Hepatic dysfunction in multiple systems organ failure as a manifestation of altered cell-cell interaction.

F. B. Cerra*, M. West, T. R. Billiar, R. T. Holman, R. Simmons

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

7 Scopus citations

Abstract

Multiple organ failure continues to be the primary cause of death after trauma and sepsis. This clinical syndrome follows shock and resusitation and the transition from a hypermetabolic response to a syndrome of progressive organ failures and death. Risk factors include: perfusion deficits, persistent foci of dead or injured tissue, an uncontrolled focus of infection, the presence of the respiratory distress syndrome, and preexisting fibrotic liver disease. The imitation of the syndrome represents the clinical manifestation of hepatic failure. It is hypothesized that this hepatic failure results from paracrine amplification with Kupffer cell induced hepatocyte cytotoxicity. The best treatment remains prevention and rapid control of risk factors including restoration of oxygen transport and aggressive nutrition support. There seems to be no treatment "magic bullet" either experimentally or clinically once the syndrome has occurred.

Original languageEnglish
Pages (from-to)563-573
Number of pages11
JournalProgress in clinical and biological research
Volume308
StatePublished - 1989
Externally publishedYes

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