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FIGURE 8.25. Pathogenesis of diverticulitis.
significant because they may cause upper GI bleeding
that is difficult to localize. They are far less likely to cause
diverticulitis.
ECKEL’S DIVERTICULUM This is a common true
M
diverticulum that occurs on the antemesenteric aspect of
the ileum, usually within 2 feet of the ileocecal valve. It is
a remnant of the Vitelline duct. The Rule of 2 refers to the
fact that Meckel’s diverticulum occurs in 2% of the population, it is 2 feet proximal to the ileocecal valve, it is 2
inches long, and it is symptomatic in only 2% of adults
(Figure 8.26). It is clinically important because it can cause
three conditions; Meckel’s diverticulitis, gastrointestinal
hemorrhage, and small bowel obstruction.
Meckel’s Diverticulitis Signs and symptoms are similar
to those of acute appendicitis. Meckel’s diverticulitis is thus
an important item in the differential diagnosis.
Gastrointestinal Hemorrhage The mucosa of Meckel’s
diverticulum may contain heterotopic gastric mucosa that
secretes acid. This produces a peptic ulcer in the adjacent
normal ileal mucosa, which may sometimes lead to major
hemorrhage and rarely to perforation. Techniques that
help demonstrate the presence of Meckel’s diverticulum
99m
include enteroclysis and radionucleotide scan with
Tcpertechtinate, which is taken up by heterotopic gastric
mucosa if present.
Small Bowel Obstruction In rare cases, the apex of a
Meckel’s diverticulum may be attached to the underside of
the umbilicus through a persistent cord remnant of the
Vitelline duct. Small bowel volvulus around this cord is a
rare complication.
TABLE 8.8. Complications of Diverticular Disease
Localized pericolic abscess
Free perforation and generalized peritonitis
Sigmoid obstruction
Colovesical or colovaginal fistula and sequelae
Ureteric obstruction or coloureteric fistula
Pylephlebitis and liver abscess
Lower gastrointestinal hemorrhage
P athophysiology ................................................................................................................................. 269
FIGURE 8.26. Meckel’s diverticulum. The diverticulum (arrow)
originates from a collapsed segment of ileum in the right lower
quadrant. This barium small bowel examination was performed
to look for metastatic melanoma, and the Meckel’s diverticulum
was incidentally found. (Courtesy of Henry Goldberg, MD.)
DIVERTICULOSIS OF THE SMALL INTESTINE Diverticulosis of the small intestine is usually seen in conjunction with
other underlying conditions such as abnormalities of
the myenteric plexus and/or smooth muscle, and in the
pseudo-obstruction syndrome. These are most common in
the jejunum. Their clinical significance lies in their association with pseudo-obstruction and potential to cause malabsorption syndrome due to bacterial overgrowth within
their lumen.
PATHOGENESIS AND GENETICS
OF COLON POLYPS AND
COLORECTAL CANCER
Although the exact cause of colorectal cancer is incompletely understood, significant advances in molecular
genetics in the last 5 to 10 years have improved our understanding of the mechanism of carcinogenesis. Colorectal
cancer is the second most common cause of cancer death
in North America and in Western Europe after cancer of
the lung. Approximately 55,000 deaths and 134,000 new
cases of colon cancer are predicted each year.
20
Etiology
It is now generally accepted that colorectal cancer develops
as a multistep process. The epithelial cell receives multiple
hits, first from environmental factors that damage the DNA,
then with sequential genetic alterations within the cell
involving oncogenes and tumor-suppressor genes. Four
factors that have been found to have significance in the etiology of colorectal cancer are diet, genetic predisposition,
premalignant conditions, and molecular genetics.
Dietary Factors
An association has been described between high fat intake
and colorectal cancer. The likelihood is that cancer will
develop more often when more than 5% of the diet is
made up of fat. Not all fats are implicated in this equation,
but the polyunsaturated and saturated fats are the primary
culprits. Monounsaturated fats do not pose the same risk.
Some theories have been advanced regarding the mechanism that makes a high-fat diet carcinogenic, including the
carcinogenic effect of increased bile acids in the colon and
the release of tumor-promoting prostaglandins. The exact
mechanism is as yet unknown.
