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These drugs can be used orally or topically. A combination
of oral and rectal administration may be required.
Steroids While steroids are the mainstay of acute
therapy, they are associated with severe toxicity. Less toxic,
newly developed drugs (e.g., budesonide) may prove
useful. Steroids should be used at the lowest possible dose
and for the shortest period necessary. Steroids block the
production and effects of cytokines and other inflammatory mediators. The use of steroids, particularly in the
presence of abdominal masses and fistulas, may mask
abdominal signs of severe sepsis. Steroids may be administered orally or rectally.
Immunomodulatory Agents Four immunomodulatory
drugs are in use: azathioprine (AZA), 6-mercaptopurine
(6-MP), methotrexate (MTX), and cyclosporine. The beneficial effect of AZA and 6-MP is slow, developing in 3 to
4 months. Hence, these agents are useful only as maintenance therapy to reduce recurrence rates. MTX is particularly useful in patients who are refractory to AZA.
Cyclosporine is the most controversial choice because it is
associated with serious systemic toxicity (i.e., renal failure,
upper GI bleeding, bowel infarction). Cyclosporine may
be a useful drug to treat pyoderma gangrenosum.
Antibiotics Clarithromycin, ciprofloxacin, and
metronidazole are currently used in inflammatory
bowel disease therapy. Metronidazole has been shown to
prolong postresection remission.
I
NDICATIONS FOR SURGICAL THERAPY Surgery is
reserved for complications of Crohn’s disease or for failure
of medical treatment. Possible complications of CD
include: acute abdomen due to acute ileitis, obstruction,
fistula, perforation, hemorrhage, growth retardation,
ureteral obstruction, or anorectal disease. Acute abdomen
due to acute ileitis was discussed earlier (see Acute Presentation, under Crohn’s Disease, earlier in this chapter).
Obstruction Intestinal obstruction is the most
common indication for surgery in CD. The indication for
operation may be complete obstruction or, more frequently,nonresolving incomplete obstruction. The guiding
principle of surgical treatment in bowel obstruction due to
CD is to conserve as much intestine as possible. There is no
advantage to extending resection beyond macroscopic
disease. The practice of performing frozen sections to
determine microscopically free margins has been abandoned. Any segment of normal intestine measuring 10cm
or longer between skip lesions should be preserved.
Narrowings due to burnt-out Crohn’s can be treated with
stricturoplasty. This procedure is used primarily in patients
with multiple short fibrotic strictures, particularly those
vulnerable to short bowel syndrome. Strictures as long as
15 to 20cm can be treated with stricturoplasty. Operated
sites should be biopsied to exclude lymphoma or carcinoma.
Fistula Enteroenteral fistulas that are asymptomatic
require no surgical correction. Often, however, fistulas are
either associated with sepsis or involve other organs (e.g.,
bladder, vagina, uterus). Sometimes enterocutaneous fistulas may develop and cause severe abdominal wall excoriation. Surgical management of fistulas requires excision of
the bowel from which the fistula arises and drainage of any
associated abscess.
Perforation Perforation is a rare complication of CD
and requires emergency operation, appropriate resection,
and drainage.
Hemorrhage Massive, life-threatening hemorrhage is a
rare but important complication of CD, especially Crohn’s
colitis. Selective angiography is useful to localize areas of
bleeding. Operative treatment requires resection of the
involved segment of bowel.
Growth Retardation Approximately 25% of children
with CD have growth retardation. If aggressive medical and
nutritional therapy fails to reverse growth retardation,
resection of the diseased bowel is indicated.
Ureteral Obstruction The ureter may become
obstructed either because of a retroperitineal abscess or
retroperitoneal fibrosis. The treatment for abscess is
drainage with or without bowel resection. In the case
of fibrosis, extensive ureterolysis may be necessary.
Anorectal Disease Perineal abscesses and fistulas are
treated with conservative surgery without performing
large excisions.
F
AILURE OF MEDICAL THERAPY Failure to achieve
remission in severe CD involving the small or large bowel
is an indication for surgery, particularly when patients
cannot tolerate medication or develop complications from
drug therapy. Severe perianal disease that recurs frequently
or fails to respond to local surgery is an indication for
surgery. While bowel conservation is a top priority in small
intestinal resection, the same is not true for colonic
resection. Stricturoplasty, for example, is not indicated
in colonic stricture. Pancolonic disease requires total proctocolectomy with Brook’s ileostomy. Continent ileostomy,
either the Kock’s type or pelvic, is contraindicated.
