Patterns of Fat Stranding

Transcription

1 Residents Section Pattern of the Month Thornton et al. Patterns of Fat Stranding Residents Section Pattern of the Month Residents inradiology Patterns of Fat Stranding Eavan Thornton 1 Mishal Mendiratta-Lala ettina Siewert Ronald L. Eisenberg Thornton E, Mendiratta-Lala M, Siewert, Eisenberg RL Keywords: abdomen, CT, fat stranding DOI: /JR Received February 1, 2010; accepted after revision December 14, ll authors: Department of Radiology, eth Israel Deaconess Medical Center, Harvard Medical School, 330 rookline ve, oston, M ddress correspondence to R. L. Eisenberg (rleisenb@bidmc.harvard.edu). WE This is a Web exclusive article. JR 2011; 197:W1 W X/11/1971 W1 merican Roentgen Ray Society I n the setting of abdominal pain, whether acute or chronic, CT is helpful, and frequently essential, in discovering the underlying cause. Fat stranding is a common finding on CT of the abdomen and, when present, it directs the radiologist s attention to the site of pathology. However, there is a wide differential for this pattern. The following logical approach to abdominal fat stranding on CT can lead to the formulation of a succinct and accurate differential diagnosis: 1. What is the location of the fat stranding? 2. What other structures are involved in the process? 3. re there other characteristic CT findings of the diagnostic possibilities that suggest the most likely cause? Fat stranding refers to an abnormal increased attenuation in fat, (in the mesentery, omentum, retroperitoneum, or subcutaneous fat). The underlying pathophysiologic process is increased edema and engorgement of lymphatics. bdominal fat stranding can produce various appearances. Whereas mild inflammation may cause a subtle hazy increased attenuation of the fat (ground-glass like), increasing severity of the inflammation can produce a reticular pattern, with more well-defined linear areas of increased attenuation. reticulonodular appearance can also be observed frequently in association with neoplastic disease. Fat Stranding djacent to Thickened Loops of owel Diseases Originating in the Mesentery or Omentum Disease processes originating in the mesentery or omentum result in minimal bowel wall thickening and a disproportionate amount of adjacent fat stranding. These findings help to narrow the differential diagnosis to one of four conditions that cause acute abdominal pain: diverticulitis, acute appendicitis, epiploic appendagitis, and omental infarction. cute diverticulitis Occlusion of the neck of a diverticulum leads to inflammation with subsequent erosion and microperforation. Diverticula typically occur in the sigmoid colon but can develop in any portion of the large bowel and less frequently in the small bowel. In acute diverticulitis, the inflammatory process occurs in relation to the diverticulum, which protrudes through the wall of the bowel into the perienteric fat. Consequently, fat stranding is observed adjacent to focally thickened colon or small bowel adjacent to a diverticulum or a focally thickened segment with diverticula. Fat stranding and bowel wall thickening can be seen in varying degrees from minimal to extensive in acute diverticulitis (Fig. 1); however, intramural diverticulitis with minimal fat stranding can also occur. Other CT findings that have been described in acute diverticulitis are the comma sign (accumulation of fluid on the root of the sigmoid mesentery) and the centipede sign (engorgement of the mesenteric vessels). Small-bowel diverticula usually are seen to arise from the duodenum but can arise less frequently from the jejunum and ileum. These small-bowel diverticula can become inflamed, resulting in acute diverticulitis in a similar manner to the large bowel. Meckel diverticulum is the term for a congenital outpouching in the distal ileum at the site of an unobliterated yolk stalk. The well-known rule of 2s applies to this condition it is seen in 2% of the population, occurs 2 feet (61 cm) from the ileocecal valve, and is 2 inches (5 cm) long. Meckel diverticulum can be lined with gastric mucosa, which can potentially become ulcerated. Meckel diverticulum can also become inflamed in a manner similar to that in the colon (Fig. 2). JR:197, July 2011 W1

