of the Large Intestine
- Constipation or obstipation.
- Abdominal distention and sometimes tenderness.
- Abdominal pain.
- Nausea and vomiting (late).
- Characteristic x-ray findings.
Approximately 15% of intestinal obstructions in adults
occur in the large bowel. The obstruction may be in any portion
of the colon but most commonly is in the sigmoid. Complete colonic
obstruction is most often due to carcinoma; volvulus, diverticular
disease, inflammatory disorders, benign tumors, fecal impaction,
and miscellaneous rare problems account for the remainder (Table 30–4). Adhesive bands seldom
obstruct the colon, and intussusception is uncommon in adults.
Table 30–4. Causes
of Colonic Obstruction in Adults. |Favorite Table|Download (.pdf)
Table 30–4. Causes
of Colonic Obstruction in Adults.
|Cause||Relative Incidence (%)*|
|Carcinoma of colon||65|
Obstruction by a lesion at the ileocecal valve produces the symptoms
and signs of small bowel obstruction. The pathophysiology of more
distal colonic obstruction depends on the competence of the ileocecal
valve (Figure 30–4). In 10–20% of
individuals, the ileocecal valve is incompetent, and colonic pressure
is relieved by reflux into the ileum. If the colon is not decompressed
through the ileocecal valve, a closed loop is formed between the
valve and the obstructing point. The colon distends progressively
because the ileum continues to empty gas and fluid into the obstructed
segment. If luminal pressure becomes very high, circulation is impaired
and gangrene and perforation can result. The wall of the right colon
is thinner than that of the left colon and its luminal caliber is
larger, so the cecum is at greatest risk of perforation in these
circumstances (law of Laplace). In general, if the cecum acutely
reaches a diameter of 10–12 cm, the risk of perforation
The role of the ileocecal valve in obstruction of the
colon. The obstruction is in the upper sigmoid. A: The
ileocecal valve is competent, creating a closed loop between the
obstruction and the valve. Tension in the closed loop is increased
further by emptying of gas and fluid from the ileum into the colon. B: The
ileocecal valve is incompetent. Reflux into the ileum is permitted.
The colon is relieved of some of its distention, and the small bowel
has become distended.
Simple mechanical obstruction of the colon may develop insidiously.
Deep, visceral, cramping pain from obstruction of the colon is usually
referred to the hypogastrium. Lesions of the fixed portions of the
colon (cecum, hepatic flexure, splenic flexure) may cause pain that
is felt immediately anteriorly. Pain originating from the sigmoid
is often located to the left in the lower abdomen. Severe, continuous
abdominal pain suggests intestinal ischemia or peritonitis. Borborygmus
may be loud and coincident with cramps. Constipation or obstipation
is a universal feature of complete obstruction, though the colon
distal to the obstruction may empty after the initial symptoms begin.
Vomiting is a late finding and may not occur at all if the ileocecal
valve prevents reflux. If reflux decompresses the cecal contents into
the small intestine, the symptoms of small bowel as well as large
bowel obstruction appear. Feculent vomiting is a late manifestation.
Physical examination discloses abdominal distention and tympany,
and peristaltic waves may be seen if the abdominal wall is
thin. High-pitched, metallic tinkles associated with rushes and
gurgles may be heard on auscultation. Localized tenderness or a
tender, palpable mass may indicate a strangulated closed loop. Signs
of localized or generalized peritonitis suggest gangrene or rupture
of the bowel wall. Fresh blood may be found in the rectum in intussusception
and in carcinoma of the rectum or colon. Sigmoidoscopy may disclose
a neoplasm. Colonoscopy may be diagnostic and perhaps therapeutic
in some patients with strictures or neoplasms.
The distended colon frequently creates a “picture frame” outline
of the abdominal cavity. The colon can be distinguished from the
small intestine by its haustral markings, which do not cross the
entire lumen of the distended colon. A contrast enema or CT scan
with rectal contrast will confirm the diagnosis of colonic obstruction
and identify its exact location. Water-soluble contrast medium should
be used if strangulation or perforation is suspected. Barium should
not be given orally in the presence of suspected colonic obstruction.
A CT scan with rectal contrast is the most useful single test for
large bowel obstruction because it can yield information regarding
the location and etiology of the bowel obstruction.
Large Bowel Obstruction
Large bowel obstruction is frequently slow in onset, causes less
pain, and may not cause vomiting in spite of considerable distention.
Elderly patients with no history of abdominal surgery or prior attacks
of obstruction frequently have carcinoma of the large bowel. Plain
abdominal x-rays and contrast studies are helpful in establishing
Paralytic ileus may be a result of peritonitis or trauma to the back
or pelvis. The abdomen is silent, and abdominal cramping is not
present. There may be tenderness. Plain films show a dilated colon.
Contrast enema may be required to exclude an obstruction.
Acute pseudo-obstruction of the colon (Ogilvie syndrome)
is massive colonic distention in the absence of a mechanically obstructing
lesion (Figure 30–5). It is a severe
form of ileus and arises in bedridden patients who have serious
extraintestinal illness (renal, cardiac, respiratory) or trauma
(eg, vertebral fracture). Aerophagia and impairment of colonic motility by
drugs are contributing factors. Abdominal distention without pain
or tenderness is the earliest manifestation, but later symptoms
mimic those of true obstruction. Plain x-rays of the abdomen show
marked gaseous distention of the colon. Although the entire colon
may contain gas, the distention is typically localized to the right
colon, with a cutoff at the hepatic or splenic flexure. Contrast
enema proves the absence of obstruction, but instillation of radiopaque
material should cease as soon as the dilated colon is reached.
Plain radiograph demonstrating the dilated colon with
pseudoobstruction (Ogilvie syndrome).
(Courtesy of Dr. Santhat Nivatvongs.)
Conservative treatment with nasogastric suction and enemas may
succeed in resolving colonic pseudoobstruction. Neostigmine is highly
effective in treating colonic pseudoobstruction. It should be avoided
in patients with a mechanical colonic obstruction, bradycardia,
bronchospasm, or renal insufficiency. If the cecum is markedly dilated,
the risk of perforation is high, and direct intervention must be prompt.
Colonoscopic decompression is the method of choice if an expert
is available. Initial success is claimed in 90% of patients,
but recurrence is common (25% or more). Often, it is possible
to place a tube into the proximal colon during colonoscopy to maintain
decompression. Placement of a decompressive tube per rectum under
fluoroscopic guidance has been described recently. Another alternative
is cecostomy, performed either in the standard open fashion or by
an endoscopic percutaneous method, similar to the technique for
gastrostomy, using laparoscopic assistance.
