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Department of Radiology
Seth G.S. Medical College and K.E.M. Hospital, Mumbai , India
Interventional Case Record
Interventional Case Record
Sharp retrograde recanalization of an occluded collateral hepatic vein in Budd Chiari syndrome
Sharp retrograde recanalization of an occluded collateral hepatic vein in Budd Chiari syndrome
George Budd, a British internist, described three cases of hepatic vein thrombosis due to abscess-induced phlebitis in 1845, and Hans Chiari, an Austrian pathologist, added the first pathologic description of a liver with “obliterating endophlebitis of the hepatic veins” in 1899.
Contributed by : Amruta Varma
Contributed by : Amruta Varma
Introduction:
Introduction:
Budd-Chiari Syndrome (BCS) is a rare but serious condition characterized by obstruction of hepatic venous outflow, typically due to thrombosis of the hepatic veins or inferior vena cava. This obstruction can lead to significant hepatic congestion, portal hypertension, and liver dysfunction. The clinical presentation varies widely, from acute, rapidly fatal disease to chronic, progressive portal hypertension, ascites, cachexia, and cirrhosis; thus making early diagnosis and intervention crucial in management . Traditional portocaval or mesoatrial bypass shunts have offered some success, but with high rates of complications. Hepatic vein stenting has emerged as a vital therapeutic option for patients with BCS, particularly in those with non-cirrhotic disease and adequate liver function. The procedure aims to restore venous patency, alleviate symptoms and prevent the progression of liver damage.
Budd-Chiari Syndrome (BCS) is a rare but serious condition characterized by obstruction of hepatic venous outflow, typically due to thrombosis of the hepatic veins or inferior vena cava. This obstruction can lead to significant hepatic congestion, portal hypertension, and liver dysfunction. The clinical presentation varies widely, from acute, rapidly fatal disease to chronic, progressive portal hypertension, ascites, cachexia, and cirrhosis; thus making early diagnosis and intervention crucial in management . Traditional portocaval or mesoatrial bypass shunts have offered some success, but with high rates of complications. Hepatic vein stenting has emerged as a vital therapeutic option for patients with BCS, particularly in those with non-cirrhotic disease and adequate liver function. The procedure aims to restore venous patency, alleviate symptoms and prevent the progression of liver damage.
In this report, we present a case of a young man , presenting with complaints of ascites and deranged liver function secondary to Budd-Chiari syndrome. The patient was treated with stenting from a collateral hepatic vein with good clinical outcome.
In this report, we present a case of a young man , presenting with complaints of ascites and deranged liver function secondary to Budd-Chiari syndrome. The patient was treated with stenting from a collateral hepatic vein with good clinical outcome.
Case Presentation:
Case Presentation:
A 36 year old man presented with complaints of jaundice and abdominal distention in the month of January 2024 and was given conservative management. The patient presented again with history of one episode of hematemesis in August for the evaluation of which MRI of the abdomen with MR venogram was done. Besides gross ascites, this revealed intrahepatic veno-venous collaterals (Fig. 1), suggestive of Budd-Chiari syndrome. His laboratory parameters showed increase in total bilirubin ( 5 mg/dl) and direct bilirubin ( 3.1 mg/dl),platelet counts – 2 lakhs/cumm, Haemoglobin was 6.1 gm% and INR was 1.08 IU.
A 36 year old man presented with complaints of jaundice and abdominal distention in the month of January 2024 and was given conservative management. The patient presented again with history of one episode of hematemesis in August for the evaluation of which MRI of the abdomen with MR venogram was done. Besides gross ascites, this revealed intrahepatic veno-venous collaterals (Fig. 1), suggestive of Budd-Chiari syndrome. His laboratory parameters showed increase in total bilirubin ( 5 mg/dl) and direct bilirubin ( 3.1 mg/dl),platelet counts – 2 lakhs/cumm, Haemoglobin was 6.1 gm% and INR was 1.08 IU.