2 Thornton et al. Epiploic appendagitis Epiploic appendages are fat-containing peritoneal pouches typically between cm in length that arise from the serosal surface of the colon except the rectum, to which they are attached by a vascular stalk. They are arranged in two rows along the taenia longitudinales that extend from the cecum to the rectosigmoid junction. Epiploic appendages generally cannot be seen on CT unless they are inflamed or surrounded by free fluid. Each epiploic appendage is supplied by two arteries and one vein. ecause of their limited blood supply combined with their shape and mobility, they are prone to develop torsion, and ischemic or hemorrhagic infarc tion. Epiploic appendagitis most commonly affects the sigmoid colon. Rarely, it may occur in a hernial sac. The characteristic CT finding of acute epiploic appendagitis is an oval fatty mass, with a well-circumscribed hyperattenuated rim that represents the inflamed lining of the visceral peritoneum about the epiploic appendage (Fig. Fig. 1 Diverticulitis. Coronal reformatted image shows diverticulum (long arrow) arising from distal descending colon with mild surrounding fat stranding (short arrows). 3). Frequently there is also a central high-density dot that represents a thrombosed or engorged central vessel. However, the central dot sign is not required to make the diagnosis. Epiploic appendagitis usually presents with acute relatively severe abdominal pain in men predominantly in their 40s or 50s. ecause it is a self-limited disease, making the correct diagnosis avoids an unnecessary exploratory laparoscopy. CT findings generally take longer to resolve than the symptoms. lthough fatty changes will decrease in size on subsequent scans, abnormal CT Fig. 2 Meckel diverticulitis., Coronal reformatted image shows blind-ending tubular structure with hyperenhancing wall arising from ileum (long arrows), which represents inflamed Meckel diverticulum. There is mild surrounding fat stranding (short arrow)., Sagittal reformatted image shows origin of Meckel diverticulum (long arrows), which is surrounded by fat stranding (short arrow). W2 JR:197, July 2011

3 Patterns of Fat Stranding Fig. 3 Epiploic appendagitis in left lower quadrant. xial image shows oval fatty mass with well-circumscribed hyperattenuated rim, which represents inflamed lining of visceral peritoneum (arrow) with mild fat stranding in this location. Note that adjacent colonic wall is not thickened. Fig. 4 Omental infarction. Contrast-enhanced axial image shows focal rounded area of fat stranding in omentum in left upper quadrant (arrows). This subsequently resolved on follow-up abdominal CT scan obtained for another reason. findings have been described up to 18 months after the initial presentation. Epiploic appendages may completely calcify after the ischemic insult and result in calcified peritoneal loose bodies. Omental infarct Omental infarction is a rare cause of acute abdominal pain. Unlike epiploic appendagitis, which mainly affects adults, approximately 15% of cases of omental infarction occur in children. ecause of its supply by multiple collateral vessels (primarily branches of the right and left gastroepiploic arteries), the omentum infarcts less frequently than the small or large bowel. Infarction can be due to torsion of the right omental leaf or venous thrombosis or insufficiency. Predisposing factors to the development of an omental infarction include obesity, congestive heart failure, recent abdominal surgery, trauma, and strenuous activity. Omental infarction usually presents clinically with acute abdominal pain in the right upper or lower quadrant. On CT, there is usually a solitary non enhancing omental mass with heterogeneous fatty attenuation. The mass is centered on the omentum, frequently located deep in relation to the rectus abdominis muscle, and either anterior to the transverse colon or anteromedial to the ascending colon (Fig. 4). In contrast with acute diverticulitis, omental infarction is not usually associated with bowel wall thickening. Only rarely in omental infarction does the colonic wall become thickened due to spread of the inflammation from the omentum along its attachments on the tenia omentalis of the colon. Distinction from acute diverticulitis can be made by absence of an adjacent diverticulum, abscess, and bowel wall thickening. Omental infarction and epiploic appendagitis can have similar appearances on CT. In an omental infarct, there is no central dot sign. Moreover, omental infarction is most likely if the process occurs near the right colon or cecum, whereas epiploic appendagitis is more commonly seen in relation to the sigmoid and left colon. Omental infarction also tends to produce a larger abnormality in the fat (> 5 cm) than epiploic appendagitis. Differentiating these two conditions does not alter the treatment of the patient because both are managed conservatively. Therefore, some authors recommend the use of the umbrella term intraabdominal focal fat infarction when these two conditions cannot be reliably distinguished on CT. JR:197, July 2011 W3

