Interventional Radiology in the Pediatric Liver Transplant Patient

Abstract

Liver transplantation now plays a major role in the treatment of end-stage liver disease in children. Reduced-size liver transplant surgical techniques have allowed increasing numbers of children to undergo liver transplantation. As more children are undergoing liver transplantation, there is a growing need for radiologic diagnosis of and intervention in post-transplantation complications in these patients.

REDUCED-SIZE LIVER TRANSPLANT ANATOMY

Liver transplantation has evolved into an effective and widely accepted treatment of end-stage liver disease in infants and children, with 10-year actuarial patient survival rates as high as 76%. ^{1 2} Common indications for liver transplantation include extrahepatic biliary atresia, metabolic disease, fulminant hepatic failure, cryptogenic cirrhosis, intrahepatic cholestasis, chronic hepatitis, cystic fibrosis and tumors. ¹ Most liver transplant patients experience postoperative complications at some time. ^{3 4} Interventional radiologists are playing an increasing role in the diagnosis and management of these complications in pediatric patients.

The limited availability of size-matched donor whole organs has led to the development of reduced-size liver transplant techniques that are now widely used to treat end-stage liver disease in infants and children. ^{4 5 6} Knowledge of the unique surgical anatomy of the reduced-size liver transplant is essential to assess and treat pediatric liver transplant patients. Reduced-size liver transplants are based on the surgical segmental anatomy described by Couinaud and Bismuth. ^{6 7 8} This classification scheme divides the liver into vertical and oblique planes forming eight segments that are separated vertically by the three main hepatic veins and transversely by a plane drawn from the right to left portal veins (Fig. 1 ). Each segment is a functional unit containing a single discrete segmental duct, artery, and portal vein. This scheme allows division or resection of the liver by functional segment(s) and creates a framework for reduced-size transplants. Reduced-size transplants include left lobar transplants (segments 2-4), left lateral segmental transplants (segments 2 and 3), and right lobar transplants (segments 5-8). The left lobar and left lateral segmental grafts are most commonly used in children; the lateral segmental transplant is most commonly used in smaller children as body size dictates the amount of liver tissue necessary for adequate hepatic function. ^{5 6 7 8 9} The left lateral segment or left lobe may also be resected from a living donor for transplantation into a child.

Figure 1.

Segmental liver anatomy. IVC, inferior vena cava; PV, portal vein.

The surgical anatomy in these reduced-size grafts differs from adult whole graft transplant anatomy in that they have a cut surface, an enteric Roux-en-Y loop for biliary drainage, and an alteration in the position and number of hepatic vessels (Fig. 2 ). ¹⁰ A cut surface is created as the whole donor liver is divided and the left lateral segment or left lobe is prepared for transplantation. The bile ducts and individual vessels are sutured for the resection. Fibrin glue may be applied to the cut surface of the liver for hemostasis. Five anastomoses are performed for standard liver transplantation: one portal venous, one hepatic arterial, one biliary, and two caval anastomoses. The arterial anastomosis may vary depending on the donor or recipient anatomy, but most commonly the anastomosis is end to end between the donor celiac axis or hepatic artery and the recipient hepatic artery. The donor and recipient portal veins are ideally attached via an end-to-end anastomosis unless the recipient portal vein is thrombosed. In this case, the recipient superior mesenteric vein can be anastomosed to the portal vein via an interposition graft. If the donor portal vein is too short or if the recipient portal vein is atretic, an interposition graft can be used to ensure adequate length for anastomosis. Biliary reconstruction is achieved with an end-to-side choledochojejunostomy. A biliary stent is not routinely placed. A caval sparing ``piggyback'' technique is used for the caval anastomosis for cadaveric organ and living donor transplantation. ^{11 12} The recipient inferior vena cava (IVC) remains intact, and the infrahepatic portion of the donor IVC is oversewn. The recipient hepatic veins are joined, forming a wide-mouthed channel to receive the venous outflow of the graft. This makes for only a single IVC anastomosis. ^{11 12}

Figure 2.

Reduced-size allografts. (A) Left lobar transplant (segments 2-4). (B) Left lateral segment transplant (segments 2 and 3). In A and B: BD, bile duct; HA, hepatic artery; PV, portal vein; RL, Roux-en-Y loop; LHV, left hepatic vein. In A: MHV, middle hepatic vein.

The reduced-size allograft occupies the vacated recipient hepatic fossa but with some displacement to the left. The neo-porta hepatis is located on the right posterolateral aspect of the allograft (Fig. 3 ).

Figure 3.

Left lateral segment liver transplant in a 2-year-old boy. Axial computed tomography (CT) image showing the posterolaterally positioned neo-porta hepatis with the most superior portion of the Roux-en-Y loop adjacent ( white arrow ), portal vein ( small black arrow ) cut edge ( small black arrowheads ), hepatic artery ( large black arrow ), and IVC ( large black arrowhead ).

ARTERIAL COMPLICATIONS

Hepatic arterial thrombosis is the most common vascular complication following liver transplantation, ¹³ occurring in 4-12% of adult liver transplantations ¹⁴ and in as many as 50% of pediatric liver transplantationss. ^{2 13} With newer surgical techniques and improved postoperative medical management, the rate of pediatric hepatic arterial thrombosis has been reported to be as low as 9%. ¹³ Thrombosis is more likely to occur in children because the small arterial size makes the anastomosis technically difficult. ¹³ Clinically, patients with arterial thrombosis may present with hepatic dysfunction or failure and/or biliary sepsis. Occasionally, patients may be asymptomatic. ^{13 15} Cross-sectional imaging may show bilomas or infarcts suggesting hepatic arterial occlusion (Fig. 4 ). Cholangiography may demonstrate focal or diffuse biliary abnormalities as 84% of patients with hepatic arterial thrombosis have biliary abnormalities. ¹⁶ Doppler sonography shows absence of arterial flow at the porta hepatis, decreased resistive indices (<0.5), and systolic acceleration times of 0.08 seconds or longer in the intrahepatic arterial branches. ^{17 18} Arteriography remains the ``gold standard'' for confirmation of thrombosis (Fig. 4 ). Extrahepatic hepatopetal collateral vessels have been seen in 30% of children with hepatic arterial thrombosis and may prevent graft loss in these children (Fig. 4 ). ^{16 19}

Figure 4.

Hepatic arterial thrombosis. (A) Axial CT image in a patient with a whole liver transplant shows multiple wedge-shaped low-attenuation areas within the liver. (B) Aortogram demonstrates only the stump of the common hepatic artery ( arrow ). (C) Later phase of the aortogram demonstrates reconstitution of the intrahepatic arterial branches via extrahepatic collateral vessels ( arrowheads ).

Most cases of acute thrombosis require emergent operation for revascularization and surgical revision of the anastomosis. If the arterial thrombosis is detected early, there is a high rate of graft survival with these surgical techniques. ²⁰ There are few reports of successful percutaneous thrombolysis or thrombolysis with angioplasty for treatment of hepatic arterial thrombosis. ^{3 12} We have had no experience with these percutaneous techniques.

Hepatic arterial stenosis can lead to arterial thrombosis. Stenoses generally occur at or within a few centimeters of the arterial anastomotic site. ¹⁷ Stenosis that occurs shortly after transplantation has been attributed to surgical trauma to vessels, extrinsic compression, differences in vessel caliber that require oblique anastomoses, kinking resulting from excessive vessel length, and rejection. ²¹ Because arterial stenosis can lead to thrombosis, diagnosis and treatment are essential. Doppler arterial findings that can suggest stenosis include slow systolic upsweep and a dampened systolic Doppler shift in the artery distal to the stenosis associated with a low resistive index ^{17 18} (Fig. 5 ). Angiography remains the gold standard for diagnosis. Signs and symptoms are related to biliary ischemia and are similar to those seen with arterial thrombosis. Hepatic arterial stenosis can be surgically treated, but this could endanger the graft. Percutaneous transluminal angioplasty has been reported to be successful in treating hepatic arterial stenoses in adults and in a limited number of pediatric patients. ^{21 22 23} Caution should be used if performing percutaneous transluminal angioplasty in the immediate postoperative period to avoid vessel rupture.