Cecal perforation, described earlier, is a potentially lethal complication.
Partially obstructive lesions of the colon may be complicated by
acute colitis in the bowel proximal to the obstruction; it is probably
a form of ischemic colitis secondary to impaired mucosal blood flow
in the distended segment.
An operation is almost always required. The primary goals of
treatment are resection of all necrotic bowel and decompression
of the obstructed segment. Removal of the obstructing lesion is
a secondary goal, but a single operation to accomplish both objectives
is preferred whenever possible.
Colonoscopic balloon dilation with endoluminal stent placement
across obstructing benign strictures or neoplasms may be performed
in selected circumstances. Stent placement may allow for decompression
of the obstruction as a bridge to elective resection. Stents may
be considered also for palliation in patients whose life expectancy
is less than 6 months, which is the expected patency of a colonic
stent placed for malignancy. Laser photocoagulation of an obstructing
cancer, especially in the rectum, may enlarge the lumen to permit
an elective operation later under better circumstances, and occasionally
a patient with advanced cancer may avoid operation entirely. Permanent
diverting colostomy may be the only possible choice in a debilitated patient
with unresectable obstructing rectal cancer.
Obstructing lesions of the right colon are resected
in one stage, with ileotransverse colostomy if the patient’s condition
is good. If the patient’s condition is precarious or if
the colon has perforated, the bowel is resected but no anastomosis
is done; an ileostomy is established, and anastomosis is performed
at a second operation. Unresectable lesions may be bypassed.
Obstructing lesions of the left colon are best treated
by resection in patients who seem likely to tolerate this procedure.
After resection has been achieved, anastomosis may be postponed
and a temporary end colostomy created (two-stage procedure; Figure 30–6). Alternatively, intraoperative colonic
lavage has previously been advocated to cleanse the colon well enough
so that primary anastomosis can be performed safely. In this setting,
subtotal colectomy results in similar morbidity and mortality as
on-table lavage and still permits a one-stage procedure using healthy
bowel. If the proximal bowel is healthy, a primary anastomosis with
a proximal defunctioning (diverting) loop ileostomy may be possible. Two other
options may be entertained. A colonic stent may be deployed preoperatively
to decompress the obstructed bowel, allowing for an elective resection
under better circumstances. Alternatively, in unfavorable circumstances,
a diverting transverse colostomy may utilized. However, a serious
disadvantage is the need for three operations if this approach is
elected: (1) colostomy, (2) resection of the obstructing lesion
with anastomosis, and (3) closure of the colostomy.
Primary resection for diverticulitis of the colon. The
affected segment (shaded) has been divided at its distal end. If
primary anastomosis is to be done, the proximal margin (dotted line)
is transected, and the bowel is anastomosed end to end. If a two-stage
procedure will be used, a colostomy is formed at the proximal margin,
and the distal stump is oversewn (Hartmann procedure, as shown)
or exteriorized as a mucous fistula. The second stage consists of
colostomy takedown and anastomosis.
The prognosis depends upon the age and general condition of the
patient, the extent of vascular impairment of the bowel, the presence
or absence of perforation, the cause of obstruction, and the promptness
of surgical management. The overall mortality rate is about 20%.
Cecal perforation carries a 40% mortality rate. Obstructing
cancer of the colon has a worse prognosis than nonobstructing cancer
because it is more likely to be locally extensive or metastatic
to nodes or distant sites.
Baron TH: Expandable metal stents for the treatment
of cancerous obstruction of the gastrointestinal tract. N Engl J
Med 2001; 344:1681.
Bharucha AE et al: Acute, toxic, and chronic. Curr Treat Options Gastroenterol
Boorman P et al: Endoluminal stenting of obstructed colorectal tumours.
Ann R Coll Surg Engl 1999;81:251.
Breitenstein S et al: Systematic evaluation of surgical strategies for
acute malignant left-sided colonic obstruction. Br J Surg 2007;94:1451.
Chapman AH, McNamara M, Porter G: The acute contrast enema in
suspected large bowel obstruction: value and technique. Clin Radiol
Gooszen AW et al: Operative treatment of acute complications
of diverticular disease: primary or secondary anastomosis after sigmoid
resection. Eur J Surg 2001;167:35.
Gooszen AW et al: Prospective study of primary anastomosis following
sigmoid resection for suspected acute complicated diverticular disease.
Br J Surg 2001;88:693.
Ponec RJ, Saunders MD, Kimmey MB: Neostigmine
for the treatment
of acute colonic pseudo-obstruction. N Engl J Med 1999;341:137.
SCOTIA Study Group. Single-stage treatment for malignant left-sided
colonic obstruction: a prospective randomized clinical trial comparing
subtotal colectomy with segmental resection following intraoperative
irrigation. Br J Surg 1995;82(12):1622.
Stewart J, Diament RH, Brennan TG: Management of obstructing lesions
of the left colon by resection, on-table lavage, and primary anastomosis.
Suri S et al: Comparative evaluation of plain films, ultrasound
and CT in the diagnosis of intestinal obstruction. Acta Radiol 1999;40:422.
Tilney HS et al: Comparison of colonic stenting and open surgery for
malignant large bowel obstruction. Surg Endosc 2007;21:225.
Cancer of the
- Unexplained weakness or anemia.
- Occult blood in feces.
- Dyspeptic symptoms.
- Persistent right abdominal discomfort.
- Palpable abdominal mass.
- Characteristic x-ray findings.
- Characteristic colonoscopic findings.
- Change in bowel habits.
- Gross blood in stool.
- Obstructive symptoms.
- Characteristic x-ray findings.
- Characteristic colonoscopic or sigmoidoscopic findings.
- Rectal bleeding.
- Change in bowel habits.
- Sensation of incomplete evacuation.
- Intrarectal palpable tumor.
- Sigmoidoscopic findings.
In Western countries, cancer of the colon and rectum ranks second
after cancer of the lung in incidence and death rates. An estimated
150,000 new cases of colorectal cancer are diagnosed and over 50,000
people die of this disease in the United States each year. The overall
death rates from colorectal cancer in the United States has been
declining since the mid-1980s, perhaps related to earlier detection.
The incidence increases with age, from 0.39/1000 persons
per year at age 50 to 4.5/1000 persons per year at age
80. Carcinoma of the colon, particularly the right colon, is more common
in women, and carcinoma of the rectum is more common in men. The
distribution of cancers of the colon and rectum is shown in Figure 30–7. An apparent “proximal shift” of
cancer (increased incidence in the right colon and decreased incidence
in the rectum) in recent decades is at least partially explainable
by improved diagnostic accuracy for proximal lesions as a result
of total colonoscopy. Multiple synchronous colonic cancers (ie,
two or more carcinomas occurring simultaneously) are found in 5% of
patients. Metachronous cancer is a new primary lesion in a patient
who has had a previous resection for cancer. The cumulative risk
of metachronous colorectal cancer was 6.3% at 18 years
in one study and as high as 10% at a mean follow-up of
39 months in another series. Ninety-five percent of malignant tumors
of the colon and rectum are adenocarcinomas.
Distribution of cancer of the colon and rectum.
Genetic predisposition to cancer of the large bowel is well recognized
in persons with familial adenomatous polyposis (FAP; discussed in
the Treatment section under Polyps of the Colon & Rectum). The
most common form of hereditary colorectal cancer is hereditary
nonpolyposis colorectal cancer (HNPCC), also called Lynch
syndrome. There are four cardinal features of HNPCC: (1) earlier
average age (45 years) at onset of cancer than in the general population,
(2) the presence of HNPCC-associated cancers within the pedigree,
(3) improved survival when compared stage for stage to sporadic
cases, (4) the presence of a germline mutation in affected family
members. The gene responsible for this syndrome has been localized
to chromosome 2p, and the genetic defect is in DNA mismatch repair
genes (MLH1, MSH2, MSH6, PMS1, and PMS2).
The defects occur in the setting of microsatellite instability.
There may be other genes not as of yet identified. The Amsterdam
I and II criteria and Revised Bethesda criteria (Tables 30–5a and 30–5b) were developed
to identify patients with HNPCC. The presence of the Amsterdam criteria
defines HNPCC by history alone and the presence of any one of the
Revised Bethesda criteria warrants further investigation for HNPCC.
However, all patients with early-onset colorectal cancer should
be offered screening for a familial colorectal cancer syndrome.
First-degree relatives of patients with sporadic colorectal cancer have
a twofold to threefold increased risk of large bowel cancer, and
it is estimated that approximately 10% of cancers
of the large bowel are due primarily to an inherited genetic defect.
(Polyposis-associated familial colorectal cancer syndromes are discussed
later in chapter.)
Table 30–5a. Amsterdam
I and II Criteria. |Favorite Table|Download (.pdf)
Table 30–5a. Amsterdam
I and II Criteria.
|Amsterdam I criteria:|
|At least three relatives must have histologically verified
colorectal cancer.||(1) One must be a first-degree relative of the other two.|
|(2) At least two successive generations must be affected.|
|(3) At least one of the relatives with colorectal cancer
must have received the diagnosis before age 50.|
|Amsterdam II criteria:|
|At least three relatives must have a cancer
associated with hereditary nonpolyposis colorectal cancer (HNPCC)
(colorectal, endometrial, stomach, ovary, ureter or renal-pelvis,
brain, small bowel, hepatobiliary tract, skin (sebaceous tumors)||(1) One must be a first-degree relative of the other two.|
|(2) At least two successive generations must be affected.|
|(3) At least one of the relatives with HNPCC-associated cancer
must have received the diagnosis before age 50.|
Table 30–5b. Revised Bethesda Criteria. |Favorite Table|Download (.pdf)
Table 30–5b. Revised Bethesda Criteria.
|1. Colorectal cancer (CRC) diagnosed in individual under
age 50 years.|
|2. Presence of synchronous, metachronous colorectal or other HNPCC-associated
tumors, regardless of age.|
|3. CRC with the microsatellite instability-high (MSI-H) histology
(presence of tumor-infiltrating lymphocytes, Crohn-like lymphocytic
reaction, mucinous/signet-ring differentiation, or medullary
growth pattern) in patient 60 years of age.|
|4. CRC in one or more first-degree relatives with an HNPCC-related
tumor, with one of the cancers being diagnosed under age 50 years.|
|5. CRC diagnosed in two or more first- or second-degree relatives
with HNPCC-related tumors, regardless of age.|
Ulcerative colitis, Crohn colitis, schistosomal colitis, exposure
to radiation, and the presence of an ureterocolostomy are conditions
that predispose to cancer of the large bowel. It was previously
thought that a prior history of cholecystectomy predisposed to the
development of colorectal cancer, but this has largely been disproved.
The main behavioral risk factors for the development of advanced
colorectal neoplasia include cigarette smoking and excessive alcohol
consumption. Additional contributing factors may include obesity,
lack of dietary fiber, and excessive red meat consumption. Mitigating
factors include nonsteroidal anti-inflammatory drug (NSAID) use,
vitamin D consumption, and physical activity.
A high incidence of colorectal cancer occurs in populations that
are economically prosperous. This observation has focused attention
on environmental factors, particularly diet, in the etiology of
this tumor. Increased intake of saturated fat, increased caloric
intake, decreased dietary calcium, and decreased intake of fiber
are among the possible dietary influences. Dietary fat enhances
cholesterol and bile acid synthesis by the liver, and the amounts
of these sterols in the colon increase. Anaerobic colonic bacteria
convert these compounds to secondary bile acids, which are promoters
of carcinogenesis. Other possible mechanisms by which saturated
fat promotes colorectal cancer include changes in immunity, effects
on lipid peroxidation, and modulation of prostaglandin synthesis
through arachidonic acid metabolism. Experimental studies have suggested
that dietary fish oil, rich in unsaturated fatty acids of the omega-3
type, is protective against colorectal cancer, and the mechanism
may be inhibition of prostaglandin synthesis from arachidonic acid.
The mechanism by which dietary fiber is protective remains elusive.
Effects of fiber on fecal bulk, water content, transit time, and
pH are less important than once thought. Plant lignans in fiber
are fermented to a group of human lignans by colonic bacteria, and
these substances may be important in some way. Metabolic activity
of gut microflora is altered by dietary fiber, perhaps with important
inhibitory effects on tumor promoters such as bile acids. Another possible
mechanism is chelation of dietary iron by the phytate content of
high-fiber foods. Iron catalyzes oxidation of lipid to substances
that are genotoxic, and iron has been associated with the initiating
and promoting phases of carcinogenesis in experimental systems.
Ingested calcium affects colonic epithelial cell proliferation topically
and by absorption into the bloodstream. If these concepts are correct,
reducing dietary saturated fat and calories and increasing the intake
of calcium and fermentable fiber can minimize the risk of colorectal
cancer. Populations with a high incidence of colon cancer tend to
have low serum cholesterol levels, and average serum cholesterol
levels are higher in groups with less cancer of the colon.
