve terminal motor latency times 
are 2.0 ± 0.2 milliseconds. Prolonged values are seen in trau-
matic injuries (spinal cord) or with stretch injury from obstetric 
trauma due to prolonged labor, chronic stretch injury as seen 
in long-standing defecation disorders, sacral nerve root damage 
or chronic diseases as diabetes. This is typically measured witha special electrode taped to the index finger of the examiner, 
whereby the tip of the finger electrode stimulates the pudendal 
nerve and the recording electrode at the base of the finger mea-
sures anal sphincter contraction.
Electromyography records the change from basal electrical activ-
ity of motor units of the external sphincter and puborectalis 
muscle during activity. Patients with inappropriate or para-
doxical puborectalis contraction fail to show a relaxation of the 
muscles when asked to push. 
Imaging to Evaluate the Pelvic Floor and Colonic Transit
Endoanal ultrasound (Fig. 52.87) can be used to evaluate the 
integrity, thickness, and possible abnormalities (scars, fistulas) 
of the internal and external anal sphincter.
Defecography is a dynamic study of the anorectum and the pelvic 
floor during defecation. It provides information regarding ana-
tomic abnormalities, such as rectocele, rectal prolapse, internal 
rectal intussusception, and cul-de-sac hernia, as well as about 
functional disorders, such as nonrelaxation or paradoxical pu-
borectalis contraction, perineal descent, and the degree of rec-
tal emptying. Dynamic images are captured with fluoroscopy, 
with the rectum and the vagina opacified with radiographic 
contrast and the patient in the sitting position on a radiolucent 
commode. If magnetic resonance defecography is performed, 
the rectum is opacified with a mixture of ultrasonography gel 
and gadolinium. The advantages of MRI are high-quality im-
ages of the pelvic soft tissues and viscera and avoiding use of 
ionizing radiation. It is, however, limited by the supine posi-
tion of the patient that does not reproduce normal conditions 
of defecation (Fig. 52.88).
Colonic transit time is a test that studies colonic inertia. The pa-
tient is asked to ingest 24 radio-opaque markers contained in a 
capsule (Sitzmarks) and to refrain from using laxatives and any 
other mechanical measures that might interfere with colonic 
function. The progression of the markers through the three ar-
eas of the colon (right, left, and rectosigmoid) is studied with 
plain abdominal films that are taken every other day until day 
7. In the healthy population, 80% of the markers should be 
expelled by day 5. Patients with slow transit constipation or 
colonic inertia retain a significant portion of the markers dur-
ing the entire time of the study (Fig. 52.89). 
Rectal Prolapse (Procidentia)
Anatomy and Pathophysiology
The rectal prolapse is a circumferential, full-thickness intussuscep-
tion of the rectal wall. The degree of prolapse can vary from intrar-
ectal or internal rectal prolapse (Fig. 52.90), to intra-anal prolapse, 
to external rectal prolapse (Fig. 52.91). Rectal prolapse is an un-
common condition that occurs in about 0.5% of the general popu-
lation, with women older than 50 years 6 times more likely than 
men to develop rectal prolapse. The few men who present with 
rectal prolapse are usually younger than 40 years. Young patients 
(males and females) with prolapse often suffer from psychiatric dis-
eases, such as autism or developmental delay, and take constipat-
ing medications. The cause of rectal prolapse is still unknown, but 
some anatomic defects are commonly found in patients with total 
rectal prolapse. These defects include a diastasis of the levator ani 
muscle, an abnormally deep cul-de-sac, a redundant sigmoid colon, 
a patulous anus, and a lack of fascial attachments of the rectum 
against the sacrum. Risk factors of rectal procidentia include: age 
over 40 years, female gender, prior pelvic surgery, chronic strain-
ing and constipation, chronic diarrhea, vaginal delivery, and mul-
tiparity (however, one third of the female rectal prolapse patients 
are nulliparous), pelvic floor dysfunction and/or anatomic defects, 
neurologic diseases/injuries, and psychiatric diseases that require 
constipating medications. Rectal prolapse usually has a progressive 
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1391CHAPTER 52 Colon and Rectum 
Resting profile Squeeze EAS relax RAIR
FIG. 52.86 A normal anorectal manometry: resting and squeeze pressure curves are evident, and the exter-
nal anal sphincter relaxation when the patient is asked to push. The rectoanal inhibitory reflex is present. EAS, 
External anal sphincter.
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1392 SECTION X Abdomen
course from transient self-reducing prolapse during defecation, to 
prolapse requiring digital self-reduction, to stable prolapse that may 
present with ulceration and even nonreducible, incarcerated pro-
lapse with necrosis in the most advanced and complicated cases. 
Symptoms
Symptoms include discomfort due to the prolapsed tissue, in-
continence with drainage of mucous or blood, and constipation. 
The majority (50%–75%) of patients with evident rectal pro-
lapse complain of fecal incontinence (passive or urge inconti-
nence) that is caused by the presence of a direct conduit, by the 
chronic stretching of the sphincter due to the prolapse, and by 
persistent stimulation of the rectoanal inhibitory reflex caused 
by the prolapsed rectum. Up to one half of patients with incon-
tinence have also pudendal neuropathy with a prolonged puden-
dal nerve terminal motor latency. The other 25% to 50% of the 
patients, and in particular those with intrarectal prolapse, report 
constipation or obstructed defecation (feeling of an incomplete 
rectal evacuation during defecation) that results from the “tele-
scoping” of the bowel on itself creating a functional blockage 
that worsens with straining (Fig. 52.90B,C) or by the presence 
of a concomitant rectocele. 
Diagnosis and Differential Diagnosis
On physical exam, true rectal prolapse must be differentiated 
from prolapsed rectal mucosa or prolapsed hemorrhoids: the 
full-thickness rectal prolapse has concentric folds, whereas pro-
lapsed hemorrhoids or rectal mucosa is characterized by radial 
folds, with grooves along hemorrhoid cushions. At rest, typical 
findings include a patulous anus with a lax sphincter. Exami-
nation is performed in the office with the patient in standard 
left lateral decubitus or in the sitting or squatting position dur-
ing straining. If the prolapse cannot be observed in the office 
setting, the patient can be asked to make a “selfie” at home 
to document the prolapse. Proctoscopic examination demon-
strates redundant tissue and, in 10% to 15% of patients, an an-
terior solitary rectal ulcer. Proctoscopy may indicate erythema 
at 5 to 6 cm, which is the leading edge of the prolapse. Fluo-
roscopic or MRI defecography is an additional test to confirm 
the diagnosis of rectal prolapse and provides more informa-
tion regarding coexisting disorders, such as rectocele, cysto-
cele, vaginal vault prolapse, enterocele, and sigmoidocele (Fig. 
52.92). Colonoscopy should be always performed to exclude 
the presence of CRC or other colonic pathology. A colonic 
transit study is performed in patients with a lifelong history 
of constipation in order to differentiate constipation due to 
obstructed defecation from constipation due to slow colonic 
transit. The two frequently coexist. Endoanal ultrasound usu-
ally shows a thickening of the internal anal sphincter. 
External sphincter
Pubo rectalis muscle
Inernal sphincter
-2.8-2.8
2.8A B
FIG. 52.87 Endoanal ultrasound. (A) The arch-shaped hyperechoic puborectalis muscle appears as a whitish 
structure. (B) The hypoechoic internal sphincter (black arrow) and the hyperechoic external sphincter (white 
arrow) are shown.50
mm
[P]
[F]
FIG. 52.88 A magnetic resonance imaging image of rectal prolapse.
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1393CHAPTER 52 Colon and Rectum 
Day 5 Day 7Day 3
A B C
FIG. 52.89 Colonic transit study: plain abdominal films at 3, 5, and 7 days after ingestion of radiopaque 
 markers. Note that at day 5, the majority of the radio-opaque markers are within the pelvis; however, by day 7, 
most markers have passed.
B C
A
FIG. 52.90 (A) The internal rectal prolapse of a male patient is nicely demonstrated by defecography. (B and 
C) Progression of the internal rectal prolapse.
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1394 SECTION X Abdomen
FIG. 52.91 A patient with a huge external rectal prolapse. (Courtesy of 
G. Sarzo, MD, Hospital Sant Antonio, Department of Surgery, Padova Italy.)
Internal rectal
prolapse
 Sigmoidocele
FIG. 52.92 Defecography of a young male patient who presents with 
internal rectal prolapse (white arrow) and sigmoidocele (black arrow).
Nonoperative Management
Prolapse-associated symptoms of constipation and fecal inconti-
nence can be palliated with medical treatment, in order to im-
prove quality of life. Adequate fluid intake, fiber supplements, and 
stool softeners can treat constipation. Sugar or salt can be used 
topically to reduce rectal mucosal edema and facilitate reduction 
of the prolapsed tissue. Enemas and suppositories may be helpful 
to assist in defecation. 