Figure 5.

Hepatic arterial stenosis with progression to thrombosis. (A) Pulsed Doppler sonogram of the intrahepatic arterial waveform showing a slow systolic upsweep ( small arrow ), dampened systolic Doppler shift, and high end-diastolic velocity ( large arrow ) indicating low resistive index. (B) Axial CT performed 2 weeks later shows a whole liver transplant with multiple wedge-shaped low-attenuation areas consistent with infarcts. (C) Aortogram performed the next day shows only a stump of the common hepatic artery consistent with thrombosis ( arrow ).

Hepatic arterial pseudoaneurysms can occur but are rare and potentially fatal complications in liver transplant patients. ²⁴ They can occur in the extrahepatic hepatic artery at the hepatic arterial anastomotic site as a result of technical factors or infection or can involve the intrahepatic hepatic artery as a result of biopsy or infection (Fig. 6 ). Ruptured pseudoaneurysms can be fatal. Clinically, patients may be asymptomatic or may present with gastrointestinal bleeding or infection. ²⁴ If a liver transplant patient has hemobilia or gastrointestinal bleeding and negative endoscopy, angiography is indicated to exclude a pseudoaneurysm. ²⁴ These lesions may be treated surgically or embolized with percutaneous transcatheter techniques (Fig. 6 ).

Figure 6.

Hepatic artery pseudoaneurysm. (A) Axial CT in a patient with a whole liver transplant showing a large enhancing mass with peripheral thrombus ( arrowheads ) in the expected location of the hepatic artery. (B) Selective common hepatic artery injection shows a large pseudoaneurysm arising at the expected location of the hepatic arterial anastomosis ( arrows ) with intact intrahepatic arterial flow ( arrowheads ). (C) Following coil embolization, a large portion of the pseudoaneurysm has been thrombosed. (D) CT examination performed 2 months later demonstrates complete resolution of the pseudoaneurysm. (Courtesy of F. Glen Seidel, M.D., Kansas City, MO.)

VENOUS COMPLICATIONS

Portal Venous Complications

The incidence of portal venous thrombosis and stenosis in children following liver transplantation ranges from 0 to 33%. ^{25 26 27} This complication rate is higher than the 1 to 13% complication rate reported in adults. ⁶ Multiple factors influence this higher complication rate in children, including the type of graft utilized (cadaveric versus living donor), the recipient portal vein size, the type of anastomosis used, and the position of the graft. ^{25 27} In patients with cadaveric reduced-size liver transplants, the donor portal vein is generally of adequate length to anastomose directly with the recipient portal vein. The donor portal vein may be too short in patients undergoing living-donor left lateral segment transplants, and an interposition graft may be required for anastomosis. The complex reconstruction involved in this process leads to the increased complication rate for the living-donor transplants requiring interposition grafts. The material used for the interposition graft also affects the rate of thrombosis, with cryopreserved iliac vein grafts yielding a significantly increased rate of thrombosis. ²⁵ Portal veins measuring 2 to 4 mm are not uncommon in recipient patients with biliary atresia. This small portal venous size can lead to technical difficulties with the portal venous anastomosis. Slight twisting of the left lateral segment grafts is allowed in the vacated recipient hepatic fossa, which can also lead to an increase in the rate of portal venous thrombosis. ²⁵

