CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE

 
943

142 
INFLAMMATORY AND ANATOMIC
DISEASES OF THE INTESTINE,
PERITONEUM, MESENTERY,
AND OMENTUM
JOHN F. KUEMMERLE

  CONGENITAL STRUCTURAL ABNORMALITIES

Meckel Diverticulum
A Meckel diverticulum, which is the most common congenital anomaly of
the gastrointestinal (GI) tract, is present in 2% to 3% of the population and
is more common in men.1 Meckel diverticulum occurs when the omphalo-
mesenteric or vitelline duct connecting the fetal yolk sac to the primordial
gut fails to close during development. Located on the antimesenteric border,
the Meckel diverticulum is commonly found within about 100 cm of the
ileocecal valve and typically is 1 to 10 cm in size. Heterotopic tissue is found
in about 50% of Meckel diverticula, most commonly gastric or pancreatic
tissue.2 The presence of heterotopic tissue correlates with the development
of symptomatic complications, with a lifetime risk of about 6%.

Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
944 CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE
FIGURE 142-1.  Meckel diverticulum. Nuclear medicine imaging with 99mTn pertechne-
tate scan shows tracer uptake in a Meckel diverticulum (arrow in left panel) and in the
stomach and bladder. Barium radiography in the same patient also shows the Meckel
diverticulum (arrow in right panel).
CLINICAL MANIFESTATIONS
The complications from a Meckel diverticulum include bleeding, obstruc-
tion, diverticulitis, and perforation. Bleeding can occur when the production
of acid from heterotopic gastric mucosa causes ileal ulcerations. Obstruction
can result from volvulus around the diverticulum, intussusception of the
diverticulum into the intestine, or herniation of the diverticulum and adja-
cent intestine. Inguinal, femoral, and umbilical hernias all can occur. Repeated
and chronic inflammation at the neck of the diverticulum and nearby ileum
also can lead to intestinal fibrosis and bowel obstruction. The most common
complications are intestinal bleeding in children and obstruction in adults.
DIAGNOSIS
The diagnosis of a Meckel diverticulum can be challenging. Radionuclide
imaging with sodium pertechnetate (99mTn) can be used in cases of bleeding
because both normal and heterotopic gastric mucosa take up the tracer (Fig.
142-1). This test has high sensitivity and specificity in children but higher
rates of false-positive and false-negative tests in adults. Crohn disease
(Chapter 141) and other ileal inflammatory diseases can yield false-positive
results. Radiographic imaging with a barium small bowel follow-through
typically is not helpful because the diverticulum does not fill with barium
contrast. Angiography can visualize the vestigial vitelline artery that arises
from the superior mesenteric artery or a superior mesenteric artery branch
that directly feeds the diverticulum or adjacent ileum. Both small bowel
capsule endoscopy (Chapter 134) and double-balloon enteroscopy can iden-
tify a Meckel diverticulum during the evaluation of obscure bleeding.
TREATMENT AND PROGNOSIS  CLINICAL MANIFESTATIONS
The management of bleeding, obstruction, or perforation that occurs in
association with a Meckel diverticulum is open or laparoscopic surgical resec-
tion of the diverticulum and possibly of adjacent ulcerated and bleeding
ileum.3 The surgical resection of a Meckel diverticulum incidentally identified
at the time of surgery for another condition is controversial given the low
lifetime risk of complications but can be considered in young men, patients
with large diverticula, or patients with suspected heterotopic tissue. After
identification and treatment, the prognosis is excellent because the Meckel
diverticulum is removed, and the risk of complications is eliminated.
Intestinal Atresia and Stenosis, Malrotation,
Gastroschisis, and Omphalocele
The congenital disorders of intestinal atresia and stenosis, malrotation, gas-
troschisis, and omphalocele disorders usually present early in infancy and
Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
FIGURE 142-2.  Sigmoid volvulus. Plain abdominal radiograph shows the presence of
a sigmoid volvulus (arrow).
childhood, but sometimes the diagnosis of stenosis or malrotation may be
made in adulthood. With the exception of pyloric stenosis, significant long-
term morbidity and mortality are associated with these anomalies even after
surgical correction. Patients with malrotation or gastroschisis typically
present with complications of their surgery, including adhesions, bowel
obstruction, or abdominal wall hernias. Patients with intestinal atresia and
resulting short gut syndrome also have significant morbidity and mortality
related to intestinal failure.
  ACQUIRED STRUCTURAL DISORDERS
Volvulus
Intestinal volvulus, which is pathologic twisting of the intestine around the
mesentery, can result in obstruction of the proximal bowel. Mesenteric
involvement may lead to vascular compromise, bowel necrosis with resulting
perforation, and peritonitis. The most susceptible regions for volvulus are
the sigmoid colon, cecum, and occasionally the transverse colon with
an estimated annual incidence of two to six cases per 100,000.4 Elderly
persons, especially individuals who are institutionalized, are at the highest
risk. Small bowel volvulus is uncommonly observed in U.S. adults but can
result from preexisting anomalies such as malrotation or congenital bands of
Ladd.
Volvulus can present with symptoms and signs of acute bowel obstruction
(Chapter 132), including pain that may be out of proportion to physical find-
ings. Nausea and vomiting are usually present. The presentation can also be
more insidious or intermittent with constipation, laxative use, and a previ-
ously recognized dilated colon. Physical findings include abdominal disten-
tion, tympanic percussion, rebound, guarding, and rigidity. Escalating pain
and tenderness can indicate colonic ischemia and perforation.
DIAGNOSIS
The diagnosis of colonic volvulus can be made using abdominal radiographs,
which demonstrate a distended colon, loss of haustrations, and a typical
“bent inner tube” sign with the apex in the right upper quadrant of the
abdomen (Fig. 142-2). In cases of a cecal volvulus, the dilated cecum is
observed in the epigastrium or in the left upper quadrant. A water-soluble
contrast enhanced radiograph can identify the point of obstruction due to
volvulus.
 CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE
TREATMENT AND PROGNOSIS  CLINICAL MANIFESTATIONS,
Patients with colonic volvulus should have nothing per oral cavity (NPO)
with nasogastric (NG) tube decompression and receive appropriate fluid
volume resuscitation. In the absence of complete obstruction or signs of
ischemia or perforation, patients with a sigmoid volvulus can undergo emer-
gent colonoscopy and attempted reduction, which is successful in up to 75%
of cases.5 Surgical intervention is indicated for volvulus involving the cecum,
transverse colon, or small intestine, as well as after colonoscopic reduction of
a sigmoid volvulus because of the risk of recurrence. The mortality rate is about
9% for sigmoid volvulus, 7% for cecal volvulus, and about 17% for combined
sigmoid and cecal volvulus or transverse colon volvulus.6
Intussusception
Intestinal intussusception occurs when a segment of bowel invaginates into
the adjacent distal intestine and results in bowel obstruction and ischemia.
Intussusception usually involves just the small intestine, but it can also
present as small intestinal intussusception into the colon. Although intus-
susception is a common cause of small bowel obstruction in pediatric
patients, especially after rotavirus vaccination (Chapter 380), it is rare in
adults and accounts for only about 5% of small bowel obstruction. The cause
of intussusception is infrequently identified in children, but a cause can be
identified in about 90% of adult cases.7 Typical precipitating causes in adults
include inflammatory bowel disease (Chapter 141), postoperative adhesions,
Meckel diverticula, feeding tubes, and small intestinal polyps and tumors
(including leiomyomas, neurofibromas, and lymphomas).
CLINICAL MANIFESTATIONS
Most patients present with symptoms of partial bowel obstruction, including
pain, nausea, and vomiting, and some patients have diarrhea with occult or
overt bleeding. The clinical picture can be confusing when the patient has
intermittent symptoms from a spontaneously resolved event. A mass may be
palpable on examination. Passage of “currant jelly” stools is characteristic of
intussusception, especially in children.
DIAGNOSIS
The diagnosis of intussusception is usually made using computed tomogra-
phy (CT), which reveals a characteristic alternating high- and low-attenuation
target-like or sausage-shaped lesion that represents the invaginated intestinal
segments. However, because of the confusing presentation of intussusception
in adults, a combination of plain radiographs, upper GI series, and barium
enema frequently is required for an adequate evaluation.
TREATMENT AND PROGNOSIS
Colonic intussusceptions are treated surgically in adults because of the
high likelihood that a colonic malignancy is the causative lesion.8 For small
intestinal intussusception, pneumatic reduction is successful in children and
has been tried in adults in whom no other significant causative lesion is
present. However, adults with small intestinal intussusception frequently
have an underlying pathological cause, so their treatment consists primarily
of surgical intervention and bowel resection, which not only resolves the
obstruction but also provides a diagnosis of the causative lesion. If the pre-
disposing cause can be diagnosed and corrected, the prognosis is good,
and recurrence rates are low. If the underlying cause is not fully correctable
such as with neurofibromatosis (Chapter 417) or adhesions, intussuscep-
tions may recur.
Hernias
Anatomically, hernias comprise a herniated viscus, the hernial sac (internal
wall of the hernia lined by peritoneum), and the hernial ring. Whereas
an external hernia occurs when the viscus lies outside the abdomen, an
internal hernia occurs when the viscus lies in an abnormal location within
the abdominal cavity. Secondary hernias can occur at previous sites of
incision or injury. Incisional, inguinal, and umbilical hernias comprise
90% of all hernias.9 Hernias are common and occur in about 5% of the popu-
lation within their lifetimes. For inguinal hernias alone, the lifetime cumula-
tive incidence is estimated to be 43% in men and 6% in women.10 By
comparison, femoral, umbilical, and incisional hernias occur twice as often
in women.
Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
945
 
DIAGNOSIS, AND TREATMENT  
OF SPECIFIC HERNIAS 
Epigastric hernias occur at sites of congenital weakness in the midline
between the xiphoid and umbilicus along the linea alba. Small epigastric
hernias may be asymptomatic or difficult to identify. Larger epigastric hernias
can present as nodules, sometimes with tenderness. Multiple hernias may be
present. They can be repaired surgically if symptomatic or if complications are
present.
Umbilical hernias occur in association with obesity, in multiparous women,
and in patients with ascites. They present as a protuberant mass palpable at
the umbilicus. Incarceration of small bowel or omentum is common, and stran-
gulation occurs in about one third of umbilical hernias. Umbilical hernias can
be repaired surgically if they are symptomatic or associated with complica-
tions, but ascites should be controlled for the hernia repair to succeed.
Groin hernias present with bulging in this region, particularly with Valsalva
maneuvers. Whereas direct inguinal hernias occur at the site of weakness at
the base of the Hesselbach triangle, indirect inguinal hernias occur lateral
to the Hesselbach triangle. Both direct and indirect inguinal hernias are above
the inguinal ligament. Femoral hernias occur below the inguinal ligament in
the femoral canal. Pain is typically mild, but more severe pain or colicky
abdominal pain suggests incarceration or strangulation. Palpation can reveal
the presence of a groin hernia that increases in size with standing or increased
intra-abdominal pressure, such as a Valsalva maneuver, but palpation may be
difficult in obese patients. In unclear cases, CT imaging can be helpful. The
differential diagnosis of an inguinal bulge also includes adenopathy, lipoma
or other tumors, testicular torsion of an undescended testicle, and abscess.
Femoral hernias should be repaired when first diagnosed because of their risk
for strangulation, but watchful waiting is an acceptable option for men with
minimally symptomatic inguinal hernias. A1  The treatment of symptomatic
groin hernias is surgical, now usually by open mesh-based techniques or lapa-
roscopic repair, which appear to provide equivalent results. A2  Because the
presence of strangulation can reliably be made only at surgery, more severe
symptoms warrant early surgical intervention.
Pelvic hernias occur through a weakened pelvic floor and are sixfold more
common in women, especially with advancing age. The most common form
is an obturator hernia, but less common forms include a sciatic hernia through
the sciatic foramen or perineal hernias through the pelvic floor musculature.
Most obturator hernias present with acute bowel obstruction. A tender mass
may be palpable near the obturator canal on rectal or vaginal examination.
Inner thigh pain on internal rotation of the hip may be present in 50% of
patients. Diagnosis can be aided using CT imaging. The treatment is surgical.
Incisional hernias can develop after 1% to 4% of laparotomy incisions. Inci-
sional hernias may cause chronic abdominal discomfort, especially with
maneuvers that increase intra-abdominal pressure. Repair is usually performed
with prosthetic mesh.
More rare hernias include lumbar hernias (which are more common in men
and after surgery for trauma), Spigelian hernias occurring through the linea
semilunaris in elderly patients, and internal hernias that occur when an intra-
peritoneal organ protrudes into a separate compartment within the abdomen.
Some hernias occur in surgically created defects or because of congenital
defects (e.g., paraduodenal, pericecal, or foramen of Winslow). Up to 15% of
internal hernias occur through mesenteric or omental defects. Most patients
present with intermittent symptoms of pain and bowel obstruction or stran-
gulation. Radiologic studies can be of variable assistance. The differential diag-
nosis should include volvulus, adhesions, and tumors. Surgery is needed to
reduce the herniated viscus and close any defect.
  INFLAMMATION OF THE INTESTINE AND COLON
Appendicitis
Appendicitis is the most common intra-abdominal pathology that requires
emergency surgery. The lifetime prevalence of appendicitis is 8.7% in men
and 6.9% in woman. Lifetime rates of appendectomy are higher, 12% in men
and 23% in women, because the diagnosis may be difficult to confirm nonin-
vasively and because of the practice of operating on patients in whom the
condition is highly suspected.
About one third of patients have luminal obstruction of the vermiform
appendix, most commonly caused by an appendicolith but also occasionally
by lymphoid hyperplasia or tumors, including carcinoid tumors (Chapter
232). Gangrenous appendicitis is almost always associated with luminal
obstruction.
946 CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE
 

TABLE 142-1  DIFFERENTIAL DIAGNOSIS OF ACUTE

APPENDICITIS
SURGICAL CAUSES
Intestinal obstruction
Intussusception
Acute cholecystitis
Mesenteric adenitis (especially from adenoviral infection; Chapter 365)
Meckel diverticulitis
Right-sided colonic diverticulitis
UROLOGIC CAUSES
Right nephrolithiasis
Right pyelonephritis
GYNECOLOGIC CAUSES
Ectopic or tubal pregnancy
Ruptured or torsed ovarian cyst
Right-sided salpingitis or tubo-ovarian abscess
MEDICAL CAUSES
Yersinia (Chapter 312) or Campylobacter (Chapter 303) enterocolitis
Crohn ileitis FIGURE 142-3.  Appendicitis. A computed tomography scan shows an inflamed
Pneumonia appendix with a diameter greater than 1 cm (arrow) consistent with acute, uncompli-
Diabetic ketoacidosis cated appendicitis. (Courtesy of Charlene Prather, MD.)
Herpetic neuralgia (especially right 10th and 11th nerves)
Porphyria
Tuberculous colitis

