Gastrointestinal Imaging Flashcards
Liver Anatomy
The Couinaud classification divides the liver into eight segments. Because each segment is self-contained, an individual segment can be completely resected without disturbing the other segments.
Numbering of hepatic segments is clockwise when looking at a frontal/coronal view.
Each hepatic segment features its own: (Central portal triad including branches of the portal vein, hepatic artery, and bile duct. Peripheral venous drainage to the hepatic veins and ultimately the IVC.)
The caudate lobe drains directly to the IVC, not into the hepatic veins. The caudate lobe is spared in early cirrhosis since the direct drainage to the IVC spares the caudate from increased venous pressures due to portal hypertension. This leads to compensatory hypertrophy of the caudate lobe, which is a typical morphologic change of early cirrhosis.
Liver CT
A “routine” contrast-enhanced abdominal CT is acquired in the portal venous phase of enhancement, typically obtained 70 seconds following intravenous contrast administration.
A portal venous phase CT reveals characteristic attenuation alterations and/or morphologic changes of diffuse liver disease, such as hepatic steatosis and cirrhosis. Most metastatic tumors are not hypervascular (although a few notable exceptions will be subsequently discussed) and can also generally be detected on the portal venous phase. Of note, rarely some breast cancers may be isoattenuating on the portal venous phase and more conspicuous on unenhanced CT.
Most benign and malignant primary liver masses are hypervascular and thus most conspicuous in the arterial phase of enhancement. The arterial phase begins approximately 20-25 seconds after intravenous contrast injection. Many authors advocate that optimal conspicuity of a hypervascular liver lesion is obtained in the late arterial phase, which is between 9 and 16 seconds after abdominal aortic enhancement, or approximately 35 seconds after intravenous injection.
Liver MRI
Compared to CT, MRI of the liver displays the same patterns of contrast enhancement but has superior lesion-to-liver contrast. MRI also does not impart ionizing radiation.
MRI is able to obtain dynamic post-contrast images in multiple phases without any penalty in radiation exposure. In- and out-of-phase gradient imaging allows detection of intractyoplasmic lipid, which is seen in hepatic steatosis. Additionally, advanced techniques such as diffusion-weighted imaging may show potential for clinical use.
Fatty liver (hepatic steatosis)
Nonalcoholic fatty liver diease can be divided into steatosis and steatosis with associated inflammatory activity (steatohepatitis). Overall, greater than 15% of the population is afflicted with nonalcoholic fatty liver disease (NAFLD), which is a component of the metabolic syndrome of obesity, insulin resistance, and dyslipidemia. Ultimately, steatohepatitis may progress to cirrhosis.
CT can determine if steatosis is present and can provide a rough gauge as to its severity. In- and out-of-phase MRI imaging can more accurately quantify the degree of steatosis, although liver biopsy is the gold standard and best evaulates for the presence of inflammatory and early fibrotic change. By the time imaging can detect morphologic changes of cirrhosis, the changes may be irreversible.
On unenhanced CT, the liver should be slightly hyperattenuating relative to the spleen. The traditional teaching is that steatosis is present if the liver attenuates at least 10 Houndsfield units (HU) less than the spleen, although new work suggests that even a single HU of relative hypoattenuation compared to the spleen may represent hepatic steatosis.
On contrast-enhanced CT, evaluation of hepatic steatosis is much less reliable compared to unenhanced CT due to different contrast uptake rates of the liver and the spleen. However, the liver is considered diffusely hypoattenuating if it attenuates at least 25 HU less than the spleen in the portal venous phase.
In- and out-of-phase GRE MRI is a sensitive imaging technique to evaluate for the presence of (and to quantify the degree of) hepatic steatosis.
Variations in portal venous supply may cause geographic regions that are more or less affected by fatty change. Focal fat does not have any mass effect, vessels characteristically run through it, and it tends to occur in the following typical locations.
Amyloid
Abnormal extracellular deposition of amyloid protein in the liver can cause focal or diffuse areas of decreased attenuation on CT imaging.
Wilson disease
Wilson disease causes high levels of copper to accumulate in the basal ganlgia, cornea, and liver due to an autosomal recessive genetic defect. The liver may be hyperattenuating on CT with multiple nodules, eventually leading to hepatomegaly and cirrhosis.
Hepatic Iron Overload
There are two pathways to excess hepatic iron accumulation. Accumulation within hepatocytes is seen in hemochromatosis. Uptake within the reticuloendothelial system (RES) causes hepatic Kupffer cell iron overload, as seen in hemosiderosis. Regardless of the etiology, the iron-overloaded liver is hypointense on all MRI sequences, relative to the paraspinal muscles as an internal control. Hemochromatosis is the most common cause of iron overload, due to a genetic defect causing increased iron absorption. Excess iron is unable to be stored in the RES, so the spleen and bone marrow are not affected. Treatment of hemochromatosis is phlebotomy.
Hemosiderosis is excess iron stored within the reticuloendothelial system, which may be due to frequent blood transfusions or defective erythrocytosis. Treatment of hemosiderosis is with iron chelators, not phlebotomy.
Hemosiderosis is excess iron stored within the reticuloendothelial system, which may be due to frequent blood transfusions or defective erythrocytosis. Treatment of hemosiderosis is with iron cheltors, not phlebotomy.
Hemosiderosis is a precursor to secondary hemochromatosis. Secondary hemochromatosis is hepatic damage from iron overload after the RES system becomes saturated from prolonged hemosiderosis.
In clinical practice, the distinction between hemosiderosis and secondary hemochromatosis often overlaps. Many authors recommend against the term “secondary hemochromatosis” in favor of describing the primary disease (e.g., thalassemia) with secondary iron overload.
Hypoattenuating liver: The liver is considered hypoattenuating if it attenuates less than the spleen on an unenhanced CT. (Fatty liver (hepatic steatosis) is by far the most common cause of a diffusely hypoattenuating liver. Hepatic amyloid is rare and may cause either focal or diffuse hepatic hypoattenuation.)
Hyperattenuating liver: The normal unenhanced attenuation of the liver is 30 to 60 HU. An absolute attenuation greater than 75 HU is considered hyperattenuating. (Iron overload is by far the most common cause of a hyperattenuating liver. Medications (e.g. amiodarone, gold, and methotrexate). Copper overload (Wison disease). Glycogen excess)
Viral Hepatitis
Patients with viral hepatits often have a normal CT scan. Viral hepatitis may cause nonspecific CT findings, such as gallbladder wall thickening or periportal edema (fluid on both sides of the portal veins).
