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Updated: Jun 24, 2026

Visualization and Analysis of Blood Flow and Oxygen Consumption in Hepatic Microcirculation: Application to an Acute Hepatitis Model
Published on: August 4, 2012
Transient hepatic attenuation differences and focal liver lesions: sump effect due to primary arterial hyperperfusion
Stefano Colagrande1, Nicoletta Centi, Silvia Pradella
1Department of Clinical Physiopathology, Section of Radiodiagnostics, University of Florence, Firenze, Italy. stefano.colagrande@unifi.it
Objective:
To analyze at computed tomography (CT) examination the "sump effect," a particular type of transient hepatic attenuation differences, related primarily to an increase in arterial flow without any accompanying decrease in portal flow.
Methods:
We retrospectively evaluated all biphasic upper abdomen CT examinations (1283 in 807 patients) performed from the year 2003 to the year 2006 and selected and organized those with at least 1 transient hepatic attenuation differences. Of these, we enrolled patients with lobar/multisegmental arterializations surrounding focal lesion(s), without CT portal hypoperfusion signs, in the study group. We assessed histology, number, site, diameter, and volume of causing focal lesion(s); site, extension, and attenuation of arterial area; greater visibility of feeding artery branches ipsilateral to causal focal lesion; and presence of aberrant left hepatic artery. Thirty patients with normal liver represented the control group.
Results:
Fifteen of the 99 patients with transient hepatic attenuation differences presented with sump effect. In our series, this phenomenon was always related to hypervascular inflammatory and benign lesion(s) with overall average diameter of 8 +/- 4 cm inscribed in arterial area. Attenuation of arterial enhanced areas were significantly higher than the contralateral parenchyma and control patients' parenchyma, with frequent hypertrophy of ipsilateral arterial feeding branches and/or aberrant left hepatic artery visibility.
Conclusions:
Siphonage seems to be primary hyperperfusion area determined by arterial bed enlargement, induced by inscribed large hypervascular inflammatory/benign lesion(s).
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