P
ROGNOSIS It is estimated that 70% of patients with
CD require surgical treatment. Postresection recurrence
rates are high and endoscopically 70% recur within 1 year.
If defined by the need for reoperation, however, some 25%
to 30% have recurrent disease within 5 years, and 40% to
45% develop recurrent disease within 20 years.
25
Neither
medical nor surgical therapy can cure CD. A partnership
C linical D isorders and Management .................................................................................................. 289
between patient, physician, gastroenterologist, and surgeon
is required to provide optimum care.
CHRONIC ULCERATIVE COLITIS
Clinical Presentation
The predominant clinical picture in a patient with chronic
ulcerative colitis (CUC) is one of rectal bleeding and diarrhea. The stools are watery, containing blood, mucous, and
pus, and may be frequent.Tenesmus and rectal urgency are
frequent symptoms. Most patients complain of abdominal
pain. The onset may be either mild, characterized by
bloody diarrhea, or fulminant with fever, abdominal pain,
and tenderness. Abdominal examination in severe cases
shows tenderness with or without rebound tenderness.
Rectal examination may show superficial anal fissures
from severe diarrhea, and blood may be present on the
examining finger. Sigmoidoscopy should be performed as
part of the physical examination. The rectal mucosa is
usually erythematous and bleeds on contact; in severe
cases, it has been aptly described as “bleeding velvet.” Paradoxically, rectal ulcers are not frequently seen in CUC,
whereas rectal involvement in Crohn’s disease is often
associated with longitudinal ulcers in the rectal mucosa.
Investigations
FIGURE 8.39. Colonoscopy in a patient with chronic ulcerative
colitis shows extensive polyposis. (Courtesy of John Cello, MD.)
colon with irregular interface between luminal gas and the
edematous mucosa. Dilatation of the colon and small
bowel may be present.
Laboratory Findings
Anemia, leukocytosis,and elevated sedimentation rates are
usually present. In fulminant disease, severe leukocytosis,
and bandemia are present. Severe diarrhea may lead
to hypokalemia, hypoproteinemia, and significant contraction of the extracellular fluid volume. Stool studies
may be necessary to exclude salmonellosis and shigellosis.
Campylobacter and C. difficile infections must also be
excluded.
Colonoscopy
If sigmoidoscopy suggests the presence of CUC,
colonoscopy will be needed to show the extent of colon
involvement, the presence of pseudopolypi (Figure 8.39),
and to facilitate biopsy. Following colonoscopy, barium
enema may or may not be necessary to obtain additional
information. Colonoscopy must be performed with great
care in severe disease because of the danger of perforation.
Colonoscopy should not be performed in the presence of
toxic megacolon or toxic colitis.
Radiology
PLAIN FILMS In patients with severe disease, plain
films of the abdomen may show edematous, thickened
ARIUM ENEMA Barium enema should be performed
B
carefully to avoid overinflation and should be avoided if
toxic colitis or toxic megacolon is present. The mucosa is
granular, thickened, with superficial ulcers. Haustral folds
are lost, and the colon is foreshortened if disease has been
longstanding. Pseudopolyps may be present (Figure 8.40).
PIRAL CT Spiral CT with 3-D reconstruction may
S
be useful when barium enema is too risky to perform.
Clinical Management
CUC is treated medically, with surgery reserved for
medical failure or complications.
Medical Therapy
The medical therapy for CUC is the same as that described
above for Crohn’s disease. When only the rectum is
involved, steroid retention enemas are used first in combination with oral preparation of 5-ASA. Systemic corticosteroid therapy is reserved for cases in which local
therapy fails. Disease beyond the rectum is treated with
oral prednisone in mild cases or intravenous prednisone
in severe cases. Once remission is achieved, maintenance
therapy is usually instituted, using 5-ASA preparations
(e.g., mesalazine, olsalazine).
