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ploic appendage torsion or spontaneous thrombosis of the epiploic appendage central draining vein resulting in vascular occlusion and focal inflammation [5–7, 12, 13]. In some cases of epiploic appendagitis, inflammation may be present without any vascular impairment [6, 14, 15].
The reported age range for primary epiploic appendagitis is 12–82 years, with a peak in incidence in the fifth decade. Primary epiploic appendagitis is more common in obese patients and women [3, 4]. Primary epiploic appendagitis occurs more frequently in the sigmoid colon than in the cecum or ascending colon and is uncommon in the transverse colon [3, 5, 16]. Epiploic appendages may cause incarcerated hernia; a case has been reported of an epiploic appendagitis within an incisional hernia sac [10].
Primary epiploic appendagitis usually presents as an abrupt onset of focal abdominal pain in the lateral lower quadrants, is nonmigratory, and worsens with cough and abdominal stretching [2, 3, 11, 17]. Appetite and bowel function are usually unchanged; nausea and vomiting are rare [6, 16]. On physical examination, the patient will present with localized tenderness without significant guarding or rigidity. The patient also may have a lowgrade fever [3, 18]. WBC count is usually normal or slightly elevated [2]. Heavy exercise has been reported as a predisposing factor [2, 4, 6].
Primary epiploic appendagitis is difficult to diagnose clinically because of the lack of pathognomonic clinical features and can simulate a case requiring surgery [3, 4].
Epiploic Appendagitis: An Entity Frequently Unknown to Clinicians—Diagnostic Imaging, Pitfalls, and Look-Alikes
Ana Teresa Almeida1
Lina Melão Barbara Viamonte Rui Cunha José Miguel Pereira
Almeida AT, Melão L, Viamonte B, Cunha R, Pereira JM
1All authors: Department of Radiology, Faculdade de Medicina da Universidade do Porto, Hospital São João, Alameda Professor Hernâni Monteiro, 4200-451 Porto, Portugal. Address correspondence to L. Melão (lina_melao@hotmail.com).
Gastrointest ina l Imaging • Review
AJR 2009; 193:1243–1251
0361–803X/09/1935–1243
© American Roentgen Ray Society
Epiploic appendages, also known as epiploicae appendices, are 50–100 pedunculated fatty structures arranged in two separate
longitudinal rows next to the anterior and posterior tenia coli over the external aspect of the colon [1–4]. Epiploic appendages extend from the cecum to the rectosigmoid junction and are covered by the peritoneum [1, 4–8]. The greatest concentration of epiploic appendages is in the cecum and sigmoid colon but spares the rectum [5, 9]. Epiploic appendages are between 1–2 cm thick, 0.5–5 cm long, and larger on the left side of the colon than on the right side [3]. Each epiploic appendage is supplied by one or two small end arteries branching from the vasa recta longa of the colon and is drained by a tortuous vein passing through its narrow pedicle [2–4]. Their limited blood supply, together with their pedunculated shape and excessive mobility, make epiploic appendages prone to torsion and ischemic or hemorrhagic infarction [1, 2, 4, 8, 10].
Epiploic AppendagitisAppendagitis is a term denoting primary
or secondary inflammation of the epiploic appendages [6].
Primary Epiploic AppendagitisPrimary epiploic appendagitis is an ischemic
infarction of an epiploic appendage and an uncommon cause of abdominal pain that has been recognized relatively recently [11]. Primary epiploic appendagitis is caused by epi
Keywords: appendagitis, appendicitis, diverticulitis, omental infarction
DOI:10.2214/AJR.08.2071
Received November 8, 2008; accepted after revision April 12, 2009.
This article was prepared based on an educational exhibit that won the Magna Cum Laude award at the 2007 annual meeting of the European Society of Gastrointestinal and Abdominal Radiology.
