1280 SECTION X Abdomen

TABLE 49-11 Small Intestinal Gastrointestinal Tumor Classification

GROUP PRIMARY TUMOR SIZE* REGIONAL LYMPH NODE METASTASIS† DISTANT METASTASIS‡ MITOTIC RATE
Stage I T1 or T2 N0 M0 Low
Stage II T3 N0 M0 Low
Stage IIIA T1 N0 M0 High
T4 N0 M0 Low
Stage IIIB T2 N0 M0 High
T3 N0 M0 High
T4 N0 M0 High
Stage IV Any T N1 M0 Any rate
Any T Any N M1 Any rate

*T1 Tumor ≤2 cm
T2 Tumor >2 cm but not >5 cm
T3 Tumor >5 cm but not >10 cm
T4 Tumor >10 cm in greatest dimension
†
N0 No regional lymph node metastasis
N1 Regional lymph node metastasis
‡
M0 No distant metastasis
M1 Distant metastasis
Adapted from Edge SB, Byrd DR, Compton CC, et al, editors: AJCC cancer staging manual, ed 7, New York, 2010, Springer, pp 181–189.

Imatinib is also a first-line treatment for unresectable and Metastatic Neoplasms

metastatic GISTs with characteristic tumor biology (Fig. 49-38).
Genotyping is standard of care for patients with advanced or
metastatic GIST. Standard-dose therapy (400 mg daily) is recom-
mended as no survival advantage is offered by increasing the dose
unless the patient has an exon 9 mutation. A European trial
determined that patients with exon 9 mutations exhibited a
dose-dependent decrease in risk of progression. Therefore, in this
select group of patients, imatinib 400 mg twice per day should
be given.
New molecular targeted therapies may provide better treat-
ments for patients with genetic mutations and GISTs. In phase 3
clinical trials evaluating imatinib dosing in patients with meta-
static GIST, there was no objective response in patients who carry
the D842V PDGFRα mutation. A recent phase 2 trial evaluated
dasatinib, an oral tyrosine kinase inhibitor of c-kit, PDGFR, ABL
(Abelson murine leukemia viral oncogene homologue), and the
proto-oncogene Src with a distinct binding affinity for c-kit and
PDGFR, and showed that it has significant activity (as judged by
CT response rates) in imatinib- and sunitinib-refractory GISTs;
however, dasatinib did not meet the predefined 6-month
progression-free survival rate of 30% in the population of patients.
In vitro studies suggest that dasatinib may provide the best
response in patients with a D842V PDGFRα mutation and could
prove to be useful in this particular subset of patients.
Regorafenib is a second-generation tyrosine kinase inhibitor
that targets c-kit, RET, BRAF, VEGFR, PDGFR, and fibroblast
growth factor receptor. It is currently Food and Drug Administra-
tion approved and may be an effective treatment for advanced
GISTs after failure of either imatinib or sunitinib. Nilotinib is a
second-generation tyrosine kinase inhibitor active in chronic
myeloid leukemia and has an inhibitory effect on c-kit and PDGF.
Phase 3 trials have shown minimal differences between this drug
and imatinib and sunitinib. Sorafenib is a VEGF, c-kit, PDGFR,
and BRAF inhibitor and has been effective in imatinib- and
sunitinib-resistant tumors. The combination of imatinib and
doxorubicin has shown some benefit in patients with wild-type
GISTs.
Metastatic tumors involving the small bowel are much more
common than primary neoplasms. The most common metastases
to the small intestine are those arising from other intra-abdominal
organs, including the uterine cervix, ovaries, kidneys, stomach,
colon, and pancreas. Small intestinal involvement is by direct
extension or implantation of tumor cells. Metastases from extra-
abdominal tumors are rare but may be found in patients with
adenocarcinoma of the breast and carcinoma of the lung. Cuta-
neous melanoma is the most common extra-abdominal source to
involve the small intestine, with involvement of the small intes-
tine noted in more than 50% of patients dying of malignant
melanoma (Fig. 49-39). Common symptoms include anorexia,
weight loss, anemia, bleeding, and partial bowel obstruction.
Treatment is palliative resection to relieve symptoms or, occa-
sionally, bypass if the metastatic tumor is extensive and not ame-
nable to resection. Interventional, nonoperative strategies for
palliation of malignant bowel obstruction include endoscopic
and radiologic placement of self-expandable metal stents, which
are potential options to improve quality of life in patients with
very poor performance status who may not tolerate a surgical
procedure. Gastrostomy and jejunostomy tubes also may be
placed to provide palliative decompression when other palliative
methods are not possible.
DIVERTICULAR DISEASE
Diverticular disease of the small intestine is relatively common. It
may be manifested as true or false diverticula. A true diverticulum
contains all layers of the intestinal wall and is usually congenital.
False diverticula consist of mucosa and submucosa protruding
through a defect in the muscle coat and are usually acquired
defects. Small bowel diverticula may occur in any portion of the
small intestine. Duodenal diverticula are the most common
acquired diverticula of the small bowel, and Meckel’s diverticulum
is the most common true congenital diverticulum of the small
bowel.

