[Adjuvant therapy of peritonitis with taurolidine. Modulation of mediator liberation]

Despite aggressive surgical treatment, prompt antibiotic therapy, and modern intensive care, up to one half of patients still die of diffuse peritonitis. There must be a distinction between infection as a microbiological phenomenon and sepsis as a complex, deleterious, inflammatory host response. Physiologic and metabolic changes during the latter process by taxonomically different organisms or different sources of infection are often clinically indistinguishable. Taurolidine, an amino acid derivate, seems to cover a variety of effects in peritonitis. As secondary peritonitis is associated with a significant cytokine release that is compartementalized in the peritoneal cavity, taurolidine is bactericidal, antiendotoxic, and antiadherent locally and, on the other hand, may modulate the systemic cytokine-mediated inflammatory response after being adsorbed systemically by the peritoneum. Current management of peritonitis can clear the peritoneal cavity of microorganisms and their products but patients continue to die of uncontrolled cytokine-induced systemic inflammation. In patients that undergo daily staged, planned relaparotomies they should not only be treated locally by taurolidine but also systemically by intravenous administration. The latter should, as a sort of sequential therapy, be continued, especially when the peritoneal cavity has been closed after a series of relaparotomies.