摘要
目的 进一步探讨成人肝海绵状血管瘤 (cavernoushemangiomasoftheliver,CHL)的血供和介入治疗。方法 近来有人报道少数门静脉供血的CHL病例通过门静脉插管栓塞治疗取得满意的疗效 ,并对通常认为的CHL血供完全来自肝动脉的观点提出了质疑。为求得一科学合理的解释 ,作者复习了肝脏的血管胚胎发生学和组织学、CHL的病理改变以及相关的文献 ,并结合 2 0 0 0～ 2 0 0 2年曾作过的CHL血液动力学研究结果作进一步探讨。结果 CHL系肝脏血窦于胚胎阶段的发育障碍所致。病理学上 ,CHL是由多数扩张的异常血窦构成 ,窦腔大小不一 ,且与CHL的血液动力学变化密切相关 (呈反比例关系 )。病理所示的均一细小异常血窦 (直径小于 5 0 μm)所构成的CHL常显示为高流量。于肝动脉造影或经肝动脉注入对比剂CT增强扫描 (CTHA)时 ,瘤体可快速地被含对比剂的动脉血液充盈 ,经常呈浓密的显影或增强 ,同时并可引起异常血窦腔内压增加 ;当其内压超过与其相连接的门静脉小支内压时 ,充盈于异常血窦内的含对比剂动脉血液即可逆流入这些门静脉小支 ,也即肝动脉 门静脉短路 (APVS)。上述表现也可见于一些中等流量的CHL ,病理证实这些瘤体周边有许多细小的异常血窦。反之 ,病理所示的大径异常血窦 (直径大于 5 0 0 μm)所构成的CHL常?
Objective To further explore the blood supply and interventional therapy of adult cavernous hemangiomas of the liver (CHL).Methods Recently some authors reported that a satisfactory effect resulted from transcatheter portal venous embolization was obtained in few cases of CHL with blood supply of portal vein,and raised an objection to the standpoint that CHL was commonly supplied by hepatic artery completely.In order to get a scientific and reasonable explanation for it,this paper reviewed the vascular embryology and histology of the liver,the pathologic features of CHL as well as the relative literature,and combined with the investigation results of blood dynamic changes of CHL that had been performed in 2000～2002 by us.Results CHL was caused by the arrested development of hepatic sinusoids at the embryonic stage.Pathologically,CHL was consisted of a lot of enlarged abnormal sinusoids,which were variant in size and closely related with the hemodynamic changes of CHL (in inverse proportion).The CHL consisted of even and tiny abnormal sinusoids (diameter less than 50 μm) pathologically usually presented a high flow.During the hepatic artery angiography or CTHA,it was rapidly filled by the arterial blood containing contrast media and frequently showed dense opacification or enhancement.Simultaneously this could result in increased pressure of abnormal sinusoids.When the sinusoidal pressure exceeded that of the connecting portal venules,the arterial blood containing contrast media filled in the abnormal sinusoids could lead to retrograde flow in the portal venules.That was arterial-portal venous shunts (APVS).These appearances described as above could also occur in some CHL with intermediate flow,in which many tiny abnormal sinusoids located in the peripheral area were identified pathologically.On the contrary,the CHL consisted of larger abnormal sinusoids (diameter more than 500 μm) pathologically usually presented a low flow.During the hepatic artery angiography or CTHA,it was filled very slowly by the arterial blood containing contrast media and was difficult to opacify or enhance.Simultaneously this could result in a low pressure of abnormal sinusoids.When the sinusoidal pressure was lower than that of the connecting portal venules,the portal venous blood containing contrast media could easily flow into the abnormal sinusoids and make it enhanced during the direct or indirect portography (or CTAP).Conclusion CHL is really a congenital venous malformation.All the CHL with high flow and some CHL with intermediate flow are surely supplied by the hepatic artery and drained primarily by the peripheral branches of portal vein.However,in few CHL with marked lower flow,the portal vein should become a primary supply vessel,so a direct or indirect portography (or CTAP) must often be taken to identify the diagnosis.Thereby,the technique of transcatheter embolization of CHL including the aim,indication,approach,and the used sclerotic or embolic drugs,etc,should also be reconsidered in order to improve its therapeutic efficacy.
出处
《中华放射学杂志》
CAS
CSCD
北大核心
2004年第7期746-750,共5页
Chinese Journal of Radiology
关键词
肝海绵状血管瘤
血供
介入治疗
栓塞治疗
Hemangioma,cavernous
Neoplasms,liver
Malformations,venous
Blood supply
Embolization,therapeutic