Candidiasis
Systemic fungal infection may seed the liver (and commonly the spleen as well) due to portal venous drainage of infected bowel. CT shows multiple tiny hypoattenuating microabscesses in the liver and the spleen, which may be rim-enhancing.
Candidiasis is almost always seen in immunocompromised patients.
The differential diagnosis for multiple tiny hypoattenuating hepatic lesions includes metastatic disease, lymphoma, biliary hamartomas, and Caroli disease.
Abscess
Hepatic abscess is most commonly caused by a bowel process and resultant infectious nidus carried through the portal system to the liver. Common causes include diverticulitis, appendicitis, Crohn disease, and bowel surgery. E. coli is the most common organism. A primary hepatobiliary infection, such as ascending cholangitis, may be a less common cause.
Imaging features of hepatic abscess may mimic metastasis, appearing as a ring-enhancing mass on CT. On MRI, there is typically central hyperintensity on T2-weighted images with an irregular wall that enhances late. Perilesional enhancement may be present.
Echinococcal disease
Hepatic echinococcus is caused by ingestion of the eggs of Echinococcus granulosus, which is endemic in the Mediterranean basin and associated with sheep-raising. Echinococcal eggs can develop into hydatid cysts.
On CT, a hydatid cyst is a well-defined hypoattenuating mass featuring a characteristic floating membrane or an associated daughter cyst. Peripheral calcification may be present.
Cirrhosis
Cirrhosis is caused by repeated cycles of injury and repair, which can be due to metabolic (alcohol, steatohepatitis, hemochromatosis, or Wilson disease), infectious (chronic hepatitis B or C), or inflammatory (primary biliary cirrhosis or primary sclerosing cholangitis) etiologies. The hallmarks of cirrhosis are fibrosis and attempted, disorganized regeneration.
The micronodular form of cirrhosis is most often due to metabolic causes.
The macronodular form of cirrhosis is most often post-viral (hepatitis B or C).
One of the earliest signs of cirrhosis is expansion of the preportal space. Atrophy of the medial segment of the left hepatic lobe in early cirrhosis causes increased fat anterior to the right main portal vein. Enlargement of the caudate lobe is a specific sign of cirrhosis. Specifically, a caudate to right lobe size ratio >0.65 highly suggests cirrhosis. As previously discussed, the caudate drains directly to the IVC, not via the hepatic veins, which results in compensatory caudate hypertrophy. The empty gallbladder fossa sign results when hepatic parenchyma surrounding the gallbladder is replaced with periportal fat.
Portal hypertension causes splenomegaly, portosystemic collaterals, and varices. Gallbladder wall thickening is due to hypoalbuminemia and resultant edema. Gamna-Gandy bodies are splenic microhemorrhages, which appear hypointense on GRE.
Pathway to hepatocellular carcinoma
In the setting of cirrhosis, hepatocellular carcinoma (HCC) is thought to develop in a sequence from regenerative nodule to dysplastic nodule to HCC. Regenerative and dysplastic nodules cannot be reliably differentiated on imaging; and high-grade dysplastic nodules cannot be reliably differentiated from low-grade HCC.
Regenerative nodule: A regenerative nodule is completely supplied by the portal vein and is not premalignant. A regenerative nodule should not enhance in the arterial phase. (Most regenerative nodules show low signal intensity on T2-weighted images, with variable signal intensity on T1-weighted images. Rarely, a regenerative nodule may be hyperintense on T1-weighted images due to glycogen deposition. On contrast-enhanced MRI, most regenerative nodules enhance to the same (or slightly less) degree as the adjacent hepatic parenchyma.)
Dysplastic nodule: Unlike a regenerative nodule, a dysplastic nodule is premalignant. However, most dysplastic nodules do not demonstrate arterial phase enhancement (unless high grade), since blood supply is still from the portal vein. (Dysplastic nodules are variable in signal intensity on T1-weighted images. Most dysplastic nodules are hypointense on T2-weighted images, although high-grade dysplastic nodules may be T2 hyperintense. Contrast-enhanced MRI shows low-grade dysplastic nodules to be iso-enhancing relative to liver and thus indistinguishable from regenerative nodules. High grade dysplastic nodules may demonstrate arterial enhancement and be indistinguishable from well-differentiated hepatocellular carcinoma.)
A siderotic nodule is an iron-rich regenerative or dysplastic nodule. A siderotic nodule is hypointense on T1 and T2-weighted images and hyperattenuating on CT. A siderotic nodule is rarely, if ever, malignant.
Hepatocellular Carcinoma
Hepatocellular carcinoma (HCC) is the most common primary liver tumor. Cirrhosis is the major risk factor for development of HCC. A hypervascular liver mass in a patient with cirrhosis or chronic hepatitis is an HCC until proven otherwise.
Alpha-feto protein (AFP) is elevated in approximately 75% of cases of HCC.
Arterial phase enhancement is the characteristic imaging feature of HCC. However, between 10 and 20% of HCCs are hypovascular and thus slightly hypoenhancing relative to surrounding liver on arterial phase imaging.
The classic CT or MRI appearance of HCC is an encapsulated mass that enhances on arterial phase and washes out on portal venous phase. HCC may be difficult to detect on non-contrast or portal venous phase CT. On unenhanced MRI, HCC is characteristically slightly hyperintense on T2-weighted images relative to surrounding liver. (The nodule in a nodule appearance describes an enhancing nodule within a dysplastic nodule and represents an early HCC).
HCC is locally invasive and tends to invade into the portal and portal veins, IVC, and bile ducts. In contrast, metastases to the liver are much less likely to be locally invasive.
Treatment options for HCC include partial hepatectomy, orthotopic liver transplantation, percutaneous ablation, and transcatheter embolization.
Fibrolamellar HCC
Fibrolamellar carcinoma is a subtype of HCC that occurs in young patients without cirrhosis.
The tumor tends to be large when diagnosed, but has a better prognosis than typical HCC. Unlike in HCC, AFP is not elevated.
On MRI, fibrolamellar HCC is a large, heterogenous mass. A fibrotic central scar is classic, which is hypointense on T1 and T2-weighted images (in contrast, focal nodular hyperplasia feature a T2 hyperintense scar that enhances late). Capsular retraction may be seen in 10%.
Unlike HCC, the fibrolamellar subtype does not have a capsule, although there may be a pseudocapsule of peripherally compressed normal hepatic tissue.
Hepatic Metastases
Although metastases are supplied by branches of the hepatic artery induced by tumoral angiogenesis, most metastases are hypovascular and best appreciated on portal venous phase (in contrast to HCC, which is hypervascular and best visualized on late arterial phase).