A
B that may contribute to cholangitis and pancreatitis, respectively,
FIGURE 49-39 A, Barium radiograph shows target lesions consistent
with metastatic melanoma of small bowel (arrow). B, Gross specimen
demonstrating metastatic melanoma to the small bowel. (A, Courtesy
Dr. Melvyn H. Schreiber, The University of Texas Medical Branch,
Galveston, TX. B, Courtesy Dr. Mary R. Schwartz, Baylor College of
Medicine, Houston, TX.)
Duodenal Diverticula
Incidence and Cause
First described by Chomel, a French pathologist, in 1710, diver-
ticula of the duodenum are relatively common, representing the
second most common site for diverticulum formation after the
CHAPTER 49 Small Intestine 1281
colon. The incidence of duodenal diverticula varies, depending on
the age of the patient and method of diagnosis. Upper gastroin-
testinal radiographic studies identify duodenal diverticula in 1%
to 5% of all studies, whereas endoscopic retrograde cholangiopan-
creatography identifies 9% to 23% of cases. Previous autopsy
series report the incidence as being approximately 15% to 20%.
Duodenal diverticula occur twice as often in women as in men
and are rare in patients younger than 40 years. They have been
classified as congenital or acquired, true or false, and intraluminal
or extraluminal. Extraluminal duodenal diverticula are consider-
ably more common than intraluminal diverticula, are acquired,
and consist of mucosal or submucosal outpouchings herniated
through a muscle defect in the bowel wall. Intraluminal duodenal
diverticula (also known as windsock diverticula) are congenital
and occur as a single saccular structure that is connected to the
entire circumference or part of the wall of the duodenum to create
a duodenal web. Incomplete recanalization of the duodenum
during fetal development leads to intraluminal diverticula, which
are exceedingly rare. In general, extraluminal diverticula usually
occur within the second portion of the duodenum (62%) and less
commonly in the third (30%) and fourth (8%) portions. They
rarely occur in the first part of the duodenum (<1%). When they
occur in the second portion, most (88%) are noted on the medial
wall around the ampulla (i.e., periampullary), 8% are seen poste-
riorly, and 4% occur on the lateral wall.
Clinical Manifestations
The important thing to remember is that the overwhelming
majority of duodenal diverticula are asymptomatic and are usually
noted incidentally by an upper gastrointestinal series for an unre-
lated problem (Fig. 49-40). Upper gastrointestinal endoscopy
identifies approximately 75% of duodenal diverticula, and the use
of a side-viewing scope further increases the success rate. The
diagnosis may be suggested by plain abdominal films showing an
atypical gas bubble; CT can identify large diverticula by the pres-
ence of a mass-like structure interposed between the duodenum
and pancreatic head containing air, air-fluid levels, fluid contrast
material, or debris. Magnetic resonance cholangiopancreatogra-
phy is particularly helpful to demonstrate the relationship of the
diverticulum to the biliary and pancreatic ducts and associated
pathologic changes in the biliary system and pancreas. Hemor-
rhage in diverticula is best diagnosed by a combination of angi-
ography and scanning with 99mTc-labeled red blood cells; however,
surgery should not be delayed to obtain imaging in the event of
hemorrhage in a hemodynamically unstable patient. Less than 5%
of duodenal diverticula will require surgery because of a complica-
tion of the diverticulum itself. Major complications of duodenal
diverticula include obstruction of the biliary or pancreatic ducts
and hemorrhage, perforation, and, rarely, blind loop syndrome.
Iatrogenic injuries, most commonly acquired during endoscopic
instrumentation of an asymptomatic diverticulum, can lead to
perforation or hemorrhage.
Only those diverticula associated with the ampulla of Vater are
significantly related to complications of cholangitis and pancre-
atitis. In these patients, the ampulla usually enters the duodenum
at the superior margin of the diverticulum rather than through
the diverticulum itself. The mechanism proposed for the increased
incidence of complications of the biliary tract is the location of
the perivaterian diverticulum, which may produce mechanical
distortion of the common bile duct as it enters the duodenum,
resulting in partial obstruction and stasis. Hemorrhage can be
1282 SECTION X Abdomen
FIGURE 49-40 Large diverticulum arises from the second portion of
the duodenum. (Courtesy Dr. Melvyn H. Schreiber, The University of
Texas Medical Branch, Galveston, TX.)
caused by inflammation, leading to erosion of a branch of the
superior mesenteric artery. Perforation of duodenal diverticula has
been described but is rare. Finally, stasis of intestinal contents
within a distended diverticulum can result in bacterial overgrowth,
malabsorption, steatorrhea, and megaloblastic anemia (i.e., blind
loop syndrome). Symptoms related to duodenal diverticula in the
absence of any other demonstrable disease usually are nonspecific
epigastric complaints that can be treated conservatively and may
actually prove to be the result of another problem not related to