290 ................................................................................................................ Small and L arge Intestine
A
B
FIGURE 8.40. Manifestations of CUC. (A) Pseudopolyps (arrows) produce multiple filling defects in this
barium-filled descending colon. These are seen in chronic ulcerative colitis in the acute phase and as
part of the healing spectrum. (B) The entire colon is foreshortened and has lost its normal haustral
pattern, a condition known as “lead pipe colon,” due to long-standing chronic ulcerative colitis.
(Courtesy of Henry I. Goldman, MD.)
C linical D isorders and Management .................................................................................................. 291
TABLE 8.12. Chronic Ulcerative Colitis: Indications for Surgery
Emergent
䊏
Perforation
䊏
Hemorrhage (6–8 U of blood/24 h)
䊏
Toxic colitis that is nonresponsive to 72–84h of maximal
medical therapy
䊏
Toxic megacolon that is nonresponsive to 24–48h of maximal
medical therapy
Elective
䊏
Failure of or intolerance to medical therapy
䊏
Dysplasia
䊏
Carcinoma
Surveillance for Cancer
Colonoscopic surveillence for cancer is recommended
after 7 years of pancolitis or 10 years of left-sided colitis.
Colonoscopy and multiple random biopsies, as well as
biopsies of any suspicious lesions are performed every 1 to
2 years. If dysplasia is found, colonoscopy and biopsy are
repeated in 2 months. If dysplasia persists, colectomy is
recommended.
Surgical Treatment
The indications for surgery are complications and failure
of medical therapy (Table 8.12).
Other alternatives—including total procolocolectomy
with continent (Kock) ileostomy or abdominal colectomy
with ileoproctostomy—are less appealing. The latter, of
course, does not eliminate the risk of cancer in the rectal
mucosa.
Emergency surgery may be indicated for toxic colitis,
toxic megacolon, perforation, or hemorrhage.
Toxic Colitis Toxic colitis, or fulminant colitis, affects
5% to 15% of patients with CUC. Toxic colitis may represent the initial presentation of disease in approximately
one-third of patients with CUC. It carries a mortality rate
of 8% to 10%, which rises more than 25% if the colitis is
accompanied by perforation.
26
Clinical features include
fever, abdominal pain and tenderness with signs of peritonitis, absent bowel sounds, distension, and leukocytosis
with bandemia. Steroid therapy inhibits the full clinical
expression of peritonitis, and this fact must always be borne
in mind. Other causes of acute colitis should be excluded,
especially Clostridium difficile enterocolitis. Plain films of
the abdomen show ileus of the small intestine but no megacolon. Free peritoneal fluid may be present. The presence
of free air, of course, indicates that perforation has
occurred, In which case barium enema and colonoscopy
must be avoided.
This complication, like toxic megacolon, is best
managed by a team approach between the surgeon and
gastroenterologist. A decision is made how to administer
REOPERATIVE MANAGEMENT Preoperative manage-
P
ment requires correction of any fluid deficit, hypokalemia,
and anemia. Preoperative total parenteral nutrition is indicated in elective settings where the patient has evidence of
malnutrition. Because most patients have been on steroids,
a perioperative steroid regimen is administered, with
100mg of cortisol intramuscularly or intravenously just
before the operation, followed by 50 to 100 mg every 6 h
during surgery. Postoperatively, the steroid dose can be
decreased by half each day from postoperative day 1 until
maintenance doses are reached. Thereafter, a steroid tapering program is started until the patient is completely off the
drug. Preoperatively, intraoperatively and postoperatively,
careful monitoring of the volume status, serum potassium,
and blood pressure should be performed.
PERATIVE MANAGEMENT Elective surgery is indicated
O
when the patient’s condition is refractory to treatment,
when severe extraintestinal manifestations develop, or
when risk for cancer is identified. The current operation of
choice is total colectomy, mucosal protectomy, and ileoanal anastomosis using a reservoir ileal pouch (Figure
8.41). The preferred pouch is a 30-cm duplicated J (15cm
per limb). Other pouch constrictions are the Sand W-types.
The operation removes all mucosa susceptible to CUC
and cancer development, avoids permanent ileostomy, and
maintains anal continence. Successful outcome can be
expected in at least 95% of patients.
