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Diffuse peritoneal soft tissue nodules
Peritoneal carcinomatosis (ovarian, stomach, colon and pancreas most common)
Mesothelioma (20-40% is abdominal)
Aortic dissection: how to identify false lumen
False lumen is usually larger and commonly contains a thrombus.
"Beak sign": junction of dissection flap with the false lumen wall produces an acute angle
Spigelian hernia
Just lateral to lower rectus abdominal muscles. Through a defect in the aponeurosis of internal oblique and transversalis abdominal muscles. 
Tends to have smaller opening and therefore is more prone to strangulation
Causes of increased liver attenuation
Amiodarone toxicity (deposition of Iodine compounds)
Hemochromatosis (primary or secondary. MRI can confirm)
Liver metastases
Can look like anything. Most common are well-defined, low density, solid mass w/ vague peripheral enhancement.
Other patterns:
  • Hypovascular tumors - best seen on PV phase. Colon cancer, classically.
  • Hypervascular tumors - best seen on arterial phase. Carcinoid, choriocarcinoma, melanoma, pancreatic islet cell, pheo, RCC, thyroid are most common.
  • Common cystic/necrotic primaries -  mucinous colon, lung cancer, melanoma, carcinoid.
  • Calcified - mucinous adenoCa, osteosarc, chondrosarc. 
Hepatocellular carcinoma
80% occur in cirrhotic livers. >50y/o. Increased AFP. HepB+C common risk factors. 
3 growth patterns: solitary, diffuse infiltrative, multinodular. A dominant mass surrounded by satellites is characteristic.
Arterial phase enhancement is characteristic: homogenous when <3cm; heterogenous in larger tumors.
Invasion of portal vein and IVC common.
Fibrolamella carcinoma
Slow growing tumor in a healthy liver. <40y/o. AFP normal.
Non-con: large, low-atten, lobulated mass w/ well-defined margins.
Post-con: enhances heterogenously in arterial and PV phases. Becomes more homog and stays on delayed scans.
Fibrous tissue bands separate mass into islands, often coalescing in central scar, which may calcify. Scar more evident on delayed scans.
Hepatic lymphoma
Liver involved in >50% of pts w/ lymphoma. Hard to see on CT though.
Diffuse infiltration may cause only hepatomegaly.
Most characteristic is multiple well-defined, large, homogenous, low-density nodules.
Numerous small nodules resembling microabscesses occur w/ Hodkin's.
Adenopathy usually present. Spleen usually involved.
Hepatic Adenoma
Rare and benign, but risk for major hemorrhage.
Most often young women on OCP, men taking steroids, and glycogen storage disease.
Tx = surgery due to risk of rupture or malignant transformation.  
Non-con: often isodense. (Made of hepatocytes). Sometimes may fill w/ fat. Intratumoral hemorrhage in 25-40%.
Arterial phase: early, homog enhancement. 
PV/delayed: Rapid washout, so becomes near isodense.
No uptake of tech99m sulfur colloid (paucity of Kupffer cells).
Solitary in 70-80%. Multiple in glycogen storage dz, liver adenomatosis.
Focal nodular hyperplasia (liver)
Contains all normal liver cell types. 2nd most common benign liver tumor (after cavenous hemangioma). 
Benign; no Tx.
Bright, homogeneously enhancing mass on arterial phase. Hypodense central scar in arterial and venous phase. Enchancement of central scar in delayed phase. Main lesion near isodense on portal phase.

Cavernous hemangioma
Most common benign liver tumor. 2nd most common focal mass (after mets). Any age, F>M.
Large, thin-walled, blood-filled vascular spaces lined by epithelium and have fibrous septa. Slow blood flow, so hold onto contrast.
Non-con: well-defined, vessel-density mass.
Arterial phase: early, peripheral nodules of enhancement, equal to aorta.
PV phase: Progressive fill-in from periphery, becoming uniform.
Delayed: prolonged enhancement. (20-30 min).
May get thrombosis.
Small ones may enhance homog, like HCC and vascular mets. Look for slow washout.
Most stay same size.
If questionable appearance, tagged RBC usually diagnostic.
Amebic abscess
Usually solitary and in the right lobe. 
Well-defined, enhancing wall; sometimes nodular.
