High Prevalence of Work-related Musculoskeletal Disorders and Limited Evidence-based Ergonomics in Orthopaedic Surgery: A Systematic Review.

BACKGROUND: The Centers for Disease Control defines work-related musculoskeletal disorders as disorders of the nerves, muscles, tendons, joints, spinal discs, and cartilage that are caused or exacerbated by the environment or nature of work. Previous meta-analyses have characterized work-related musculoskeletal disorders among interventionists, general surgeons, and other surgical subspecialties, but prevalence estimates, prognosis, and ergonomic considerations vary by study and surgical specialty. QUESTIONS/PURPOSES: (1) What is the career prevalence of work-related musculoskeletal disorders in orthopaedic surgeons? (2) What is the treatment prevalence associated with work-related musculoskeletal disorders in orthopaedic surgeons? (3) What is the disability burden of work-related musculoskeletal disorders in orthopaedic surgeons? (4) What is the scope of orthopaedic surgical ergonomic assessments and interventions? METHODS: A systematic review of English-language studies from PubMed, MEDLINE, Embase, and Scopus was performed in December 2022 and reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Studies that presented prevalence estimates of work-related musculoskeletal disorders or assessed surgical ergonomics in orthopaedic surgery were included. Reviews, case reports, gray literature (conference abstracts and preprints), and studies with mixed-surgeon (nonorthopaedic) populations were excluded. The search yielded 5603 abstracts; 24 survey-based studies with 4876 orthopaedic surgeons (mean age 48 years; 79% of surgeons were men) were included for an analysis of work-related musculoskeletal disorders, and 18 articles were included for a descriptive synthesis of ergonomic assessment. Quality assessment using the Joanna Briggs Institute Tool revealed that studies had a low to moderate risk of bias, largely because of self-reporting survey-based methodology. Because of considerable heterogeneity and risk of bias, prevalence outcomes were not pooled and instead are presented as ranges (mean I 2 = 91.3%). RESULTS: The career prevalence of work-related musculoskeletal disorders in orthopaedic surgeons ranged from 37% to 97%. By anatomic location, the prevalence of work-related musculoskeletal disorders in the head and neck ranged from 4% to 74%; back ranged from 9% to 77%; forearm, wrist, and hand ranged from 12% to 54%; elbow ranged from 3% to 28%; shoulder ranged from 3% to 34%; hip and thigh ranged from 1% to 10%; knee and lower leg ranged from 1% to 31%; and foot and ankle ranged from 4% to 25%. Of orthopaedic surgeons reporting work-related musculoskeletal disorders, 9% to 33% had a leave of absence, practice restriction or modification, or early retirement, and 27% to 83% received some form of treatment. Orthopaedic surgeons experienced biomechanical, cardiovascular, neuromuscular, and metabolic stress during procedures. Interventions to improve orthopaedic surgical ergonomics have been limited, but have included robotic assistance, proper visualization aids, appropriate use of power tools, and safely minimizing lead apron use. In hip and knee arthroplasty, robotic assistance was the most effective in improving posture and reducing caloric expenditure. In spine surgery, proper use of surgical loupes was the most effective in improving posture. CONCLUSION: Although the reported ranges of our main findings were wide, even on the low end of the reported ranges, work-related musculoskeletal disability among orthopaedic surgeons appears to be a substantial concern. We recommend that orthopaedic residency training programs incorporate surgical ergonomics or work injury lectures, workshops, and film review (alongside existing film review of surgical skills) into their curricula. We suggest hospitals engage in shared decision-making with surgeons through anonymous needs assessment surveys to implement wellness programs specific to surgeons' musculoskeletal needs. We urge institutions to assess surgeon ergonomics during routine quality assessment of novel surgical instruments and workflows. LEVEL OF EVIDENCE: Level III, prognostic study.

Graft Augmentation of Rotator Cuff Repair Improves Load to Failure But Does Not Affect Stiffness or Gap Formation: A Meta-analysis of Biomechanical Studies.