Portal venous thrombosis occurring in the immediate postoperative period requires emergent surgical thrombectomy or retransplantation. Late occurring portal venous thrombosis and stenosis were treated in the past with retransplantation, venous reconstruction, or portacaval shunting. ^{28 29 30} The Rex shunt (superior mesenteric vein to left intrahepatic portal vein bypass) is now the surgical treatment of choice for late post-transplantation extrahepatic portal venous thrombosis with patent intrahepatic portal venous branches. ^{31 32} Percutaneous transhepatic venoplasty with or without metallic stent placement has become the treatment of choice for portal venous stenoses following reduced-size liver transplantation. ^{23 28 29 30 33} Patients with late portal venous complications present from 2 to 48 months after transplantation with signs of portal hypertension-splenomegaly, ascites, and variceal bleeding. The diagnosis of portal venous stenosis or thrombosis may be made with sonography or magnetic resonance angiography, but angiography is required for confirmation and can be performed in anticipation of treatment (Fig. 7 ). Pediatric patients with portal venous thrombosis have not been successfully treated with percutaneous techniques because of the inability to cross the thrombosed anastomotic site. ^{28 29 30} Funaki et al ^{28 29 30} reported a series of 19 pediatric patients with segmental transplants who underwent percutaneous transhepatic venoplasty for portal vein stenoses. Five of these patients required stent placement at the time of the initial procedure for elastic stenoses that were not responsive to venoplasty alone. Seven patients who underwent initial venoplasty returned with recurrent stenoses and required stent placement. The portal veins in these 12 patients and 7 patients who underwent venoplasty alone remained patent with a mean follow-up time of 46 months. This study is important for two reasons. First, children with portal venous stenoses can be successfully treated with percutaneous venoplasty with or without metallic stent placement. Second, metallic stents can be successfully deployed in the portal venous systems of growing children with an excellent outcome.

Figure 7.

Portal vein stenosis. (A) Transverse sonogram of a left lateral segment transplant demonstrating marked narrowing of the portal vein in the expected location of the venous anastomosis ( arrow ) with poststenotic dilatation of the portal vein ( arrowheads ). (B) Transhepatic portal angiogram showing the marked stenosis in the portal vein ( arrow ) with the poststenotic dilatation ( arrowheads ). (C) Following balloon angioplasty with a 9-mm balloon, significant stenosis and pressure gradient were still present, necessitating stent placement. (D) Injection performed after venoplasty and 10-mm stent placement demonstrating a decrease in the caliber of the stenosis. The gradient across the stenosis following angioplasty and stent placement was 5 mm Hg.

Hepatic Venous-Inferior Vena Caval Complications

IVC stenosis or thrombosis is seen in less than 1% of liver transplantations. ³ Causal factors include anastomotic technical difficulties and/or extrinsic compression. Extrinsic compression on the graft in children occurs frequently because liver graft volumes may be greater than preoperative liver volumes and mesenteric edema and bowel wall edema from portal venous cross-clamping can lead to an increase in intra-abdominal volume before abdominal closure. If the abdomen is then closed, thromboses may occur. Portal venous occlusion has been reported in one patient and portal venous, hepatic arterial, and hepatic venous occlusions have been reported in another patient as a result of increased abdominal pressure following reduced-size liver transplantation. ³⁴ After reopening of the surgical wound and release of abdominal pressure, flow was reestablished in the portal vein spontaneously in both patients. Hepatic arterial thrombectomy reestablished hepatic arterial and venous flow in the other. ³⁴

Patients with stenosis or thrombosis of the IVC present clinically with Budd-Chiari-like symptoms if the venous obstruction includes the hepatic venous return or may present with truncal edema if the obstruction is below the level of the hepatic venous confluence. Acute hepatic necrosis is the most severe result of hepatic outflow obstruction. Hepatic venous occlusion is increased in frequency in living-donor or split-liver transplants when donor hepatic veins are anastomosed to recipient hepatic veins or IVC. Therefore, great care must be taken at the time of transplantation in constructing these anastomoses so that the orifice size of the donor and recipient veins is well matched and the graft is positioned so that posterior rotation of the graft will not cause venous occlusion and outflow obstruction.

