Mesentery, Omentum, Peritoneum:

Inflammatory, Infectious Diseases and 102

Pseudo Lesions

Farnoosh Sokhandon, Peyman Borghei, and Ali Shirkhoda

Peritoneum with its two main components of visceral affect the peritoneum resulting in tumor-like lesions.
and parietal is considered to be the largest and the most Some of these include mesenteric fibromatosis, inflam-
complexly arranged serous membrane in the body. matory pseudotumor, retractile mesenteritis, and
The space between the parietal peritoneum lining Castleman’s disease. In this chapter, various inflamma-
the abdominal wall and the visceral peritoneum tory and infectious conditions of the peritoneum are
enveloping the solid and hollow abdominal organs is discussed and example of each is illustrated. This will
called peritoneal cavity. It consists of the greater sac, be followed by a discussion on various tumor-like lesions
and the omental bursa or lesser sac situated behind the (psuedotumors), and diagnostic pitfalls in the peritoneum.
stomach. Fluid dynamics, respiratory motion, gravity,
and anatomic barriers dictate direct spread of disease
processes within the peritoneal cavity and their appear- Inflammatory and Infectious Conditions of
ance on cross-sectional imaging (Shirkhoda and the Peritoneum
Leyendecker 2011).
On CT and MR imaging, the peritoneum is often Peritoneal Inflammation (Peritonitis)
visible as a thin line, which is smooth, non-enhancing,
and without nodularity. Thickening or enhancement Peritoneal inflammation due to infectious or nonin-
of the peritoneal lining is best seen on contrast-enhanced fectious causes may result in acute or chronic
CT or on enhanced fat-suppressed T1-weighted MR peritonitis. Acute infectious peritonitis is typically
images (Shirkhoda and Leyendecker 2011). Peritoneum seen in bowel perforation, diverticulitis, appendicitis,
is a target for a variety of pathologic conditions originat- retained foreign objects (Fig. 102.1), severe cholecys-
ing within or outside of the abdomen. The most common titis, or it may also result from tuberculous peritonitis
involving tumor is metastasis from various sources such (Fig. 102.2). Bacterial peritonitis may also result from
as ovaries in women and gastrointestinal tract in men. peritoneal instrumentation such as peritoneal dialysis,
However, there are various inflammatory and infectious paracentesis, and surgery or penetrating abdominal
diseases and a variety of other conditions that may also trauma. Spontaneous bacterial peritonitis can occur
in the setting of alcoholic cirrhosis or other forms of
chronic liver disease (Lata et al. 2009).
F. Sokhandon (*) Noninfectious causes of diffuse or localized perito-
Department of Radiology, William Beaumont Hospital, Royal
nitis include pancreatitis (Fig. 102.3) and systemic
Oak, MI, USA
diseases such as systemic lupus erythematosus (SLE).
P. Borghei
In patients with SLE, peritonitis may be accompanied
Department of Radiology, University of Alabama at
Birmingham, Birmingham, AL, USA by development of ascites, pleural and pericardial
effusions. Chemical peritonitis may occur as a result
A. Shirkhoda
Department of Radiology, University of California, Irvine, CA, of hemoperitoneum or bile leak. Hemoperitoneum
USA usually happens in patients with abdominal trauma,

B. Hamm, P. R. Ros (eds.), Abdominal Imaging, DOI 10.1007/978-3-642-13327-5_172, 1577

# Springer-Verlag Berlin Heidelberg 2013
1578 F. Sokhandon et al.

b
Fig. 102.2 A 28-year-old woman with large amount of reactive
ascites due to peritoneal tuberculosis. Notice thickening and
minimal nodularity of the peritoneum (arrows)

