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Pancreatic parenchyma

Pancreatic necrosis A diffuse or focal area(s) of nonviable pancreatic parenchyma, typically associated with peripancreatic fat necrosis. [Pg.57]

As new imaging tools have become available, such as CT and MRI, many attempts have been made to evaluate imaging criteria for assessing the severity of acute pancreatitis. The first severity index of acute pancreatitis was developed in 1990 by Balthazar et al. (B2). The CT Scoring Index (CTSI) is a 10-point system based on the degree and the type of changes in pancreatic parenchyma and peripancreatic tissues as well as the extent of pancreatic necrosis. The majority of studies confirm its clinical utility for prediction of severity of AP (K6, LI, M20, S14, VI) however, some authors report CT to be ineffective (L13, L14). [Pg.67]

Due to the above mentioned rotations of the stomach, the presumptive duodenum will bend into a C shape and will be displaced to the right until it lies against the dorsal body wall and becomes secondarily retroperitoneal. A system of digestive glands develops from endodermal buds of the duodenum, including the liver parenchyma, the gall bladder and their ducts (derived from the hepatic diverticulum), as well as the pancreatic parenchyma and its ducts (derived from the fusion of the dorsal and ventral pancreatic ducts) (Fig. 3.1). [Pg.110]

US will reveal pancreatic cysts. On CT these cysts will have lower attenuation than the normal pancreatic parenchyma, and calcifications might be seen with unenhanced and enhanced CT (Choyke et al. 1990 Hough et al. 1994). [Pg.159]

CT may demonstrate duct dilatation, focal areas oflow attenuation in the pancreatic parenchyma that correspond to fluid collections (King et al. 1995). Necrosis is recognized as a focal or diffuse area of non-enhancing pancreatic tissue. The pancreas can he enlarged or normal. Other findings include extra-pancreatic fluid collections located in the anterior pararenal space, lesser sac, lesser omentum, and transverse mesocolon. Peripancreatic fat stranding and pancreatic pseudocyst are sometimes encountered (Geier et al. 1990). [Pg.163]

MDCT of the pancreas is performed using triphasic acquisition obtained prior to, and biphasic acquisition after, intravenous contrast material injection (Freeny 2005). It has been shown that an arterial-phase scan (similar in timing to the typical arterial-phase scan of the hver) is not of value for detection of pancreatic adenocarcinoma (Fletcher et al. 2003 Graf et al. 1997). Pancreatic adenocarcinoma, which is by far the most common pancreatic tumor, is hypovascular and shows only little to no contrast to the minimally enhancing pancreatic parenchyma in the early arterial phase. Lu et al. (1996) implemented a two-phase CT protocol evalu-... [Pg.408]

As mentioned, the most important differential diagnosis of a main-duct-type IPMT is chronic pancreatitis. The typical CT features indicative of IPMT are the bulging papilla, diffuse pancreatic duct dilatation without stricture, no circumscribed pancreatic duct stones, and solid contrast-enhanced nodules. Pancreatic gland atrophy may be present in IPMT and chronic pancreatitis as well, but pancreatic parenchyma classifications are almost always absent in IPMT. [Pg.417]

Pancreatic necrosis occurs in patients with severe acute pancreatitis detected through perfusion defects in the contrast-enhanced CT. Therapeutic method of choice is surgical necrosectomy percutaneous drainage is not suitable. On the other hand, the differentiation of sterile from infected pancreatic necrosis is done by percutaneous sampling of the necrotic pancreatic parenchyma with a small-gauge needle (20 G). [Pg.529]

The course of pancreatic fibrosis in rats induced by dibutyltin dichloride was studied 2-36 weeks after single i.v. treatment of rats with dose of 6 or 8 mgkg-1. The pancreatic fibrosis induced by Bu2SnCl2 differs from other experimental models of acute pancreatitis. Extensive infiltration is present in fibrotic areas without pancreatic atrophy or lipomatosis. The presence of chronic inflammatory lesions characterized by the destruction of exocrine parenchyma and fibrosis, and in the later stages the endocrine parenchyma, indicates a chronic pancreatitis45. [Pg.1688]