The diagnosis of occlusion of the IVC and/or hepatic veins can be made sonographically and confirmed with angiography if necessary (Fig. 8 ). If the occlusion is technical in nature, related to an underlying stenosis, treatment with percutaneous transluminal angioplasty (PTA) with or without stent placement can be successful. Repeat dilatation(s) may be necessary to achieve long-term patency (Fig. 9 ). Of a series of six patients who successfully underwent IVC PTA for IVC stenoses, only one remained asymptomatic without repeated intervention. ³⁵ Thrombosis related to extrinsic compression must be surgically treated. Retransplantation may be necessary if the thrombosis cannot be treated successfully.

Figure 8.

Inferior vena cava thrombosis. Venogram obtained 1 week after transplantation demonstrates slow flow within the opacified portion of the IVC with a meniscus ( arrow ) at the superior portion of the contrast column indicating acute thrombosis. Filling of retroperitoneal collaterals is also seen.

Figure 9.

Recurrent IVC thrombosis following IVC stent placement. (A) Venogram demonstrating caval thrombosis with filling only of retroperitoneal collaterals. The IVC stent is seen superiorly ( arrow ). (B) Following balloon angioplasty, caval flow is restored with a gradient of 4 mm Hg.

BILIARY COMPLICATIONS

Biliary tract complications after liver transplantation are common and are a significant cause of technical morbidity after orthotopic liver transplantation. ^{9 26 36} The incidence of biliary complications in children after liver transplantation ranges from 11.5% to 38%. ^{2 37 38} Bile leaks and biliary tract obstruction occur most commonly.

The etiology of biliary complications is multifactorial and includes vascular, technical, and immunologic factors. ³⁶ Because the allograft bile duct relies solely on hepatic arterial flow, hepatic arterial thrombosis or stenosis can lead to biliary stricture and/or necrosis either at the anastomosis or in any portion of the donor biliary tree. ³⁹ Technical difficulties leading to biliary complications are difficult to delineate because of the widely varied surgical techniques and materials used at the anastomotic site. Immunologic mechanisms such as ABO incompatibility between allograft and patient may lead to an increase in the incidence of biliary strictures. ⁴⁰ Infection with cytomegalovirus and chronic rejection may also play significant roles in the development of biliary strictures. ^{9 39}

Bile leaks are generally discovered in the immediate postoperative period and can occur at the biliary enteric anastomosis (50%), from the cut edge of the allograft (35%), or as a result of perforation of the Roux limb of the jejunum (15%). ³⁷ Early postoperative hepatic arterial thrombosis leads to global allograft ischemia with intrahepatic biliary ductal disruption and resultant bile lakes or multiple intrahepatic and extrahepatic strictures. ³⁹ Fifty percent of biliary leaks result from hepatic arterial thrombosis in the immediate postoperative period. ³⁹ These patients may present with fulminant hepatic necrosis, bile leak, or relapsing bacteremia. ^{13 15} Cross-sectional imaging may show a collection adjacent to the anastomotic site (Fig. 10 ). Percutaneous transhepatic cholangiography may demonstrate anastomotic biliary leaks as contrast extravasation out of the expected location of the biliary tree and/or bowel. Placement of a biliary stent should decompress the biliary tree and allow closure of the leaking bile duct nonoperatively. Bile leaks associated with arterial thrombosis are more difficult to manage because of the associated bile duct necrosis, and despite biliary stent placement these patients may require retransplantation. If the extrahepatic bile collection is large, a percutaneous drainage catheter should also be placed into the biloma.

Figure 10.

Biliary-enteric anastomotic leak. (A) Axial CT image of a left lateral segment transplant demonstrating a mixed attenuation collection ( arrows ) adjacent to the neo-porta hepatis in the location of the biliary enteric anastomosis. (B) A more cephalad axial CT image demonstrates continuation of the collection superiorly along the cut surface ( arrows ). A cholangiogram (not shown) demonstrated leakage of contrast material from the biliary enteric anastomosis into the collection.