TABLE 142-2  SCORING SYSTEM FOR ACUTE APPENDICITIS*

VARIABLE
Symptoms Migration of pain to the right iliac fossa
Anorexia
Nausea or vomiting
Signs Tenderness in right lower quadrant
Rebound of pain
Elevation of temperature (≥37.3°C)
Laboratory Leukocytosis (WBC count >10,000/µL)
Shift to the left (>75% neutrophils)
Total score
*An aggregate score of 5 or 6 is compatible with the diagnosis of acute appendicitis. A score of 7 or
8 indicates a probable appendicitis, and a score of 9 or 10 indicates a very probable acute
appendicitis.
WBC = white blood cell.
Adapted from Alvarado, A. A practical score for the early diagnosis of acute appendicitis. Ann Emerg
Med. 1986;15:557-564.
CLINICAL MANIFESTATIONS AND DIAGNOSIS
The differential diagnosis of appendicitis is extensive (Table 142-1).11 Current
guidelines for diagnosis include characteristic history and physical findings
of abdominal pain; localized tenderness; or other signs of acute appendicitis,
including increased right lower quadrant pain with cough, pain with flexion
and internal rotation of the hip, pain with passive extension of the right hip,
and increased right lower quadrant pain during palpation of the left lower
quadrant. Laboratory evidence of inflammation include leukocytosis, greater
than10,000/µL but usually less than 18,000/µL unless perforation has
occurred, with left shift, and elevated markers (Table 142-2) such as the
C-reactive protein or procalcitonin level. However, none of these tests are
accurate enough to make or exclude the diagnosis of appendicitis.12 The pre-
ferred diagnostic test is multidetector CT (Fig. 142-3), which has a sensitivity
and specificity of at least 94% A3  and perhaps higher, and can also detect per-
foration (Fig. 142-4). Ultrasonography is less sensitive and specific, 83% and
93%, respectively, but is useful when CT is contraindicated, such as in preg-
nant women or a suspected ectopic pregnancy.
TREATMENT AND PROGNOSIS
When acute appendicitis is suspected, emergent surgical consultation and
appendectomy are indicated. Laparoscopic appendectomy is increasingly
used in preference to open appendectomy because of lower rates of postop-
erative complications and a more rapid return to normal eating and activity. A4  Diverticulitis of the Colon
Preoperative antibiotics (e.g., cefotetan, 2 g intravenously, or cefoxitin, 2 g
intravenously followed by three postoperative doses or ticarcillin–clavulanic
VALUE
1
1
1
2
1
1
2
1
10
FIGURE 142-4.  Appendicitis. A computed tomography scan shows appendicitis
complicated by perforation with abscess formation (arrow). (Courtesy of Charlene
Prather, MD.)
acid) reduce infectious complications in otherwise uncomplicated appendi-
citis. Because perforation of the appendix increases the risk of mortality from
0.0002% to 3% and increases the morbidity rate from 3% to 47%, the tradi-
tional approach is that a negative laparotomy is an acceptable trade-off to
missing true appendicitis. A nonoperative approach using antibiotics to treat
uncomplicated appendicitis can reduce routine surgical morbidity but at the
expense of about a 2% risk of rupture and 1% risk of gangrenous appendici-
tis. A5  For a perforated appendix with abscess formation, immediate appen-
dectomy yields similar results to a strategy of percutaneous ultrasound- or
CT-guided drainage, intravenous (IV) antibiotics, and laparoscopic appen-
dectomy about 10 weeks later. A6  In the setting of perforation, once-daily
dosing with ceftriaxone and metronidazole for 7 to 10 days is as good as
triple-dose therapy. A7 
Complications develop in more than 15% of patients, with an overall mor-
tality rate of about 3% in patients with perforated appendicitis. Complica-
tions are uncommon in surgically treated nonperforated appendicitis.
Patients who have appendectomies for suspected but not confirmed appen-
dicitis have a prognosis that depends on whether they had an underlying
disease, such as Crohn (Chapter 141) or carcinoid (Chapter 232).
Colonic diverticula are technically pseudodiverticula. They form when the
colonic mucosa and submucosa herniate through the muscularis propria of

Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
 CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE
FIGURE 142-5.  Sigmoid diverticulosis. The colonoscopic appearance of sigmoid diver-
ticulosis coli.
the colon. A spectrum of problems can result from diverticulosis, including
diverticulitis, which is an infected diverticulum, or diverticular bleeding,
which is manifested as acute lower GI bleeding (Chapter 135). Diverticular
disease (Fig. 142-5 and E-Fig. 142-E1) affects about 10% of middle-aged
adults and increases in prevalence up to about 80% in elderly adults.
Colonic diverticula form at the site where the nutrient artery, the vasa
recta, penetrates the muscularis propria. Diverticulosis in Western popula-
tions is most common in the left colon and has been thought to be associated
with the low-fiber content of the typical Western diet, although recent epi-
demiologic studies cast doubt on this hypothesis. Diverticulosis can occur
anywhere in the colon, however, and it is more commonly observed in the
right colon in Asian populations.
The lifetime risk of diverticulitis is up to 25%.13 Diverticulitis is thought to
occur when impacted material in the diverticulum compresses the blood
supply, thereby resulting in a microperforation. Diverticulitis can be compli-
cated further by free perforation, abscess, or fistula formation.
CLINICAL MANIFESTATIONS
The majority of patients with colonic diverticulosis are asymptomatic.
Patients with diverticulitis commonly present with localized pain, fever, and
anorexia. The pain may radiate to the back, flank, or suprapubic region.
Nausea and vomiting, constipation or diarrhea, or urinary symptoms may be
variably present. Physical examination typically reveals left lower quadrant
tenderness, sometimes with localized guarding or a palpable mass. Rebound
tenderness or peritoneal signs should suggest the presence of free perforation.
Visible diverticular bleeding is rare in the setting of acute diverticulitis. Leu-
kocytosis is present. When the acutely inflamed diverticulum is adjacent to
the bladder, sterile pyuria may be found.
DIAGNOSIS
The diagnosis of acute diverticulitis can be confirmed in the appropriate
setting by leukocytosis and an ultrasound examination or a CT scan showing
diverticulosis coli with localized inflammation of the colonic wall and peri-
colic fat at the site of acute diverticulitis. A CT scan also can demonstrate free
perforation, abscess, or fistula formation (Fig. 142-6). Because of the
increased risk of perforation, invasive testing such as barium enema or colo-
noscopy is contraindicated when a diagnosis of acute diverticulitis is being
entertained. The differential diagnosis of acute diverticulitis includes inflam-
matory bowel disease (Chapter 141), gastroenteritis, appendicitis, and colon
cancer (Chapter 193) with perforation.
TREATMENT  anti-inflammatory drugs (NSAIDs), potassium chloride preparations, vaso-
Uncomplicated acute diverticulitis can be treated with antibiotics. A 7- to
10-day course of oral antibiotics (e.g., ciprofloxacin 750 mg twice daily and
metronidazole 500 mg four times daily), perhaps after a single IV dose of
Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
947
FIGURE 142-6.  Diverticulitis. A computed tomography scan shows acute diverticulitis
with perforation. An abscess (arrow) is seen presenting as an air-filled collection. (Cour-
tesy of Charlene Prather, MD.)
antibiotics, is as effective and safe as hospitalization for IV antibiotics. A8 
Patients who can tolerate clear liquids can be treated in the outpatient setting
with gradual advancement of their diet. Patients who are unable to tolerate
eating should be admitted to the hospital for IV fluids and antibiotics (e.g.,
levofloxacin 750 mg daily and metronidazole 500 mg every 6 hours or
piperacillin–tazobactam 3.375 g every 6 hours).
Although the risks associated with one episode of uncomplicated diverticu-
litis are low, with a mortality rate that is less than 1%, complicated diverticulitis,
defined as diverticulitis with abscess, fistula formation, free perforation, or
obstruction, is associated with increased inpatient morbidity in up to 25% of
cases and has a mortality rate as high as 5%. Furthermore, these risks increase
with a second episode of complicated diverticulitis. Elective segmental colec-
tomy typically has been recommended to patients after 2 to 3 episodes of
complicated diverticulitis and in young patients even after a first episode.
However, recent evidence suggests that the risk of complicated diverticulitis
after recovery from uncomplicated diverticulitis is only about 5% and is lower
not higher after subsequent episodes of uncomplicated diverticulitis. As a
result, prophylactic surgery is not indicated in patients whose diverticulitis is
uncomplicated and can be medically treated.14 Patients with diverticulitis with
abscess formation require percutaneous CT-guided drainage and subsequent
surgery, usually laparoscopic, typically after 6 weeks. Acute diverticulitis can
be complicated by colitis or late stricture formation. About 40% of patients
with complicated diverticulitis have significant morbidity, and their mortality
rate is about 6%, but it is only about 2% in patients without perforation. There
is no convincing evidence that a high-fiber diet prevents recurrent diverticular
disease15 or that nuts or any particular foods should be favored or avoided.
Other Intestinal Inflammatory Conditions
SMALL INTESTINAL ULCERS
Most primary idiopathic ulcers are found in the mid- to distal ileum, where
they can be solitary or multiple. A careful history is necessary to exclude other
precipitating causes of small intestinal ulcers, including drug exposure and
other systemic diseases (Table 142-3). Pathologically, these ulcers can be
differentiated from Crohn disease or chronic ulcerative jejunoileitis by the
absence of granulomas. Barium contrast studies including enteroclysis can
make the diagnosis, and CT or magnetic resonance enterography can also be
helpful. In the absence of bowel obstruction, wireless capsule endoscopy is
often the preferred test. Therapy with anti-inflammatory or immunosuppres-
sive medications has not proven helpful. Therapy is typically directed to
complications, including perforation and obstruction, with segmental surgi-
cal resection. However, the risk of ulcer recurrence is high.
Drug-induced ulcerations are common and can result from nonsteroidal
active medications, antimetabolites, and cocaine. Wireless capsule endos-
copy can make the diagnosis (Fig. 142-7). NSAID-induced injury is similar
to Crohn disease, with transmural injury and the risk of stricture formation.
Treatment is aimed at avoiding the offending agent, if possible. Unlike for
 CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE
 
947.e1

E-FIGURE 142-1.  Colonic diverticula. An abdominal flat plate shows residual barium

in diverticula scattered throughout the colon. (Courtesy of Charlene Prather, MD.)

Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
948 CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE
FIGURE 142-7.  Nonsteroidal anti-inflammatory drug (NSAID)—induced enteropathy.
The wireless capsule endoscopy appearance of a jejunal ulceration (arrow) caused by
NSAID use.
TABLE 142-3  CAUSES OF SMALL INTESTINAL ULCERS
CATEGORY CAUSES
Acidic Meckel diverticulum, Zollinger-Ellison syndrome
Drug-induced Potassium chloride, NSAID, antimetabolite
Idiopathic Primary ulcer, Behcet disease
Infectious Tuberculosis, typhoid, Yersinia infection, Strongyloides
superinfection
Inflammatory Crohn disease, SLE, chronic jejunoileitis
Metabolic Uremia
Neoplastic Malignant histiocytosis, lymphoma, adenocarcinoma
Radiation Radiation enteritis
Vascular Mesenteric vascular insufficiency, vasculitis, arteritis
NSAID = nonsteroidal anti-inflammatory drug; SLE = systemic lupus erythematosus.
gastric ulceration, data are conflicting as to whether the concomitant use of
a proton pump inhibitor mitigates or exacerbates the condition.16
A variety of systemic conditions also can manifest with small intestinal
ulcerations. Patients with Crohn disease (Chapter 141) can cause ulcers of
any portion of the GI tract. Systemic lupus erythematosus (Chapter 266),
rheumatoid arthritis (Chapter 264), scleroderma (Chapter 267), polyarteri-
tis nodosa (Chapter 270), and Henoch-Schönlein purpura (Chapter 270)
can present with small intestinal ulcerations that are thought to be secondary
to microthrombosis and vasculitis. Mesenteric vasculitis presents as nausea,
vomiting, fever, and GI bleeding.
Behçet disease (Chapter 270) is a systemic process that causes intestinal
ulcers, typically in the ileocecal region, in fewer than 1% of cases. Although
symptoms are similar to those of Crohn disease, pathologically Behçet
disease-related ulcers are deep and do not have surrounding inflammation or
granulomas. The optimal treatment of this disease has yet to be delineated.
Patients frequently are treated with immunomodulators (Chapter 270), and
surgery is reserved for ulcer-related complications.
Sarcoidosis (Chapter 95) uncommonly involves the intestine. Its presenta-
tion is similar to Crohn disease, with small and large intestinal ulceration and
Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
noncaseating granulomas. Patients commonly have nausea, vomiting, diar-
rhea, abdominal pain, and protein-losing enteropathy. Treatment is targeted
to controlling the systemic disease.
Mycobacterium tuberculosis (Chapter 324) typically involves the distal
ileum and cecum. A waxing and waning course can mimic the symptoms and
location commonly seen in Crohn disease. The diagnosis is suspected based
on a history of exposure, particularly in endemic regions, and confirmed by
colonoscopy with biopsy, stains, and culture. Treatment is as for disseminated
tuberculosis (Chapter 324).
Histoplasma capsulatum (Chapter 332) presents with ulcerations and pol-
ypoid masses that mimic tumors, typically in an immunocompromised
patient. Patients present with diarrhea, bleeding, and obstruction. The granu-
lomas seen on biopsy must be differentiated from Crohn disease, tuberculo-
sis, and sarcoidosis. Treatment involves managing the systemic infection.
Neutropenic enterocolitis, or typhlitis (E-Fig. 142-E2), is an inflammation of
the intestine or colon, usually during the neutropenic phase 10 to 14 days
after high-dose induction chemotherapy.17 It involves right lower quadrant
abdominal pain, distention, and diarrhea, sometimes with bleeding. These
findings in of themselves are nonspecific and are similar to Clostridium
difficile–associated colitis (Chapter 296), ischemic colitis (Chapter 143), or
pseudo-obstruction (Chapter 136). Diagnosis is based on typical CT scan
findings of thickened bowel wall; bowel distention, especially of the cecum;
and associated inflammatory changes. Treatment is conservative, with bowel
rest and decompression when bowel dilation is present, and broad-spectrum
antibiotics. Leukocyte-stimulating agents are often used to reverse the neu-
tropenia (Chapter 167). Treatment of bleeding is supportive with transfu-
sions and correction of any coagulopathy. Surgery is indicated in the setting
of intractable bleeding or perforation. The symptoms resolve rapidly with
resolution of neutropenia.
VISCERAL ANGIOEDEMA
Visceral angioedema can be idiopathic, or it can be a complication of
hereditary and acquired C1 esterase inhibitor deficiency (Chapter 252),
hypocomplementemia, drugs (especially angiotensin-converting enzyme
inhibitors), or foods. Patients with GI angioedema commonly present with
abdominal pain and distention, nausea, vomiting, and diarrhea. Some patients
also have evidence of mucous membrane swelling, hives, wheezing, or
dyspnea. On CT scan, thickened, fluid-filled loops of small bowel and ascites
may also be seen. Symptoms commonly occur episodically, persist for 1 to 3
days and may recur periodically. The diagnosis is established by discontinuing
the implicated drug or food, low serum levels of C4, low C1 esterase quantita-
tive levels, or reduced C1 esterase functional activity. C1 esterase inhibitor
deficiency can be treated successfully with C1 inhibitor therapy (Chapter
252).
RADIATION ENTERITIS
Radiation injury (Chapters 20 and 140) can occur in the small or large intes-
tine as a result of therapy for gynecologic, urologic, rectal, or retroperitoneal
tumors. Acute injury, which can occur during the course of treatment, is
associated with nausea, diarrhea, and abdominal or rectal discomfort. The
risk is related to radiation dose. Chronic injury typically presents 6 months
to 2 years after treatment and presents with progressive bowel obstruction
owing to continued inflammation and fibrosis.18 Patients with radiation proc-
titis present with rectal pain, bleeding, and occasionally diarrhea.
Acute radiation injury is usually self-limited to the period of treatment, but
up to 5% of patients can progress to chronic radiation injury to the small
intestine, and up to 15% of patients experience chronic radiation proctitis.
Radiation enteritis and stricture formation can be seen on barium radio-
graphs or CT scans. The characteristic neovascularization pattern of telangi-
ectasias from radiation proctitis is seen on endoscopy.
One third to half of patients develop bleeding, which can be minor and
intermittent or more substantial. Whereas patients who do not require trans-
fusion have a 70% chance of remission, patients with chronic radiation enteri-
tis who need transfusion have a low rate of remission (20%) and have
subsequent high morbidity and even mortality rates. Less invasive treatment
options include sucralfate enemas. Several small studies suggest a benefit
from endoscopic argon plasma coagulation.
An algorithmic approach emphasizing specific approaches, as outlined
earlier, to each specific symptom, can improve outcome compared with
routine clinical care. A9  Surgery, which can be required in up to one third of
patients with strictures or bleeding, is associated with a high complication
rate and should be avoided if possible.19
 CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE
 