Carcinogenesis in the large bowel and elsewhere is a long, multistep
process. Colorectal cancer involves multiple genetic alterations,
ie, oncogene activation, including K-ras point
mutation, c-myc amplification and overexpression,
and c-src kinase activation. Tumor-suppressor gene
inactivation is also important; these events may include point mutations
in the APC gene (adenomatous polyposis coli, at
chromosome 5q21), the DCC gene (deleted in colorectal
carcinoma, on chromosome 18q), and TP53 (on chromosome
17). Genetic damage is initiated by carcinogenic agents. In addition,
DNA microsatellite instability has been demonstrated to be another pathway
for colorectal carcinogenesis. Promoters, such as bile acids, may
stimulate growth of a benign neoplasm, and it may be that still
other promoters cause malignant change to occur. There is evidence
that estrogen may have a protective effect for the development of
colon cancer. Aspirin and other NSAIDs, particularly the cyclooxygenase-2
inhibitors, may also reduce the incidence of and mortality rate
from colorectal cancer by inhibition of the prostaglandins implicated
in immune suppression and the promotion of metastasis. The use of
such agents is the subject of several clinical trials for the chemoprevention
of colon cancer.
Cancer of the colon and rectum spreads in the following ways:
Carcinoma grows circumferentially and may completely encircle
the bowel before it is diagnosed; this is especially true in the
left colon, which has a smaller caliber than the right. It takes
about 1 year for a tumor to encircle three fourths of the circumference
of the bowel. Longitudinal submucosal extension occurs with invasion
of the intramural lymphatic network, but it rarely goes beyond 2
cm from the edge of the tumor unless there is concomitant spread
to lymph nodes. As the lesion extends radially, it penetrates the outer
layers of the bowel wall, and it may extend by contiguity into neighboring
structures: the liver, the greater curvature of the stomach, the
duodenum, the small bowel, the pancreas, the spleen, the bladder,
the vagina, the kidneys and ureters, and the abdominal wall. Cancer
of the rectum may invade the vaginal wall, bladder, prostate, or
sacrum, and it may extend along the levators. Subacute perforation
with inflammatory attachment of bowel to an adjacent viscus may be
indistinguishable from actual invasion on gross examination.
Lymphovascular invasion may allow tumor cells be carried via
the portal venous system to establish hepatic metastases. Tumor
embolization also occurs through lumbar and vertebral veins to the
lungs and elsewhere. Rectal cancer spreads through tributaries of
the hypogastric veins. Metastases to ovaries are mostly hematogenous;
they are found in 1–10.3% of women with colorectal
cancer. Venous invasion occurs in 15–50% of cases
even though it does not always cause distant metastases. An attempt
is made to avoid producing hematogenous metastases during operation
by minimizing manipulation of the tumor prior to ligation of the
Lymph Node Metastasis
This is the most common form of tumor spread (Figure
30–8). Longitudinal spread via extramural lymphatics
is an important mechanism. Rectal cancer metastasizes proximally
to the mesorectal, iliac, and inferior mesenteric lymph nodes, and radially
along lymphatics to the pelvic side walls, where obturator nodes
can become involved. The lymphatic drainage of the tumor must be
removed in curative operations, and some nodal involvement will
be found in over half of the specimens. Over the past several years,
sentinel lymph node mapping for colorectal cancer has been under
investigation in an effort to improve identification of candidates
for adjuvant chemotherapy. However, results have been inconsistent
with several large single and multi-institutional studies demonstrating
an unacceptably high false-negative rate with the technique. The
completeness of lymph node evaluation as reflected in the total
number of lymph nodes examined at the time of colectomy for cancer
is associated with survival. The size of the lesion bears little
relationship to the degree of nodal involvement. The more anaplastic
the lesion, the more likely that lymph node metastasis will occur. Up
to 10–25% of T1 rectal cancers may harbor occult
lymph node metastases.
Lymphatic drainage of the colon. The lymph nodes (black)
are distributed along the blood vessels to the bowel.
“Seeding” may occur when the tumor has extended
through the serosa and tumor cells enter the peritoneal cavity, producing
local implants or generalized abdominal carcinomatosis. Large metastatic
deposits in the pelvic cul-de-sac are palpable as a hard shelf (Blumer
Malignant cells shed from the surface of the tumor can be swept
along in the fecal current. Implantation more distally on intact
mucosa occurs rarely, if ever, but viable exfoliated cells presumably
can be trapped in an anastomotic suture or staple line during operation.
Adenocarcinoma of the colon and rectum has a median doubling
time (the time required for the tumor to double in volume) of 130
days, suggesting that at least 5 years—and often 10–15
years—of silent growth are required before a cancer reaches
symptom-producing size. During this asymptomatic phase, diagnosis
depends on routine examination.
The value of routine screening of asymptomatic populations
who lack high-risk factors for development of large bowel cancer
has been established. Screening should be initiated at age 50. The
goals of screening are detection of early cancers and prevention
of cancer by finding and removing adenomas. The screening recommendations
of the American Society of Colon and Rectal Surgery are listed in (Table 30–6). Screening for occult
blood detects has been shown to have a survival benefit in a US
prospective trial of occult blood testing followed by colonoscopy
in those with positive tests. Improved survival in the screened
group was related to a lower percentage of advanced cancers—the lesions
that more commonly prove fatal. It is not clear whether the survival
benefit in this study should be attributed mainly to the tests for
occult blood or the colonoscopy, because the latter test alone might
have achieved the same outcome. Four case-control studies have demonstrated
that sigmoidoscopy is associated with a reduced mortality for colorectal
cancer. However, its utility as a screening test for colorectal
neoplasia is limited by the amount of colon visualized with a 70
cm sigmoidoscope. Cancer mortality is reduced for lesions within
the reach of the sigmoidoscope but not in the area beyond the reach
of the sigmoidoscope. Therefore, flexible sigmoidoscopy should be
used in conjunction with radiographic evaluation of the more proximal colon
or annual fecal occult blood testing. Dissatisfaction with the poor specificity of guaiac slide tests has
led to development of alternative methods, including immunochemical
fecal occult blood tests and fecal tests for DNA mutations. If fecal
occult blood testing is positive, total colonoscopy should be performed.
As a screening test, flexible sigmoidoscopy, when normal, should be
repeated every 5 years. Alternatively, total colonoscopy can be
performed as the initial examination, since all roads eventually
lead to colonoscopy for diagnosis or therapy (as in the case of
a lesion on barium enema).