Operative Repair
The goals of surgery are to eliminate the prolapse and correct the 
anatomic and functional abnormalities. The approach can be trans-
abdominal or transperineal. None have shown a clear superiority 
in terms of recurrence rates which vary between 13% and 31%. 
The choice of procedure is based upon the patient’s comorbidities, 
the patient’s age and bowel function, and the surgeon’s preference.
Abdominal procedures. The rationale of the intraabdominal 
approach is to perform a fixation of the rectum with the goal of 
providing adequate upward tension to prevent a recurrence, but at 
the same time allowing appropriate evacuatory movements during 
defecation. The abdominal approach can be performed via open 
or minimally invasive approaches (laparoscopic or robotic). Both 
have equivalent clinical and functional results, recurrence rates 
(4%–8%), and morbidity (10%–33%). Laparoscopy offers ben-
efits in terms of pain control, hospital stay, and recovery time. The 
advantages offered by robotic rectal prolapse repair are the ease in 
suturing and tying and improved visualization of the deep pelvis. 
The rectum must be dissected, retracted intraabdominally, and 
fixed to the presacral fascia with sutures (posterior rectopexy). In 
these cases, a simultaneous resection of the redundant sigmoid can 
be performed in selected patients with coexisting constipation. A 
mesh can be utilized to increase scarring and improve fixation of 
the rectum posteriorly or anteriorly. With the posterior mesh recto-
pexy, the rectum is mobilized posteriorly and laterally down to the 
levator ani muscles, and a mesh is fixed to the presacral fascia, be-
low the sacral promontory, and to the rectum laterally (Fig. 52.93). 
This technique is associated with significant improvement in fecal 
incontinence in 20% to 60% of patients but has a 20% rate of 
postoperative complications and is associated with a 2% to 5% re-
currence rate. The more recently described ventral mesh rectopexy 
is a technique that involves a limited anterior rectal mobilization 
and a mesh suspension to the sacral promontory. The mesh is fixed 
to the anterior wall of the rectum and suspended to the sacral 
promontory (Fig. 52.94). Advantages of this technique are the im-
provement in postoperative incontinence and constipation, with 
few cases of de novo postoperative constipation, and low compli-
cation and recurrence rates (3%–5%).49 In published series, many 
different types of mesh and fixation devices are used: nonabsorb-
able or biologic grafts, tacks, sutures, or staples to fix the mesh. 
Mesh-related complications include erosion usually into the va-
gina, infection and pelvic sepsis, bowel obstruction, and mesh 
detachment and/or migration. In theory, with the use of biologic 
mesh, the risk of infection or erosion may be lower, and the risk of 
recurrence higher, but recent literature 49 shows no statistical im-
provement in recurrence and complication rates between biologic 
and nonabsorbable mesh. The follow-up for studies using biologic 
mesh is, however, short. 
Perineal approach. Perineal procedures allow for the resection 
of the prolapse without concomitant fixation. They are recom-
mended for the elderly or medically unfit patients and are thought 
to be associated with a lower operative morbidity and mortality 
but with higher recurrence rates. Recent reviews and trials have, 
however, concluded that there are no significant differences in re-
currence and reoperation rates between perineal and abdominal 
approaches. Therefore, perineal procedures may have to be consid-
ered an option for all patients with rectal prolapse. The “Altemeier 
procedure” or perineal proctectomy or proctosigmoidectomy is a 
true rectosigmoidectomy. The prolapse is exteriorized, it is grasped 
with Allis clamps, and a full-thickness circumferential incision 
is made through the rectum 1 cm above the dentate line. The 
peritoneal cavity is entered anteriorly and the redundant sigmoid 
colon is extracted transanally (Fig. 52.95). The levator muscles 
are visualized and can be plicated posteriorly in order to reinforce 
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1395CHAPTER 52 Colon and Rectum 
the pelvic floor and restore the anorectal angle (levatorplasty or 
Parks postanal repair). A handsewn or stapled coloanal anastomo-
sis is then performed. The operation can be done under epidural 
anesthesia, with minimal postoperative pain. This technique al-
lows for the resection of redundant bowel, it has low complication 
rates, and, especially when levator plication is done, it is associated 
with low recurrence rates (10%). For patients with a short (mobilized and the 
mesh is fixed to the presacral fascia. (B) The mesh is fixed to both sides of the rectum.
FIG. 52.94 Ventral mesh rectopexy. The mesh is attached to the an-
terior rectal wall and the sacral promontory. (Courtesy of G. Sarzo, MD, 
Hospital Sant Antonio, Department of Surgery, Padova Italy.)
FIG. 52.95 The Altemeier procedure or perineal proctectomy. The re-
dundant rectosigmoid colon is resected through a transperineal approach 
and a hand-sewn coloanal anastomosis is performed.
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1396 SECTION X Abdomen
good results in cases of obstructed constipation, but the onset of 
chronic proctalgia and stool urgency with postoperative inconti-
nence have often been reported. Other complications of transrec-
tal stapled repair are staple-line bleeding and, rarely, staple-line 
disruption and rectovaginal fistula (overall morbidity rate from 
7%–21%). Because of the high rate of serious complications and 
poor functional outcome, this is not recommended by the ASCRS 
Clinical Practice Guidelines. 
Solitary Rectal Ulcer
Solitary rectal ulcer syndrome (SRUS) is a rare chronic benign 
disorder characterized by a combination of symptoms, clinical 
findings, and histologic abnormalities. Twenty percent of patients 
have a single ulcer, while 40% of patients have multiple ulcers. 
The remainder have nonspecific lesions such as hyperemic mucosa 
or pseudopolyps.
SRUS is a disorder of young adults (30–40 years), with a slight 
female predominance. The cause is multifactorial and includes in-
ternal rectal prolapse and abnormal/paradoxical contraction of the 
puborectalis muscle. These two conditions result in trauma and 
compression of the anterior rectal wall on the upper anal canal 
during straining and defecation, with resulting mucosal ischemia 
and, in some cases, ulceration. Symptoms reported by patients 
with SRUS include rectal bleeding, prolonged excessive straining, 
incomplete defecation/tenesmus, mucous discharge, perineal and 
abdominal pain, and constipation. Up to one quarter of patients 
are asymptomatic.
Physical examination and anoscopy demonstrate an intrarectal 
prolapse and a 1 to 1.5-cm ulcer of the anterior rectal wall 3 to 
10 cm from the anal verge that is sometimes difficult to differenti-
ate from a rectal cancer. Histologic examination of biopsies shows 
characteristic findings: fibromuscular obliteration of the lamina 
propria, hypertrophied muscularis mucosae with muscular fibers 
between the crypts, and glandular crypt abnormalities. These spe-
cific findings differentiate SRUS from cancer and other inflamma-
tory lesions such as IBD, ischemic colitis, and infectious proctitis.
For patients with mild to moderate symptoms and no significant 
mucosal prolapse, medical treatment is usually effective. It consists 
of patient education and behavioral modification: high-fiber diet, 
stool softeners and bulking laxatives, avoidance of straining and/or 
anal digitations, minimizing time on the toilet, and the use of su-
cralfate, corticosteroid, and/or mesalamine enemas. Surgery is rare-
ly indicated and is reserved only for highly symptomatic patients 
absolutely unresponsive to medical treatment. Surgical options in-
clude local excision of the ulcer, treatment of the rectal prolapse, or 
a defunctioning stoma for patients who have failed other options. 
Unfortunately, many patients with SRUS continue to have symp-
toms of anorectal dysfunction regardless of the treatment. 
Rectocele
A rectocele is a bulging of the anterior wall of the rectum into 
the posterior wall of the vagina. The most common risk factors 
are advanced age, history of pregnancy and vaginal childbirth, 
increasing body mass index, chronically elevated intraabdominal 
pressure, and a history of hysterectomy. The cause of rectocele is 
multifactorial and may be explained by a muscular and/or neuro-
logic damage to the rectovaginal septum (usually due to obstetric 
trauma) and due to the effect of chronic straining on the endo-
pelvic fascia and on the posterior wall of the vagina. It can be 
associated with other pelvic organ prolapses. Most rectoceles are 
asymptomatic, but when they become symptomatic, the cardinal 
symptom is difficulty in rectal emptying and the need to press 
against the posterior wall of the vagina or against the perineum 
in order to complete the rectal emptying (obstructed defecation). 
