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  Vol. 131 No. 10, October 1996 TABLE OF CONTENTS
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Pancreas Graft Loss Caused by Intra-abdominal Infection

A Risk Factor for a Subsequent Pancreas Retransplantation

Enrico Benedetti, MD; Christoph Troppmann, MD; Angelika C. Gruessner, MS, PhD; David E. R. Sutherland, MD, PhD; David L. Dunn, MD, PhD; Rainer W. G. Gruessner, MD, PhD

Arch Surg. 1996;131(10):1054-1060.


Abstract

Objective
To investigate whether previous pancreas graft loss caused by intra-abdominal infection is a risk factor for a subsequent pancreas retransplantation.

Design
Retrospective case-series analysis.

Setting
Large university hospital.

Patients
Of 97 pancreatic retransplantations (July 1, 1985 to June 30, 1994), 13 (13%) were performed after previous pancreas grafts had been lost because of intra-abdominal infection.

Main Outcome Measures
Cause of retransplant graft loss; patient survival.

Results
Of 13 cases of pancreatic retransplantations performed after previous grafts had been lost because of intra-abdominal infection, 12 (92%) were again complicated by intra-abdominal infection. Of these 12 retransplantation infections, 10 were caused by the same microbial species that had caused failure of the previous graft 1 to 5 years earlier (8 required graft pancreatectomy [mortality rate, 25%], and 2 were successfully treated) and 2 were caused by different microbial species (both required graft pancreatectomy [mortality rate, 0%]). In 1 of the 13 retransplantations, prophylactic antimicrobial treatment was directed at the microbial species that had caused failure of the previous graft; no recurrent intra-abdominal infection developed.

Conclusions
Intra-abdominal infection after a previous pancreas transplantation is a risk factor for recurrence of infection by the same microbial species after a subsequent retransplantation. For the selected patients who are considered for retransplantation in spite of their previous graft loss caused by intra-abdominal infection, periretransplantation antimicrobial prophylaxis should include a prolonged course of an agent directed against the previously identified microbial species.

Arch Surg. 1996;131:1054-1060



Author Affiliations

From the Department of Surgery, University of Minnesota, Minneapolis.



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