Fig. 102.3 Inflammation of transverse mesocolon and thicken-

ing of the adjacent colon (arrows) in a 57-year-old man with
Fig. 102.1 55 year old woman, status post-omentectomy with acute pancreatitis. P = Pancreas, r = right kindney
gossypiboma (retained sponge) resulting in localized thickened
peritoneum (focal peritonitis; “arrows”) encapsulating the
infected foreign object Also patients who have undergone recent percutane-
ous transhepatic cholangiopancreatography (PTC)
aneurysm, or tumor rupture. It results in reactive may show abnormal peritoneal enhancement due to
inflammation of the peritoneum and as a result bile peritonitis. Inflammation of the peritoneum
peritoneal enhancement may be seen on imaging. is indistinguishable on imaging from peritoneal
Both infectious and noninfectious causes of metastasis. The distinction between peritonitis and
peritonitis show peritoneal enhancement on con- peritoneal carcinomatosis is generally based on
trast-enhanced MRI or CT scan. For example, clinical presentation and laboratory values. Also
patients with pancreatitis commonly show upper a mesh, which may be used during the course of
abdominal peritoneal enhancement due to chemical surgery for hernia repair, should not be mistaken for
irritation of the peritoneum by pancreatic enzymes. peritoneal enhancement (Fig. 102.4).
Mesentery, Omentum, Peritoneum: Inflammatory, Infectious Diseases and Pseudo Lesions 1579

Fig. 102.4 This 49-year-old a b

man received a mesh (arrows)
as part of his anterior
abdominal wall hernia repair.
The high-density curvilinear
appearance of mesh can mimic
localized peritoneal
enhancement

a b

Fig. 102.5 Peritoneal

sarcoidosis. A 42-year-old
woman with pulmonary hilar
nodes and nodular thickening
of peritoneum (arrows)
underwent percutaneous core
biopsy of peritoneum and the
diagnosis of sarcoidosis was
confirmed

Peritoneal Sarcoidosis large omental and mesenteric masses (Fig. 102.6), and
“Dry type” is characterized by diffuse fibrous peritoneal
Sarcoidosis is a relatively common systemic disorder thickening (Jadvar et al. 1997).
characterized by noncaseating granuloma formation. Findings in all three forms may be associated with
It is of unknown etiology and infrequently involves low-attenuating abdominal adenopathy. Presence of
peritoneum (Warshauer and Lee 2004). Ascites in typical thoracic findings is very helpful in narrowing
the setting of sarcoidosis is often secondary to the differential diagnosis. However, such findings may
hepatic or cardiac disease rather than true peritoneal be absent in approximately 50% of cases with abdom-
involvement (Lubner and Pickhardt 2009). In case of inal disease (Pickhardt and Bhalla 2005).
peritoneal involvement, sarcoidosis could cause
noninfectious peritonitis and findings may mimic
peritoneal tuberculosis or peritoneal carcinomatosis. Ascites and Infectious Peritonitis in
Imaging appearence is nonspecific and may include Patients with Pseudomembranous Colitis
simple to bloody ascites with or without infiltration,
thickening, and enhancement of peritoneum (Lubner Pseudomembranous colitis is a condition in which
and Pickhardt 2009) (Fig. 102.5). an insult to normal gut flora commonly caused
by antibiotics allows colonization of the colon by
Clostridium difficile and production of its toxins. The
Tuberculous Peritonitis toxins are responsible for a spectrum of clinical pre-
sentations ranging from watery diarrhea and abdomi-
Tuberculous peritonitis is usually a result of direct nal pain to fever, sepsis, and toxic megacolon. In
extension from bowel or nodal disease. CT manifesta- a subset of patients with indolent or subacute infection,
tions of tuberculous peritonitis are divided into three pancolitis results in severe leakage of serum albumin
different types. The “Wet type” is characterized by through the damaged bowel mucosa causing severe
ascites (Fig. 102.2), “Fibrotic type” is characterized by hypoalbunemia which indirectly causes ascites.
1580 F. Sokhandon et al.

