CT of Nonneoplastic Hepatic Vascular and Perfusion Disorders

Torabi, Maha; Hosseinzadeh, Keyanoosh; Federle, Michael P.

doi:10.1148/rg.287085067

Cited by 131 publications

(107 citation statements)

References 38 publications

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“…Radyologlar tanı için hastalığa yönelik görüntüleme bulguları ile klinik belirtilere aşina olmalıdır. Sirotik karaciğer dışındaki lokal risk faktörleri inflamasyon, neoplazm, kan hastalıkları,iatrojenik girişimler, ilaç kullanımı gibi nedenlerdir [1,2]. Fokal inflamatuar durumlar arasında akut (Resim 3a, b) veya kronik pankreatit, kolesistit, kolanjit, karaciğer absesi, mantar enfeksiyonları gibi patolojiler sayılmaktadır.…”

Section: Karaciğerin Vasküler Hastalıklarıunclassified

“…Benign ya da malign nedenli hepatopankreatikobilier sistem cerrahi veya perkütan girişimleri, karaciğer nakil operasyonu, Vitamin C eksikliği gibi metabolik nedenler, Orak hücreli anemi vb. hematolojik hastalıklar da PVT nedenleri arasında yer almaktadır [1]. PVT'da benign-malign tromboz ayrımı tedavi kararı için önem taşımaktadır.…”

Section: Karaciğerin Vasküler Hastalıklarıunclassified

“…Karaciğerin %75'i portal venden %25'i ise hepatik arter dallarından beslenmektedir (1). Venöz drenaj ise sağ, orta ve sol hepatik venler aracılığı ile inferior vena kava'ya olmaktadır (Resim 1).…”

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Karaciğerin Vasküler Hastalıkları

Elmas¹,

Harman²

2016

Trd Sem

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Section: Karaciğerin Vasküler Hastalıklarıunclassified

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Karaciğerin Vasküler Hastalıkları

Elmas¹,

Harman²

2016

Trd Sem

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“…Radiological imaging-guided intervention, such as embolisation, is performed if there is rapid development of life-threatening portal hypertension or high-output cardiac failure. If embolisation fails, surgery is often necessary [2,8].…”

Section: Imaging Features Of Hepatic Vascular Shuntsmentioning

confidence: 99%

“…The unique dual blood supply of the liver (approximately 75% portal venous and 25% arterial) means there is a compensatory relationship between the two sources. When vascular compromise occurs, it causes a macroscopic opening of the shunts between the hepatic arteries, the portal veins and the hepatic veins through physiological anastomoses, which become abnormally enlarged [1][2][3]. The purpose of this pictorial review is to illustrate the imaging appearances of hepatic vascular shunts on multidetector CT (MDCT) with sonographic and conventional angiographic correlation.…”

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confidence: 99%

Hepatic vascular shunts: embryology and imaging appearances

Bhargava

Vaidya

Kolokythas

et al. 2011

BJR

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ABSTRACT. The purpose of this pictorial review is to understand the embryological basis of the development of congenital hepatic vascular shunts and to review the multimodality imaging appearances of congenital and acquired hepatic vascular shunts. Hepatic vascular shunts are commonly seen in imaging. Familiarity with their characteristic appearances is important in order to accurately characterise these shunts and diagnose the underlying disorders. Intrahepatic vascular shunts are common; all intrahepatic vessels are associated with the formation of shunts. These include arterioportal (AP), portosystemic and arteriosystemic venous shunts. Rarely, systemic venous (i.e. hepatic vein to hepatic vein) shunts and portal-to-portal communications are seen [1]. The unique dual blood supply of the liver (approximately 75% portal venous and 25% arterial) means there is a compensatory relationship between the two sources. When vascular compromise occurs, it causes a macroscopic opening of the shunts between the hepatic arteries, the portal veins and the hepatic veins through physiological anastomoses, which become abnormally enlarged [1][2][3]. The purpose of this pictorial review is to illustrate the imaging appearances of hepatic vascular shunts on multidetector CT (MDCT) with sonographic and conventional angiographic correlation. EmbryologyIn the fifth week of intrauterine life, there are three major paired veins in the abdomen: the vitelline or omphalomesenteric veins, the umbilical veins and the cardinal veins. The vitelline veins form the hepatic sinusoids. The left vitelline vein subsequently involutes and the blood is diverted into the right vitelline vein, which enlarges and forms the hepatocardiac portion of the inferior vena cava (IVC). Derivatives of the vitelline veins also form the hepatic and portal vein. The entire right umbilical vein and a portion of the left umbilical vein also degenerate. The persistent portion of the left umbilical vein connects to the right vitelline vein via the ductus venosus (Figure 1). The hepatic artery arises from the aorta and follows the mesentery [4,5].In antenatal circulation, oxygenated blood from the placenta returns to the foetus via the umbilical vein and flows through the ductus venosus into the IVC (Figure 2a). At birth, there is functional closure of the umbilical arteries, veins and the ductus venosus. Following atrophy, these form the medial umbilical ligaments, the ligamentum teres and the ligamentum venosum, respectively. Post-natal anatomy consists of inflow into the liver through the hepatic artery and portal vein, with the outflow through the hepatic veins (Figure 2b) [5].There is potential for intrahepatic shunts to develop when the ductus venosus remains patent, from failure of right upper vitelline vein regression, from a varix of the portal vein connecting to the hepatic/systemic venous circulation, from focal persistence of the most superior aspect of the vitelline veins or from arteriovenous malformations or neoplasms [6,7].

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