Transient Hepatic Attenuation Differences THAD

THAD is associated with numerous intrahepatic vascular conditions, particularly intrahepatic shunts.

Intrahepatic shunts can be divided into arterio-portal, arteriosystemic, and portosystemic, depending on the vascular connection. APS are the most common form of intrahepatic shunts, and are commonly associated with HCC or with iatrogenic causes, such as liver biopsy (Fig. 25) or radio-frequency (RF) ablation (Fig. 26). In APS a direct communication between the feeding arterial vessels of the neoplasm and the draining portal venules leads to increased arterial flow around the tumor [29].

Early enhancement of portal vein branches during the arterial phases of CT and MR dynamic studies is often indicative of APS. APS can sometimes be seen in association with small heman-giomas and seems to be related to the hyperdy-namic vasculature of this tumor. APS are common in liver cirrhosis, due to the damaged hepatic flow (Figs. 27,28), and can be a source of potential confusion with HCC, especially when they appear as small, round areas during the arterial phase (Figs. 29,30).

Non-tumoral round APS show signal loss after SPIO administration, comparable to that occurring in the normal liver parenchyma. Homogeneous uptake of hepatospecific contrast agents such as Gd-BOPTA is generally observed, resulting in an isointense appearance relative to the normal parenchyma (Fig. 3o f, g) [48]. Well-differentiated small HCC may demonstrate the same enhancement behavior and the same uptake after SPIO and hepatospecific contrast agents. As a result, differential diagnosis may be difficult and biopsy or strict follow-up should be performed.

Direct communication between the portal vein and systemic veins results in intrahepatic por-tosystemic venous shunts. These are frequent in the setting of liver cirrhosis with portal hypertension, and may be accompanied by extrahepatic portosystemic collateral circulation.

THAD can be classified according to morphology (sectoral, segmental, and lobar), etiology (as a result of benign or malignant tumors, arteriopor-tal shunting, liver cirrhosis, or venous thrombosis), or pathogenesis (due to low portal inflow, phl-ogosis, or sump effect). In the absence of a direct relationship to neoplasm, the most common cause of THAD is thrombosis of the portal vessels. The most frequent etiopathogenesis is therefore low portal inflow due to obstruction or compression of the portal vein [21]. Low portal inflow could be a result of APS. In this case, diversion of the portal flow by arterial flow under higher pressure results in relatively low portal flow and induces compensatory collateral arterial flow which intensifies and perpetuates the phenomenon. Thus, when THAD is related to APS there is no portal block, but rather a mixing of arterial and venous blood. This pathogenesis is frequently seen in hemangioma and HCC [9], as well as in arterial phenomena not associated with focal liver lesions.

Sectoral THAD are usually triangular in shape. If the lesion is present in the medial portion, low flow is induced by compression and the THAD is fan-shaped. However, if the lesion is central the low flow is usually related to thrombosis or APS and the THAD is wedge-shaped [21] (Fig. 31). On the other hand, it is well known that APS arising in the context of cirrhosis may produce THAD that sometimes display a round or pseudo-round morphology (the axial section of the conical shape may appear round or oval). Thus, THAD is poorly distinguishable from small HCC in cirrhotic patients, or from hypervascular metastases in non-cirrhotic patients [11]. Occasionally, THAD may occur as a prelude to an otherwise occult focal lesion [12] and can sometimes mask the underlying lesion.

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    Can a liver biopsy cause transient hepatic attenuation?
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