4 Thornton et al. Fig. 5 Small bowel ischemia due to superior mesenteric vein thrombosis., There is abnormal loop of ileum in right lower quadrant (thick arrows). Wall of affected bowel is thickened with low-density center representing submucosal edema. There is mild surrounding fat stranding (thin arrows)., Filling defect in superior mesenteric vein (arrow) represents thrombus. Rim of enhancement around thrombus represents enhancing vessel wall, and fat stranding around affected vessel is due to edema. Diseases Originating in the owel owel ischemia Ischemia and infarction of the gastrointestinal tract are a heterogeneous group of disorders that have the unifying theme of hypoxia of the small bowel or colon. Ischemic bowel disease results from acute or chronic insufficiency of blood flow to the bowel and may result in severe complications, such as infarction and perforation. Improvements in cross-sectional imaging can provide earlier and more precise diagnosis, which is the key to reducing the morbidity and mortality of this potentially fatal condition. Patients with acute intestinal ischemia most often present with abdominal pain and other nonspecific symptoms, such as nausea, vomiting, diarrhea, and bloating. The diagnosis of acute bowel ischemia is often one of exclusion after more common abnormalities including bowel obstruction, appendicitis, diverticulitis, cholelithiasis, peptic ulcer disease, and gastroenteritis have been eliminated from consideration. cute bowel ischemia is more common in the geriatric population, especially in those with comorbid cardiovascular disease and other systemic dysfunction. mong the multiple causes of primary bowel ischemia are vascular occlusive processes, such as embolic disease, arterial or venous thrombosis, and nonocclusive disease related to hypotension or hypovolemia. Secondary bowel ischemia can occur in the setting of small-bowel obstruction, incarcerated hernia, or volvulus. CT can accurately show ischemic bowel segments and often aids in determining the primary underlying cause as well as important coexistent findings or complications. The various morphologic changes on CT in acute bowel ischemia include wall thickening, which may be hypoattenuating when there is submucosal edema (Fig. 5) or hyperattenuating when there is intramural hemorrhage from a reperfusion injury. Other findings are bowel dilatation, lack of bowel wall enhancement, mesenteric fat stranding (Fig. 5), vascular engorgement, ascites, pneumatosis (Fig. 6), and portal venous gas (Fig. 6). In cases of complicated bowel obstruction, the visualization of mesenteric fat stranding, mesenteric fluid, and ascites can strongly suggest the diagnosis of partial or transmural bowel ischemia [1]. If two of these three findings are present, the specificity of this diagnosis is reported to be about 95% [1]. However, the single best predictor of ischemia is lack of bowel wall enhancement. In the case of strangulating closed loop obstruction seen as a C- or U-shaped W4 JR:197, July 2011

5 Patterns of Fat Stranding C D Fig. 6 Ischemia of right colon., Locules of portal venous gas are seen in liver (arrows)., There is pneumatosis of right colon (arrows). C, ir is also seen in distal branches of ileocolic vein (arrows). D, Extensive fat stranding is seen in right iliac fossa (arrows). loop with two transition points, CT may show mild circumferential intramural high attenuation, a target sign, or pneumatosis in the wall of the incarcerated bowel. In addition, there may be mesenteric haziness, engorged mesenteric structures, or mesenteric fluid in the attached small-bowel mesentery [2]. In large bowel ischemia, paracolic fat stranding and even paracolic fluid collections may result from superinfection of ischemic colonic segments. These findings have been reported in 61% and 37% of cases of ischemic colitis, respectively, even if there has been no transmural necrosis of the bowel wall [3]. Colon cancer with perforation cute perforation of the colon associated with colon cancer may cause fat stranding that is difficult to differentiate from that seen with acute diverticulitis. The degree of bowel wall thickening can be a helpful differential feature because the mural thickening in malignant perforation of the colon tends to be more severe than in diverticulitis (Fig. 7). The bowel wall thickening is of soft-tissue attenuation and does not display the target sign or mural stratification signifying bowel wall edema that is seen in inflammatory processes or ischemia (Fig. 7). Other associated findings suggesting perforated colon cancer include adjacent lymphadenopathy, distant metastases, and shouldering (i.e., the abrupt transition from the intraluminal component of the tumor to the adjacent normal mucosa, forming a shouldered edge). Nevertheless, in some cases, CT cannot differentiate between the two conditions and endoscopic correlation is required. Infectious enteritis and colitis In both these conditions, acute inflammation can cause variable CT findings depending on the organism, ranging from marked small-bowel wall thickening resembling Crohn disease to diffuse edema with more marked mesenteric stranding in Salmonella infections and giardiasis. The many causative agents include parasites, protozoa, bacteria, and viruses. JR:197, July 2011 W5

