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Background Indications for deltoid ligament repair in bimalleolar equivalent ankle fractures are unclear. This study compared radiographic outcomes in bimalleolar equivalent ankle fractures undergoing open reduction internal fixation (ORIF) +/− deltoid ligament repair. Methods A retrospective review of 1024 ankle fractures was performed. Bimalleolar equivalent injuries treated with ORIF +/− deltoid ligament repair were included. Radiographic assessment was performed preoperatively, and at three months postoperatively. Results One hundred and forty-seven ankle fractures met inclusion criteria with 46 undergoing deltoid ligament repairs. There was a significant decrease in medial clear space (1.93 ± 0.65 mm vs. 2.26 ± 0.64 mm, p = 0.01), and tibiofibular clear space (3.89 ± 1.20 mm vs. 4.87 ± 1.37 mm, p = 0.0001) at 3 months postoperative in the deltoid repair group compared to the no repair group. When syndesmotic fixation was performed, there were no differences between groups. Conclusion Deltoid ligament repair in bimalleolar equivalent ankle fractures resulted in reduced medial clear space, and tibiofibular clear space in the early postoperative period. These differences were small and remained within established normal limits. Level of clinical evidence Level III, retrospective cohort study.

Background: The goal of the study was to compare radiographic and functional outcomes between conventional closed syndesmotic reduction and screw fixation with open reduction, direct repair of the anterior inferior tibiofibular ligament (AiTFL) and screw fixation. We hypothesized that open reduction with restoration of the AiTFL would provide an improved reduction with better radiographic and functional outcomes. Methods: Fifty consecutive patients with OTA 44-C ankle fractures were enrolled. Treatment was nonrandomized and based on surgeon preference. Patients were treated with either open reduction, suture-anchor AiTFL repair, and screw fixation (ART group), or conventional closed reduction of the syndesmosis followed by screw fixation (CR group). The primary outcome measure was anteroposterior (AP) displacement of the fibula on CT scan at 3 months postoperatively. Secondary outcome measures included the Maryland Foot Score, the American Orthopaedic Foot & Ankle Society (AOFAS) Ankle Hindfoot Score, and the Foot and Ankle Outcome Score (FAOS). Results: Mean AP difference between injured and noninjured ankles was decreased in the ART group compared with the CR group (0.7 ± 0.3 mm vs 1.5 ± 0.3 mm, P = .008). No differences were observed between groups in overall scores for secondary outcome measures. The ART group displayed a significant difference in Maryland Foot Shoe subscore at 12 months (ART = 9.5 vs CR = 8.3, P = .03) and FAOS Quality of Life subscore at 12 months (64.1 compared to 38.3, P = .04). Conclusion: Open anatomic syndesmotic repair resulted in improved radiographic outcomes compared with closed reduction. Cosmesis was worse at 6 weeks compared to the CR group; however, quality of life and shoewear were improved in the ART group at 1 year postoperatively. Level of Evidence: Level II, prospective comparative study.

OBJECTIVES Acute limb compartment syndrome, a complication of musculoskeletal trauma, results in muscle necrosis and cell death. Carbon monoxide, liberated from the carbon monoxide-releasing molecule-3, has been shown protective in a rat model of compartment syndrome. The purpose of this study was to test the effect of carbon monoxide-releasing molecule-3 in a preclinical large animal model of compartment syndrome, with the ultimate goal of developing a pharmacologic adjunct treatment for compartment syndrome. DESIGN Animal research study. SETTING Basic research laboratory in a hospital setting. SUBJECTS Male Yorkshire-Landrace pigs (50-60 kg). INTERVENTIONS Pigs underwent 6 hours of intracompartmental pressure elevation by infusing fluid into the anterior compartment of the right hind limb. Carbon monoxide-releasing molecule-3 was administered systemically (2 mg/kg, IV) at fasciotomy, followed by 3-hour reperfusion. MEASUREMENTS AND MAIN RESULTS Muscle perfusion, inflammation, injury, and apoptosis were assessed in the skeletal muscle. Systemic leukocyte activation was assessed during compartment syndrome and reperfusion. Elevation of hind limb intracompartmental pressure resulted in significant microvascular perfusion deficits (44% ± 1% continuously perfused capillaries in compartment syndrome vs 76% ± 4% in sham; p < 0.001), increased tissue injury (ethidium bromide/bisbenzimide of 0.31 ± 0.07 in compartment syndrome vs 0.17 ± 0.03 in sham; p < 0.05), apoptosis (fluorescence in vivo/bisbenzimide of 0.26 ± 0.06 in compartment syndrome vs 0.13 ± 0.03 in sham; p < 0.05), and systemic leukocyte activation (14.7 relative luminescence units/10 polymorphonuclear leukocytes in compartment syndrome vs 1.0 ± 0.1 in baseline; p < 0.001). Systemic application of carbon monoxide-releasing molecule-3 at fasciotomy increased the number of continuously perfused capillaries (68% ± 3%; p < 0.001), diminished tissue injury (ethidium bromide/bisbenzimide of 0.13 ± 0.04; p < 0.05), apoptosis (fluorescence in vivo/bisbenzimide of 0.12 ± 0.03; p < 0.05), and blocked systemic leukocyte activation (3.9 ± 0.3 relative luminescence unit/10 polymorphonuclear leukocytes; p < 0.001). CONCLUSIONS Administration of carbon monoxide-releasing molecule-3 at fasciotomy offered protection against compartment syndrome-induced microvascular perfusion deficit, tissue injury, and systemic leukocyte activation. The data suggest the potential therapeutic application of carbon monoxide-releasing molecule-3 to patients at risk of developing compartment syndrome.

