Injury-related Factors Research Articles

Patient Outcomes After Peripheral Nerve Injury Depend on Bimanual Dexterity and Preserved Use of the Affected Hand

Background Little is known about how peripheral nerve injury affects human performance, behavior, and life. Hand use choices are important for rehabilitation after unilateral impairment, but rarely measured, and are not changed by the normal course of rehabilitation and daily life. Objective To identify the relationship between hand use (L/R choices), motor performance, and patient-centered outcomes. Methods Participants (n = 48) with unilateral peripheral nerve injury were assessed for hand use via Block Building Task, Motor Activity Log, and Edinburgh Handedness Inventory; dexterity (separately for each hand) via Nine-Hole Peg Test, Jebsen Taylor Hand Function Test, and a precision drawing task; patient-centered outcomes via surveys of disability, activity participation, and health-related quality of life; and injury-related factors including injury cause and affected nerve. Factor Analysis of Mixed Data was used to explore relationships between these variables. The data were analyzed under 2 approaches: comparing dominant hand (DH) versus non-dominant hand (NH), or affected versus unaffected hand. Results The data were best explained by 5 dimensions. Good patient outcomes were associated with NH performance, DH performance (separately and secondarily to NH performance), and preserved function and use of the affected hand; whereas poor patient outcomes were associated with preserved but unused function of the affected hand. Conclusion After unilateral peripheral nerve injury, hand function, hand usage, and patient life arise from a complex interaction of many factors. To optimize rehabilitation after unilateral impairment, new rehabilitation methods are needed to promote performance and use with the NH, as well as the injured hand.

Longitudinal Associations Between Persistent Post-Concussion Symptoms and Blood Biomarkers of Inflammation and CNS-Injury After Mild Traumatic Brain Injury.

The aim of our study was to investigate the biological underpinnings of persistent post-concussion symptoms (PPCS) at 3 months following mild traumatic brain injury (mTBI). Patients (n = 192, age 16-60 years) with mTBI, defined as Glasgow Coma Scale (GCS) score between 13 and 15, loss of consciousness (LOC) <30 min, and post-traumatic amnesia (PTA) <24 h were included. Blood samples were collected at admission (within 72 h), 2 weeks, and 3 months. Concentrations of blood biomarkers associated with central nervous system (CNS) damage (glial fibrillary acidic protein [GFAP], neurofilament light [NFL], and tau) and inflammation (interferon gamma [IFNγ], interleukin [IL]-8, eotaxin, macrophage inflammatory protein-1-beta [MIP]-1β, monocyte chemoattractant protein [MCP]-1, interferon-gamma-inducible protein [IP]-10, IL-17A, IL-9, tumor necrosis factor [TNF], basic fibroblast growth factor [FGF]-basic platelet-derived growth factor [PDGF], and IL-1 receptor antagonist [IL-1ra]) were obtained. Demographic and injury-related factors investigated were age, sex, GCS score, LOC, PTA duration, traumatic intracranial finding on magnetic resonance imaging (MRI; within 72 h), and extracranial injuries. Delta values, that is, time-point differences in biomarker concentrations between 2 weeks minus admission and 3 months minus admission, were also calculated. PPCS was assessed with the British Columbia Post-Concussion Symptom Inventory (BC-PSI). In single variable analyses, longer PTA duration and a higher proportion of intracranial findings on MRI were found in the PPCS group, but no single biomarker differentiated those with PPCS from those without. In multi-variable models, female sex, longer PTA duration, MRI findings, and lower GCS scores were associated with increased risk of PPCS. Inflammation markers, but not GFAP, NFL, or tau, were associated with PPCS. At admission, higher concentrations of IL-8 and IL-9 and lower concentrations of TNF, IL-17a, and MCP-1 were associated with greater likelihood of PPCS; at 2 weeks, higher IL-8 and lower IFNγ were associated with PPCS; at 3 months, higher PDGF was associated with PPCS. Higher delta values of PDGF, IL-17A, and FGF-basic at 2 weeks compared with admission, MCP-1 at 3 months compared with admission, and TNF at 2 weeks and 3 months compared with admission were associated with greater likelihood of PPCS. Higher IL-9 delta values at both time-point comparisons were negatively associated with PPCS. Discriminability of individual CNS-injury and inflammation biomarkers for PPCS was around chance level, whereas the optimal combination of biomarkers yielded areas under the curve (AUCs) between 0.62 and 0.73. We demonstrate a role of biological factors on PPCS, including both positive and negative effects of inflammation biomarkers that differed based on sampling time-point after mTBI. PPCS was associated more with acute inflammatory processes, rather than ongoing inflammation or CNS-injury biomarkers. However, the modest discriminative ability of the models suggests other factors are more important in the development of PPCS.