Parenchyma adjacent to the wall may enchance too, causing double-rim target appearance.
Right lower lobe effusion/infiltrate possible.
Serology positive in 95%.
Hydatid cyst
Echinococcus larvae. 
May be unilocular, contain daughter cysts, or be calcified, depending on stage of growth.
Wall calcified in 50%. Lyering debris common; floating membranes sometimes. 
Daughter cysts = cysts within a cyst.
Mirizzi syndrome
Gallstone in cystic duct causing obstruction of common bile duct, either by direct compression or inflammation.
Slow-growing. From bile duct epithelium. Can be mass-forming, periductal infiltrative, or intraductal growing.
Hypovascular and fibrotic, so poor and slow enchancement. 10-20 min delay ideal.
Mass-forming: homogenous with irregular borders and low attenuation. Weak periph enhancement. Peripheral bile ducts usually obstruction and dilated. 
Periductal infiltrating: involved ducts are narrowed with thick walls; peripheral ducts dilated.
Primary sclerosing cholangitis
70% of pts have U.C. 
Progressive fibrosis of bile ducts, causing obstruction, cholestasis and biliary cirrhosis.
Multiple segmental strictures w/ wall thickening alternating w/ normal segments: "beaded" appearance.
Primary biliary cirrhosis
Chronic progressive cholestatic liver disease characterized by nonsuppurative destruction of interlobular bile ducts.
Liver failure in 7-10 yrs. 95% female. Often 40-50yrs old.  antimitochondrial Ab+.  Often have other autoimmune disease (Thyroiditis, scleroderma, rheumatoid arthritis, Sjögren syndrome)
Hepatomegaly, lace-like fibrosis, and regenerative nodules (3-10mm). 
More lymphadenopaty than other causes of chronic liver disease.
Oriental cholangiohepatitis
Recurrent pyogenic cholangitis assoc w/ pigmented stones and multifocal biliary strictures and dilatations. 
Assoc w/ Clonorchis sinensis and Ascaris lumbricoides infections. Immigrants from asia.
Dilated bile ducts w/ enhancing walls are filled with stones and pus.
Klatskin tumor
Cholangiocarcinoma at confluence of right and left hepatic bile ducts.
Often present too late for resection.
Choledochal cysts
Congenital dilitation of the biliary tree. Usually found in childhood.
Risk of stones and cholangiocarcinoma.
Type 1: 70%. Localized dilitation of CBD.
Type 2: Diverticulum from CBD or common hepatic duct.
Type 3: Choledochocoele - dilation of intramural part of CBD, bulging into lumen of duodenum.
Type 4: 20%. Cystic dilitation of intrahepatic bile ducts assoc w/ sacular dilitation of CBD.
Type 5: Caroli's disease
Caroli's disease
Congenital, saccular dilatation of the intrahepatic biliary tree, cholangitis, and gallstone formation without cirrhosis or portal HTN. 
High risk of bile duct carcinoma (7%). 
CT shows cystic dilatation of the intrahepatic biliary tree, w/ focal areas of tubular and saccular enlargement.
Gas or contrast in the biliary tree causes
Gallstone fistula
Cholecystoduodenal fistula
Perforated ulcer
Choledochalduodenal fistula
Choledochalenteric fistula
Signs of acute cholecystitis
  • Gallbladder distended to 4-5cm
  • Wall thickened >3mm and indistinct. May enhance.
  • Subserosal edema and stranding in nearby tissue
  • Increased bile density >20 HU indicates stasis, pus, hemorrhage or debris
  • Early phase increased attenuation of adjacent liver suggests hyperemia and inflammation
  • Pericholecystic fluid is assoc w/ perforation and abscess

Emphysematous cholecystitis: air in lumen or wall. Bad.
Porcelein gallbladder
Calcification of bladder wall in assoc w/ chronic cholecystitis. Calcs can be broad and continuous or multiple and punctate.
25% get carcinoma, so always remove; even when no symptoms.