OBJECTIVE. Epiploic appendagitis is an ischemic infarction of an epiploic appendage caused by torsion or spontaneous thrombosis of the epiploic appendage central draining vein. When it occurs on the right side of the abdomen, it can mimic appendicitis and rightsided diverticulitis; whereas when it occurs on the left side of the abdomen, it is often mistaken for sigmoid diverticulitis. The purpose of this article is to review the diagnostic imaging of this entity.
CONCLUSION. Epiploic appendagitis is selflimited and spontaneously resolves without surgery within 5–7 days. Therefore, it is imperative for radiologists to be familiar with this entity.
Almeida et al.Imaging of Epiploic Appendagitis
Gastrointestinal ImagingReview
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Rightsided primary epiploic appendagitis is often confused with acute appendicitis or rightsided diverticulitis; whereas leftsided primary epiploic appendagitis is often confused with sigmoid diverticulitis [3, 4, 18].
In the past, diagnosis of epiploic appendagitis was often the result of an unexpected finding during an exploratory laparotomy [3]. Today, this condition is usually diagnosed by ultrasound or CT, with the latter more sensitive and specific. Although ultrasound has the advantage of correlating the location of the lesion with the location of maximum tenderness, CT
should be used to confirm the fatty nature of the lesion before making a definite diagnosis of primary epiploic appendagitis. With the increasing use of CT for assessing cases of acute abdominal pain, the diagnosis of epiploic appendagitis is now more common [18, 19].
Primary epiploic appendagitis is selflimited in the majority of patients and spontaneously resolves within 5–7 days. Rarely, acute epi ploic appendagitis may result in adhesion, bowel obstruction, intussusception, intraperitoneal loose bodies, peritonitis, or abscess formation [3, 5]. Primary epiploic appendagitis does not require surgery, and treatment is based on the patient’s symptoms [4, 5, 7, 13, 15]. Misdiagnosis may lead to unwarranted surgery, medical treatment, and hospitalization [4].
Secondary Epiploic AppendagitisIn secondary epiploic appendagitis, the
epiploic appendage is inflamed because of another process, such as diverticulitis, appendicitis, pancreatitis, or cholecystitis. Management of secondary epiploic appendagitis is based on treatment of the primary abnormality [1, 2, 4, 7].
Imaging FindingsThe diagnosis of acute epiploic appendagi
tis primarily relies on crosssectional CT, although ultrasound and MRI are occasionally used [11, 19].
CTIn CT of a healthy patient, the epiploic ap
pendages blend in with the surrounding pericolic fat but become apparent when surrounded by ascites (Fig. 1) or inflammation [3, 5, 8]. An infarcted or inflamed epiploic appendage on CT appears as a 1–4 cm ovoid pericolic lesion with fat density surrounded by inflammatory changes and abuts the anterior colonic wall [1, 3, 5, 11, 15]. Primary epiploic appendagitis may have a lobular appearance because of two or more affected, contiguous epiploic appendages with hyperattenuated rings lying in proximity [19].
A 2–3 mm hyperdense rim surrounding the ovoid mass on CT (hyperattenuating ring sign) represents the inflamed visceral peritoneal covering of the epiploic appendage and is diagnostic of primary epiploic appendagitis [13, 15]. The hyperdense rim surrounding the ovoid mass on CT corresponds to the hypoechoic halo on ultrasound [13, 15, 19] (Figs. 2–6). Thickening of the parietal peritoneum secondary to the spread of inflammation may be observed [3, 5–7].
Fat stranding is more pronounced than wall thickening because the paracolonic inflammatory changes are disproportionately more severe than the mild local reactive thickening of the adjacent colonic wall (Figs. 2–6). Wall thickening of the adjacent side of the colon is asymmetric [1, 4, 8] (Figs. 2 and 3).
A central, hyperattenuating, illdefined round area (“central dot sign”) or a longitudinal linear area corresponds to engorged or thrombosed central vessels or central areas of hemorrhage or fibrosis (Figs. 2–4). Although the presence of a central dot or linear area is useful for diagnosis, their absence does not exclude the diagnosis of acute epiploic appendagitis [4–6, 11, 19, 20].
