Abnormal liver perfusion, also known as transient liver density difference [1], refers to the difference of blood perfusion among hepatic segments, subsegments and hepatic lobes caused by various reasons. The causes of abnormal liver perfusion are diverse, the mechanism is complex, and the imaging manifestations are not characteristic. It is of great clinical significance to be familiar with various imaging manifestations of hepatic perfusion abnormalities and correctly distinguish between physiological and pathological hepatic perfusion abnormalities. In order to improve the ability of diagnosis and differentiation of liver diseases, the authors reviewed the reports about abnormal hepatic perfusion (HPD) in recent years.
1 Historical origin of abnormal hepatic perfusion
198 1 year, Inamoto[2] found a low-density area of non-neoplastic liver segment during routine enhanced CT examination, which may be due to the decrease of portal vein blood flow; In 1982, Itai[3] reported the transient abnormal enhancement phenomenon of hepatic segment in arterial phase during enhanced CT scanning, which was called transient liver density difference. 1988 reported that the signal of liver segment was abnormal during MR examination, showing a long T 1 T2 signal shadow. Ultrasound examination found that the liver region corresponding to some cases was oblique hypoechoic region, and hepatic arteriography was clear. 1984, when Matsui[5] examined the patients with liver tumor by DSA, he found a dye-deficient area in the normal subcapsular liver tissue outside the tumor area. After detailed study, it was found that the dye area in the liver segment was an abnormal enhancement area during CT-enhanced arterial phase. Zhou Kangrong, a domestic scholar, clearly put forward transient abnormal perfusion of liver in 1996 [1]; 1997, Gryspeerdt et al. [6] first put forward the concept of hepatic perfusion disorder. He systematically studied and reviewed the liver density difference in multi-slice spiral CT enhanced scanning [1], and proposed diseases related to HPD formation, which were more comprehensive, more specific and more comprehensive than those proposed by Itai and Matsui. In 2006, CT findings of 128 cases of transient hepatic perfusion abnormality were analyzed retrospectively by satellite. At present, most scholars advocate naming it after abnormal hepatic perfusion.
2 Imaging manifestations of abnormal hepatic perfusion
2. 1CT performance
2. 1. 1 CT manifestations of abnormal high-density perfusion: enhanced scanning showed transient wedge-shaped, triangular, quasi-circular, irregular high-density shadow of hepatic parenchyma in arterial phase, uniform density, clear edge, clear and narrow transition zone between surrounding liver tissues and no displacement of vascular system. Abnormal high-density perfusion shows vascular shadow, and the portal vein phase recovers to equal density, which can be single or multiple. Abnormal hyperperfusion often occurs under the liver capsule, around the superficial part of the liver, liver lesions, and can also involve liver segments, subsegments and liver lobes.
2. 1.2 CT manifestations of abnormal low-density perfusion: On enhanced scanning, the hepatic parenchyma showed wedge-shaped and triangular low-density shadows with uniform density, sharp boundary or unclear boundary with surrounding tissues, but rarely spherical, and recovered to equal density in portal vein; Abnormal hypoperfusion often occurs in sickle ligament, venous ligament, near gallbladder fossa and superficial parts of liver.
2. 1.3 CT plain scan manifestations of abnormal hepatic perfusion: CT plain scan mostly showed isodensity, and a few showed wedge-shaped or triangular low-density areas.
2.2MRI features: During dynamic contrast-enhanced scanning of abnormal liver perfusion, the enhancement and distribution features are similar to those of CT. In arterial phase, high perfusion shows short signal T 1, while low perfusion shows long signal T 1. Most of them display equal signal T 1 and equal signal T2 in plain scan, and a few can display long signal T 1.
2.3 DSA findings: Wedge-shaped and triangular hepatic segments can be seen in hepatic arteriography, which can be located around or adjacent to liver-related lesions. If portal vein occlusion exists, indirect portography can show that the staining in the corresponding area is missing or weakened; Hepatic vein occlusion and ectopic vascular variation will have corresponding angiographic manifestations [7].
2.4 Ultrasonography: Search the literature, there is no literature report about ultrasound and liver perfusion abnormality, only the report that CT and MRI compare with ultrasound in the study of liver perfusion abnormality [6].
3 Causes and mechanisms of abnormal hepatic perfusion
3. 1 Physiological liver perfusion abnormality:
3. 1. 1 Physiological hyperperfusion abnormality of liver: The liver is an organ receiving double blood supply, and the blood supply is very rich. In addition to the blood supply of hepatic artery and portal vein, there are anatomical variations of blood supply, which may be the main reason for the abnormal physiological hyperperfusion of liver. Such as variation of hepatic artery in hepatic segment or subsegment, vagal drainage vein, etc. Typically, the gallbladder artery originates from the hepatic artery in the colon triangle and then reaches the gallbladder neck. Most of the gallbladder reaching the left edge of the gallbladder neck is divided into two branches, one to the attachment surface (liver surface) of the gallbladder and the other to the liver under the capsule. The other branch is located under the peritoneum on the free surface of the gallbladder. In addition, gallbladder artery can also originate from right hepatic artery, left hepatic artery or middle hepatic artery of vagus nerve, and even common hepatic artery, proper hepatic artery and gastroduodenal artery. In addition, gallbladder vagus nerve instead of hepatic artery and parahepatic artery of vagus nerve are both specific blood supply arteries of liver parenchyma in a certain range, and they are the only arterial blood supply pipeline in this area or liver tissue [8]. Sometimes the liver parenchyma around the gallbladder fossa receives blood supply from the gallbladder artery at the same time, which is called deep hepatic artery, which increases the arterial perfusion in this part [9]. Therefore, physiological liver hyperperfusion abnormalities mostly occur in gallbladder fossa, ligament attachment, anterior hilum, posterior margin of the second segment and anterior and posterior margin of the third segment, subcapsular area of the liver and other specific parts [10]. Some vagal drainage veins, such as accessory gallbladder vein, vagal right gastric vein, cystic vein, etc. [1 1], which drains into the hepatic sinus and forms the "third access to the liver". These ectopic drainage veins enter the hepatic sinus directly through the systemic venous system rather than the portal vein system. Therefore, in the late stage of artery, the blood containing contrast agent in the liver of these drainage veins enters the hepatic sinus earlier than the portal vein, resulting in abnormal physiological perfusion or staining of the liver in the corresponding area [1 1].
3. 1.2 Physiological hypoperfusion abnormality of liver: In normal physiological state, the blood supply of hepatic portal vein accounts for about 75~80%, while that of hepatic artery accounts for about 20%~25%. Portal vein is mainly composed of splenic vein and superior mesenteric vein. In the early stage of enhanced scanning of arteries by CT and MRI of liver, the contrast agent and portal vein blood returning through spleen and gastrointestinal tract have not been fully and evenly mixed, which may lead to abnormal physiological hypoperfusion of liver. This is a transient perfusion abnormality and then tends to be uniform [10].
3.2 Pathological abnormal liver perfusion: