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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
Interventional radiological treatment of left hepatic vein-IVC anastomotic stenosis:in in a liver transplant recipient
Interventional radiological treatment of left hepatic vein-IVC anastomotic stenosis:in in a liver transplant recipient
Contributed by : Salman Mapara
Contributed by : Salman Mapara
Introduction:
Introduction:
Living donor liver transplantation (LDLT) is an established therapeutic modality for adults and children with end stage liver disease and congenital hepato biliary disease, especially in countries where deceased donors for liver transplantation (LT) are not available and where the waiting lists for orthotopic liver transplantation are too long for critically ill patients with end stage liver disease. [1] Liver transplantation can be complicated by stenosis of the hepatic venous or inferior vena cava outflow. Venous outflow stenosis occurs at rates of 1 to 6% depending on the type of anastomosis. Stenoses can develop acutely because of technical problems or can present much later after the transplant due to intimal hyperplasia or perianastomotic fibrosis. [4,5] Common clinical presentations include hepatic dysfunction, liver engorgement, ascites, abdominal pain, and occasionally variceal bleeding. Treatment can generally be accomplished via a transjugular approach, but percutaneous transhepatic access may be needed when the anastomosis cannot be catheterized from jugular access. Angioplasty can achieve technical success in restoring anastomotic patency in close to 100% of cases, but restenosis is frequent. Repeat angioplasties may be needed. In adults and paediatric patients with adult sized hepatic veins, stenting may be a better option. Resolution of clinical signs and symptoms is seen in 73 to 100% of cases. Major complications are uncommon, with stent migration being one of the more difficult complications to manage.
Living donor liver transplantation (LDLT) is an established therapeutic modality for adults and children with end stage liver disease and congenital hepato biliary disease, especially in countries where deceased donors for liver transplantation (LT) are not available and where the waiting lists for orthotopic liver transplantation are too long for critically ill patients with end stage liver disease. [1] Liver transplantation can be complicated by stenosis of the hepatic venous or inferior vena cava outflow. Venous outflow stenosis occurs at rates of 1 to 6% depending on the type of anastomosis. Stenoses can develop acutely because of technical problems or can present much later after the transplant due to intimal hyperplasia or perianastomotic fibrosis. [4,5] Common clinical presentations include hepatic dysfunction, liver engorgement, ascites, abdominal pain, and occasionally variceal bleeding. Treatment can generally be accomplished via a transjugular approach, but percutaneous transhepatic access may be needed when the anastomosis cannot be catheterized from jugular access. Angioplasty can achieve technical success in restoring anastomotic patency in close to 100% of cases, but restenosis is frequent. Repeat angioplasties may be needed. In adults and paediatric patients with adult sized hepatic veins, stenting may be a better option. Resolution of clinical signs and symptoms is seen in 73 to 100% of cases. Major complications are uncommon, with stent migration being one of the more difficult complications to manage.
Here, we will review the case of post operative hepatic vein anastomosis site stenosis and associated liver failure which was managed by endovascular treatment of stenosis with reversal of liver failure.
Here, we will review the case of post operative hepatic vein anastomosis site stenosis and associated liver failure which was managed by endovascular treatment of stenosis with reversal of liver failure.
A nine-year-old boy with history of jaundice with treatment by complementary and alternative medicine (CAM). He was evaluated at our hospital and found to have liver cirrhosis and portal hypertension with low serum ceruloplasmin levels, negative for viral markers and autoimmune conditions. He was further diagnosed with chronic liver failure (Wilson’s related) associated with ascites and grade II encephalopathy without gastric bleeding or peritonitis. His hepatoportal Doppler showed changes of portal hypertension, chronic liver disease and ascites. His total and direct bilirubin and liver function parameter levels were raised (Total bilirubin was 8.8 mg/dL, AST was 300 U/L) and CTP score was 13 and MELD score was 30.
A nine-year-old boy with history of jaundice with treatment by complementary and alternative medicine (CAM). He was evaluated at our hospital and found to have liver cirrhosis and portal hypertension with low serum ceruloplasmin levels, negative for viral markers and autoimmune conditions. He was further diagnosed with chronic liver failure (Wilson’s related) associated with ascites and grade II encephalopathy without gastric bleeding or peritonitis. His hepatoportal Doppler showed changes of portal hypertension, chronic liver disease and ascites. His total and direct bilirubin and liver function parameter levels were raised (Total bilirubin was 8.8 mg/dL, AST was 300 U/L) and CTP score was 13 and MELD score was 30.
In view of his worsening condition. a living donor liver transplant surgery done with donor left liver from mother and removal of recipient liver. LHV to IVC, hepatic artery, bile duct and LPV anastomosis were done by multispecialty transplant team at our hospital. From post operative Day 2, the patient was on steroids and antibiotics as well during which he developed fungal infection (Cryptococcus laurentii). Post operative Doppler revealed mild anastomotic site stenosis at left hepatic vein- IVC site (Figure 1 and 2).
In view of his worsening condition. a living donor liver transplant surgery done with donor left liver from mother and removal of recipient liver. LHV to IVC, hepatic artery, bile duct and LPV anastomosis were done by multispecialty transplant team at our hospital. From post operative Day 2, the patient was on steroids and antibiotics as well during which he developed fungal infection (Cryptococcus laurentii). Post operative Doppler revealed mild anastomotic site stenosis at left hepatic vein- IVC site (Figure 1 and 2).
Figure 1 (left) Colour doppler image showing anastomotic site stenosis and turbulent colour flow (arrowhead)
Figure 2 (right) Pulsed waveform images showing reduced PSV with lost typical waveform of hepatic vein.
The Patient was having rising trends of liver parameters and bilirubin level. Hence, transjugular liver biopsy and hepatic venous pressure gradient measurement were planned on day 18 of surgery.
The Patient was having rising trends of liver parameters and bilirubin level. Hence, transjugular liver biopsy and hepatic venous pressure gradient measurement were planned on day 18 of surgery.
The venogram was performed by 6F sheath from right IJV access and through this a 4F H1 catheter was guided into the left hepatic vein and hepatic venous pressure gradient was done showing 2 mmHg gradient (more than 5 mmHg is significant). Following this. an Amplatzer ultra stiff wire access was established and the sheath was exchanged for 7F Balkin access. Following this, transjugular lover biopsy (TJLB) was done. (Figure 3).
The venogram was performed by 6F sheath from right IJV access and through this a 4F H1 catheter was guided into the left hepatic vein and hepatic venous pressure gradient was done showing 2 mmHg gradient (more than 5 mmHg is significant). Following this. an Amplatzer ultra stiff wire access was established and the sheath was exchanged for 7F Balkin access. Following this, transjugular lover biopsy (TJLB) was done. (Figure 3).
Figure 3 Showing transjugular liver biopsy from transplant left hepatic vein.
Over the next few days, the patient developed thrombocytopenia. His liver parameters were in rising trends. Liver biopsy reports show acute liver changes.
Over the next few days, the patient developed thrombocytopenia. His liver parameters were in rising trends. Liver biopsy reports show acute liver changes.
His Doppler evaluation shows moderate left hepatic vein-IVC anastomosis site stenosis.
His Doppler evaluation shows moderate left hepatic vein-IVC anastomosis site stenosis.
Interventional technique:
Interventional technique:
The patient was planned for DSA venogram SOS stenting. Through a 6F sheath, a right IJV access was obtained and through this using glidewire a 4F H1 catheter an IVC gram and left hepatic venogram was performed. Simultaneously the pressure changes were recorded at right atrium, IVC and in left hepatic vein. (figure 4 and video A).
The patient was planned for DSA venogram SOS stenting. Through a 6F sheath, a right IJV access was obtained and through this using glidewire a 4F H1 catheter an IVC gram and left hepatic venogram was performed. Simultaneously the pressure changes were recorded at right atrium, IVC and in left hepatic vein. (figure 4 and video A).
video A.mp4Figure 4 (left)- Left hepatic venogram images showing anastomotic site stenosis.
Video A (right)- Venogram demonstrating the anastomosis site stenosis of LHV and IVC.
The hepatic venous pressure gradient was significant (5.5 mmHg) and there was moderate anastomotic site stenosis. The glidewire was exchanged for Amplatz ultra stiff wire accords the stenosis and a 8F long sheath access was achieved. Over the stiff wire and using this sheath access a 10mm x 25 mm balloon mounted stent was deployed at anastomotic site (figure 5 and 6).