The central dot may have high attenuation because the infarcted tissue tends to calcify. Calcification may be eggshell in shape and may become detached and appear as a peritoneal loose body in the abdominal cavity [1, 3, 16, 21]. The calcified tissue may reattach itself to a surface, such as the lower aspect of the spleen, in which case it is called a “parasitized epiploic appendage” [3]. The smooth surface and calcified consistency of the epiploic appendage help to distinguish it from a metastatic lesion (Fig. 7).
UltrasoundAt the site of maximum tenderness, a non
compressible hyperechoic small ovoid or round solid mass of adipose tissue is seen be
Fig. 1—54-year-old man with hepatic cirrhosis. Unenhanced CT image shows several epiploic appendices (arrowhead) outlined by ascites. Arrow indicates normal central vein.
A
Fig. 2—Epiploic appendagitis in 46-year-old man.A and B, Axial contrast-enhanced CT images show severe fat stranding (arrowhead) and fatty ovoid mass (curved arrow) with hyperattenuated rim and central dot (thin straight arrow). Associated thickening of colonic wall (open arrow) is mild.
B
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tween the colon and the abdominal wall in the anterior or anterolateral compartment of the abdomen [1, 6, 22] (Fig. 8). In most cases, a mass effect is seen either on the adjacent bowel or in the anterior parietal peritoneum. Changes to the colonic wall are not seen [12]. The lesion is adherent to the colonic wall, is frequently surrounded by a hypoechoic border (Fig. 8), and does not have central blood flow on Doppler ultrasound [4, 12]. The absence of a Doppler signal because of a lack of blood flow as a result of torsion in epiploic appendagitis is a useful finding to differentiate epiploic appendagitis from acute diverticulitis [12].
MRIThe involved epiploic appendage is hyper
intense on unenhanced T1weighted imaging but is slightly less intense than normal peritoneal fat. Epiploic appendages show marked loss of signal on fatsuppressed T2weighted
images, confirming the fatty nature of the lesion [23].
In epiploic appendagitis, the thin peripheral rim and the perilesional inflammatory changes appear hypointense on T1weighted imaging, appear hyperintense on T2weighted imaging, and show marked enhancement on contrastenhanced T1weighted fatsuppressed images, whereas the central draining vein usually has low signal on both T1weighted and T2weighted imaging [23].
Differential DiagnosisIn epiploic appendagitis, there is much
more fat stranding than bowel wall thickening. In patients with acute abdominal pain, the finding of fat stranding that is disproportionate suggests a relatively narrow differential diagnosis: diverticulitis; omental infarction; appendicitis; and, less commonly, mesenteric panniculitis and primary tumors and metastases to the omentum.
DiverticulitisDiverticula are herniations of the mucosa
and submucosa through the muscular layers of the bowel wall in areas of bowel wall weakness (between the mesenteric and antimesenteric taeniae) and high pressure gradient (caused by dehydrated stools) [8, 24]. Diverticula occur at the point where blood vessels (vasa recta) penetrate the colon wall [24].
Diverticulitis occurs when a diverticulum becomes obstructed, with subsequent focal inflammation, diverticular distention, localized ischemia, and perforation [24]. Typically, perforation of the colonic wall is confined and restricted, leading to peridiverticular and extracolonic inflammation that is more severe than the inflammation of the colon itself [8]. However, the course of the disease may be complicated by abscess formation, hemorrhage, pneumoretroperitoneum, fistula formation, and postinflammatory stenosis.
Fig. 3—Primary epiploic appendagitis in 23-year-old man with clinical diagnosis of presumed colonic diverticulitis. Axial contrast-enhanced CT scan shows pericolonic fatty lesion surrounded by hyperattenuating ring (thick arrow) containing central hyperattenuating area (thin arrow) corresponding to thrombosis and hemorrhagic changes and very mild thickening of colonic wall (open arrow).