Fig. 102.6 Mass-like a b

thickening of omentum
(arrows) due to tuberculous
peritonitis

Intraperitoneal Hemmorrhage

Intraperitoneal hemorrhage can be idiopathic, related

to rupture of a known vascular lesion, neoplastic or
posttraumatic (Lucey et al. 2005). It usually presents
with acute abdominal pain and distension and if severe,
may present with hypovolemic shock. CT and MRI
can very well demonstrate blood within the peritoneal
cavity, while ultrasound can be used to detect
small hemorrhage within the cul-de-sac as seen in
ruptured ovarian cyst or ectopic pregnancy (Hertzberg
et al. 1999).
CT scan is usually the primary imaging modality for
evaluation of acute abdominal pain. Based on the
origin, extent, and age of bleeding, the CT appearance
Fig. 102.7 This patient with portal hypertension, ascites, and varies (Fig. 102.8). Acute blood manifests as layering
splenomegaly has developed numerous collaterals (arrows) within dense material within the dependent aspect of the
the greater omentum mimicking inflammation or tumor infiltration peritoneal cavity with the low-density serum on
the non-dependent aspect. If the imaging is performed
Although ascites is not uncommon in pseudo- following several hours, a hyperdense focus (sentinel
membranous colitis, it is not considered well-known clot) might be seen at the origin of the bleeding – a clue
characteristic of this condition (Rybolt et al. 1989). that can be used to find the source of hemorrhage
Patients with pseudomembranous colitis could also (Mortele et al. 2003).
develop transmural colonic inflammation with micro- MRI imaging can be used when there is a concern
perforations and as a result develop infectious for rupture of an intra-abdominal pathology and for
peritonitis (Tsourous et al. 2007). In cases of infectious characterization of the primary lesion. Specifically
peritonitis, diffuse thickening and enhancement of MRI is helpful when an underlying liver lesion is the
peritoneum with or without focal loculated fluid may source of intraperitoneal hemorrhage. Based on the
be observed. Care should be exercised when dealing chronicity, the intraperitoneal hemorrhage may appear
with density change in peritoneum. In patients with high signal intensity on T1- and mixed signal
with portal hypertension or portal vein thrombosis, intensity on T2-weighted images (Casillas et al.
occasionally presence of numerous collateral vessels 2000). Occasionally on CT and MRI, intraperitoneal
in the omentum can mimic inflammation or tumor hemorrhage mimics infiltrative processes such as
infiltration (Fig. 102.7). lymphoma (Fig. 102.9).
Mesentery, Omentum, Peritoneum: Inflammatory, Infectious Diseases and Pseudo Lesions 1581

Fig. 102.8 Acute bleed from left gastric artery (arrow) into the
lesser and greater omental sac

Peritoneal Pseudo-lesions/Pseudotumors

Mesenteric Fibromatosis (Desmoid Tumor)

c
Mesenteric desmoid tumor or aggressive fibromatosis
is considered a benign proliferative condition with
tendency for local recurrence (Kawashima et al.
1994). It is often seen in association with familial
adenomatous polyposis (FAP) or Gardner’s syndrome.
These lesions can present as well-defined or irregular
mesenteric masses mimicking malignancies
(Fig. 102.10).
Small bowel mesentery is the most common site
for the origin of intra-abdominal fibromatosis. Other
mesenteric structures such as omentum, ileocolic
mesentery, transverse or sigmoid mesocolon, and
ligamentum teres may also be the site of origin for
this pseudo-mass lesion. The age distribution is
between 14 and 75 years and occurs most commonly
in 20–30-year-old women. Most cases of this condition Fig. 102.9 Spontaneous intraperitoneal hemorrhage due to rup-
tured mesenteric aneurysms. Contrast-enhanced CT and
manifest sporadically, and there is no gender or race T2-weighted MR image show massive intraperitoneal bleed.
predilection (Burke et al. 1990). 3D reconstruction of CT angiogram shows the cause to be
If the epicenter of abnormality is in the mesocolon, mesenteric aneurysms (arrows)
involvement of a segment of colon may be seen
on imaging. Infiltration of mesenteric fibromatosis compromise and ischemic small bowel with mucosal
into the adjacent small bowel loops occasionally ulcerations (Church 1998).
causes partial or complete small bowel obstruction. The imaging appearance is directly related to histo-
Mesenteric vascular encasement may result in vascular logic characteristics of the lesion and vascularity.
1582 F. Sokhandon et al.

Fig. 102.10 This 25-year-old a b

female with history of
Gardner’s syndrome, status
post-total colectomy for
familial adenomatous
polyposis, presents with
mesenteric and subcutaneous
masses that were proven to
represent desmoid tumors