A second dietary risk factor may be a diet low in fiber.
Countries with a high-fiber diet have a lower incidence of
colon cancer, but how the high-fiber diet protects against
cancer is unknown. One plausible theory is that a highfiber diet increases transit time through the colon. As a
corollary, a low-fiber diet prolongs transit time, increasing
mucosal exposure to luminal carcinogens.
A number of substances are said to be protective.These
include vitamins A, C, and E; b-carotenes; calcium; sele-
nium; dithiothiones; thioethers; and terpenes. These substances are believed to act by reducing the generation of
free-oxygen radicals at the mucosal surface.
Genetic Predisposition
About 15% of colorectal cancer is familial. The transmission is most obvious in familial adenomatous polyposis
(see below). But other nonpolyposis hereditary conditions
are also known. These include the cancer family syndrome
(CFS), or Lynch syndrome II, and hereditary site-specific
colon cancer (HSSCC), or Lynch syndrome I. In Lynch
syndrome II, the cancers tend to be located in the proximal colon and are associated with noncolon cancers such
as endometrial cancer. Lynch syndrome I is similar but not
associated with extracolonic cancers. Even in the absence
of these predisposing syndromes, first-degree relatives
carry a risk that is two to three times higher than the
general population.
Premalignant Conditions
Several hereditary and nonhereditary premalignant conditions of the colon are recognized.
A
DENOMATOUS POLYPS Colon cancer often develops
from polyps. The polyp to cancer sequence is depicted in
Figure 8.27.
F
AMILIAL ADENOMATOUS POLYPOSIS Familial adeno-
matous polyposis (FAP) is the best known premalignant condition (Figure 8.28). It is inherited as a
dominant autosomal disorder with a genetic defect on
chromosome 5, close to the q21 locus. The defective gene
has been called the adenomatous polyposis coli or APC
gene.
Colorectal cancer develops in all patients with FAP
before age 40 years if untreated. Infants in affected families have congenital hypertrophy of the retinal pigment
epithelium as early as 3 months of age.
21
This abnormality predicts FAP with an accuracy of 97%. Polyps begin to
appear at puberty, but the average age of diagnosis of a
new patient with FAP is 29 years.
FAP includes two other syndromes characterized by
varying extracolonic manifestations.
Gardner’s Syndrome Gardner’s syndrome is characterized by colonic polyposis, sebaceous cysts,desmoid tumors,
and osteomas of the mandible and skull.
Turcot’s Syndrome Turcot’s syndrome is characterized
by colonic polyposis and brain tumors (medulloblastoma
or glioma).
270 ................................................................................................................ Small and L arge Intestine
A
B
FIGURE 8.27. Polyp to cancer sequence. (A) Diagrammatic representation of the transition from
normal colonic mucosa to adenomatous polyp, carcinoma in situ and invasive carcinoma. These stages
of cancer development are shown in the photomicrographs demonstrating (B) benign adenomatous
polyp, (C) high-grade dysplasia and carcinoma in situ, and (D) early invasive carcinoma. (Courtesy of
Linda D. Ferrell, MD.)
CHRONIC ULCERATIVE COLITIS In CUC involving the
entire colon, the incidence of colon cancer is 1% per year
after 10 years, that is, the cumulative incidence of cancer by
20 years is 10%.
22
The cancers are more advanced at the
time of diagnosis, most being Duke C or D lesions. Dys-
Molecular Genetics
The process of carcinogenesis involves: (1) alteration in
proto-oncogene expression and (2) deletion of tumor suppressor genes.
plasia predates the development of colon cancer. Once dysplasia is diagnosed, colectomy is the best way to prevent the
development of cancer.
Alteration in Proto-Oncogenes
Proto-oncogenes are human genes containing DNA
ROHN’S DISEASE The incidence of cancer in CD is
C
lower than in CUC, estimated at 7% over 20 years of
disease, including cancers in both the small and large intes-
23
The incidence of cancer in the large bowel is much
tine.
lower.