the diverticulum itself.
Treatment
Most duodenal diverticula are asymptomatic and benign; when
they are found incidentally, they should be left alone. For symp-
tomatic duodenal diverticula, treatment consists of removal of the
diverticulum, which can be accomplished endoscopically or surgi-
cally. Appropriate classification of these diverticula guides man-
agement. All intraluminal duodenal diverticula require treatment
as recurrence of symptoms is certain. Curative treatment consists
of removal of the intraluminal diverticulum by laparotomy and
duodenotomy or by endoscopic resection. Large (>3 cm) or
obstructing intraluminal duodenal diverticulum does not pre-
clude endoscopic resection, but an endoscopic approach in the
setting of massive hemorrhage or perforation with intra-abdominal
contamination secondary to intestinal contents is discouraged.
These entities are relatively rare and often require a multidisci-
plinary approach to determine the best treatment strategy.
Extraluminal duodenal diverticula should be resected in the
setting of symptomatic disease or need for urgent surgery, such as
free perforation or hemorrhage. Several operative procedures have
been described for the treatment of the symptomatic extraluminal
duodenal diverticula. The most common and effective treatment
is diverticulectomy, which is most easily accomplished by per-
forming a wide Kocher maneuver that exposes the duodenum.
The diverticulum is then excised, and the duodenum is closed in
a transverse or longitudinal fashion, whichever produces the least
amount of luminal obstruction. Because of the proximity of the
ampulla, careful identification of the ampulla is essential to
prevent injury to the common bile duct and pancreatic duct. For
diverticula embedded deep within the head of the pancreas, a
duodenotomy is performed, with invagination of the diverticu-
lum into the lumen, which is then excised, and the wall is closed
(Fig. 49-41A-C). Alternative methods that have been described
for duodenal diverticula associated with the ampulla of Vater
include an extended sphincteroplasty through the common wall
of the ampulla in the diverticulum (Fig. 49-41D-F). Laparoscopic
duodenal diverticulectomy has been determined to be safe and
effective in patients with symptomatic and noncomplicated (i.e.,
not perforated or bleeding) diverticula. An endoscopic stapler is
most commonly used to traverse and to resect the diverticulum
at its base, and an omental patch reinforcement can be placed over
the staple line.
The treatment of a perforated diverticulum may require pro-
cedures similar to those described for patients with massive
trauma-related defects of the duodenal wall. The perforated diver-
ticulum should be excised and the duodenum closed with a serosal
patch from a jejunal loop. If the surrounding inflammation is
severe, it may be necessary to divert the enteric flow away from
the site of the perforation with a gastrojejunostomy or duodeno-
jejunostomy. Interruption of duodenal continuity proximal to the
perforated diverticulum may be accomplished by pyloric closure
with suture or a row of staples. If the diverticulum is posterior
and perforates into the substance of the pancreas, operative repair
may be difficult and dangerous. Wide drainage with duodenal
diversion may be all that is feasible in such cases. Great care should
be taken if the perforation is adjacent to the papilla of Vater.
Jejunal and Ileal Diverticula
Incidence and Cause
Diverticula of the small bowel are much less common than duo-
denal diverticula, with an incidence ranging from 0.1% to 1.4%
in autopsy series and 0.1% to 1.5% in upper gastrointestinal
studies. Jejunal diverticula are more common and are larger than
those in the ileum. These are false diverticula, occurring mainly
in an older age group (after the sixth decade of life). These diver-
ticula are multiple, usually protrude from the mesenteric border
of the bowel, and may be overlooked at surgery because they are
embedded within the small bowel mesentery (Fig. 49-42). The
cause of jejunoileal diverticulosis is thought to be a motor dys-
function of the smooth muscle or the myenteric plexus, resulting
in disordered contractions of the small bowel, generating increased
intraluminal pressure and herniation of the mucosa and submu-
cosa through the weakest portion of the bowel (i.e., the mesenteric
side).
Clinical Manifestations
Jejunoileal diverticula are usually found incidentally at laparot-
omy or during an upper gastrointestinal study (Fig. 49-43); the
great majority remain asymptomatic. Acute complications, such
as intestinal obstruction, hemorrhage, and perforation, can occur
but are rare. Chronic symptoms include vague chronic abdominal
pain, malabsorption, functional pseudo-obstruction, and chronic
low-grade gastrointestinal hemorrhage. Acute complications are
diverticulitis with or without abscess or perforation, gastrointes-
tinal hemorrhage, and intestinal obstruction. Stasis of intestinal
flow with bacterial overgrowth (blind loop syndrome), caused by
the jejunal dyskinesia, may lead to deconjugation of bile salts and
 CHAPTER 49 Small Intestine 1283