Other symptoms include the sensation of a vaginal bulge, urinary 
and/or sexual dysfunction, constipation, and in some cases fecal 
incontinence. The mechanism of incontinence is thought to be 
due to fecal trapping within the rectal pocket allowing for post-
defecatory leakage, an associated mucosal prolapse that impairs 
anal closure or overflow incontinence. The diagnosis of rectocele is 
mainly clinical and based on physical examination. Digital vaginal 
and rectal examinations shows a bulging in the posterior vaginal 
wall and in the anterior rectal wall during straining that can be 
associated with the prolapse of other pelvic organs and with an-
terior cystocele. Associated stress urinary incontinence is assessed 
by making the patient cough or perform Valsalva maneuver with 
a full bladder.
On defecography, the rectocele appears as a bulging of the rec-
tal wall toward the vagina. A rectocele is graded as small if it is 
less than 2 cm, moderate if it is between 2 and 4 cm, and large 
if it is larger than 4 cm in size (Fig. 52.97). This test also gives 
B
C D
A
E
FIG. 52.96 The Delorme procedure. The mucosal layer is infiltrated 
with epinephrine containing solution (A), incised (B), and stripped off 
the underlying muscularis (C). Plication of the muscularis propria is per-
formed (D).The operation concludes with an anastomosis between the 
proximal and distal mucosal edges (E).
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1397CHAPTER 52 Colon and Rectum 
information about the possible trapping of contrast within the 
rectocele during defecation and about the possible association 
with an enterocele or sigmoidocele. It is important to realize that 
the degree of anatomic distortion often does not correlate with the 
degree of functional impairment and symptoms. Dynamic MRI 
and MRI defecography are limited by the fact that they are per-
formed with the patient in the supine position (i.e., not in the 
normal upright position for defecation). The balloon expulsion 
tests can identify the inability to expel an inflated balloon from the 
rectum after 4 minutes of sitting on a commode. Asymptomatic 
rectoceles do not need treatment, while patients with a symptom-
atic rectocele are initially managed with a bowel regimen and fiber 
products in order to improve defecation. Only selected patients 
with markedly symptomatic rectoceles unresponsive to medical 
treatment are candidates for surgery. The goal of surgery is to re-
move the redundant tissue of the rectocele and to strengthen the 
rectovaginal septum.
The transvaginal approach, preferred by gynecologists, allows 
for a better visualization and access to the levator muscles. A lo-
cal anesthetic with epinephrine or vasopressin is injected below 
the vaginal mucosa to dissect the tissue and for hemostasis. The 
vaginal epithelium is opened in the posterior midline to the upper 
level of the defect; the fibromuscular layer is exposed and plicated 
in the midline with vertically or transversely placed sutures. The 
puborectalis can be reapproximated. The surplus vaginal epithe-
lium is cut off if necessary and sutured with absorbable sutures.An endorectal repair is performed by colorectal surgeons, with 
the patient in prone jackknife position. A local anesthetic plus 
epinephrine or vasopressin is injected in the submucosal plane to 
dissect the tissue and for hemostasis. A T-shaped or midline inci-
sion is made in the rectal mucosa just above the dentate line. Two 
lateral mucosal flaps are developed on either side of the midline 
to a level proximal to the rectocele. The excess rectal mucosa is 
excised. The underlying muscularis layer is exposed and plicated 
with transversely placed absorbable sutures and the mucosal edges 
are then approximated with absorbable sutures. The transperineal 
rectocele repair is performed by a transverse incision across the 
bulbocavernosus and transverse perineal muscles; the two limbs 
of the puborectalis muscle are reapproximated. A mesh can be 
placed in order to reinforce the plasty. This approach is indicated 
especially in patients with associated fecal incontinence, because a 
concomitant sphincteroplasty or levatorplasty can be performed. 
Constipation
Constipation is a frequent condition that can affect more than 
50% of population over 65, but in a small subset of patients, 
constipation may present at younger age. Several medical con-
ditions can contribute to constipation, including metabolic, 
endocrine, neurologic, and psychiatric disorders. In adults, 
new-onset constipation is always a worrisome symptom and the 
primary cause must be excluded. Hypothyroidism and medica-
tion-induced constipation are common causes. The presence 
of colorectal malignancies and other cause of colonic obstruc-
tion must be excluded with colonoscopy. Patients should be 
counseled to increase fluid intake up to 1.5 to 2  L/day and 
to increase the fiber content in diet. Polyethylene-based solu-
tions (e.g., MiraLAX), probiotics, and over-the-counter prod-
ucts may be helpful. Stimulant laxatives such as bisacodyl or 
senna should not be used long-term. A locally acting chloride 
channel activator (lubiprostone; Amitiza), a guanylate cyclase 
agonist (Linzess), and/or a serotonin 5-HT4 agonist (Moteg-
rity) can all be used to treat symptoms of constipation. Long-
term constipation, resistant to medical treatment and laxatives, 
should be further investigated. According to Rome IV criteria, 
functional constipation is diagnosed if (1) there are at least 
two of the following symptoms, during at least 25% of defeca-
tions, for at least 3 months50: straining, lumpy, or hard stools; 
a sensation of incomplete evacuation; sensation of anorectal 
obstruction/blockage; need for manual maneuvers to facilitate 
defecation (e.g., digital evacuation, support of the pelvic floor); 
or fewer than three spontaneous bowel movements per week; 
(2) loose stools rarely present without the use of laxatives; and 
(3) there are insufficient criteria for irritable bowel syndrome. 
In the presence of obstructed defecation symptoms, defecog-
raphy, anorectal manometry, balloon expulsion testing, and 
electromyography can exclude the presence of pelvic floor dis-
orders. Measuring the colonic transit time with the use of radi-
opaque markers (Sitzmark) can establish the diagnosis of slow 
transit constipation or colonic inertia. Slow transit constipa-
tion can have a neuropathic origin, even if a specific histologic 
change has not yet been demonstrated. The frequency of bowel 
movements varies in these patients from one to two per week 
to one per month. Some patients are unable to have a complete 
bowel movement in the absence of laxatives or colonic enemas. 
Severe constipation is associated with abdominal distension, 
abdominal pain, and nausea, and these symptoms can so af-
fect the quality of a patient’s life that they can be absolutely 
miserable. Chronic symptoms can be present from childhood 
or adolescence. Slow transit constipation can present with a 
megacolon on plain x-ray (Fig. 52.98); a water-soluble enema 
or colon CT can show a redundant, hypotonic colon, and colo-
noscopy similarly demonstrates a dilated hypotonic colon. In 
a subset of patients, the colon can be normal and not dilated 
at radiologic examination. In these patients, the diagnosis and 
the decision to initiate surgical treatment can be challenging. 
In highly symptomatic patients with slow transit constipation 
who failed aggressive medical therapy and whose quality of life 
is severely impaired, surgical treatment is indicated. Abdominal 
 colectomy with IRA (total abdominal colectomy with ileo-
rectal anastomosis [TAC-IRA] or colectomy with ileorectal 
Vagina
Rectocele
Rectum
Anal canal
FIG. 52.97 A defecating proctogram. Both the vagina and the rectum 
are opacified. The rectocele is clearly evident.
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1398 SECTION X Abdomen
anastomosis [CIRA]) is an operation that has demonstrated 
good clinical improvement with acceptable morbidity. It can 
be performed with minimally invasive techniques. Despite 
postoperative diarrhea that occurs in 5% to 15%, abdominal 
pain (30%–50%), small bowel obstruction (10%–20%), fecal 
incontinence, and recurrence of constipation (10%–30%) that 
have been reported in long-term follow-up, most patients are 
satisfied with functional results following colectomy and IRA.
Segmental colon resections based on transit time measure-
ments are no longer recommended. The extreme therapeutic solu-
tion proposed to patients with intractable constipation is a perma-
nent ostomy, usually an ileostomy.
SELECTED REFERENCES
American Society of Colon & Rectal Surgeons Clinical Practice 
Guidelines published in Diseases of the Colon & Rectum. 
Available through a link to the Clinical Practice Guidelines 
on the journal website https://journals.lww.com/dcrjournal/p
ages/default.aspx.
Specifically referred to in this chapter are the Clinical Prac-
tice Guidelines for (1) Enhanced Recovery after Colon and 
Rectal Surgery, (2) the Use of Bowel Preparation in Elective 
Colon and Rectal Surgery, (3) Colon Volvulus and Acute Co-
lonic Pseudo-obstruction, (4) the Management of Inherited 
Polyposis Syndromes, (5) the Surgical Treatment of Patients 
with Lynch Syndrome, (6) the Treatment of Colon Cancer, (7) 
the Management of Rectal Cancer, (8) the Surveillance of Pa-
tients after Curative Treatment of Colon and Rectal Cancer, 
(9) the Treatment of Rectal Prolapse, (10) the Evaluation and 
Management of Constipation, as well as (11) The Consensus 
Statement of Anorectal Physiology Testing and Pelvic Floor 
Terminology.
.