Pancreatitis findings
focal or diffuse enlargement
decreased density of parenchyma due to edema
Blurring of the margins by inflammation
Fat stranding, blurring of fat planes with thickening of involved retroperitoneal fascia
Fluid collections
Pancreated pseudocyst
Well-defined round or oval collections of fluid with a clearly identifiable fibrous capsule. The fluid collection must remain present for approximately 6 weeks for the fibrous capsule to form and for the fluid collection to qualify being identified as a pancreatic pseudocyst
Pancreatic adenocarcinoma findings
  • Hypodense mass (96% of patients), which enhances minimally compared with normal pancreatic parenchyma. Biopsy frequently needed to confirm.
  • Calcifications are rarely associated with adenocarcinoma. 
  • Location: head (60%), body (15%), tail (5%), and are diffuse throughout the pancreas in 20% May be subtle, appearing as focal enlargement of the pancreas with loss of surface lobulation.
  • Pancreatic and/or common bile duct  are commonly dilated proximal to the tumor.
  • Atrophy of pancreatic tissue may occur proximal to the tumor.
  • Signs of acute or chronic pancreatitis may be simultaneously present.
Pancreatic adenocarcinoma resectability and non-resectability signs
Isolated pancreatic mass +/- pancreatic and/or bile duct dilatation.
Combined bile and pancreatic ducta dilatation without an identifiable mass.
Enlarged lymph nodes do NOT preclude resection.

Extension of tumor beyond the margins of the pancreas.
Invasion of adjacent organs (spleen, stomach, and duodenum).
Involvement of celiac axis; superior mesenteric artery; or portal, splenic, or superior mesenteric veins; involvement includes the following signs:
  • Thickening of the vessel walls
  • Soft tissue obscuring the normally sharp definition of the vessel by perivascular fat; (also seen in pancreatitis)
  • Deformity of the vessel by adjacent tumor
  • Enlargement of collateral vessels
  • Absence of vessel enhancement
  • Metastases to the liver (usually hypodense and poorly enhancing)
  • Ascites, which is presumptive evidence of peritoneal carcinomatosis
Pancreatic islet cell tumors

Functioning tumors produce clinical syndromes and are found early. Malginant potential: insulinoma 10%, gastrinoma 60%, and glucagonoma 80%.
NON-functional tumors present with mass effect and up to 80% are malignant.

CT findings:
Small tumors (<4cm) are homogenous and isodense. Enhance brightly and usually uniformly during arterial phase.
Large tumors (6–20 cm) are usually heterogeneous with calcification, cystic degeneration, necrosis, vascular invasion, and direct tumor extension into adjacent structures
Pancreatic lymphoma
Primary pancreatic lymphoma is rare. Usually, it instead invades from peripancreatic lymphadenopathy.

CT findings:
  • Focal tumor that is well circumscribed with homogeneous attenuation less than muscle and that enhances weakly but uniformly is characteristic.
  • Diffuse infiltration of the pancreas resembles pancreatitis but without clinical evidence of pancreatitis.
  • Peripancreatic lymphadenopathy that extends into and displaces the pancreas is characteristic of secondary pancreatic lymphoma
  • A bulky mass with no or minimal dilatation of the pancreatic duct strongly favors lymphoma over adenocarcinoma.
  • Lymphadenopathy below the level of the renal veins is seen with lymphoma but not with pancreatic adenocarcinoma.
Metastases to pancreas
Unusual. Most common with melanoma and AdenoCa of kidney, lung, and breast.
  • Most are round or ovoid with smooth, discrete margins.
  • Equal frequency in all portions of the pancreas.
  • Most (75%) demonstrate heterogeneous contrast enhancement.
  • Multiple nodules in 5% to 17%
Intraductal Papillary Mucinous Neoplasm
Secrete tons of mucin into the pancreatic ducts, producing progressive dilation of the main pancreatic duct and cystic ectasia of the branch pancreatic ducts.
Arise from epithelium lining ducts.
Tumors in the main duct often cause marked diffuse or segmental dilation of the duct with parenchymal atrophy.
Cystic ectasia of branch ducts produces a “bunch-of-grapes” appearance that bulges the contour of the pancreas.
Intraductal papillary solid masses are seen within the dilated pancreatic ducts and may bulge into the lumen of the duodenum at the papilla.
Tumors in the branch ducts produce a multicystic mass. Most common in the uncinate process. 