Carbon monoxide (CO)- and hydrogen sulphide-releasing molecules (CORM-3 and GYY4137, respectively) have been shown to be potent antioxidant and antiinflammatory agents at the tissue and systemic level. We hypothesized that both CORM-3 and GYY4137 would reduce the significant organ dysfunction associated with abdominal compartment syndrome (ACS).Randomized trial was conducted where ACS was maintained for 2 hours in 27 rats using an abdominal plaster cast and intraperitoneal COHepatocellular death and the number of activated leukocytes within postsinusoidal venules were significantly increased in rats with ACS (16-fold increase, 17-fold leukocyte activation, respectively, P 0.05). Administration of CORM-3 or GYY4137 resulted in a significant decrease of both parameters (P = 0.03 and P = 0.009). ACS resulted in an increase in markers of renal and liver injury; CORM-3 or GYY4137 partially restored levels to those seen in sham animals. Myeloperoxidase was significantly elevated in the ACS group in lung, liver, and small intestine (P = 0.0002, P = 0.01, and P = 0.08, respectively). CORM-3 treatment, but not GYY4137, was able to completely block the response (65 ± 11 U/ml and 92 ± 18 U/ml, respectively versus 110 ± 10U/ml in the ACS group, lung tissue).We have demonstrated the effect of two molecules, CO and hydrogen sulphide, on tempering the reperfusion-associated metabolic and organ derangements in ACS. CORM-3 demonstrated a greater effect than GYY4137 and was able to restore most of the measured parameters to levels comparable to sham.

Ischemia-reperfusion (IR) is a limb- and life-threatening complication of acute limb ischemia and musculoskeletal trauma. Carbon monoxide-releasing molecules (CORMs) have recently been shown to protect microvascular perfusion and to reduce inflammation and injury in various ischemic animal models. The purpose of this study was to examine the effects of water-soluble CORM-3 on the extent of IR-induced muscle injury.Wistar rats were randomized into three groups: sham (no ischemia), IR + CORM-3 (10 mg/kg intraperitoneally), and IR + inactive CORM-3 (iCORM-3; 10 mg/kg intraperitoneally). No-flow ischemia was induced by the application of a tourniquet to the hind limb for 2 hours; tourniquet release commenced the reperfusion phase. Both CORM-3 and iCORM-3 were injected immediately after tourniquet release. Temporal changes in microvascular perfusion, cellular tissue injury (ethidium bromide and bisbenzimide staining), and inflammatory response (leukocyte recruitment) within the extensor digitorum longus muscle were assessed using intravital video microscopy every 15 minutes for a total of 90 minutes after initiation of reperfusion. Systemic levels of tumor necrosis factor-α were also measured.Hind limb IR resulted in (1) a significant no-reflow phenomenon followed by progressive increase in microvascular perfusion deficit (21% ± 2% continuously perfused capillaries in IR vs 76% ± 4% in sham [P .001]; 52% ± 8% nonperfused capillaries in IR vs 13% ± 2% in sham at 90 minutes of reperfusion [P .001]), (2) tissue injury (ethidium bromide and bisbenzimide staining of 0.52 ± 0.07 in IR vs 0.05 ± 0.03 in sham at 90 minutes of reperfusion [P .001]), (3) leukocyte recruitment (13.7 ± 0.9 adherent leukocytes/30 seconds/1000 μmCORM-3 displays potent protective and anti-inflammatory effects in an experimental model of hind limb IR, suggesting a potential therapeutic application of CORMs in treatment of ischemic conditions.

© 2020 Elsevier Ltd Background: Observational studies have suggested that accelerated surgery is associated with improved outcomes in patients with a hip fracture. The HIP ATTACK trial assessed whether accelerated surgery could reduce mortality and major complications. Methods: HIP ATTACK was an international, randomised, controlled trial done at 69 hospitals in 17 countries. Patients with a hip fracture that required surgery and were aged 45 years or older were eligible. Research personnel randomly assigned patients (1:1) through a central computerised randomisation system using randomly varying block sizes to either accelerated surgery (goal of surgery within 6 h of diagnosis) or standard care. The coprimary outcomes were mortality and a composite of major complications (ie, mortality and non-fatal myocardial infarction, stroke, venous thromboembolism, sepsis, pneumonia, life-threatening bleeding, and major bleeding) at 90 days after randomisation. Patients, health-care providers, and study staff were aware of treatment assignment, but outcome adjudicators were masked to treatment allocation. Patients were analysed according to the intention-to-treat principle. This study is registered at ClinicalTrials.gov (NCT02027896). Findings: Between March 14, 2014, and May 24, 2019, 27 701 patients were screened, of whom 7780 were eligible. 2970 of these were enrolled and randomly assigned to receive accelerated surgery (n=1487) or standard care (n=1483). The median time from hip fracture diagnosis to surgery was 6 h (IQR 4–9) in the accelerated-surgery group and 24 h (10–42) in the standard-care group (p

