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(BQ) The book delivers detailed imaging of all areas of the abdomen and pelvis—including the liver and biliary system, pancreas, GI tract, spleen, mesentery/omentum/peritoneum, kidney and urinary system, retroperitoneum and adrenal glands, and abdominal wall—helps readers understand relevant anatomy and identify pathologies.
CLINICAL HISTORY 34-yUJr-old man presenting with left upper quadrant pain FIGURE 80A FIGURE soc FIGURE SOB FIGURE SOD FINDINGS Axial CECf (A) demonstrates two geographic of low attenuation These lesions are best demonstrated on hypo-attenuating areas in the spleen Axial T2-WI (B) shows an additional round lesion more inferiorly, which bas bright DIAGNOSIS Splenic infarcts CECT image During the acute stage, infarcts are ill-defined and heterogeneously hyperdense due to areas of hemorrhage within them MRI best shows the internal hemorrhage on the Tl-WI, as in this case As an infarct begins to fibrose, it will appear better demarcated and may cause contraction of the sWTOunding nmmal spleen When serial CT scans demonstrate progressive liquefaction and necrosis with outward extension, developing subcapsular hemorrhage, and free peritoneal hematoma, the possibility ofimpending rupture or superimposed infection should be considered DISCUSSION There are multiple causes for splenic infarcts, including emboli, hematologic diseases, portal hypertension, and iatrogenic causes In patients younger than 40 years, hemoglobinopathies are the most common cause of splenic infarction Infarcts can have a variety of CT appearances ranging from the classic peripheral wedgeshaped defect to focal round lesions and ill-defined areas Even though infarcts are typically wedge-shaped, on axial images, they may appear round, as in this case, depending on how the wedge shaped area is "cut" on the image; this is more commonly seen in infarcts in the superior and inferior aspects of the spleen Coronal or sagittal reformatted images would show best the true wedgeshaped configuration of the abnormality signal On the fat-suppressed axial Tl-WI (C), one lesion has a spontaneously bright curvilinear central area No enhancement is seen on the gadolinium-enhanced, fat-suppressed axial Tl-WI (D) DIFFERENTIAL DIAGNOSIS Splenic laceration, fracture 103 CLINICAL HISTORY 37-year-old woman presenting with known steatohepatitis and alcohol abuse FIGURE 81A FIGURE B1C FIGURE 818 FIGURE FINDINGS Axial MRI demonstrate marked enlargement of the lateral segment of the left lobe of the liver and concomitant decrease in the size of the right liver lobe An illdefined wedge-shaped area within the medial segment of the left liver lobe shows increased signal intensity on the axial 1'2-WI (A), decreased signal intensity on the fat-suppressed axial Tl-WI (B), and delayed enhancement on gadoliniumenhanced, fat-suppressed axial Tl-WI (C and D) Hepatic vessels are seen traversing through this region without the evidence of distortion Also note the capsular retraction adjacent to the abnormal area DIFFERENTIAL DIAGNOSIS Hepatocellular carcinoma, intrahepatic cholangiocarcinoma DIAGNOSIS Confluent hepatic fibrosis 104 810 DISCUSSION Confluent hepatic fibrosis can present as a masslike area (14%) in patients with underlying cirrhosis, especially primary sclerosing cholangitis It typically affects the anterior segments of the right lobe and medial segments of the left lobe Confluent hepatic fibrosis usually has a wedgeshaped appearance, but in some patients, the entire segment might be involved The typical appearance of confluent hepatic fibrosis is an area of low signal intensity on Tl-WI and high signal intensity on T2-WI It usually demonstrates delayed enhancement on gadolinium-enhanced images The typical geographic pattern of involvement and retraction of the ovttlying hepatic capsule can be helpful in diagnosing this condition Possible explanations for the hyperintense appearance of confluent fibrosis on T2-WI are a relative reduction in the signal of the remaining liver parenchyma due to increased iron deposition, edema due to venous thrombosis, or most likely, inflammatory changes within the fibrosis CLINICAL HISTORY 22-year-old man presenting with abdominal pain and tenderness FIGURE FIGURE 82A 828 FINDINGS Axial CECT images (A-D) demonstrate highdensity ascites as well as a thick enhancing peritoneum There are also omental and retroperitoneal lymph nodes DIFFERENTIAL DIAGNOSIS Peritoneal carcinomatosis, malignant mesothelioma DIAGNOSIS Tuberculosis peritonitis and omentitis DISCUSSION Although tuberculosis is unusual in Western countries, there has been an increased incidence of tuberculosis due to the large number of chronically immunosuppresse patients due to transplantation mv infection, and other causeA Extrapulmonary tuberculosis has proportionally also increased, FIGURE 82C FIGURE 820 reaching up to 15% of new cases of tuberculosis documented in the United States Furt:hermore, in only 15% ofcases ofabdom- inal tuberculosis, there is pulmonary disease Ascites due to tuberculosis has high attenuation (20 to 4S lRJ) due to the high protein and cellular contentB also demonstrates peritoneal thickm:i:ng, enhancement, and sometimes nodularity corresponding to the tuberculomas present in it Omental caking can be seen in up to 82% of patients with abdominal tuberculosis Peritoneal carcinomatosis is very difficult to distinguish from tuberculou.s peritonitis except for the fact that, in the latter, there is history of a known malignancy Peritoneal mesothelioma can also produce some of the findings seen in tuberculous peritonitis, but the peritoneal thickening is much more pronounced, and the ascites is less massive than in tuberculosis cr 105 CLINICAL HISTORY 49-year-old man with chronic affective disorder presenting with lower abdominal pain FIGURE 83A FIGURE B3C 838 FIGURE 830 FIGURE FINDINGS Axial (A and B), coronal reformatted (C), and sagittal reformatted (D) CECT images demonstrate innumerable microcysts in the cortex and medulla of both kidneys DIFFERENTIAL DIAGNOSIS Glomerulocystic kidney disease, autosomal recessive polycystic kidney disease, autosomal dominant polycystic kidney disease DIAGNOSIS Chronic lithium nephropathy DISCUSSION Chronic lithium nephropathy is a progressive condition causing interstitial fibrosis and dilatation of distal tubules with formation of microcysts These microcysts are identified in 63% of renal biopsy specimens of 106 patients on chronic lithium therapy The cysts are present in both the cortex and the medulla and measure to mm in size Progressive decrease in renal function is seen in chronic lithium nephropathy On the other hand, glomerulocystic kidney disease, occurring in sporadic or familial forms, is characterized by cystic dilatation of Bowman's capsule; the cysts are therefore entirely cortical in distribution, a key distinguishing factor Patients with autosomal recessive polycystic kidney disease (ARPKD) present in the early life with multiple small renal cysts in massively enlarged kidneys The juvenile form of ARPKD presents in adolescence with associated findings of portal hypertension The kidneys of patients with autosomal dominant polycystic kidney disease harbor multiple cysts, but oflarger size (several centimeters) 84 FIGURE CLINICAL HISTORY 26-year-old woman presenting with an asymptomLJtic vaginal bulge 84A FIGURE 84C ,, / •' • ;l'i' - • , ~" _