ERCP shows characteristic communication between the dilated main pancreatic duct and the multicystic dilatation of the branch pancreatic ducts.
Side branch has good prognosis. Main branch has higher risker of malignant degeneration.
Pancreatic pseudocysts
Low-density collections of fluid, cellular debris, or blood
Distinct walls are well defined and of variable thickness. Calcifications are occasionally present in the cyst wall.
Most are unilocular. Some contain a few septa.
Signs of pancreatitis are usually present
Mucinous cystic neoplasm (pancreas)
Middle aged women (95%).
Multiloculated cysts with thin septa. Usually 6 or less, bigger than 2cm.
Fluid attenuation varies from water to hemorrhage.
Size range 2-36cm; avg 6-10cm.
Most common in the tail
Do not communicate with the ductal system
Require surgical resection, but have excellent prognosis
Serous cystadenoma (pancreas)
No malginant potential. Contain clear fluid. 
Classically: a well-circumscribed mass of innumerable small cysts in the pancreatic head without biliary dilatation.  If cysts are tiny, looks like a spongy, solid lesion w/ central scar, often w/ central calcification. If cysts larger, has honeycomb appearance.
Unilocular form may be indistinguishable from mucinous cystic neoplasm. Lobulated contour, absence of wall enhancement, and location in the pancreatic head favor serous cystadenoma.
Causes of splenic cysts
  • Post traumatic 80%. After laceration, hematoma, infection. End stage of hematoma. Fibrous wall of varying thickness; internal debris and fluid levels common; Calcification in the wall in 30%.
  • Congenital epidermoid cysts: true cysts with epithelial-lined walls. Well defined, spherical, and usually unilocular with thin walls.  Sometimes have internal debris. No contrast enhancement occurs. Calcification in the walls uncommon.
  • Echinococcal cysts: can look like the above types. Rare in the U.S. Often have daughter cysts at the periphery and ringlike calcifications in mother and daughter walls. Can have high density hydatid 'sand' debris. 
  • Pancreatic pseudocysts can dissect into the splenic hilum 
Differential of multiple small, low-density lesion in the spleen
  • Microabscesses. immunocompromised patients w/ opportunistic infections like: Candida, aspergillus, cryptococcus, histoplasma, TB, pneumocystis carinii, CMV.
  • Lymphoma
  • Kaposi's sarcoma
  • Sarcoidosis
  • Metastases 
Splenic metastases
Melanoma (50%), lung, breast, and ovarian carcinomas. 
Most appear as ill-defined, low-density nodules with some degree of peripheral enhancement 
Melanoma commonly causes well-defined cystic metastases.
Benign solid renal tumor that arises from the proximal tubule. Men in their 60s. Can't distinguish from RCC though, so Tx is surgery.
Classic CT features: homogeneous attenuation w/ contrast and a central, sharply marginated, stellate, low‐attenuation scar. (RCC can do the same though)
Can also have heterogeneous attenuation, necrosis, and hemorrhage like RCC.
Renal Angiomyolipoma
Benign tumor composed of blood vessels, smooth muscle, and fat. Dysplastic vessels are prone to aneurysm, so bleeds common. 
Sporadic: middle-aged women.
Multifocal and bilateral: Tuberous sclerosis.
CT findings:
Presense of fat (<-20HU) is diagnostic.
Hemorrhage common
May not have fat and look like RCC; AML is suggested if the lesions are homogeneous high attenuation on unenhanced CT and show homogeneous increased density on enhanced CT.
Transitional cell carcinoma
90% in bladder. The rest in renal pelvis or ureter. 
CT findings:
Isodense on non-con. Variable, but usually poor enhancement.
  • Single or multiple filling defects (35%) in the renal pelvis have a smooth surface or a stippled papillary pattern  
  • Filling defects within dilated calyces obstructed at the infundibulum (26%). A “phantom” calyx fails to opacify and may be associated with a focal delayed or increasingly dense lobar nephrogram
  • Absent or decreased contrast excretion (13%) is caused by long‐standing obstruction at the ureteropelvic junction.
  •  Diffuse hydronephrosis with renal enlargement (6%) is seen with tumor obstruction at the ureteropelvic junction.
  • Large tumors invade the renal sinus fat and infiltrate into the parenchyma. Differentiation from RCC may be difficult.