FIGURE 8.41. Elective surgery for ulcerative colitis includes total
colectomy with mucosal protectomy and ileo-anal anastomosis
using an ileal pouch and protective divided ileostomy. (Adapted
from Schwartz SI, ed: Principles of Surgery, 6th ed. New York:
McGraw Hill, 1994:1247.)
292 ................................................................................................................ Small and L arge Intestine
maximum medical therapy, to follow the patient with
frequent abdominal examinations, and to operate if no
improvement is seen in 48 to 72h. Treatment consists of:
1. Nasogastric suction.
2. Fluid administration monitored by urine output and
central venous pressure or pulmonary artery pressure
measurements.
3. Maximum doses of intravenous steroids (hydrocortisone 100 to 300mg/24 h, or, if the patient does not
respond to steroids, ACTH by intravenous drip at
120 U/24 h).
4. Intravenous antibiotics, usually triple antibiotics
consisting of ampicillin, aminoglycoside, and
metronidazole.
On this regimen, approximately 60% to 75% of
patients improve. The 25% to 40% who do not improve
require an emergency proctocolectomy with concurrent or
subsequent mucosal protectomy and ileo-anal anastomosis with pelvic reservoir. A temporary diverting loop
ileostomy is often necessary. If perforation has occurred,
the procedure must be staged by first performing total
abdominal colectomy (Figure 8.42), followed by the pelvic
operation several weeks later.
Toxic Megacolon This complication consists of fulmi-
nant colitis associated with persistent dilatation of the
TABLE 8.13. Essentials: Toxic Megacolon in Chronic Ulcerative
Colitis
Incidence: 5%
Precipitating factors
䊏
Hypokalemia
䊏
Opiates or anticholinergics
䊏
Barium enema, colonoscopy
Clinical picture
䊏
Frequent bloody diarrhea
䊏
Fever, tachycardia
䊏
Abdominal distention
䊏
Abdominal tenderness (may be masked by steroid therapy)
X-ray findings
䊏
Dilated transverse colon (>6 cm)
䊏
Ileus
Management
䊏
Initial conservative treatment
➢ Nasogastric tube
➢ Intravenous fluids
➢ Intravenous steroids (hydrocortisone 100 mg q 6 h)
➢ Broad-spectrum antibiotics
䊏
If no improvement in 24–48 h, total abdominal colectomy
with ileostomy
䊏
Definitive treatment is delayed mucosal proctectomy,
ileo-anal anastomosis with ileal pouch
Prognosis
䊏
50% respond to medical therapy; 50% of these will
ultimately require surgery
䊏
Postoperative mortality rate of 10%–15%
FIGURE 8.42. Total abdominal colectomy. In treatment for
emergent complications of ulcerative colitis, a total abdominal
colectomy with ileostomy is performed and the divided rectum
is brought out as a stoma. (Adapted from Schwartz SI, ed:
Principles of Surgery, 6th ed. New York: McGraw Hill, 1994:1247.)
colon. The essentials are summarized in Table 8.13. Colonic
dilatation is assessed by measuring the diameter of the
transverse colon in a supine abdominal x-ray film (Figure
8.43). Transverse colon diameter in excess of 6cm represents dilatation. On the same film, the size of the cecum
should also be noticed. The clinical picture and management is the same as for toxic colitis, except that there is
more urgency in toxic megacolon because of potential
complications. Thus, if the patient fails to improve
clinically, and dilatation does not subside within 24 to
48h, emergency operation is indicated. The principles of
operative management are similar to those for toxic colitis.
Factors that precipitate toxic megacolon include the
use of opiates or anticolinergic drugs, hypokalemia, and
recent colonoscopy or barium enema.
Perforation Perforation is a dreaded and potentially
lethal complication of CUC. It can complicate both toxic
colitis and toxic megacolon. The incidence of perforation
in toxic megacolon has been reported to be as high as
27
Physical findings may be masked by steroid therapy,
33%.
but free peritoneal air is present on plain abdominal films.
Immediate abdominal colectomy and Brook’s ileostomy are
indicated. Rectal mucosectomy, construction of a pelvic
pouch, and ileo-anal anastomosis are postponed to a
second operation weeks or months after colectomy.