Fig. 4—Acute epiploic appendagitis with hyperattenuating center in 31-year-old woman. Axial contrast-enhanced CT image shows lesion (arrow) that abuts sigmoid colon and has central focal area of hyperattenuation with surrounding inflammation.
Fig. 5—40-year-old man with acute epiploic appendagitis with hyperattenuating ring sign (thick arrow) adjacent to left colon without significant involvement of colonic wall. Severe and disproportionate fat stranding (thin arrow) is seen nearby.
Fig. 6—Acute epiploic appendagitis (arrow) with hyperattenuating ring sign adjacent to sigmoid colon without significant involvement of colonic wall in 52-year-old man.
Fig. 7—CT image shows small calcified body (arrow) adjacent to normal epiploic appendices, probably residual to anterior epiploic appendagitis in 59-year-old man.
Fig. 8—Sonogram in 22-year-old man shows hyperechoic small mass (asterisk) surrounded by hypoechoic border (arrow) corresponding to hyperattenuating ring on CT scans at site of maximum tenderness, located anteriorly between colon and abdominal wall.
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Diverticula can be found anywhere in the colon, but the majority are located in the distal descending and sigmoid colon; hence, most cases (95%) of diverticulitis are located in the left side of the abdomen. A minority of diverticula (5%) are located on the right side of the abdomen, which for unknown reasons has a predilection for patients of Asian descent. The transverse colon is rarely affected, whereas the rectum is completely spared from diverticula formation [8].
The most common CT finding of acute diverticulitis is paracolic fat stranding. Other typical CT findings include an illdefined or blurry diverticulum in the region where the fat stranding is most pronounced (Figs. 9 and 10); mild wall thickening (usually < 5 mm), commonly more pronounced on the side of the offending diverticulum and usually affecting a large colonic segment greater than 5 cm (Figs. 9 and 10); thickened base of the sigmoid mesocolon with fluid (“comma sign”) (Figs. 9 and 10); and engorged vessels supplying the affected segment (“centipede sign”) [8]. Other findings detected by CT include pericolic abscess, smallbowel obstruction, free intraperitoneal or extraperitoneal gas, colovesical fistula, thrombosis of the mesenteric or portal veins caused by pyophlebitis, and hepatic abscess formation. In some instances, small localized collections of gas are identified adjacent to the colonic wall and indicate localized pericolic perforation [17] (Figs. 11 and 12). In cases of complicated diverticulitis, surgical management may be required.
Features that help discern the differential diagnosis—Although their clinical manifestations are similar, acute epiploic appendagitis tends to occur in younger patients, whereas acute diverticulitis frequently affects older patients (> 50 years). Patients with diverticulitis are more likely to experience nausea, vomiting, fever, rebound tenderness, and more diffuse lower abdominal pain. Only a minority (7%) of patients with acute epiploic appendagitis have leukocytosis, whereas most patients with acute diverticulitis have an elevated WBC count [5].
In cases of acute epiploic appendagitis, the involved colonic segment is short; however, in cases of acute diverticulitis, a lengthy segment of thickened colonic wall is a typical CT feature [8].
The classic complications of diverticulitis (extramural abscesses, sinus tract and fistula formation, bowel obstruction, perforation, and peritonitis) are rare in the setting
of acute epiploic appendagitis [5, 17] (Figs. 11 and 12).
Features that complicate the differential diagnosis—Both epiploic appendagitis and acute diverticulitis frequently present with a sudden focal leftsided tenderness. Moreover, the two conditions can be seen simultaneously because the inflammation from an acute diverticulitis may extend to involve the epiploic appendages [4, 5, 7] (Fig. 12).
Omental InfarctionThe greater omentum consists of a four
layered fold of peritoneum that covers the colon and small bowel in the peritoneal cavi
ty, acting as a barrier to generalized spread of intraperitoneal infection or tumor. It contains fat and vascular structures (Fig. 13).