P athophysiology ................................................................................................................................. 271
sequences homologous to those of acute transforming
retroviruses. They normally exist in inactive form. Their
activation, it has been suggested, contributes to malignant
transformation. The oncogenes of greatest interest are the
myc and ras families. In colon cancer, c-myc levels are
C
D
FIGURE 8.27. Continued
272 ................................................................................................................ Small and L arge Intestine
A
B
FIGURE 8.28. Familial multiple polyposis. (A) Discrete polyps occur separated by large surfaces of
normal colonic mucosa. (B) In other cases, the entire surface of the colon may be covered with
grape-like polyps. (Reprinted with permission from Fenoglio–Priese CM, et al., eds. Gastrointestinal
Pathology: An Atlas and Text. Philadelphia: Raven Press, 1989.)
P athophysiology ................................................................................................................................. 273
FIGURE 8.29. Proposed sequence of molecular genetic events in evolution of colon cancer. APC gene
abnormalities lead to disruption of normal cell-to-cell adhesions and hyperproliferative epithelium.
The K-ras gene is associated with adenoma formation, but loss of the p53 gene is required for conversion of an adenoma to adenocarcinoma. Distant metastases are associated with allelic loss of 17p and
18q. Abbreviation: APC, adenomatous polyposis coli.
elevated. In 40% to 50% of primary colon cancer cases, ras
point mutations have been found. Ras gene mutations are
an early event and occur in 58% of adenomas larger than
1 cm. Enhanced expression of ras gene product correlates
with depth of tumor invasion.
Deletion of Tumor Suppressor Genes
Allelic losses occur at chromosome locations 5q, 17p, and
18q. Some 20%–36% of sporadic colon cancers have lost
CLINICAL DISORDERS AND MANAGEMENT
SMALL BOWEL OBSTRUCTION
Clinical Presentation
Simple Obstruction
The approximate site of a simple small bowel obstruction
will be evident from the patient’s presenting signs and
symptoms. Vomiting and abdominal distension are present in all small bowel obstruction but differ considerably
depending on whether the obstruction is in the high or
low bowel (Table 8.9). Evidence from x-rays however, is
apparent only in low small bowel obstruction.
alleles at the 5q location. The familial polyposis gene is
found at locus 5q21. The p53 gene is a major tumor suppressor gene located on chromosome 17p, and point
mutations of p53 are believed to be implicated in the
development of colon cancer. Another gene involved at
locus 18q has been termed the DCC gene, that is, deleted
in colon cancer.
Figure 8.29 illustrates the proposed sequence of
molecular genetic events in the evolution of colon
cancer.
IGH SMALL BOWEL OBSTRUCTION The presenting
H
symptoms of high small bowel obstruction are colicky
upper abdominal pain and profuse, bilious vomiting. The
onset of vomiting is close to the onset of pain, and the
vomitus is nonfeculent. On physical examination, vital
signs are normal except late in the course, when dehydration is present. Distension,if present, is not prominent. The
patient will be dehydrated if protracted vomiting has
occurred. An abdominal scar from previous operation is
usually present. Abdominal tenderness is absent, and bowel
sounds are hyperactive, the crescendos of which coincide
with attacks of colicky pain.
TABLE 8.9. Comparison of High and Low Small Bowel
Obstruction
High Low
Vomiting Early, severe Late, feculent
Rapid dehydration Slow dehydration
Electrolyte imbalance Little electrolyte
imbalance
Distension Absent or minimal Significant,
midabdominal
Abdominal x-ray Little or no finding Distended loops of
bowel
Air fluid levels
Ladder formation
OW SMALL BOWEL OBSTRUCTION Colicky, midab-
L
dominal pain, vomiting, and abdominal distension are the
presenting symptoms of low small bowel obstruction. The
interval between onset of pain and vomiting lengthens as
the site of obstruction is more distal. Vomiting may be feculent. No gas or feces will have been passed through the
rectum for variable periods of time. An abdominal scar
may be present. Potential hernial sites in the abdominal
wall and groin area should be carefully examined, especially
the femoral hernia site beneath the midinguinal point.
Abdominal tenderness is minimal or absent, and rectal
examination is normal.