PURPOSE: To examine the biomechanical properties of rotator cuff repair with graft augmentation (RCR-G) with regard to ultimate load to failure, gap displacement, and stiffness. METHODS: A systematic review was performed by searching PubMed, the Cochrane library, and Embase using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines to identify studies that analyzed the biomechanical properties of RCR-G. The search string implemented used the concepts "rotator cuff" and "graft," and "biomechanical" OR "cadaver." Meta-analysis was performed to provide a quantitative comparison of the 2 techniques. Primary outcome measures were ultimate load to failure (N), gap displacement (mm), and stiffness (N/mm). RESULTS: Our initial search yielded 1,493 articles for review. Following screening for inclusion criteria, 8 studies were included in the meta-analysis, including a total of 191 cadaveric specimens (106 RCR-G, 85 RCR). The pooled analysis from 6 studies reporting on ultimate load to failure revealed a statistically significant difference in favor of RCR-G compared with RCR (P < .001). Pooled analysis from 6 studies reporting on gap displacement failed to reveal a difference between RCR-G and RCR (P = .719). Pooled analysis from 4 studies reporting on stiffness failed to reveal a difference between RCR-G and RCR (P = .842). CONCLUSIONS: Graft augmentation of RCR in vitro resulted in significantly increased ultimate load to failure, with no influence on gap formation or stiffness. CLINICAL RELEVANCE: The biomechanical advantage of RCR with graft augmentation demonstrated via increased ultimate load to failure in cadaveric studies may provide an explanation for the decreased RCR retear rates and improved patient reported outcomes reported in the clinical literature regarding graft augmentation.

Evaluation of immunogenicity and reactogenicity of COVID-19 vaccines in pregnant women.

OBJECTIVE: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in pregnancy is associated with increased risk of adverse maternal and perinatal outcomes. Vaccines are highly effective at preventing severe coronavirus disease 2019 (COVID-19), but there are limited data on COVID-19 vaccines in pregnancy. This study aimed to investigate the reactogenicity and immunogenicity of COVID-19 vaccines in pregnant women when administered according to the 12-week-interval dosing schedule recommended in the UK. METHODS: This was a cohort study of pregnant women receiving COVID-19 vaccination between April and September 2021. The outcomes were immunogenicity and reactogenicity after COVID-19 vaccination. Pregnant women were recruited by phone, e-mail and/or text and were vaccinated according to vaccine availability at their local vaccination center. For immunogenicity assessment, blood samples were taken at specific timepoints after each dose to evaluate nucleocapsid protein (N) and spike protein (S) antibody titers. The comparator group comprised non-pregnant female healthcare workers in the same age group who were vaccinated as part of the national immunization program in a contemporaneous longitudinal cohort study. Longitudinal changes in serum antibody titers and association with pregnancy status were assessed using a two-step regression approach. Reactogenicity assessment in pregnant women was undertaken using an online questionnaire. The comparator group comprised non-pregnant women aged 18-49 years who had received two vaccine doses in primary care. The association of pregnancy status with reactogenicity was assessed using logistic regression analysis. RESULTS: Overall, 67 pregnant women, of whom 66 had received a mRNA vaccine, and 79 non-pregnant women, of whom 50 had received a mRNA vaccine, were included in the immunogenicity study. Most (61.2%) pregnant women received their first vaccine dose in the third trimester, while 3.0% received it in the first trimester and 35.8% in the second trimester. SARS-CoV-2 S-antibody geometric mean concentrations after mRNA vaccination were not significantly different at 2-6 weeks after the first dose but were significantly lower at 2-6 weeks after the second dose in infection-naïve pregnant compared with non-pregnant women. In pregnant women, prior infection was associated with higher antibody levels at 2-6 weeks after the second vaccine dose. Reactogenicity analysis included 108 pregnant women and 116 non-pregnant women. After the first dose, tiredness and chills were reported less commonly in pregnant compared with non-pregnant women (P = 0.043 and P = 0.029, respectively). After the second dose, feeling generally unwell was reported less commonly (P = 0.046) in pregnant compared with non-pregnant women. CONCLUSIONS: Using an extended 12-week interval between vaccine doses, antibody responses after two doses of mRNA COVID-19 vaccine were found to be lower in pregnant compared with non-pregnant women. Strong antibody responses were achieved after one dose in previously infected women, regardless of pregnancy status. Pregnant women reported fewer adverse events after both the first and second dose of vaccine. These findings should now be addressed in larger controlled studies. © 2022 The Authors. Ultrasound in Obstetrics & Gynecology published by John Wiley & Sons Ltd on behalf of International Society of Ultrasound in Obstetrics and Gynecology.

