Kneeling tolerance following intramedullary nailing or plate fixation of uncomplicated distal tibia fractures.

INTRODUCTION: Distal tibia fractures often occur in younger, high demand patients, though the literature surrounding management remains contentious. This study sought to quantitatively determine differences in kneeling ability and self-reported knee function in patients managed with either intramedullary nailing (IMN) or open reduction internal fixation (ORIF) with compression plating following distal tibia fracture to assist in the preoperative consent process. HYPOTHESIS: There is no difference in kneeling tolerance following either tibial nailing or plate fixation of distal tibia fractures. MATERIAL AND METHODS: Retrospective sampling of public hospital data with outpatient prospective functional testing were completed. The primary outcome measure was the Kneeling Test (KT). Secondary outcome measures were The Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) and the Forgotten Joint Score (FJS) for the knee joint. There were 28 patients recruited (18 IMN and 10 ORIF) with a mean age of 44years. Mean overall follow-up was 13.3months (range 8-25, SD 3.6). All fractures had completely healed without postoperative complication. RESULTS: The IMN affected limb had a significantly worse overall kneeling function than their non-affected limb (mean KT: 70.4 vs. 94.9 respectively, p<0.005) Additionally, the IMN group performed significantly worse when compared to the ORIF group (mean KT 70.4 vs. 92.5 respectively, p<0.005). No significant differences (p>0.05) in kneeling function existed for the ORIF group when comparing affected to non-affected limbs. Secondary outcome analysis showed significantly worse overall WOMAC and FJS in the IMN group compared to the ORIF group (mean WOMAC 19.3 vs. 6.9 respectively, p=0.040; mean FJS 38.3 vs. 75.9 respectively, p=0.005). DISCUSSION: The use of intramedullary nailing for the treatment of distal tibia fracture results in a mean reduction of 20% in kneeling tolerance in comparison to ORIF. The resulting kneeling tolerance is comparable to that of patients post-total knee arthroplasty. The present findings should assist in the consent process for patients with high kneeling demands in sportive, professional or cultural pastimes. LEVEL OF EVIDENCE: IV; retrospective cohort study with quantitative outcome measurement.

Activated Protein C Protects against Murine Contact Dermatitis by Suppressing Protease-Activated Receptor 2.

Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with excessive inflammation and defective skin barrier function. Activated protein C (APC) is a natural anticoagulant with anti-inflammatory and barrier protective functions. However, the effect of APC on AD and its engagement with protease activated receptor (PAR)1 and PAR2 are unknown. Methods: Contact hypersensitivity (CHS), a model for human AD, was induced in PAR1 knockout (KO), PAR2KO and matched wild type (WT) mice using 2,4-dinitrofluorobenzene (DNFB). Recombinant human APC was administered into these mice as preventative or therapeutic treatment. The effect of APC and PAR1KO or PARKO on CHS was assessed via measurement of ear thickness, skin histologic changes, inflammatory cytokine levels, Th cell phenotypes and keratinocyte function. Results: Compared to WT, PAR2KO but not PAR1KO mice displayed less severe CHS when assessed by ear thickness; PAR1KO CHS skin had less mast cells, lower levels of IFN-γ, IL-4, IL-17 and IL-22, and higher levels of IL-1ß, IL-6 and TGF-ß1, whereas PAR2KO CHS skin only contained lower levels of IL-22 and IgE. Both PAR1KO and PAR2KO spleen cells had less Th1/Th17/Th22/Treg cells. In normal skin, PAR1 was present at the stratum granulosum and spinosum, whereas PAR2 at the upper layers of the epidermis. In CHS, however, the expression of PAR1 and PAR2 were increased and spread to the whole epidermis. In vitro, compared to WT cells, PAR1KO keratinocytes grew much slower, had a lower survival rate and higher para permeability, while PAR2KO cells grew faster, were resistant to apoptosis and para permeability. APC inhibited CHS as a therapeutic but not as a preventative treatment only in WT and PAR1KO mice. APC therapy reduced skin inflammation, suppressed epidermal PAR2 expression, promoted keratinocyte growth, survival, and barrier function in both WT and PAR1KO cells, but not in PAR2KO cells. Conclusions: APC therapy can mitigate CHS. Although APC acts through both PAR1 and PAR2 to regulate Th and mast cells, suppression of clinical disease in mice is achieved mainly via inhibition of PAR2 alone. Thus, APC may confer broad therapeutic benefits as a disease-modifying treatment for AD.

Late-Onset Dysphagia From Hardware Migration After Anterior Cervical Discectomy and Fusion: An Unusual Cause and Review of Literature.

Post-operative dysphagia is the most common complication following anterior cervical discectomy and fusion (ACDF), with reports varying from 1% to 79%. We report a case of a 63-year-old female patient complaining of dysphagia presenting 9 years post surgery. The cause of dysphagia is often multifactorial with the true aetiology poorly understood. One potentially life-threatening cause of post-operative dysphagia is hardware migration associated with pharyngoesophageal perforation. This patient presents a unique case of a conservatively managed hardware migration with delayed onset dysphagia after 8 years of minimal symptoms. On further investigation, barium swallow identified a freely mobile screw in the oesophageal submucosa, rotating on swallowing. Retrieval of the screw was achieved transcervically with no visible perforation and resolution of dysphagia occurred 1 week post-operatively. Understanding the aetiology with early diagnosis and appropriate management of delayed hardware migration are paramount in reducing patient morbidity and potential life-threatening otolaryngologic complications.