C linical D isorders and Management .................................................................................................. 293
Yersenia Enteritis
The pathogen Yersenia enterocolitica typically causes ter-
minal ileitis and mesenteric adenitis that simulate acute
appendicitis. But it can also cause gastroenteritis and
colitis and even liver and spleen abscesses. Diagnosis
can be made by culturing the pathogen from stool and/or
by measuring blood antibody titer, which rises and
falls with the course of the disease. Effective antibiotic
therapy is provided by trimethoprim-sulfamethoxazole or
doxycycline.
Campylobacter Enteritis
The pathogen is Campylobacter jejuni. This common
infection is transmitted by contaminated water, milk, or
undercooked poultry. The usual picture is similar to that
of viral gastroenteritis, although severe enterocolitis with
bloody diarrhea—resembling CD or CUC—can develop.
Diagnosis is made by microscopic (darkfield or phasecontrast) examination of stool, or by culturing the Gramnegative rod from stool or blood. The treatment of choice
is oral erythromycin.
FIGURE 8.43. Colonic dilatation in toxic megacolon. This supine
abdominal x-ray, taken because the patient had abdominal pain
and distention and known acute ulcerative colitis, shows a
greatly dilated colon. The colon contour lacks the usual haustral
pattern and, in the transverse colon (arrows), an irregular
contour is present, suggesting ulceration. This patient had systemic signs and symptoms as well as laboratory values consistent
with the term toxic megacolon. (Courtesy of Henry I. Goldberg,
MD.)
Hemorrhage Massive hemorrhage is an indication for
surgery in fewer than 5% of cases. Hemorrhage requiring
6 to 8U of blood transfusion per 24h should be treated
with emergency colectomy or proctocolectomy.
OTHER INFLAMMATORY DISEASES OF
THE SMALL AND LARGE BOWEL
Specific infections of the small and large intestine are very
common in developing countries but less so in North
America and Europe. They must be differentiated from
Crohn’s disease or chronic ulcerative colitis. Causes include
bacteria, viruses, parasitic infestations, or fungal infections.
Typhoid
Typhoid, caused by Salmonella typhi, is endemic in regions
with poor public health services. The disease is an acute
systemic infection with high fever. In the GI tract, the
infection concentrates on Peyer’s patches, causing severe
enteritis and colitis with ulcerations. Gross hemorrhage or
perforation can occur. Diagnosis is established by demonstrating high titer of agglutinins for the O and H antigens
in samples of blood or feces. The drug therapy of choice
is chloramphenicol or trimethoprim-sulfamethoxazole
(TMP-SMX). Parenteral amoxicillin is a second choice.
Perforation requires immediate surgery, but in severe
disease limited to the ileum and cecum that does not
rapidly respond to antibiotic therapy, early operation
before perforation develops may prove lifesaving.
Shigella
Shigella organisms cause bacillary dysentery. Four groups
of shigella are the major pathogens. They include S. dysen-
teriae, S. flexneri, S. boydii, and S. sonnei. The major organ
affected is the colon. The stool contain large amounts
of PNMs and blood. Treatment includes rehydration,
ampicillin therapy, and avoidance of opiates. Ampicillinresistant organisms are treated with TMP-SMX.
Tuberculosis
Bacterial Enterocolitis
Bacteria may infect either the small bowel, the colon, or
both.
Primary tuberculosis of the intestine is rare and is caused
by Mycobacterium tuberculosis. The cecum and terminal
ileum are most commonly involved, but the ascending
colon, jejunum, duodenum, stomach, esophagus, and
294 ................................................................................................................ Small and L arge Intestine
sigmoid colon may also be involved. Complications
include hemorrhage, perforation, fistula formation, and
malabsorption. If an operation is carried out, the findings
are similar to those in CD, and resection should be conservative. The mainstay of therapy is, of course, the use of
antituberculosis drugs.
Clostridium Difficile Enterocolitis
Clostridium difficile elaborates a toxin that causes
pseudomembranous enterocolitis. The most common precipitating cause is antibiotic therapy, particularly with oral
clindamycin, ampicillin, cephalosporins, and several
others. Antibiotic therapy leads to unopposed proliferation of C. difficile and invasion of the colonic mucosa. The
clinical findings are severe watery diarrhea (15–30 stools
per day), associated with abdominal pain and high fever.
