Somatostatin in the Management of Gastrointestinal Fistulas: A Multicenter Trial A. J. TORRES, J. I. LANDA, M. M. AZCOITA, ET AL Archives of Surgery 127:97–99, 1992

Somatostatin is a naturally occurring 14‐amino acid peptide that exhibits strong inhibitory effects on gastrointestinal hormone secretion. This results in a decrease in gastric and hepatobiliary secretory outputs. The presence of gastrointestinal fistulas may lead to “short‐gut” syndrome and malabsorption in the absence of replacement of fluid and protein losses. This may, in turn, result in the development of malnutrition and immune system suppression that in many cases, lead to sepsis and death. Total parenteral nutrition (TPN) has been the mainstay of gastrointestinal fistula therapy, allowing maintenance of nitrogen balance and resulting in decreased fistula output. This therapeutic modality has allowed many fistulas to heal without surgical intervention. To determine whether somatostatin would improve fistula closure rates, 40 patients with postoperative gastrointestinal fistulas were randomized either to a group treated with TPN alone or to a group treated with TPN and a continuous intravenous infusion of somatostatin. Both groups received standard supportive and local care. All patients had fistula outputs greater than 150 mL/day and had undergone an abdominal operation during a 10‐month period in 1988. Patients included in the study had simple fistulas demonstrated radiologically that had a single tract without distal obstruction. Patients who developed fistulas early in the postoperative period with very high outputs (>1000 mL/48 h) because of anastomotic leaks and patients with diabetes (>30 IU insulin/ day), intra‐abdominal sepsis, intra‐abdominal foreign body, or fistulas at cancer sites were excluded from the study. The distribution of fistulas in both groups was similar. Most patients had fistulas originating in the small bowel (n = 30) and pancreas (n = 7), and there were a small number (n = 3) of ileocolic fistulas. Once patients were enrolled in the study, they were randomly assigned to either a control group that received TPN alone or to a group that received TPN and somatostatin. The latter group was initially treated with TPN only for a few days, until positive nitrogen balance was achieved, and then somatostatin infusion was initiated (250 μg/h). Somatostatin infusion was terminated if there was no fistula output for 48 hours. If fistula healing was not achieved after 20 days of somatostatin infusion, its use was reviewed. After 15 days of treatment, patients treated with TPN alone who demonstrated less than a 30% decrease in fistula output were crossed over to the somatostatin treatment group. Overall, 83% of fistulas healed. Although there was no significant difference in closure rates between the two groups, patients receiving somatostatin healed their fistulas 7 days earlier than did the control group of patients (13.9 ± 1.8 vs 20.4 ± 3, p <.05). In addition, there were fewer complications in the treatment group, perhaps because of a shorter hospital stay and fewer days receiving TPN. Somatostatin appears to be a useful adjunct to TPN in the therapy of gastrointestinal fistulas.