6 Thornton et al. Fig. 7 Colon carcinoma with perforation., Focally thickened segment of sigmoid colon, which is of soft-tissue attenuation, represents colon carcinoma with shouldering (short arrow). There is moderate fat stranding in region of carcinoma, secondary to perforation (long arrow)., This image shows free intraperitoneal air (arrow) distant from site of perforation. Infectious enteritis and colitis are typically diagnosed clinically and do not require CT for detection. However, these conditions may be identified at CT in patients in whom the clinical symptoms are not straightforward. On CT, infectious enteritis or colitis can produce thickening of the bowel wall with submucosal edema (mural stratification or the target sign when the bowel loop is imaged in cross-section) (Fig. 8). scites and fat stranding may also be present. Multiple air-fluid levels in the colon may be produced by increased fluid and liquid feces. Clinical and laboratory testing are required to identify the causative pathogen. Pseudomembranous colitis, which is caused by colonic overgrowth of Clostridium difficile, can result in severe thickening of the wall of the colon. When this is the case, the appearance of the colon may be similar to that of an accordion. The accordion sign refers to positive oral contrast seen between the extremely thickened colonic haustra. However, this CT sign is not specific for pseudomembranous colitis and can be also seen in ischemia, cirrhosis, and infectious types of colitis caused by cytomegalovirus, cryptosporidiosis, and salmonellosis. Inflammatory bowel disease Inflammatory bowel disease includes both ulcerative colitis and Crohn disease, each of which has different CT findings with some overlap. Ulcerative colitis primarily affects the colon (most commonly the rectum and left colon), occasionally also involving the terminal ileum with backwash ileitis. Exclusive involvement of the right colon is rare in this condition. In contrast, Crohn disease usually affects the small bowel (almost always the terminal ileum) (Fig. 9), with or without colonic or anal involvement. owel wall thickening is the most common CT finding in both conditions (Fig. 9). The wall thickening in Crohn disease is generally eccentric and segmental, unlike the usually diffuse symmetric colonic thickening in ulcerative colitis, with asymmetric inflammation often occurring along the mesenteric border or in patchy distribution. In Crohn disease, the bowel wall can range from normal or mildly thickened to severely thickened. In Crohn disease, pseudodiverticula develop on the antimesenteric border of the colon opposite regions of fibrosis and scarring. CT finding that is more common in ulcerative colitis is the halo sign, which is due to the deposition of submucosal fat that results in a low-attenuation ring in the bowel wall. In inflammatory bowel disease, fat stranding can be seen when the inflammatory process extends from the bowel into the fat or involves the fat exclusively. Hazy (groundglass) fat stranding in the mesentery in Crohn disease results in a misty mesentery, with increased attenuation of the mesenteric fat. Mesenteric lymphadenopathy, al- Fig. 8 Infectious pancolitis. Entire colon is diffusely thickened (short arrows). There is mild fat stranding (long arrows) in pericolonic region. W6 JR:197, July 2011

7 Patterns of Fat Stranding Fig. 9 Crohn disease., Coronal reformatted image shows thickened terminal ileal wall (short arrows) and coned cecum. Small mesenteric nodes are also present in right iliac fossa (long arrows)., Coronal reformatted image shows mild fat stranding around abnormal thickened terminal ileum (arrows). C, xial image of right lower quadrant again shows thickening of terminal ileum, with abscess formation deep in pelvis (thick arrows), with diffuse infiltration of surrounding fat (thin arrows). C though nonspecific, occurs more commonly in Crohn disease (Fig. 9). Fibrofatty proliferation in the mesentery, which is defined as the asymmetric proliferation of fat usually along the mesenteric border, is seen almost exclusively in Crohn disease. It is usually seen adjacent to an affected loop of small bowel. It has been described as the creeping fat sign, given how the fat proliferation extends toward the root of the mesentery. Fibrofatty proliferation of the perirectal fat, in which the fatty proliferation is seen around the entire circumference of the rectum, can develop in both Crohn disease and ulcerative colitis as well as in pseudomembranous and radiation colitis. CT may also show such complications of inflammatory bowel disease as abscesses (Fig. 9), fistulas, strictures (seen mainly in Crohn disease), and toxic colitis (more common in ulcerative colitis). Toxic colitis refers to a thickened, often dilated, transverse colon, which frequently has adjacent mild to moderate fat stranding. Toxic colitis is a surgical emergency because of the high risk of perforation. cute appendicitis cute appendicitis occurs after obstruction of the appendiceal lumen, usually by a fecalith but may be due to lymphoid hyperplasia, foreign bodies, parasites, or tumors. acteria within the appendix multiply, invade the wall of the appendix, and cause transmural inflammation. s the appendix becomes increasingly dilated, the development of JR:197, July 2011 W7

