ObjectiveTo assess the long-term incidence of venous complications, including portal vein and hepatic vein stenoses, in both whole cadaveric and reduced-size cadaveric and living related liver transplants in a pediatric population, and to assess the therapeutic modalities in the treatment of these lesions. Summary Background DataA shortage in appropriate-sized liver grafts for pediatric patients led to the use of segmental liver grafts, which became the predominant graft used in 325 of 600 (54%) transplants at the authors' institution. To assess the long-term impact of this strategy, the authors examined the incidence of late (Ͼ90 days) venous complications and the efficacy of all therapeutic interventions. MethodsSix hundred pediatric liver transplants were performed in 325 patients, with reduced-size or split (RSS; n ϭ 207), living related (LRD; n ϭ 118), or full-size cadaveric grafts (FS; n ϭ 275) from 1988 to 2000. All transplants identified with late portal vein or vena caval stenoses or thromboses from a cohort of 524 grafts with survival greater than 90 days were reviewed for demographics, symptoms, therapeutic intervention, recurrence, morbidity, and mortality. ResultsFifty lesions were identified in 49 patients (38 portal vein and 12 hepatic vein-cava stenoses). Sex distribution was similar between portal vein and hepatic vein to cava, as was the mean patient age. Portal vein stenoses occurred in 32 LRD, 3 RSS, and 3 FS, while hepatic vein-cava stenoses occurred in 2 LRD, 8 RSS, and 2 FS. In the 38 portal vein stenoses, 9 had prior perioperative portal vein and/or 5 hepatic artery thrombectomies. Portal vein stenoses were identified after bleeding (17/38), ascites (6/38), increased liver function tests (6/38), splenomegaly (5/38), or screening ultrasound (4/38). Portal vein stenosis was associated most often with cryopreserved vein for portal conduits. Excluding conduits, the incidence of late portal vein complications was reduced to 1%. Lesions became symptomatic at a mean of 50.8 Ϯ 184.2 months posttransplant. All patients underwent venous angioplasty with a 66% (25/38) success rate, while 7 of 25 required further angioplasty and stenting. In the 13 unsuccessful angioplasties, 8 required surgical shunts for complete portal vein thrombosis. Recurrence occurred in 9 patients: all were amenable to stenting. Nine patients (24%) eventually died of sepsis (4) and surgical deaths at shunt or retransplant (5). Hepatic vein-cava stenoses occurred after a mean of 37.2 Ϯ 35.2 months, presenting with ascites (n ϭ 10), increased liver function tests (n ϭ 2), and splenomegaly (n ϭ 2). All patients were diagnosed by venogram and managed by balloon dilatation alone (n ϭ 6) or stented (n ϭ 4), with an 80% (10/12) success, with two late recurrences amenable to repeat angioplasty or stenting. Long-term survival was 80% at 1 year. ConclusionsThe use of segmental grafts without venous conduits is not associated with a significant rate of long-term venous complication. When late venous complications do occur, venous angiop...

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Neovascularization is a feature of a variety of pathological processes. We compared the characteristics of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) on migration and proliferation of human umbilical vein endothelium (HUVEC). Both VEGF and bFGF induced endothelial cell migration at similar concentrations (1/2 max. VEGF = approximately 1.0 ng/ml, bFGF = approximately 5.0 ng/ml). However, VEGF-stimulated migration was two-fold greater than bFGF at 1 and 10 ng/ml (p < 0.05). In contrast, bFGF induced proliferation four-fold more effectively than VEGF (1/2 max. 1 ng/ml and 1.4 ng/ml respectively). Checkerboard migration assays for bFGF showed a predominantly chemokinetic pattern, whereas VEGF was predominantly chemotactic. VEGF and bFGF were not synergistic in monolayer proliferation and migration assays. Three angiogenesis inhibitors, alpha-interferon, TNP-470, and platelet factor-4, inhibited VEGF and bFGF induced cell migration. These results indicate that VEGF and bFGF are chemoattractants that stimulate endothelial migration by different mechanisms and that both can be inhibited by known angiogenesis inhibitors.

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Hypothesis: Multiple centers have reported on bile duct injuries after cholecystectomy, but few have reported on the impact of concomitant vascular injuries. Design: Twenty-seven life-threatening complex injuries (CIs) (Bismuth level III, IV, or V or combined arterialductal injuries) were retrospectively compared with 22 noncomplex injuries (NCs) (level I or II). Setting: Tertiary referral center. Main Outcome Measures: The incidence and level of biliary and arterial injuries and their resulting morbidity and mortality. Results: Bismuth classifications of all injuries were as follows: level I in 6 patients (12%), II in 19 (39%), III in 12 (24%), IV in 8 (16%), and V in 4 (8%). Diagnosis was based on peritonitis (n = 13 [27%]), endoscopic retrograde pancreatography (n = 19 [39%]), and percutane-ous transhepatic cholangiography (n = 7 [14%]). Delayed referral was more common in levels I through IV (100 days) than in level V (15 days) (PϽ.001). Repairs were attempted in level IV (75%), III (67%), V (25%), and II (11%). Thirteen arterial injuries (26%) occurred irrespective of ductal injury level: I (n=1), II (n=3), III (n=1), IV (n=5), and V (n=3). There was, however, a higher incidence of repairs before referral in the CI group (59% vs 5%; PϽ.01), with resulting higher rates of complication (70% vs 23%; PϽ.01). Five deaths occurred in the CI group vs 1 in the NC group (P =.14). In univariate analysis, the presence of arterial injury vs no arterial injury was a predictor of mortality (5 [38%] of 13 patients vs 1 [3%] of 36 patients; PϽ.001). Conclusion: Bile duct injuries after cholecystectomy can be morbid and lethal with the incidence of arterial injury grossly underestimated.