Phenotyping Depression After Mild Traumatic Brain Injury: Evaluating the Impact of Multiple Injury, Gender, and Injury Context.

The chronic mental health consequences of mild traumatic brain injury (TBI) are a leading cause of disability. This is surprising given the expectation of significant recovery after mild TBI, which suggests that other injury-related factors may contribute to long-term adverse outcomes. The objective of this study was to determine how number of prior injuries, gender, and environment/context of injury may contribute to depressive symptoms after mild TBI among deployed United States service members and veterans (SMVs). Data from the Long-term Impact of Military-Relevant Brain Injury Consortium Prospective Longitudinal Study was used to assess TBI injury characteristics and depression scores previously measured on the Patient Health Questionnaire-9 (PHQ-9) among a sample of 1456 deployed SMVs. Clinical diagnosis of mild TBI was defined via a multi-step process centered on a structured face-to-face interview. Logistical and linear regressions stratified by gender and environment of injury were used to model depressive symptoms controlling for sociodemographic and combat deployment covariates. Relative to controls with no history of mild TBI (n = 280), the odds ratios (OR) for moderate/severe depression (PHQ-9 ≥ 10) were higher for SMVs with one mild TBI (n = 358) OR: 1.62 (95% confidence interval [CI] 1.09-2.40, p = 0.016) and two or more mild TBIs (n = 818) OR: 1.84 (95% CI 1.31-2.59, p < 0.001). Risk differences across groups were assessed in stratified linear models, which found that depression symptoms were elevated in those with a history of multiple mild TBIs compared with those who had a single mild TBI (p < 0.001). Combat deployment-related injuries were also associated with higher depression scores than injuries occurring in non-combat or civilian settings (p < 0.001). Increased rates of depression after mild TBI persisted in the absence of post-traumatic stress disorder. Both men and women SMVs separately exhibited significantly increased depressive symptom scores if they had had combat-related mild TBI. These results suggest that contextual information, gender, and prior injury history may influence long-term mental health outcomes among SMVs with mild TBI exposure.

METTL3 boosts mitochondrial fission and induces cardiac fibrosis after ischemia/reperfusion injury.

METTL3, an RNA methyltransferase enzyme, exerts therapeutic effects on various cardiovascular diseases. Myocardial ischemia-reperfusion injury (MIRI) and subsequently cardiac fibrosis is linked to acute cardiomyocyte death or dysfunction induced by mitochondrial damage, particularly mitochondrial fission. Our research aims to elucidate the potential mechanisms underlying the therapeutic actions of METTL3 in MIRI, with focus on mitochondrial fission. When compared with Mettl3flox mice subjected to MIRI, Mettl3 cardiomyocyte knockout (Mettl3Cko) mice have reduced infarct size, decreased serum levels of myocardial injury-related factors, limited cardiac fibrosis, and preserved myocardial ultrastructure and contractile/relaxation capacity. The cardioprotective actions of Mettl3 knockout were associated with reduced inflammatory responses, decreased myocardial neutrophil infiltration, and suppression of cardiomyocyte death. Through signaling pathway validation experiments and assays in cultured HL-1 cardiomyocytes exposed to hypoxia/reoxygenation, we confirmed that Mettl3 deficiency interfere with DNA-PKcs phosphorylation, thereby blocking the downstream activation of Fis1 and preventing pathological mitochondrial fission. In conclusion, this study confirms that inhibition of METTL3 can alleviate myocardial cardiac fibrosis inflammation and prevent cardiomyocyte death under reperfusion injury conditions by disrupting DNA-PKcs/Fis1-dependent mitochondrial fission, ultimately improving cardiac function. These findings suggest new approaches for clinical intervention in patients with MIRI.

αPD-1 immunotherapy promotes IL-17A production and promotes the formation of acute radiation-induced lung injury.