948.e1

E-FIGURE 142-2.  Computed tomography scans showing neutropenic colitis. The left scan shows a thickened cecal wall (arrow). Eight days later, a follow-up scan shows resolution
(right scan). (Courtesy of Charlene Prather, MD.)

Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
 CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE
  PERITONEAL DISORDERS
Peritonitis
Peritonitis, which is a local or generalized inflammation that involves the
visceral and parietal peritoneum, can occur as a primary or secondary process.
Primary peritonitis in adults is the spontaneous infection of ascites in a
patient with cirrhosis (Chapter 153) in the absence of an overt intra-
abdominal source. The use of acid-suppressive therapy appears to increase
the risk of developing spontaneous bacterial peritonitis threefold in hospital-
ized patients with cirrhosis.
Secondary peritonitis develops when disease or injury to the intestine
results in bacterial contamination from a perforated viscus (e.g., peptic ulcer
disease, appendicitis, diverticulitis, penetrating trauma, or iatrogenic), from
iatrogenic causes (e.g., peritoneal dialysis [Chapter 131] or surgical contami-
nation), from granulomatous disease (e.g., tuberculosis or fungal infections),
or from chemical or aseptic exposures (e.g., bile, urine, or radiographic
barium).20
CLINICAL MANIFESTATIONS AND DIAGNOSIS
Abdominal pain is the hallmark of peritonitis. It can be sudden in onset in
the setting of a perforated viscus or more insidious in nature in the setting of
granulomatous or chemical causes. Patients with peritonitis typically lie
supine with flexed knees and exhibit shallow breathing. Physical examination
reveals a distended abdomen with tenderness to palpation, localized or gen-
eralized guarding, and rigidity. Associated symptoms include fever, nausea,
vomiting, and leukocytosis with a left shift. Some patients with bacterial
peritonitis rapidly develop septic shock (Chapter 108).
Granulomatous peritonitis has a more insidious presentation, and 70% of
patients have symptoms for 4 months before diagnosis. Systemic symptoms
include fever, malaise, anorexia, and weight loss. The abdomen is diffusely
tender. Leukocytosis can be absent.
Patients with tuberculous peritonitis often have a positive skin test result
or infiltrates on their chest radiograph. The peritoneal fluid typically has a
high protein level (<3 g/dL), a low glucose (<30 mg/dL), and elevated leu-
kocytes (<250 cells/µL); fluid stains and cultures are unhelpful, but poly-
merase chain reaction–based tests can be diagnostic. The laparoscopic
appearance of tuberculous peritonitis is characteristic, with fibrous masses
from the parietal peritoneum and granulomas.
Plain abdominal radiographs may show evidence of paralytic ileus, and
free air under the diaphragm on upright views confirms the presence of a
perforated viscus. CT scan is more sensitive, 70% to 100%, than plain radio-
graphs for detecting free air and may also demonstrate the underlying cause
(Fig. 142-8).
In young patients, appendicitis and a perforated duodenal ulcer (Chapter
139) are common causes. In older patients, perforated diverticula and cancer
(Chapter 193) are more common. In young women, tubal pregnancy and a
ruptured tubo-ovarian abscess must be considered (Chapters 285 and 299).
FIGURE 142-8.  Peritonitis. A computed tomography scan in a patient with peritonitis
showing a thickened duodenal wall from a perforated duodenal ulcer found at the time
of surgical exploration. (Courtesy of Charlene Prather, MD.)
Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
949
Secondary peritonitis is usually caused by a mixed flora of bacteria, including
Escherichia coli, Streptococcus faecalis, Pseudomonas aeruginosa, Klebsiella mira-
bilis, Bacteroides fragilis, Clostridium spp., and anaerobic streptococci.
TREATMENT AND PROGNOSIS 
Treatment of acute suppurative peritonitis relies on prompt adequate resus-
citation with IV fluids and broad-spectrum IV antibiotics. Treatment regimens
include: piperacillin–tazobactam, 3.375 g every 6 hours; ampicillin–sulbactam,
3.0 g every 6 hours; ciprofloxacin, 400 mg every 12 hours, and metronidazole,
1 g every 12 hours; levofloxacin, 750 mg every 24 hours; cefepime, 2 g every 12
hours, and metronidazole, 1 g every 12 hours; or imipenem–cilastatin sodium,
500 mg every 6 hours. Early diagnosis and surgical intervention for acute peri-
tonitis from perforated viscus is critical. The mainstay of treatment for tubercu-
lous peritonitis is at least 6 months of a multidrug regimen (Chapter 324).
Chemical aseptic peritonitis can be complicated by secondary bacterial
infection. Treatment is similar to that of acute suppurative peritonitis, with
intervention to control the source of peritoneal contamination.
The outcome of peritonitis depends on its cause as well as the rapidity of
treatment. The mortality rate can be as low as 15% in patients who have cor-
rectable causes, such as a perforated appendix, and who do not develop
multiorgan failure before treatment but as high as 50% for postoperative infec-
tive peritonitis.
PERITONITIS AS A COMPLICATION OF CHRONIC AMBULATORY
PERITONEAL DIALYSIS
The most common complication of chronic ambulatory peritoneal dialysis is
infectious peritonitis from bacterial contamination (Chapter 131), which
commonly results from poor technique.21 In contrast to polymicrobial acute
suppurative peritonitis, peritonitis complicating chronic ambulatory perito-
neal dialysis is typically monomicrobial with gram-positive cocci in the
majority of cases and gram-negative species in the remainder of cases. Fungal
peritonitis is rare. Symptoms can be milder than in other forms of peritonitis,
with patients often presenting with diffuse abdominal pain, low-grade fever,
and leukocytosis. The exchange fluid is characteristically turbid and may be
the only sign of infection. The diagnosis is based on these physical findings,
turbid dialysate with less than 100 leukocytes/µL, and a positive dialysate
culture that determines the microbe involved. Treatment is with intraperito-
neal antibiotics. The dialysis catheter should be removed in the setting of an
inadequate response to therapy, fungal or tuberculous peritonitis or concomi-
tant skin infection.
ADHESIONS
Peritoneal adhesions, which are the most commonly observed cause of bowel
obstruction,22 can occur at any time after a laparotomy. Patients who have had
intra-abdominal infection, ischemia, and peritonitis are at increased risk.
Patients present with complete or incomplete bowel obstruction, which is
usually manifested as colicky abdominal pain, nausea, and vomiting (includ-
ing feculent vomiting), abdominal distention, and an absence of flatus or
stooling. Bowel obstruction can be diagnosed on plain radiographs or CT
scan from the presence of dilated bowel and air-fluid levels, with decom-
pressed bowel distal to the site of obstruction (Fig. 142-9). Treatment of
bowel obstructions is with NG tube decompression and fluid resuscitation.
A nonoperative approach can be attempted in cases of partial bowel obstruc-
tion or in patients who have had numerous prior laparotomies, which make
surgical exploration more complicated. However, urgent laparotomy for lysis
of adhesions must be performed before bowel ischemia develops. In patients
