Postoperative Pancreatic Fistula Following Traumatic Splenectomy: A Morbid and Costly Complication.

INTRODUCTION: Development of clinically relevant postoperative pancreatic fistula (CR-POPF) in adult splenectomies following trauma occur in 1%-3% of cases. We hypothesized that the use of sutures in splenic hilum ligation compared to staples was associated with a reduced rate of CR-POPF incidence. METHODS: Adult trauma patients (age ≥17 y) that underwent nonelective splenectomy from 2010 to 2020 were retrospectively evaluated from the trauma registries of all three adult level 1 trauma centers in Indiana. Patients were excluded if they were pregnant, currently incarcerated, expired within 72 h of admission, or had a pancreatic injury diagnosed preoperatively or intraoperatively. A Firth logistic regression using a penalized-maximum likelihood estimate for rare events was used for univariate predictive modeling (SPSS 28.0) of surgical technique on CR-POPF development. RESULTS: Four hundred nineteen adult splenectomies following trauma were conducted; 278 were included. CR-POPF developed in 14 cases (5.0%). Sutures alone were used in 200 cases: seven developed CR-POPF (3.5%). Staples alone or in combination with sutures were used in 74 cases: seven developed CR-POPF (9.5%). There was no statistically significant difference between the use of sutures alone compared to the use of staples alone (P = 0.123) or in combination (P = 0.100) in CR-POPF incidence. CONCLUSIONS: Our 10-y retrospective review of CR-POPF finds the complication to be rare but morbid. This study was underpowered to show any difference in surgical technique. However, we do propose a new institutional norm that CR-POPF develop in 5% of splenectomies after trauma and conclude that further study of optimal technique for emergent splenectomy is warranted.

Glucocorticoid attenuates the anabolic effects of parathyroid hormone on fracture repair.

Long-term use of glucocorticoid (GC) not only reduces bone mass and strength, which leads to a greater risk of fracture, but also hinders fracture repair. In this study, we produced open fractures in GC-treated mice and investigated the effects of human parathyroid hormone 1-34 (hPTH) on fracture repair. Swiss-Webster mice were randomly divided into five groups. Three groups of GC-treated mice were given prednisolone, which was slowly released from subcutaneously implanted pellets at the rate of 1.4 mg/kg/day. Placebo pellets were implanted into the animals in two placebo groups. Three weeks later, osteotomies at the midshaft femora were performed and intramedullary pins were inserted to stabilize the fracture site under general anesthesia. Following fracture surgery, three GC groups were treated subcutaneously with vehicle, PTH at a low dose (40 ug/kg/day), and PTH at a high dose (80 ug/kg/day), respectively. Two placebo groups were given vehicle and PTH at a dose of 40 ug/kg/day, respectively. Radiographs, dual-energy X-ray absorptiometry, and mechanical testing (four-point bending) were used to evaluate fracture repair at 4 weeks after fracture surgery. Callus development, endochondral ossification, and recovery of mechanical strength at the fracture sites in GC animals treated with vehicle were significantly suppressed compared to placebo animals. Normally, PTH accelerates fracture repair. In GC-treated mice, PTH fails to improve endochondral ossification and mechanical properties compared to vehicle treatment, suggesting that the anabolic effect of PTH on fracture healing can be attenuated by GC administration in mice.