Biliary Complications of Orthotopic Liver Transplantation

Tung, Bruce Y.; Kimmey, Michael B.

doi:10.1159/000016918

Cited by 115 publications

(110 citation statements)

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“…Though uncommon, biliary casts are most frequently described in liver transplant patients [1][2][3][4] . The etiology of cast development is not fully known, but it is likely to be multifactorial with biliary sludge being a prerequisite for cast formation.…”

Section: Introductionmentioning

confidence: 99%

“…The etiology of cast development is not fully known, but it is likely to be multifactorial with biliary sludge being a prerequisite for cast formation. Bile duct damage and ischemia, hemolysis, cholangitis, fasting, total parenteral nutrition (TPN) and recent surgery are thought to be implicated in cast, pathogenesis via sludge development [3,4] . We describe a diabetic man who developed a biliary cast after cholecystectomy.…”

Section: Introductionmentioning

confidence: 99%

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Heterogeneity of endoscopy negative heartburn: Epidemiology and natural history

Katsinelos

Kountouras²,

Chatzimavroudis

et al. 2008

WJG

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A 76-year-old diabetic man underwent cholecystectomy for gangrenous calculous cholecystitis. His postoperative course was complicated by the development of Candida albicans esophagitis necessitating antifungal therapy, and total parenteral nutrition (TPN) for 1 5 d . S e ve n w e e k s a f t e r c h o l e c y s t e c t o my, h e presented with cholangitis. Endoscopic retrograde cholangiopancreatography (ERCP) demonstrated extrahepatic filling defects. Despite endoscopic extraction of a biliary cast, cholestasis remained unchanged. Oral administration of ursodeoxycholic acid (UDCA), 750 mg/d, resulted in normalization of liver function tests. We, therefore, propose for the first time, combined endoscopic plus UDCA treatment for the management of biliary cast syndrome.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Heterogeneity of endoscopy negative heartburn: Epidemiology and natural history

Katsinelos

Kountouras²,

Chatzimavroudis

et al. 2008

WJG

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“…Initial treatment of the syndrome should be endoscopic biliary sphincterotomy and cast extraction. In cases where it is not possible to completely remove the casts, nasobiliary drainage placement has been proposed to clean up bile ducts [3]. Also, ursodeoxycholic acid has been used as complementary treatment in difficult or recurrent cases [22,23,26].…”

Section: Discussionmentioning

confidence: 99%

“…been described almost exclusively in liver transplant patients, more often during the first years of orthotopic liver transplant, when graft preservation techniques were less advanced [1][2][3]. Nowadays, the prevalence of bile duct filling defects due to sludge or casts is reported to be around 3 % [4].…”

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confidence: 99%

Endoscopic Management of Biliary Cast Syndrome Post Hepatic Trauma

López-Rosés¹

2017

GHOA

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Biliary cast syndrome is a rare disorder that is characterized by the presence of casts in the biliary ducts, causing obstruction leading to infection and hepatic and ductal damage. The syndrome is more commonly reported in liver transplant patients, being very unusual in other situations. We report a case in a patient that suffered a severe hepatic trauma that was successfully managed by endoscopic therapy. IntroductionThe biliary cast syndrome is a rare phenomenon that develops due to precipitation of amorphous material in the bile ducts, forming casts that lead to obstruction with consequent infection and damage to liver parenquima and duct. The syndrome has DiscussionThe formation of casts of the bile ducts (biliary cast syndrome) is caused by mechanisms not clearly understood, that involve factors such as ischemia, infection, hemolysis and liver surgery among others. These casts are made up primarily of calcium bilirrubinate, cholesterol crystals and mucus [5]. Recently, by using scanning electron microscopy and hematoxilin and eosin staining, studies showed that cast also contains blood vessels and collagen fibers [11,12]. From a theoretical standpoint, any situation that increases the viscosity of bile or decreases bile flow, may lead to the formation of casts. The vast majority of cases reported occurred in liver transplant patients, especially during the first few years of application of the technique, where graft preservation methods were less sophisticated than today. Some studies have linked the formation of the casts with the existence of faulty reconstructions of the biliary tract, which would cause injury to the biliary epithelium and trigger the precipitation of material in it. This in combination with infection and a cholesterol-saturated bile, play a role in the formation of casts after transplantation [7]. Moreover, the presence of ischemia is believed to be one of the main triggers of this syndrome, because it has been shown that the presence of casts after liver transplantation was accompanied by hepatic artery occlusion in 30% of cases [4]. Also, some drugs used post transplant, such as cyclosporine, may contribute to the emergence of casts, by inhibiting the secretion of bile, causing a functional bile stasis [8]. Furthermore, the presence of foreign bodies such as T tubes or prosthesis may act as a nidus for formation of stones or sludge [13]. Systemic bacterial or fungal infection, which causes intrahepatic cholestasis may also be a predisposing factor to the formation of casts in the bile ducts after liver transplantation [14]. Finally, many others have been associated as risk factors for the formation of biliary casts, such as, hepatic artery stenosis or thrombosis, biliary strictures, renal replacement therapy, ischemia-reperfusion injury, prolonged cold preservation, prolonged warm ischemia, hemolysis, pregnancy or AIDS virus infection [15][16][17][18].Casts can also occur in non-transplant patients, although that is extremely unusual; only a few cases have been published to...