A B C

Retroduodenal
diverticulum

Papilla in orifice
D of diverticulum E F
FIGURE 49-41 A-C, Treatment of a diverticulum protruding into the head of the pancreas. The duodenum
is opened vertically. A clamp is used to invert the diverticulum into the lumen, where it is excised, and the
posterior wall defect is closed. D-F, Management of the unusual duodenal diverticula that arise in the peri-
ampullary location. A tube stent should be placed into the common bile duct and passed distally into the
duodenum to facilitate identification and later dissection of the sphincter of Oddi. The diverticulum is inverted
into the lumen of the duodenum. The round opening in the wall of the base of the diverticulum is the site
at which the ampullary structures were freed by a circumferential incision. E, Line of division of the base of
the diverticulum (heavy broken line), which is accomplished by free-hand dissection. After the diverticulum
has been removed, the stent and enveloping papilla are protruded into the defect left by the division of the
base of the diverticulum. The mucosa and muscle wall of the papilla are then sewn circumferentially to the
wall of the duodenum. (Adapted from Thompson JC: Atlas of surgery of the stomach, duodenum, and small
bowel, St. Louis, 1992, Mosby–Year Book, pp 209–213.)

uptake of vitamin B12 by the bacterial flora, resulting in steator-

rhea and megaloblastic anemia, with or without neuropathy.