with chronic abdominal pain, surgical exploration for the intent of lysing
adhesions without clear evidence of obstructing adhesions should be avoided.
Patients who develop postoperative adhesions can progress to bowel obstruc-
tion and develop recurrent adhesions despite surgical lysis of the adhesions.
Data suggest that oxidized regenerated cellulose and hyaluronate carboxy-
methylcellulose adhesion barriers can safely reduce clinically relevant conse-
quences of adhesions. A10 
PERITONEAL CARCINOMATOSIS AND MALIGNANT ASCITES
Peritoneal carcinomatosis results when malignancy spreads throughout the
peritoneal cavity and eventually encases the viscera. The cause can be primary
tumors of the peritoneal cavity (e.g., mesothelioma and sarcoma), dissemina-
tion of an intra-abdominal malignancy (e.g., gastric, colon, pancreatic,
950 CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE
FIGURE 142-9.  Small bowel obstruction. A computed tomography scan shows dilated,
fluid-filled small bowel (white arrow) and a nondilated colon (black arrow) in a patient
with a small bowel obstructions from adhesions in the midileum found at the time of
surgical exploration. (Courtesy of Charlene Prather, MD.)
FIGURE 142-10.  Malignant ascites. A computed tomography scan shows ascites (large
arrow) in a patient with gastric cancer (small arrow). (Courtesy of Charlene Prather, MD.)
ovarian, or neuroendocrine tumors), lymphomas, metastatic spread from
extra-abdominal malignancy (e.g., breast, lung, or melanoma), and pseudo-
myxoma peritonei (a rare condition with gelatinous peritoneal implants from
mucinous neoplasms of the appendix or ovary).
CLINICAL MANIFESTATIONS AND DIAGNOSIS
The presentation of peritoneal carcinomatosis is nonspecific, with complaints
of abdominal pain, anorexia, nausea, vomiting, malaise, and weight loss.
Ascites is the most common physical finding. Malignant ascites is rare,
accounting for less than 10% of cases of ascites.
Although ultrasound examination may document ascites, CT is preferred
to identify carcinomatosis and the origin of the underlying cause (Fig. 142-
10). Diagnostic paracentesis can be performed to obtain cell count and dif-
ferential, culture, and cytologic examination. A serum to ascites albumen
ratio of less than 1.1 mg/dL suggests malignant ascites, but the differential
diagnosis also includes pancreatic ascites (Chapter 144), nephrotic syn-
drome (Chapter 121), and peritoneal tuberculosis. Laparoscopy can disclose
the typical tumor implant stubbing the peritoneum. Biopsy and appropriate
stains can verify the presence of mesothelioma (Chapters 99 and 191) by
detecting hyaluronic acid on Alcian stain in a specimen that has a negative
carcinoembryonic antigen stain and no mucin on a periodic acid-Schiff stain.
By contrast, carcinomas have no hyaluronic acid but show mucin and have a
positive carcinoembryonic antigen stain.
Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
TABLE 142-4  MESENTERIC DISEASES
PRIMARY INFLAMMATORY DISEASE
Panniculitis
Retractile mesenteritis
CYSTS
Developmental
Traumatic
Neoplastic
Infectious
TUMORS
Benign tumors
Lipoma
Leiomyoma
Hemangioma
Malignant tumors
Liposarcoma
Leiomyosarcoma
Rhabdomyosarcoma
Metastatic tumor
Mesenteric fibromatosis
TREATMENT AND PROGNOSIS 
Treatment is typically palliative owing to the late presentation of disease.
Malignant ascites responds poorly to diuretic therapies, and repeated thera-
peutic paracentesis may be needed. Recent data suggest some benefit from
cytoreductive surgery and hyperthermic intraperitoneal chemotherapy.23
  DISEASES OF THE MESENTERY AND OMENTUM
The differential diagnosis of mesenteric and omental disorders include a
variety of rare disorders, including inflammation, cysts, and tumors that can
be benign or malignant (Table 142-4).
Mesenteric panniculitis presents in middle or later age with a slight male
predilection. Symptoms typically include nonspecific abdominal pain, weight
loss, nausea, vomiting, and low-grade fever, but patients occasionally can
present with an acute abdomen. A palpable mass is felt in the majority of
patients. The diagnosis can be confirmed by CT scan. Lesions should be
biopsied to exclude malignancy but generally are not amenable to complete
resection. Significant improvement in the symptoms of this generally self-
limited process has been reported with progesterone, corticosteroids, aza-
thioprine, or cyclophosphamide, but evidence to recommend their general
use is lacking.
Mesenteric and omental cysts and solid tumors are rare disorders. Patients
present with a constellation of nonspecific symptoms. They can be identified
with CT scan. Surgical resection will provide the definitive diagnosis and
determine whether a benign or malignant condition is present.
Mesenteric fibromatosis (desmoid tumors) is a rare noninflammatory condi-
tion that may be associated with familial adenomatosis coli (Chapter 193)
and Gardner syndrome (Chapter 193). Fibromatoses are locally aggressive
tumors that may present as stable or rapidly growing intraabdominal masses.
They have a high rate of recurrence after incomplete surgical resection, in
patients with multicentric disease, or if precipitated by surgical trauma itself.
Grade A References
A1. Fitzgibbons RJ Jr, Giobbie-Hurder A, Gibbs JO, et al. Watchful waiting vs repair of inguinal hernia
in minimally symptomatic men: a randomized clinical trial. JAMA. 2006;295:285-292.
A2. Karthikesalingam A, Markar SR, Holt PJ, et al. Meta-analysis of randomized controlled trials com-
paring laparoscopic with open mesh repair of recurrent inguinal hernia. Br J Surg. 2010;97:4-11.
A3. Kim K, Kim YH, Kim SY, et al. Low-dose abdominal CT for evaluating suspected appendicitis.
N Engl J Med. 2012;366:1596-1605.
A4. Ohtani H, Tamamori Y, Arimoto Y, et al. Meta-analysis of the results of randomized controlled
trials that compared laparoscopic and open surgery for acute appendicitis. J Gastrointest Surg.
2012;16:1929-1939.
A5. Varadhan KK, Neal KR, Lobo DN. Safety and efficacy of antibiotics compared with appendicec-
tomy for treatment of uncomplicated acute appendicitis: meta-analysis of randomised controlled
trials. BMJ. 2012;344:e2156.
 A6. St Peter SD, Aguayo P, Fraser JD, et al. Initial laparoscopic appendectomy versus initial nonopera-
tive management and interval appendectomy for perforated appendicitis with abscess: a prospec-
tive, randomized trial. J Pediatr Surg. 2010;45:236-240.
A7. St Peter SD, Tsao K, Spilde TL, et al. Single daily dosing ceftriaxone and metronidazole vs standard
triple antibiotic regimen for perforated appendicitis in children: a prospective randomized trial.
J Pediatr Surg. 2008;43:981-985.
A8. Biondo S, Golda T, Kreisler E, et al. Outpatient versus hospitalization management for uncompli-
cated diverticulitis: a prospective, multicenter randomized clinical trial (DIVER Trial). Ann Surg.
2014;259:38-44.
A9. Andreyev HJ, Benton BE, Lalji A, et al. Algorithm-based management of patients with gastrointes-
tinal symptoms in patients after pelvic radiation treatment (ORBIT): a randomised controlled trial.
Lancet. 2013;382:2084-2092.
A10. ten Broek RP, Stommel MW, Strik C, et al. Benefits and harms of adhesion barriers for abdominal
surgery: a systematic review and meta-analysis. Lancet. 2014;383:48-59.