Sigmoidoscopy shows a confluent pseudomembrane covering an erythematous and swollen mucosa. Diagnosis is
further established by showing C. difficile cytotoxin in the
stool and culturing the organism from stool. Occasionally,
pseudomembranous colitis may cause toxic megacolon or
perforation, requiring colectomy.
Viral Diseases
Several viruses cause gastroenteritis, which is rarely of
surgical interest. Rotavirus, Norwalk virus, enteric
adenovirus, and others are involved.
Parasitic Infestations
Intestinal Amebiasis
The pathogen Entamoeba histolytica, transmitted by
oral-fecal contact, can cause three forms of disease:
amebic dysentery, amebic colitis, and intestinal ameboma.
Amebic colitis may be severe; it causes severe bloody and
mucousy diarrhea, abdominal pain, high fever, toxicity,
and high leukocytosis. Sigmoidoscopy shows typical
amebic ulcers, which are small with white caps. Ameba
may be recovered from their exudate. Colonic dilatation
may develop, resulting in a picture similar to that of toxic
megacolon in CUC. The distinction is critical, however,
because steroid therapy for amebic colitis leads to perforation. Amebic colitis is treated with metronidazole and
tetracycline. Other antiamebic drugs include paromomycin (Humatin®), dehydroemetin, and iodoquinol.
Very rarely colectomy may be necessary. Intestinal
ameboma may rarely cause intestinal obstruction
requiring resection.
Fungal Infection
Actinomycosis
The infection is due to actinomycetes, Gram-positive,
nonacid-fast filamentous organisms. Typically, the ileum,
cecum, and ascending colon are involved. Multiple sinuses
may form within the abdomen and into the skin. The characteristic and diagnostic finding is the presence of sulfur
granules in the discharging pus. The disease is treated with
high doses of penicillin. Right hemicolectomy may be
necessary to remove the diseased bowel for cure.
Nocardiosis
The pathogen is Nocardiae, Gram-positive branching filamentous organisms. Abdominal nocardiosis resembles
actinomycosis and is characterized by abscess, granuloma,
and sinus formation. The treatment of choice is sulfonamides. Surgical intervention may be necessary to drain
abscesses and excise fistulas.
NEOPLASMS OF THE SMALL INTESTINE
Neoplasms of the small intestine comprise about 3% of
all gastrointestinal tumors. They tend to be associated
with neoplasms elsewhere. Benign lesions are the most
common, but they are rarely symptomatic unless they
cause intussusception or bleeding. Lymphomas and
adenocarcinomas are the most common tumors. In
general, lymphomas are more common distally and their
incidence declines more proximally in the small intestine.
Adenocarcinomas have the opposite distribution.
Benign Neoplasms
Solitary Polyps
Both villous and adenomatous polyps occur but very
rarely. The most common site is the duodenum. Large
periampullary villous adenomas nearly always have a
malignant component, which is often difficult to detect on
biopsy.Solitary polyps are asymptomatic unless they cause
intussusception or bleeding. They are then treated by
limited resection.
Leiomyomas
These benign tumors are usually asymptomatic. Bleeding
is rare unless malignant degeneration is present.
Multiple Polyps
PEUTZ–JEGHERS SYNDROME An inherited disorder of
multiple polyposis, Peutz–Jeghers syndrome is associated
with skin pigmentation. Patients often have café-au-lait
pigmentation in the circumoral area and in the buccal
mucosa. The lesions rarely become malignant, but they
can cause bleeding or obstruction when they are treated
with resection.
C linical D isorders and Management .................................................................................................. 295
MULTIPLE HAMARTOMATOUS POLYPS These polyps are
usually asymptomatic.
F
AMILIAL ADENOMATOUS POLYPOSIS These polyps
occur as part of Gardner’s syndrome (see section on
familial adenomatous polyps of the colon).
J
UVENILE POLYPS Also known as retention polyps,
juvenile polyps are benign and are probably hamartomas.
They may cause bleeding or intussusception in childhood.
Malignant Tumors
Primary Tumors
LYMPHOMA Primary lymphoma is probably the most
common malignant lesion of the small intestine. It is most
common in the ileum but may occur in the jejunum in
association with celiac disease. These tumors present clinically with colicky abdominal pain, anorexia, weight loss,
and sometimes anemia. They may also present with small
bowel obstruction and intussusception. Rarely, lymphomas
may cause perforation. Treatment includes limited small
bowel resection followed by whole abdominal radiation
and/or chemotherapy.
