于本文中,作者将由于肝动脉和门静脉血流的功能性重新分配而形成的肝内动脉-门静脉分流(intrahepatic arterial-portal venous shunts, IHAPVSs),皆定义为功能性肝内动脉-门静脉分流(functional IHAPVSs或F-IHAPVSs)；以此从概念上区别于由于肝内动脉-门静脉瘘或直接交通而形成的器质性肝内动脉-门静脉分流(organic IHAPVSs或O-IHAPVSs),如伴发于进展期肝细胞癌和其他恶性肝脏肿瘤的O-IHAPVSs以及伴发于先天性肝脏血管畸形、遗传性出血性毛细血管扩张症和肝脏外伤(包括医源性损伤)等的O-IHAPVSs。在F-IHAPVSs中,最常见的是由于各种原因使向肝性门静脉血流减少而致肝动脉血流代偿性(或继发性)增多所形成的F-IHAPVSs,其形成机制分为3类：经肝窦性,如伴发于肝硬化的F-IHAPVSs；窦后性,如伴发于布加综合征患者急性期的F-IHAPVSs；窦前性,如伴发于胃肠道出血性休克患者的F-IHAPVSs。另一种F-IHAPVSs常见于一些原发性肝动脉血流增多的肝脏疾患,如伴发于富血型肝海绵状血管瘤、血供丰富的小肝细胞癌和肝胆炎性病变等的IHAPVSs,皆归之于F-IHAPVSs范畴；然而,此类F-IHAPVSs的形成机制是随其基础疾病而不同。临床上,依据下列3个要点可作出F-IHAPVSs的影像诊断：①首先是伴有肝内动脉-门静脉瘘或直接交通的各种肝脏疾病(已如上述)的临床和影像学表现皆已经被排除；②肝动脉DSA动脉期像上显示门静脉早显的特征性表现；或(和)③肝脏CT/MR动态增强成像动脉期像上显示一过性肝实质强化(THPE),特别是如同时见到门静脉早显,则可确认为F-IHAPVSs无疑。但是,在鉴别诊断上,F-IHAPVSs必须仔细地与O-IHAPVSs、肝脏迷走静脉或体循环的异常向肝性引流静脉等所引起的局部肝实质灌注作鉴别；此外,伴发于肝硬化的小THPE如呈现为孤立小结节状时,则需谨慎地与小的肝细胞癌灶作鉴别。%In this paper, all the intrahepatic arterioportal shunts (IHAPSs) that result from the functional redistribution of hepatic arterial and portal venous blood flow are defined as functional IHAPSs (F-IHAPSs) so as to make the differentiation from organic IHAPSs (O-IHAPSs) that result from the intrahepatic arterioportal fistula or direct communication, such as those IHAPSs that are associated with advanced hepatocellular carcinoma (HCC) and other malignant hepatic tumors as well as those IHAPSs that are accompanied by congenital hepatic vascular malformations, hereditary hemorrhagic telangioectasia (HHT) and liver trauma (including iatrogenic injury), etc. In F-IHAPSs, the most common one is formed by the compensatory (or secondary) increase of arterial blood flow that is caused by the decrease of hepatopetal portal blood flow due to a variety of reasons; its formation mechanisms can be divided into three categories:(1) trans-sinusoidal type, such as the F-IHAPSs that is associated with cirrhosis;(2) post-sinusoidal type, such as the F-IHAPSs that is accompanied with the acute stage of Budd-Chiari syndrome; and (3) pre-sinusoidal type, such as the F-IHAPSs that occurs along with the gastrointestinal hemorrhagic shock. Another kind of F-IHAPSs has been commonly seen in some hepatic diseases that have primary increase of hepatic arterial blood flow, including hypervascular hepatic cavernous hemangioma, small hepatocellular carcinoma that has rich blood supply, hepatobiliary inflammatory diseases, etc.;and in this paper they are all classified as F-IHAPSs category, however, the formation mechanisms of such F-IHAPSs vary with their basic diseases. Clinically, imaging diagnosis of F-IHAPSs can be made based on the following three signs:(1) all kinds of hepatic diseases that have concomitant intrahepatic arterioportal fistula or direct communication, as mentioned above, have been definitely excluded:(2) hepatic artery DSA reveals early visualization of portal vein in arterial phase, known as the characteristic sign of F-IHAPSs;and/or: (3) hepatic dynamic enhanced CT/MR scanning demonstrates transient enhancement of liver parenchyma in arterial phase, especially early visualization of portal vein is also present; in this case the diagnosis of F-IHAPSs can be undoubtedly confirmed. However, in making differential diagnosis, F-IHAPSs must be carefully differentiated from O-IHAPSs, local hepatic parenchymal perfusion caused by hepatic aberrant vein or by abnormal hepatopetal draining vein from systemic circulation, etc. In addition, when cirrhosis-related transient hepatic parenchymal enhancement presents as a solitary small nodule, differentiation with small HCC should be taken into consideration. In order to provide the readers with a complete and up-to-date understanding of F-IHAPSs, the relevant example illustrations, figures and graphics are accompanied with the text.
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