FIGURE 49-42 Multiple large jejunal diverticula located in the mesen-
tery in an older patient presenting with obstruction secondary to an
enterolith. (Adapted from Evers BM, Townsend CM Jr, Thompson JC:
Small intestine. In Schwartz SI, editor: Principles of surgery, ed 7, New
York, 1999, McGraw-Hill, p 1248.)
Treatment
For incidentally noted, asymptomatic jejunoileal diverticula, no
treatment is required. Treatment of complications of obstruction,
bleeding, and perforation is usually by intestinal resection and
end-to-end anastomosis. Patients presenting with malabsorption
secondary to the blind loop syndrome and bacterial overgrowth
in the diverticulum can usually be given antibiotics. Obstruction
may be caused by enteroliths that form in a jejunal diverticulum
and are subsequently dislodged and obstruct the distal intestine.
This condition may be treated by enterotomy and removal of the
enterolith, or sometimes the enterolith can be milked distally into
the cecum. When the enterolith causes obstruction at the level of
the diverticulum, bowel resection is necessary. When a perforation
of a jejunoileal diverticulum is encountered, resection with reanas-
tomosis is required because lesser procedures, such as simple
closure, excision, and invagination, are associated with greater
1284 SECTION X Abdomen

FIGURE 49-44 Omphalomesenteric remnant persisting as a fibrous

cord from the ileum to the umbilicus.

FIGURE 49-43 Multiple jejunal diverticula demonstrated by a barium

contrast upper gastrointestinal study. (Courtesy Dr. Melvyn H. Sch-
reiber, The University of Texas Medical Branch, Galveston, TX.)

mortality and morbidity rates. Laparoscopic bowel resection with

reanastomosis is a safe option in minimally contaminated surgical
fields. In extreme cases, such as diffuse peritonitis, enterostomies
may be required if judgment dictates that reanastomosis may be
risky.

Meckel’s Diverticulum
Incidence and Cause
Meckel’s diverticulum is the most commonly encountered con-
genital anomaly of the small intestine, occurring in about 2% of
the population. It was reported initially in 1598 by Hildanus and
then described in detail by Johann Meckel in 1809. Meckel’s
diverticulum is located on the antimesenteric border of the ileum
45 to 60 cm proximal to the ileocecal valve and results from
incomplete closure of the omphalomesenteric, or vitelline, duct.
An equal incidence is found in men and women. Meckel’s diver-
ticulum may exist in different forms, ranging from a small bump
that may be easily missed to a long projection that communicates FIGURE 49-45 Common presentation of a Meckel’s diverticulum pro-
with the umbilicus by a persistent fibrous cord (Fig. 49-44) or, jecting from the antimesenteric border of the ileum.
much less commonly, a patent fistula. The usual manifestation is
a relatively wide-mouthed diverticulum measuring about 5 cm in common symptomatic presentation in children 2 years of age or
length, with a diameter of up to 2 cm (Fig. 49-45). Cells lining younger. This complication may be manifested as acute massive
the vitelline duct are pluripotent; therefore, it is not uncommon hemorrhage, anemia secondary to chronic bleeding, or a self-
to find heterotopic tissue within the Meckel’s diverticulum, the limited recurrent episodic event. The usual source of the bleeding
most common of which is gastric mucosa (present in 50% of all is a chronic acid-induced ulcer in the ileum adjacent to a Meckel’s
Meckel’s diverticula). Pancreatic mucosa is encountered in about diverticulum that contains gastric mucosa.
5% of diverticula; less commonly, these diverticula may harbor Another common presenting symptom of Meckel’s diverticu-
colonic mucosa. lum is intestinal obstruction, which may occur as a result of a
volvulus of the small bowel around a diverticulum associated with
Clinical Manifestations a fibrotic band attached to the abdominal wall, intussusception,
Most Meckel’s diverticula are benign and are incidentally discov- or, rarely, incarceration of the diverticulum in an inguinal hernia
ered during autopsy, laparotomy, or barium studies (Fig. 49-46). (Littre hernia). Volvulus is usually an acute event and, if allowed
The most common clinical presentation of Meckel’s diverticulum to progress, may result in strangulation of the involved bowel. In
is gastrointestinal bleeding, which occurs in 25% to 50% of intussusception, a broad-based diverticulum invaginates and then
patients who present with complications; hemorrhage is the most is carried forward by peristalsis. This may be ileoileal or ileocolic