The hepatic venous pressure gradient was significant (5.5 mmHg) and there was moderate anastomotic site stenosis. The glidewire was exchanged for Amplatz ultra stiff wire accords the stenosis and a 8F long sheath access was achieved. Over the stiff wire and using this sheath access a 10mm x 25 mm balloon mounted stent was deployed at anastomotic site (figure 5 and 6).
Figure 5 (left)Showing long sheath (8 Fr) over the stiff wire with balloon mounted stent over it.
Figure 6 (right) Fluoroscopic image showing deployment of balloon mounted stent over the stenosis.
Post stenting venogram shows resolution of the stenosis and hepatic venous pressure gradient was less than 1mmHg (Figure 7, 8 and video B).
Post stenting venogram shows resolution of the stenosis and hepatic venous pressure gradient was less than 1mmHg (Figure 7, 8 and video B).
Figure 7 (left) Left hepatic venogram showing resolution of anastomotic site stenosis after stent placement.
Figure 8 (right) Fluoroscopic image showing stent in situ at LHV-IVC anastomosis.
video B.mp4Video B-Venogram demonstrating post stenting of anastomotic site at LHV and IVC.
Doppler images show typical hepatic venous waveform and patent stent. (Figure 9 and 10).
Doppler images show typical hepatic venous waveform and patent stent. (Figure 9 and 10).
Figure 9 (left) Pulsed waveform images showing normal PSV with typical waveform of left hepatic vein.
Figure 10 (right) Colour doppler image showing normal anastomotic site and laminar colour flow (arrowhead).
Post procedure, there was improvement in liver profile with generalised improvement with improved clearance of tacrolimus immunosuppressant. His CTP score reduced from 15 to 9B, MELD score reduced from 30 to 15 with subsequent reduction of bilirubin to 2.1 mg/dL and AST to 98 U/L at 6 weeks on discharge.
Post procedure, there was improvement in liver profile with generalised improvement with improved clearance of tacrolimus immunosuppressant. His CTP score reduced from 15 to 9B, MELD score reduced from 30 to 15 with subsequent reduction of bilirubin to 2.1 mg/dL and AST to 98 U/L at 6 weeks on discharge.
Discussion:
Discussion:
Living-donor liver transplantation (LDLT) has provided a solution to the severe lack of cadaver grafts for the replacement of liver afflicted with end-stage cirrhosis, fulminant disease, or inborn errors of metabolism. Vascular complications remain the most serious complications and a common cause for graft failure after hepatic transplantation. Doppler ultrasound remains the primary radiological imaging modality for the diagnosis of such complications. Liver transplantation has become a common operation and although results are often very good, the various vascular anastomoses can become compromised. Fortunately, these complications can usually be managed by interventional techniques. The key role of interventional techniques was nicely illustrated in the study by Cavallari and coworkers in which mortality after interventional graft salvage procedures was 11.1% compared with 41.6% mortality for those patients managed by retransplantation.[1] This current article will focus on compromise of the venous outflow (due to either hepatic vein or inferior vena cava stenosis), which can lead to significant morbidity and even death.
Living-donor liver transplantation (LDLT) has provided a solution to the severe lack of cadaver grafts for the replacement of liver afflicted with end-stage cirrhosis, fulminant disease, or inborn errors of metabolism. Vascular complications remain the most serious complications and a common cause for graft failure after hepatic transplantation. Doppler ultrasound remains the primary radiological imaging modality for the diagnosis of such complications. Liver transplantation has become a common operation and although results are often very good, the various vascular anastomoses can become compromised. Fortunately, these complications can usually be managed by interventional techniques. The key role of interventional techniques was nicely illustrated in the study by Cavallari and coworkers in which mortality after interventional graft salvage procedures was 11.1% compared with 41.6% mortality for those patients managed by retransplantation.[1] This current article will focus on compromise of the venous outflow (due to either hepatic vein or inferior vena cava stenosis), which can lead to significant morbidity and even death.