Introduction This study was designed to measure early postoperative outcomes of plate vs. nail fixation for humeral shaft fractures. Patients and methods Patients ≥18 years who underwent plate or nail fixation for low-energy humeral shaft fractures between 2005–2016 were identified from the National Surgical Quality Improvement Program (NSQIP). Multivariable regression was used to compare postoperative outcomes using propensity score adjustment to account for differences between fixation groups. Variables included in the propensity score were age, American Society of Anesthesiologists (ASA) class, hypertension, steroid use, cancer, functional status, chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), and sex. Results Plate fixation was used in 1418 patients (70.6%), while nail fixation was used in 591 (29.4%). Patients undergoing nail fixation were more likely to be older, have a higher American Society of Anesthesiologists (ASA) class, and have comorbidities. Mean operative time was statistically longer in the plate fixation group (130 +/−62 min vs. 102 +/−54 min). After propensity score adjustment, type of fixation was not a significant predictor of major or minor complications, length of stay, or readmission. However, nail fixation was a significant predictor of mortality following propensity score adjustment (OR 3.15, 95% Confidence interval 1.26–7.85). Conclusion Patients undergoing intramedullary nail fixation tended to be older patients with more comorbidities, suggesting that surgeons are selecting nail fixation in patients who may not be ideal surgical candidates. Although LOS, complications, and readmission rates were higher in the nail group, this difference was not statistically significant following propensity score adjustment. However, nail fixation remained an independent predictor of 30-day mortality following adjustment. This suggests that nail fixation may not be a safer surgical option in patients with multiple medical co-morbidities and low-energy humeral shaft fractures.

© 2019 John Wiley & Sons Ltd Objective: Limb compartment syndrome (CS), a complication of trauma, results in muscle necrosis and cell death; ischemia and inflammation contribute to microvascular dysfunction and parenchymal injury. Carbon monoxide-releasing molecule-3 (CORM-3) has been shown to protect microvascular perfusion and reduce inflammation in animal models of CS. The purpose of the study was to test the effect of CORM-3 in human in vitro CS model, allowing exploration of the mechanism(s) of CO protection and potential development of pharmacologic treatment. Methods: Confluent human vascular endothelial cells (HUVECs) were stimulated for 6 h with serum isolated from patients with CS. Intracellular oxidative stress (production of reactive oxygen species (ROS)) apoptosis, transendothelial resistance (TEER), polymorphonuclear leukocyte (PMN) activation and transmigration across the monolayer in response to the CS stimulus were assessed. All experiments were performed in the presence of CORM-3 (100 μM) or its inactive form, iCORM-3. Results: CS serum induced a significant increase in ROS, apoptosis and endothelial monolayer breakdown; it also increased PMN superoxide production, leukocyte rolling and adhesion/transmigration. CORM-3 completely prevented CS-induced ROS production, apoptosis, PMN adhesion, rolling and transmigration, while improving monolayer integrity. Conclusion: CORM-3 offers potent anti-oxidant and anti-inflammatory effects, and may have a potential application to patients at risk of developing CS.

Objectives To determine whether patients with AO/OTA 43-B anterior impaction tibial plafond fractures have worse clinical outcomes, and an increased risk of progression to ankle arthrodesis. Design Retrospective cohort study. Setting Level 1 academic trauma center. Patients One hundred sixty-eight patients were included in the study, all of whom had tibial plafond fractures. Intervention Study patients underwent external fixation and/or open reduction internal fixation (ORIF) as indicated by fracture/injury pattern. Main outcome measurements Arthrodesis rate. Results AO 43-B Anterior impaction tibial plafond fractures have an increased risk of progression to arthrodesis when compared to AO 43-B nonanterior impaction type fractures (19.4% vs 8%). Conclusions AO 43-B anterior impaction tibial plafond fractures have a worse clinical outcome compared to AO 43-B nonanterior impaction fractures. These fractures also confer increased risk of progression to arthrodesis. Conflicts of interest The authors have no conflict of interests to declare.