Table 30–6. American Society of Colon and Rectal
Surgeons Guidelines for Colorectal Cancer Screening.1,2 |Favorite Table|Download (.pdf)
Table 30–6. American Society of Colon and Rectal
Surgeons Guidelines for Colorectal Cancer Screening.1,2
|Risk||Procedure||Onset (Age, yr)||Frequency|
|I. Low Risk|
|A. Asymptomatic—no risk factors||Fecal occult blood testing and flex-sig||50||FOBT yearly. Flex-sig every 5 years|
|B. Colorectal cancer in none of first-degree relatives||Total colon examination (colonoscopy or double-contrast barium
enema and proctosigmoidoscopy||50||Every 5–10 years|
|II. Moderate Risk (20–30% of
|A. Colorectal cancer in first-degree relative, age 55 or
younger, or two or more first-degree relatives of any ages||Colonoscopy||40, or 10 yrs. before the youngest case in the family, whichever
is earlier||Every 5 years|
|B. Colorectal cancer in a first-degree relative over the
age of 55||Colonoscopy||50, or 10 yrs. before the age of the case, whichever is earlier||Every 5–10 years|
|C. Personal history of large (> 1 cm) or multiple
colorectal polyps of any size||Colonoscopy||One year after polypectomy||If recurrent polyps—1 year|
|If normal—5 years|
|D. Personal history of colorectal malignancy—surveillance
after resection for curative intent||Colonoscopy||1 year after resection||If normal—3 years|
|If still normal—5 years|
|If abnormal—as above|
|III. High Risk (6–8 percent of people)|
|A. Family history of hereditary adenomatous polyposis||Flex-sig; consider genetic counseling and genetic testing||12–14 (Puberty)||Every 1–2 years|
|B. Family history of hereditary nonpolyposis
colon cancer||Colonoscopy; consider genetic counseling and
genetic testing||21–40||Every 2 years|
|C. Inflammatory bowel disease|
|1. Left-side colitis||Colonoscopy||15th||Every 1–2 years|
|2. Pancolitis||Colonoscopy||8th||Every 1–2 years|
Screening colonoscopy has been widely recognized to save lives
by preventing the development of colorectal cancer. However, as
a screening test, it is operator dependent. The incidence of missed
polyps may be as high as 10% and related to the duration
of time the operator spends during the examination. In addition,
the yield particularly for small lesions may be augmented by new
technologies such as high-definition video and chromoendography.
Yet there is still controversy regarding the cost effectiveness
of routine colonoscopic screening when compared to other modalities.
More recently, fecal immunohistochemical testing and fecal DNA
testing has been studied with great interest, as they may potentially
have improved rates of sensitivity and specificity when compared
to fecal occult blood tests. The principle advantage of these tests
is the potential for improved population participation rates when
compared to invasive modalities such as flexible sigmoidoscopy with
air-contrast barium enema or colonoscopy.
The need for colonoscopic screening of patients in high-risk
groups has been established, but the timing of initial evaluations
must be individualized. Children with possible FAP should have annual
or biannual sigmoidoscopy (then colonoscopy as indicated) starting
at puberty. Biannual colonoscopy beginning at age 21 is the recommendation
for members of families with HNPCC. Colonoscopy every year is probably
the best advice for patients with ulcerative colitis for longer
than 10 years. People with a history of colorectal cancer in one
first-degree relative should undergo colonoscopy starting by age
50 years or at an age 10 years younger than the age at which the
index relative was diagnosed.
Symptoms in patients with large bowel cancer depend upon the
anatomic location of the lesion, its type and extent, and upon complications,
including perforation, obstruction, and hemorrhage. Marked systemic
manifestations such as cachexia are indications of advanced disease.
The average delay between the onset of symptoms and definitive therapy is
7–9 months; both patients and physicians are responsible.
The right colon has a large caliber and a thin and distensible
wall, and the fecal content is fluid. Because of these anatomic
features, carcinoma of the right colon may attain large size before
it is diagnosed. Patients often see a physician for complaints of
fatigue and weakness due to severe anemia. Unexplained microcytic
hypochromic anemia should always raise the question of carcinoma
of the colon. Gross blood may not be visible in the stool, but occult blood
may be detected. Patients may complain of vague right abdominal
discomfort, which is often postprandial and may be mistakenly attributed
to gallbladder or gastroduodenal disease. Alterations in bowel habits
are not characteristic of carcinoma of the right colon, and obstruction
is uncommon. In about 10% of cases, the first evidence
of the disease is discovery of a mass by the patient or the physician.
The left colon has a smaller lumen than the right,
and the feces are semisolid. Tumors of the left colon can gradually occlude
the lumen, causing changes in bowel habits with alternating constipation
and increased frequency of defecation (not true watery diarrhea).
Partial or complete obstruction may be the initial picture. Bleeding
is common but is rarely massive. The stool may be streaked or mixed
with bright red or dark blood, and mucus is often passed together with
small blood clots.
In cancer of the rectum, the most common symptom
is the passage of bright red blood with bowel movements (hematochezia).
Bleeding is usually persistent; it may be slight or (rarely) copious.
Blood may or may not be mixed with stool or mucus. Predictions of
an anal source of bleeding based on color and pattern are unreliable. Whenever persistent
rectal bleeding occurs, even in the presence of hemorrhoids, cancer
must be ruled out. There may be tenesmus (an ineffectual
urge to evacuate the rectum).
Physical examination is important to determine the extent of
local disease, to identify distant metastases, and to detect diseases
of other organ systems that may influence treatment. The supraclavicular
areas should be carefully palpated for metastatic nodes. Examination
of the abdomen may disclose a mass, enlargement of the liver, ascites,
or engorgement of the abdominal wall veins if there is portal obstruction.
If a mass is palpated, its location and extent of fixation are important.
Distal rectal cancers can be felt as a flat, hard, oval or encircling
tumor with rolled edges and a central depression. Its extent, the
size of the lumen at the site of the tumor, and the degree of fixation
should be noted. Blood may be found on the examining finger. Vaginal
and rectovaginal examination will yield additional information on
the extent of the tumor. Retrorectal nodes may be palpable. Rigid
proctoscopic examination is essential to accurately determine the location
of the tumor within the rectum in order to inform subsequent treatment
Urinalysis, leukocyte count, and hemoglobin determination should
be done. Serum proteins, calcium, bilirubin, alkaline phosphatase,
and creatinine should be measured if clinically indicated.