Overall venous outflow complications are relatively uncommon. Stenosis of the inferior vena cava (IVC) is reported to occur in less than 2% of liver transplants.[2] Stenosis of the hepatic vein (HV) outflow is slightly more common, but the incidence varies with the type of transplant. In a review of 600 paediatric liver transplants, the rates of HV stenosis were 1% for whole liver grafts and 2% for living related grafts, but 4% for reduced size or split grafts. [3] The piggyback type of anastomosis is said to reduce problems with anastomotic stenosis. In one review of 264 piggyback transplants only 2 cases (0.8%) of delayed HV obstruction occurred [4]; however, in another series of piggyback transplants the HV stenosis rate was 3.4%.[5] On the other hand, HV stenosis is more likely to occur after living related transplants because of the different ways these are anastomosed. In living related transplants, a patch of the donor IVC is usually not removed as can be done in cadaveric donors. Egawa and coworkers [6] reported HV stenosis in 3 of 48 (6%) children post living related donor transplants. There are different causes of outflow obstruction, which will vary with both the type of transplant and the length of time elapsed since the operation. If the obstruction occurs acutely, it is often due to a technical problem such as too tight of an anastomosis, donor-recipient size mismatch, twisting of the veins, or an abnormal intimal flap. Anastomotic stenoses presenting in delayed fashion are more likely to be secondary to perivascular fibrosis or intimal hyperplasia. Obstruction does not necessarily need to occur right at the anastomosis. Graft edema may cause hepatic enlargement and extrinsic impression on the IVC thus obstructing caval and/or HV outflow. Normal morphologic change of the liver may also cause problems. Partial liver grafts show considerable growth after implantation and this morphologic change may lead to twisting of the veins.
Overall venous outflow complications are relatively uncommon. Stenosis of the inferior vena cava (IVC) is reported to occur in less than 2% of liver transplants.[2] Stenosis of the hepatic vein (HV) outflow is slightly more common, but the incidence varies with the type of transplant. In a review of 600 paediatric liver transplants, the rates of HV stenosis were 1% for whole liver grafts and 2% for living related grafts, but 4% for reduced size or split grafts. [3] The piggyback type of anastomosis is said to reduce problems with anastomotic stenosis. In one review of 264 piggyback transplants only 2 cases (0.8%) of delayed HV obstruction occurred [4]; however, in another series of piggyback transplants the HV stenosis rate was 3.4%.[5] On the other hand, HV stenosis is more likely to occur after living related transplants because of the different ways these are anastomosed. In living related transplants, a patch of the donor IVC is usually not removed as can be done in cadaveric donors. Egawa and coworkers [6] reported HV stenosis in 3 of 48 (6%) children post living related donor transplants. There are different causes of outflow obstruction, which will vary with both the type of transplant and the length of time elapsed since the operation. If the obstruction occurs acutely, it is often due to a technical problem such as too tight of an anastomosis, donor-recipient size mismatch, twisting of the veins, or an abnormal intimal flap. Anastomotic stenoses presenting in delayed fashion are more likely to be secondary to perivascular fibrosis or intimal hyperplasia. Obstruction does not necessarily need to occur right at the anastomosis. Graft edema may cause hepatic enlargement and extrinsic impression on the IVC thus obstructing caval and/or HV outflow. Normal morphologic change of the liver may also cause problems. Partial liver grafts show considerable growth after implantation and this morphologic change may lead to twisting of the veins.
The signs and symptoms of hepatic vein stenosis may be similar to those of portal hypertension. Ascites, increasing abdominal girth, and weight gain is one of the commonest presentations. The patient may also have shortness of breath from either hydrothorax or massive ascites. Variceal bleeding may also be the initial presentation. Abdominal pain is another common symptom and may relate to either the ascites or the engorgement and distension of the liver. Rarely fatigue and weight loss associated with protein losing enteropathy can be the primary presentation of hepatic vein obstruction.[7] On physical examination the liver will feel enlarged and firm. Abdominal distension from ascites may be significant. When IVC stenoses occur they usually occur above the HV anastomosis. Thus, IVC stenoses often present with hepatic dysfunction or symptoms similar to the HV stenoses. Isolated IVC stenosis below the hepatic veins may present with lower extremity edema and ascites but without hepatic enlargement or dysfunction. A severe stenosis of the IVC can lead to IVC thrombosis, which may cause more severe lower extremity edema.[8] Laboratory findings of hepatic dysfunction can help confirm the clinical suspicion or may precede symptoms or physical findings. There is one situation in which the liver function tests may not parallel the clinical symptoms. Isolated stenosis of the right hepatic vein after piggyback transplantation has been reported to cause development of ascites despite relatively preserved liver function.[9] Another laboratory manifestation of HV outflow obstruction is decreased clearance of transplant immunosuppressive drugs like tacrolimus, resulting in higher trough levels. In one study,[10] 50% of 28 cases with HV stricture had increased trough levels of tacrolimus. Elevated serum creatinine may occur in cases of IVC obstruction.