Omental infarctions are rare because abundant collateral vessels perfuse the omentum [25]. The cause of omental infarction is unclear but may be similar in pathophysiology to the cause of primary epiploic appendagitis [9]. Omental infarction occurs when there is an interruption of arterial blood supply to the omentum, possibly because of omental torsion, venous insufficiency due to trauma, or spontaneous thrombosis of the omental veins [5, 26]. Rightsided epiploic vessels are involved in 90% of the cases and are thought to be caused
A
Fig. 9—61-year-old man with diverticulitis.A and B, Axial contrast-enhanced CT images show mild stranding of pericolonic fat (asterisk). Fuzzy (thick arrow, B) and normal diverticula (thin arrows) are seen.
B
A
Fig. 10—52-year-old woman with diverticulitis.A and B, Transverse contrast-enhanced CT images show engorgement of vasa recta feeding sigmoid colon (“centipede sign,” open arrow, B). Notice mild wall thickening of colon, with fuzzy (curved arrow, A) and normal (thin arrows) diverticula and fluid by side of root of sigmoid mesentery (arrowhead, B). “Comma sign” (thick arrow, A) and disproportionate fat stranding (asterisk, A) are also seen.
B
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by the omentum being longer and more mobile on the right side [21]. Precipitating factors include obesity, recent abdominal surgery, strenuous activity, congestive heart failure, digitalis administration, and abdominal trauma [5, 12, 27]. However, most cases of omental infarction are idiopathic [16] (Fig. 13).
Omental infarctions are usually localized to the right upper and lower quadrants and clinically mimic cholecystitis and appendicitis, respectively [16, 26, 28]. A few cases of leftsided omental infarction have also been described [28].
Omental infarction more commonly affects elderly obese patients, with a slight predilection for men [16]. Omental infarction usually presents with acute abdominal pain with normal or mildly elevated WBC count. Other presenting symptoms include nausea, vomiting, anorexia, diarrhea, and fever [21].
CT findings of omental infarction range from a subtle, focal, hazy softtissue infiltration of the omentum [25, 29] to a solitary large, cakelike, nonenhancing, heterogeneous, and highattenuating fatty mass centered in the great omentum [8, 13, 21] (Figs. 14–17). Omental infarctions are usually located in the right upper or lower quadrants, deep in relation to the abdominal wall, anterior to the transverse colon, or anteromedial to the ascending colon. Colonic involvement depends on the anatomic location of the infarcted omentum relative to the colon [8, 11, 13, 26] (Figs. 14–16). Reactive bowel wall thickening may occur, although the inflammatory process in the omentum is usually disproportionately more severe [8, 21, 26]. Omental torsion is implicated as a cause of omental infarction when a whirled pattern of concentric linear strands is seen on CT [21].
In most cases of omental infarction, the process is selflimited, but surgery may be
indicated if symptoms persist or an associated abscess develops [27].
Features that help discern the differential diagnosis—Unlike acute epiploic appendagitis, which predominantly affects adults (> 20 years), omental infarction can occur in pediatric patients (15% of cases) [5].
On CT, omental infarction lacks the hyperattenuating ring and central dot seen in epiploic appendagitis [2, 5, 21, 28].
The focal lesion in acute epiploic appendagitis is often less than 5 cm long, may have a lobular appearance, and is frequently found adjacent to the sigmoid colon. The lesion in omental infarction is larger than that of epiploic appendagitis (averaging a diameter of up to 7 cm), cakelike, centered in the omentum, and commonly located medial to the cecum or the ascending colon [4–6, 19, 21].
The pain in acute epiploic appendagitis is typically in the inferior abdomen, whereas the pain in omental infarction is more common in the right side of the abdomen.
Features that complicate the differential diagnosis—The CT findings in both epiploic appendagitis and omental infarction may
overlap and the two entities cannot be differentiated. Nevertheless, the clinical relevance of such differentiation is limited because both conditions are selflimited and tend to resolve spontaneously [4, 28]. Treatment is conservative unless the infarcted omentum becomes infected [2].