8 Thornton et al. Fig. 10 cute appendicitis., xial contrast-enhanced scan shows fat stranding (black arrows) adjacent to dilated appendix (9 mm in diameter) with hyperenhancing wall (white arrow)., Coronal reformatted image in same patient shows fat stranding extending to right psoas muscle (black arrows). ppendix is dilated (white arrow) with hyperenhancing wall. venous engorgement leads to arterial ischemia and inflammation. If left untreated, the appendiceal wall will infarct and subsequently perforate, often resulting in the development of an abscess in the lower abdomen or pelvis. The most specific CT finding for acute appendicitis is a dilated fluid-filled appendix with a diameter 6 mm (Fig. 10). Other direct findings on CT include an abnormally thickened appendiceal wall, with contrast enhancement (Fig. 10) and periappendicular fat stranding. The fat stranding around the appendix is disproportionate to the adjacent mild bowel wall thickening in established acute appendicitis (Fig. 10). Thickening of the cecal pole may also be present. The appendix may be difficult to locate, particularly in thin individuals. Severe fat stranding in the right iliac fossa, even in the Fig. 11 Postoperative changes in patient who had undergone resection of sigmoid carcinoma several days before CT. There is extensive fat stranding in pelvis (short arrows) in region of suture line (long arrow). absence of significant thickening of the ileum or cecum, is highly suggestive of acute appendicitis. This should lead to a careful search for the appendix, including the use of multiplanar reformatted images. Postoperative changes in the mesentery, subcutaneous fat, and omentum Focal fat stranding adjacent to the surgical bed is extremely common after recent abdominal surgery (Fig. 11). Fat Stranding djacent to a Solid Organ Peripancreatic Fat Stranding: cute Pancreatitis Pancreatitis is most frequently caused by the ingestion of alcohol or by an obstructing calculus in the lower portion of the common bile duct near the ampulla (70% of cases). Other less common causes include trauma, post-ercp, drugs, viruses (such as mumps), hypertriglyceridemia, hypercalcemia, and hyperparathyroidism. cute pancreatitis classically presents with severe central upper abdominal pain that radiates to the back. Patients can be hemodynamically unstable if there is severe necrosis of the pancreatic parenchyma. On CT, the pancreas appears enlarged. The pancreatic parenchyma may not enhance after IV contrast administration in the setting of pancreatic necrosis, which can be focal (Fig. 12) or diffuse. In addition to fat stranding in the peripancreatic tissues, other secondary findings W8 JR:197, July 2011

9 Patterns of Fat Stranding Fig. 12 cute necrotizing pancreatitis., There is severe peripancreatic fat stranding (thick arrows). Focal area of parenchyma in pancreatic neck is not enhancing due to necrosis (thin arrows)., Severe fat stranding extends from peripancreatic region to left paracolic gutter and anterior pararenal space (arrows). There is residual enhancing pancreatic parenchyma in head of pancreas (arrowheads). Fig. 13 ilateral acute pyelonephritis. Contrastenhanced coronal reformatted image shows bilateral striated nephrograms and ill-defined wedged-shaped areas of low density in upper poles of both kidneys, radiating from papilla to cortical surface (arrows). include free fluid in the paracolic gutters and pleural effusions. Complications of acute pancreatitis can be identified on CT. These include pseudoaneurysm formation, venous thrombosis, peripancreatic fluid collections, and pancreatic abscess formation (usually occurs 4 weeks or more after the onset of acute pancreatitis), pancreatic pseudocyst formation (at least 6 weeks after the onset of acute pancreatitis), and hemorrhage from erosion into adjacent splenic or pancreaticoduodenal arteries or rupture of a pseudoaneurysm. Infection of necrotic pancreatic tissue, which is the most common cause of mortality in patients with acute pancreatitis, has no specific imaging findings and needs to be excluded by imaging-guided aspiration or biopsy. Diffuse Perinephric Fat Stranding Without hydronephrosis: acute renal inflammatory or infectious disease Renal inflammatory disease includes acute pyelonephritis with or without abscess formation and emphysematous pyelonephritis. cute pyelonephritis usually results from the retrograde spread of bacteria from the lower urinary tract system into the renal parenchyma; less frequently it may occur via hematogenous spread. Typical clinical symptoms include fever, flank pain, frequency, and dysuria. cute bacterial pyelonephritis is more common in women and in patients with impaired immune systems secondary to diabetes, organ transplantation, or HIV IDS. Imaging usually is not required to make the diagnosis. However, if the clinical presentation is atypical, the infection is severe, or the patient is not responding to antibiotic therapy, CT is the most sensitive imaging modality that can be performed. Unenhanced CT is used to assess for underlying stone disease, whereas dynamic contrastenhanced CT is required to evaluate the renal parenchyma. In acute pyelonephritis, the nephrographic phase of contrast enhancement is superior for depicting the extent of the process. Typically ill-defined wedge-shaped areas of low density are noted radiating from the papilla to the cortical surface (Fig. 13). These wedge-shaped areas are thought to represent sites of poor- or nonfunctioning parenchyma due to vasospasm, tubular obstruction, or inter- JR:197, July 2011 W9