Hypervascular metastases (best seen on arterial phase) classically include: (Neuroendocrine tumors, including pancreatic neuroendocrine tumors and carcinoid. Renal cell carcinoma. Thyroid carcinoma. Melanoma. Sarcoma.)
Colorectal and pancreatic adenocarcinoma metastases are typically hypovascular and can be usually diagnosed on portal venous imaging.
Calcifications can be seen in mucinous colorectal tumors or ovarian serous tumors. Calcification within a metastatic lesion may imply a better prognosis.
On MRI, metastatic lesions tend to be hypointense on T1-weighted images and hyperintense on T2-weighted images. Blood products and melanin (as in melanoma) are T1 hyperintense.
Pseudocirrhosis describes the macronodular liver contour resulting from multiple scirrhous hepatic metastases, which may mimic cirrhosis. Treated breast cancer is the most common cause of this appearance. Capsular retraction, although not always seen, is characteristic of pseudocirrhosis, and when present suggests pseudocirrhosis over cirrhosis.
Hepatic lymphoma
Primary hepatic lymphoma is very rare. Lymphomatous involvement of the liver tends to be secondary to systemic disease, with associated splenomegaly and lymphadenopathy.
Epithelioid hemangiothelioma
Epithelioid hemangioendothelioma is a rare vascular malignancy that characteristically causes multiple spherical subcapsular masses that can become confluent. The individual masses may have a halo or target appearance. Epithelioid hemagioendothelioma is one cause of capsular retraction.
Hepatic capsular retraction
Capsular retraction is a focal convexity of the normally convex external liver contour.
Metastatic tumor (more commonly post-treatent)
Fibrolamellar hepatocellular carcinoma (10% of cases of fibrolamellar HCC).
Hepatocellular carcinoma (capsular retraction has been reported but is uncommon).
Epithelioid hemangioendothelioma.
Intrahepatic cholangiocarcinoma.
Confluent hepatic fibrosis (wedge-shaped fibrosis seen in cirrhosis, most commonly the medial segment of the left hepatic lobe or the anterior segment of the right hepatic lobe).
Focal Nodular Hyperplasia
Focal Nodular Hyperplasia (FNH) is disorganized liver tissue with no malignant potential. It is primarily seen in asymptomatic women and is not associated with oral contraceptives.
FNH has a characteristic central “scar” which does not contain fibrotic tissue and is therefore not a true scar. Instead, the central area consists of T2-hyperintense ductules and venules, and demonstrates delayed enhancement. FNH does not have a capsule.
FNH can be difficult to see without contrast on CT and T1- and T2-weighted MRI sequences. FNH avidly enhances during the arterial phase, then washes out very quickly. The portal venous phase will often show just the unenhanced scar, which enhances late.
Kupffer cells and bile duct epithelium are both present. Kupffer cells may be confirmed by a sulfur colloid study (1/3 of the time) and bile duct cells can be seen on a HIDA scan.
Hemangioma
A hepatic hemangioma is a benign mass composed of disorganized endotheliallined pockets of blood vessels, supplied by a branch of the hepatic artery at the periphery.
Hemangioma is more common in females and uncommon in cirrhosis. When a known hemangioma is sequentially followed in a patient with early cirrhosis, the hemangioma involutes as the liver becomes more cirrhotic.
Hemangiomas may range in size from <1 cm to >10 cm. Giant hemangiomas tend to have a nonenhancing central area representing cystic degeneration.
A virtually pathognomonic imaging feature is periphera, discontinuous, progressive, nodular enhancement. The attenuation (or signal intensity on MR) of the enhancement is identical to the aorta and features gradual centripetal fill-in on later phases.
The unenhanced CT appearance of a hemangioma is a nonspecific hypoattenuating liver mass.
Hepatic Adenoma
Hepatic adenoma is a benign hepatic neoplasm containing hepatocytes, scattered Kupffer cells, and no bile ducts.
Adenomas are much more common in females, especially with prolonged oral contraceptive use. When seen in males, adenoma may be associated with anaboic steroids.
Adenomas have a relatively high risk of hemorrhage, which is often the presenting symptom. For this reason, incidentally discovered adenomas are usually resected.
Multiple hepatic adenomas are seen in von Gierke disease (type I glycogen storage disease).
A pseudocapsule may be present, which tends to enhance late.
Adenomas lack portal venous drainage and thus are hypervascular on arterial phase. The presence of microscopic fat, when present, is best seen on in- and out-of-phase MRI. Intralesional hemorrhage may cause T1 hyperintensity. Adenomas may be difficult to differentiate from other hypervascular liver lesions in the absence of fat or hemmorrhage.
Budd-Chiari
Budd-Chiari is hepatic venous outflow obstruction, which can be thrombotic or non-thrombotic. Budd-Chiari may be due to hypercoagulative states including hematological disorders, pregnancy, oral contraceptives, malignancy, infection, and trauma. It is very rare to have primary Budd-Chiari due to congenital hepatic veins anomaly, as pictured below.
Acute Budd-Chiari presents with a clinical triad of hepatomegaly, ascites, and abdominal pain.
Direct vascular findings include lack of flow within hepatic veins, thrombus in the hepatic veins/IVC, and the formation of collateral vessels.
Acute intraparenchymal findings include an edematous peripheral liver with sparing of the caudate lobe. The caudate is spared as it drains directly into the IVC.
Progressive liver failure may result in chronic disease, producing caudate lobe hypertrophy and atrophy of peripheral liver with prominent regenerative nodules.
Veno-occlusive diease
Veno-occlusive disease (VOD) is destruction of post-sinusoidal venules, with patent hepatic veins. VOD is seen in bone marrow transplant patients, possibly due to chemotherapy.
Imaging findings are nonspecific. Periportal edema, narrowing of the hepatic veins, hepatomegaly, and heterogenous hepatic enhancement have been reported. In contrast to Budd-Chiari, the caudate lobe is not spared.
Cardiac Hepatopathy
Cardiac hepatopathy is passive hepatic congestion from heart failure, constrictive pericarditis, or right-sided valvular disease, which ultimately may lead to cirrhosis.
Imaging clues are enlarged hepatic veins and IVC, with reflux of intravenous contrast from the right atrium into the IVC and hepatic veins. The liver is typically enlarged and demonstrates mottled enhancement. Ascites is usually present.
Biliary hamartomas (von Meyenburg complexes)
Biliary hamartomas are incidental small cystic lesions that do not communicate with the biliary tree, caused by embryologic failure of normal bile duct formation.
Biliary hamartomas tend to be smaller and more irregularly shaped than simple cysts.
