Effects of Prostaglandin E1 on Patients Undergoing Major Gastrointestinal Surgery.

Abstract

The aim of this study was to investigate the clinical effects of prostaglandin E1 (PGE1) in patients who underwent surgery for gastrointestinal (GI) trauma, perforation, or obstruction. PGE1 is thought to enhance intestinal blood supply and reduce GI complications during the postoperative period. The medical records of 889 patients undergoing major GI surgery were reviewed retrospectively. Propensity score matching was performed to adjust for any baseline differences. Clinical outcomes, including early GI function recovery, postoperative complications, and length of hospital stay, were evaluated in all patients. In 278 paired patients, selected nutritional, immunologic, and inflammatory variables were compared based on PGE1 administration. After propensity score 1:1 matching, the baseline characteristics were similar for both groups. PGE1 was associated with prompt postoperative GI function recovery, including first bowel movement [2.6 ± 0.9 vs 3.1 ± 1.0 days after surgery in patients with and without PGE1 treatment, risk ratio 0.51, 95% confidence interval (CI) 0.41-0.65, P < 0.001] and first feeding within postoperative day 3 [179 (64.39%) vs 152 (54.68%); risk ratio 0.61, 95% CI 0.42-0.90, P = 0.012]. A lower overall postoperative complication rate, including infectious complications [45 (16.2%) vs 68 (24.5%); odds ratio 0.60, 95% CI 0.39-0.91, P = 0.010] and major complications [23 (8.3%) vs 48 (17.3%); odds ratio 0.43, 95% CI 0.26-0.73, P = 0.001], was noted in patients with PGE1 treatment than in patients without PGE1 treatment. Furthermore, the immunologic and inflammatory variable C-reactive protein on postoperative day 3 was reduced by PGE1 treatment (52.5 ± 36.4 vs 89.6 ± 42.4 mg/L; P = 0.037, t test). PGE1 is associated with beneficial clinical effects, such as prompt postoperative GI function recovery and reduced overall postoperative complications after emergency GI surgery, which may be attributed to a reduced inflammatory response.