Fig 1 MRI of the abdomen shows prominent middle hepatic vein distal to the occlusion (top arrow) and intrahepatic veno-venous collateral (bottom arrow).
Interventional technique:
Interventional technique:
Percutaneous transhepatic access was obtained under US and DSA guidance using a Chiba needle. Injection of contrast showed occlusion of the common trunk of left and middle hepatic veins with multiple intrahepatic venous collaterals (Fig. 2).
Percutaneous transhepatic access was obtained under US and DSA guidance using a Chiba needle. Injection of contrast showed occlusion of the common trunk of left and middle hepatic veins with multiple intrahepatic venous collaterals (Fig. 2).
Fig. 2 DSA showing left hepatic vein ( left arrow) and collateral (right arrow).
Multiple attempts were made to cross the lesion through the transhepatic access , however these were futile. Through a right internal jugular vein access, the inferior vena cava was entered . A 10x 40 mm balloon was inflated in the retrohepatic portion of IVC as a guidance to target while crossing the occlusion through the transhepatic route ( Video 1) , however it was not successful.
Multiple attempts were made to cross the lesion through the transhepatic access , however these were futile. Through a right internal jugular vein access, the inferior vena cava was entered . A 10x 40 mm balloon was inflated in the retrohepatic portion of IVC as a guidance to target while crossing the occlusion through the transhepatic route ( Video 1) , however it was not successful.
video 1.mp4Video 1 10x 40 mm angioplasty balloon catheter inflated in retrohepatic portion of IVC as a guidance to target while crossing the occlusion through the transhepatic route .
Following this, attempts through the transjugular approach were made using a long chiba needle to cross the hepatic vein ostial lesion. However these were futile as the angle between the IVC and hepatic vein was acute. . An attempt was made to target the collateral through the IVC. (Video 2) . After confirming the backflow in chiba needle, injection of contrast confirmed that the tip was in a collateral. A 0.014” Nitrex wire was negotiated through it (Fig 3) and an H1 catheter was advanced over it.
Following this, attempts through the transjugular approach were made using a long chiba needle to cross the hepatic vein ostial lesion. However these were futile as the angle between the IVC and hepatic vein was acute. . An attempt was made to target the collateral through the IVC. (Video 2) . After confirming the backflow in chiba needle, injection of contrast confirmed that the tip was in a collateral. A 0.014” Nitrex wire was negotiated through it (Fig 3) and an H1 catheter was advanced over it.
video 2.mp4
Video 2 (left) Targeting the collateral using the long chiba needle via the trans jugular route
Fig 3 (right)– 0.014” wire negotiated through the long chiba needle with tip of the wire in the collateral.
Preliminary dilation was done using a 5 x 40 mm angioplasty balloon catheter and a balloon mounted 10x 37 mm stent was deployed with the distal end in the collateral and proximal end in the IVC ( Video 3) .
Preliminary dilation was done using a 5 x 40 mm angioplasty balloon catheter and a balloon mounted 10x 37 mm stent was deployed with the distal end in the collateral and proximal end in the IVC ( Video 3) .
video 3.mp4Video 3 Deployment of the balloon mounted stent with it’s distal end in the intrahepatic venovenous collateral
Post stenting balloon angioplasty was done using 10 x 40 mm balloon. An angiogram was performed which showed good flow through the stent ( Video 4). The transhepatic track was embolized using a pushable coil (Fig. 4) .
Post stenting balloon angioplasty was done using 10 x 40 mm balloon. An angiogram was performed which showed good flow through the stent ( Video 4). The transhepatic track was embolized using a pushable coil (Fig. 4) .
video 4.mp4
Video 4 Final post stenting DSA showing good opacification of the stent.
Fig 4 Embolization of the track with the pushable coil.
Post stenting liver function tests were done after one month. These revealed normal total bilirubin levels - 0.5 mg/dl. A Doppler study was done after 15 days which showed good flow through the stent (Fig. 5). A Triple phase CT performed after one month revealed good opacification of the stent and complete absence of the ascites. (Fig. 6)
Post stenting liver function tests were done after one month. These revealed normal total bilirubin levels - 0.5 mg/dl. A Doppler study was done after 15 days which showed good flow through the stent (Fig. 5). A Triple phase CT performed after one month revealed good opacification of the stent and complete absence of the ascites. (Fig. 6)
Fig 5 Post stenting doppler suggestive good flow through the stent.
Fig. 6 Post stenting 1 month follow up Triple phase CT suggestive of patent stent with disappearance of the ascites
Discussion:
Discussion:
BCS denotes a heterogeneous group of diseases characterized by hepatic venous outflow obstruction at the level of hepatic veins or inferior vena cava resulting in portal hypertension (1) . The right hepatic vein drains directly into the IVC; left and middle hepatic veins often unite to drain the rest of the liver in approximately 80% of the cases. Small accessory hepatic veins from the pericaval liver segments drain directly into the IVC . The intrahepatic venovenous collaterals and the hepatic vein occlusion can be appreciated well on imaging modalities like ultrasonography, triple phase CT and MRI (2).
BCS denotes a heterogeneous group of diseases characterized by hepatic venous outflow obstruction at the level of hepatic veins or inferior vena cava resulting in portal hypertension (1) . The right hepatic vein drains directly into the IVC; left and middle hepatic veins often unite to drain the rest of the liver in approximately 80% of the cases. Small accessory hepatic veins from the pericaval liver segments drain directly into the IVC . The intrahepatic venovenous collaterals and the hepatic vein occlusion can be appreciated well on imaging modalities like ultrasonography, triple phase CT and MRI (2).
Formation of intrahepatic venovenous collateral vessels in patients with hepatic venous obstruction is the body’s own compensatory mechanism to decompress the liver, and if these collateral vessels are adequate, it can explain the absence of symptoms in these patients (3). The significance of intrahepatic collateral vessels in the treatment of patients with BCS was mentioned by Baijal et al (4), who observed in patients with combined hepatic vein and IVC obstruction that recanalization of the IVC alone can be an effective treatment option if at least one large hepatic vein or collateral vessel opens into the IVC below the level of its obstruction.
Formation of intrahepatic venovenous collateral vessels in patients with hepatic venous obstruction is the body’s own compensatory mechanism to decompress the liver, and if these collateral vessels are adequate, it can explain the absence of symptoms in these patients (3). The significance of intrahepatic collateral vessels in the treatment of patients with BCS was mentioned by Baijal et al (4), who observed in patients with combined hepatic vein and IVC obstruction that recanalization of the IVC alone can be an effective treatment option if at least one large hepatic vein or collateral vessel opens into the IVC below the level of its obstruction.
Intrahepatic collateral vessels reroute the obstructed hepatic venous system into the IVC and share a common ostium with an accessory hepatic vein, providing a venovenous collateral vessel formation (5). A good understanding of this compensatory intrahepatic collateral vessel formation and its mapping with US and color Doppler studies are key factors in the consideration of this recanalization option for suitable patients. Endovascular recanalization of the compromised ostium of these collateral vessels indirectly facilitates the body’s own compensatory mechanism. (6) The limitation of this procedure is that it is feasible only in cases of adequate intrahepatic collateral vessel formation with ostial stenosis/occlusion and a failed standard hepatic vein recanalization procedure.
Intrahepatic collateral vessels reroute the obstructed hepatic venous system into the IVC and share a common ostium with an accessory hepatic vein, providing a venovenous collateral vessel formation (5). A good understanding of this compensatory intrahepatic collateral vessel formation and its mapping with US and color Doppler studies are key factors in the consideration of this recanalization option for suitable patients. Endovascular recanalization of the compromised ostium of these collateral vessels indirectly facilitates the body’s own compensatory mechanism. (6) The limitation of this procedure is that it is feasible only in cases of adequate intrahepatic collateral vessel formation with ostial stenosis/occlusion and a failed standard hepatic vein recanalization procedure.