Autosomal dominant polycystic liver disease (ADPLD)
40% of patients with autosomal dominant polycystic kidney disease (ADPKD) have a similar disease process in the liver, called ADPLD. Even in severe disease, hepatic failure is rare.
On imaging, there are innumerable nonenhancing simple cysts throughout the liver.
Liver Trauma
The liver is the second most commonly injured solid organ due to blunt trauma, second to the spleen. The CT description and grading of liver injury is similar to splenic injury.
The American Association for the Surgery of Trauma (AAST) classification describes hepatic injury based on findings at laparotomy.
The MDCT injury grading scale is based on CT findings and is more commonly used by radiologists. It is similar to the MDCT grading scale for splenic trauma.
MDCT hepatic trauma
Grade 1: Superficial laceration or subcapsular hematoma <1 cm in size.
Grade 2: Laceration or subcapsular/intraparenchymal hematoma >1 and <3 cm in size.
Grade 3: Laceration or subcapsular/intraparenchymal hematoma >3 cm in diameter.
Grade 4: Massive hematoma >10 cm, or destruction/devascularization of one hepatic lobe.
Grade 5: Destruction or devascularization of both hepatic lobes.
MRCP
Magnetic resonance cholangiopancreatography (MRCP) is an abdominal MRI acquired with heavily T2-weighted sequences that increase the contrast between T2 hyperintense stationary fluid in the biliary tract and surrounding structures.
Fast spin echo sequences are most commonly used for MRCP acquisition. Various techniques can be employed to optimize imaging including breath-hold sequences and respiratory-triggered sequences.
Heavily T2-weighted sequences primarily image the biliary tree.
Sequences with intermediate T2 (TE 80-100ms) are best suited for visualization of the biliary ductal system and surrounding tissue, in particular to evaluate extraluminal structures.
Advantages of MRCP over ERCP include: MRCP has the ability to see extra-luminal findings. MRCP can visualize excluded (obstructed) ducts. MRCP is non-invasive.
Disadvantages of MRCP compared to ERCP include: MRCP does not allow for concurrent therapeutic intervention. MRCP does not actively distend the biliary ductal system with contrast. MRCP has worse spatial resolution compared to ERCP.
Contrast-enhanced MRCP can also be performed with fat-saturated T1-weighted imaging after injection of gadolinium contrast agents that have biliary excretion, such as gadoxetic acid disodium (Eovist, Bayer Healthcare, Germany) and gadobenate dimeglumine (Multihance, Bracco Diagnostics). These agents shorten T1 relaxation, resulting in T1 hyperintense biliary fluid, but require a 20-45 minute delay prior to imaging to allow time for biliary excretion.
Choledochal Cysts
Type I choledochal cyst: Fusiform common bile duct dilation
Type II choledochal cyst: Extrahepatic saccular dilation
Type III choledochal cyst: Dilation of intraduodenal bile duct.
Type IV choledochal cyst: Multiple segments dilated
Type V choledochal cyst: Intrahepatic dilation = Caroli disease
Choledochal cysts are thought to represent a heterogenous group of disease with a common end pathway of intrahepatic or extrahepatic biliary ductal dilation.
The Todani system divides the cysts into types I-V based on their number, distribution, and morphology.
Most choledochal cysts are diagnosed in childhood, but less commonly may be a new diagnosis for an adult. Clinijcally, choledochal cysts can present with nonspecific abdominal pain or may be found incidentally.
Choledochal cysts are often resected due to increased cholangiocarcinoma risk, which can be as high as 25%.
In contrast to biliary hamartomas, choledochal cysts do communicate with the biliary tree.
Type I Choledochal Cyst
A type I choledochal cyst, representing extrahepatic dilation of the common bile duct, is the most common type of extrahepatic cyst.
Caroli Disease (Type V choledochal cyst)
Caroli disease represents saccular dilation of the intrahepatic bile ducts, which may be segmental or diffuse. Caroli disease may be associated with polycystic kidneys.
Caroli syndrome is Caroli disease plus hepatic fibrosis.
The central-dot sign describes the small branches of the portal veink and hepatic artery bridging the dilated bile ducts, which look like a central dot on contrast-enhanced CT.
Biliary Anatomical Variants
Low insertion of cystic duct - With a low insertion of the cystic duct, the surgeon may misidentify the common duct as the cystic duct if the patient undergoes choleycystectomy, possibly leading to inadvertent common duct litigation.
Aberrant right posterior duct - An aberrant right posterior duct is only important if the patient is a right hepatic lobe liver donor, as the two right hepatic ducts need to be anastomosed separately in the recipient.
Acute Choleycystitis
Choleycystitis is inflammation and localized infection secondary to obstruction of the gallbladder neck or cystic duct.
Calculous choleycystitis is caused by a gallstone which blocks the cystic duct.
Acalculous choleycystitis is a functional obstruction of the cystic duct without a culprit stone. It is typically seen in ICU patients.
Acute choleycystitis is typically diagnosed by ultrasound, but similar criteria can be applied to CT: (Gallbladder wall thickening >3 mm (a nonspecific finding). Pericholeycystic fluid or inflammatory changes in the pericholeycystic fat. Gallbladder hyperemia. Gallbladder calculi (although not all gallstones are radiopaque; ultrasound is more sensitive).
Complications of acute choleycystitis include gangrenous choleycystitis, gallbladder perforation, and emphysematous choleycystitis.
Gangrenous choleycystitis is due to increased intraluminal pressure, leading to gallbladder wall ischemia. On imaging, the gallbladder wall thickening may be notably asymmetric and intraluminal membranes may be present. Due to the increased risk of perforation, treatment is emergent choleycystectomy or choleycystostomy.
Acute gallbladder perforation has a very high mortality due to generalized bile peritonitis. Subacute perforation may lead to a pericholeycystic abscess and chronic perforation may cause a choleycystoenteric fistula.
Emphysematous cholecystitis is a severe complication of acute cholecystitis caused by gas-forming bacteria. Gas may be present either within the lumen or the wall of the gallbladder. The typical patient susceptible to emphysematous cholecystitis is an elderly diabetic. Treatment of emphysematous cholecystitis is most often emergent cholecystectomy or cholecystostomy, although treatment can be conservative in patients with a very high surgicla risk.
Porcelain Gallbladder
Porcelain gallbladder describes a peripherally calcified gallbladder wall, thought to be a sequela of chronic cholecystitis.
Porcelain gallbladder is associated with a (somewhat controversial) increased risk of gallbladder carcinoma. Typically, a porcelain gallbladder is an indication for non-emergent cholecystectomy.
Ascending Cholangitis
Obstruction of the biliary tree, most commonly due to choledocholithiasis, may cause ascending cholangitis, which presents with the clinical triad of fever, abdominal pain, and jaundice (Charcot’s triad).