10 Thornton et al. stitial edema. They have a lobar distribution and may be unifocal, multifocal, or bilateral. The striated nephrogram bands of alternating high- and low-density parallel to the axes of the tubules, characteristic of acute pyelonephritis is thought to be due to obstructed tubules with intervening normal tubules (Fig. 13). Perinephric fat stranding is usually seen immediately adjacent to the abnormal areas in the renal parenchyma because of an inflammatory reaction with leukocytes forming an infection or infarction (Fig. 14). In addition to abnormalities within the renal cortex and medulla, there may be inflammatory changes in the Gerota fascia and renal sinuses as well as thickening of the urothelium. Fig. 14 cute pyelonephritis of left kidney. On this unenhanced image, there is diffuse mild perinephric fat stranding (arrows). Contrast-enhanced CT was not performed subsequently due to renal failure. In diffuse pyelonephritis, there is renal enlargement, poor enhancement, and poor excretion of contrast material in proportion to the severity of infection. Soft-tissue filling defects in the collecting system may represent inflammatory debris, blood clots, or sloughed tissue from papillary necrosis. Microabscesses may appear as nonenhancing fluid collections within abnormal areas of parenchyma. Emphysematous pyelonephritis is a rare life-threatening fulminant necrotizing infection of the renal parenchyma. It is caused by gas-forming organisms, predominantly Escherichia coli, Proteus species, or Klebsiella pneumoniae. It primarily affects patients with poorly controlled diabetes or severe immune suppression. Immediate treatment with surgical débridement or percutaneous drainage is mandatory to reduce mortality. Typical CT findings include extensive destruction of the renal parenchyma, which contains mottled or streaky regions of gas, and perinephric fat stranding. With hydronephrosis: acute urinary obstruction cute obstruction of the upper urinary collecting system results in a proximal increase in pressure that produces ureteral dilation, hydronephrosis, and forniceal rupture. The obstruction can gradually cause decreased diastolic blood flow over several days, which may lead to reduction or even cessation of urine excretion because of impaired renal function. Unenhanced CT of the abdomen is useful in identifying an obstructing stone within the renal pelvis or ureter. CT detects all calculi regardless of calcium content, with the exception of stones formed during indavir treatment in the management of HIV. If there is an obstructing ureteral calculus, the dilated ureter can be followed inferiorly to a focal area of high attenuation that represents the obstructing stone (Fig. 15). Uric acid stones have attenuation values of between 300 and 400 HU, whereas calcium-containing stones have higher attenuation. Ureteral calculi frequently lodge in one of the three narrowest sites in the ureter: the ureteropelvic junction, the location where the ureter crosses the iliac vessels, and at the ureterovesical junction (Fig. 15). complication of ureteral obstruction is forniceal rupture. Other signs of urinary tract obstruction include dilatation of the intrarenal collecting system, swelling of the ipsilateral kidney, and perinephric fat stranding (Fig. 15). stone lodged in the ureter often is surrounded by a thin circumferential rim of soft-tissue attenuation. fter contrast administration, there is a delayed nephrogram because of decreased renal perfusion. If delayed images are obtained, a dense persistent nephrogram can be seen on the obstructed side. With chronic hydronephrosis: xanthogranulomatous pyelonephritis Xanthogranulomatous pyelonephritis is an uncommon chronic infection, usually caused by E. coli and Proteus mirabilis, which results from long-standing urinary obstruction by a staghorn calculus. It classically occurs in middle-aged women who have a history of recurrent urinary tract infections, flank pain, and low-grade fever. The affected kidney is hydronephrotic and functions poorly, if at all. The typical CT findings of xanthogranulomatous pyelonephritis include renal enlargement, staghorn calculus, poor or no renal function, and multiple round low-attenuation masses. Pathologically, these low attenuation masses represent either dilated calyces or focal areas of parenchymal destruction filled with pus or debris. Histologically, these fluid filled cavities are lined by lipid-laden macrophages. djacent organs may become involved in the inflammatory process, and extension into the perinephric space results in perinephric fat stranding. W10 JR:197, July 2011