Bile leaks from the cut surface are visualized most commonly with cross-sectional imaging and may be seen with percutaneous transhepatic chelangiography if the nonoccluded bile duct leading to the leak fills adequately with contrast material (Fig. 11 ). Placement of a percutaneous catheter directly into the biloma should allow nonoperative closure of the leak.

Figure 11.

Biloma after transplantation. Axial CT image of a living related left lateral segment liver transplant obtained 2 weeks after transplantation showing a large biloma adjacent to the cut surface of the liver ( arrows ).

Biliary strictures at the anastomotic site often occur relatively late in the post-transplantation course and can occur years after the initial surgery. These strictures occur as a result of fibrosis at the anastomotic site and may not be related to hepatic arterial thrombosis. Anastomotic strictures without associated hepatic arterial thrombosis can occur in the immediate postoperative period but are likely to be technical in nature, resulting from surgical ligation of a biliary duct in patients with reduced-size grafts (Fig. 12 ). Patients with anastomotic strictures present with a cholestatic profile on liver function tests, evidence of biliary obstruction on biopsy, or may have frank cholangitis. Sonography may or may not show a dilated biliary tree.

Figure 12.

Biliary obstruction presumed secondary to ligation of a biliary duct. (A) Longitudinal sonogram obtained 2 weeks after transplantation demonstrating marked biliary ductal dilatation ( arrows ). (B) Cholangiogram showing ductal dilatation and complete obstruction at the biliary-enteric anastomosis ( arrow ). Crossing the anastomosis was difficult. (C) Following angioplasty with a 3-mm balloon and biliary drainage catheter placement, contrast material passes freely into the Roux-en-Y loop.

In our institution, biliary strictures are managed with percutaneous drainage techniques. Access to the biliary tree is obtained using sonographic guidance into a primary or secondary biliary radicle for opacification of the biliary tree. In reduced-size grafts, a midline subxiphoid approach is most often used. Contrast injection with appropriate angulation demonstrates the anastomotic stricture. It is important to review the type of transplant used (either whole or reduced size) to ensure opacification of all ducts because undrained obstructed ducts may not be opacified on the cholangiogram (Fig. 13 ). If the initial access site is not optimal to gain access for intervention, repuncture with sonographic or fluoroscopic guidance into a more appropriately positioned duct is performed (Fig. 14 ). After crossing the anastomotic stricture using a 0.018-inch guide wire, exchange is made for a 0.035-inch guide wire, over which the stricture is balloon dilated if needed with balloon sizes ranging from 3 to 6 mm in diameter. The balloon is inflated two to three times to maximum tolerated pressure for approximately 1 minute per inflation (Fig. 15 ) (unlabeled use of a commercial product). Caution should be used if considering PTA in fresh anastomoses to avoid rupture. Then 6 to 14 French transanastomotic internal external biliary drainage catheters are placed. Smaller catheters are used in fresh anastomoses and in smaller children. Because recurrent strictures can occur, the largest size catheter deemed appropriate is used.

Figure 13.

Whole liver transplant with atrophy of the right lobe. (A) Axial CT image showing a whole liver transplant with hypertrophy of the left lobe ( large arrows ) and atrophy of the right lobe ( small arrows ). Biliary ductal dilatation is seen in both lobes ( arrowheads ). (B) Initial puncture into the left-sided ducts via a midline subxiphoid approach shows a focal stricture at the junction of the segment 2 and 3 ducts ( large arrow ) and an anastomotic stricture ( small arrow ). (C) Subsequent puncture of the right lobe for continuing fevers following left-sided drainage shows ductal dilatation and a focal anastomotic stricture ( arrow ).

Figure 14.

