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The role of MR in the early diagnosis of acute osteomyelitis is well known. In the context of florid cellulitis, abnormalities of marrow signal are not uncommon, although they are often non-specific. Marrow oedema and enhancement in the context of deep cellulitis might reflect either reactive marrow oedema or true osteomyelitis. More specific signs lend favour to the diagnosis of osteomyelitis: these include focal bone destruction, periosteal reaction and sequestra. The observation of an extramedullary fat-fluid sign is also a specific sign for osteomyelitis, as illustrated in the following case report. This sign is an indication of cortical breach and, thus, in the setting of infection and in the absence of trauma confirms the presence of osteomyelitis. To our knowledge, this additional specific sign of osteomyelitis has not been previously reported on MR.

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Fig. 3. Illustration demonstrating the cyst coursing deep to the vascular structures and extending into the perineurium of the tibial nerve (looped) underneath the divided medial head of gastrocnemius muscle.

Multimodality imaging plays a major role in the diagnosis of cholecystic and choledochal vascular disorders. The presentation of these conditions ranges from acute and potentially fatal to asymptomatic and incidental. Gallbladder hemorrhage, ischemia, and hemobilia may complicate acute cholecystitis and may also occur in other clinical settings. The radiological appearances of gangrenous cholecystitis, gallbladder hemorrhage, hemobilia, vascular malformations, and gallbladder torsion will be presented. The vascular anatomy of the bile ducts and gallbladder will be reviewed with particular reference to the communication of the choledochal and cholecystic venous drainage with the portal venous system. The imaging features of the unique vascular conditions arising as a result of this connection to the portal system will be illustrated (Table 1). | ARTERIAL SUPPLY AND VENOUS DRAINAGE OF THE GALLBLADDERThe gallbladder is supplied by both small vessels from the hepatic bed and the cystic artery, which usually arises from the right hepatic artery. The cystic artery runs toward the gallbladder in Calot's triangle, the boundaries of which are formed by the liver, common hepatic duct, and cystic duct (Figure 1a). The cystic artery passes posterior to the common hepatic duct to reach the neck of the gallbladder. 1 Variations in the artery origin are common and it may arise from the common hepatic artery (26%), from the left hepatic artery (5%), or gastroduodenal artery (2%). Rarely, it may arise from the superior pancreaticoduodenal, right gastric, celiac trunk, or superior mesenteric arteries. 1 It may also course anterior to the cystic duct and bile duct. Thrombosis of the

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A variety of patterns of enhancement of liver lesions and liver parenchyma is observed in the hepatobiliary phase (HBP) of gadoxetic acid-enhanced MRI. It is becoming increasingly apparent that many lesions may exhibit HBP enhancement. Much of the literature regarding the role of gadoxetic acid-enhanced MRI in characterising liver lesions is dichotomous, focusing on whether lesions are enhancing or non-enhancing in the HBP, rather than examining the patterns of enhancement. We provide a pattern-based description of HBP enhancement of liver parenchyma and of liver lesions. The role of OATP1B3 transporters, hepatocyte function and lesion composition in influencing patterns of HBP hyperintensity are discussed.

A case of intracranial extraosseous 99mTc MDP uptake is presented, which was found on CT to be due to dystrophic gyral calcification characteristic of Sturge-Weber syndrome (SWS). The imaging characteristics of SWS are described. The possibility of extraosseous MDP uptake should be considered when unusual or atypical 'hot spots' are seen on bone scanning.