11 Patterns of Fat Stranding Fig. 15 Obstructing ureteral stone. Prone unenhanced CT images of abdomen in patient with right flank pain and hematuria., There is moderate right hydronephrosis (long arrows) and mild perinephric fat stranding due to edema (short arrow)., Dilated right ureter with mild fat stranding (arrow). C, Lodged in right vesicoureteric junction, 4-mm calculus (arrow) is causing obstruction of right ureter. Pericholecystic Fat Stranding: cute Cholecystitis cute cholecystitis is caused by a calculus that obstructs the neck of the gallbladder or the cystic duct. Similar to the sequence of events in acute appendicitis, the gallbladder initially becomes distended with bile that cannot drain into the common bile duct. Venous engorgement of the wall of the gallbladder ensues, followed by arterial insufficiency and ischemia. The resulting inflammation can be detected on CT by the presence of pericholecystic fat stranding (Fig. 16). Emphysematous cholecystitis is of concern when gas-forming organisms cause intramural gas in the gallbladder lumen, wall, or pericholecystic tissues in the absence of an abnormal communication between the biliary tree and the gastrointestinal tract or recent instrumentation of the biliary tree (Fig. 17). C Fig. 16 cute cholecystitis., There is low-density gallstone in gallbladder (arrow)., Wall of gallbladder is thickened (thin arrows), and there is mild pericholecystic fat standing (thick arrows). JR:197, July 2011 W11

12 Thornton et al. Fig. 17 Emphysematous cholecystitis in patient with diabetes., Multiple small hyperdense foci in gallbladder represent gallstones (thin arrow). There is severe pericholecystic fat stranding (thick arrows)., There is locule of air in lumen of gallbladder (thin arrow). Inflammatory process has extended to hepatic flexure of colon, causing thickening of colonic wall (arrowheads). Thick arrow indicates gallstones lying dependently in gallbladder. The offending gallstones frequently cannot be detected on CT. However, the presence of pericholecystic fat stranding is evidence for an underlying inflammatory process (Figs. 16). Thickening of the gallbladder wall can often be detected (Fig. 16). Sclerosing Mesenteritis Sclerosing mesenteritis is an idiopathic fibroinflammatory disorder that affects the smallbowel mesentery. It can be categorized on the basis of the predominant histologic process as mesenteric panniculitis (chronic inflammation), mesenteric lipodystrophy (fat necrosis), and retractile mesenteritis (fibrosis). Sclerosing mesenteritis has varying appearances on CT, from a well-defined soft-tissue mass containing areas of fat attenuation to an ill-defined area of increased attenuation in the root of the small-bowel mesentery (Fig. 18). This rare condition, seen in patients in the sixth and seventh decades of life, has a poorly understood association with underlying malignancy and may rarely be a paraneoplastic condition. Usually self-limiting with a favorable prognosis, sclerosing mesenteritis is characterized by a chronic nonspecific inflammation and fibrosis of the adipose tissue of the bowel mesentery. The clinical, imaging and intraoperative findings are imperative to complement the diagnosis of the nonspecific histologic features, which can also be seen in lymphomas or in the soft tissues adjacent to infiltrating carcinomas. Unlike most tumors, the changes of sclerosing mesenteritis occur around the mesenteric vessels and do not displace them. However the mass does displace loops of bowel. The CT appearance of a fat ring sign a thin radiolucent rim of fat between the mesenteric vessel and the mass in the mesentery has been reported as an indication of sclerosing mesenteritis. Small lymph nodes less than 5 mm in diameter are often scattered throughout the mass in sclerosing mesenteritis. The fat ring sign may also be seen in relation to these small nodules and differentiate them from lymphoma and other causes of malignant lymphadenopathy. hyperattenuating stripe partially surrounding the mass is also suggestive of panniculitis. Calcification is uncommon in sclerosing mesenteritis. Mesenteric metastases from a small-bowel carcinoid tumor may simulate sclerosing mesenteritis, presenting as an infiltrating soft-tissue mass in the root of the mesentery, with associated desmoplastic reaction and calcification. Calcification is more common in carcinoid tumors and is present in up to 70% of cases. This neuroendocrine tumor typically arises from the distal il- W12 JR:197, July 2011