The signs and symptoms of hepatic vein stenosis may be similar to those of portal hypertension. Ascites, increasing abdominal girth, and weight gain is one of the commonest presentations. The patient may also have shortness of breath from either hydrothorax or massive ascites. Variceal bleeding may also be the initial presentation. Abdominal pain is another common symptom and may relate to either the ascites or the engorgement and distension of the liver. Rarely fatigue and weight loss associated with protein losing enteropathy can be the primary presentation of hepatic vein obstruction.[7] On physical examination the liver will feel enlarged and firm. Abdominal distension from ascites may be significant. When IVC stenoses occur they usually occur above the HV anastomosis. Thus, IVC stenoses often present with hepatic dysfunction or symptoms similar to the HV stenoses. Isolated IVC stenosis below the hepatic veins may present with lower extremity edema and ascites but without hepatic enlargement or dysfunction. A severe stenosis of the IVC can lead to IVC thrombosis, which may cause more severe lower extremity edema.[8] Laboratory findings of hepatic dysfunction can help confirm the clinical suspicion or may precede symptoms or physical findings. There is one situation in which the liver function tests may not parallel the clinical symptoms. Isolated stenosis of the right hepatic vein after piggyback transplantation has been reported to cause development of ascites despite relatively preserved liver function.[9] Another laboratory manifestation of HV outflow obstruction is decreased clearance of transplant immunosuppressive drugs like tacrolimus, resulting in higher trough levels. In one study,[10] 50% of 28 cases with HV stricture had increased trough levels of tacrolimus. Elevated serum creatinine may occur in cases of IVC obstruction.
Doppler examinations in a patient with HV stenosis will show decreased mean velocities in both the hepatic veins and portal vein. The hepatic vein wave form will be very dampened when there is an outflow obstruction.[6] Typically the Doppler waveform in a normal hepatic vein is triphasic, but after transplantation the waveform is often biphasic even without any other signs or symptoms of flow obstruction.[11] However, when significant stenosis develops, the waveform usually degrades to a monophasic pattern. Other findings may include reversal of HV flow, accelerated flow with aliasing just beyond the stenosis, and visualization of the stenosis on gray scale imaging. Although Doppler ultrasound is useful, venography and pressure measurements are still considered to be the gold standard. Venography should be done whenever the diagnosis of venous outflow compromise is suspected. This is partially because the symptoms of outflow obstruction may be nonspecific. Anywhere from 3 to 20 mm Hg has been the threshold of abnormality. A gradient greater than 10 mm Hg is one commonly used threshold. [13,14] However, in a series by Weeks and coworkers, 15 the initial gradients ranged from 3 to 14 mm Hg. The significance of these stenoses was validated both by presenting symptoms and the response to treatment.
Doppler examinations in a patient with HV stenosis will show decreased mean velocities in both the hepatic veins and portal vein. The hepatic vein wave form will be very dampened when there is an outflow obstruction.[6] Typically the Doppler waveform in a normal hepatic vein is triphasic, but after transplantation the waveform is often biphasic even without any other signs or symptoms of flow obstruction.[11] However, when significant stenosis develops, the waveform usually degrades to a monophasic pattern. Other findings may include reversal of HV flow, accelerated flow with aliasing just beyond the stenosis, and visualization of the stenosis on gray scale imaging. Although Doppler ultrasound is useful, venography and pressure measurements are still considered to be the gold standard. Venography should be done whenever the diagnosis of venous outflow compromise is suspected. This is partially because the symptoms of outflow obstruction may be nonspecific. Anywhere from 3 to 20 mm Hg has been the threshold of abnormality. A gradient greater than 10 mm Hg is one commonly used threshold. [13,14] However, in a series by Weeks and coworkers, 15 the initial gradients ranged from 3 to 14 mm Hg. The significance of these stenoses was validated both by presenting symptoms and the response to treatment.