Because they have the same common denominator of spontaneous fatty tissue
AFig. 11—45-year-old man with intraabdominal abscess. Contrast-enhanced CT image shows intraabdominal fluid–air collection (arrow). Diverticulitis was proven at surgery.
B
Fig. 12—52-year-old man with left-side diverticulitis.A–D, Contrast-enhanced CT images (A and C) with magnified images (B and D) show intraabdominal free air in large quantities (asterisk, A and C). Severe fat stranding, comma sign (curved arrow, A and B), and diverticula (thin arrows, A and B) are seen. Note intraabdominal fluid–air collection (open arrow, C and D) and secondary epiploic appendagitis (solid arrow, C and D).
C D
Fig. 13—Normal greater omentum in 63-year-old woman. Axial contrast-enhanced CT image shows normal layer of fat attenuation between transverse colon and anterior abdominal wall (arrow).
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necrosis, epiploic appendagitis and omental infarction have recently been proposed to be regrouped under the same new term, “intraabdominal focal fat infarction” or
“IFFI,” to stress that the differentiation is not clinically important and that the management of the two entities is conservative [9, 30].
AppendicitisIn the Western world, appendicitis is the
most common cause of acute abdominal pain that requires surgical intervention [31, 32]. The cause in the majority of cases is obstruction of the lumen of the appendix secondary to fecaliths, lymphoid hyperplasia, foreign bodies, parasites, and tumors [33]. After mechanical obstruction, the continued secretion of mucus results in luminal distention, venous engorgement, arterial compromise, and tissue ischemia. Luminal bacteria multiply and invade the appendiceal wall, causing transmural inflammation. Appendiceal infarction, microperforation, and extension of inflammation to the parietal peritoneum and adjacent structures are possible sequelae of appendicitis [8, 31, 33].
Appendicitis can affect all ages, although it is relatively rare at extremes of age, with the greatest incidence in the second decade of life [32, 33]. Appendicitis usually presents as a periumbilical pain of less than 5 days in duration and migrates to the right lower quadrant, associated with peritoneal irritation, anorexia, nausea, vomiting, diarrhea, and temperature greater than 37.5°C [34]. The WBC count may be elevated, but this is not seen in all cases of appendicitis.
Acute appendicitis presents on CT images as a thick fluidfilled appendix (> 6 mm outertoouter wall), with intramural gas, appendiceal wall thickening (wall thickness ≥ 3 mm), and a stratified appearance that may hyperenhance after contrast material administration [31, 35]. Endoluminal appendicoliths are present in one third of patients with appendicitis; their presence increases the likelihood of appendiceal perforation [31, 33]. Occasionally, an appendicolith may be identified in an otherwise normalappearing appendix [27].
Other associated CT signs of appendicitis are adjacent bowel wall thickening, cecal apical thickening (“cecal bar” and arrowhead signs), adjacent fat stranding, right lateral conal thickening, the presence of an abscess, and lymphadenopathy [8, 31, 32, 34] (Figs. 18 and 19).
Periappendicular fat stranding is typically mild to moderate, but the diagnosis of appendicitis is strongly implicated when severe fat stranding is found in the absence of substantial cecal or ileal thickening. A careful search for a thickened or focally perforated appendix will often confirm the diagnosis of appendicitis [8].
Features that help discern the differential diagnosis—Appendicitis affects all ages,
A B
B
Fig. 14—Acute omental infarction in 68-year-old woman.A–C, Ultrasound images show hyperechoic, nonmobile mass (arrows, A and C) located between anterior wall and colon.D, Axial contrast-enhanced CT image shows oval lesion with heterogeneous attenuation (arrow) separated from colon in right lower quadrant.
C D
Fig. 15—Omental infarction in 71-year-old man. CT image shows heterogeneous, cakelike fatty mass centered in omentum located in right upper quadrant anterior to and continuous with ascending colon (arrow). Reactive bowel wall thickening (arrowhead ) is seen.