13 Patterns of Fat Stranding Fig. 18 Sclerosing mesenteritis. (Courtesy of Kane R, oston M), There is moderate fat stranding in mesentery above mesenteric mass (arrows)., Mesenteric mass displaces loops of small bowel (thin arrows). There is dystrophic calcification (black arrow), uncommon finding in this condition. Diffuse mild mesenteric fat stranding is also seen (thick arrows). eum, and adjacent loops of bowel may have thickened walls, which can be due to either infiltration of the tumor or ischemia that is caused by sclerosis of mesenteric vessels. Patients can become symptomatic with sweating, flushing, and diarrhea when the tumor metastasizes to the liver. Therefore, if hypervascular liver metastases are seen on CT with elevated levels of urinary 5-hydroxy indoleacetic acid along with a calcified mesenteric mass, radiating mesenteric strands, and adjacent bowel wall thickening, the diagnosis of carcinoid is favored. bdominal Tuberculosis Tuberculosis is reemerging globally, partly due to the increasing incidence of HIV IDS infection and the increased use of immunosuppressant drugs. In the abdomen, tuberculosis mimics such conditions as inflammatory bowel disease, malignancy, and other infectious diseases. bdominal tuberculosis is usually caused by ingestion of bacilli in infected sputum or contaminated food. It can affect the bowel, mesenteric lymph nodes, solid viscera, and peritoneum. The ingested bacilli cause caseating necrosis in the intestine, followed by spread to the mesenteric lymph nodes, which may rupture into the peritoneum and produce tuberculous peritonitis. Tuberculosis may also reach the abdomen via hematogenous spread of the bacilli from a distant source of infection, such as the lungs. Intestinal involvement is a rare manifestation of tuberculosis but is a common form of the disease within the abdomen. The most common sites of intestinal tuberculosis are the terminal ileum and cecum (90% of cases). The disease causes circumferential thickening of the bowel wall, with adjacent mild fat stranding and lymphadenopathy. In advanced ileocecal disease, small-bowel loops may become adherent in the right iliac fossa. lthough isolated tuberculous involvement of the peritoneum is rare, it frequently occurs in association with widespread abdominal disease. Peritoneal tuberculosis may affect the peritoneal cavity, mesentery, and omentum. The most frequent form (90% of cases) is the wet type with ascites or pockets of loculated fluid (Fig. 19). The dry type is characterized by fat stranding in the mesentery, dense adhesions, and adenopathy. In the fibrotic-fixed type, omental thickening produces large masses that may be mistaken for a tumor. Fat stranding can be seen in any of these three types (Fig. 19). t times, the clinical and radiologic differentiation between tuberculous peritonitis and peritoneal carcinomatosis can be challenging because there is a significant overlap of CT findings. normal chest radiograph does not exclude tuberculous peritonitis because only 15% of patients with abdominal involvement also have evidence of pulmonary disease. The liver and spleen are the main abdominal organs that become involved in miliary tuberculosis. On CT, microabscesses appear as diffuse low-density focal lesions in the liver and spleen. Isolated involvement of the abdominal viscera is rare, and these organs are almost JR:197, July 2011 W13

14 Thornton et al. Fig. 19 Tuberculous peritonitis (wet type)., There is extensive fat stranding of greater omentum (long arrows). Peritoneum is thickened and hyperenhancing (short arrows), and pockets of fluid are present (arrowheads), There is moderate ascites (long arrow) and enhancement of thickened peritoneum (short arrows). always affected as part as of a multifocal or disseminated disease. Peritoneal Carcinomatosis and Primary Peritoneal Tumors Peritoneal carcinomatosis is a common metastatic manifestation of many organ-based malignancies, particularly carcinomas of the gastrointestinal tract and ovaries. Primary neoplasms of the peritoneum occur much less frequently than metastatic peritoneal involvement from a known or occult primary tumor. However, these rare primary lesions (peritoneal mesothelioma, papillary serous carcinoma, desmoplastic small round cell tumor, benign and malignant mesenchymal tumors, Fig. 20 Peritoneal carcinomatosis (serous adenocarcinoma of ovary). There is moderate ascites (long arrows) in paracolic gutters and nodularity and fat stranding in omentum (short arrows). and lymphoproliferative disorders) should be considered in the absence of a known or suspected malignancy. Nevertheless, even if there is no known underlying malignancy, metastatic disease from an occult gastrointestinal, ovarian, or other primary carcinoma is probably more likely than a primary peritoneal tumor. The prognosis is poor with both conditions. Neoplastic involvement of the peritoneal space generally appears on CT as a soft-tissue process, which may have associated ascites (Fig. 20). n infiltrative tumor can produce an appearance of generalized fat stranding within the peritoneal cavity. dditional findings of primary peritoneal tumors may include a cystic component or cystic necrosis, calcification, prominent contrast material enhancement, and fat attenuation. Conclusion Fat stranding on abdominal CT examinations is a common finding that may be related to numerous conditions. y assessing the location and pattern of the fat stranding and other CT findings, it is possible to accurately narrow the differential diagnosis. References 1. Zalcman M, Sy M, Donckier V, Closset J, Gansbeke DV. Helical CT signs in the diagnosis of intestinal ischemia in small-bowel obstruction. JR 2000; 175: althazar EJ, irnbaum, Megibow J, Gordon R, Whelan C, Hulnick DH. Closed-loop and strangulating intestinal obstruction: CT sign. Radiology 1992; 185: althazar EJ, Yen C, Gordon R. Ischemic colitis: CT evaluation of 54 cases. Radiology 1999; 211: W14 JR:197, July 2011