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“…174,175 Evidence now shows that preservation injury of the biliary tree is a very complex phenomenon.…”

Section: Bile Duct Cell Injury: Long-lasting Phase Of Reperfusion Injurymentioning

confidence: 99%

Untitled

2001

Liver Transpl

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In liver transplantation, it is currently hypothesized that nonparenchymal cell damage and/or activation is the major cause of preservation-related graft injury. Because parenchymal cells (hepatocytes) appear morphologically well preserved even after extended cold preservation, their injury after warm reperfusion is ascribed to the consequences of nonparenchymal cell damage and/or activation. However, accumulating evidence over the past decade indicated that the current hypothesis cannot fully explain preservation-related liver graft injury. We review data obtained in animal and human liver transplantation and isolated perfused animal livers, as well as isolated cell models to highlight growing evidence of the importance of hepatocyte disturbances in the pathogenesis of normal and fatty graft injury. Particular attention is given to preservation time-dependent decreases in high-energy adenine nucleotide levels in liver cells, a circumstance that (1) sensitizes hepatocytes to various stimuli and insults, (2) correlates well with graft function after liver transplantation, and (3) may also underlie the preservation timedependent increase in endothelial cell damage. We also review damage to bile duct cells, which is increasingly being recognized as important in the long-lasting phase of reperfusion injury. The role of hydrophobic bile salts in that context is particularly assessed. Finally, a number of avenues aimed at preserving hepatocyte and bile duct cell integrity are discussed in the context of liver transplantation therapy as a complement to reducing nonparenchymal cell damage and/or activation. (Liver Transpl 2001;7: 381-400.)A lthough the use of University of Wisconsin (UW) solution has permitted an increase in mean preservation time, the incidence of graft dysfunction still persists, 1,2 contributing significantly to a more than 20% per year mortality rate for patients in liver transplantation centers in the United States. 3 In addition, when storage time exceeds 10 to 12 hours, such late posttransplantation complications as biliary strictures occur in more than 25% of liver transplant recipients. [4][5][6] To prevent or minimize graft dysfunction and posttransplantation complications, it is essential to fully understand the importance of individual liver cell types in graft injury induced by cold storage and reperfusion. Insight into the cellular and molecular basis of these injuries will lead to the development of better intervention strategies, which is very important because graft dysfunction results in increased morbidity and enhances mortality rates. 7,8 Moreover, up to 30% of patients with graft dysfunction need retransplantation as early as within the first 3 months after transplantation, 2,7,8 which increases the demand on an already short pool of donor organs.According to morphological studies, cold preservation leads to injuries of nonparenchymal cells, whereas liver parenchymal cells appear well preserved. It is currently hypothesized that sinusoidal endothelial cell impairment, 9-11 activatio...

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Biliary Complications of Orthotopic Liver Transplantation

Cited by 115 publications

References 57 publications

Heterogeneity of endoscopy negative heartburn: Epidemiology and natural history

Heterogeneity of endoscopy negative heartburn: Epidemiology and natural history

Endoscopic Management of Biliary Cast Syndrome Post Hepatic Trauma

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