Beck DE, Wexner SD, Rafferty RF, eds. Gordon and Nivatvongs 
Principles and Practice of Surgery for the Colon, Rectum, and 
Anus. 4th ed. New York: Thieme Publishers; 2018.
This text provides excellent anatomic illustrations and detailed 
descriptions of all aspects of diseases of the colon, rectum, 
and anus.
.
Haggitt RC, Glotzbach RE, Soffer EE, et  al. Prognostic factors 
in colorectal carcinomas arising in adenomas: implications for 
lesions removed by endoscopic polypectomy. Gastroenterology. 
1985;89:328–336.
Description of Haggitt criteria, a classification for polyps with 
adenocarcinoma that assesses malignant potential according 
to the depth of invasion.
.
Sagar PM, Hill AG, Knowles CH, et  al. Keighley & Williams’ 
Surgery of the Anus, Rectum and Colon. 4th ed. Boca Raton, 
FL: CRC Press; 2019.
The most recently published two-volume textbook of colon 
and rectal surgery, with an international list of contributors.
.
Steele SR, Hull TL, Hyman N, et al. The ASCRS Textbook of Colon 
and Rectal Surgery. 3rd ed. New York: Springer; 2016.
This text is sponsored by the American Society of Colon and 
Rectal Surgeons (ASCRS), with chapters written by recog-
nized authorities in their field, including an excellent chapter 
onthe molecular basis of colorectal cancer and inherited syn-
dromes written by Dr. Matthew Kalady.
.
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Clostridium difficile infection in the United States. N Engl J 
Med. 2015;372:2369–2370.
 22. Loo VG, Davis I, Embil J, et  al. Association of Medical 
Microbiology and Infectious Disease Canada treatment prac-
tice guidelines for Clostridium difficile infection. JAMMI. 
2018;3:71–92.
 23. Miller MA, Louie T, Mullane K, et al. Derivation and valida-
tion of a simple clinical bedside score (ATLAS) for Clostridium 
difficile infection which predicts response to therapy. BMC 
Infect Dis. 2013;13:148.
 24. Furuya-Kanamori L, Doi SA, Paterson DL, et al. Upper ver-
sus lower gastrointestinal delivery for transplantation of fecal 
microbiota in recurrent or refractory Clostridium difficile 
infection: a collaborative analysis of individual patient data 
from 14 studies. J Clin Gastroenterol. 2017;51:145–150.
 25. Bartlett JG. Bezlotoxumab—a new agent for Clostridium dif-
ficile infection. N Engl J Med. 2017;376:381–382.
 26. Ferrada P, Callcut R, Zielinski MD, et  al. Loop ileostomy 
versus total colectomy as surgical treatment for Clostridium 
difficile–associated disease: an Eastern Association for the 
Surgery of Trauma multicenter trial. J Trauma Acute Care Surg. 
2017;83:36–40.
 27. Yngvadottir Y, Karlsdottir BR, Hreinsson JP, et al. The inci-
dence and outcome of ischemic colitis in a population-based 
setting. Scand J Gastroenterol. 2017;52:704–710.
 28. Brandt LJ, Feuerstadt P, Longstreth GF, et al. ACG clinical 
guideline: epidemiology, risk factors, patterns of presentation, 
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 29. Tseng J, Loper B, Jain M, et al. Predictive factors of mortality 
after colectomy in ischemic colitis: an ACS-NSQIP database 
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 30. Dienstmann R, Vermeulen L, Guinney J, et  al. Consensus 
molecular subtypes and the evolution of precision medicine in 
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 31. Dongre A, Weinberg RA. New insights into the mechanisms 
of epithelial-mesenchymal transition and implications for 
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 32. He X, Hang D, Wu K, et  al. Long-term risk of colorectal 
cancer after removal of conventional adenomas and serrated 
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 33. Click B, Pinsky PF, Hickey T, et al. Association of colonos-
copy adenoma findings with long-term colorectal cancer inci-
dence. JAMA. 2018;319:2021–2031.
 34. Kikuchi R, Takano M, Takagi K, et al. Management of early 
invasive colorectal cancer. Risk of recurrence and clinical 
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 35. Brosens LA, Offerhaus GJ, Giardiello FM. Hereditary 
colorectal cancer: genetics and screening. Surg Clin North Am. 
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 36. Stoffel EM, Mangu PB, Limburg PJ, et  al. Hereditary 
colorectal cancer syndromes: American Society of Clinical 
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the familial risk-colorectal cancer: European Society for 
Medical Oncology clinical practice guidelines. J Oncol Pract. 
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 36a. Amin MB, Edge SB, Greene, Fl et al: AJCC Cancer Staging 
Manual 8th edition, American College of Surgeons, NY: 
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 37. Acuna SA, Chesney TR, Ramjist JK, et al. Laparoscopic ver-
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analysis of quality of surgical resection outcomes. Ann Surg. 
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 38. Pisano M, Zorcolo L, MerliC, et  al. WSES guidelines on 
colon and rectal cancer emergencies: obstruction and perfora-
tion. World J Emerg Surg. 2017;13:36; 2018.
 39. Amelung FJ, Borstlap WAA, Consten ECJ, et al. Propensity 
score-matched analysis of oncological outcome between stent 
as bridge to surgery and emergency resection in patients 
with malignant left-sided colonic obstruction. Br J Surg. 
2019;106:1075–1086.
 40. Sauer R, Becker H, Hohenberger W, et al. Preoperative versus 
postoperative chemoradiotherapy for rectal cancer. N Engl J 
Med. 2004;351:1731–1740.
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1400 SECTION X Abdomen
 41. Habr-Gama A, Perez RO, Nadalin W, et  al. Operative ver-
sus nonoperative treatment for stage 0 distal rectal cancer fol-
lowing chemoradiation therapy: long-term results. Ann Surg. 
2004;240:711–717.
 42. Ryan R, Gibbons D, Hyland JM, et  al. Pathological 
response following long-course neoadjuvant chemoradio-
therapy for locally advanced rectal cancer. Histopathology. 
2005;47:141–146.
 43. Sylla P, Rattner DW, Delgado S, et al. NOTES transanal rectal 
cancer resection using transanal endoscopic microsurgery and 
laparoscopic assistance. Surg Endosc. 2010;24:1205–1210.
 44. Penna M, Hompes R, Arnold S, et al. Transanal total mesorec-
tal excision: international registry results of the first 720 cases. 
Ann Surg. 2017;266:111–117.
 45. Frasson M, Flor-Lorente B, Rodriguez JL, et al. Risk factors for 
anastomotic leak after colon resection for cancer: multivariate 
analysis and nomogram from a multicentric, prospective, national 
study with 3193 patients. Ann Surg. 2015;262:321–330.
 46. Martellucci J. Low anterior resection syndrome: a treatment 
algorithm. Dis Colon Rectum. 2016;59:79–82.
 47. Andre T, de Gramont A, Vernerey D, et  al. Adjuvant fluo-
rouracil, leucovorin, and oxaliplatin in stage II to III colon 
cancer: updated 10-year survival and outcomes according to 
BRAF mutation and mismatch repair status of the MOSAIC 
Study. J Clin Oncol. 2015;33:4176–4187.
 48. Grothey A, Sobrero AF, Shields AF, et al. Duration of adju-
vant chemotherapy for stage III colon cancer. N Engl J Med. 
2018;378:1177–1188.
 49. Consten EC, van Iersel JJ, Verheijen PM, et al. Long-term out-
come after laparoscopic ventral mesh rectopexy: an observational 
study of 919 consecutive patients. Ann Surg. 2015;262:742–747.
 50. Mearin F, Lacy BE, Chang L, et  al. Bowel disorders. 
Gastroenterology; 2016 18;S0016-5085(16)00222-5. doi: 
10.1053/j.gastro.2016.02.031. Online ahead of print.
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1400.e1CHAPTER 52 Colon and Rectum 
VIDEO 52.1 The technique of transanal minimally invasive surgery 
(TAMIS)
VIDEO 52.2 The technique of transanal total mesorectal excision 
(TaTME)
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52 - Colon and Rectumthe rectum, is a membra-
nous layer that is an extension of the inferior peritoneal reflection 
and extends to the perineal body. This fascial layer separates the 
rectum from the previously mentioned anterior structures and is 
considered as the anterior border of a TME.
Blood Supply, Lymphatic Drainage, and Innervation of the 
Rectum
The blood supply to the rectum is derived from the superior, 
middle, and inferior rectal (hemorrhoidal) arteries. All three rectal 
arteries are connected with a strong anastomotic network, which 
helps avoid rectal ischemia after dividing the superior rectal ar-
teries during anterior resections (Fig. 52.12). The superior rectal 
artery is the end branch of the IMA. It usually divides into left 
and right branches that run posteriorly downward. The middle 
rectal arteries are paired vessels derived from the internal iliac ar-
teries to the lower rectum through the lateral columns. They are 
not considered a major blood supply to the rectum and are found 
inconstantly. They can be inadvertently injured when dissecting 
the lateral ligaments. The inferior rectal arteries are branches of 
the internal pudendal arteries and generally supply the anus distal 
to the dentate line.