Access for the interventions is generally taken form the internal jugular access will provide the best overall approach to study either HV or IVC anastomoses since it provides a good trajectory to cannulate the target veins and there is very little associated morbidity with jugular access. If the HV obstruction prevents HV catheterization from the jugular access, an alternative approach is to do a percutaneous transhepatic puncture into the peripheral aspects of the obstructed hepatic vein, which can usually be done using ultrasound guidance. Similarly, caval stenoses can usually be catheterized from the jugular access, but if the IVC is completely obstructed, a catheter may need to be passed from a femoral venous access to define the caudal extent of the obstruction. Attempts to cross the obstruction may be more successful from the femoral access since the cava provides support for the catheter and prevents some of the wire buckling that occurs in the right atrium when trying to cross the obstruction from above. If unable to cross the IVC stenosis, sharp recanalization may be necessary.[8] This involves passing a needle across the obstruction while aiming at a balloon or snare placed on the other side of the obstruction. This technique should be restricted to short obstructions and cases where the needle can be passed in a straight line toward the target without significant angulation or curvature.[14]
Access for the interventions is generally taken form the internal jugular access will provide the best overall approach to study either HV or IVC anastomoses since it provides a good trajectory to cannulate the target veins and there is very little associated morbidity with jugular access. If the HV obstruction prevents HV catheterization from the jugular access, an alternative approach is to do a percutaneous transhepatic puncture into the peripheral aspects of the obstructed hepatic vein, which can usually be done using ultrasound guidance. Similarly, caval stenoses can usually be catheterized from the jugular access, but if the IVC is completely obstructed, a catheter may need to be passed from a femoral venous access to define the caudal extent of the obstruction. Attempts to cross the obstruction may be more successful from the femoral access since the cava provides support for the catheter and prevents some of the wire buckling that occurs in the right atrium when trying to cross the obstruction from above. If unable to cross the IVC stenosis, sharp recanalization may be necessary.[8] This involves passing a needle across the obstruction while aiming at a balloon or snare placed on the other side of the obstruction. This technique should be restricted to short obstructions and cases where the needle can be passed in a straight line toward the target without significant angulation or curvature.[14]
The next step is to open the stenosis and balloon angioplasty is usually the first approach. The balloon needs to be slightly oversized compared with the vessel diameter and often a high-pressure balloon will be needed to adequately open the anastomosis. For tough strictures that fail to dilate with standard percutaneous transluminal angioplasty (PTA) balloons, cutting balloons can be useful. Because of the high incidence of restenosis, stenting is an attractive option. While stenting may be preferable in adults, there is some debate about their use in paediatric patients. Venous stents can develop intimal hyperplasia and thus are not totally protective against restenosis. In addition, there is concern that stents will not grow in size with the child and could end up creating a relative narrowing of the HV. However, it should be recognized that the HVs may be adult size if the liver is derived from an adult donor. Rerksuppaphol and coworkers[16] suggest that stenting is superior even in paediatric cases. If an adult size stent (10 mm or greater diameter) can be deployed, the concern about growth of the child is probably a moot point. If the hepatic veins are small (< 8 mm in size), then stenting may not be the best option and instead repeated PTA is probably a better strategy. For both HV and IVC stenting, using a stent with large interstices is commonly recommend to avoid blocking HV flow if the stent ends up partially or completely over the HV or HV branches. Another theoretic problem with jailing the HV with an IVC stent is that future interventions would be made more difficult if a separate HV stenosis should develop. Use of balloon expandable stents is sometimes recommended for HV stenoses because they have higher radial strength compared with self-expanding stents and generally can be placed more precisely. This assertion is supported by comparing the 92% clinical success of the Stanford group [5] using Palmaz stents to the 72% clinical success reported by Ko and coworkers [17] using self-expanding stents.