Fig. 16—Omental infarction in 65-year-old man. CT image shows solitary heterogeneous and high-attenuation fatty mass centered in omentum (arrow) located deep in relation to rectus abdominis muscle and anterior to transverse colon.
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unlike acute epiploic appendagitis, which predominantly affects adults (> 20 years). Appendicitis has a more typical clinical presentation with periumbilical pain migrating to the right lower quadrant and is associated with anorexia and nausea. Patients with acute epiploic appendagitis usually do not present with significant guarding or rigidity on physical examination. Most patients with acute appendicitis have an elevated WBC count, whereas only a minority of patients with acute epiploic appendagitis have leukocytosis.
A definitive CT diagnosis of appendicitis can be made with the identification of an abnormal appendix or a calcified appendicolith
in association with pericecal inflammation [33]. Doppler ultrasound shows increased blood flow in contrast to absent blood flow in epiploic appendagitis [4, 12, 20].
Features that complicate the differential diagnosis—Classic presentation of acute appendicitis occurs in only 50–60% of patients, and the diagnosis may be missed or delayed in cases without the classic presentation [33]. In cases of perforated appendicitis, with peritonitis and abscess formation, the appendix may be difficult to see on imaging studies [8]. In early or mild appendicitis, the appendix may remain normal in size [35], and inflammatory stranding of the periappendicular fat may be the only finding.
Mesenteric PanniculitisMesenteric panniculitis is a subgroup of
sclerosing mesenteritis, consisting of nonspecific chronic inflammation and fibrosis of the fatty tissue of the bowel mesentery. Depending on the predominant tissue type in the mesenteric lesion, sclerosing mesenteritis can be categorized into three subgroups: mesenter
AFig. 17—Omental infarction in 51-year-old man. Transverse contrast-enhanced CT image shows inhomogeneous, ill-defined ovoid-shaped fatty mass (thin arrow) centered in greater omentum distant from descending colon wall (thick arrow).
B
Fig. 18—28-year-old man with appendicitis.A and B, Transverse unenhanced CT images show thickened appendix (short arrow) surrounded by marked fat stranding (asterisk). Note high-density appendicolith (long arrow, B).
A B
Fig. 19—24-year-old man with appendicitis.A, Axial contrast-enhanced CT image shows dilated appendix with abnormally enhanced wall (arrow).B and C, Longitudinal (B) and transverse (C) ultrasound images show enlarged (12 mm) appendix (arrow, C) that is noncompressible with hyperreflective adjacent fat (asterisk, C) suggesting local inflammation. Line in B indicates thickness of appendix.D, CT scan after IV and oral contrast administration in a different patient (41-year-old man) with appendicitis shows thickened appendiceal wall with wall enhancement (arrow) and fat stranding. Note enlargement of right vesical wall (arrowhead) caused by inflammatory process.
C
D
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ic panniculitis if inflammation pre dominates over fibrosis, mesenteric lipodystrophy if fat necrosis is the predominant process, and retractile mesenteritis if fibrosis and retraction predominate [5, 36, 37]. Retractile mesenteritis is considered the final, more invasive stage of mesenteric panniculitis complicated by fibrosis and retraction [36]. Progression from mesenteric panniculitis to retractile mesenteritis is difficult to predict but fortunately is rare [29]. In most patients, the condition consists of a mixture of chronic inflammation, fat necrosis, and fibrosis [8].
Most cases of mesenteric panniculitis occur in middle or late adulthood (mean age, ~ 60 years), with a slight male predominance [5, 37]. Mesenteric panniculitis may be entirely asymptomatic, but clinical manifestations may be related to the inflammation or its mass effect and include acute abdominal pain, fever, nausea, vomiting, diarrhea, and weight loss [5, 36, 37]. Mesenteric panniculitis can be found in 0.6% of all patients under
going abdominal CT for various indications. The pathogenesis is uncertain but can be associated with autoimmune disease, a paraneoplastic process, trauma, previous surgery, druginduced disease, infection, and thrombosis of mesenteric vessels [37].