IntroductionAnnually, millions of adults suffer hip fractures. The mortality rate post a hip fracture is 7%–10% at 30 days and 10%–20% at 90 days. Observational data suggest that early surgery can improve these outcomes in hip fracture patients. We designed a clinical trial—HIP fracture Accelerated surgical TreaTment And Care tracK (HIP ATTACK) to determine the effect of accelerated surgery compared with standard care on the 90-day risk of all-cause mortality and major perioperative complications.Methods and analysisHIP ATTACK is a multicentre, international, parallel group randomised controlled trial (RCT) that will include patients ≥45 years of age and diagnosed with a hip fracture from a low-energy mechanism requiring surgery. Patients are randomised to accelerated medical assessment and surgical repair (goal within 6 h) or standard care. The co-primary outcomes are (1) all-cause mortality and (2) a composite of major perioperative complications (ie, mortality and non-fatal myocardial infarction, pulmonary embolism, pneumonia, sepsis, stroke, and life-threatening and major bleeding) at 90 days after randomisation. All patients will be followed up for a period of 1 year. We will enrol 3000 patients.Ethics and disseminationAll centres had ethics approval before randomising patients. Written informed consent is required for all patients before randomisation. HIP ATTACK is the first large international trial designed to examine whether accelerated surgery can improve outcomes in patients with a hip fracture. The dissemination plan includes publishing the results in a policy-influencing journal, conference presentations, engagement of influential medical organisations, and providing public awareness through multimedia resources.Trial registration numberNCT02027896; Pre-results.

Objectives:. Compartment syndrome (CS) is one of the most devastating consequences of musculoskeletal trauma. The pathophysiology of CS includes elevation of intracompartmental pressure (ICP), causing damage to the microcirculation, decreased oxygen delivery, tissue anoxia, and cell death. CS is a combined ischemic and inflammatory condition that induces the systemic inflammatory cascade. In complete ischemia, within the first hour of reperfusion, a peak in the pro-inflammatory cytokine, tumor necrosis factor alpha (TNF-α) has been previously reported. The purpose of this study was to examine the suspected systemic inflammatory cytokine/chemokine release in response to CS, and to evaluate the microvascular dysfunction, tissue injury, and inflammatory response following the neutralization of pro-inflammatory cytokines TNF-α and/or interleukin-1 beta (IL-1β). Methods:. Twenty-eight male Wistar rats were randomly assigned into 5 groups: Sham (no CS), CS (with isotype control), CS+TNF-α neutralizing antibody (NA), CS+IL-1β NA, CS+Combo (both TNF-α and IL-1β NA). CS was induced by elevation of ICP above 30 mm Hg through an infusion of isotonic saline into the anterior compartment of the hind limb for 2 hours; NA were administered just prior to fasciotomy. Microvascular perfusion, cellular tissue injury, and inflammatory response within the extensor digitorum longus muscle were assessed using intravital video microscopy for 45 minutes after fasciotomy. Systemic levels of 24 different cytokines/chemokines were also measured, using the xMAP Luminex technology. Results:. Of the 24 cytokines/chemokines sampled, 6 were significantly elevated from their baseline levels, and included the pro-inflammatory cytokines TNF-α, IL-1β, growth-related oncogene/keratinocyte chemoattractant (GRO/KC), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1 alpha (MIP-1α), and the anti-inflammatory cytokine IL-10. CS resulted in a significant decrease in microvascular perfusion, from 75 ± 2% continuously perfused capillaries in the sham to 31 ± 4% in CS (P

Pelvic fractures in women significantly disrupt the pelvic floor, which may cause stress urinary incontinence (SUI) or pelvic organ prolapse (POP). Our objective was to assess the incidence of operative treatment for SUI and POP after pelvic fracture.We used administrative data from Ontario, Canada, to conduct a retrospective cohort study. Female patients who underwent operative repair of a pelvic fracture between 2002 and 2010 were identified. The primary outcomes were the subsequent surgical treatment of SUI or POP. To compare the incidence with that of the general population, patients who had operative repair of a pelvic fracture were matched (1:2) to a person in the general population (with a propensity score to account for measurable potential confounders). Our primary analysis was a Cox proportional hazards model to compare hazard ratios (HR) in subjects with a pelvic facture and those without.We identified 390 female patients with a median age of 47 (IQR 30-67) years. Our median follow-up period was 5.9 (4.1-8.3) years. The absolute risk of SUI surgery after pelvic fracture was 3.3 % (13 out of 390) compared with 1.0 % (8 out of 769) in the matched general population sample. The HR for SUI surgery was 5.8 (95 % CI 2.2-15.1). The absolute risk of POP surgery after pelvic fracture was 1.8 % (7 out of 390) compared with 0.9 % (7 out of 769) in the matched general population. The HR for POP surgery was 2.3 (95 % CI 0.9-5.8).Among patients who had a pelvic fracture requiring operative repair, there appears to be a significantly increased chance of surgery for SUI, but not for POP.