Measurement of stool weight and quantitative fecal fat excretion on three consecutive days during a balanced diet are common screening tests for both pancreatic insufficiency and other pathologies that result in malabsorption. However, these tests are insensitive and nonspecific for pancreatic malfunction Steatorrhea occurs only after loss of more than 90% of exocrine parenchyma, and other causes of malabsorption (e.g., celiac sprue or Crohn s disease) may also induce abnormal fecal fat excretion of more than 7 g/day or more than 5 g/100 g. [Pg.284]

Higher contrast material flow rates have been shown to be advantageous. Tublin et al. (1999) showed that a flow rate of 5 ml s is superior to 2.5 ml s regarding enhancement of the pancreas and the fiver parenchyma. Many authors recommend using a flow rate of 4-5 ml s to optimize pancreatic enhancement and tumor-to-pancreas contrast Schueller at eh (2006) demonstrated that an even higher flow rate of 8 ml s (compared with the standard flow rate of 4 ml s ) has its merits. They demonstrated that a flow rate of 8 ml s results in better enhancement of the pancreas, but not of the typically hypovascular adenocarcinomas, which resulted in a higher tumor-to-pancreas contrast. [Pg.409]

Pancreas. Typically, the pancreas is surrounded by various organs like the stomach, liver, transverse colon, kidney, or major vessels. In particular, needle biopsy of small suspect masses in the pancreatic head is therefore usually regarded as technically sophisticated, and CT guidance preferred instead of ultrasound (Fig. 37.5). For differentiation of the tumor from surrounding normal parenchyma or inflammation, a contrast-enhanced CT scan obtained in an arterial phase should generally be performed prior to the intervention. The most common access route is from an anterior approach and often... [Pg.517]

Fig. 16.4a,b. A 48-year-old man with pancreatic cancer presented with persistent neutropenia and thrombocytopenia. Patient was referred for partial splenic embolization (PSE) in an attempt to increase white blood ceil and platelet counts prior to additional chemotherapy. Pre-embolization axial CT image of the abdomen (a) shows splenomegaly. CT scan performed 4 months after PSE (b) shows massive necrosis of splenic parenchyma. Within 2 weeks of partial splenic embolization, the platelet count normalized (379,000/mm )... [Pg.214]

Fig. 11.18a,b. Dynamic helical CT of a hypervascular liver metastasis from non-functioning malignant neuroendocrine pancreatic tumor, a The primary tumor (arrow) and the liver metastasis (arrowhead) are similarly enhanced during the arterial phase of liver enhancement. The parenchyma around the metastasis is less dense than the normal left liver lobe due to steal phenomena. This finding is transitory and not depicted in the later phases of the dynamic study (b)... [Pg.162]

In general, the vascularity of metastases is classified according to their contrast behavior in the arterial-dominant phase scan. Metastases which are hyperdense to normal liver parenchyma in this phase are called hypervascular . Hypervascular metastases are less frequently than hypovascular metastases in the liver and typically originate from renal cell carcinomas, carcinoids, pancreatic islet cell carcinomas, sarcomas, pheochromocytomas, melanomas, thyroid carcinomas, chorion carcino-... [Pg.284]


See other pages where Pancreatic parenchyma is mentioned: [Pg.47]    [Pg.279]    [Pg.169]    [Pg.169]    [Pg.159]    [Pg.160]    [Pg.36]    [Pg.409]    [Pg.410]    [Pg.410]    [Pg.505]    [Pg.215]    [Pg.47]    [Pg.279]    [Pg.169]    [Pg.169]    [Pg.159]    [Pg.160]    [Pg.36]    [Pg.409]    [Pg.410]    [Pg.410]    [Pg.505]    [Pg.215]    [Pg.169]    [Pg.1321]    [Pg.150]    [Pg.243]    [Pg.418]    [Pg.504]    [Pg.132]    [Pg.159]    [Pg.215]    [Pg.158]    [Pg.212]    [Pg.214]    [Pg.219]   


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