The superior rectal vein drains the upper two thirds of the 
rectum, draining into the IMV and portal system. The lower 
rectum and anus drain into the middle and inferior rectal veins, 
which are connected to the internal iliac and systemic circula-
tion. This drainage pattern explains the higher rate of lung me-
tastases observed with low rectal cancers as compared to mid and 
Peritoneum
Investing fascia of rectum
Presacral fascia
Rectosacral fascia
Denonvilliers fascia
FIG. 52.10 Fascial relationships of the rectum. (From Gordon PH, Nivatvongs S, ed. Principles and Practice of 
Surgery for the Colon, Rectum and Anus. 2nd ed. St. Louis: Quality Medical Publishing; 1999:10.)
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1329CHAPTER 52 Colon and Rectum 
upper rectal cancers, which are much more likely to metastasize 
to the liver.
The lymph from the upper two thirds of the rectum drains 
upward toward the inferior mesenteric and paraaortic nodes. The 
lower part of the rectum drains in two directions, cephalad toward 
the inferior mesenteric nodes and laterally and inferiorly toward 
the internal iliac nodes. Below the dentate line, lymph drains to-
ward the inguinal lymph nodes.
The sympathetic innervation of the rectum is derived from 
sympathetic nerves exiting at the level of L1–3, forming the su-
perior hypogastric plexus (Fig. 52.13). At the level of the sacral 
promontory, they divide into left and right hypogastric nerves, 
traveling on both sides of the pelvis. These nerves supply the rec-
tum and send branches to supply the genitourinary system ante-
riorly. When performing pelvic operations, it is important to be 
aware of these nerves and avoid injuring them if possible. A high 
IMA ligation injuring the superior hypogastric plexus or severing 
the hypogastric nerves near the sacral promontory may result in 
sympathetic dysfunction characterized by retrograde ejaculation 
in men. Division of the lateral stalks too close to the pelvic side-
wall may injure the pelvic plexus and nervi erigentes and cause 
erectile dysfunction, impotence, and atonic bladder. Injury to 
the periprostatic plexus when dissecting anteriorly can also cause 
sexual and bladder dysfunction. 
Pelvic Floor Anatomy
The pelvic floor or diaphragm supports the pelvic organs and, 
together with the anal sphincter, regulates defecation. The pelvic 
diaphragm resides between the sacrum, obturator fascia, ischial 
spines, and pubis. The levator ani muscle, which makes up the 
floor, consists of three subdivisions: the pubococcygeus, iliococcy-
geus, and the puborectalis (Fig. 52.14). The pubococcygeus forms 
the levator hiatus, which ellipses the top of the anal canal, urethra, 
and vagina in women and the dorsal vein in men. The puborectalis 
originates in the lower part of the symphysis pubis and courses 
parallel to the anorectal junction, forming a U-shaped sling of stri-
ated muscle posterior to the rectum. The puborectalis is in a state 
of constant contraction, increasing the anorectal angle, a factor 
critical to the maintenance of fecal continence. Relaxation of the 
puborectalis straightens the anorectal angle and permits defeca-
tion. Puborectalis dysfunction is an important cause of defecation 
disorders. 
PHYSIOLOGY OF THE COLON
Absorption of Fluid and Electrolytes
The major functions of the colon are water absorption and elec-
trolyte exchange. This process converts succus from the terminal 
ileus into formed stool that is stored in the rectal reservoir until it 
can be excreted at a convenient time. The body has the ability to 
adapt and sustain life without a colon, making it uniquely differ-
ent to small bowel. The problems associated with colonic patients 
provide a simplistic view of colonic function—individuals with 
a diverting ileostomy are at particular risk for dehydration and 
electrolyte derangement.
By surface area, the colon is the most efficient site of absorp-
tion in the GI tract. It has the ability to absorb up to 5 L of fluid 
per day; however, only 1 to 2 L are generally excreted from the 
ileum. By the time succus reaches the terminal ileum, most of 
the nutrients have been absorbed, leaving a mix of electrolyte-rich 
fluid, bile salts, and some proteins and starches that have resisted 
digestion. Approximately 90% of the fluid in succus is reabsorbed 
in the colon, and the total volume of water in stool is only ∼150 
mL/day. The colon’s ability to absorb sodium is equally impressive. 
Succus in the ileum has a sodium concentration of 200 mEq/L 
that is reduced to approximately 30 mEq/L in rectal stool.
Sodium and chloride are actively absorbed via Na+/H+, Na+/
K+, and Cl−/HCO3
− exchange. Water is passively absorbed and 
follows sodium along an osmotic gradient. Potassium chloride and 
bicarbonate are actively secreted into the lumen. 
Rectum
Inferior hypogastric
(pelvic) plexus
Lateral ligaments
Right middle rectal artery
Left middle rectal artery
Left and right branches
of superior rectal artery
Parasympathetic
nervi erigentes
Mesorectum
Right hypogastric nerve
Presacral fascia
Presacral veins
Bladder
Denonvillier fascia
Seminal vesicles
FIG. 52.11 Cross-section of mesorectum and surrounding structures. (From Netz U, Galandiuk S. Clinical 
anatomy for procedures involving the small bowel, colon, rectum and anus. In: Fischer JE, Ellison EC, Upchurgh 
Jr. GR, et al., eds. Fischer’s Mastery of Surgery. 7th ed. Philadelphia: Wolter Kluwer; 2019.)
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1330 SECTION X Abdomen
Secretion
The physiologic role of colon secretion is demonstrated in patients 
with chronic renal failure. Uremic patients can remain normoka-
lemic while ingesting a normal amount of potassium before re-
quiring dialysis. This phenomenon is associated with a compensa-
tory increase in colonic secretion and fecal excretion of potassium. 
Aldosterone promotes colonic potassium secretion, and this effect 
is blocked by spironolactone.
Many forms of colitis are associated with increased potassium 
secretion, such as inflammatory bowel disease (IBD), cholera, and 
shigellosis. In addition, some forms of colitis impair colonic absorp-
tion or produce secretion of chloride, such as collagenous and mi-
croscopic colitis and congenital chloridorrhea. Chloride is secreted 
by colonic epithelium at a basalrate, which is increased in patho-
logic conditions such as cystic fibrosis and secretory diarrhea.
Colonic secretion of H+ and bicarbonate is coupled to the ab-
sorption of Na+ and Cl−, respectively. It is through these exchang-
ers that the colon is linked to systemic acid-base metabolism. The 
supply of H+ and bicarbonate for these exchangers is catalyzed 
by colonic carbonic anhydrase. Changes in systemic pH induce 
changes in the activity of carbonic anhydrase, eliciting elimination 
of H+ or bicarbonate as needed to bring the systemic pH back to 
normal. 
Urea Recycling
Colonic bacteria are rich in urease, which is important for urea 
recycling. Since mammalian cells do not produce urease, this pro-
cess relies on the symbiotic relationship found in a healthy co-
lonic lumen. Ammonia is the by-product of urea metabolism, and 
its absorption depends on the concentration of bacteria present 
and the intraluminal pH. Antibiotics and lactulose decrease the 
amount of ammonia absorbed by lowering the concentration of 
bacteria and reducing the pH, respectively. Absorbed ammonia is 
transported to the liver.
Urea recycling is not beneficial in cases of liver failure. When 
the liver cannot reuse the urea nitrogen absorbed by the colon, 
ammonia crosses the blood-brain barrier and produces “false” 
neurotransmitters, which results in hepatic coma. 
Vasculature of the rectum (posterior view)
Internal iliac vein
Superior vesical vein
Obturator vein
Superior rectal artery and vein
(from inferior mesenteric vessels)
Inferior rectal vein
Internal pudendal vein
in pudendal canal
Inferior vesical vein
Perimuscular rectal
venous plexus
Communication between
internal and external
rectal plexus
Left internal iliac artery
Median sacral artery and vein
(from aorta and inferior vena cava)
Bladder
Subcutaneous part of external anal sphincter
Left common iliac artery
Common iliac vein
Middle rectal vein
Internal rectal plexus
Inferior pubic ramus
Internal anal sphincter
External anal sphincter
Peritoneum
External rectal plexus
Obturator artery
Umbilical artery
Middle rectal artery
Internal pudendal artery
and vein in pudendal canal
Obturator internus
Inferior rectal
artery and vein
Iliococcygeus
(part of levator ani)
Pubococcygeus
(part of levator ani)
Ischioanal fossa
Pectinate
line
FIG. 52.12 Vasculature of the rectum, posterior view. (From Drake RL, Vogl AW, Mitchell AWM, et al. Gray’s 
Atlas of Anatomy. 2nd ed. Philadelphia: Churchill Livingstone, an imprint of Elsevier; 2015.)