On imaging, the key finding is hyperenhancement and thickening of the walls of the bile ducts, often with a common bile duct stone present. On ultrasound, debris within the biliary system may be apparent.
Initial treatment is antibiotics and fluid resuscitation. Endoscopic biliary intervention may be necessary if the patient does not respond to conservative management.
Primary Sclerosing Cholangitis
Primary sclerosisng cholangitis (PSC) is idiopathic inflammation and destruction of bile ducts
PSC is associated with ulcerative colitis (UC) and is more common in males. (Most (75%) patients with PSC have UC, while only a few (4-5%) of patients with UC have PSC)
Biliary imaging shows a characteristic beaded, irregular appearance of the common bile duct and intrahepatic bile ducts.
PSC appears similar to HIV-cholangiopathy, although cholangitis in HIV patients is more commonly associated with papillary stenosis.
Long-term complications of PSC include cirrhosis, cholangiocarcinoma, and recurrent biliary infections. Cross-sectional imgin is better at evaluating for these complications compared to ERCP.
Primary Biliary Cirrhosis
Primary biliary cirrhosis (PBC is inflammation and destruction of smaller bile ducts compared to PSC. PBC affects middle-aged women and often initially presents with pruritus.
Similar to PSC, chornic PBC can lead to hepatic cirrhosis.
AIDS cholangitis (AIDS cholangiopathy)
Patients with acquired immunodeficiency syndrome are susceptible to biliary infection with Cryptosporidium and CMV, which clinically present with right upper quadrant pain, fever, and elevated LFTs.
The imagin of AIDS cholangitis appears nearly identical to primary sclerosing cholangitis, with multiple strictures and a beaded appearance of the bile ducts. A distinguishing feature of AIDS cholangitis is papillary stenosis, which is not typically seen in PSC.
Recurrent Pyogenic Cholangitis (Oriental cholangiohepatitis)
Recurrent pyogenic cholonagitis, also known as Oriental cholangiohepatitis, is thought to be caused by the parasite Clonorchis sinensis, which leads to pigment stone formation, biliary stasis, and cholangitis. Nutritional deficiency may also play a role. The disease typically affects patients indigenous to Southeast Asia. Clinically, patients present with recurrent jaundice and fevers.
Recurrent pyogenic cholangitis features an imaging triad of: 1) Pneumobilia. 2) Lamellated bile duct filling defects. 3) Intrahepatic and extrahepatic bile duct dilation and strictures.
Patients with recurrent pyogenic cholangitis have an increased risk of cholangiocarcinoma.
Biliary Cystadenoma
Biliary cystadenoma is a benign neoplasm, occuring predominantly in middle-aged women. Biliary cystadenoma may be quite large at presentation and cause nonspecific symptoms such as abdominal pain, nausea, vomiting, and obstructive jaundice.
Biliary cystadenoma does not communicate with the biliary system.
On imaging, biliary cystadenoma appears as a large, multiloculated, cystic mass. The presence of septations distinguishes cystadenoma from a simple cyst. The septations may mimic an echinococcal cyst. In contrast to hepatic abscess or necrotic metastasis, a thick enhancing wall is not a feature of cystadenoma.
Although benign, cystadenoma may uncommonly recur after resection.
Malignant degeneration to biliary cystadenocarcinoma has been reported but is rare. The presence of a large solid component or thick calcification should raise concern for cystadenocarcinoma.
Cholangiocarcinoma
Cholangiocarcinoma is a highly malignant tumor of the biliary ductal epithelium.
A hilar tumor (at the confluence of the right and left intrahepatic biliary ducts), known as a Klatskin tumor, is the most common form of cholangiocarcinoma. In contrast, peripheral cholangiocarcinoa is rare.
Cholangiocarcinoma tends to obstruct bile ducts and cause intrahepatic ductal dilation. Eventually, the obstruction may lead to lobar atrophy.
Risk factors for development of cholangiocarcinoma include: Choledochal cyst(s). Primary sclerosing cholangitis. Familial adenomatous polyposis syndrome. Clonorchis sinensis infection. Thorium dioxide (alpha-emitter contrast agent), not used since the 1950s. Thorium dioxide is also associated with angiosarcoma and HCC.
On cross-sectional imaging, cholangiocarcinoma typically presents as an intrahepatic mass at the confluence of the central bile ducts (Klatskin tumor), with resultant bile duct dilation and capsular retraction. Tumor fingers often extend into the bile ducts.
Gallbladder carcinoma
Gallbladder carcinoma is rare and is usually due to chronic gallbladder inflammation.
Gallstones and concomitant chronic cholecystitis are typically present. Porcelain gallbladder, a result of chronic cholecystitis, is thought to be a risk factor for gallbladder cancer, although this is controversial.
Gallbladder carcinoma most commonly presents as scirrhous infiltrating mass that invades through the gallbladder wall into the liver. Less commonly, gallbladder carcinoma may appear as a polypoid mass. Very rarely it can present as mural thickening.
Tumor spread is via direct extension into the liver, although lymphatic and hematogenous metastasis are also common.
Prognosis is generally poor, although small polypoid lesions may undergo curative resection.
Metastasis to the Gallbladder
Melanoma has a propensity to metastasize to the gallbladder.
Overview of Pancreatic Neoplasms
Adenocarcinoma (ductal adenocarcinoma)
Pancreatic ductal adenocarcinoma makes up 80-90% of all pancreatic tumors. It is typically seen in patients over age 60, with a slight male predominance. Risk factors include smoking, alcohol, and chronic pancreatitis.
A pancreatic-mass CT includes unenhanced, late arterial phase, and portal venous phase images. The late arterial phase (pancreatic parenchymal phase) has the greatest conspicuity for detecting the hypoenhancing tumor against the background enhancing pancreas.
The most common location of ductal adenocarcinoma is the pancreatic head.
The classic appearance is a hypodense (CT), T1 hypointense (MR), ill-defined, hypovascular mass causing ductal obstruction and atrophy of the pancreatic tail. The double duct sign describes dilation of both the pancreatic duct and the common bile duct.
Since pancreatic adenocarcinoma is almost alsways associated with a dilated pancreatic duct, an alternative diagnosis should be strongly considered if there is a pancreatic mass with no ductal dilation, such as: Autoimmune pancreatitis. Groove Pancreatitis. Cystic pancreatic tumor. Neuroendocrine tumor. Duodenal gastrointestinal stromaltumor (GIST). Peripancreatic lymph node. Pancreatic metastasis (e.g., renal cell, thyroid, or melanoma). Lymphoma.