Nonoperative management of anterior shoulder instability can result in high rates of recurrent instability and pain at long-term follow-up.

BACKGROUND: Data on the long-term outcomes of nonoperative treatment of anterior shoulder instability are lacking, particularly for the US population. The purpose was to (1) describe the characteristics of patients with anterior shoulder instability treated nonoperatively, (2) assess the long-term outcomes of nonoperative management in a US population, and (3) identify risk factors for poor outcomes following nonoperative management. METHODS: A geographic cohort of >500,000 subjects was used to identify patients treated nonoperatively for anterior shoulder instability. Only patients aged <40 years at the time of initial instability with minimum 10-year follow-up were included. Medical records were reviewed to obtain demographic characteristics, physical examination findings, clinical history data, imaging results, treatment details, and clinical and/or radiographic progression. Recurrent pain, recurrent instability, and the development of symptomatic osteoarthritis (OA) were the primary outcomes evaluated. RESULTS: The study included 254 patients (73% male) with a median age of 19 years (range, 16-26 years) at the time of initial instability. At median 17-year follow-up, 37.5% experienced recurrent instability, 58.4% had recurrent pain, and 12.2% had symptomatic OA development. Factors associated with recurrent pain at final follow-up were multiple instability events prior to presentation (hazard ratio [HR], 2.43; P < .01) and increased pain at the initial visit (HRs of 0.79 for mild, 1.74 for moderate, and 1.39 for severe; P < .01); patients with multiple instability events prior to presentation also had an increased risk of recurrence (P < .01). Factors increasing the risk of the development of symptomatic OA included increased pain at the initial visit (P = .05), seizure disorder (HR, 27.01; P < .01), and smoking (HR, 5.15; P < .01). CONCLUSIONS: At long-term follow-up of 17 years, a high rate of poor outcomes was observed following nonoperative management of anterior shoulder instability. Overall, 37.5% of patients experienced recurrent shoulder instability, 58.4% had recurrent shoulder pain, and 12.2% had symptomatic OA development. Risk factors associated with adverse clinical outcomes included increased pain at the initial visit, recurrent instability prior to presentation, seizure disorder, and smoking.

TDP43 proteinopathy is associated with aberrant DNA methylation in human amyotrophic lateral sclerosis.

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by motor neurone (MN) degeneration and death. ALS can be sporadic (sALS) or familial, with a number of associated gene mutations, including C9orf72 (C9ALS). DNA methylation is an epigenetic mechanism whereby a methyl group is attached to a cytosine (5mC), resulting in gene expression repression. 5mC can be further oxidized to 5-hydroxymethylcytosine (5hmC). DNA methylation has been studied in other neurodegenerative diseases, but little work has been conducted in ALS. AIMS: To assess differences in DNA methylation in individuals with ALS and the relationship between DNA methylation and TDP43 pathology. METHODS: Post mortem tissue from controls, sALS cases and C9ALS cases were assessed by immunohistochemistry for 5mC and 5hmC in spinal cord, motor cortex and prefrontal cortex. LMNs were extracted from a subset of cases using laser capture microdissection. DNA from these underwent analysis using the MethylationEPIC array to determine which molecular processes were most affected. RESULTS: There were higher levels of 5mC and 5hmC in sALS and C9ALS in the residual lower motor neurones (LMNs) of the spinal cord. Importantly, in LMNs with TDP43 pathology there was less nuclear 5mC and 5hmC compared to the majority of residual LMNs that lacked TDP43 pathology. Enrichment analysis of the array data suggested RNA metabolism was particularly affected. CONCLUSIONS: DNA methylation is a contributory factor in ALS LMN pathology. This is not so for glia or neocortical neurones.