FIGURE 49-46 Barium radiograph demonstrates an asymptomatic
Meckel’s diverticulum (arrow). (Courtesy Dr. Melvyn H. Schreiber, The
University of Texas Medical Branch, Galveston, TX.)
and be manifested as acute obstruction associated with an urge to
defecate, early vomiting, and occasionally the passage of the classic
currant jelly stool. A palpable mass may be present. Although
reduction of an intussusception secondary to Meckel’s diverticu-
lum can sometimes be performed by barium enema, the patient
should still undergo resection of the diverticulum to negate sub-
sequent recurrence of the condition.
Diverticulitis accounts for 10% to 20% of symptomatic pre-
sentations. This complication is more common in adult patients.
Meckel’s diverticulitis, which is clinically indistinguishable from
appendicitis, should be considered in the differential diagnosis of
a patient with right lower quadrant pain. Progression of the diver-
ticulitis may lead to perforation and peritonitis. When the appen-
dix is found to be normal during exploration for suspected
appendicitis, the distal ileum should be inspected for the presence
of an inflamed Meckel’s diverticulum.
Neoplasms can also occur in a Meckel’s diverticulum, with
NET as the most common malignant neoplasm (77%). Other
histologic types include adenocarcinoma (11%), which generally
originates from the gastric mucosa, and GIST (10%) and lym-
phoma (1%).43
Diagnostic Studies
The diagnosis of Meckel’s diverticulum may be difficult. Plain
abdominal radiography, CT, and ultrasonography are rarely helpful.
In children, the single most accurate diagnostic test for Meckel’s
diverticula is scintigraphy with sodium 99mTc-pertechnetate. The
99m
Tc-pertechnetate is preferentially taken up by the mucus-
secreting cells of gastric mucosa and ectopic gastric tissue in the
diverticulum (Fig. 49-47). The diagnostic sensitivity of this scan
has been reported as high as 85%, with a specificity of 95% and
an accuracy of 90% in the pediatric age group.
CHAPTER 49 Small Intestine 1285
Stomach
Meckel's
diverticulum
Bladder
FIGURE 49-47 A 99mTc-pertechnetate scintigram from a child demon-
strates a Meckel’s diverticulum clearly differentiated from the stomach
and bladder. (Courtesy Dr. Melvyn H. Schreiber, The University of Texas
Medical Branch, Galveston, TX.)
In adults, however, the sensitivity of 99mTc-pertechnetate scan
falls to 63% because of the presence of less gastric mucosa in the
diverticulum compared with that noted in the pediatric age group.
The sensitivity and specificity can be improved by the use of
pharmacologic agents. Cimetidine may be used to increase the
sensitivity of scintigraphy by decreasing the peptic secretion, but
not the radionuclide uptake, and retarding the release of pertech-
netate from the diverticular lumen, thus resulting in higher radio-
nuclide concentrations in the wall of the diverticulum. In adult
patients, when nuclear medicine findings are normal, barium
studies should be performed. False-negative results can occur
because of inadequate gastric mucosal cells, inflammatory changes
causing edema or necrosis, presence of outlet obstruction of the
diverticulum, or low hemoglobin levels. In false-negative cases,
mesenteric arteriography or double-balloon endoscopy can be
helpful. In patients with acute hemorrhage, angiography is some-
times useful. Nevertheless, surgical intervention should not be
delayed to obtain imaging for a patient with signs and symptoms
of hemorrhage and hemodynamic instability.
Treatment
The treatment of a symptomatic Meckel’s diverticulum should be
prompt surgical intervention with resection of the diverticulum
or resection of the segment of ileum bearing the diverticulum.
Segmental intestinal resection is required for treatment of patients