Lesions with high collagen stroma are usually hematopoiesis, Erdheim-Chester disease, sarcoidosis,
homogeneous in appearance. Lesions with myxoid and cavitating mesenteric lymph node syndrome may
stroma appear hypoattenuating on CT, while also simulate this process on imaging.
lesions with alternating collagen and myxoid areas
appear striated and/or heterogeneous. Depending
on the amount of vascularity, CT and MRI may Sclerosing Mesenteritis
demonstrate variable degrees of enhancement (Levy
et al. 2006). Sclerosing mesenteritis is an idiopathic disorder
characterized by tumor-like masses within the mesen-
tery. It has various appearances and is also known
Inflammatory Pseudotumor as mesenteric panniculitis, retractile mesenteritis,
mesenteric lipodystrophy, lipogranuloma of the mesen-
Inflammatory pseudotumor is an unusual chronic tery, sclerosing lipogranulomatosis, and primary lipo-
inflammatory process that most often manifests sclerosis of the mesentery (Riddel et al. 2003). Although
before adulthood and involves the orbit and lungs. sclerosing mesenteritis usually involves the small bowel
Occasional involvement of the mesentery and mesentery, it can also involve the mesocolon (Ng et al.
peritoneal cavity (Bonnet et al. 1996) has also 1992; Han et al. 1986). The average age at presentation
been described. This condition might be a sequela is reported to be 60 years and there is a significant male
of chronic infection, prior surgery or trauma predilection (Emory et al. 1997). Patients are usually
(Levy et al. 2006). symptomatic with nonspecific abdominal pain and
Lesions can present as infiltrative or well-defined distention, weight loss, vomiting, diarrhea, and occa-
masses. The imaging characteristics are nonspecific sionally fever of unknown origin. It is occasionally
and include an isodense to hypodense mass on discovered as an incidental finding (Fig. 102.11).
CT with mild enhancement on post-contrast The process usually presents as a soft tissue
images (Levy et al. 2001; Slavotinek et al. 2000). or mixed fat and soft tissue attenuation on CT
The pattern of enhancement might be homogeneous with variable degrees of enhancement (Fig. 102.12).
or heterogeneous, while larger lesions may demon- It may involve mesenteric vessels; however, there
strate central necrosis. MR features also include is usually preservation of a fatty collar around
nonspecific T1-hypointense and T2-hyperintense the vessels, a finding that has been referred to
signal with variable degrees of enhancement (Torzilli as the fat ring sign (Sabate et al. 1999; Valls
et al. 2001). 2000). The mass may appear speculated with radiat-
Occasionally systemic or organ-based diseases ing strands of fibrosis surrounding the lesion.
involve the peritoneum. Conditions such as eosino- Punctate or coarse calcifications may also be present
philic gastroenteritis, amyloidosis, extra medullary (Levy et al. 2006).
Mesentery, Omentum, Peritoneum: Inflammatory, Infectious Diseases and Pseudo Lesions 1583

The affected mesentery is usually thickened and fibrosis. Histological evaluation of these lesions
shortened. Kinking and fixation of the adjacent small shows a loose myxomatous component. A fibrous
bowel loops may occur. There is usually no direct capsule is usually present in these cases (Kawashima
extension to the adjacent small bowel loops; et al. 1993).
rather involvement is by retraction and shortening of
the small bowel mesentery. If abnormality is severe
enough, it may cause partial or complete small Pseudomyxoma Peritonei
bowel obstruction, and as a result patients
present with associated symptoms. Rare cases of Pseudomyxoma peritonei is a rare clinical syndrome
sclerosing mesenteritis have been reported with which is characterized by accumulation of voluminous
a hypoattenuating cystic appearance on CT scan mucinous ascites throughout the peritoneal cavity. It is
(Johnson et al. 1997). Lesions usually contain chronic a slowly progressive process and is usually the result
nonspecific inflammatory cells, fat necrosis, and of mucinous adenocarcinoma of the appendix pre-
senting as a mucocele with spread to the peritoneal
cavity (Fig. 102.13). It may also occur as a complica-
tion of ovarian mucinous neoplasm. The primary
tumor of the appendix or ovary is typically inconspic-
uous at the time of diagnosis. Although it does not
metastasize through the lymphatics or blood vessels,
if left untreated it usually spreads throughout the
peritoneal surfaces by following the pathway of flow
of peritoneal fluid and also the gravity.
In cases of peritoneal carcinomatosis deposits of
mucinous tumor in the right and left subphrenic spaces
and omentum are most commonly seen (Fig. 102.14).
Although deposition of the mucinous tumor cells on
bowel surfaces is uncommon, it can be seen at the
ileocecal region, the rectosigmoid junction, and the gas-
Fig. 102.11 Mesenteric panniculitis incidentally discovered on tric antrum.
CT as a confined area of hazy fat at the root of mesentery
(arrows)

Fig. 102.12 Sclerosing mesenteritis in a 65-year-old man with Fig. 102.13 Pseudomyxoma peritonei from ruptured appendiceal
chronic abdominal pain. CT study shows the mass (arrow) with mucin producing carcinoma. Notice the bulky nature of peritoneal
development of calcification and mesenteric retraction involvement
1584 F. Sokhandon et al.