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1331CHAPTER 52 Colon and Rectum 
Recycling Bile Salts
The colon absorbs bile acids that escape absorption by the 
terminal ileum. Bile acids are passively transported across the 
colonic epithelium by nonionic diffusion. When the colonic 
 absorptive capacity is exceeded, colonic bacteria deconjugate 
bile acids. Deconjugated bile acids can then interfere with 
sodium and water absorption, leading to secretory, or cho-
leretic, diarrhea. Choleretic diarrhea is seen early after right 
hemicolectomy as a transient phenomenon and more perma-
nently after extensive ileal resection. This diarrhea can often be 
effectively treated by administration of cholestyramine, which 
binds to bile acids. 
Pelvic extensions of the prevertebral nerve plexus (anterior view)
Pelvic splanchnic
nerves
(preganglionic
parasympathetics
from S2 to S4) 
Prevertebral plexus
Right hypogastric
nerve
Ganglion impar
Piriformis
Coccygeus
(ischiococcygeus)
Abdominal aorta
Left common iliac artery
Gray ramus communicans
Left lumbar sympathetic trunk
Superior
gluteal nerve
Pudendal nerve
Coccygeal plexus
Sacral splanchnic
nerves to inferior
hypogastric plexus
(postganglionic
sympathetic)
Inferior hypogastric
plexus
Left hypogastric
nerve
Sacral splanchnic
nerves to inferior
hypogastric plexus
(postganglionic
sympathetic) 
Pelvic splanchnic
nerves
(preganglionic
parasympathetics
from S2 to S4) 
Iliococcygeus
(part of levator ani)
Pubococcygeus
(part of levator ani)
Lumbosacral trunk
Right common iliac artery
Right lumbar sympathetic trunk 
Superior hypogastric plexus
Superior gluteal
nerve
Greater sciatic
foramen
FIG. 52.13 Pelvic nerve plexus. (From Drake RL, Vogl AW, Mitchell AWM, et al. Gray’s Atlas of Anatomy. 2nd 
ed. Philadelphia: Churchill Livingstone, an imprint of Elsevier; 2015.)
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1332 SECTION X Abdomen
Colonic Flora, Fermentation, and Short-Chain Fatty Acids
Large bowel contents have a concentration of 1011 to 1012 bacte-
rial cells per gram, contributing approximately 50% of fecal mass. 
Over 400 bacterial species, mostly anaerobic, are present in the 
colon. Bacteroides species are obligate anaerobes that comprise 
two thirds of the total colonic bacteria. Other species commonly 
found in the colonic flora are the following facultative anaerobes: 
Escherichia, Klebsiella, Proteus, Lactobacillus, and Enterococci. 
These bacteria feed on proteins sloughed from the bowel wall and 
undigested complex carbohydrates. In turn, colonocytes and gut-
associated lymphoid tissue rely on the colonic flora for nutrients.
The main source of energy for intestinal bacteria is dietary fiber, 
composed of complex carbohydrates (i.e., starches and nonstarch 
polysaccharides). However, not all complex carbohydrates are 
fermented in the same manner. Dietary recommendations (i.e., 
“adding fiber”) generally refer to bulking agents, such as lignin and 
psyllium, which are nonabsorbable and nonfermentable by co-
lonic bacteria. Bulking agents decrease intracolonic pressures and 
increase colonic transit time, which help prevent the formation of 
colonic diverticula and minimize colonic exposure to toxins.
For the fermentable complex carbohydrates available, colonic 
flora produce short-chain fatty acids (SCFAs). Butyrate, an SCFA, 
is the principal source of nutrition for the colonocyte. Because 
mammalian cells do not produce butyrate, the colonic epithe-
lium and luminal bacteria form an essential and elegant symbi-
otic relationship. Antibiotics disrupt this cohabitation—decreased 
bacteria leads to less butyrate, which, in turn, negatively affects 
colonocyte function leading to diarrhea. Likewise, mucosal atro-
phy is seen after fecal diversion (i.e., diversion colitis). The other 
physiologic effects of SCFAs on the colon include stimulation of 
blood flow, mucosal cell renewal, and regulation of intraluminal 
pH for homeostasis of the bacterial flora.
The role of SCFAs on homeostasis extends beyond the colon. 
Besides butyrate, two other SCFAs, acetate and propionate, are 
produced in the colon, with acetate being the most common of 
all three. Over 90% of the SCFAs produced are absorbed. Hepa-
tocytes metabolize SCFAs for use in gluconeogenesis, and muscle 
cells oxidize acetate to generate energy. Additionally, acetate is the 
primary substrate for cholesterol synthesis. The production of ac-
etate is reduced by nonabsorbable, nonfermentable dietary fiber, 
such as psyllium, which in turn has a beneficial effect on cholester-
ol levels. Similarly, propionate, which has a glycolytic role in the 
liver, may also lower serum lipid levels by inhibiting cholesterol 
synthesis. Butyrate may also play an important role in maintain-
ing cellular health by arresting the proliferation of neoplastic colo-
nocytes while paradoxically being trophic for normal colonocytes.
The end products of fermentation are SCFAs and gas—carbon 
dioxide, methane, and hydrogen. In additionto nonstarch poly-
saccharides, colonic bacteria ferment poorly absorbed starches and 
proteins from the upper GI tract. Although highly variable from 
person to person, the gases produced by bacterial fermentation 
compose approximately 50% of flatus, with the remainder con-
sisting of swallowed air.
Protein fermentation (i.e., putrefaction) results in the forma-
tion of potentially toxic metabolites, including phenols, indoles, 
and amines. The production of these toxins is inhibited in in-
testinal bacteria by the presence of carbohydrate energy sources. 
This process becomes accentuated more distally in the colon as 
Muscle fibers
over central
tendon of
perineum
Gluteus
maximus
Anococcygeal
ligament
Puborectalis
Pubococcygeus
Ileococcygeus
Levator ani
External anal
sphincter
Subcutaneous
Superficial
FIG. 52.14 The pelvic musculature and innervation from below. The deep anal sphincter muscles are hidden 
under the superficial part. (From Netz U, Galandiuk S. Clinical anatomy for procedures involving the small bowel, 
colon, rectum and anus. In: Fischer JE, Ellison EC, Upchurgh Jr. GR, et al., eds. Fischer’s Mastery of Surgery. 
7th ed. Philadelphia: Wolter Kluwer; 2019.)
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1333CHAPTER 52 Colon and Rectum 
carbohydrate sources become scarcer. These end products of bac-
terial metabolism can lead to mucosal injury and reactive hyper-
proliferation, which have been hypothesized to promote carcino-
genesis. 
Probiotics and Prebiotics
Probiotics can be defined as dietary supplements that contain live 
cultures of bacteria and/or yeast that are beneficial to colonic and 
host function. The two most widely used agents are Lactobacillus 
and Bifidobacterium. Studies have indicated that probiotics may 
have widespread health benefits, including stimulation of im-
mune function, anti-inflammatory effects, and suppression of en-
teropathogenic colonization.1 In addition, they may increase the 
digestibility of dietary proteins and enhance absorption of amino 
acids. Probiotics have been shown to prevent Clostridium difficile–
associated diarrhea, but there are insufficient data to recommend 
probiotics for the primary prevention of C. difficile infection 
(CDI).1 Indications for probiotics use are evolving. Currently, 
there are a small number of studies to support the role of probiot-
ics for the following colorectal conditions: necrotizing enteroco-
litis in neonates, ulcerative colitis (UC), pouchitis, and constipa-
tion. Further research is needed, but the evidence for probiotic use 
in various settings is encouraging.
Prebiotics are nutrients that support the growth of probiotic 
bacteria. Prebiotics are nondigestible oligosaccharides (e.g., inu-
lin) that help the host by stimulating the growth of certain species 
of beneficial intestinal bacteria. There is a growing body of data 
suggesting health benefits; however, there is currently little evi-
dence to guide recommendations for their use. 
Colonic Motility
In the colon, there is extrinsic and intrinsic innervation made up 
by the autonomic nervous system and enteric nervous system, re-
spectively. The autonomic nervous system is comprised of para-
sympathetic and sympathetic innervation. Parasympathetic inner-
vation is excitatory, and it reaches the colon via the vagus nerve and 
the rectum via the sacral nerves (S2–S4) through the pelvic plexus. 