GENERAL REFERENCES
For the General References and other additional features, please visit Expert Consult
at https://expertconsult.inkling.com.

Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
 CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE
GENERAL REFERENCES
1. Park JJ, Wolff BG, Tollefson MK, et al. Meckel diverticulum: the Mayo Clinic experience with 1476
patients (1950-2002). Ann Surg. 2005;241:529-533.
2. Uppal K, Tubbs RS, Matusz P, et al. Meckel’s diverticulum: a review. Clin Anat. 2011;24:416-422.
3. Ruscher KA, Fisher JN, Hughes CD, et al. National trends in the surgical management of Meckel’s
diverticulum. J Pediatr Surg. 2011;46:893-896.
4. Martin MJ, Steele SR. Twists and turns: a practical approach to volvulus and intussusception. Scand
J Surg. 2010;99:93-102.
5. Tan KK, Chong CS, Sim R. Management of acute sigmoid volvulus: an institution’s experience over
9 years. World J Surg. 2010;34:1943-1948.
6. Halabi WJ, Jafari MD, Kang CY, et al. Colonic volvulus in the United States: trends, outcomes, and
predictors of mortality. Ann Surg. 2014;259:293-301.
7. Potts J, Al Samaraee A, El-Hakeem A. Small bowel intussusception in adults. Ann R Coll Surg Engl.
2014;96:11-14.
8. Varban OA, Ardestani A, Azagury DE, et al. Contemporary management of adult intussusception:
who needs a resection? World J Surg. 2013;37:1872-1877.
9. Jensen KK, Kjaer M, Jorgensen LN. Abdominal muscle function and incisional hernia: a systematic
review. Hernia. 2014;18:481-486.
10. Zendejas B, Ramirez T, Jones T, et al. Incidence of inguinal hernia repairs in Olmsted County, MN:
a population-based study. Ann Surg. 2013;257:520-526.
11. Rao KS, Prabhakar J, Sudhakar W. Progress in the diagnosis of appendicitis. Ann Surg. 2015;
261:e88-e89.
12. Yu CW, Juan LI, Wu MH, et al. Systematic review and meta-analysis of the diagnostic accuracy of
procalcitonin, C-reactive protein and white blood cell count for suspected acute appendicitis. Br J
Surg. 2013;100:322-329.
Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
951.e1
13. Shahedi K, Fuller G, Bolus R, et al. Long-term risk of acute diverticulitis among patients with
incidental diverticulosis found during colonoscopy. Clin Gastroenterol Hepatol. 2013;11:
1609-1613.
14. Morris AM, Regenbogen SE, Hardiman KM, et al. Sigmoid diverticulitis: a systematic review.
JAMA. 2014;311:287-297.
15. Unlu C, Daniels L, Vrouenraets BC, et al. A systematic review of high-fibre dietary therapy in diver-
ticular disease. Int J Colorectal Dis. 2012;27:419-427.
16. Chan FK. Proton pump inhibitors and nonsteroidal anti-inflammatory drug-related lower gastroin-
testinal adverse events. Clin Gastroenterol Hepatol. 2014;12:904-906.
17. Shafi MA, Bresalier RS. The gastrointestinal complications of oncologic therapy. Gastroenterol Clin
North Am. 2010;39:629-647.
18. Theis VS, Sripadam R, Ramani V, et al. Chronic radiation enteritis. Clin Oncol (R Coll Radiol).
2010;22:70-83.
19. Shadad AK, Sullivan FJ, Martin JD, et al. Gastrointestinal radiation injury: prevention and treat-
ment. World J Gastroenterol. 2013;19:199-208.
20. Weledji EP, Ngowe MN. The challenge of intra-abdominal sepsis. Int J Surg. 2013;11:290-295.
21. Segal JH, Messana JM. Prevention of peritonitis in peritoneal dialysis. Semin Dial. 2013;26:
494-502.
22. ten Broek RP, Issa Y, van Santbrink EJ, et al. Burden of adhesions in abdominal and pelvic surgery:
systematic review and met-analysis. BMJ. 2013;347:f5588.
23. Brucher BL, Piso P, Verwaal V, et al. Peritoneal carcinomatosis: cytoreductive surgery and HIPEC—
overview and basics. Cancer Invest. 2012;30:209-224.
951.e2 CHAPTER 142  INFLAMMATORY AND ANATOMIC DISEASES OF THE INTESTINE
REVIEW QUESTIONS
1. An 18-year-old college freshman reports to the Student Health Center. He
complains of a 12-hour history of abdominal pain and fever. He complains
of anorexia, nausea, and vomiting. He denies diarrhea and blood per
rectum. His past history is unremarkable. His family history is notable for
heart disease, hypertension, and diverticulosis coli. On physical examina-
tion, he is febrile to 38° C. His abdomen has normal bowel sounds but is
tender in the right lower quadrant with rebound tenderness. On labora-
tory examination, his WBC count is elevated at 11,000/µL with a left shift.
His urinalysis reveals 1+ protein. The most likely diagnosis in this patient
is
A. acute colonic diverticulitis.
B. ulcerative colitis.
C. acute appendicitis.
D. Behçet disease.
E. nephrolithiasis and renal colic.
Answer: C  This patient has an acute appendicitis. He has typical presenting
signs and symptoms. Acute diverticulitis typically presents at an older age,
and it most commonly localizes to the left side of the abdomen. Although
ulcerative colitis presents at this age, its symptoms are typically bloody diar-
rhea and tenesmus. This patient does not have the multisystem presentation
that is common for Behçet disease, in which small bowel involvement is rare.
His normal urinalysis result makes a diagnosis of nephrolithiasis and renal
colic unlikely.
2. A 64-year-old woman reports to the emergency department with a com-
plaint of 2 days of left lower quadrant pain, fever, and diarrhea, as well as
nausea and vomiting. She denies recent travel and antibiotic use. She
admits to many years of constipation and uses laxatives intermittently. Her
past history is notable for hypertension and glaucoma. Her medications
include hydrochlorothiazide 25 mg/day and eye drops for glaucoma. Her
family history is positive for hypertension, diabetes mellitus, and coronary
artery disease. Her physical examination is notable for temperature of
37.6° C, and a heart rate of 105 beats/min. Heart examination shows a
regular tachycardia and a grade 2/6 midsystolic murmur. Her abdomen is
soft with tenderness in the left lower quadrant. There is no distention or
involuntary rebound. On digital rectal examination, there is no stool in
the rectal vault, and you palpate internal hemorrhoids. The most like diag-
nosis is
A. Meckel diverticulum.
B. acute colonic diverticulitis.
C. Crohn colitis.
D. colonic intussusception.
E. acute intestinal obstruction.
Answer: B  This patient has the typical presenting signs and symptoms of
sigmoid colon diverticulitis. Complications from Meckel diverticulum, such
as right lower quadrant pain from ulceration and bleeding, are not present.
Crohn colitis can occur in this age group, but the presentation usually is more
insidious with diarrhea and abdominal pain. The patient does not have the
symptoms of bowel obstruction or the currant jelly stools that are typical of
colonic intussusception.
3. An 82-year-old man is referred to the emergency department from a
nursing home. He complains of abdominal distension and progressive
constipation. He has not passed flatus or stool for 2 days. His history is
notable for dementia and a prior stroke. He has used laxatives for constipa-
tion for many years. His other medications include clopidogrel and
aspirin. He is allergic to intravenous contrast dye. On examination, you
find he is afebrile with a blood pressure of 155/93 mm Hg and a tachy-
cardia of 110 beats/min. His abdomen is distended and tympanic to per-
cussion, with a diffuse tenderness. Bowel sounds are decreased. A small
amount of stool in the rectal vault is brown but Hemoccult positive. Labo-
ratory tests reveal a lactate of 2 and a normal WBC and Hgb levels. The
next step in his management is
A. exploratory laparotomy.
B. abdominal radiographs.
C. bleeding scan.
D. mesenteric angiography.
E. barium upper GI series.
Downloaded for FK Unisba (mahasiswa17fkunisba@unisba.ac.id) at Universitas Islam Bandung from ClinicalKey.com by Elsevier on May 26, 2018.
For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
Answer: B  This patient has a sigmoid volvulus. A volvulus is commonly seen
in institutionalized patients and in patients with a history of chronic constipa-
tion and laxative use. The presence of a volvulus or intestinal obstruction
from other causes can be investigated cost effectively using plain radiographs
as the initial imaging modality. There is no massive gastrointestinal (GI)
bleeding to warrant a bleeding scan, angiography, or upper GI series.
4. A 55-year-old woman presents to your office complaining of vague
abdominal pain and fatigue. Her past history is notable for osteoarthritis.
She is postmenopausal and on hormone replacement therapy. Her medi-
cations also include ibuprofen 600 mg tid. She has noted intermittent
black tarry stools. Physical examination is unremarkable. Laboratory
examination reveals Hgb 8.7 g/dL with an MCV 79. You obtain and
esophagogastroduodenoscopy (EGD) and a colonoscopy for her anemia
and abdominal complaints. EGD is normal, and she has mild sigmoid
diverticulosis coli. The most likely cause of her anemia is
A. diverticular bleeding.
B. gastric ulcer bleeding.
C. Meckel diverticulum.
D. Crohn disease.
E. NSAID-induced enteropathy.
Answer: E  This patient has nonsteroidal anti-inflammatory drug (NSAID)–
induced enteropathy. The episodes of melena are suggestive of ulceration and
bleeding from the upper gastrointestinal (GI) tract, but peptic ulcer disease
was not seen on EGD. She regularly uses NSAIDs, which can be a cause of
secondary small intestinal ulcerations. Meckel diverticulum and bleeding are
more rare than NSAID-induced enteropathy. Although sigmoid diverticuli
were identified on colonoscopy, diverticular bleeding presents as massive
lower GI bleeding, not melena. Crohn disease can present with anemia and
bleeding, but melena is rare.
5. A 63-year-old man presents to your office with a complaint of 5 months
of a poor appetite, a 35-lb weight loss, and low grade fevers up to 37.4° C.
Over the past month, he has noted increasing abdominal girth and tender-
ness. He has been otherwise healthy and takes no medications. His family
history is notable for stroke. He denies tobacco use. He drinks two glasses
of wine each night. He retired at age 55 years and has traveled extensively
throughout Southeast Asia. On physical examination, you note that his
abdomen is markedly distended and diffusely tender. Bowel sounds are
normal, but a fluid wave is present. Findings of the laboratory examina-
tion, including a comprehensive metabolic profile and complete blood
count, are normal. A diagnostic paracentesis reveals protein, 3.5 g/dL;
neutrophils, 800/µL; glucose, 20 mg/dL; and amylase, 50 IU/L. No bac-
teria are seen on stain, and fluid cultures show no growth. The most likely
diagnosis for this man’s ascites is
A. alcoholic cirrhosis.
B. pancreatic ascites.
C. nephrotic syndrome.
D. metastatic lung cancer.
E. tuberculous peritonitis.
Answer: E  This patient has tuberculous peritonitis, which characteristically
presents insidiously in patients who have been exposed to tuberculosis, as
this patient probably was exposed during extensive travel in endemic regions
like Southeast Asia. The ascites is typically high in protein and neutrophils
and low in glucose. The patient’s alcohol use and the characteristics of his
ascites make alcoholic cirrhosis an unlikely cause. The ascitic fluid amylase
level is normal, so pancreatic ascites is unlikely. Ascitic fluid in adult patients
with the nephrotic syndrome is low in protein and is associated with hypo-
albuminemia and heart failure. The characteristics of his ascites are not
typical of metastatic carcinomatosis.