Several histologic subtypes of lymphoma exist,
including:
1. Diffuse large- or small-cell lymphoma.
2. Immunoproliferative intestinal disease (IPSID
lymphoma).
3. Mucosa-associated lymphoid tumors (MALT).
4. Multiple lymphoid polyposis.
5. Enteropathy-associated T cell lymphoma.
A
DENOCARCINOMA Adenocarcinoma is more com-
mon in the jejunum. It remains asymptomatic for a long
period and, by the time surgery is performed, the tumor is
invasive and 80% has metastasized (Figure 8.44). Treatment is resection of the involved bowel and its mesentery.
The 5-year survival rate is 15% to 35%.
28
Adenocarcinoma
may occur in the bypassed segment of bowel when bypass
is used to treat Crohn’s disease.
C
ARCINOID TUMOR See Chapter 5 for a full discussion
of carcinoid tumors of the small intestine. A characteristic
small intestinal carcinoid tumor is shown in Figure 8.45.
L
EIOMYOSARCOMA Leiomyosarcoma can occur any-
where in the small intestine and tends to cause bleeding from
central ulceration of the mucosa overlying it. Less commonly,
leiomyosarcoma may cause obstruction. The major mode of
spread is hematogenous. Treatment is segmental resection.
Recently, imatinib mesylate has been shown to be effective in
the treatment of stromal tumors of the gastrointestinal tract.
29
Other types of sarcoma can also occur. In HIV/AIDS, Kaposi
sarcoma may develop in the small intestine.
Metastatic Disease
The most common metastatic tumor in the small intestine
is malignant melanoma. Approximately 50% of patients
dying from melanoma have secondary tumors in the submucosa of the small intestine. Other neoplasms that may
metastasize to the small intestine include breast, lung,
kidney, and cervix. Useful palliation can be achieved by
resection if bleeding or obstruction occurs.
COLORECTAL CANCER
Colon cancer has a doubling time of 130 days and may
remain asymptomatic for 5 to 10 years. When it becomes
symptomatic, the clinical picture varies depending on
whether the tumor is located in the right colon, the left
colon, or the rectum. Colon cancer may be of the polypoid, ulcerating, or napkin-ring type (Figure 8.46).
Clinical Presentation
Carcinoma of the Right Colon
Because of the large caliber of the right colon and the fluid
nature of the intestinal contents, carcinoma of the right
colon does not frequently produce obstruction, and the
tumor can become large in size. The clinical presentation
may include:
1. Iron-deficiency anemia causing fatigue and weakness.
2. Right-sided abdominal pain.
3. Abdominal mass discovered by the patient or by the
physician in routine physical examination.
4. Obstruction of the ileocecal valve causing low small
bowel obstruction.
5. Obstruction of the base of the appendix causing acute
appendicitis (rare presentation).
When a patient over 40 years of age, particularly a man,
presents with unexplained iron-deficiency anemia, carcinoma of the right colon must be excluded. Bleeding is
usually occult, but when it is gross, the stools become
melanotic, and the patient may not suspect bleeding.
Occasionally, patients present with advanced disease
including liver metastasis and ascites.
Carcinoma of the Left Colon
Because the left colon has a smaller diameter, the stools in
it are more solid, and the lesion is more distal, carcinoma
of the left colon causes symptoms earlier than cancer of
the right colon. The clinical presentation may include
the following symptoms:
1. A change in bowel habits develops, usually
constipation.
296 ................................................................................................................ Small and L arge Intestine
A
B
FIGURE 8.44. (A) Adenocarcinoma of the colon with invasion of the muscularis propria. (B) Some
colon cancers are mucin-producing, in which case the prognosis is worse. (Courtesy of Linda D. Ferrell,
MD.)
C linical D isorders and Management .................................................................................................. 297
A
B
FIGURE 8.45. (A) Carcinoid tumor of the small intestine causes a characteristic knuckling, due to
fibrosis. (B) Carcinoid tumors are formed from nests of uniform cells with small round nuclei. (Courtesy
of Linda D. Ferrell, MD.)
298 ................................................................................................................ Small and L arge Intestine
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