Sympathetic innervation is, conversely, inhibitory. Sympathetic fi-
bers originate from lumber ventral roots (L2–L5), postganglionic 
hypogastric nerves, and the splanchnic nerves (T5–T12), which 
reach the colon and rectum through perivascular plexuses (see also 
the section on Colon Anatomy).
The intrinsic colonic nervous system consists of the myenteric 
(Auerbach) plexus and the submucosal (Meissner) plexus. These plex-
us regulate colonic motility, as well as colonic blood flow, absorption, 
and secretion. The interstitial cells of Cajal are the primary pace-
maker cells governing the function of the enteric nervous system and 
are important for colonic motility. Most motility is involuntary and 
is divided into two primary patterns: (1) low-amplitude propagated 
contractions (LAPCs) and (2) high- amplitude propagated contrac-
tions (HAPCs). LAPCs allow mixing, which promotes optimal 
absorption and are bursts of short-duration contractions. HAPCs 
propagate colonic contents distally in a coordinated fashion, and 
their role lies in shifting large quantities of contents through the co-
lon one to three times per day. Other factors affecting motility are 
circadian rhythms and food ingestion. 
Defecation
Normal defecation requires adequate colonic transit time, stool 
consistency, and fecal continence. The frequency of defecation is 
just as variable among individuals as is their perception of abnor-
mal stool frequency. The definitions of diarrhea and constipation 
differ by individual patients and providers; therefore, reporting 
stool frequency and consistency provides a clearer understanding 
of defecation patterns.
Many factors influence colonic transit rate. Colonic transit is 
longer in women than in men and longer in premenopausal than 
in postmenopausal women. Supplementation with nonstarch 
polysaccharides shortens colonic transit time in individuals with 
idiopathic constipation. 
PREOPERATIVE EVALUATION
Nutritional and Risk Assessment
Over the last 20 years since the original work on the National 
Veterans’ Administration Surgical Risk Study, few parameters 
have been as reliable at predicting postoperative complications as 
the preoperative serum albumin level. Unfortunately, this labora-
tory value is seldom obtained preoperatively in elective surgery 
patients and therefore needs to be explicitly ordered. There are 
numerous preoperative indices such as POSSUM, CR-POSSUM, 
and the ACS-NSQIP calculators and others that have been used 
to predict operative risk. If operating on a patient with a condi-
tion such as diverticulitis, or IBD, the addition of an inflamma-
tory marker such as C-reactive protein (CRP) may be beneficial. 
In general, patients with an albumin less than 3 are considered 
higher risk. Some studies suggest that preoperative correction of 
risk factors may result in improved postoperative outcomes. There 
is a growing field of immunonutrition suggesting that consump-
tion of nutritional supplements rich in arginine may, in fact, boost 
the immune system and lead to a reduction in postoperative infec-
tious complications, such as surgical site infection (SSI).2
Patients who are at particularly high risk are those who have 
chronic partial bowel obstruction and cancer and those who have 
lost a significant amount of weight (greater than 10% of body 
weight) in unintentional weight loss. 
Preoperative Bowel Preparation
As human feces can have as much as 1012 bacteria/gram, colon 
surgery has been associated with a higher rate of SSI than small 
bowel and upper GI surgery. Issues of antibiotic prophylaxis have 
focused upon the choice of an antibiotic with an appropriate 
spectrum, administration prior to making the surgical incision, 
and discontinuation of the antibiotic postoperatively. Over the 
last 20 years, performing or omitting preoperative bowel prepara-
tion has been a cyclical phenomenon. The reader is referred to the 
American Society of Colon & Rectal Surgeons’ Clinical Practice 
Guidelines for the Use of Bowel Preparation in Elective Colon 
and Rectal Surgery for a more in-depth coverage of this issue. 
Studies suggest that mechanical bowel preparation alone is not 
beneficial prior to colon resection. These recommendations were 
based upon findings that bowel preparation generally led to fluid 
and electrolyte abnormalities that, in turn, led to large volumes offluid administration during surgery and subsequent bowel edema 
and ileus. In addition, bowel preparation is poorly tolerated in the 
elderly and in those with multiple medical comorbidities. Lower 
volume bowel preparations generally have higher patient compli-
ance. Higher rates of spillage of liquid as opposed to more formed 
stool at the time of surgery following mechanical bowel prepa-
ration was thought to be the cause of the higher observed rates 
of SSI. However, for many surgeons performing rectal resection, 
either with minimally invasive or open techniques, particularly 
when inserting intraluminal staplers for the purpose of creating 
intestinal anastomoses, it was felt to be more convenient and safer 
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1334 SECTION X Abdomen
to have the large bowel free of solid particulate matter. Recently, 
large administrative database studies have demonstrated that the 
combination of a mechanical and an oral antibiotic bowel prepa-
ration is associated with a very low rate of postoperative infectious 
complications in patients undergoing colorectal surgery. Gener-
ally, many surgeons believe that a formal mechanical bowel prepa-
ration is not required for patients undergoing surgery for IBD 
since these patients are already having numerous liquid bowel 
movements. Bowel preparation is also not used for patients with 
partial obstruction. 
Planning Intestinal Stomas
When operating on a patient in whom there may be a need for 
a diverting stoma (e.g., patients with Crohn disease, diverticular 
 disease, intestinal obstruction, and low rectal cancer), it is al-
ways wise to mark the patient for a preoperative stoma site. Most 
 patients do not have an ideal abdomen. The area of the abdomen 
that usually is chosen for a stoma, the infraumbilical fat mound 
(Fig. 52.15), may not look the same in a patient who is sitting up 
as it does when they are recumbent. In many patients, there are 
skin folds that may prevent a stoma bag from sealing properly. It 
is essential to mark the patients in a sitting position and to avoid 
old scars and any skin folds that may interfere with adherence of 
a stoma appliance. Fig. 52.16 shows how important it is to avoid 
skin folds that would interfere with a normal adherence of a stoma 
appliance and how this can be underestimated if the patient is 
supine.
Stoma Types
Many different types of stoma configurations can be chosen at 
the time of surgery. Stomas can be differentiated by whether they:
	•	 	are	small	bowel	stomas	or	colostomies
	•	 	drain	stool	or	urine
	•	 	are	temporary	or	permanent
	•	 	are	end,	loop,	or	end-loop	stomas.
Temporary stomas are often chosen to aid in anastomotic heal-
ing or in the presence of sepsis or other conditions, when it is not 
considered not safe to perform an unprotected anastomosis. Loop 
ileostomies are often chosen for temporary diversion due to their 
lack of odor, ease of care, and ease of closing. Loop descending or 
sigmoid colostomies can similarly easily be closed. Transverse loop 
colostomies should seldom be used, as they are large, very prone 
to prolapse, and can be difficult to maintain pouch adherence, 
frequently being located in an area around the patient’s belt line 
or mid-upper abdomen.
Temporary diversion can be performed for a number of situ-
ations. Most often, temporary diversion is used to aid in healing 
of distal anastomosis. Alternatively, diversion of the fecal stream 
is sometimes recommended in patients undergoing treatment of 
distal pathology, such as anal squamous cell carcinoma, in order 
to make the treatment (e.g., chemoradiation) more tolerable. In 
these scenarios, a diverting stoma is anticipated to be closed after 
healing of the anastomosis or after conclusion of treatment. Each 
of the three different types of stomas (end, loop, and end loop) has 
advantages and disadvantages. The consistency and amount of 
stoma effluent can differ significantly depending on:
	•	 	whether	the	small	bowel	or	the	colon	is	selected	for	stoma	con-
struction
FIG. 52.15 Demonstration of the infraumbilical fat mound that is the 
ideal stoma site in many patients, here showing marking for a descend-
ing colostomy.
A B
FIG. 52.16 Patient referred following surgery for ischemic colitis without preoperative stoma marking. (A) 
Patient in supine position. (B) Patient sitting up. Note the colostomy “disappears” within folds of her abdominal 
wall making pouching extremely difficult.
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1335CHAPTER 52 Colon and Rectum 
	•	 	if	the	colon	is	selected,	upon	which	site	of	the	colon	is	selected	
for stoma construction
	•	 	what	types	of	treatment	(radiation)	the	patient	has	undergone
	•	 	previous	bowel	resection(s)	the	patient	may	have	had. 
Colostomy
Ascending colostomies tend to have a higher amount of liquid 
effluent, while descending and left-sided colostomies are usually 
preferable, as most of the colon is in circuit, allowing for more 
colonic water absorption, with a more formed effluent, while still 
providing proximal diversion.
With the increasing body mass index of patients in the United 
States today, creating a well-functioning stoma can be a challenge. 
