British Journal of Radiology 74 (2001),273-275 © 2001 The British Institute of Radiology
Pseudolesion in segment IV of the liver adjacent to the falciform ligament caused by drainage of the paraumbilical vein: demonstration by power Doppler ultrasound
S Kobayashi, MD
O Matsui, MD
and
T Gabata, MD
Department of Radiology, Kanazawa University School of Medicine, 13-1, Takara-machi, Kanazawa, 920-8641, Japan
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Abstract
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A case of a pseudolesion in segment IV of the liver, adjacent to the falciform ligament, was observed on conventional CT and CT during arterial portography. The pseudolesion was caused by drainage of the paraumbilical vein. Power Doppler ultrasound was helpful in recognizing this pseudolesion by depicting that the paraumbilical vein was connected to vessels in this area. Although the direction of flow could not be determined, power Doppler ultrasound is a useful method for confirming non-invasively the aetiology of pseudolesions in this area.
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Introduction
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Various pseudolesions have been reported on CT during arterial portography (CTAP). Most of these pseudolesions are attributed to extraportal hepatopetal flow other than flow in the hepatic arteries. To determine their aetiology, selective arteriography or selective CT arteriography is performed to opacify the aberrant or extraportal venous flow [1–3]. In some cases, however, it is difficult to demonstrate the venous flow that causes the pseudolesion.
We describe a pseudolesion in segment IV of the liver, adjacent to the falciform ligament, owing to hepatopetal flow in the paraumbilical vein and confirmed by a combination of CTAP and non-invasive power Doppler ultrasound (Power Vision 6000, Toshiba Co., Tokyo, Japan). We discuss the advantages of confirming by ultrasound the hepatopetal flow except for flow in the portal vein.
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Case report
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A 37-year-old woman with pulmonary haemangioendothelioma was admitted to hospital for examination and treatment of liver metastases. Three focal lesions were observed in the liver on abdominal CT. Two of these lesions, in segments IV and VII, appeared hypodense on pre-contrast CT, showed ring-like enhancement on dynamic contrast enhanced CT and appeared isodense on post-contrast CT. These lesions appeared hypointense on T1 weighted MRI and hyperintense on T2 weighted MRI. On CTAP, these two lesions showed portal perfusion defects, but on CT during hepatic arteriography (CTHA) they showed a ring of contrast opacification. These two lesions were diagnosed as metastases from the pulmonary haemangioendothelioma. The third lesion was in the anteromedial edge of segment IV, adjacent to the falciform ligament, and appeared isodense on pre-contrast CT, hypodense on dynamic enhanced CT and isodense on post-contrast CT (Figure 1
). This lesion was isointense on the T1 and T2 weighted MR images. On CTAP, the lesion showed a portal perfusion defect, while on CTHA it appeared hypodense compared with the surrounding liver parenchyma (Figures 2 and 3). Because of the specific position in the liver and because no signal intensity change was seen on MRI, we suspected this lesion to be a pseudolesion caused by hepatopetal flow of the paraumbilical vein, which runs within the falciform ligament toward the liver parenchyma of segment IV. Power Doppler ultrasound showed a blood vessel directly connecting the liver parenchyma of segment IV with the extrahepatic space where the falciform ligament is located (Figures 4a,b). Unfortunately, we failed to show the vessel on colour Doppler imaging and pulse Doppler imaging. However, by combining the finding of a portal perfusion defect observed on CTAP with the power Doppler ultrasound appearances we could attribute this lesion to hepatopetal flow in the paraumbilical vein.
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Figure 1. Contrast enhanced CT shows a rounded area of hypoattenuation in the anteromedial edge of segment IV of the liver, adjacent to the falciform ligament.
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Figure 2. CT during arterial portography shows a rounded portal perfusion defect at the anteromedial edge of segment IV of the liver, adjacent to the falciform ligament.
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Figure 3. CT obtained during common hepatic arteriography (CTHA) shows hypoattenuation at the anteromedial edge of segment IV of the liver, adjacent to the falciform ligament. Because of the irregular perfusion of contrast medium, the liver shows irregular non-tumorous stain on CTHA.
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Figure 4. (a) Power Doppler image shows a vessel connecting the hepatic parenchyma at the anteromedial edge of segment IV of the liver, adjacent to the falciform ligament, and extrahepatic soft tissue of the abdominal wall (arrow). (b) The vessel observed in (a) is directly connected to the vessels in the hepatic parenchyma on the anteromedial edge of segment IV of the liver, adjacent to the falciform ligament (arrow), and is shown in the extrahepaticsoft tissue of the abdominal wall (arrowhead).
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Discussion
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The anteromedial edge of segment IV of the liver, adjacent to the falciform ligament, is a well recognized site for pseudolesions demonstrated on CTAP [4–7]. Focal fatty infiltration is also occasionally observed in this area [7, 8]. In the cirrhotic liver, a venous anastomosis showing hepatofugal flow between the intrahepatic portal vein and the systemic vein, known as the paraumbilical vein or vein of Sappey, arises from the hepatic parenchyma at the anteromedial edge of segment IV of the liver, adjacent to the falciform ligament [9, 10]. In normal liver without portal hypertension, this venous flow is usually not conspicuous and does not modify the imaging findings. However, the hepatopetal flow of the paraumbilical vein is increased in some cases, and the liver parenchyma adjacent to the falciform ligament then shows portal perfusion defects on CTAP [11]. The reason the paraumbilical vein shows hepatopetal flow in some normal livers is still not known. Such differences in the focal hepatic parenchymal blood supply are related to the occurrence of focal fatty liver observed in this area [8]. The aetiology of focal fatty infiltration in this area is also not clear.
To opacify and confirm the hepatopetal flow of the paraumbilical vein draining into segment IV of the liver on arteriography or CT arteriography, one must perform right or left internal thoracic arteriography or CT during internal thoracic arteriography [11]. With this procedure, however, there is a risk of thrombosis of the carotid and/or vertebral artery.
On the other hand, demonstration of flow within the paraumbilical vein directly connecting to the hepatic parenchyma around the falciform ligament by colour and/or power Doppler ultrasound confirms that the portal perfusion defect seen on CTAP is a pseudolesion caused by this venous drainage without resorting to an invasive procedure [12].
We could not demonstrate the hepatopetal flow of the paraumbilical vein by colour Doppler ultrasound because of the noise artefact caused by the motion of the heart. Power Doppler ultrasound demonstrated a blood vessel directly connecting the extrahepatic soft tissue of the abdominal wall to the hepatic parenchyma of segment IV around the falciform ligament. Unfortunately, we failed to depict the pulse Doppler signal of this vessel.
Because the anteromedial edge of segment IV of the liver around the falciform ligament is located relatively near to the heart, noise caused by the heart affects Doppler imaging. Although power Doppler imaging cannot show the flow direction, it is effective because it better detects a low volume and low velocity flow than does colour Doppler imaging [13, 14]. In this case, once the existence of the blood vessel directly connecting the hepatic parenchyma and extrahepatic area was shown, it was easy to estimate the flow direction of this vessel by referring to the CTAP findings. In our opinion, if a portal perfusion defect is seen on CTAP in the anteromedial edge of segment IV of the liver around the falciform ligament, it is sufficient to show a blood vessel connecting this hepatic area and extrahepatic area by power Doppler ultrasound to confirm that this detect is a pseudolesion.
Received for publication August 17, 2000.
Revision received October 16, 2000.
Accepted for publication October 26, 2000.
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Abstract
Introduction
