Adverse effect of smoking on surgical site infection following ankle and calcaneal fracture fixation: a meta-analysis.

Purpose: Studies have reported conflicting findings on the relationship between smoking and surgical site infection (SSI) post fixation for ankle and calcaneal fractures. This meta-analysis explored the effect of smoking on SSI incidence following open reduction and internal fixation (ORIF) of these fractures. Methods: Full-text studies on smoking's influence on post-ORIF SSI rates for closed ankle and calcaneal fractures were sourced from the PubMed, Embase, and Cochrane databases, with no consideration given to language or publication date. Study quality was appraised using the Newcastle-Ottawa Scale. Odds ratios (OR) and the corresponding 95% CIs were determined using random-effects models. This meta-analysis adhered to the PRISMA guidelines and was registered with PROSPERO (CRD42023429372). Results: The analysis incorporated data from 16 cohort and case-control studies, totaling 41 944 subjects, 9984 of whom were smokers, with 956 SSI cases. Results indicated smokers faced a higher SSI risk (OR: 1.62; 95% CI: 1.32-1.97, P < 0.0001) post ORIF, with low heterogeneity (I 2 = 26%). Smoking was identified as a significant deep SSI risk factor (OR: 2.09; 95% CI: 1.42-3.09; P = 0.0002; I 2 = 31%). However, the subgroup analysis revealed no association between smoking and superficial SSI (OR: 1.05; 95% CI: 0.82-1.33; P = 0.70; I 2 = 0%). Conclusion: Smoking is associated with increased SSI risk after ORIF for closed ankle and calcaneus fractures. Although no clear link was found between superficial SSI and smoking, the data underscore the negative influence of smoking on deep SSI incidence.

Is smoking a risk factor for complications following total ankle arthroplasty? A meta-analysis.

BACKGROUND: Smoking has long been recognized as a risk factor for impaired wound and bone healing, particularly in the context of ankle and foot surgery. Despite numerous studies exploring the association between smoking and complications following ankle replacement, there remains significant inconsistency in their findings. Therefore, this meta-analysis study aims to elucidate whether smoking increases the rate of complications after total ankle arthroplasty (TAA), providing valuable insights for clinical management. METHODS: A comprehensive systematic search was conducted in the PubMed, Embase, and Wiley databases to identify relevant English studies on the influence of smoking on postoperative complications following ankle replacement without any restrictions on publication dates. The quality of the included studies was assessed using the Newcastle-Ottawa Scale. Random-effect models were used to calculate odds ratios (OR) and 95 % confidence intervals (CI). This study adhered to PRISMA guidelines for transparent reporting and was registered with PROSPERO. RESULTS: The analysis incorporated data from 12 retrospective cohort studies, totaling 17331 subjects, 2580 of whom were smokers and 791 complications following TAA. The findings revealed a statistically significant disparity in wound-related complications (OR: 2.26; 95 % CI: 1.13-4.50; P = .02), particularly evident in current smokers with an OR of 3.30 (95 % CI: 2.12-5.14; P < .00001). However, we lacked sufficient evidence to substantiate an association between smoking and complications related to the prosthesis (OR: 1.09; 95 % CI: 0.77-1.53; P = .64) or systemic complications (OR: 1.18; 95 % CI: 0.10-14.13; P = .90) following TAA. CONCLUSIONS: Smoking, especially current smoking, is associated with increased wound complication risk post-operation for total ankle arthroplasty. Despite a lack of definitive evidence on the optimal timeframe for smoking cessation before surgery, discontinuing smoking appears to be a prudent measure to mitigate these complications.

The Association between Red Blood Cell Distribution Width and Mortality Risk after Hip Fracture: A Meta-Analysis.

Background and Objectives: Hip fractures in the elderly pose a considerable health risk and cause concern. Red blood cell distribution width (RDW) is a valuable marker for identifying patients at high risk of age-related mortality and various disorders and diseases. However, its association with poor patient outcomes following hip fractures has yet to be fully established. Hence, the purpose of this meta-analysis was to investigate and gain a better understanding of the relationship between RDW levels and the risk of mortality after hip fractures. Materials and Methods: PubMed, Embase, Web of Science, and other databases were comprehensively searched until April 2023 to identify relevant studies. The meta-analysis included observational studies finding the association between RDW at admission or preoperation and short-term and long-term mortality rates following hip fractures. The results were presented in terms of odds ratios (ORs) or hazard ratios (HRs) with corresponding 95% confidence intervals (CIs). Results: This meta-analysis included 10 studies involving 5834 patients with hip fractures. Patients with preoperative RDW of over 14.5% had higher risks of 1-year (OR: 5.40, 95% CI: 1.89-15.48, p = 0.002) and 3-month (OR: 2.91, 95% CI: 1.42-5.95, p = 0.004) mortality. Higher admission or preoperative RDW was significantly associated with an 11% higher mortality risk after 1 year (HR: 1.11, 95% CI: 1.06-1.17, p < 0.00001). Patients with higher preoperative RDW had a significantly higher risk of 6-month mortality, which was three times that of those with lower preoperative RDW (OR: 3.00, 95% CI: 1.60-5.61, p = 0.0006). Higher preoperative RDW was correlated to a higher 30-day mortality risk (OR: 6.44, 95% CI: 3.32-12.47, p < 0.00001). Conclusions: Greater RDW values at admission or before surgery were associated with a higher risk of short-term and long-term mortality following hip fractures. Because RDW can be easily measured using a routine blood test at a low cost, this parameter is promising as an indicator of mortality in elderly patients with hip fractures.

The scavenging chemokine receptor ACKR2 has a significant impact on acute mortality rate and early lesion development after traumatic brain injury.

The atypical chemokine receptor ACKR2 promotes resolution of acute inflammation by operating as a scavenger receptor for inflammatory CC chemokines in several experimental models of inflammatory disorders, however its role in the brain remains unclear. Based on our previous reports of increased expression of inflammatory chemokines and their corresponding receptors following traumatic brain injury (TBI), we hypothesised that ACKR2 modulates neuroinflammation following brain trauma and that its deletion exacerbates cellular inflammation and chemokine production. We demonstrate increased CCL2 and ACKR2 mRNA expression in post-mortem human brain, whereby ACKR2 mRNA levels correlated with later times post-TBI. This data is consistent with the transient upregulation of ACKR2 observed in mouse brain after closed head injury (CHI). As compared to WT animals, ACKR2-/- mice showed a higher mortality rate after CHI, while the neurological outcome in surviving mice was similar. At day 1 post-injury, ACKR2-/- mice displayed aggravated lesion volume and no differences in CCL2 expression and macrophage recruitment relative to WT mice. Reciprocal regulation of ACKR2 and CCL2 expression was explored in cultured astrocytes, which are recognized as the major source of CCL2 and also express ACKR2. ACKR2 mRNA increased as early as 2 hours after an inflammatory challenge in WT astrocytes. As expected, CCL2 expression also dramatically increased at 4 hours in WT astrocytes but was significantly lower in ACKR2-/- astrocytes, possibly indicating a co-regulation of CCL2 and ACKR2 in these cells. Conversely, in vivo, CCL2 mRNA/protein levels were increased similarly in ACKR2-/- and WT brains at 4 and 12 hours after CHI, in line with the lack of differences in cerebral macrophage recruitment and neurological recovery. In conclusion, ACKR2 is induced after TBI and has a significant impact on mortality and lesion development acutely following CHI, while its role in chemokine expression, macrophage activation, brain pathology, and neurological recovery at later time-points is minor. Concordant to evidence in multiple sclerosis experimental models, our data corroborate a distinct role for ACKR2 in cerebral inflammatory processes compared to its reported functions in peripheral tissues.

Tin triggers suicidal death of erythrocytes.

Suicidal erythrocyte death or eryptosis is characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine (PS) exposure at the erythrocyte surface. Triggers of eryptosis include increase in cytosolic Ca(2+) activity, formation of ceramide and energy depletion. Excessive eryptosis contributes to several anemic conditions. Intoxication with inorganic tin(II) may lead to anemia. The present study therefore explored whether tin influences eryptosis. To this end, erythrocytic phosphatidylserine exposure was estimated from annexin V-binding, cell volume from forward scatter, cytosolic Ca(2+) activity from Fluo3 fluorescence, ceramide formation from binding of fluorescent antibodies and cytosolic ATP utilizing a luciferin-luciferase assay kit. Under control conditions, eryptosis was observed in less than 5% of the erythrocytes. Exposure to tin (1-100 microm) significantly increased the percentage of PS-exposing erythrocytes and decreased cell volume. The effect was paralleled by an increase in the cytosolic Ca(2+) concentration, ceramide formation and a decrease of intracellular ATP concentration. In conclusion, tin triggers eryptosis, an effect at least partially due to Ca(2+ )entry, ceramide formation and ATP depletion. The effect could contribute to tin-induced anemia.