The next step is to open the stenosis and balloon angioplasty is usually the first approach. The balloon needs to be slightly oversized compared with the vessel diameter and often a high-pressure balloon will be needed to adequately open the anastomosis. For tough strictures that fail to dilate with standard percutaneous transluminal angioplasty (PTA) balloons, cutting balloons can be useful. Because of the high incidence of restenosis, stenting is an attractive option. While stenting may be preferable in adults, there is some debate about their use in paediatric patients. Venous stents can develop intimal hyperplasia and thus are not totally protective against restenosis. In addition, there is concern that stents will not grow in size with the child and could end up creating a relative narrowing of the HV. However, it should be recognized that the HVs may be adult size if the liver is derived from an adult donor. Rerksuppaphol and coworkers[16] suggest that stenting is superior even in paediatric cases. If an adult size stent (10 mm or greater diameter) can be deployed, the concern about growth of the child is probably a moot point. If the hepatic veins are small (< 8 mm in size), then stenting may not be the best option and instead repeated PTA is probably a better strategy. For both HV and IVC stenting, using a stent with large interstices is commonly recommend to avoid blocking HV flow if the stent ends up partially or completely over the HV or HV branches. Another theoretic problem with jailing the HV with an IVC stent is that future interventions would be made more difficult if a separate HV stenosis should develop. Use of balloon expandable stents is sometimes recommended for HV stenoses because they have higher radial strength compared with self-expanding stents and generally can be placed more precisely. This assertion is supported by comparing the 92% clinical success of the Stanford group [5] using Palmaz stents to the 72% clinical success reported by Ko and coworkers [17] using self-expanding stents.
Complications fortunately are uncommon. The rate of major complications has been reported to be 0% in several series. [12,20,22] Minor complication occur in about 10% of cases and include transient hypotension and arrhythmias.[12] Hypotension can occur because the large PTA balloons can occlude the IVC and decrease venous return to the heart, particularly in young paediatric patients. If partial stent migration occurs during the procedure and if it has not extended too far into the IVC, the stent can be stabilized by deploying another stent in better position to lock the first stent in place.[15] If excessive migration occurs, attempts should be made to snare and retrieve the stent. Leaving a migrated stent in the right atrium can have disastrous consequences.
Complications fortunately are uncommon. The rate of major complications has been reported to be 0% in several series. [12,20,22] Minor complication occur in about 10% of cases and include transient hypotension and arrhythmias.[12] Hypotension can occur because the large PTA balloons can occlude the IVC and decrease venous return to the heart, particularly in young paediatric patients. If partial stent migration occurs during the procedure and if it has not extended too far into the IVC, the stent can be stabilized by deploying another stent in better position to lock the first stent in place.[15] If excessive migration occurs, attempts should be made to snare and retrieve the stent. Leaving a migrated stent in the right atrium can have disastrous consequences.
Stenosis of the venous outflow of liver transplants is uncommon, but when it does occur it can cause significant symptoms and hepatic dysfunction. Fortunately, endovascular techniques allow these to be treated with little risk and a high degree of efficacy.
Stenosis of the venous outflow of liver transplants is uncommon, but when it does occur it can cause significant symptoms and hepatic dysfunction. Fortunately, endovascular techniques allow these to be treated with little risk and a high degree of efficacy.