Both early and late complications can occur with stoma construc-
tion. Remember, a stoma should look good at the end of an 
 operation! This is your best opportunity to address issues of stoma 
construction. One should not make the error of hoping that a sub-
optimal-appearing stoma will improve postoperatively. While ede-
ma secondary to obstruction may improve, ischemia does not and 
will only worsen over time. If there is doubt about stoma viability, 
construct the stoma prior to closing the abdomen, when revision 
is easy. A key aspect to creating a good stoma is to create a large 
enough aperture in the abdominal wall to allow the stoma to reach 
to the skin without tension, but not to create such a wide opening 
that the patient will develop a hernia at the site. Typically, creating 
an aperture that will admit two fingers is adequate (Fig. 52.17). In 
addition, one should ensure that the patient is marked for a stoma 
site preoperatively, as was discussed earlier. It is important to cre-
ate a muscle-splitting stoma aperture within the rectus muscle and 
sharply divide the rectus sheath (Fig. 52.18). In creating a colos-
tomy in an obese patient, especially with the left side of the colon, 
one frequently has to perform the same central vascular ligation as 
one does for a cancer resection merely to achieve the same degree 
of mobilization and mobility to enable the colon to reach to the 
 abdominal wall in a tension-free manner. This can particularly be 
true with patients who have a very rigid abdominal wall and those 
with a very thick layer of subcutaneous tissue. In constructing an 
end colostomy, typically this does not need to protrude more than 
0.5 to 1 cm above the level of the abdominal skin. However, there 
are some circumstances where the patient may be expected to have 
a more liquid effluent (e.g., due to receiving chemotherapy), and 
one may wish to have the stoma protrude more to permit easier 
pouch placement and adherence. In the presence of a liquid efflu-
ent, a protruding “spout-like” stoma is always easier to maintain 
pouch adherence compared with a flatter stoma. In the obese pa-
tient, it is sometimes easier to construct an end-loop colostomy 
than an end colostomy if complete fecal diversion is required. This 
is constructed in a similar fashion as a loop-end ileostomy (see 
later),whereby a loop of mesentery is brought up, rather than an 
end of mesentery. Remember, traditional loop colostomies are not 
always completely diverting. If one wishes total diversion, an end-
loop stoma, with tacking of the distal limb in close proximity of 
the stoma site, may be a preferable option. Also remember that, in 
obese individuals, the thinnest part of the abdominal wall is often 
in the upper abdomen. 
Ileostomy
As with colostomy, an ileostomy can be constructed as an end 
ileostomy, loop, or end-loop ileostomy (Fig. 52.19). Ileostomies 
are generally favored by colorectal surgeons for fecal diversion as 
they are easier to construct, especially in obese individuals, usually 
easier to close, and do not risk compromising the marginal vessels 
of the colon that are so important to the viability of low and ultra-
low colorectal and coloanal anastomoses. Ileostomy effluent usu-
ally has no odor, in contrast to colostomy effluent, which usually 
has odor associated with colonic flora. However, in contrast to a 
colostomy, an ileostomy will empty continuously and has a high 
rate of associated chemical dermatitis due to the more alkaline pH 
associated with small bowel effluent as opposed to the stool of the 
colon. There is also a much higher risk of dehydration with an 
ileostomy, which is a frequent reason for hospital readmission fol-
lowing elective colorectal surgery. Prior to hospital discharge, one 
should ensure that the 24-hour stoma output is less than 1000 mL. 
FIG. 52.17 A stoma aperture that admits two fingers is typically of ad-
equate size to allow the bowel and mesentery to pass without tension. 
In cases of obstruction or an obese mesentery, a larger aperture will be 
needed.
FIG. 52.18 In making the stoma aperture in the abdominal wall, the 
rectus muscle is split and the rectus sheath is divided sharply. In laparo-
scopic cases, one can cut down directly on the trocar inserted through 
this site.
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1336 SECTION X Abdomen
If the output is greater than this amount, the patient is at high risk 
of hospital readmission.
In patients in whom temporary ileostomy diversion is contem-
plated, wrapping the segment of diverted bowel in hyaluronate-
carboxymethylcellulose membrane (Seprafilm) at the time of 
stoma creation facilitates stoma closure. Loop ileostomy is often 
performed at the time of ileal pouch–anal anastomosis (IPAA) 
in patients who are immunosuppressed and in those in whom 
there is tension on the anastomosis. It is also performed in cases 
of low colorectal and coloanal anastomosis following neoadjuvant 
chemoradiation, in some patients in whom complex pelvic recon-
structions are performed (e.g., redo rectovaginal fistula repairs, 
repair of cloacal defects) and in other cases when temporary fecal 
diversion is desired. Laparoscopic-assisted diversion is particularly 
convenient for these cases. 
ENHANCED RECOVERY PROTOCOLS
The last edition of this textbook reported that protocols for en-
hanced recovery after surgery had not been widely implemented. 
Since that time, there has been much attention to enhanced re-
covery protocols (ERPs) in colorectal surgery with widespread 
dissemination and implementation in the community. These 
protocols, also called fast-track or enhanced recovery after surgery 
protocols, have been shown to reduce complications, length of 
stay, and cost of care without increasing readmission rates. Pro-
tocols include a bundle of components affecting the preopera-
tive, intraoperative, and postoperative phases of care. The factors 
that comprise a single protocol are numerous and heterogeneous 
between centers, thus making it difficult to identify the most 
beneficial components in a bundled protocol. In 2017, the 
American Society of Colon and Rectal Surgeons (ASCRS) and 
the Society of American Gastrointestinal and Endoscopic Sur-
geons published evidence-based guidelines for the components 
of ERPs.3
Preoperative Interventions
Counseling before surgery to set expectations on milestones 
and discharge criteria is considered a cornerstone of successful 
ERPs. If an ostomy is a part of the planned operation, marking, 
education, and counseling on dehydration should be started in 
the preoperative period. Ostomy creation is an independent risk 
factor for increased postoperative length of stay, and structured 
education has been shown to mitigate this risk. Additionally, de-
hydration is the most common reason for readmission after an 
ileostomy creation.
Prehabilitation or increasing the patient’s physical condition-
ing before elective surgery may be considered for patients with 
 deconditioning or multiple comorbidities. The evidence to sup-
port prehabilitation is in evolution but appears promising. 
Preadmission Nutrition and Bowel Preparation
There is strong evidence to support the recommendation of a clear 
liquid diet up until 2 hours before the induction of anesthesia. 
However, there is weaker evidence to support the use of per os 
carbohydrate loading prior to surgery.
Mechanical bowel preparation alone has not shown to be ben-
eficial (strong recommendation based on high-quality evidence, 
1A). In the United States, mechanical bowel preparation plus oral 
antibiotics preparation has become the preferred preparation to 
reduce complications, including SSIs, especially when left-sided 
and rectal resections are anticipated. In the American Society 
of Colon & Rectal Surgeons Clinical Practice Guidelines for 
the Use of Bowel Preparation in Elective Colon and Rectal Sur-
gery, this practice was given a strong recommendation based on 
moderate-quality evidence, 1B. Interestingly, a recent random-
ized controlled trial found no evidence to support this practice 
for elective colon resection compared to no bowel preparation 
as a mechanism to reduce SSIs or postoperative morbidity.4 It is 
important to note that the majority of reported studies, including 
this one, were performed in patients undergoing colon as op-
posed to rectal resections. 
Perioperative Interventions
ERPs commonly involve preset orders for the preoperative, intra-
operative, and postoperative care for all patients. Standardization 
requires collaborative buy-in from different stakeholders, which 
helps avoid confusion and promotes timely adherence to care.
Colorectal surgery patients have up to a 20% risk of develop-
ing a SSI postoperatively. Bundles of care aimed at SSI reduction 
have shown SSI rates to be significantly reduced. These bundles 
include some, if not all, of the following measures: preoperative 
chlorhexidine shower, mechanical bowel preparation with oral an-
tibiotics, prophylactic antibiotic administration within 1 hour of 
incision, the use of wound protectors during surgery, changing 
gown, gloves, and instruments before fascial closure, euglycemia, 
and normothermia. The degree to which each element impacts the 
reduction of SSIs is unclear.
There is strong evidence to support the use of multimodal, 
opioid-sparing, pain management plans starting before the induc-
tion of anesthesia. Minimizing opioids is associated with earlier 
return of bowel function and shorter length of stay. Acetamino-
phen, nonsteroidal antiinflammatory drugs (NSAIDs), and gaba-
pentin have all been incorporated into various ERPs. Transverse 
abdominis plane block with local anesthetic, including liposomal 
bupivacaine, have shown promising results. Epidural analgesia is 
generally recommended for open, but not laparoscopic, colorec-
tal surgery.
FIG. 52.19 The Intraoperative photo showing the “matured” loop 
 ileostomy protruding 2 to 3 cm above the abdominal wall. The distal limb 
at skin level is located inferiorly.
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