OBJECTIVES To examine the protective effects of carbon monoxide (CO), liberated from a novel CO-releasing molecule (CORM-3), on the function of compartment syndrome (CS)-challenged muscle in a rodent model, thus providing for a potential development of a pharmacologic adjunctive treatment for CS. METHODS Wistar rats were randomized into 4 groups: sham (no CS), CS, CS with inactive CORM-3 (iCORM-3), and CS + CORM-3 (10 mg/kg intraperitoneally). CS was induced by elevation of intracompartmental pressure to 30 mm Hg through an infusion of isotonic saline into the anterior compartment of the hind limb for 2 hours. Both CORM-3 and iCORM-3 were injected immediately after fasciotomy. Microvascular perfusion, cellular tissue injury, and inflammatory response within the extensor digitorum longus muscle were assessed using intravital video microscopy 45 minutes after fasciotomy. Systemic levels of tumor necrosis factor alpha (TNF-α) were also measured. RESULTS Elevation of intracompartmental pressure resulted in significant microvascular perfusion deficits (23% ± 2% continuously perfused capillaries in CS vs. 76% ± 4% in sham, P < 0.0001; 55% ± 2% nonperfused capillaries in CS vs. 13% ± 2% in sham, P < 0.0001), significant increase in tissue injury (ethidium bromide/bisbenzimide of 0.31 ± 0.05 in CS vs. 0.05 ± 0.03 in sham, P < 0.0001) and adherent leukocytes (13.7 ± 0.9 in CS vs. 1.8 ± 0.5 in sham, P < 0.0001), and a progressive rise in systemic TNF-α. CORM-3 (but not iCORM-3) treatment restored the number of continuously perfused capillaries (57% ± 5%, P < 0.001), diminished tissue injury (ethidium bromide/bisbenzimide of 0.07 ± 0.01, P < 0.001), reversed the CS-associated rise in TNF-α, and decreased leukocyte adherence (0.6 ± 0.3, P < 0.001). CONCLUSIONS CORM-3 displays a potent protective/anti-inflammatory action in an experimental model of CS, suggesting a potential therapeutic application to patients at risk of developing CS.

© 2017 Elsevier Ltd Background Reoperation rates are high after surgery for hip fractures. We investigated the effect of a sliding hip screw versus cancellous screws on the risk of reoperation and other key outcomes. Methods For this international, multicentre, allocation concealed randomised controlled trial, we enrolled patients aged 50 years or older with a low-energy hip fracture requiring fracture fixation from 81 clinical centres in eight countries. Patients were assigned by minimisation with a centralised computer system to receive a single large-diameter screw with a side-plate (sliding hip screw) or the present standard of care, multiple small-diameter cancellous screws. Surgeons and patients were not blinded but the data analyst, while doing the analyses, remained blinded to treatment groups. The primary outcome was hip reoperation within 24 months after initial surgery to promote fracture healing, relieve pain, treat infection, or improve function. Analyses followed the intention-to-treat principle. This study was registered with ClinicalTrials.gov, number NCT00761813. Findings Between March 3, 2008, and March 31, 2014, we randomly assigned 1108 patients to receive a sliding hip screw (n=557) or cancellous screws (n=551). Reoperations within 24 months did not differ by type of surgical fixation in those included in the primary analysis: 107 (20%) of 542 patients in the sliding hip screw group versus 117 (22%) of 537 patients in the cancellous screws group (hazard ratio [HR] 0·83, 95% CI 0·63–1·09; p=0·18). Avascular necrosis was more common in the sliding hip screw group than in the cancellous screws group (50 patients [9%] vs 28 patients [5%]; HR 1·91, 1·06–3·44; p=0·0319). However, no significant difference was found between the number of medically related adverse events between groups (p=0·82; appendix); these events included pulmonary embolism (two patients [

