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Jeong-Sik Yu, South Korea Radiology, 2001

Jeong-Sik Yu, South Korea Radiology, 2001. Bile Duct Injuries Leading to Portal Vein Obliteration after Transcatheter Arterial Chemoembolization in the Liver: CT Findings and Initial Observations. P urpose.

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Jeong-Sik Yu, South Korea Radiology, 2001

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  1. Jeong-Sik Yu, South Korea Radiology, 2001 Bile Duct Injuries Leading toPortal Vein Obliteration afterTranscatheter ArterialChemoembolization in theLiver: CT Findings and InitialObservations

  2. Purpose • To document CT findings of TACE–induced, localized bile duct injuries leading toportal vein branchobliteration in the liver and to elucidate the clinical implicationswith retrospective review of the authors’ experiences.

  3. Materials and Methods • 381 patients (the CT reports of 381 pre-TACE and 1,307post-TACE follow-up CT ,between September 1996and June 2000) • 42 patientshad developed TACE-related intrahepaticbile duct dilatation, and/or cyst formationwith or without segmental or lobar parenchymal infarction or atrophic changes. • 120 patients were excluded for no pre-TACE or follow-up CT data were available.

  4. Our routineprotocol for TACE • 1–20 mL of iodized oil and 10–50 mg of doxorubicin hydrochloride,the dose dependent on the size, extent, and vascularityof the tumor, and gelatin spongefragments are administered. • Liver functiontests: measure serumaminotransferase and alkaline phosphatase levels (performed 1 or 2 days after TACE).

  5. The time of follow-up CT The first follow-up CT was 3 or 4 weeks after TACE. if no tumor recurrence or newly developed tumors,further follow-up CT were performed 3and 6 months after TACE(during follow-up CT, live fuction was also tested).

  6. The imaging criteria of bile duct injury • disproportionately dilated bile duct with lobar or segmental distribution that developed after TACE or a newly developedcystic lesion accompanied by segmentalbile duct dilatation.

  7. The location of bile duct injuries • In 22 of the 42 patients,the bile duct injuries were localized andlimited to small subsegmental branchesand the identification of the portal veinwas not possible in the intensely opaquearea of iodized oil uptake, with or without segmental infarction or necrosis resulting from selective TACE.

  8. Exclusion cases • Another 5 patients had tumor thrombosis in dilatedportal veins, and another 4 werethought to have direct bile duct invasioncaused by tumor progression during thefollow-up period. • After exclusion of thesecases, a total of 11 patients (six men andfive women aged 32–62 years) were selected for detailed analysis.

  9. The classification of bile duct dilatation • The bile duct dilatation was graded as mild or marked,as compared with the diameter of theadjacent portal veins at pre-TACE CT. • Mild dilatation was defined as an increased diameter of the bile duct smallerthan the diameter of the adjacent portalvein . • When the dilatedbile duct diameter was similar to orgreater than those of the adjacent portalveins , it is marked dilatation.

  10. The recorded clinical results ①finaldiagnosis of the treated tumor; ②previoushistory of abdominal surgery or underlying liver disease; ③time between TACE and the total number of TACE ④bile duct, portal vein, liver parenchymachanges atCT; ⑤serum alkalinephosphatase levels; ⑥the injection location of the catheter tip; ⑦the amount of doxorubicin hydrochloride andiodized oil ; ⑧the useof gelatin sponge fragments;

  11. Results • The clinical data and CT findings of the11 patients with TACE-induced intrahepatic bile duct injuries adjacent to thefirst- or second-order branches of the intrahepatic portal vein are summarized inTable 1. • one TACE has 6 patients(5patients with metastatic tumors,one with hepatocellular carcinoma),two sessions in 4 patients (patients 1, 3, 8, and 11), three sessionsin 1 patient (patient 10).

  12. Results • 8 patients (73%) had a newly developed linear, low-attenuating area alongside the portal tract ,was suggestive of marked dilatation . • Three patients (27%) had mild dilatation. • The widths of the linear low-attenuating areas were greater than those of the corresponding portal vein branches (Figs 1, 2).

  13. The time of appearanceof bile ductdilatation • Within 1 month afterTACE, 9 patients(82%) had bile duct dilatation (mild=4,marked=5). • 11 and 16 weeksafter TACE, 2 patients had bile duct injury. • The time-relatedprogression of bile duct dilatation waswell demonstrated on the CT scans obtained in three patients (patients 1, 3,and 7) (Fig 1).

  14. Figure 1 (Patient 1) Chemoembolization of multiple nodular hepatocellular carcinomas in a 55-year-old man with chronic hepatitis B

  15. 10 patients (91%) had marked narrowing or obliteration ofthe first- (n=4) or second-order branches(n = 6) of the intrahepatic portalvein, with progressive atrophy of the corresponding hepatic parenchyma in 9 patients (82%) (Figs 1, 2).