The most familiar chemical marker for cancer of the large bowel
is carcinoembryonic antigen (CEA), a glycoprotein found
in the cell membranes of many tissues, including colorectal cancer.
Some of the antigen enters the circulation and is detected by radioimmunoassay
of serum; CEA is also detectable in various other body fluids, urine, and
feces. Elevated serum CEA is not specifically associated with colorectal
cancer; abnormally high levels are also found in sera of patients
with other gastrointestinal cancers, nonalimentary cancers, and
various benign diseases. CEA levels are high in 70% of
patients with cancer of the large intestine, but less than half
of patients with localized disease are CEA-positive. CEA does not,
therefore, serve as a useful screening procedure, nor is it an accurate
diagnostic test for colorectal cancer in a curable stage. CEA is
helpful in detecting recurrence after curative surgical resection;
if high CEA levels return to normal after operation and then rise
progressively during the follow-up period, recurrence of cancer
Chest films should be obtained routinely. Barium enema examination
is a radiographic means of diagnosing cancer of the colon and is
mainly of historical importance, but unnecessary in patients who
have undergone complete colonoscopy. Carcinoma of the left colon
appears as a fixed filling defect, with an annular (“apple
core”) configuration. Lesions of the right colon may appear
as a constriction or an intraluminal mass. These are the typical
findings of locally advanced carcinoma and earlier stages of the
disease may produce less characteristic filling defects that should
be investigated with colonoscopy. Artifacts (stool, spasm) can resemble
carcinoma. Barium should not be administered by mouth if there is
evidence of carcinoma of the colon, especially on the left side,
since it may precipitate acute large bowel obstruction.
CT scans of the chest, abdomen, and pelvis with oral, intravenous,
rectum contrast are essential in patients with cancer of the colon.
They are informative for identifying the primary tumor location,
assessing extramural extension in patients with colon or rectal
cancer and for detecting metastatic disease in distant organs or
regional lymph node basin (Figure 30–9).
In many situations a combined resection of the primary lesion with
the metastatic lesion (eg, hepatic) can be performed. MRI may be
useful for this purpose as well. PET/CT scans are useful
for detecting recurrences and metastatic disease but are probably
not necessary as part of the routine initial evaluation. Detection
of liver metastases by CT scan and other methods is discussed further
in Chapter 24.
CT scan images. A: Primary, circumferential
carcinoma of the sigmoid colon (arrow). B: Hepatic metastasis
Fifty to sixty-five percent of colorectal cancers are within
the reach of a 70 cm flexible sigmoidoscope. Only 20% can
be seen with a rigid sigmoidoscope. The typical cancer is raised,
red, centrally ulcerated, and may bleed. Mobility of the lesion
can be determined by manipulation with the tip of the instrument.
The size of the lumen should be noted, and the sigmoidoscope should
be passed beyond the lesion to inspect the proximal bowel if possible.
The tumor should be biopsied.
Endoscopic examination of the entire colon should be performed
in every patient with suspected or known cancer of the colon or
rectum if the intention is curative treatment. Colonoscopy allows
for tissue diagnosis, evaluation for synchronous lesions, and opportunity
for ink-spot tattoo marking of the colon for tumor localization. When complete colonoscopy
cannot be performed, the evaluation of the colon may be completed
by CT colonography or air-contrast barium enema.
Endorectal ultrasound for the evaluation of a newly diagnosed
rectal cancer is performed using either a rigid or flexible probe.
In the United States, endorectal ultrasound is one of the principal
diagnostic tests for the clinical evaluation of rectal cancer. However, recently
there has been increasing interest in high-resolution pelvic MRI
for the determination of surgical resection margin status and lymph
An initial erroneous diagnosis is made in as many as 25% of
patients with cancer of the colon and rectum after gastrointestinal
symptoms appear. Symptoms may be attributed mistakenly to disease
of the upper gastrointestinal tract, particularly gallstones or
peptic ulcer. Chronic anemia may be attributed to a primary hematologic
disorder if fecal occult blood testing is not done. Acute pain in
the right side of the abdomen owing to carcinoma can simulate appendicitis.
Most errors are made when the clinical findings are ascribed
to benign disease, and patients may even be operated upon for benign
anorectal conditions in the presence of undetected cancer. Cancer
must be sought out in every patient with recent onset of significant
rectal bleeding even if there are obvious hemorrhoids.
Carcinoma may be difficult to distinguish from diverticular disease;
colonoscopy is useful in these cases. Other colonic diseases—including
ulcerative colitis, Crohn colitis, ischemic colitis, and amebiasis—usually
can be diagnosed by colonoscopy, sigmoidoscopy, or barium enema.
Symptoms should be attributed to irritable bowel syndrome only after
neoplasm has been ruled out.
Treatment consists of wide surgical resection of the lesion and
its regional lymphatic drainage. Resection of the primary tumor
may be indicated, even if unresectable distant metastases have occurred,
in order to prevent obstruction or bleeding and allow for maximization
of systemic therapy.
The abdomen is explored to determine resectability of the tumor
and to search for distant metastases, and associated abdominal disease.
Care is taken not to contribute to spread of the tumor by unnecessary
palpation. The cancer-bearing portion of colon is mobilized and
removed according to anatomic criteria based on the vascular distribution
of the segment of colon containing the tumor. The extent of resection
of the colon and mesocolon for cancers in various locations and
the methods for restoration of continuity are shown in Figure 30–10.
Extent of surgical resection for cancer of the colon
at various sites. The cancer is represented by a black disk. Anastomosis
of the bowel remaining after resection is shown in the small insets.
The extent of resection is determined by the distribution of the
regional lymph nodes along the blood supply. The lymph nodes may
contain metastatic cancer.
For cancer of the rectum, the choice of operation depends on the
location of the lesion within the rectum, the extent of tumor invasion
into the rectal wall, histopathologic features such as the degree
of differentiation or presence of lymphatic or venous invasion,
and the patient’s size, habitus, and general condition.
Preoperative evaluation and staging by digital rectal examination,
proctoscopy, endorectal ultrasound, CT and or MRI, is essential
in order to tailor the treatment to the patient. Preservation of
the anal sphincter and avoidance of colostomy are desirable if possible.
The principal procedures for rectal tumors are as follows:
Resection of the Rectum
This operation, performed through an abdominal incision, is the
curative procedure of choice provided a margin of 1–2 cm
or more of normal bowel can be resected below the lesion but above
the dentate line. The proximal extent of resection should include the
sigmoid colon as it makes for a poor replacement for the rectum
due to hypertrophy of the muscle and common presence of diverticula.
