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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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Imaging of Epiploic Appendagitis

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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Almeida et al.

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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Imaging of Epiploic Appendagitis

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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Almeida et al.

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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Imaging of Epiploic Appendagitis

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

AJR:193, November 2009 1251

Imaging of Epiploic Appendagitis

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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