274 ................................................................................................................ Small and L arge Intestine
A
B
FIGURE 8.30. Simple bowel obstruction. (A) Supine radiographs are provided of a patient with a
simple small bowel obstruction due to a postoperative adhesion. The bowel is identified as small
bowel because of its central location, the presence of plicae circularis, which cross the entire air-filled
lumen, and multiple sharp turns of small bowel segments. Notice that no air is seen in the colon. (B)
Upright x-ray demonstrates multiple air-fluid levels in distended loops of bowel, a classic appearance
of distal small bowel obstruction. (Courtesy of Henry I. Goldman, MD.)
Strangulated Obstruction
The presence of strangulation may be difficult to detect in
complete small bowel obstruction, but historical and physical clues may be present. When recording the medical
history, the most suggestive finding is the progression of
colicky pain to constant and more intense pain. Fever and
tachycardia may develop but are relatively late signs. The
most significant physical finding is the presence of abdominal tenderness, which may or may not be associated with
early rebound tenderness. Despite these distinctions, it
should be noted that some 35% of strangulated obstructions are unsuspected before operation, underscoring the
importance of early operation in all patients with complete small bowel obstruction. The old adage still holds
true: “Never let the sun rise or set on complete bowel
obstruction.”
Investigations
Laboratory Studies
Laboratory findings are normal in the early stages. Later,
hemoconcentration and some leukocytosis may develop.
Electrolytes are usually normal in distal small bowel
obstruction, but hypokalemia and hypochloremia may
occur in high obstruction. Serum amylase levels are infre-
quently elevated and usually in the presence of strangulation. When strangulation is present, marked leukocytosis
with a shift to the left occurs. Blood gases may show metabolic acidosis.
Abdominal X-Ray
Abdominal x-rays should include supine and upright
views. The findings in simple obstruction (Figure 8.30) are:
1. Dilated loops of small intestine with air–fluid levels, a
finding that may be absent when the level of obstruction is high in the small intestine.
2. No air in the colon if complete obstruction is present,
although gas may be present in the rectum and
sigmoid, especially if sigmoidoscopy was performed
before x-rays.
The findings suggesting that strangulation has occurred
are:
1. Thumbprinting and loss of mucosal pattern.
2. Air in the bowel wall or in the portal vein and its
branches.
3. Free air in the peritoneum if perforation has occurred.
C linical D isorders and Management .................................................................................................. 275
Management
All patients with complete mechanical small bowel
obstruction need an emergent operation. Patients with
incomplete obstruction can be treated expectantly with
nasogastric suction and hydration. Long intestinal tubes
(e.g., Miller–Abbot) are sometimes successful, but they are
cumbersome and may not be well tolerated by the patient.
Serial plain films of the abdomen should be obtained daily
or more often and, if the obstruction becomes complete,
an emergency operation is necessary.
In complete small bowel obstruction, rapid fluid and
electrolyte resuscitation and early surgery are required.
The management steps are described below.
Preoperative
A nasogastric tube is inserted and placed to suction early
to prevent aspiration and reduce distension. Fluid and
electrolyte resuscitation is commenced, as patients with
small bowel obstruction have significant contraction of
the extracellular volume. The fluid deficit should be corrected with either normal saline or lactated Ringer solution. A Foley catheter is inserted into the bladder to
monitor urine output, which should be maintained at
50 cc/h or more, as an index of adequacy of hydration.
When dehydration is severe or when the patient has
serious cardiopulmonary disease, central venous or pulmonary artery pressure may need to be monitored. Most
patients with low small bowel obstruction have normal
electrolyte measurements. Despite this, potassium chloride should be administered as soon as adequate urine
output is established, because hypokalemia develops with
hydration. Patients with high small bowel obstruction may
have severe hypokalemia, hypochloremia, and even metabolic alkalosis. Correction of these abnormalities is best
accomplished with saline solution and potassium chloride.
Analgesia should be provided with either morphine
or pethidine once a decision is made to operate. Broadspectrum perioperative antibiotics should be administered.
Operation
The optimal time to operate is as soon as fluid and electrolyte resuscitation is complete. The type of incision
depends on the cause of obstruction and on any preexisting abdominal scars. Wide exposure is necessary. A useful
way to identify the site of obstruction is to locate the
collapsed bowel and follow it proximally to the site of
obstruction and proximal distension. Adhesion bands
should be lysed, and if the obstruction is due to tumor or
foreign body, these should be dealt with appropriately. If
frank gangrene is present, the gangrenous bowel must be
resected.