Conversely, if the double duct sign is present but no mass is visible, one should still be suspicious for pancreatic adenocarcinoma. Approximately 10% of cases will be isoattenuating relative to pancreas in the pancreatic parenchymal (late arterial) phase and thus extremely difficult to directly detect.
Most cancers present at an advanced, unresectable stage. Unresectable tumors show encasement (>180° circumference) of the SMA, extensive venous invasion, or evidence of metastasis.
For lower-stage tumors, complete surgical resection is the only chance for cure. A resectable tumor features no evidence of celiac, SMA, or portal venous invasion. Limited extension to the duodenum, distal stomach, or CBD does not preclude resection, as these structures are resected during the Whipple procedure. Limited venous extension may be resectable.
Acinar cell carcinoma
Acinar cell carcinoma is a rare, aggressive variant of pancreatic adenocarcinoma, exclusively seen in elderly males.
The malignant cells produce a large amoutn of lipase to cause the clinical triad of lipase hypersecretion syndrome: Subcutaneous fat necrosis; bone infarcts causing polyarthralgias; and eosinophilia.
Cystic Pancreatic Epithelial Neoplasms
Serous cystadenoma
Mucinous cystic neoplasm
Solid and papillary epithelial neoplasm (SPEN)
Intraductal papillary mucinous neoplasm (IPMN)
Serous Cystadenoma
Serous cystadenoma is a benign tumor that occurs in elderly women and has been nicknamed the grandmother tumor.
It consists of many small cysts (>6 cysts that are <2 cm) that may have a solid appearance on CT due to apposition of many cyst walls. MRI is useful to show the cystic nature of the lesion.
Serous cystadenoma is hypervascular, unigque among cystic pancreatic tumors.
Unlike adenocarcinoma, serous cystadenoma does not cause pancreatic duct dilation or tail atrophy.
A classic imaging feature is central stellate calcification.
Mucinous cystic neoplasm
Mucinous cystic neoplasm affects middle-aged women and has therefore been nicknamed the mother tumor.
Mucinous cystic neoplasm is benign, but does have malignant potential. Treatment is typically resection due to malignant potential.
The tumor consists of a single or a few large cysts (<6 cysts that are >2 cm) and typically occurs in the pancreatic body and tail.
Mucinous cystic neoplasm has a capsule. The only other pancreatic tumor with a capsule is SPEN.
Solid and Papillary Epithelial Neoplasm
Solid and papillary epithelial neoplasm (SPEN) occurs in young women and children and is nicknamed the daughter tumor. It may be a rare cause of abdominal pain.
It has low malignant potential and is typically resected.
On imaging, SPEN appears as a large mass with heterogenous solid and cystic areas. Hemorrhage is typical. SPEN features a capsule, as does mucinous cystic neoplasm.
Intraductal Papillary Mucinous Neoplasm (IPMN)
Intraductal papillary mucinous neoplasm (IPMN) occurs most commonly in elderly males and is nicknamed the grandfather tumor, although these tumros exhibit the greatest age and sex variability of the cystic pancreatic neoplasms.
IPMN featrues a spectrum of biological behavior from benign to indolent to aggressive carcinoma. IPMNs may arise from the main pancreatic duct or a sidebranch. The main duct IPMNs have greater malignant potential.
The classic appearance on endoscopy is a fish-mouth papilla pouring out mucin. Cross-sectional imaging shows a cystic intrapancreatic lesion in contiguity with the duct or sidebranch. Any nodular or enhancing component should raise concern for malignancy.
The recommended imaging follow-up and criteria for resectability are controversial. Current guidelines published in 2006 recommend following simple pancreatic cysts <1 cm annually by imaging (typically MR). However, up to 40% of elderly males have a pancreatic cyst, suggesting that they may be an acquired condition of aging rather than a premalignancy.
In general, a suspected IPMN is resected if it is >3 cm in size, if there is a mural nodule, or if there is associated dilation of the pancreatic duct to >10 mm.
Pancreatic Endocrine Neoplasms
Pancreatic neuroendocrine tumors may be hyperfunctioning or non-hyperfunctioning.
Hyperfunctioning tumors come to clinical attention due to symptoms of endocrine excess.
Non-hyperfunctioning tumors tend to be larger at diagnosis. These tumors may undergo cystic change and should be considered in the differential of a cystic pancreatic neoplasm. There is often central necrosis and calcification in these large tumors as well.
Pancreatic endocrine tumors tend to be hypervascular and are best seen in the late arterial phase. Most are solid unless large. A hypervascular liver mass with an associated pancreatic mass is most likely a metastatic pancreatic endocrine neoplasm.
Insulinoma
Insulinoma is the most common pancreatic endocrine tumor. Due to symptoms of hypoglycemia, insulinomas tend to present early and have the best prognosis of all neuroendocrine tumors, with only 10% demonstrating malignant behavior.
The Whipple triad describes the clinical symptoms of insulinoma: Hypoglycemia, clincial symptoms of hypoglycemia, and alleviation of symptoms after administration of glucose.
Gastrinoma
Gastrinoma causes hypersecretion of gastric acid resulting in Zollinger-Ellison syndrome. Gastrinoma is the second most common pancreatic tumor. Gastrinoma is associated with multiple endocrine neoplasia (MEN) type 1. When associated with MEN-1, gastrinomas tend ot be multiple and located in the duodenum rather than the pancreas.
The gastrinoma triangle describes the typical location of gastrinomas, in an area bounded by the junction of the cystic duct and CBD, the duodenum inferiorly, and the neck/body of the pancreas medially.
High gastrin levels may cause formation of carcinoid tumors in the stomach, which may regress after the gastrinoma is resected.
Other pancreatic endocrine tumors
Glucagonoma is the third most common pancreatic tumor. Prognosis is poor. VIPoma and somatostatinoma are very rare and also have poor prognosis.
Normal pancreatic ductal anatomy
Normally, the main pancreatic duct drains to the major papilla (the ampulla of Vater) through the duct of Wirsun, while the duct of Santorini drains to the minor papilla.
Mnemonic for normal anatomy: Santorini is superior and drains to small (minor) papilla.
The following anatomy is always constant, regardless of whether an anomaly is present: 1) The common bile duct always drains to the major papilla where it meets the duct of Wirsung. 2) The main pancreatic duct alsways drains the pancreatic tail. 3) The duct of Santorini always drains to the minor papilla.
Pancreas divisum
Pancreas divisum is the most common congenital pancreatic anomaly. It is caused by failure of fusion of ventral and dorsal pancreatic ducts. The ventral duct (Wirsung) only drains a portion of the pancreas while the majority of the pancreatic exocrine gland output is drained through the smaller duct of Santorini into the minor papilla.
