Fibula Nail Outcomes in Soft Tissue Compromised Ankle Fractures.

BACKGROUND: To determine the clinical outcomes following fibula nail fixation and to identify the indication for the use of fibula nails in lower limb fractures. METHODS: Retrospective study of adult patients from 2 major trauma centers (MTCs) and 9 trauma units (TUs) who underwent fibula nail fixation for AO/OTA 44 fractures between January 1, 2018, and October 31, 2020. Outcome measures included infection, metalwork complications, nonunion or malunion, time to union, and length of inpatient hospital stay. RESULTS: Ninety-five patients were included, with a mean age of 66 years; 57.9% of patients were female. The average body mass index was 30. Sixty-nine patients (72.6%) sustained a Weber B and 24 (27.4%) sustained a Weber C fracture. In addition, 26.3% were open fractures and all patients had soft tissue compromise affecting the lateral malleolus. The calculated infection rate for fibula nail was 4.2% and metalwork complication rate was 5.2%. The nonunion and malunion rate was 8.4% and rate of removal of hardware was 2.1%. The average time to union was 12.5 weeks, and length of inpatient stay was 9.4 days (SD 10). CONCLUSION: This multicenter study demonstrates that use of a fibula nail appears to be a safe approach to treating patients who have a physiologically higher risk of surgery, poor skin condition, and a complex fracture pattern. LEVEL OF EVIDENCE: Level III, case-control study.

Loss of cilia causes embryonic lung hypoplasia, liver fibrosis, and cholestasis in the talpid3 ciliopathy mutant.

Sonic hedgehog plays an essential role in maintaining hepatoblasts in a proliferative non-differentiating state during embryogenesis. Transduction of the Hedgehog signaling pathway is dependent on the presence of functional primary cilia and hepatoblasts, therefore, must require primary cilia for normal function. In congenital syndromes in which cilia are absent or non-functional (ciliopathies) hepatorenal fibrocystic disease is common and primarily characterized by ductal plate malformations which underlie the formation of liver cysts, as well as less commonly, by hepatic fibrosis, although a role for abnormal Hedgehog signal transduction has not been implicated in these phenotypes. We have examined liver, lung and rib development in the talpid(3) chicken mutant, a ciliopathy model in which abnormal Hedgehog signaling is well characterized. We find that the talpid(3) phenotype closely models that of human short-rib polydactyly syndromes which are caused by the loss of cilia, and exhibit hypoplastic lungs and liver failure. Through an analysis of liver and lung development in the talpid(3) chicken, we propose that cilia in the liver are essential for the transduction of Hedgehog signaling during hepatic development. The talpid(3) chicken represents a useful resource in furthering our understanding of the pathology of ciliopathies beyond the treatment of thoracic insufficiency as well as generating insights into the role Hedgehog signaling in hepatic development.