Radiotherapy (RT) is essential in the treatment of thoracic neoplasms. Immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1) have significantly improved the clinical management of non-small cell lung carcinoma (NSCLC). This study aimed to investigate the impact of combining anti-PD-1 (αPD-1) immunotherapy with radiotherapy on lung injury. Additionally, it investigates the role and mechanism of interleukin (IL)-17A, a pro-inflammatory cytokine involved in immune regulation, in lung injury arising from this combination treatment. Experiments were conducted using a PD-1 deficient mouse model to simulate acute radiation-induced lung injury. Inbred female BALB/c wild-type (WT) mice and PD-1-/- mice were divided into six groups: WT group, PD-1-/- group, WT_LIR + IgG group, PD-1-/-_LIR + IgG group, WT_LIR + αIL-17A group, and PD-1-/-_LIR + αIL-17A group. The mice were subjected to 8 Gy × 3 irradiation in both lungs. Various methods including histological scoring, immunofluorescence, qPCR, and flow cytometry were employed to analyze the role of IL-17A in lung injury and the effect of PD-1 gene deletion on the severity of radiation-induced lung injury. The PD-1-/-_LIR mice exhibited evident radiation-induced lung injury after receiving 8 Gy × 3 doses in both lungs. The expression level of IL-17A peaked at 2 weeks. Lung injury-related factors IFN-γ, TNF-α, IL-6, and RORγt in the PD-1-/-_LIR groups increased 2 weeks after irradiation. The CD4+ and CD8+ T cells in lung tissue of the PD-1-/-_LIR mice significantly increased. Post αIL-17A administration, the incidence of alveolitis in the treatment group decreased, the expression levels of lung injury-related factors IFN-γ, TNF-α, IL-6, RORγt, TGF-β1, and IL-17A decreased, and the CD4+ and CD8+ T cells in lung tissue significantly declined. Throughout the observation period, the survival rate of the mice in the treatment group was significantly higher than that of the isotype control group (60% vs 0%, P = 0.011). Combining αPD-1 immunotherapy with radiotherapy in mice can induce radiation-induced lung injury, with IL-17A playing a critical role in this process. αIL-17A administration significantly mitigated radiation-induced lung injury caused by the combination of αPD-1 immunotherapy and radiotherapy, improving mouse survival. This finding offers a promising treatment target for lung injury resulting from the combination of αPD-1 immunotherapy and radiotherapy.

Mechanistic insights into aniline-induced liver injury: Role of the mmu_circ_26984/Myh9/NLRP3 axis and modulation by N-acetylcysteine

Aniline is a widely used chemical. Chronic or high-dose exposure to aniline can lead to hepatocellular damage. Although the hepatic pathogenicity of aniline has been established in previous studies, studies involving pathogenic genes during aniline-induced liver injury are limited. Our study first discovered and identified the role and mechanism underlying a new circRNA mmu_circ_26984 in aniline-induced chemical liver injury. Further, we discuss the protective effect of N-acetylcysteine (NAC) in this pathway. After constructing in vitro and in vivo models of aniline treatment, we screened the circRNA with significant differences in expression in AML12 cells from control and aniline-treated groups by circRNA microarray analysis. Next, using RNA pulldown, liquid chromatography-mass spectrometry (LC-MS), and RNA immunoprecipitation, we analyzed the relationship between mmu_circ_26984 and myosin heavy chain 9 (Myh9). Subsequently, we determined the specific mechanism of action of mmu_circ_26984 and Myh9 in aniline-induced liver injury and the protective effect of NAC against aniline-induced liver injury process using Cell Counting Kit-8, Western blot, RNA extraction, a reverse transcription quantitative polymerase chain reaction (RT-qPCR), fluorescence in situ hybridization, immunohistochemistry, and immunofluorescence. The expression of mmu_circ_26984 was significantly increased in liver tissues and AML12 cells of aniline-treated mice compared with the control group. This high expression of mmu_circ_26984 increased the expression of injury-related inflammatory factors, such as NLRP3, Caspase-1, IL-18, and IL-1β in vivo and ex vivo, which exacerbated the level of liver injury. The interaction of mmu_circ_26984 with Myh9 also affected the course of liver injury. Mmu_circ_26984 overexpression and reduced treatment affected the levels of Myh9 expression in AML12 cells, as well as downstream inflammatory factors associated with injury, such as NLRP3. In addition, NAC reduced the process of liver injury mediated by the mmu_circ_26984/Myh9/NLRP3 axis. In conclusion, mmu_circ_26984 is a potential molecular marker and therapeutic target in the process of aniline-induced liver injury that can mediate aniline-exposure-induced liver injury via modulation of the mmu_circ_26984/Myh9/NLRP3 axis, and NAC can effectively attenuate the effect of this liver injury.

The Need to Rethink Harm Reduction for People Using Drugs Alone to Reduce Overdose Fatalities