Pancreas divisum may be a cause of pancreatitis due to obstruction at the minor papilla from a Santorinicele. A Santorinicele is a focal dilation of the terminal duct of Santorini.
The crossing sign describes the CBD crossing over the main duct to join the duct of Wirsung.
Annular pancreas
Annular pancreas is a rare congenital anomaly where a portion of the pancreas wraps completely around the duodenum, secondary to incomplete rotation of the bentral pancreatic bud.
In an adult, annular pancreas can cause pancreatitis, peptic ulcer disease, and duodenal obstruction. In a neonate, it can cause duodenal obstruction and is in the differential for the double bubble sign.
Common channel syndrome/ pancreatobiliary maljunction
Normally the common bile duct and duct of Wirsung both drain to the major papilla, where there is usually a thin septum separating these two systems.
In common channel syndrome, also known as pancreaticobiliary maljunction, the distal CBD and pancreatic duct are missing the septum, allowing refulcx between the two systems.
Common channel syndrome may be in the spectrum of choledochal cyst disease witht he common channel representing a very mild form of choledochocele. Common channel syndrome may predispose to cholangiocarcinoma, but this is rare and controversial.
Systemic diseases that affect the pancreas
Pancreatic manifestations of von Hippel-Lindau - von Hippel-Lindau is an inherited multisystemic disease with icnreased risk of multiple malignancies and formation of cysts in various organs including the pancreas. Pancreatic neoplasms seen in von Hippel-Lindau include serous cystadenoma and pancreatic neuorendocrine tumors.
Cystic fibrosis (CF) - Cystic fibrosis (CF) is the most common cause of childhood pancreatic atrophy. CF can cause either fatty atrophy of the pancreas or pancreatic cystosis (diffuse replacement of the pancreas with innumerable cysts)
Schwachman-Diamond - Schwachman-Diamond is a rare inherited disorder characterized by diffuse fatty replacement of the pancreas, resultant pancreatic exocrine insufficiency, neutropenia, and bone dysplasia. Schwachman-Diamond is the second most cause of childhood pancreatic atrophy.
Obesity and exogenous steroid use - Both obesity and steroids can cause fatty atrophy of the pancreas.
Intrapancreatic accessory spleen
Intrapancreatic accessory spleen is a gening mimic of a hypervascular pancreatic neoplasm.
On imaging, an intrapancreatic spleen typically is a small (1-3 cm), well-defined mass usually found in the pancreatic tail. It follows the density, signal intensity, and enhancement of the spleen on all CT and MRI sequences.
MRI is usually diagnostic. Either technetium-99m sulfur colloid or technetium-99m RBC scintigraphy can confirm the diagnosis in ambiguous cases.
Pancreatitis
Pancreatitis is inflammation of the pancreas, which may be due to a wide variety of etiologies that share a final common pathway of premature activation of pancreatic enzymes and resultant autodigestion of pancreatic parenchyma.
Pancreatitis may range in severity from mild self-limited disease to necrotizing pancreatitis resulting in multi-organ failure and death.
Imaging of pancreatitis is optimally performed in the pancreatic parenchymal phase (late arterial; ~40 seconds after contrast injection), which is the most sensitive timing to detect subtle areas of decreased enhancement suggestive of necrosis.
CT is key for pancreatitis imaging. In addition to often identifying an etiology of the pancreatitis, CT can grade severity, detect complications, and guide possible percutaneous interventions.
CT imaging is not indicated in patients with clinical diagnosis of mild acute pancreatitis, especially if they are improving. CT imaging may be negative or show a mildly edematous pancreas in these cases.
Acute Pancreatitis
Acute pancreatitis is most commonly caused by alcohol or an obstructing gallstone.
Acute pancreatitis can be classified either with the Balthazar grading system or by the CT severity index.
Balthazar grading system: A. Normal-appearing pancreas, B. Focal or diffuse pancreatic enlargement, C. Mild peripancreatic inflammatory changes, D. Single fluid collection, E. Two or more fluid collections. (0% mortality, 4% morbidity for grades A, B, and C; 14% mortality, 54% morbidity for grades D and E (a fluid collection is a poor prognostic indicator).
CT severity index (CTSI) integrates the Balthazar grading system wiht the degree of necrosis: Assigns 0-4 points for Balthazar A-E, with 0 points for Balthazar A and 4 points for Balthazar E. Adds 0-6 points for necrosis to create a total score from 0-10. 0 points: 0% necrosis; 2 points: <30% necrosis, 4 points: 30-50% necrosis, 6 points: >50% necrosis. CTSI 0-3: 3% mortality, 8% morbidity; CTSI 7-10: 17% mortality, 92% morbidity
Acute pancreatitis pancreatic and peripancreatic complications
Pancreatic necrosis: On imaging, pancreatic necrosis appears as a focal or diffuse area of nonenhancing pancreatic parenchyma. Evaluation of necrosis is best performed 48-72 hours after onset of acute pancreatitis. Late arterial phase imaging has the highest sensitivity for detecting pancreatic necrosis. Patients with pancreatic necrosis are at increased risk for infection and severe morbidity.
Fluid collections: Peripancreatic fluid may resolve or may evolve either into peripancreatic abscess or pseudocyst
Pseudocyst: A pancreatic pseudocyst is a collection of pancreatic enzymes and fluid enclosed by a fibrous wall lacking an epithelial lining. The fibrous wall usually takes about 4-6 weeks to mature.
Pancreatic abscess: Pancreatic abscess is a purulent collection featuring thicker, more irregular walls compared to a pseudocyst. Gas locules may be present within the abscess.
Acute pancreatitis extrapancreatic complications
Extrapancreatic pseudocyst may occur nearly anywhere below the diaphragm and should always be considered in the differential of a cystic structure in a patient with history of pancreatitis. In particular, an intrasplenic pseudocyst may lead to intrasplenic hemorrhage.
Perihilar renal inflammation, which may lead to venous compression or thrombosis.
Bowel involvement, especially of the transverse colon.
Acute pancreatitis secondary inflammation of adjacent vessels
Secondary inflammation of adjacent vessels can cause vascular complications:
Arterial bleeding, most commonly due to erosion into the splenic artery.
Pseudoaneurysm, most commonly of the splenic artery.
Venouse thrombosis, most commonly splenic vein thrombosis, which may lead to portal hypertension.
Chronic pancreatitis
Chronic pancreatitis, most commonly from long-term alcohol abuse, causes irreversible pancreatic damage. (A much less common cause of chronic pancreatitis is pancreas divisum)
Calcifications in the distribution of the pancreatic duct are pathognomonic for chronic pancreatitis.