What's known on the subject? and What does the study add? Hydrogen sulphide (H2S) has recently been classified as a member of the gasotransmitter family. Its physiological and pathophysiological effects are rapidly expanding with numerous studies highlighting the protective effects of H2S on ischaemia-reperfusion injury (IRI) in various organ systems, e.g. heart, liver, CNS and lungs. The mechanisms behind its protective effects reside in its vasodilatory, anti-inflammatory and anti-oxidant characteristics. These specific mechanistic profiles appear to be different across different tissues and models of IRI. We recently showed that supplementation of preservation solutions with H2S during periods of prolonged cold renal storage and subsequent renal transplantation leads to a massive and significant survival, functional and tissue protective advantage compared with storage in standard preservation solution alone. However, there have only been a few studies that have evaluated the effects of H2S against warm renal IRI; although these studies have focused primarily upon shorter periods of warm renal pedicle clamping, they have shown a clear survival benefit to H2S supplementation. The present study adds to the existing literature by evaluating the effects of H2S in a model of warm IRI with clinically relevant, prolonged warm ischaemia-reperfusion times (1 h ischaemia, 2 h reperfusion). We show an unprecedented view into real-time renal and hepatic perfusion with intravital microscopy throughout the reperfusion period. We show, for the first time, that supplemental H2S has multiple protective functions against the warm IRI-induced tissue damage, which may be clinically applicable to both donation after cardiac death models of renal transplantation, as well as to uro-oncological practices requiring surgical clamping of the renal pedicle, e.g. during a partial nephrectomy. OBJECTIVE • To determine the protective role of supplemental hydrogen sulphide (H2S) in prolonged warm renal ischaemia-reperfusion injury (IRI) using real-time intravital microscopy (IVM). MATERIALS AND METHODS • Uninephrectomised Lewis rats underwent 1 h of warm ischaemia and 2 h of reperfusion during intraperitoneal treatment with phosphate buffer saline (IRI, n= 10) or 150 µmol/L NaHS (IRI+H2S, n= 12) and were compared with sham-operated rats (n= 9). • Blood was collected for measurement of serum creatinine (Cr), alanine aminotransferase (ALT) and aspartate aminotransferase (AST). • IVM was performed to assess renal and hepatic microcirculation. • Kidneys were sectioned for histology and real-time quantitative polymerase chain reaction for markers of inflammation. RESULTS • The mean (sd) Cr concentration raised to 72.8 (2.5) µmol/L after IRI from 11.0 (0.7) µmol/L (sham) but was partially inhibited with H2S to 62.8 (0.9) µmol/L (P < 0.05). • H2S supplementation during IRI increased renal capillary perfusion on IVM, and improved acute tubular necrosis and apoptotic scores on histology (P < 0.05). • Supplemental H2S decreased expression of the pro-inflammatory markers toll-like receptor 4, tumour necrosis factor α, interleukin 8, C-C chemokine receptor type 5, interferon γ and interleukin 2 (P < 0.05). • Distant organ (liver) dysfunction after renal IRI was limited with H2S supplementation: blunting of the ALT and AST surge, decreased hepatic sinusoidal vasodilation, and decreased leukocyte infiltration in post-sinusoidal venules (P < 0.05). • H2S supplementation directly inhibited interleukin 8-induced neutrophil chemotaxis in vitro (P < 0.05). CONCLUSIONS • These findings are the first to show the real-time protective role of supplemental H2S in prolonged periods of warm renal IRI, perhaps acting by decreasing leukocyte migration and limiting inflammatory responses. • The protective effects of H2S suggest potential clinical applications in both donors after cardiac death models of renal transplantation and oncological practices requiring vascular clamping.

Aims Compartment syndrome results from increased intra-compartmental pressure (ICP) causing local tissue ischaemia and cell death, but the systemic effects are not well described. We hypothesised that compartment syndrome would have a profound effect not only on the affected limb, but also on remote organs. Methods Using a rat model of compartment syndrome, its systemic effects on the viability of hepatocytes and on inflammation and circulation were directly visualised using intravital video microscopy. Results We found that hepatocellular injury was significantly higher in the compartment syndrome group (192 PI-labelled cells/10-1 mm3, standard error of the mean (sem) 51) compared with controls (30 PI-labelled cells/10-1 mm3, sem 12, p < 0.01). The number of adherent venular white blood cells was significantly higher for the compartment syndrome group (5 leukocytes/30s/10 000 μm2, sem 1) than controls (0.2 leukocytes/30 s/10 000 μm2, sem 0.2, p < 0.01). Volumetric blood flow was not significantly different between the two groups, although there was an increase in the heterogeneity of perfusion. Conclusions Compartment syndrome can be accompanied by severe systemic inflammation and end organ damage. This study provides evidence of the relationship between compartment syndrome in a limb and systemic inflammation and dysfunction in a remote organ. Cite this article: Bone Joint J 2016; 98-B:1132–7.

Abdominal compartment syndrome (ACS) is associated with an increased rate of multiple organ dysfunction and is an independent marker for mortality. Our objective was to develop an animal model to study the mechanisms of tissue and microvascular injury associated with ACS at the microscopic level.ACS was established in rats with CO₂ insufflation at 20 mm Hg for 2 h, with an abdominal cast. Sinusoidal perfusion, inflammatory response, and cell death were quantified in exteriorized livers. Respiratory and renal dysfunction were assessed biochemically and morphologically. Myeloperoxidase levels, a marker of neutrophil activation, were measured in the liver, lung, and small intestine.Continuously perfused sinusoids were significantly lower in the ACS group (81.4 ± 2.2% versus 99.6% ± 0.50), with an increase in nonperfused and intermittently perfused sinusoids (P0.05). Hepatocellular death and the number of activated leukocytes in postsinusoidal venules showed 7- and 18-fold increases, respectively, in the ACS group (P0.05). A significant increase in blood urea nitrogen levels in experimental rats was also observed. Myeloperoxidase levels were found to be 8-fold higher in lungs of ACS rats relative to control (P0.05), as well as statistically significant increase in the pCO₂ and decrease in pH of ACS rats.We have successfully developed a model of ACS with documented evidence of renal and respiratory dysfunction. In addition, we have microscopy-confirmed evidence of early inflammatory changes and perfusion deficits in the liver with a concomitant increase in cell death in the ACS group.