Background: During the ongoing opioid epidemic, Cuyahoga County (second largest in Ohio) reported overdose mortality rates (54/per 100,000) higher than the national average. Prior research demonstrates that people who use drugs often use alone but there is minimal research on people who died of overdose while using alone. The objective of this study is to examine sociodemographic, toxicologic, and injury characteristics, and emergency medical response to overdose decedents who died using drugs alone. Method: Data from the Cuyahoga County Medical Examiner’s Office (2016–2020, N = 2944) on unintentional overdose deaths in adults was tabulated including socio-demographic, toxicologic, and injury-related information. Decedents using drugs alone were identified and compared to those not using alone via Chi-square and Fisher’s exact tests. We further fit a multivariate logistic regression model to evaluate socio-demographic, toxicologic, and injury-related factors associated with increased odds of using alone. All results are reported with 95% confidence intervals. Result: Among decedents, 75% (n = 2205) were using drugs alone. Decedents using alone were more likely to be using drugs at home (p = 0.001) or be found dead at the scene (p < 0.001) and less likely to receive naloxone (p < 0.001) have other person/bystander, not using, present (p = 0.002). Using drugs at home (aOR = 1.61[1.19–2.20]) was associated with higher odds of using alone; and being married (aOR = 0.57[0.38–0.86]), having history of illicit drug use (aOR = 0.25[0.08–0.81]) and other person present, who was not using (aOR = 0.58[0.42–0.79]) were associated with lower odds of using alone. Conclusion: New harm reduction approaches targeting people using drugs alone are needed to reduce overdose deaths.

56 Genetic Models for Long-Term Neurocognitive Outcomes in Pediatric Medulloblastoma and Traumatic Brain Injury

Objective:Children who suffer from brain insults (i.e., traumatic brain injury (TBI), chemotherapy and radiation treatment for brain tumors) are susceptible to late-emerging cognitive sequelae. Even with similar neurological risk variables, variability in long-term cognitive outcomes remains an area of investigation for researchers of acquired brain injury. Given the potential for genetic factors to influence response to chemoradiation, researchers have examined associations between germline, inherited, single nucleotide polymorphisms (SNPs), and neurocognitive outcomes for cancer survivors. Children who sustain an uncomplicated mild TBI generally recover without long-term neuropsychological consequences. However, TBI survivors have overlapping mechanism categories with cancer survivors through secondary injury variables that can be influenced by genomic variation (e.g., oxidative stress and neuroinflammation). Furthermore, the study of genomic vulnerability is limited in heterogenous groups of pediatric TBI survivors. This study aims to identify associations between genotype and long-term neurocognitive outcomes for acquired brain injury survivors by utilizing machine learning to uncover pathophysiological similarities and differences between groups.Participants and Methods:Fourteen brain tumor survivors, 139 traumatic brain injury survivors, and 63 healthy, age-matched controls completed the Letter N-back task to obtain performances on core neurocognitive skills (attention, working memory, and processing speed). Ten targeted genotypes were examined across five pathophysiological pathways (neurotransmission, oxidative stress, neuroinflammation, plasticity, growth and repair, and folate metabolism). Data were trained and tested utilizing three regression machine learning models. Mean estimated error and R2 were generated for each neurocognitive outcome. A feature importance score for models with positive variance was generated to determine how predictive a given SNP is for neurocognitive outcomes.Results:Genotype only accounted for a small amount of variance in cognitive outcomes when all clinical groups were combined. The mean absolute error for the best-fitting models from analyses where all groups were combined decreased when groups were examined separately; however, the differences in model R2 values were not significant. The relationship between brain tumor survivors and processing speed performance depended on genotype. Two SNPs had positive feature importance at the interaction level (rs58225473 and rs1801394). These SNPs are located on the CACNB2 and MTR genes and have functional consequences for neurotransmission and folate metabolism. Models of traumatic brain injury survivors did not explain positive variance and could not be examined for feature importance. Additionally, even when removing the only mechanism of action that should not be relevant for TBI survivors (folate metabolism polymorphisms), the TBI models still did not explain positive variance.Conclusions:Findings of the importance of two key SNPs on MTR and CACNB2 genes align with recent systematic reviews, which found associations between these polymorphisms and neuropsychological outcomes in more than one group or cohort of pediatric cancer survivors. Models for TBI survivors were limited by the heterogeneity of the group and ceiling effects on performance. An understanding of genetic vulnerabilities influenced by treatment and injury-related factors in acquired brain injury will inform our understanding of the developing and recovering childhood brain. The current study is an initial contribution to this goal and highlights the utility of machine learning methodology for future studies that examine the influence of genetic heterogeneity in pediatric acquired brain injury.

Cataracts after Ophthalmic andNonophthalmic Trauma Exposure inService Members, U.S. Armed Forces.

IntroductionWe aimed to identify injury-related risk factors for secondary cataract incidence after eye and brain injury and polytrauma. We also examined the effect of direct and indirect eye injury management on cataract diagnosis and treatment. Prevention or mitigation strategies require knowledge of the causes and types of combat injuries, which will enable more appropriate targeting of resources toward prevention and more efficient management of such injuries. Data were gathered from the Military Health System using the Military Health System Management and Analysis Reporting Tool (M2) between 2017 and 2021 from inpatient and outpatient Service Members (SMs) (active duty and National Guard). The date of the first cataract diagnosis was tracked to estimate the annual incidence rate, and it was longitudinally linked to any prior diagnosis of ocular trauma (OT), traumatic brain injury (TBI), or polytrauma to calculate the relative risk. International Classification of Disease codes, 10th Revision, were used to identify those diagnosed with cataracts, TBI, and polytrauma. Defense and Veterans Eye Injury and Vision Registry data were used to examine SMs who sustained ocular injuries from 2003-2020 and who may have had cataract surgery following a cataract diagnosis. The relative risk of traumatic cataract formation from OT, TBI, and polytrauma are 5.71 (95% CI, 5.05-6.42), 2.32 (95% CI, 2.03-2.63), and 8.95 (95% CI, 6.23-12.38), respectively. Traumatic cataracts in SMs more commonly result from open-globe injuries (70%) than closed-globe injuries (30%). By specific sub-injury type, traumatic cataracts occur most frequently from intraocular foreign bodies (22%). More than 400 patients in the cohort suffered from TBI and traumatic cataracts, more than 300 from OT and cataracts, and more than 20 from polytrauma and cataracts. The battlefield is the riskiest environment for trauma exposure, with 62% of OT occurring in combat. There was a statistically significant difference between the mean visual acuity value before cataract surgery (M = 1.17, SD = 0.72) and the mean visual acuity value after cataract surgery (M = 0.44, SD = 0.66, P < .001). Traumatic cataracts often occur in SMs who sustain ocular injuries. New to the literature is that relationships exist between traumatic cataract formation and nonglobe trauma, specifically TBI and polytrauma. Ocular injury calls for an ophthalmic examination. A low threshold should exist for routine ocular exam consultation in the setting of TBI and polytrauma. Separately, polytrauma patients should undergo a review of systems questions, particularly questions about the ocular and visual pathways. A positive response to screening warrants further investigation of possible ocular pathology, including traumatic cataract formation. Cataract surgery is an effective treatment in improving the vision of SMs who suffer from traumatic cataracts. Constant effort must be made to limit occurrences of occupation-related traumatic cataracts.

Characterizing depression after traumatic brain injury using a symptom-oriented approach

BackgroundProgress in addressing depression after traumatic brain injury (TBI) has been limited. Traditional approaches to measuring depression classify individuals with diverse symptoms as having the same problem. We adopted a novel, symptom-oriented approach to characterize post-TBI depression, emphasizing specific symptoms rather than the number of symptoms. MethodsWe assessed depressive symptoms cross-sectionally in 393 participants with moderate-severe TBI (range 0.4–35.4 years post-injury; M = 12.6) using the Inventory of Depression and Anxiety Symptoms – Expanded Version (IDAS-II). We analyzed symptoms of DSM-5 major depressive disorder (MDD), separating compound symptoms into sub-symptoms. We quantified depression heterogeneity across 16 specific symptoms and explored associations between each symptom and personal, injury-related, treatment, and functional/psychosocial outcome factors. Results28 % of participants self-reported a current depression diagnosis, and 35 % met DSM-5 symptom criteria for MDD. Depressed participants (according to either self-reported diagnosis or MDD symptom criteria) were more likely to endorse each specific depressive symptom, including those that overlap with TBI. Post-TBI depression was highly heterogeneous, with 84–91 % of depressed participants (depending on classification method) showing a unique symptom profile not shared with any other individual. The most common symptom profile was shared by only three individuals. This heterogeneity was meaningful, as specific depressive symptoms had distinct associations with personal, injury-related, treatment, and outcome factors. LimitationsCross-sectional design. We only analyzed DSM-5 MDD symptoms, and some symptoms were assessed using only one item. ConclusionsA symptom-oriented approach to post-TBI depression captures the individual's unique profile of depressive symptoms, which relate differently to outcomes and other factors. We recommend future studies investigating post-TBI depression analyze specific symptoms alongside overall depression scores.

Musculoskeletal Injuries in Table Tennis during Competition: A Systematic Review.

The study aimed to investigate the incidence of musculoskeletal injuries among table tennis players and identify their associated risk factors. We conducted a literature search in online databases using relevant search terms related to "table tennis" and "injury". To compare the rate of injuries according to player-related variables, we extracted information on sex, level of games, circumstances of injury, and duration of sport absence after injury. Furthermore, we calculated the odds ratios based on the number of injuries according to variables. Eight articles included 873 professional table tennis players, revealing an overall musculoskeletal injury rate of 3.6% (31 musculoskeletal injuries). The incidence was 10.0 injuries per 1,000 playing hours (range, 0-27.0). The rate of musculoskeletal injuries for female and male players were 3.2% and 3.8%, respectively, and those for Summer Olympic Games, Asian Games, and domestic national games was 4.8%, 15.4%, and 0%, respectively. More than half (52%) of injuries occurred during training, and most injuries (64%) were of a nature that did not cause time loss. This review provides valuable information about the incidence of musculoskeletal injuries in table tennis competitions. However, owing to the limitations of this study in identifying injury-related risk factors, future studies analyzing comprehensive variables are required.

PEDF inhibits LPS-induced acute lung injury in rats and promotes lung epithelial cell survival by upregulating PPAR-γ

BackgroundThe progression of acute lung injury (ALI) involves numerous pathological factors and complex mechanisms, and cause the destruction of epithelial and endothelial barriers. Pigment epithelium-derived factor (PEDF) is an angiogenesis inhibitor and a potential anti-inflammatory factor. The purpose of this study was to investigate the effect of PEDF on lipopolysaccharide (LPS)-induced ALI in rats.MethodsIn vivo, pathological and injury related factors examination were performed on rat lung to investigate the effect of PEDF on ALI. In vitro, the effect of PEDF on inflammatory injury and apoptosis of lung epithelial type II RLE-6TN cell was evaluated, and the expression of inflammatory factors and related pathway proteins and PPAR-γ (in the presence or absence of PPAR-γ inhibitors) were analyzed.ResultsIn vivo results showed that PEDF inhibited the inflammatory factor expression (TNF-α, IL-6 and IL-1β) and progression of ALI and reduced lung cell apoptosis in rats. In vitro results showed that PEDF could effectively inhibit LPS-stimulated inflammatory damage and apoptosis of RLE-6TN cells. PEDF inhibited the RLE-6TN cell injury by enhancing the expression of PPAR-γ.ConclusionsPEDF is an anti-inflammatory factor, which can inhibit apoptosis of lung epithelial cells by upregulating the expression of PPAR-γ and reducing LPS-induced ALI in rats.

Identifying risk factors for osteonecrosis after talar fracture.

To identify patient, injury, and treatment factors associated with development of avascular necrosis (AVN)following talar fractures, with particular interest in modifiable factors. Retrospective chart review. 21 US trauma centers and 1 UK trauma center. 2,220 patients with talar neck and/or body fractures. Open reduction internal fixation of talar neck and body fractures. Development of AVN. Infection, nonunion, and arthritis were secondary outcomes. 796 patients (408 M; 388 F; age 18-81, avg 38.6) with 796 (532R; 264L) fractures were included and were classified as Hawkins 1(51), IIA(71), IIB(113), III(158), IV(40), neck plus body (177), body (188). 336/798 developed AVN (42%), more commonly following any neck fracture (47.0%) vs isolated body fracture (26.1%, p<0.001). More severe Hawkins' classification, combined neck and body fractures, body mass index (BMI), tobacco smoking, right-sided fractures, open fracture, dual anteromedial and anterolateral surgical approaches, and associated medial malleolus fracture were associated with AVN. After multivariate regression, fracture type, tobacco smoking, open fractures, dual approaches, age, and BMI remained significant.Excluding late cases (>7 days), time to joint reduction for Hawkins type IIB-IV neck injuries was no different for those who developed AVN or not. AVN rates for reduction of dislocations within 6 hours of injury vs >6 hours were 48.8% and 57.5%, respectively. Complications included 60 (7.5%) infections and 70 (8.8%) nonunions. 42% of all patients developed AVN, with talar neck fractures, more displaced fractures and open injuries having higher rates. Injury-related factors are most prognostic of AVN risk. Surgical technique to emphasize anatomical reduction, without iatrogenic damage to remaining blood supply is essential. Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.

Factors associated with racial and ethnic disparities in chronic pain after acute traumatic injury

BackgroundChronic pain represents a substantial health burden and source of disability following traumatic injury. This study investigates factors associated with racial and ethnic disparities in chronic pain.MethodsProspective, longitudinal, panel study....

Risk factors for bacterial infection following replantation of zone 1 amputation

Purpose: Bacterial infection is a critical complication influencing the survival of a replanted digit. This study aimed to identify risk factors for bacterial infection following zone 1 replantation. Methods: A retrospective chart review was conducted on patients who underwent zone 1 replantation from January 2016 to November 2022. The factors included in the comparative analysis were patient demographics (age, sex), past medical history (hypertension, diabetes mellitus), smoking, types of injury, degree of contamination, source of trauma, fractures, number of vascular anastomoses, use of salvage therapies, and the use of vein grafts. A bacterial infection was diagnosed based on observation of visible inflammatory signs with the results of culture studies. Results: In total, 313 patients were selected. Thirty-eight cases of bacterial infection were identified, which accounted for 12.1% of total patients. Methicillin-resistant &lt;i&gt;Staphylococcus epidermidis&lt;/i&gt; (MRSE) was the most prevalent bacterium (63.2%, 24 of 38 cases). The patient and injury-related factors showed no significant differences, but the number of vein anastomoses and use of salvage therapy were significantly correlated with the occurrence of bacterial infection. Conclusion: Performing fewer vein anastomoses appears to increase the likelihood of a salvage procedure, and subsequently increases the risk of bacterial infection by an increased need for direct wound manipulation after zone 1 replantation. Infections caused by MRSE were more commonly identified than those by &lt;i&gt;Aeromonas hydrophilia&lt;/i&gt;, which is a commonly known pathogen in medicinal leeches.

Prediction of fracture nonunion leading to secondary surgery in patients with distal femur fractures.

Several previously identified patient-, injury-, and treatment-related factors are associated with the development of nonunion in distal femur fractures. However, the predictive value of these factors is not well defined. We aimed to assess the predictive ability of previously identified risk factors in the development of nonunion leading to secondary surgery in distal femur fractures. We conducted a retrospective cohort study of adult patients with traumatic distal femur fracture treated with lateral locking plate between 2009 and 2018. The patients who underwent secondary surgery due to fracture healing problem or plate failure were considered having nonunion. Background knowledge of risk factors of distal femur fracture nonunion based on previous literature was used to form an initial set of variables. A logistic regression model was used with previously identified patient- and injury-related variables (age, sex, BMI, diabetes, smoking, periprosthetic fracture, open fracture, trauma energy, fracture zone length, fracture comminution, medial side comminution) in the first analysis and with treatment-related variables (different surgeon-controlled factors, e.g. plate length, screw placement, and proximal fixation) in the second analysis to predict the nonunion leading to secondary surgery in distal femur fractures. We were able to include 299 fractures in 291 patients. Altogether, 31/299 fractures (10%) developed nonunion. In the first analysis, pseudo-R2 was 0.27 and area under the receiver operating characteristic curve (AUC) was 0.81. BMI was the most important variable in the prediction. In the second analysis, pseudo-R2 was 0.06 and AUC was 0.67. Plate length was the most important variable in the prediction. The model including patient- and injury-related factors had moderate fit and predictive ability in the prediction of distal femur fracture nonunion leading to secondary surgery. BMI was the most important variable in prediction of nonunion. Surgeon-controlled factors had a minor role in prediction of nonunion.

Functional Outcomes at 6 and 12 Months Post-Injury in a Trauma Centre Population with Moderate-to-Severe Traumatic Injuries.

This study aims to evaluate the global functional outcomes after moderate-to-severe traumatic injury at 6 and 12 months and to examine the sociodemographic and injury-related factors that predict these outcomes. A prospective cohort study was conducted in which trauma patients of all ages with a New Injury Severity Score > 9 who were discharged alive from two regional trauma centres in Norway over a one-year period (2020) were included. The Glasgow Outcome Scale Extended (GOSE) score was used to analyse the functional outcomes. Regression analyses were performed to investigate the predictors of the GOSE score. Follow-up assessments were obtained from approximately 85% of the 601 included patients at both time points. The mean (SD) GOSE score was 6.1 (1.6) at 6 months and 6.4 (1.6) at 12 months, which corresponds to an upper-moderate disability. One-half of the patients had a persistent disability at 12 months post-injury. The statistically significant predictors of a low GOSE score at both time points were more pre-injury comorbidity, a higher number of injuries, and higher estimated rehabilitation needs, whereas a thorax injury with an Abbreviated Injury Scale ≥ 3 predicted higher GOSE scores. A high Glasgow Coma Scale score at admission predicted a higher GOSE score at 6 months. This study strengthens the evidence base for the functional outcomes and predictors in this population.

COMT Val158Met and BDNF Val66Met Single-Nucleotide Polymorphisms Are Not Associated With Emotional Distress One Year After Moderate-Severe Traumatic Brain Injury.

Emotional distress is a common, but poorly addressed, feature of moderate-severe traumatic brain injury (TBI). Previously identified sociodemographic, psychological, and injury-related factors account for only a small proportion of the variability in emotional distress post-TBI. Genetic factors may help to further understand emotional distress in this population. The catechol-O-methyltransferase (COMT) Val158 and brain-derived neurotrophic factor (BDNF) 66Met single-nucleotide polymorphisms (SNPs) have been identified as possible contributory factors to outcomes after TBI. We investigated whether the COMT Val158 and BDNF 66Met SNPs were associated with emotional distress 1 year after moderate-severe TBI, and whether these associations were moderated by age, sex, and TBI severity (as measured by the duration of post-traumatic amnesia [PTA]). Moderate-severe TBI survivors (COMT, n = 391; BDNF, n = 311) provided saliva samples after admission to a TBI rehabilitation hospital. At a follow-up interview ∼1 year after injury, participants completed a self-report measure of emotional distress (Hospital Anxiety and Depression Scale; HADS). Multiple linear regression models were constructed for each SNP to predict total scores on the HADS. Neither COMT Val158 nor BDNF 66Met carriage status (carrier vs. non-carrier) significantly predicted emotional distress (COMT, p = 0.49; BDNF, p = 0.66). Interactions of SNP × age (COMT, p = 0.90; BDNF, p = 0.93), SNP × sex (COMT, p = 0.09; BDNF, p = 0.60), SNP × injury severity (COMT, p = 0.53; BDNF, p = 0.87), and SNP × sex × age (COMT, p = 0.08; BDNF, p = 0.76) were also non-significant. Our null findings suggest that COMT Val158 and BDNF 66Met SNPs do not aid the prediction of emotional distress 1 year after moderate-severe TBI, neither in isolation nor in interaction with age, sex and injury severity. The reporting of null findings such as ours is important to avoid publication bias and prompt researchers to consider the challenges of single-gene candidate studies in understanding post-TBI outcomes. Analyses in larger samples that incorporate multiple genetic factors and their relevant moderating factors may provide a greater understanding of the role of genetics in post-TBI emotional distress.

Occult Pneumothorax in Blunt Thoracic Trauma: Clinical Characteristics and Results of Delayed Tube Thoracostomy in a Level 1 Trauma Center

Occult pneumothorax in blunt trauma patients is often diagnosed only after computed tomography because supine chest X-ray (CXR) is preferred as an initial evaluation. However, improperly managed preexisting occult pneumothorax could threaten the vitality of patients. Therefore, this study aimed to evaluate the incidence, characteristics, risk factors, and outcomes of occult pneumothorax in a single trauma center. From 2020 to 2022, patients who were admitted to the level 1 trauma center were retrospectively investigated. Inclusion criteria focused on blunt chest trauma. Variables including demographic factors, image findings, injury-related factors, tube thoracostomy timing, and treatment results were evaluated. Of the 1621 patients, 187 who met the criteria were enrolled in the study: 32 with overt pneumothorax and 81 with occult pneumothorax. Among all of the pneumothorax cases, the proportion of occult pneumothorax was 71.7% (81/113), and its incidence in all admitted trauma victims was 5.0% (81/1621). Subcutaneous emphysema and rib fractures on supine CXR were risk factors for occult pneumothorax. Six patients underwent delayed tube thoracostomy; however, none had serious complications. Given that occult pneumothorax is common in patients with blunt chest trauma, treatment plans should be established that consider the possibility of pneumothorax. However, the prognosis is generally good, and follow-up is an alternative.

Plantamajoside alleviates acute sepsis-induced organ dysfunction through inhibiting the TRAF6/NF-κB axis

Context Plantamajoside (PMS) possesses rich pharmacological characteristics that have been applied to remedy dozens of diseases. However, the understanding of PMS in sepsis remains insufficient. Objective Role of PMS in sepsis-regulated organ dysfunction and potential mechanisms were investigated. Materials and methods Thirty C57BL/6 male mice were adaptive fed for three days and used to establish acute sepsis model by caecal ligation and perforation (CLP). These experimental mice were divided into Sham, CLP, CLP + 25 mg PMS/kg body weight (PMS/kg), CLP + 50 mg PMS/kg and CLP + 100 mg PMS/kg (n = 6). The pathological and apoptotic changes of lung, liver and heart tissues were observed via HE and TUNEL staining. The injury-related factors of lung, liver and heart were detected by corresponding kits. ELISA and qRT-PCR were applied to assess IL-6/TNF-α/IL-1β levels. Apoptosis-related and TRAF6/NF-κB-related proteins were determined using Western blotting. Results All doses of PMS enhanced the survival rates in the sepsis-induced mouse model. PMS remitted sepsis-mediated lung, liver and heart injury through prohibiting MPO/BALF (70.4%/85.6%), AST/ALT (74.7%/62.7%) and CK-MB/CK (62.3%/68.9%) levels. Moreover, the apoptosis index (lung 61.9%, liver 50.2%, heart 55.7% reduction) and IL-6/TNF-α/IL-1β levels were suppressed by PMS. Furthermore, PMS lowered TRAF6 and p-NF-κB p65 levels, whereas TRAF6 overexpression reversed the protective influences of PMS in organ injury, apoptosis and inflammation triggered by sepsis. Discussion and conclusions PMS suppressed sepsis-induced organ dysfunction by regulating the TRAF6/NF-κB axis, and PMS treatment may be considered as a novel strategy for sepsis-caused damage in future.