  • Advanced disease shows extrarenal extension, regional lymph node involvement, and distant metastases to lungs and bone. TCC may rarely invade the renal vein and inferior vena cava.
  • Calcification occurs in up to 5% of tumors. It may appear coarse, punctate, linear, granular, or stippled and indistinct.
Renal medullary carcinoma
Aggressive infiltrative tumor that arises from the collecting tubules of the renal medulla. (RCC is from convoluted tubules of cortex.)
Ill-defined, nonencapsulated margins
Extends into renal sinus, replacing fat and protruding into collecting system
Large tumors are expansile and indistinguishable from RCC
Renal metastases: common sources and appearance
Sources: lung, breast, and GI adenocarcinomas.
Appearance: multiple bilateral low-attenuation renal nodules most common. Can also be solitary exophytic masses with colon Ca and melanoma.
Differential for multiple renal cysts
Multiple simple cysts, ADPKD, multicystic dysplastic kidney, von Hippel–Lindau disease, tuberous sclerosis, and acquired renal cystic disease (such as from dialysis)
Autosomal dominant polycystic kidney disease
Most pts present w/ HTN and renal failure ages 30-50. 
Associated w/ berry aneurysms in circle of Willis (10-15%)
CT findings:
  • Cysts of varying size in renal parenchyma w/ progressive bilateral increase in renal volume
  • Cysts in other organs: mostly liver (30-50%) and pancreas (10%)
  • Cysts often complicated by hemorrhage and may have calcified walls and/or high internal attenuation
  • Renal stones (20-40%) 
Multicystic dysplastic kidney
Nonhereditary renal dysplasia.
Multiple thin-walled cysts that do not communicate w/ collecting system. At birth, kidney is enlarged. Progressively shrinks with time and often calcifies.
Opposite kidney has UPJ obstruction or other anomaly in 30%
Von-Hippel Lindau
Autosomal dominant.
Characterized by: Cerebellar, spinal cord and retinal hemangioblastomas; Renal and pancreatic cysts; RCC; Pheochromocytoma. 
 RCC in 30-45%.  Pheo in 30% (bilateral in 50% of those)
Tuberous sclerosis (renal)
Autosomal dominant.
Multiple and bilateral renal AMLs; cutaneous, retinal, and cerebral hamartomas. The renal lesions are commonly detected in infancy and childhood.
Acquired renal cystic disease
Pts on chronic HD get innumerable cysts in their native kidneys. >90% of pts on HD for 5-10 are affected.
Cysts are lined by hyperplastic and dysplastic epithelium. Complications by hemorrhage w/ calcification of cyst walls is common.
Cysts usually regress within months of renal transplant.
Acute pyelonephritis
Symptoms usually resolve in patients with uncomplicated pyelonephritis within 72 hours of antibiotic therapy. Patients who fail to improve should be imaged.
CT signs of acute bacterial infection of the kidneys include:
Wedge‐shaped areas of mottled decreased parenchymal enhancement, similar to renal infarct. 
A striated pattern of linear alternating increased and decreased densities on enhanced scans is particularly characteristic.
High‐density areas of parenchyma on unenhanced scans indicate parenchyma hemorrhage caused by inflammation and ischemia.
Perirenal fat stranding and thickening of the renal fascia.
Severe localized infection (focal pyelonephritis, acute focal bacterial nephritis, lobar nephronia) produces a poorly defined, mottled, low‐density mass without distinct liquefaction. These phlegmons may resolve completely, result in a scar, or evolve into an abscess.
Emphysematous pyelonephritis is a severe type of diffuse pyelonephritis that occurs in patients with diabetes or urinary obstruction. Gas in renal parenchyma and signs of renal inflammation. Emergency nephrectomy is usually the treatment of choice.
Emphysematous pyelitis refers to gas confined to the renal pelvis and calyces. This finding may be found with infection, trauma, instrumentation, or fistula and lacks the dire implications of gas within the renal parenchyma.
Abscess: collection of pus and liquefied tissue within the kidney or with spread into the perirenal space. Fluid collection (10–30 H) with an enhancing rim. Gas may be present, esp in patients with diabetes. Large abscesses require catheter or surgical drainage
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