Skip to main content
Log in

Bile canaliculi are defective in hepatic involvement of organ failure and recovery of liver function is due to their secondary regeneration

  • Original
  • Published:
Intensive Care Medicine Aims and scope Submit manuscript

Abstract

Objective

To investigate the morphological changes in the liver in patients with organ failure and hyperbilirubinemia and to correlate them to the outcome.

Design

A case series prospective study.

Setting

Intensive care units of two general hospitals.

Patients

Twelve patients in organ failure with predominant hepatic involvement, aged 16 to 69 years (mean 56 years).

Interventions

Liver biopsy was performed on all patients 3–15 days after organ failure. A second biopsy was also performed on all four surviving patients, as well as on 3 patients just before death at a mean time of 16 days (6–32) and 31 days (14–55), respectively, after the first biopsy. The samples were studied by electron microscopy and findings were assessed according to Rappaport's designation.

Measurements and main results

In the first biopsy it was shown that in zone III there was complete degeneration of bile canaliculi and hepatocytes in contrast to zone I. The grade of histological severity for zone III is positively correlated to the bilirubin concentration (p=0.001). In the specimens from the second biopsy, it was shown that numerous, newly formed secondary bile canaliculi per 20 consecutive hepatocytes had developed in zone III in the surviving patients, whereas there was a complete absence of such canaliculi in the patients who died (mean±SD: 9.6±3.2 vs 0).

Conclusions

It appears that the destruction of primary bile canaliculi is a striking anatomical defect in patients with organ failure and impaired bilirubin excretion. The restoration of liver function coincides with adequate formation of new secondary bile canaliculi in zone III, giving credence to the hypothesis that this formation is an important structural change responsible for the improvement in liver function.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. Tugwell P, Williams AO (1977) Jaundice associated with lobar pneumonia. QJM 46:97–118

    Google Scholar 

  2. Zimmerman HJ, Fang M, Utili R, Seeft LB, Hoofnagle J (1979) Jaundice due to bacterial infection. Gastroenterology 77:362–374

    Google Scholar 

  3. Bank JG, Foulis AK, Ledingham I McA, Macsween RNM (1982) Liver function in septic shock. J Clin Pathol 35:1249–1252

    Google Scholar 

  4. Nakatani T, Kobayashi K (1991) Posttraumatic jaundice, its mechanism from a view point of hepatic mitochondrial function. Nippon Geka Gakkai Zasshi 92:441–447

    Google Scholar 

  5. Sarfeh IJ, Balint JA (1978) The clinical significance of hyperbilirubinemia following trauma. J Trauma 18:58–62

    Google Scholar 

  6. Marubayashi S, Dohi K, Ochi K, Kawasaki T (1986) Role of free radicals in ischemic rat liver cell injury: prevention of damage by α-tocopherol administration. Surgery 99:184–192

    Google Scholar 

  7. Nordstrom G, Seeman T, Hasselgren PO (1985) Beneficial effect of allopurinol in liver ischemia. Surgery 97: 679–684

    Google Scholar 

  8. Utili R, Abernathy CO, Zimmerman HJ (1976) Cholestatic effects ofEscherichia coli endotoxin on the isolated perfused rat liver. Gastroenterology 70:248–253

    Google Scholar 

  9. Gourley GR, Chesney PJ, Davis JP, Odell GB (1981) Acute cholestasis in patients with toxic-shock syndrome. Gastroenterology 81:928–931

    Google Scholar 

  10. Lefkowitch JH, Mendez L (1986) Morphologic features of hepatic injury in cardiac disease and shock. J Hepatol 2:313–327

    Google Scholar 

  11. Brough AJ, Bernstein J (1974) Conjugated hyperbilirubinemia in early infancy. Hum Pathol 5:507–516

    Google Scholar 

  12. Ruokonen E, Takala J, Kari A, Alhava E (1991) Septic shock and multiple organ failure. Crit Care Med 19:1146–1151

    Google Scholar 

  13. Rappaport AM (1976) The microcirculatory acinar concept of normal and pathological hepatic structure. Beitr Pathol 157:215–243

    Google Scholar 

  14. Schwartz DB, Bone RC, Balk RA, Szidon JP (1989) Hepatic dysfunction in the adult respiratory distress syndrome. Chest 95:871–875

    Google Scholar 

  15. te-Boekhorst T, Urlus M, Doesburg W, Yap SH, Goris RJ (1988) Etiologic factors of jaundice in severely ill patients. J Hepatol 7:111–117

    Google Scholar 

  16. Lefkowitch JH (1982) Bile ductular cholestasis: an ominous histopathologic sign related to sepsis and “cholangitis lenta”. Hum Pathol 13:19–24

    Google Scholar 

  17. Shoemaker WC, Szanto PB, Fitch LB, Brill NR (1964) Hepatic physiologic and morphologic alterations in shock. J Am Coll Surg 118:828

    Google Scholar 

  18. Alverdy JC, Aoys E, Moss G (1988) Total parenteral nutrition promotes bacterial translocation from the gut. Surgery 104:185–190

    Google Scholar 

  19. Marshall J, Lee C, Meakins JL, Michel RP, Christou NV (1987) Kupffer cell modulation of the systemic immune response. Arch Surg 122:191

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Douzinas, E.E., Vamvasakis, E., Rigas, K. et al. Bile canaliculi are defective in hepatic involvement of organ failure and recovery of liver function is due to their secondary regeneration. Intensive Care Med 22, 553–558 (1996). https://doi.org/10.1007/BF01708095

Download citation

  • Received:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF01708095

Key words

Navigation