Surgical experience of deeply jaundiced patients with bile duct obstruction

Armstrong, Carrie; Dixon, J. M.; Taylor, T. V.; Davies, G C

doi:10.1002/bjs.1800710326

Cited by 166 publications

(74 citation statements)

References 30 publications

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“…The consequences of jaundice are complex and involve a variety of physiologic derangements, including immunosuppression as well as hepatic fibrosis. In particular, patients with jaundice have a predisposition to infection and increased morbidity and mortality (1,2). Altered function of a number of immune effector cells has been implicated in the pathophysiology of jaundice.…”

mentioning

confidence: 99%

Biliary Obstruction Selectively Expands and Activates Liver Myeloid Dendritic Cells

Bleier

Katz

Chaudhry

et al. 2006

The Journal of Immunology

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Obstructive jaundice is associated with immunologic derangements and hepatic inflammation and fibrosis. Because dendritic cells (DCs) play a major role in immune regulation, we hypothesized that the immunosuppression associated with jaundice may result from the functional impairment of liver DCs. We found that bile duct ligation (BDL) in mice expanded the myeloid subtype of liver DCs from 20 to 80% of total DCs and increased their absolute number by >15-fold. Liver myeloid DCs following BDL, but not sham laparotomy, had increased Ag uptake in vivo, high IL-6 secretion in response to LPS, and enhanced ability to activate T cells. The effects of BDL were specific to liver DCs, as spleen DCs were not affected. Expansion of liver myeloid DCs depended on Gr-1+ cells, and we implicated monocyte chemotactic protein-1 as a potential mediator. Thus, obstructive jaundice selectively expands liver myeloid DCs that are highly functional and unlikely to be involved with impaired host immune responses.

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confidence: 99%

Biliary Obstruction Selectively Expands and Activates Liver Myeloid Dendritic Cells

Bleier

Katz

Chaudhry

et al. 2006

The Journal of Immunology

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“…1 Whereas in experienced centers, postoperative mortality has been reduced from 20% to 5%, morbidity remains as high as 50%. 2,3 Most complications have a septic etiology and are considered to be related with translocation of endotoxin from the intestinal lumen into the portal and systemic circulation where an inflammatory cascade is triggered.…”

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confidence: 99%

Interleukin-1 receptor type I gene-deficient bile duct-ligated mice are partially protected against endotoxin

et al. 2002

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Cholestatic liver injury is associated with an increased susceptibility toward endotoxininduced toxicity. To determine the role of interleukin 1 (IL-1) herein, extrahepatic cholestasis was induced by bile duct ligation (bdl) in IL-1 receptor type I gene-deficient (IL-1R ؊/؊ ) mice, which are unresponsive to IL-1␣ and IL-1␤, and normal IL-1R ؉/؉ mice. Bdl elicited increases in hepatic IL-1␣ and IL-1␤ messenger RNA (mRNA) and protein. Hepatocellular injury at 2 weeks after bdl was similar in IL-1R ؊/؊ and IL-1R ؉/؉ mice as shown by clinical chemistry and histopathology. Administration of endotoxin to cholestatic mice at 2 weeks after bdl was associated with enhanced cytokine release, more severe liver damage, and occurrence of death when compared with sham-operated mice. Endotoxin effects in shamoperated IL-1R ؊/؊ and IL-1R ؉/؉ mice were largely similar, but cholestatic IL-1R ؊/؊ mice were better protected against toxic effects of endotoxin, as reflected by lowered cytokine release, less profound liver injury, and reduced mortality. These data indicate that IL-1␣ and IL-1␤ are produced in the liver after bdl, but that these cytokines do not play a significant role in cholestatic liver damage; however, endogenous IL-1 activity is an important denominator of enhanced endotoxin sensitivity that is observed during cholestasis induced by bdl. S urgery in jaundiced patients with periampullary tumors carries an increased risk of postoperative complications. 1 Whereas in experienced centers, postoperative mortality has been reduced from 20% to 5%, morbidity remains as high as 50%. 2,3 Most complications have a septic etiology and are considered to be related with translocation of endotoxin from the intestinal lumen into the portal and systemic circulation where an inflammatory cascade is triggered. 4,5 Potential causes of translocation of endotoxin include lack of bile salts in the intestinal lumen resulting in increased bacterial translocation, 6,7 decreased function of the resident macrophages of the liver (the Kupffer cells) leading to inadequate interception of endotoxin, 6-8 and changes in plasma concentrations of lipoproteins which bind endotoxin. 9 In addition, cholestasis is associated with enhanced susceptibility toward endotoxin-induced toxicity. [9][10][11][12][13][14] Endotoxin exerts its biological effects by activating immunocompetent cells such as monocytes and macrophages. After exposure to endotoxin, these cells readily release various inflammatory mediators such as the cytokines tumor necrosis factor (TNF) and interleukin-1 (IL-1), 15 which leads to an inflammatory response. The Kupffer cells are also capable of releasing these cytokines in response to endotoxin. 16,17 IL-1␣ and IL-1␤ are pleiotropic proinflammatory cytokines that are considered to play a proximal role in initiation and regulation of the inflammatory cascade triggered in response to endotoxins or bacteremia. 15,18 Both IL-1␣ and IL-1␤ can interact with two specific cell surface receptors, the type I and type II IL-1 receptor (IL-1R), of ...

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“…Many previous studies [3][4][5][6][7] have shown that operating on patients with high bilirubin levels is worse with regard to complications but none, including a large meta-analysis, 30 have suggested a threshold below which surgery without drainage in the non-septic patient is universally acceptable. 13,[26][27][28] This cut-off level of 300 µmol/l is similar to that used in previous studies.…”

Section: Discussionmentioning

confidence: 99%

“…Surgery in jaundiced patients with pancreatobiliary tumours is associated with a higher rate of postoperative complications. [3][4][5][6][7] Complications of jaundice include haemorrhage, impaired wound healing, renal dysfunction and sepsis (cholangitis, abscesses, anastomotic dehiscence). Relief of jaundice by the percutaneous (percutaneous transhepatic biliary drainage, PTBD) or endoscopic (endoscopic retrograde cholangiopancreatogram, ERCP) route may be considered and have been reviewed in current guidelines.…”

mentioning

confidence: 99%

Fast-Track Management of Patients Undergoing Proximal Pancreatic Resection

French

Mansfield

Jaques

et al. 2009

annals

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INTRODUCTION To avoid the risk of complications of biliary drainage, a feasibility study was carried out to determine whether it might be possible to fast-track surgical treatment, with resection before biliary drainage, in jaundiced patients with proximal pancreatic/peri-ampullary malignancy.PATIENTS AND METHODS Over an 18-month period, based on their presenting bilirubin levels and other logistical factors, all jaundiced patients who might be suitable for fast-track management were identified. Data on complications and hospital stay were compared with those patients in whom a conventional pathway (with biliary drainage) was used during the same time period. Data were also compared with a group of patients from the preceding 6 months.

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Surgical experience of deeply jaundiced patients with bile duct obstruction

Cited by 166 publications

References 30 publications

Biliary Obstruction Selectively Expands and Activates Liver Myeloid Dendritic Cells

Biliary Obstruction Selectively Expands and Activates Liver Myeloid Dendritic Cells

Interleukin-1 receptor type I gene-deficient bile duct-ligated mice are partially protected against endotoxin

Fast-Track Management of Patients Undergoing Proximal Pancreatic Resection

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