In our case the recanalized intrahepatic collateral vessel shared the ostium with the middle and left hepatic veins and multiple attempts were made to recanalize the hepatic vein however, these were futile and hence hepatic collateral recanalization was done through the transjugular approach.
In our case the recanalized intrahepatic collateral vessel shared the ostium with the middle and left hepatic veins and multiple attempts were made to recanalize the hepatic vein however, these were futile and hence hepatic collateral recanalization was done through the transjugular approach.
In conclusion, understanding intrahepatic collateral vessel formation in patients with BCS is not only essential in understanding the evolution of the disease but also important in planning suitable endovascular recanalization procedures. Intrahepatic collateral vessel recanalization is a promising treatment option in suitable patients with failed hepatic vein recanalization.
In conclusion, understanding intrahepatic collateral vessel formation in patients with BCS is not only essential in understanding the evolution of the disease but also important in planning suitable endovascular recanalization procedures. Intrahepatic collateral vessel recanalization is a promising treatment option in suitable patients with failed hepatic vein recanalization.
References :
References :
1. Li T, Zhai S, Pang Z, et al. (2009) Feasibility and midterm outcomes of percutaneous transhepatic balloon angioplasty for symptomatic Budd-Chiari syndrome secondary to hepatic venous obstruction. J Vasc Surg 50:1079–1084.
1. Li T, Zhai S, Pang Z, et al. (2009) Feasibility and midterm outcomes of percutaneous transhepatic balloon angioplasty for symptomatic Budd-Chiari syndrome secondary to hepatic venous obstruction. J Vasc Surg 50:1079–1084.
2. Chaubal N, Dighe M, Hanchate V, Thakkar H, Deshmukh H, Rathod K. Sonography in Budd-Chiari syndrome. J Ultrasound Med 2006; 25:373–379.
2. Chaubal N, Dighe M, Hanchate V, Thakkar H, Deshmukh H, Rathod K. Sonography in Budd-Chiari syndrome. J Ultrasound Med 2006; 25:373–379.
3. Valla C. Hepatic vein thrombosis (Budd Chiari syndrome). Semin Liver Dis 2002; 22:5–14.
3. Valla C. Hepatic vein thrombosis (Budd Chiari syndrome). Semin Liver Dis 2002; 22:5–14.
4. Baijal SS, Roy S, Phadke RV, Agrawal DK, Kumar S, Choudhuri G. Management of idiopathic Budd-Chiari syndrome with primary stent placement: early results. J Vasc Interv Radiol 1996; 7:545–553
4. Baijal SS, Roy S, Phadke RV, Agrawal DK, Kumar S, Choudhuri G. Management of idiopathic Budd-Chiari syndrome with primary stent placement: early results. J Vasc Interv Radiol 1996; 7:545–553
5. Millener P, Grant EG, Rose S, et al. Color Doppler findings in patients with Budd-Chiari syndrome: correlation with venographic findings. AJR Am J Roentgenol 1993; 161:307–312.
5. Millener P, Grant EG, Rose S, et al. Color Doppler findings in patients with Budd-Chiari syndrome: correlation with venographic findings. AJR Am J Roentgenol 1993; 161:307–312.
6. Intrahepatic Collateral Recanalization in Symptomatic Budd-Chiari Syndrome: A Single-center Experience . Mammen, Thomas et al. Journal of Vascular and Interventional Radiology, Volume 21, Issue 7, 1119 – 1124.
6. Intrahepatic Collateral Recanalization in Symptomatic Budd-Chiari Syndrome: A Single-center Experience . Mammen, Thomas et al. Journal of Vascular and Interventional Radiology, Volume 21, Issue 7, 1119 – 1124.
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