Fig. 102.14 Peritoneal a b

carcinomatosis from ovarian
origin seen as peritoneal
depositions lateral to the liver
and in the left lower quadrant
(arrows)

On imaging, pseudomyxoma peritonei presents as

diffuse but heterogeneous peritoneal enhancement
with copious amount of mucinous ascites without sig-
nificant invasion of underlying tissues. Often scalloped
indentation of the surface of the liver and spleen is
noted. Unlike peritoneal carcinomatosis, there is a
rarely large nodular component (Levy 2009).

Endometriosis

Endometriosis is ectopic implantation of functioning

endometrial tissue outside the uterine cavity, seen in
Fig. 102.15 Endometriosis seen as solid mass in right lower
women of reproductive age. One of the common sites abdominal wall with bladder involvement (arrow). Patient has
of involvement is the serosal surface of the ovaries; history of cesarean section
other common locations are the fallopian tubes, pelvic
peritoneum, and pelvic ligaments. Implantation of
endometrial tissue in the atypical locations has also T1-weighted with mixed intensity on T2-weighted
been described, including the abdominal wall, abdomi- images. Endometrial implants can present with a low
nal peritoneum, gastrointestinal and urinary tract, and T1- and T2-weighted signal intensity rim due to periph-
also in the chest (Woodward et al. 2001; Hensen et al. eral fibrosis (Kataoka et al. 2005; Busard et al. 2010).
2006; Yantiss et al. 2001; Joseph and Sahn 1996).
Endometrial implants can be seen on the serosal surface
of other organs most commonly the peritoneal lining Splenosis
around the rectovaginal pouch (Olive and Schwartz
1993). The ectopic endometrium is responsive to ovarian Splenosis is the ectopic autotransplantation of splenic
hormones resulting in cyclic pattern of symptoms. The tissue and occurs in 16–67% of patients after traumatic
serosal implants of endometrium with recurrent cyclic splenic rupture or splenic surgery (Kok et al. 2008).
bleeding can incite inflammatory reaction resulting in Implantation usually occurs along the peritoneum in
adhesions and fibrosis. The presenting symptoms vary the abdomen and pelvis (Tsitouridis et al. 2010); how-
based on the involved organ (Sonavane et al. 2011). ever, hematogenous spread to the lung and liver has
CT findings are usually nonspecific and can appear also been reported (Pekkafali et al. 2002; Backhus and
as cystic, solid (Fig. 102.15) or mixed with or without Bremner 2006).
foci of calcification. On MRI, the appearance of Splenosis is a benign condition that could poten-
endometrioma depends on the age of hemorrhage and tially be mistaken for a neoplastic process; therefore,
stage of blood product degradation. However, the most knowledge of prior splenic injury, trauma, and
common appearance is high signal intensity on splenectomy would be beneficial to diagnose this
Mesentery, Omentum, Peritoneum: Inflammatory, Infectious Diseases and Pseudo Lesions 1585

Fig. 102.16 Splenosis. This a b

patient with remote history of
traumatic splenic rupture and
splenectomy was discovered
to have multiple peri-hepatic
and left upper quadrant
peritoneal nodules. There is
also one nodule within the
fissure for ligamentum
venosum seen on CT. Note
some of the nodules on the
liver capsule mimic
intrahepatic lesions. Contrast-
enhanced CT, T2-weighetd
MR, and post-contrast T1-
weighted fat saturated images c d
show enhancing
intraperitoneal nodules proven
also by isotope tagged RBC
study to be due to splenosis