Biliary reaccess for a more optimal angle for intervention. (A) Initial cholangiogram showing puncture of segment 3 duct with suboptimal angle of access for anastomotic crossing and portal venous filling ( arrows ). (B) Fluoroscopic repuncture of the segment 2 duct improves the angle of access for intervention. (C) Cholangiogram performed 4 months after biliary drainage catheter placement shows free passage of contrast material from the biliary tree into the Roux-en-Y loop without significant residual anastomotic narrowing. Residual narrowing at the junction of the segment 2 and 3 ducts is seen.

Figure 15.

Balloon angioplasty of a biliary-enteric anastomotic stricture. (A) Initial cholangiogram in a left lateral segment transplant shows a focal anastomotic stricture at the biliary-enteric anastomosis ( arrow ). (B) Balloon angioplasty of the stricture was performed using a 5-mm balloon inflated to maximum pressure with only a minimal residual waist seen ( arrow ).

After the drainage catheter is placed, contrast injection is performed to ensure opacification of the biliary tree and nonopacification of the portal venous or hepatic venous systems. Contrast injection is also performed to ensure that the tip of the drainage catheter is not within the blind end of the Roux-en-Y loop, which can lead to stasis and biliary obstruction. The biliary drainage catheters are capped after any signs of biliary sepsis have resolved and the patient has been afebrile for at least 48 hours. Follow-up cholangiograms are performed every 6 weeks to 3 months or as needed for evaluation of tube patency.

There is currently no consensus about the length of time a biliary stent should be left in place. ^{39 40 41} We remove a biliary stent when contrast injection demonstrates free passage and drainage of contrast material from the biliary tree into the Roux-en-Y loop in a clinically well patient with stable liver function tests (Fig. 13 ). We have not used biliary manometry or clinical trials without biliary stents across the anastomoses to determine the length of biliary stenting necessary. The time from catheter placement to removal is variable but has ranged from 2 to 8 months. We have had little experience with placement of metallic stents across resistant anastomotic strictures, but this procedure has been reported as viable in adult patients. ³

We have attempted transhepatic cholangiography in 25 pediatric liver transplant patients. Successful biliary access was obtained in 23 patients with successful biliary stent placement across anastomotic strictures in 17 patients. In one patient, access for cholangiography was obtained, but the severe stricture could not be crossed. In this case, direct intraoperative guidance for crossing the anastomosis was performed with successful stent placement in the operative suite. We were not successful at obtaining biliary access in two patients with nondilated bile ducts. Five patients had nonobstructed biliary systems, and a drainage procedure was not necessary. In eight patients, biliary drains were left in place for a mean of 4 months (range 1 to 6 months). The biliary drains were removed without evidence of recurrent stenoses with mean follow-up of 13 months (range 4 to 21 months). One patient died of unrelated causes 4 months after biliary drainage tube removal without evidence of recurrent disease. Seven patients currently have biliary drains in place with a mean dwell time of 5.5 months (range 2 to 18 months). One patient died approximately 1 month after biliary drainage catheter placement from causes related to underlying disease. With limited follow-up, restenosis requiring stent replacement has occurred in two patients. One patient had a biliary drain left in place for 4 months and the other for 8 months following biliary drainage catheter placement. These restenoses occurred 2 and 10 months, respectively, after biliary drainage catheter removal. The mechanisms leading to restenoses in these patients are not known.

BIOPSY CONSIDERATIONS

The allograft position in patients with reduced-size liver transplants is altered and may be entirely subcostal. The location of the major vessels is also altered, with the porta hepatis located on the right posterior or posterolateral aspect of the graft. If this alteration in position and anatomy is not understood, an increase in complications seen after liver biopsy will result. Sonographic localization or guidance for these biopsies is ideal, with a midline subxiphoid approach most often used.

CONCLUSIONS

Liver transplantation in children provides excellent long-term survival in children with liver failure. The continual development and improvement of interventional radiologic techniques for children who experience complications related to liver transplantation will help to improve patient and allograft survival further.