If there is any question about the viability of the
obstructed bowel, it should be wrapped in warm towels
after obstruction is relieved for 2 to 3 minutes and reinspected for color, peristaltic activity, and pulsation of
vessels at the mesentery. Other helpful techniques are
Doppler ultrasound to detect blood flow in the intestinal
wall and the fluorescein test. Fluorescein (1000 mg) is
injected intravenously over a period of 1 minute, and the
bowel is then examined under ultraviolet light using
Wood’s lamp. Gangrenous parts of the intestine have no
fluorescence. If the bowel is nonviable, or if there is serious
doubt of its viability, it should be resected and end-to-end
anastamosis performed.
If the cause of obstruction is a groin hernia, a standard
groin incision is used. It is critical that the incarcerated
bowel in a femoral or inguinal hernia be inspected for
viability. This means that, if the hernia reduces spontaneously under anesthesia, laparotomy will be necessary
through a midline incision. Otherwise, the entire procedure, including bowel resection if necessary, can be
done through the groin incision. At times, it may be
difficult to reduce a femoral hernia at operation. In such
a case, incision of the lacunar ligament (the medial boundary of the femoral ring) or division of the inguinal ligament (the anterior boundary of the femoral ring) will be
necessary.
Obstruction due to radiation enteritis presents a
special problem. Dissection may be difficult, and the possibility of unintended enterotomy could be significant.
The adhesions may be an important conduit of blood
supply to the bowel. These and other considerations
may indicate that the best course of action is to bypass
the obstruction either by entero-enterostomy or
enterocolostomy.
Some patients who have uncontrolled formation of
adhesions may have several recurrences of bowel obstruction. In these special patients, the surgeon may wish to fix
the bowel in a ladder fashion in the hope of preventing
future obstruction. Fixing is best done by threading a long
tube with an inflatable cuff at its end (e.g., the Baker tube)
into the cecum through a gastrostomy or jejunostomy. The
tube is left in place 14 to 21 days. The old technique of
Nobel plication, in which antemesenteric portions of
bowel were sutured in a ladder formation, is dangerous
because of the associated high incidence of abdominal
abscess and fistulas.
ACUTE MESENTERIC ISCHEMIA
Clinical Picture
Sudden mesenteric occlusion causes acute, severe and
diffuse noncolicky abdominal pain. The patient may have
a history of intestinal angina; recent abdominal angiography, cardiac catheterization, or cardiopulmonary bypass;
or congestive heart failure and digoxin therapy. A history
of atrial fibrillation may be an important clue. Nausea,
vomiting, and diarrhea may or may not be present.
Abdominal examination shows diffuse tenderness, but
frequently, the abdominal pain is out of proportion to the
severity of abdominal finding. The abdomen is usually not
rigid and rebound tenderness not very pronounced. Bowel
276 ................................................................................................................ Small and L arge Intestine
sounds may be hypoactive or absent, but early in the
course of the disease, they may be hyperactive.Often blood
may be seen on the physician’s finger after rectal examination. In later stages of the disease, generalized peritonitis and septic shock may develop, portending poor
outcome.
Investigation
Laboratory Findings
Severe leukocytosis, with a white blood cell count of
20,000 to 30,000/cm
3
, is a common finding. Metabolic acidosis and hemoconcentration are late findings. Other findings may include elevated serum amylase, serum inorganic
phosphate levels, and coagulation abnormalities.
Radiological Studies
Plain abdominal film details the ileus, with diffuse distension of the small intestine and colon. Specific signs of
intestinal necrosis (air in bowel wall or in portal vein
radicals) are a late sign. CT scan helps to exclude acute
pancreatitis as the cause. Specific diagnostic features of
intestinal ischemia may be shown in 25% of patients. A CT
scan is essential if the plain film does not provide definitive information for diagnosis.
