transiente Dichteunterschiede in der Leber
Transient hepatic attenuation differences (THAD) lesions refer to areas of parenchymal enhancement visible during the hepatic artery phase on helical CT. They are thought to be a physiological phenomenon caused by the dual hepatic blood supply. Occasionally, they may be associated with hepatic tumors such as hepatocellular carcinoma.
Pathology
Mechanism
Transient hepatic attenuation differences are thought to be due to a localized mismatch in hepatic arterial versus portal venous blood supply, where often there is a relative increase in hepatic arterial supply thereby giving a higher attenuation to the affected region.
Four pathogenic mechanisms have been described:
- directly by a siphoning effect (lobar multisegmental shape)
- portal hypoperfusion (sectorial shape) due to portal branch compression or infiltration
- thrombosis resulting in a portal branch blockade
- flow diversion caused by an arterioportal shunt
Compensatory relationships between two liver sources of blood supply so that arterial flow increases when portal flow decreases as a result of communication among the main vessels, sinusoids, and peribiliary venules that open in response to the autonomic nervous system and humoral factors activated by liver demand for oxygen and metabolites.
Etiology
Differences in hepatic arterial blood flow can be primary or secondary (i.e. compensatory) :
- primary: focal hypervascular lesions, variant hepatic artery anatomy, adjacent inflammation (e.g. cholelithiasis, pancreatitis)
- secondary
- decreased portal vein flow, e.g. portal vein thrombosis, extrinsic compression, liver trauma
- arterioportal shunt
Radiographic features
May be seen as areas of parenchymal enhancement usually visible only during the hepatic artery phase that is caused by the dual hepatic blood supply.
See also
- transient hepatic intensity differences (THID): the equivalent finding at MRI