Review: Microglia in motor neuron disease.

Motor Neuron Disease (MND) is a fatal neurodegenerative condition, which is characterized by the selective loss of the upper and lower motor neurons. At the sites of motor neuron injury, accumulation of activated microglia, the primary immune cells of the central nervous system, is commonly observed in both human post mortem studies and animal models of MND. Microglial activation has been found to correlate with many clinical features and importantly, the speed of disease progression in humans. Both anti-inflammatory and pro-inflammatory microglial responses have been shown to influence disease progression in humans and models of MND. As such, microglia could both contribute to and protect against inflammatory mechanisms of pathogenesis in MND. While murine models have characterized the microglial response to MND, these studies have painted a complex and often contradictory picture, indicating a need for further characterization in humans. This review examines the potential role microglia play in MND in human and animal studies. Both the pro-inflammatory and anti-inflammatory responses will be addressed, throughout the course of disease, followed by the potential of microglia as a target in the development of disease-modifying treatments for MND.

Expression of p16 and p21 in the frontal association cortex of ALS/MND brains suggests neuronal cell cycle dysregulation and astrocyte senescence in early stages of the disease.

AIMS: Cellular senescence plays a role in organismal ageing and has been linked to persistent DNA damage in age-related diseases. Brain senescence has been described in astrocytes and microglia, but it is less well understood in neurones. Evidence suggests that neurones activate a senescence-like mechanism that could contribute to neurodegeneration. We aimed to determine whether a persistent DNA damage response (DDR) and senescence activation are features of motor neurone disease (amyotrophic lateral sclerosis, ALS/MND). METHODS: We examined expression of senescence (p16 and p21) and DNA damage markers (8-OHdG and γH2AX) in motor cortex (MCx), frontal association cortex (FACx) and occipital cortex (OCx) in post-mortem tissue donated by patients with ALS/MND and controls. RESULTS: Nuclear expression of p16 and p21 was detected in glial cells; double immunofluorescence for p16/p21 and glial fibrillary acidic protein (GFAP) suggested that some of these cells were GFAP+ astrocytes. p21 nuclear expression was also found in neurones. Higher levels of p16+ (glia, P = 0.028) and p21+ (glia, P = 0.003; neurones, P = 0.008) cells were found in the FACx of ALS/MND donors but not in the MCx or OCx. Expression of p16 and p21 did not correlate with 8-OHdG or γH2AX. CONCLUSIONS: Expression of p16 and p21 in glia, mainly in astrocytes, suggests senescence induction in these cells; however, neuronal p21 expression might reflect a more general mechanism of age-related cell cycle dysregulation. The significantly higher proportion of cells expressing either p16 or p21 in the FACx of ALS/MND donors could indicate senescence activation and cell cycle dysregulation in early stages of the disease.

Neuropathological characterization of a novel TANK binding kinase (TBK1) gene loss of function mutation associated with amyotrophic lateral sclerosis.