Mesenteric panniculitis mainly involves the mesentery of the small bowel, especially at its root [25, 37, 38]. The CT findings of mesenteric panniculitis include a focal area of increased attenuation within the mesenteric fat surrounded by a thin pseudocapsule that is usually oriented to the left side [5, 37, 38]. Mesenteric panniculitis surrounds the mesenteric vessels and shows some regional mass effect by local displacement of smallbowel loops. The small softtissue nodules associated with mesenteric panniculitis are thought to correspond to lymph nodes scattered within the mesenteric mass, usually less than 5 mm in diameter [8, 26]. The “fatring sign” appears as lowdensity fat that surrounds vessels and nodules within the mesenteric mass
and represents preservation of normal fat density because of unaffected noninflamed fat [25, 26, 37, 38] (Fig. 20). The fatring sign is suggestive of mesenteric panniculitis but is nonspecific because it can be found in other entities such lymphoma [26]. Areas of fibrosis within the inflammation appear as linear bands of softtissue attenuation, resulting in spiculation that may be mistaken for a neoplastic process [5]. Calcification is uncommon and may be related to the fat necrosis [36]. The major complications of mesenteric panniculitis are related to the progressive fibrosis that may lead to shortening of the mesentery, compression of the mesenteric vessels, and bowelloop narrowing [5, 37].
Some features can help discern the differential diagnosis. Mesenteric panniculitis is not an acute abdominal condition and appears as a larger lesion. It is most commonly located in the root of the smallbowel mesentery that does not abut the colonic wall. Acute epiploic appendagitis, as the name im
A
Fig. 20—Mesenteric panniculitis in 57-year-old woman.A and B, Axial contrast-enhanced CT scans for colon cancer follow-up show soft-tissue nodules corresponding to enlarged lymph nodes within inflamed mesenteric fat (arrowheads).
B
A
Fig. 21—Well-differentiated liposarcoma in 61-year-old man.A and B, Contrast-enhanced CT scan (A) and ultrasound image (B) show well-circumscribed fatty mass (thick arrow) with enhancing capsule and internal septa that displaces mesenteric vessels (thin arrow, A).
B
A
Fig. 22—Peritoneal carcinomatosis in 52-year-old man.A and B, Axial contrast-enhanced CT scans show omental caking (asterisks, B), omental nodules (arrows), and small-volume ascites from gastric carcinoma.
B
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plies, is an acute disease seen as a small focal lesion anterior or anteromedial to the colon, abuts the colon wall, and does not involve the smallbowel mesentery [5].
Primary Tumors and MetastasesThere are many other possible causes for a
CT finding of a fatty mass or masslike lesion in the abdomen, such as liposarcoma (Fig. 21), dermoid and carcinoid tumor, lipoma, and omental metastases (Fig. 22).
Omental metastases can present as softtissue implants on peritoneal surfaces. “Omental cake” is the replacement of the omental fat by tumor infiltration and on CT appears as a thick, confluent softtissue mass closely adherent to the ventral surface of the transverse colon in the mid abdomen [25]. The presence of illdefined lesion margins, numerous lesions, a lesion centered in the omentum, and a history of primary neoplasm are useful for diagnosing omental metastasis [5] (Fig. 22). In patients with known malignancy, the diagnosis of acute epiploic appendagitis should only be made if there is a presentation with acute abdominal pain and no CT evidence of peritoneal metastatic disease elsewhere [2].
ConclusionEpiploic appendagitis is selflimiting, and
the appropriate management is conservative. In our experience, many clinicians are not familiar with this entity, and the radiologist can provide guidance for supportive management. Therefore, a noninvasive diagnosis of this relatively rare cause of acute abdomen is important for selecting the appropriate mode of management and preventing unnecessary hospital admission and surgery.
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