with bleeding because the bleeding site is usually in the ileum
adjacent to the diverticulum. Resection of the diverticulum for
nonbleeding Meckel’s diverticula can be performed with a hand-
sewn technique or stapling across the base of the diverticulum in
a diagonal or transverse line to minimize the risk for subsequent
stenosis. Reports have demonstrated the feasibility, effectiveness,
and safety of laparoscopic diverticulectomy.
Although the treatment of complicated Meckel’s diverticulum
is straightforward, the optimal treatment of Meckel’s diverticulum
noted as an incidental finding is still debated. It is generally rec-
ommended that asymptomatic diverticula found in children
during laparotomy be resected. The treatment of Meckel’s diver-
ticula encountered in the adult patient, however, remains
1286 SECTION X Abdomen
controversial. A landmark paper by Soltero and Bill44 formed the
basis of the surgical management of asymptomatic Meckel’s diver-
ticula in adults for many years. In this study, the likelihood of a
Meckel’s diverticulum becoming symptomatic in the adult patient
was estimated to be 2% or less, and given that the morbidity rates
from incidental removal were 12% at the time, the recommenda-
tion was to not remove the incidental Meckel’s diverticulum. This
study was criticized, however, because it was not a population-
based analysis. Further evidence supporting a conservative
approach to the management of the incidental Meckel’s diverticu-
lum is provided in an analysis of 244 articles by Zani and col-
leagues45 evaluating the incidence and outcomes of Meckel’s
diverticulum. In this study, a clear incidence of increased morbid-
ity associated with incidental resection was noted; in fact, it was
calculated that resection of an incidental Meckel’s diverticulum
would be required in more than 700 patients to avoid one death
related to the diverticulum. However, other studies have chal-
lenged this more conservative approach to the adult patient with
an incidental Meckel’s diverticulum. For example, an epidemio-
logic population-based study by Cullen and associates46 in 1994
initially challenged the practice of ignoring an incidentally found
Meckel’s diverticulum. A 6.4% rate of development of complica-
tions from the Meckel’s diverticulum was calculated to occur over
a lifetime. This incidence of complications did not appear to peak
during childhood, as originally thought. Therefore, the recom-
mendation from this study was that an incidentally found
Meckel’s diverticulum be removed at any age up to 80 years as
long as no additional conditions (e.g., peritonitis) make removal
hazardous. The rates of short- and long-term postoperative com-
plications from prophylactic removal were low (~2%), and death
was related to the primary operation or the general health of the
patient and not to the diverticulectomy. Furthermore, in a recent
population-based study evaluating patients from 1973 to 2006,
the mean annual incidence of malignancy in a Meckel’s diverticu-
lum was noted to be approximately 1.44 per 10 million; therefore,
the adjusted risk of cancer in the Meckel’s diverticulum was at
least 70 times higher than in any other ileal site, thus identifying
a Meckel’s diverticulum as a “hot spot” for malignant disease in
the ileum.43 Given the increased risk of malignant transformation
over a lifetime, the authors advocated for removal of an incidental
Meckel’s diverticulum.
MISCELLANEOUS PROBLEMS
Small Bowel Ulcerations
Ulcerations of the small bowel are relatively uncommon and may
be attributed to Crohn’s disease, typhoid fever, tuberculosis, lym-
phoma, and ulcers associated with gastrinoma (Table 49-12).
Drug-induced ulcerations can occur and were, in the past, attrib-