Autoimmune pancreatitis
Autoimmune pancreatitis is caused by inflammatory lymphoplasmacytic infiltrate. It is associated with Sjogren syndrome and causes elevated serum IgG-4 levels.
The typical imaging appearance of autoimmune pancreatitis is diffuse “sausage-shaged” enlargement of the entire pancreas; however a focal or segmental form may mimic a pancreatic mass.
Treatment is with steroids, which can lead to a complete resolution.
Groove pancreatitis
Groove pancreatitis is an uncommon form of focal pancreatitis fo the groove between the head of the pancreas, duodenum, and common bile duct. Groove pancreatitis usually affects young men who are heavy drinkers.
The histopathologic hallmark is fibrosis in the pancreaticoduodenal groove. Chronic inflammation of the duodenum can cause varying levels of duodenal stenosis or cystic change of the duodenal wall. Imaging reflects these findings, with duodenal thickening and cystic change often apparent. The cystic change is best appreciated on MR.
The main differential consideration is adenocarcinoma of the head of the pancreas.
Splenule
Also called an accessory spleen, a spenule is a focus of normal splenic tissue separate from the main body of the spleen, due to embyrologic failure of fusion of the splenic anlage. The most common location is the splenic hilum.
Although usually an incidental finding, the presence of a splenule does have significance in certain clinical settings. For instance, splenectomy for consumptive thrombocytopenia may not be curative if there is sufficient unresected accessory splenic tissue present. A splenule may be mistaken for a lymph node or mass when in an unusual location. As previously discussed, an intrapancreatic splenule may be mistaked for a hypervascular pancreatic mass.
A splenule should follow splenic tissue on all MRI sequences. If in doubt, a Tc-99m sulfur colloid scan or a heat-damaged Tc-99m RBC scan can be confirmatory.
Polysplenia syndrome
Polysplenia syndrome is a spectrum of anatomic disorders characterized by some degree of visceral heterotaxia in addition to multiple discrete foci of splenic tissue. Multiple spleens may be on the right or left, but are always on the same side as the stomach.
Polysplenia is usually associated with severe congenital cardiac anomalies. Most patients die in early childhood, but a few may have only minor cardiac defects and may be incidentally discovered as adults.
Polysplenia is associated with venous anomalies including interruption of the IVC with azygos or hemiazygos continuation. A less common association is a preduodenal protal vein.
Wandering spleen
A wandering spleen is a normal spleen with abnormal laxity or absence of its fixed ligamentous attachments
Wandering spleen may present clinically as an abdominal mass or may cause acute abdominal pain secondary to torsion.
Hemangioma
Hemangioma is the most common benign splenic neoplasm. Hemangioma may be solitary or multiple, and lesions tend to be small.
Splenic hemangiomas are associated with Kasabach-Merritt syndrome (anemia, thrombocytopenia, and consumptive coagulopathy) and Klippel-Trenaury-Weber syndrome (cutaneous hemangiomas, varicose veins, and extremity hypertrophy). These visceral hemangiomatosis syndromes are usually associated with phleboliths.
On CT, hemangiomas are typically iso- or hypoattenuating pre-contrast and hyperenhancing. On MR, hemangiomas are typically hyperintense on T2-weighted images and may enhance peripherally or homogenously. However, the classic pattern of discontinous nodular enhancement seen in hepatic hemangiomas is uncommon.
Nuclear medicine scintigraphy with Tc-99m labeled red blood cells would show increased activity within the lesion on delayed images. In contrast, Tc-99m sulfur colloid scanning may show either increased or decreased activity.
Hamartoma
Splenic hamartoma is a rare, benign lesion composed of malformed red pulp elements. It may be associated with tuberous sclerosis.
Splenic hamartoma is typically a well-circumscribed, iso- or hypoattenuating mass on unenhanced CT that enhances heterogenously after contrast administration. On MR, a hamartoma is iso- to slightly hyperintense on T2-weighted images, featuring heterogenous early enhancement and relatively homogenous delayed enhancement.
Congenital true (epithelial) cyst
A congenital true cyst is defined as having an epithelial lining. Interestingly, a splenic epithelial cyst may cause elevation of tumor markers including CA19-9, CA125, and CEA, despite its completely benign nature.
Unlike a post-traumatic pseudocyst, a true cyst may have septations, but mural calcification is uncommon.
Post-traumatic pseudocyst
A post-traumatic psuedocyst is the end result of evolution of a splenic hematoma.
Unlike a true (epithelial) splenic cyst, the periphery of a pseudocyst is not cellular but made of fibrotic tissue.
On imaging, a post-traumatic pseudocyst appears as a well-circumscribed, fluid-density lesion, with no peripheral enchancement.
In contrast to a true cyst, septations are uncommon but there may be mural calcification.
Evaluation of Esophageal Masses
Masses arising from the mucosa, submucosa, and extrinsic to the esophagus produce characteristic effects on the esophagus, which are usually able to be seen on imaging.
Aberrant right subclavian artery
Aberrant right subclavian artery (with a normal left arch) is seen in approximately 1% of patients and is almost always asymptomatic. The aberrant right subclavian artery travels posterior to the esophagus, where it may rarely produce dysphagia.
On an upper GI study, the resultant posterior esophageal indentation is always smooth.
Overview of Gastric bypass surgery
In order to evaluate for and accurately describe complications of Roux-en-Y gastric bypass (RYGB) surgery, it is important to be familiar with the procedure and normal postsurgical anatomy.
A small gastric pouch is created with a volume of approximately 15 to 30 cc by excluding the distal stomach from the path of food.
The Roux limb is created by transecting the jejunum approximately 35-45 cm distal to the ligament of Treitz, then bringing it up to be anastomosed to the gastric pouch via a narrow gastrojejunostomy stoma.
The current favored approach for placement of the Roux limb is antecolic (in front of the transverse colon). The Roux limb used to be placed retrocolic, which required the creation of a surgical defect through the transverse retrocolic, which required the creation of a surgical dfect through the transverse mesocolon (mesentery of the transverse colon). A retrocolic Roux limb has a higher risk of a transmesocolic hernia due to the defect in the transverse mesocolon. (Although the antecolic approach is now more commonly performed, there are many patients who have previously undergone a retrocolic approach.)
A distal side-to-side jejunojejunostomy is created to connect the pancreaticobiliary limb to the jejunum.
They RYGB leads to weight loss both from early satiety (due to small size of the gastric pouch) and malabsorption (due to surgical bypass of the proximal jejunum.)
Mesentery and Peritoneum Anatomy