References :
References :
1. Cavallari A, Vivarelli M, Bellusci R, et al: Treatment of vascular complications following liver transplantation: multidisciplinary approach. Hepatogastroenterology 48(37):179-183, 2001
1. Cavallari A, Vivarelli M, Bellusci R, et al: Treatment of vascular complications following liver transplantation: multidisciplinary approach. Hepatogastroenterology 48(37):179-183, 2001
2. Kraus TW, Rohren T, Manner M, et al: Successful treatment of complete inferior vena cava thrombosis after liver transplantation by thrombolytic therapy. Br J Surg 79:568-569, 1992
2. Kraus TW, Rohren T, Manner M, et al: Successful treatment of complete inferior vena cava thrombosis after liver transplantation by thrombolytic therapy. Br J Surg 79:568-569, 1992
3. Buell JF, Funaki B, Cronin DC, et al: Long-term venous complications after full-size and segmental pediatric liver transplantation. Ann Surg 236(5):658-666, 2002
3. Buell JF, Funaki B, Cronin DC, et al: Long-term venous complications after full-size and segmental pediatric liver transplantation. Ann Surg 236(5):658-666, 2002
4. Sze DY, Semba CP, Razavi MK, et al: Endovascular treatment of hepatic venous outflow obstruction after piggyback technique liver transplantation. Transplantation 68:446-449, 1999
4. Sze DY, Semba CP, Razavi MK, et al: Endovascular treatment of hepatic venous outflow obstruction after piggyback technique liver transplantation. Transplantation 68:446-449, 1999
5. Wang SL, Sze DY, Busque S, et al: Treatment of hepatic venous outflow obstruction after piggyback liver transplantation. Radiology 236:352- 359, 2005
5. Wang SL, Sze DY, Busque S, et al: Treatment of hepatic venous outflow obstruction after piggyback liver transplantation. Radiology 236:352- 359, 2005
6. Egawa H, Tanaka K, Uemoto S, et al: Relief of hepatic vein stenosis by balloon angioplasty after living-related donor liver transplantation. Clin Transplant 7(4):306-311, 1993
6. Egawa H, Tanaka K, Uemoto S, et al: Relief of hepatic vein stenosis by balloon angioplasty after living-related donor liver transplantation. Clin Transplant 7(4):306-311, 1993
7. Dousset B, Legmann P, Soubrane O, et al: Protein-losing enteropathy secondary to hepatic venous outflow obstruction after liver transplantation. J Hepatol 27:206-210, 1997
7. Dousset B, Legmann P, Soubrane O, et al: Protein-losing enteropathy secondary to hepatic venous outflow obstruction after liver transplantation. J Hepatol 27:206-210, 1997
8. Mindikoglu AL, Miller JS, Borge MA, et al: Post-transplant IVC occlusion and thrombosis treated with tPA, heparin, and sharp recanalization. J Gastroenterol 40:302-305, 2005
8. Mindikoglu AL, Miller JS, Borge MA, et al: Post-transplant IVC occlusion and thrombosis treated with tPA, heparin, and sharp recanalization. J Gastroenterol 40:302-305, 2005
9. Aucejo F, Winans C, Henderson JM, et al: Isolated right hepatic vein obstruction after piggyback liver transplantation. Liver Transpl 12:808- 812, 2006
9. Aucejo F, Winans C, Henderson JM, et al: Isolated right hepatic vein obstruction after piggyback liver transplantation. Liver Transpl 12:808- 812, 2006
10. Totsuka E, Hakamada K, Narumi S, et al: Hepatic vein anastomotic stricture after living donor liver transplantation. Transplant Proc 36(8): 2252-2254, 2004
10. Totsuka E, Hakamada K, Narumi S, et al: Hepatic vein anastomotic stricture after living donor liver transplantation. Transplant Proc 36(8): 2252-2254, 2004
11. Fujimoto M, Moriyasu F, Someda H, et al: Recovery of graft circulation following percutaneous transluminal angioplasty for stenotic venous complications in pediatric liver transplantation: assessment with Doppler ultrasound. Transpl Int 8(2):119-125, 1995
11. Fujimoto M, Moriyasu F, Someda H, et al: Recovery of graft circulation following percutaneous transluminal angioplasty for stenotic venous complications in pediatric liver transplantation: assessment with Doppler ultrasound. Transpl Int 8(2):119-125, 1995
12. Kubo T, Shibata T, Itoh K, et al: Outcome of percutaneous transhepatic venoplasty for hepatic venous outflow obstruction after living donor liver transplantation. Radiology 239:285-290, 2006
12. Kubo T, Shibata T, Itoh K, et al: Outcome of percutaneous transhepatic venoplasty for hepatic venous outflow obstruction after living donor liver transplantation. Radiology 239:285-290, 2006
13. Raby N, Karani J, Thomas S, et al: Stenoses of vascular anastomoses after hepatic transplantation: treatment with balloon angioplasty. AJR Am J Roentgenol 157(1):167-171, 1991
13. Raby N, Karani J, Thomas S, et al: Stenoses of vascular anastomoses after hepatic transplantation: treatment with balloon angioplasty. AJR Am J Roentgenol 157(1):167-171, 1991
14. Borsa JJ, Daly CP, Fontaine AB, et al: Treatment of inferior vena cava anastomotic stenoses with the Wallstent endoprosthesis after orthotopic liver transplantation. J Vasc Interv Radiol 10(1):17-22, 1999
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