AIMS: Mutations in TANK binding kinase gene (TBK1) are causative in amyotrophic lateral sclerosis (ALS), however correlations between clinical features and TBK1 mutations have not been fully elucidated. We aimed to identify and compare TBK1 mutations to clinical features in a cohort of ALS patients from Northern England. METHODS: TBK1 mutations were analysed in 290 ALS cases. Immunohistochemistry was performed in brain and spinal cord of one case with a novel in-frame deletion. RESULTS: Seven TBK1 variants were identified, including one novel in-frame deletion (p.85delIle). In silico analysis and literature suggested four variants were pathogenic, and three were variants of uncertain significance or benign. Post-mortem immunohistochemistry established an individual with the novel in-frame deletion had classical ALS and Type B FTLD-TDP pathology, with no changes in TBK1 staining or interferon regulatory factor IRF3. CONCLUSIONS: TBK1 mutations were present in 1.38% of our cohort, and screening showed no clear genotype-phenotype associations compared to other genetic and sporadic ALS cases. TBK1 immunohistochemistry was consistent with previously published literature and we are the first to show no differential expression of interferon regulatory factor IRF3, a downstream effector of TBK1 in the immune pathway, in the TBK1-mutant tissue, compared to controls.

Surveillance of congenital Zika syndrome in England and Wales: methods and results of laboratory, obstetric and paediatric surveillance.

The spread of the Zika virus (ZIKV) in the Americas led to large outbreaks across the region and most of the Southern hemisphere. Of greatest concern were complications following acute infection during pregnancy. At the beginning of the outbreak, the risk to unborn babies and their clinical presentation was unclear. This report describes the methods and results of the UK surveillance response to assess the risk of ZIKV to children born to returning travellers. Established surveillance systems operating within the UK - the paediatric and obstetric surveillance units for rare diseases, and national laboratory monitoring - enabled rapid assessment of this emerging public health threat. A combined total of 11 women experiencing adverse pregnancy outcomes after possible ZIKV exposure were reported by the three surveillance systems; five miscarriages, two intrauterine deaths and four children with clinical presentations potentially associated with ZIKV infection. Sixteen women were diagnosed with ZIKV during pregnancy in the UK. Amongst the offspring of these women, there was unequivocal laboratory evidence of infection in only one child. In the UK, the number and risk of congenital ZIKV infection for travellers returning from ZIKV-affected countries is very small.

The Effect of Distal Radius Fracture Location on Distal Radioulnar Joint Stability: A Cadaveric Study.

PURPOSE: To investigate whether the location of distal radius osteotomy/shortening relative to the radial insertion of the distal interosseous membrane (DIOM) is correlated with distal radioulnar joint (DRUJ) instability. We hypothesized that distal radius osteotomy and shortening proximal to the DIOM insertion would result in increased DRUJ instability because of induced laxity in the DIOM. METHODS: Osteotomies of the distal radius were performed proximal and distal to the DIOM insertion in 14 fresh-frozen cadaveric specimens. Using a volar plate, 5 conditions were tested: anatomical radius alignment; 2- and 4-mm shortening at the proximal osteotomy site; and 2- and 4-mm shortening at the distal osteotomy site. Basilar ulnar styloid osteotomy was performed to simulate triangular fibrocartilage complex (TFCC) detachment-specimens were tested with the ulnar styloid detached and the ulnar styloid fixed (to restore normal anatomy). The DRUJ stability was quantified using dorsal-volar displacement of the radius in response to 20 N of force using a force-displacement probe in neutral, pronation, and supination. Posttesting specimen dissections assessed DIOM and distal oblique bundle (DOB) anatomy. The DRUJ stability in each experimental condition was compared with a multifactor repeated measures analysis of variance with the specimen treated as the repeated factor. RESULTS: There were no significant differences in dorsal-volar translation of the radius (ie, DRUJ stability) between radial osteotomy/shortening proximal and distal to the DIOM insertion, regardless of forearm rotational position or magnitude of shortening. Five (36%) of the 14 specimens had a DOB present. There was a significant increase in DRUJ instability in the setting of TFCC detachment (via basilar ulnar styloid osteotomy). CONCLUSIONS: No difference in DRUJ stability was observed between distal radius osteotomy/shortening proximal and distal to the DIOM radial insertion, regardless of forearm rotation, magnitude of shortening, and/or TFCC detachment. CLINICAL RELEVANCE: Distal radius osteotomy and shortening did not affect DRUJ stability regardless of location relative to the DIOM insertion.