For more proximal lesions within the rectum, it is important to
excise at least 5 cm of mesorectum distal to the tumor to minimize
the chance of local recurrence from cancer in lymph nodes. The technique of total
mesorectal excision (TME) described by Heald in 1982 entails
an en bloc resection of the rectum as an intact unit with its lymphovascular
drainage contained within the fascia propria (Figure
30–11). The mesorectum tapers and diminishes at the
level of the Waldeyer fascia. TME allows for preservation of the
radial resection margins. Surgeons now recommend a “tumor-specific” sharp
mesorectal excision preserving the mesorectal fascia integrity for
at least 5 cm distal to the tumor. Widespread acceptance of this technique
has resulted in a decrease in recurrence rates of rectal cancer
from 20–30% to 5–10%. The descending
or sigmoid colon is anastomosed to the rectum. The end-to-end stapling
device facilitates very low anastomosis, sometimes even as low as
the anal canal (coloanal anastomosis). Unfortunately, such low reconstruction
can be associated with functional difficulties including seepage,
urgency, and frequent bowel movements. This improves over time (1–2 years);
however, the specific treatment should be tailored to the patient.
It may be preferable to construct a colonic J-pouch
when technically feasible to diminish the severity of these symptoms
in the first year. However, J-pouch reconstruction may be associated
with evacuation difficulties, and the relative benefits of such
a reconstruction should be considered.
Total mesorectal excision as depicted in Heald’s
Resection of the Rectum
When adequate distal margins for low anterior resection cannot
be obtained, or the patient’s functional status obviates
a sphincter-sparing approach, an abdominoperineal resection is performed.
The distal sigmoid colon, rectum, and anus are removed through combined
abdominal and perineal approaches. A permanent end colostomy is
Resection of the Colon or Rectum
Curative resections for cancer of the colon or rectum can be
carried out by laparoscopic-assisted techniques. Laparoscopic resection
has been shown to improve postoperative recovery with less pain,
faster return of bowel function, and shorter duration of hospitalization.
Initial concerns of port-site metastases from early reports have
been dispelled. A number of phase III randomized controlled clinical
trials have demonstrated that oncologic outcomes with laparoscopic
surgery are equivalent to open surgery for colon cancer. The laparoscopic
approach differs from open surgery only in the approach, but the
same oncologic resection is performed as with open surgery.
In carefully selected patients with small, well-differentiated,
superficial, mobile polypoid lesions, a full-thickness excision,
with margins greater than 1 cm, of the rectal wall containing the
tumor can be performed as definitive therapy. This technique of
resection should be limited to selected T1 lesions because patient
survival with salvage radical surgery for recurrence after local
excision of T2 and deeper lesions may be much poorer when compared
to initial radical surgery. Lymph nodes are not sampled or treated by
local excision, and success is based on adherence to strict criteria
that predict a low likelihood of nodal spread. Even T1 tumors have
been reported to be associated with a 7–14% chance
of nodal metastasis. A strategy of chemoradiation and local excision
has been reported in small case series for lesions more advanced
than T1; however, the long-term results are not well documented, and
this approach should subject to clinical trials such as one currently
ongoing sponsored by the American College of Surgeons Oncology Group
(ACoSOG). Transanal endoscopic microsurgery (TEM) is
a minimally invasive technique for the local resection of rectal
tumors, best suited for more proximal rectal lesions. The same criteria
are applied to patients for conventional local excision or TEM.
Unresectable rectal cancers can be palliated by fulguration (electrocoagulation)
or laser photocoagulation. Unfortunately, symptom relief—of
bleeding, tenesmus, and mucus discharge—in patients with
these advanced lesions is often less than anticipated. A diverting colostomy
can be performed for obstructing rectal cancer that cannot be resected.
However, in such cases, colonoscopically deployed endoluminal stents
can provide relief of obstruction even when the lumen is too small
to accommodate a pediatric colonoscope. Tumor ingrowth will cause
stent occlusion within 6–9 months, but this can be prolonged
with laser photocoagulation.
Adjuvant external beam radiation therapy, given with chemotherapy
as a radiation sensitizer has been demonstrated to reduce local
failure risk following curative surgical resection. The strategy
of preoperative treatment (neoadjuvant therapy) is
more effective than postoperative treatment for improving local
control, sphincter preservation, and reducing treatment related
toxicity. Complete clinical response has been reported to be as
high as 30% after neoadjuvant treatment; however, many
of these patients will still have pathologically detectable disease
and therefore complete clinical response does not eliminate the
need for surgical resection. Although the benefit of radiation on
decreasing local recurrence rates has been well demonstrated in
several randomized trials, only one major randomized trial has demonstrated
a benefit in survival. It should be noted, however, that the boundaries
of resection for curative intent should be based on the pretreatment evaluation
of tumor extent and not on the visible tumor after treatment. Irradiation
is not used for cancer of the colon. Intraoperative radiation therapy
at the time of curative resection is a promising method of reducing
local recurrence risk among patients with locally advance or recurrent
Chemotherapy and radiation therapy have been studied extensively
as adjuvants to curative resection of cancer of the large intestine.
Strategies are different for cancer of the colon and cancer of the
rectum. Patients with stage I lesions in either site do not benefit
from adjuvant therapy. Some stage II and stage III rectal cancer
patients have improved local control and survival with combined
neoadjuvant chemoradiation therapy followed by postoperative adjuvant
chemotherapy. Stage III colon cancer patients benefit from adjuvant
chemotherapy. Current regimens include either intravenous 5-fluorouracil
or oral capecitabine in combination with oxaliplatin as first-line therapy
(Table 30–7). Other agents effective
in the metastatic setting are currently under investigation in the
adjuvant setting. Some patients with stage II colon cancer may benefit from
adjuvant therapy, and these patients should be
enrolled into clinical trials, many of which currently use molecular
markers to help select patients for adjuvant therapy.
Table 30–7. Currently Used
Chemotherapeutic Agents Effective in the Treatment of Colon Cancer. |Favorite Table|Download (.pdf)
Table 30–7. Currently Used
Chemotherapeutic Agents Effective in the Treatment of Colon Cancer.
|Uracil and tegafur||Oral||Antimetabolite||Adjuvant Metastatic|
|Oxaliplatin||Intravenous||DNA alkylation and cross-linking||Adjuvant Metastatic|
|Irinotecan||Intravenous||Inhibit DNA repair by topoisomerase I||Metastatic|
|Bevacizumab||Intravenous||MAb to VEGF||Metastatic|
|Cetuximab||Intravenous||MAb to EGFR||Metastatic (k-ras wild type)|
|Panitumumab||Intravenous||MAb to EGFR||Metastatic|
Obstructing cancer of the left or right colon is treated by immediate
resection in good-risk patients. (See earlier section on Obstruction
of the Large Intestine.)