uted to enteric-coated potassium chloride tablets and corticoste-
roids. In addition, ulcerations of the small intestine in which no
causative agent can be identified have been described. It has been
suggested that small bowel complications from NSAIDs may be
more common than originally considered. NSAID-induced ulcers
occur more commonly in the ileum, with single or multiple
ulcerations noted. Complications necessitating operative inter-
vention include bleeding, perforation, and obstruction. In addi-
tion to ulcerations, NSAIDs are known to induce an enteropathy
characterized by increased intestinal permeability leading to
protein loss and hypoalbuminemia, malabsorption, and anemia.
Treatment of complications from small bowel ulcerations is seg-
mental resection and intestinal reanastomosis.
TABLE 49-12 Causes of Small
Intestine Ulceration
CAUSE EXAMPLES
Infections Tuberculosis, syphilis, cytomegalovirus, typhoid,
parasites, Strongyloides hyperinfection,
Campylobacter, Yersinia
Inflammatory Crohn’s disease, systemic lupus erythematosus,
celiac disease, ulcerative enteritis
Ischemia Mesenteric insufficiency
Idiopathic Primary ulcer, Behçet syndrome
Drug induced Potassium, indomethacin, phenylbutazone, salicylates,
antimetabolites
Radiation Therapeutic, accidental
Vascular Vasculitis, giant cell arteritis, amyloidosis (ischemic
lesion), angiocentric lymphoma
Metabolic Uremia
Hyperacidity Zollinger-Ellison syndrome, Meckel’s diverticulum,
stomal ulceration
Neoplastic Lymphoma, adenocarcinoma, melanoma
Toxic Acute jejunitis (β-toxin–producing Clostridium
perfringens), arsenic
Mucosal lesions Lymphocytic enterocolitis
Adapted from Rai R, Bayless TM: Isolated and diffuse ulcers of the
small intestine. In Feldman M, Scharschmidt BF, Sleisenger MH,
editors: Gastrointestinal and liver disease: Pathophysiology, diagnosis,
management, Philadelphia, 1998, WB Saunders, pp 1771–1778.
Ingested Foreign Bodies
Ingested foreign bodies, which can lead to subsequent perforation
or obstruction of the gastrointestinal tract, are swallowed, usually
accidentally, by children or adults. These include glass and metal
fragments, pins, needles, toothpicks, fish bones, coins, whistles,
toys, and broken razor blades (Fig. 49-48). Intentional ingestion
of foreign bodies is sometimes seen in the prison population and
those who are mentally unstable. For most patients, treatment is
observation, which allows the safe passage of these objects through
the intestinal tract. If the object is radiopaque, progress can be
followed by serial abdominal films. Cathartic agents are contrain-
dicated. Sharp pointed objects such as needles, razor blades, or
fish bones may penetrate the bowel wall. If abdominal pain, ten-
derness, fever, or leukocytosis occurs, immediate laparotomy and
surgical removal of the offending object are indicated. Laparot-
omy is also required for intestinal obstruction.
Small Bowel Fistulas
Despite improvements in surgical nutrition and critical care, mor-
tality from enterocutaneous fistulas remains high, 10% in recent
reports. Improvements in outcome are focused on prevention and,
when fistulas occur, prompt recognition and intervention. Multi-
disciplinary care is critical to improve enterocutaneous fistula
outcomes. Enterocutaneous fistulas are most commonly iatro-
genic, as 75% to 85% occur during surgical intervention (e.g.,
anastomotic leakage, injury of the bowel or blood supply, erosion
by suction catheters, laceration of the bowel by wire mesh or
retention suture). The remaining 15% to 25% of fistula occur-
rences are associated with predisposing conditions such as Crohn’s
disease, malignant disease, radiation enteritis, diverticulitis, intra-
abdominal sepsis, or trauma.