The most specific diagnostic investigation is abdominal angiogram, which should include the celiac artery, the
SMA, and the IMA. A lateral aortogram is useful and may
show obstruction at the origin of the SMA if present
(Figure 8.31). Angiography should be done early and is
sometimes performed on the operating table. If angiography shows no vascular occlusion, nonocclusive mesenteric
ischemia may be present, requiring continuous infusion of
vasodilators (i.e., papaverin, nitroglycerin) directly into
the SMA.
Operative Management
An algorithm for the management of acute visceral
ischemia is given in Figure 8.32. The key is not to delay
laparotomy unnecessarily. When abdominal findings
suggest generalized peritonitis, immediate exploration
should be performed, and if necessary, an on-table
angiogram obtained. The entire bowel is examined and
the area of ischemia noted (Figure 8.33). The relevant
vessel, usually the SMA or its major branches, should be
directly examined by reflecting the mesentery of the transverse colon superiorly and taking down the ligament of
Treitz.
If an embolus or thrombus is encountered, catheter
embolectomy should be performed through a transverse
arteriotomy in the SMA, after anticoagulation and after
obtaining proximal and distal control. The arteriotomy is
closed when adequate back-bleeding is present. Once circulation is re-established, the bowel should be wrapped in
warm saline sponges for several minutes and re-examined.
All infarcted bowel or bowel of questionable viability
should be resected if this will not result in short bowel syndrome (i.e., resection of more than 50% of small intestine). Otherwise, bowel of questionable viability is not
resected, primary anastomosis is completed, and a decision is made to re-explore within 24h no matter how well
the patient may look immediately postoperatively.
The most difficult decision is faced when all or most
of the small intestine is infarcted. Patients can be kept alive
with permanent total parenteral nutrition, but the most
humane course of action in the elderly may be not to resect
but close the abdomen and keep the patient comfortable
until death.
Selected patients may benefit from revascularization
procedures of the SMA, the celiac axis, or both. The best
approach is medial visceral rotation, reflecting the spleen
and pancreas medially. The procedure of choice is antegrade bypass from the supraceliac aorta using either
saphenous vein or a prosthetic graft.
In contrast to the small intestine, acute vascular
ischemia of the colon is treated with resection without
significant attempt to restore circulation. It is usually
not prudent to perform primary colo-colic anastomosis,
whereas ileo-colic anastomoses seem to pose less risk of
dehiscence.
Outcome
The mortality rate following acute mesenteric occlusion is
very high, due primarily to delay in diagnosis and treatment. The mortality rate for mesenteric thrombosis and
nonocclusive ischemia is over 50%, and that for mesenteric embolism 40%–50%.
24
LARGE BOWEL OBSTRUCTION
As mentioned earlier, carcinoma and diverticulitis account
for nearly 90% of all large bowel obstruction. Volvulus and
inflammatory bowel disease are other important causes.
Clinical Presentation
Symptoms and signs include those of mechanical obstruction as well as those of underlying disease. The pain is
crampy and suprapubic. Vomiting is a late symptom, and
the vomitus is typically feculent. Constipation and obstipation are constant features. Abdominal distension can be
prominent, especially in sigmoid volvulus. Bowel sounds
are hyperactive and high pitched.
Superimposed on these symptoms and signs are those
of the underlying disease producing the obstruction.
Patients with colon cancer may complain of a change in
bowel habits and rectal bleeding. Patients with diverticulitis may have a history of alternating diarrhea and constipation and usually have signs of the inflammatory process:
fever, tachycardia, and tenderness or mass in the left lower
quadrant. Patients with sigmoid volvulus are generally
elderly and may reside in nursing homes.
C linical D isorders and Management .................................................................................................. 277
A
FIGURE 8.31. Acute mesenteric ischemia. (A) A CT scan of the
midabdomen demonstrates thickened segments of small bowel
containing air bubbles within the wall (arrow). In this patient
with severe abdominal pain and distention, these findings, as
well as metabolic acidosis, are diagnostic of acute mesenteric
ischemia. (B) The aortogram of the same patient shows an
occluded superior mesenteric artery (arrow), the cause of the
ischemic small bowel. Compression of the celiac artery by an
B
arcuate ligament (arrowhead) is also present. (Courtesy of Henry
I. Goldman, MD.)
278 ................................................................................................................ Small and L arge Intestine
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