  16. Figure 2 ( Patient 2) Bile duct injury leading to portal vein obliteration and subsequent atrophy of the right liver lobe after TACE of a metastatic lesion in a 50-year-old woman with rectal cancer.

  17. In 8 patients (73%), narrowing of the portalvein was accompanied by marked bileduct dilatation with or without extravasated bile. • However, 3 patients (patients 5, 7, and 9) had portal vein narrowing, accompanied by mild bileductwithout extravasatedbile collection (Fig 3).

  18. Figure 3 (Patient 7) Small localized bile duct dilatation associatedwith portal vein obliteration after TACE of a metastatic lesion in a 32-year-old woman with stomach cancer.

  19. The timing of thehepatic parenchymal atrophy • from 4 to 54 week(mean ±SD, 21 weeks ±18) after TACE ( 9 patients) • One patient with mild bileduct dilatation and progressive portal veinnarrowing ,finally died owing to multiorgan failure caused by systemic carcinomatosis. • Another patients ,the bile duct dilatation hadspontaneously regressed by the follow-up CT,no remarkable parenchymal changes.

  20. The serum alkaline phosphatase level • 8 (89%) of the 9 patients, this enzyme level was elevated to more than 200 U/L ,within 1 month after TACE (Table 2, Fig 4). • In 4 patients(1, 2, 6, and 8), the enzyme level decreasedafter 1 or 2 months, 5 patients ( 3,4,7,10 and 11) had progressive elevations or fluctuations, another 2 patients(5 and 9) ,the enzyme levelincreased moderately 3 months after TACE.

  21. Table 2

  22. Figure 4

  23. Discussion • Hepatic parenchymal atrophy, a wellknown complication of TACE,is relatedto ischemic injury, especially in patientswith decreased portal venous perfusion. • The patients with portal vein thrombosis before TACE wereexcluded . • So hepatic parenchymal atrophy should be regarded as consequences of decreased portal venous perfusion after TACE.

  24. The reason for hepatic parenchymal atrophy • The results of numerous investigations have demonstratedthat biliary tree obstruction causes a decrease in portal venous inflow, which isperhaps related to the dilated intrahepatic bile duct radicles compressing thelower-pressure portal venous radicles .

  25. The extent of bile duct injury • 5 patients had bileduct dilatation that extended beyond thearea distal to the tip of the catheter .Reasons: • ①small or spastic hepatic arteries, there isthe possibility of proximal backflow ofthe embolic materials into the hepaticarteries . • ②If the catheter tipwere wedged to a small arterial branch,the positive injection pressure wouldcontribute to a proximal backflow of embolic materials into the peribiliary capillary plexus.

  26. biliary tree obstruction causes a decrease in portal venous inflow ① We believethat the dilated bile duct and the extravasated fluid collection in the Glisson capsule can gradually compress and compromise the adjacent portal vein branches. ②There is also the possibility of a periportal inflammatory process that is related to the effect of high concentrationsof chemotherapy and embolization materials without direct bile extravasation .

  27. The time between TACE and the appearance of atrophicchanges • The mean time inour study, 20weeks, was longer than thatpreviously reported by Yamashita (2–3 months after TACE),reason:the makeupof the study groups or to our exclusion ofpatients. • The degree of bile duct dilatation, severity of theperiportal inflammation, repeated TACE,and timing of the follow-up imagingcould have contributed to the timing ofovert parenchymal atrophic changes .

  28. Elevated alkaline phosphatase may be an indicator ofTACE-induced bile duct injury • Elevated enzyme factor: extrahepatic biliary tractobstruction, intrahepatic functional cholestasis,incomplete biliary obstruction . • In the present study, the majority of the patients had an elevated enzyme level of more than 200 U/L within1 month after TACE.

  29. Conclusion • ①TACE-induced bile duct injury including focal dilatation of theintrahepatic bile duct with or withoutextravasation of bile along connectivetissue sheaths of the Glisson capsule,may obliterate the adjacent portal veinbranch.

  30. serum alkaline phosphatase ismore sensitive • In 3 patients (patients 4, 7, and 11), the elevated enzyme level was checked beforethe CT appearance of bile duct dilatation,and the results suggest that a marked elevation of serum alkaline phosphatase ismore sensitive than bile duct dilatationvisualized at CT.

  31. Conclusion • ②bile duct injury leading to obliteration of the adjacent portal vein branchshould be regarded as one of the mechanisms of TACE-induced, gradual progressive parenchymal atrophic changes.

  32. Conclusion • ③Bile duct injuryassociated with theobliteration of portalvein branches may occur in the noncirrhotic liver of patients after one TACEprocedure and can be monitored bychecking the serum alkaline phosphataselevel 1 month after TACE.

  33. Limitation • Havingno reference standard such as cholangiography or pathologic findings to prove ourbeliefs.

  34. Thank you for your attention

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