Background: Closed reduction and splinting followed by outpatient management is standard of care for temporizing most ankle fractures. However, ankle fracture-dislocation potentially warrants a different approach based on the propensity for loss of reduction. The purpose of this study was to determine the rate of complications associated with closed reduction and splinting of unstable ankle fracture-dislocations. Further, we sought to determine the efficacy of immediate external fixation as an alternative to splinting in cases too swollen for acute operation. Methods: This retrospective chart review analyzed all ankle-fracture dislocations that came through a large health care system from 2008 to 2018. Patients managed with acute open reduction internal fixation (ORIF) and open fractures were excluded. In patients managed late, the cohorts were divided into those temporized with closed reduction/splinting vs external fixation. Reduction quality and splint technique were additionally assessed in splinted patients. A total of 354 closed ankle fracture-dislocations were identified: 298 patients (84%) underwent ORIF within 48 hours and were excluded; 28 (15 female/13 male, average age 46.8 years) were placed in an external fixator and 28 (22 female/6 male, average age 57.2 years) were reduced, splinted, and discharged. Results: At follow-up, 14 of the patients (50%) in the splint group developed loss of reduction and 5 of these patients (17.6%) developed anteromedial skin necrosis from skin tenting. None of the patients in the ex-fix group developed loss of reduction or skin necrosis. The rate of redislocation and the rate of development of skin necrosis was statistically higher in cases temporized with a splint versus an external fixator ( P < .01 and P = .05, respectively). Conclusion: We found that in ankle fracture-dislocations not treated with acute ORIF, splint immobilization was associated with an increased risk of complications, including redislocation and skin necrosis, when compared to a temporizing external fixator. Level of Evidence: Level III, retrospective comparative study.

We have demonstrated that enteral glutamine provides protection to the post ischemic gut and that PPARγ plays a role in this protection. Using Cre/lox technology to generate an intestinal-epithelial cell (IEC) specific PPARγ null mouse model, we now investigated the contribution of IEC PPARγ to glutamine’s local and distant organ protective effects. These mice exhibited absence of expression of PPARγ in the intestine but normal PPARγ expression in other tissues. Following one hour of intestinal ischemia under isoflurane anesthesia, wild type and null mice received enteral glutamine (60 mM) or vehicle followed by 6 hours of reperfusion or 7 days in survival experiments and compared to shams. Small intestine. liver, and lungs were analyzed for injury and inflammatory parameters. Glutamine provided significant protection against gut injury and inflammation with similar protection in the lung and liver. Changes in systemic TNFα reflected those seen in the injured organs. Importantly, mice lacking IEC PPARγ had worsened injury and inflammation and glutamine lost its protective effects in the gut and lung. The survival benefit found in glutamine treated wild type mice was not observed in null mice. Using an IEC-targeted loss-of-function approach, these studies provide the first in vivo confirmation in native small intestine and lung that PPARγ is responsible for the protective effects of enteral glutamine in reducing intestinal and lung injury and inflammation and improving survival. These data suggest that early enteral glutamine may be a potential therapeutic modality to reduce shock-induced gut dysfunction and subsequent distant organ injury.

Care management/therapeutic study, level IV; epidemiologic/prognostic study, level III.