condition. These lesions follow the attenuation and without any identifiable acute inflammatory process
enhancement pattern of the normal splenic tissue on or with mild (less than 5 mm) wall thickening of the
CT imaging with slight heterogeneous enhancement terminal ileum on imaging. Secondary mesenteric ade-
on arterial phase and homogeneous enhancement on nitis, as defined by Macari et al. is enlarged mesenteric
portal-venous phase. On MRI, these lesions are lymph nodes associated with an identifiable inflamma-
T1 hypointense and T2 hyperintense, and enhance tory condition on imaging such as celiac disease,
more avidly than the liver on post-contrast images appendicitis, or Crohn’s disease (Macari et al. 2002).
(Fig. 102.16). It has been described that intrahepatic Primary mesenteric adenitis is an infectious
splenosis demonstrates a characteristic hypointense nodal enlargement and may be caused by viruses,
rim on T1- and T2-weighted images which represent bacteria (e.g., Yersinia, Salmonella), or mycobacteria
a thin layer of fat or fibrous capsule around (Rao et al. 1997). In most cases of primary mesenteric
these lesions (De Vuysere et al. 2000; Gruen and adenitis, an underlying infectious terminal ileitis is
Gollub 1997). thought to be present (Rao et al. 1997; Jelloull et al.
1997; Lee et al. 1997; Garcia-Corbeira et al. 1995;
Koruda et al. 1988; Kunkel et al. 1984; Puylaert 1986).
Mesenteric Adenitis Secondary mesenteric adenitis could be a result of an
infectious or noninfectious process. Infectious causes
Mesenteric adenitis is defined as three or more lymph of secondary mesenteric adenitis include Clostridium
nodes with a longest diameter of 5 mm or more clus- difficile, Tuberculosis (Fig. 102.17), and nontuberculous
tered in the right lower quadrant mesentery (Macari mycobacterial infection (e.g., Mycobacterium avium
et al. 2002). Two distinct types of mesenteric adenitis Intracellular complex in immune compromised status
have been described. Primary mesenteric adenitis is as seen in AIDS patients) (Johnson et al. 2009).
defined as a right-sided mesenteric lymphadenopathy Noninfectious causes of secondary mesenteric adenitis
1586 F. Sokhandon et al.

Fig. 102.17 Mesenteric a b

adenitis secondary to ileocecal
tuberculosis. Notice
circumferential thickening of
the cecum along with
thickened adjacent mesentery
(white arrows). Note
peripheral rim enhancement of
enlarged mesenteric node
(black arrow)

include appendicitis, diverticulitis, Crohn’s disease, Church JM. Mucosal ischemia caused by desmoid tumors in
ulcerative colitis, celiac disease, immune reconstitution patients with familial adenomatous polyposis: report of four
cases. Dis Colon Rectum. 1998;41(5):661–3.
inflammatory syndrome, mesenteric panniculitis, pan- De Vuysere S, Van Steenbergen W, Aerts R, et al. Intrahepatic
creatitis, cholecystitis, and connective tissue disorders splenosis: imaging features. Abdom Imaging. 2000;25:187–9.
(Macari et al. 2002; Suri et al. 1999; Yang et al. 1999). Emory TS, Monihan JM, Carr NJ, et al. Sclerosing mesenteritis,
mesenteric panniculitis and mesenteric lipodystrophy:
a single entity? Am J Surg Pathol. 1997;21(4):392–8.
Garcia-Corbeira P, Ramos JM, Aguado JM, et al. Six cases in
Tuberculous Adenitis which mesenteric lymphadenitis due to nontyphi Salmonella
caused an appendicitis-like syndrome. Clin Infect Dis.
Four patterns of the tuberculosis-related abdominal 1995;21:231–2.
Gruen DR, Gollub MJ. Intrahepatic splenosis mimicking hepatic
adenitis have been described on imaging: (a) peripheral adenoma. AJR Am J Roentgenol. 1997;168:725–6.
rim enhancement of enlarged lymph nodes, (b) Han SY, Koehler RE, Keller FS, et al. Retractile mesenteritis
nonhomogeneous enhancement of lymph nodes, (c) involving the colon: pathologic and readiologic correla-
homogeneous enhancement, and (d) homogeneous but tion (case report). AJR Am J Roentgenol. 1986;147
(2):268–70.
nonenhancing lymph nodes (Pombo et al. 1992). The Hensen JH, Van Breda Vriesman AC, Puylaert JB. Abdominal
most common pattern has been described as peripheral wall endometriosis: clinical presentation and imaging
rim enhancement of enlarged lymph nodes (Fig. 102.17). features with emphasis on sonography. AJR.
2006;186:616–20.
Hertzberg BS, Kliewer MA, Paulson EK. Ovarian cyst rupture
causing hemoperitoneum: imaging features and the potential
for misdiagnosis. Abdom Imaging. 1999;24:304–8.
References Jadvar H, Mindelzun RE, Olcott EW, Levitt DB. Still the great
mimicker: abdominal tuberculosis. AJR Am J Roentgenol.
Backhus LM, Bremner RM. Images in clinical medicine. Intra- 1997;168:1455–60.
thoracic splenosis after remote trauma. N Engl J Med. Jelloull L, Fremond B, Dyon JF, et al. Mesenteric adenitis caused
2006;355(17):1811. by Yersinia pseudotuberculosis presenting as an abdominal
Bonnet JP, Basset T, Dijoux D. Abdominal inflammatory mass. Eur J Pediatr Surg. 1997;7:180–3.
myofibroblastic tumors in children: report of an appendiceal Johnson LA, Longacre TA, Wharton Jr KA, et al. Multiple
case and review of the literature. J Pediatr Surg. mesenteric lymphatic cysts: an unusual feature of mesenteric
1996;31:1311–4. panniculitis (sclerosing mesenteritis). J Comput Assist
Burke AP, Sobin LH, Shekitka KM, et al. Intra-abdominal Tomogr. 1997;21(1):103–5.
fibromatosis: a pathologic analysis of 130 tumors with Johnson PT, Horton KM, Fishman EK. Nonvascular mesenteric
comparison of clinical subgroups. Am J Surg Pathol. disease: utility of multidetector CT with 3D volume render-
1990;14(4):335–41. ing. Radiographics. 2009;29:721–40.
Busard MP, Mijatovic V, van Kuijk C, et al. Appearance of Joseph J, Sahn SA. Thoracic endometriosis syndrome: new
abdominal wall endometriosis on MR imaging. Eur Radiol. observations from an analysis of 110 cases. Am J Med.
2010;20(5):1267–76. 1996;100:164–70.
Casillas VJ, Amendola MA, Gascue A, et al. Imaging of Kataoka ML, Togashi K, Yamaoka T, et al. Posterior cul-de-sac
nontraumatic hemorrhagic hepatic lesions. Radiographics. obliteration associated with endometriosis: MR imaging
2000;20(2):367–78. evaluation. Radiology. 2005;234(3):815–23.
Mesentery, Omentum, Peritoneum: Inflammatory, Infectious Diseases and Pseudo Lesions 1587

