MRI of Diffuse Liver Disease

Geographic THID

THIDs originate for a variety of reasons, depending on the presence or absence of an underlying lesion. The dual portal venous–hepatic arterial blood supply allows increased arterial flow to compensate for a decrease in portal venous flow—the basic premise of a THID. Pathogenetic mechanisms of primary lesions include portal venous compression (as a result of portal branch compression or thrombosis), flow diversion (as a result of arterioportal shunt or anomalous blood supply), and effects of adjacent inflammation. Secondary causes include siphoning (increase in arterial flow), portal hypoperfusion (as a result of compression or infiltration), portal venous thrombosis (PVT), and flow diversion (as a result of an arterioportal shunt associated with an underlying lesion).

Sharp margins, arterial enhancement, and an absence of signal changes in unenhanced images usually characterize these lesions (see Fig. 2.30 ). Occlusion or truncation of vessels proximal to the capsule and distal to the lesion potentially results in a rounded appearance. Nonsectorial or amorphous morphology results from extrinsic compression (ie, subcapsular collections), anomalous vascular supply, hyperemia as a result of adjacent inflammation (ie, cholecystitis), and postprocedural changes (ie, transcutaneous biopsy or ablation). THIDs typically demonstrate no signal alteration on T2-weighted images, reflecting the isoconcentration of water protons (compared with normal liver).

Other Geographic Vascular Lesions

Other vascular etiologies resemble THIDs, such as hepatic infarct and portal venous occlusion. Hepatic infarcts are not incidental lesions and usually accompany LT, laparoscopic cholecystectomy, vasculitis, and profound hypovolemia. Temporal stability excludes infarct, which atrophies, degenerates, and may undergo necrosis. PVT also rarely manifests spontaneously and usually accompanies inflammation (ie, pancreatitis, peritonitis, diverticulitis) or malignancy. Wedge-shaped morphology and hypervascularity often associated with portal venous occlusion reiterate the appearance of a THID and direct visualization of a filling defect in a portal venous branch excludes THID. With infarction, superimposed T1 hypo- and T2 hyperintensity develop.

Because of its rare occurrence and protective dual hepatic perfusion, infarct should be realistically entertained only in appropriate clinical settings (eg, LT, laparoscopic cholecystectomy, vascular intervention; Fig. 3.2 ; see Fig. 2.52 ). Signal changes develop gradually, along with atrophy and volume loss of the affected segment. In the acute phase, only the clinical scenario and absent enhancement identify arterial infarction as the correct diagnosis.

Portal venous occlusion also rarely arises spontaneously. Identification of segmental arterial enhancement prompts inspection of the regional portal venous branches in pursuit of a filling defect ( Fig. 3.3 ). A history of visceral inflammation or malignancy (particularly HCC) increases the likelihood of portal venous occlusion. In the absence of an underlying culprit lesion—such as HCC—signal or morphologic changes are usually absent. When associated with malignancy, check for enhancement of the filling defect, which indicates tumor thrombus as opposed to bland thrombus (which does not enhance).

Geographic Steatosis/Iron Deposition

Geographic steatosis (or fatty infiltration) exhibits the same signal characteristics as its nodular counterpart ( Fig. 3.4 ). Isolated loss of signal in out-of-phase images with no mass effect on normal hepatic structures characterizes steatosis. Whereas iron deposition also lacks mass effect, the opposite signal loss pattern is observed—loss of signal in in-phase images—reflecting increasing susceptibility effects of iron as a consequence of the longer echo time (and iron deposition is usually diffuse). Enhancement equivalent to hepatic parenchyma characterizes both entities. Neither demonstrates profound signal changes in spin-echo (or FSE) images, however, because the 180-degree pulse(s) correct for phase changes (in the case of steatosis) and susceptibility artifact (in the case of iron deposition). Spin-echo images generally brandish mild relative hyperintensity as a result of fat and hypointensity from iron, respectively.