STUDY DESIGN: Immunohistochemical and behavioral study using a rat model of acute cauda equina syndrome (CES). OBJECTIVE: To determine the effect of duration of extradural cauda equina compression (CEC) on bladder, sensory, and motor functions. SUMMARY OF BACKGROUND DATA: Cauda equina syndrome is a devastating injury treated with surgical decompression. Controversy exists regarding the optimal timing of surgery. Animal models of CES have focused on motor recovery but have not evaluated pain behavior or bladder function. METHODS: A 4-mm balloon-tipped Fogarty catheter was inserted between the fifth and sixth lumbar lamina into the dorsal epidural space and inflated to compress the nerve roots at the L5 level. Maximal inflation was maintained at a constant balloon pressure of 304 Kpa for 1 or 4 hours. The catheter was inserted but not inflated in sham animals. During a 4-week period, pain behavior, bladder function, and locomotor function were assessed. Postmortem bladders and the lesion site were collected for analysis. RESULTS: Mechanical allodynia was 2-fold greater in 1-hour CEC rats than 4-hour CEC (P=0.002) and sham-operated (P=0.001) rats at 4 weeks after injury. Hind limb locomotor function was not different between groups at 4 weeks after injury. Both the 1-hour and 4-hour CEC group rats retained greater volumes of urine than the sham-operated rats throughout the 4-week period (P

The increasing incidence of hip fractures in our aging population challenges orthopedic surgeons and hospital administrators to effectively care for these patients. Many patients present to regional hospitals and are transferred to tertiary care centres for surgical management, resulting in long delays to surgery. Providing timely care may improve outcomes, as delay carries an increased risk of morbidity and mortality.We retrospectively reviewed the cases of all patients with hip fractures treated in a single Level 1 trauma centre in Canada between 2005 and 2012. We compared quality indicators and outcomes between patients transferred from a peripheral hospital and those directly admitted to the trauma centre.Of the 1191 patients retrospectively reviewed, 890 met our inclusion criteria: 175 who were transferred and 715 admitted directly to the trauma centre. Transfer patients' median delay from admission to operation was 93 hours, whereas nontransfer patients waited 44 hours (p0.001). The delay predominantly occurred before transfer, as the patients had to wait for a bed to become available at the trauma centre. The median length of stay in hospital was 20 days for transfer patients compared with 13 days for nontransfer patients (p0.001). Regional policy changes enacted in 2011 decreased the median transfer delay from regional hospital to tertiary care centre from 47 to 27 hours (p = 0.005).Policy changes can have a significant impact on patient care. Prioritizing patients and expediting transfer will decrease overall mortality, reduce hospital stay and reduce the cost of hip fracture care.L’incidence croissante des fractures de la hanche dans notre population vieillissante pose un défi aux chirurgiens orthopédistes et aux administrateurs hospitaliers qui souhaitent offrir des soins efficaces à ces patients. De nombreux patients se présentent dans des hôpitaux régionaux avant d’être transférés dans des centres de soins tertiaires pour y être opérés, ce qui retarde la chirurgie. Fournir les soins requis en temps voulu pourrait améliorer les résultats étant donné que tout retard s’accompagne d’un risque accru de morbidité et de mortalité.Nous avons effectué une revue rétrospective de tous les cas de fracture de la hanche traités dans un centre canadien de traumatologie de niveau 1 entre 2005 et 2012. Nous avons comparé les indicateurs de qualité et les résultats entre les patients transférés d’un hôpital régional et les patients admis directement au centre de traumatologie.Parmi les 1191 cas analysés rétrospectivement, 890 répondaient à nos critères d’inclusion : 175 avaient été transférés et 715 avaient été admis directement au centre de traumatologie. Le délai médian entre l’admission et la chirurgie chez les patients transférés a été de 93 heures, alors que les patients non transférés ont attendu 44 heures (Les changements de politiques peuvent avoir un impact significatif sur les soins aux patients. Prioriser les cas et accélérer les transferts réduiront la mortalité globale, abrégeront les séjours hospitaliers et réduiront les coûts associés au traitement des fractures de la hanche.

Widespread evidence exists for directed patient information interventions (eg, pamphlets) in the setting of several orthopaedic conditions and interventions. Up until now, no study had assessed the role of these interventions in the management of patients following ankle fractures.Between 2005 and 2007, 40 patients who suffered an operative ankle fracture were randomized to either a standard treatment group for an ankle fracture or an enhanced information group who received an American Academy of Orthopaedic Surgeons ankle fracture information pamphlet that explained postoperative routine at our institution and a physiotherapy handout depicting a standard protocol. Study participants were followed for 3 months clinically and radiographically. At the 6-week and 3-month intervals, study participants completed the Olerud-Molander Questionnaire and 2 questions regarding their level of satisfaction. The primary outcome measure was the Likert-scale-based survey question determining the level of satisfaction with the treating staff.Participants in the enhanced information group were more satisfied with treatment at 3 months (9.2 vs 6.3; P.001). There were significant improvements in work/activity ability at 6 weeks (P = .01), but this advantage disappeared at 3 months (P = .24). No differences in postoperative complication rates were noted.Information enhancement in the form of pamphlets can be helpful in providing patients with accessible information in the postoperative period. While they do not seem to have a sustained impact on postoperative outcomes, handouts may enhance the interaction between staff and patient at postoperative visits, improving patient satisfaction.Level I, appropriately powered randomized prospective cohort study.

BACKGROUND Traumatic spinal cord injury (SCI) triggers a systemic inflammatory response (SIR) that contributes to a high incidence of secondary organ complications, particularly after a cervical or high-level thoracic injury. Because liver plays a key role in initiating and propagating the SIR, the aim of this study was to assess the effects that SCI at differing segmental levels has on the intensity of the inflammatory response in the liver. METHODS Using male Wistar rats, clip compression SCI was performed at the 4th thoracic (T4 SCI; high-level SCI) or the 12th thoracic (T12 SCI; low-level SCI) spinal cord segment. Sham-injured rats had a partial laminectomy, but no SCI. Leukocyte recruitment to the liver, hepatic blood flow, and hepatocellular injury/death were assessed using intravital microscopy and histology. Chemokine and cytokine concentrations were assessed in the liver. Outcomes were measured at 1.5 hours, 12 hours, and 24 hours after SCI. RESULTS At 12 hours after injury, T4 SCI caused a threefold increase in hepatic leukocyte recruitment compared with T12 SCI (p < 0.05). T4 SCI induced 50% more hepatocyte injury than T12 SCI at 12 hours (p < 0.05). Hepatic blood flow decreased after SCI, but not after sham injury, and stayed decreased only after T4 SCI at 24 hours after injury. The T4 SCI-induced changes were accompanied by increases in the hepatic concentrations of interleukin-1β, leptin, interleukin 10, and cytokine-induced neutrophil chemoattractant-1 at 1.5 hours. CONCLUSIONS Our findings indicate that traumatic SCI triggers an acute SIR that contributes to hepatocellular injury. SCI-induced remote injury/dysfunction to the liver appears to be transient and is more robust after an upper thoracic SCI compared with a lower thoracic SCI.

Acute compartment syndrome (CS) is a limb-threatening disease that results from increased intracompartmental pressure. The pathophysiologic mechanisms by which this occurs are poorly understood. This study was designed to measure the effects of increased intracompartmental pressure on skeletal muscle microcirculation, inflammation and cellular injury using intravital videomicroscopy (IVVM) in a clinically relevant small animal model.We induced CS in 10 male Wistar rats (175-250 g), using a saline infusion technique. Intracompartmental pressure was controlled between 30 and 40 mm Hg and maintained for 45 minutes. After fasciotomy, the extensor digitorum longus muscle was visualized using IVVM, and perfusion was quantified. We quantified leukocyte recruitment to measure the inflammatory response. We measured muscle cellular injury using a differential fluorescent staining technique.The number of nonperfused capillaries increased from 12.7 (standard error of the mean [SEM] 1.4 ) per mm in the control group to 30.0 (SEM 6.7) per mm following 45 minutes of elevated intracompartmental pressure (CS group; p = 0.031). The mean number of continuously perfused capillaries (and SEM) decreased from 78.4 (3.2) per mm in the control group to 41.4 (6.9) per mm in the CS group (p = 0.001). The proportion of injured cells increased from 5.0% (SEM 2.1%) in the control group to 16.3% (SEM 6.8%) in the CS group (p = 0.006). The mean number of activated leukocytes increased from 3.6 (SEM 0.7) per 100 μm(2) in the control group to 8.6 (SEM 1.8) per 100 μm(2) in the CS group (p = 0.033).Early CS-induced microvascular dysfunction resulted in a decrease in nutritive capillary perfusion and an increase in cellular injury and was associated with a severe acute inflammatory component.

The liver has been shown to play a particularly important role in the initiation and progression of the early systemic inflammatory response (SIR) to spinal cord injury (SCI). The purpose of this study was to determine the time course of leucocyte recruitment to the liver, and to determine the effect of injury severity on the magnitude of leucocyte recruitment and hepatic injury.Rats were randomly assigned to one of the following groups: uninjured, sham-injured (laminectomy and no cord injury), cord compressed or cord transected. At 30 min and 90 min after SCI rats had the left lobe of their livers externalised and visualised using intravital video microscopy.Thirty minutes after injury the total number of leucocytes per post-sinusoidal venule was significantly increased after cord transection compared to that in uninjured and sham-injured rats (P0.05). Of these leucocytes, significantly more were adherent to venule walls (P0.05). At 90 min the total number of leucocytes per post-sinusoidal venule and the number of adherent and rolling leucocytes was significantly increased after cord transection and cord compression (P0.05).This is the first study to use intravital microscopy to visualise systemic inflammation in the liver following SCI. We have demonstrated immediate leucocyte recruitment to the liver within 30 min after injury and have shown that systemic inflammation increases with time after injury and with severity of injury.