Kawashima A, Fishman EK, Hruban RH, et al. Mesenteric Pickhardt PF, Bhalla S. Unusual nonneoplastic peritoneal and
panniculitis presenting as a multilocular cystic mesenteric sub-peritoneal conditions: CT findings. Radiographics.
mass: CT and MR evaluation. Clin Imaging. 1993;17 2005;25:719–30.
(2):112–6. Pombo F, Rodriguez E, Mato J, et al. Patterns of contrast
Kawashima A, Goldman SM, Fishman EK, et al. CT of enhancement of tuberculous lymph nodes demonstrated by
intraabdominal desmoid tumors: is the tumor different in computed tomography. Clin Radiol. 1992;46:13–7.
patients with Gardner’s disease? AJR Am J Roentgenol. Puylaert JB. Mesenteric adenitis and acute terminal ileitis:
1994;162:339–42. US evaluation using graded compression. Radiology.
Kok J, Lin M, Lin P, et al. Splenosis presenting as multiple 1986;161:691–5.
intra-abdominal masses mimicking malignancy. ANZ Rao PM, Rhea JT, Novelline RA. CT diagnosis of mesenteric
J Surg. 2008;78:406–7. adenitis. Radiology. 1997;202:145–9.
Koruda MJ, Bell LM, Ross III AJ. Atypical mycobacterial Riddel RH, Petras RE, Williams GT, et al. Tumors of the
mesenteric lymphadenitis in childhood presenting as an intestine. In: Atlas of tumor pathology, (3rd ser. fasc. 32).
abdominal mass. J Pediatr Surg. 1988;23:526–8. Washington, DC: Armed Forces Institute of Pathology; 2003.
Kunkel MJ, Brown LG, Bauta H, et al. Meningococcal mesen- Rybolt AH, Bennet RG, Laughon BE, et al. Protein losing
teric adenitis and peritonitis in a child. Pediatr Infect Dis. enteropathy associated with Clostridium difficile colitis.
1984;3:327–8. Lancet. 1989;1:1353.
Lata J, Stiburek O, Kopacova M. Spontaneous bacterial perito- Sabate JM, Torrubia S, Maideu J, et al. Sclerosing mesenteritis:
nitis: a severe complication of liver cirrhosis. World imaging findings in 17 patients. AJR Am J Roentgenol.
J Gastroenterol. 2009;15(44):5505–10. 1999;172(3):625–9.
Lee JH, Rhea PL, Lee JK, et al. The etiology and clinical Shirkhoda A, Leyendecker JR. The peritoneum, retroperitoneum
characteristics of mesenteric adenitis in Korean adults. and their fascial planes. In: Shirkhoda A, editor. Variants and
J Korean Med Sci. 1997;12:105–10. pitfalls in body imaging. 2nd ed. Philadelphia: Lippincott
Levy A. Peritoneum and mesentery – Part II – Pathology. Pub- Williams & Wilkins; 2011. p. 404–32.
lication date 28 Aug 2009. http://www.radiologyassistant.nl/ Slavotinek JP, Bourne AJ, Sage MR, et al. Inflammatory
en/4a6c7bba1ef26. Accessed 17 Oct 2011. pseudotumor of the pancreas in a child. Pediatr Radiol.
Levy S, Sauvanet A, Diebold M, et al. Spontaneous regression of 2000;30:801–3.
an inflammatory pseudotumor of the liver presenting as an Sonavane SK, Kantawala KP, Menias CO. Beyond the
obstructing malignant biliary tumor. Gastrointest boundaries-endometriosis: typical and atypical locations.
Endosc. 2001;53:371–4. Curr Probl Diagn Radiol. 2011;40(6):219–32.
Levy A, Rimola J, Mehrotra AK, et al. From the archives of the Suri S, Gupta S, Suri R. Computed tomography in abdominal
AFIP. Benign fibrous tumors and tumorlike lesions of tuberculosis. Br J Radiol. 1999;72(853):92–8.
the mesentery: radiologic-pathologic correclation. Radio- Torzilli G, Inoue K, Midorikawa Y, et al. Inflammatory
graphics. 2006;26:245–64. pseudotumors of the liver: prevalence and clinical impact in
Lubner MG, Pickhardt PJ. Peritoneal sarcoidosis: the role of surgical patients. Hepatogastroenterology. 2001;48:1118–23.
imaging in diagnosis. Gastroenterol Hepatol. 2009;5 Tsitouridis I, Michaelides M, Sotiriadis C, et al. CT and MRI of
(12):861–3. intraperitoneal splenosis. Diagn Interv Radiol. 2010;16
Lucey BC, Varghese JC, Soto JA. Spontaneous hemoperitoneum: (2):145–9.
causes and significance. Curr Probl Diagn Radiol. Tsourous G, Raftopoulos LG, Kafe EE, et al. A case of
2005;34(5):182–95. pseudomembranous colitis presenting with massive ascites.
Macari M, Hines J, Balthazar E, et al. Mesenteric adenitis: CT Eur J Intern Med. 2007;18:328–30.
diagnosis of primary versus secondary causes, incidence, and Valls C. Fat-ring sign in sclerosing mesenteritis. AJR Am J
clinical significance in pediatric and adult patients. AJR. Roentgenol. 2000;174(1):259–60.
2002;178:853–8. Warshauer DM, Lee JKT. Imaging manifestations of abdominal
Mortele KJ, Cantisani V, Brown DL, et al. Spontaneous intra- sarcoidosis. AJR. 2004;182:15–28.
peritoneal hemorrhage: imaging features. Radiol Clin North Woodward PJ, Sohaey R, Thomas P, et al. Endometriosis: radio-
Am. 2003;41(6):1183–201. logic-pathologic correlation. Radiographics. 2001;21:193–216.
Ng SH, Wong HF, Ko SF, et al. Retractile mesenteritis with Yang ZG, Min PQ, Sone S, et al. Tuberculosis versus lympho-
colon and retroperitoneum involvement: CT findings. mas in the abdominal lymph nodes: evaluation with contrast-
Gastrointest Radiol. 1992;17(4):333–5. enhanced CT. AJR. 1999;172:619–23.
Olive DL, Schwartz LB. Endometriosis. N Engl J Med. Yantiss RK, Clement PB, Young RH. Endometriosis of the
1993;328:1759–69. intestinal tract: a study of 44 cases of a disease that
Pekkafali Z, Karsli AF, Silit E, et al. Intrahepatic splenosis: may cause diverse challenges in clinical and pathologic
a case report. Eur Radiol. 2002;12(suppl 3):S62–5. evaluation. Am J Surg Pathol. 2001;25:445–54.