An aggressive approach to perforated cancer of the colon is advisable,
but anastomosis is often delayed based on the degree of contamination
and the health of the bowel. If contamination is severe or if bowel
health is compromised, the proximal end is exteriorized as a colostomy
(or ileostomy), and the distal end is exteriorized or closed. Secondary
anastomosis is performed after inflammation subsides. Alternatively,
the anastomosis may be performed and “covered” with
a defunctioning loop ileostomy. Closure of a loop ileostomy is a
simpler and less morbid procedure than reexploration and closure
of an end stoma.
When carcinoma of the colon has spread by contiguity to adjacent
viscera such as the small intestine, spleen, kidney, uterus, prostate,
or urinary bladder, the involved viscus—or a portion of
it—should be resected en bloc with the colon.
The clinicopathologic stage of disease is the most
important determinant of survival. In general the results of surgical treatment
are better for cancer of the colon than for cancer of the rectum,
and low rectal cancer has a worse prognosis than cancer higher in
the rectum. The Dukes classification was introduced decades ago
but has been replaced by the TNM system developed by the American
Joint Committee for Cancer. Table 30–8 lists
the definitions of TNM and the stage grouping along with the corresponding
historical Dukes classification. Clinical data are used for determination
of M, and both clinical and pathologic information is included in assessment
of T and N. Survival rates differ considerably in various series;
actuarial rates are higher than crude survival rates. Adjuvant therapy,
particularly with some of the newer agents, in addition to improved
surgical techniques, has led to 5-year survival rates of 40–80% for
stage III disease.
Table 30–8. TNM Classification of Cancer of the Colon
and Rectum.1 |Favorite Table|Download (.pdf)
Table 30–8. TNM Classification of Cancer of the Colon
|Primary Tumor (T)|
|TX||Primary tumor cannot
|T0||No evidence of primary
|Tis||Carcinoma in situ|
|T1||Tumor invades submucosa|
|T2||Tumor invades muscularis
|T3||Tumor invades through
the muscularis propria into the subserosa or into nonperitonealized
pericolic or perirectal tissues|
the visceral peritoneum, or directly invades other organs or structures|
|Regional Lymph Nodes
|NX||Regional lymph nodes
cannot be assessed|
|N0||No regional lymph
|N1||Metastasis in 1
to 3 pericolic or perirectal lymph nodes|
|N2||Metastasis in 4
or more pericolic or perirectal lymph nodes|
|N3||Metastasis in any
lymph node along the course of a named vascular trunk|
|MX||Presence of distant
metastasis cannot be assessed|
|M0||No distant metastasis|
|Stage IV||Any T||Any N||M1|
Up to 20% of patients have liver or other distant metastases
at presentation. However, in selected patients with metastases in
whom all metastatic disease can be completely resected, operation
for cure should be performed. The operative mortality rate is 1–4%.
The prognosis is adversely affected by complications such as
obstruction or perforation. The histologic features—including
the degree of differentiation of the tumor, intravascular tumor
cells, or malignant cells in the perineural space—also have
a bearing on prognosis and may influence the decision to recommend
adjuvant chemotherapy in node-negative patients.
One limitation of AJCC/TNM staging is that patients with
TNM stage may have widely different potentials for local recurrence,
distant metastasis, and survival. Ultra-staging techniques include
immunohistochemistry for markers such as cytokeratins and reverse
transcription polymerase chain reaction for CEA to look for evidence
of micrometastasis within regional lymph nodes or genotypic subset
analysis. Loss of heterozygosity at chromosome 18q (affecting expression
of DCC, Smad4, and Smad2) is predictive of a poor outcome. Other
markers of poor prognosis include loss of heterozygosity at chromosome
17p (affecting p53) and 8q, and a mutation in the BAX gene.
Favorable prognostic factors include the presence of microsatellite instability
in the genes of the mismatch repair family and increased expression
of the cyclin-dependent kinase inhibitor p21WAF1/CIP1 protein.
Further study is required before clinicians can base therapeutic
decisions on assays of these and other molecular markers.
Studies from several countries show that low-income people have
more advanced disease when diagnosed and that their stage-for-stage
survival rates are worse; these observations have not been explained
satisfactorily. An association of perioperative blood transfusions
with poorer prognosis from colorectal cancer has been found by some,
but not all, investigators; if it is genuine, the association may
reflect other effects—larger tumors requiring more extensive
surgery and transfusions, for example—rather than some
consequence of transfusion itself.
Follow-up after curative resection of cancer of the large bowel
is controversial. There are good data to support the view that periodic
colonoscopy to detect and remove adenomas after colonoscopic polypectomy
prevents subsequent cancer, and colonoscopy at 3 years is just as
beneficial as colonoscopy at 1 and 3 years after complete removal
of the index adenoma. It is not known whether these observations can
be extrapolated to follow-up after curative resection of cancer,
but in the absence of data, many clinicians perform surveillance
colonoscopy periodically for the purpose of detecting adenomas and
metachronous carcinomas. In addition, presence of a distracting
lesion may result in an increased risk for missed lesions during
colonoscopy. Other goals of follow-up are the diagnosis of recurrent
cancer or metastatic cancer. The physician should tailor the follow-up
strategy to the patient’s ability and interest in pursuing
an aggressive approach should recurrent disease be discovered. Follow-up programs
include a complete blood count, liver function tests, serum CEA
levels, chest x-rays, and CT scans in addition to colonoscopy.
If recurrent cancer or metastatic cancer is discovered, the patient
is evaluated for potential surgical resection of the lesions. This
is particularly true for hepatic or pulmonary metastases where a
survival benefit has been demonstrated. Local recurrences can be
resected, sometimes in combination with intraoperative radiation
therapy. Five-year survival rates of 25–35% after
multimodality therapy, including preoperative chemoradiation and
surgical resection with intraoperative radiation therapy, have been reported
for recurrent rectal cancer. Unfortunately, the prognosis of patients
with local recurrence is generally poor. If recurrent cancer is
suggested on the basis of rising serum CEA levels, it can usually
be located by CT, MRI, or PET scan. A second-look laparotomy is
now rarely required because of improvements in the quality of cross-sectional
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