Age-associated changes in the blood-brain barrier: comparative studies in human and mouse.

AIMS: While vascular pathology is a common feature of a range of neurodegenerative diseases, we hypothesized that vascular changes occur in association with normal ageing. Therefore, we aimed to characterize age-associated changes in the blood-brain barrier (BBB) in human and mouse cohorts. METHODS: Immunohistochemistry and Evans blue assays were used to characterize BBB dysfunction (tight junction protein expression and serum plasma protein accumulation), vascular pathology (pericyte loss and vascular density) and glial pathology (astrocyte and microglial density) in ageing neurological control human prefrontal cortex (a total of 23 cases from 5 age groups representing the spectrum of young adult to old age: 20-30 years, 31-45 years, 46-60 years, 61-75 years and 75+) and C57BL/6 mice (3 months, 12 months, 18 months and 24 months, n = 5/6 per group). RESULTS: Quantification of the tight junction protein ZO-1 within the cortex and cerebellum of the mouse cohort showed a significant trend to both increased number (cortex P < 0.001, cerebellum P < 0.001) and length (cortex P < 0.001, cerebellum P < 0.001) of junctional breaks associated with increasing age. GFAP expression significantly correlated with ageing in the mice (P = 0.037). In the human cohort, assessment of human protein accumulation (albumin, fibrinogen and human IgG) demonstrated cells morphologically resembling clasmatodendritic astrocytes, indicative of BBB dysfunction. Semiquantitative assessment of astrogliosis in the cortex expression revealed an association with age (P = 0.003), while no age-associated changes in microglial pathology, microvascular density or pericyte coverage were detected. CONCLUSIONS: This study demonstrates BBB dysfunction in normal brain ageing, both in human and mouse cohorts.

Review: Neuropathology and behavioural features of transgenic murine models of Alzheimer's disease.

Our understanding of the underlying biology of Alzheimer's disease (AD) has been steadily progressing; however, this is yet to translate into a successful treatment in humans. The use of transgenic mouse models has helped to develop our understanding of AD, not only in terms of disease pathology, but also with the associated cognitive impairments typical of AD. Plaques and neurofibrillary tangles are often among the last pathological changes in AD mouse models, after neuronal loss and gliosis. There is a general consensus that successful treatments need to be applied before the onset of these pathologies and associated cognitive symptoms. This review discusses the different types of AD mouse models in terms of the temporal progression of the disease, how well they replicate the pathological changes seen in human AD and their cognitive defects. We provide a critical assessment of the behavioural tests used with AD mice to assess cognitive changes and decline, and discuss how successfully they correlate with cognitive impairments in humans with AD. This information is an important tool for AD researchers when deciding on appropriate mouse models, and when selecting measures to assess behavioural and cognitive change.

Review: Astrocytes in Alzheimer's disease and other age-associated dementias: a supporting player with a central role.

Astrocytes have essential roles in the central nervous system and are also implicated in the pathogenesis of neurodegenerative disease. Forming non-overlapping domains, astrocytes are highly complex cells. Immunohistochemistry to a variety of proteins can be used to study astrocytes in tissue, labelling different cellular components and sub-populations, including glial fibrillary acidic protein, ALDH1L1, CD44, NDRG2 and amino acid transporters, but none of these labels the entire astrocyte population. Increasing heterogeneity is recognized in the astrocyte population, a complexity that is relevant both to their normal function and pathogenic roles. They are involved in neuronal support, as active components of the tripartite synapse and in cell interactions within the neurovascular unit (NVU), where they are essential for blood-brain barrier maintenance and neurovascular coupling. Astrocytes change with age, and their responses may modulate the cellular effects of neurodegenerative pathologies, which alone do not explain all of the variance in statistical models of neurodegenerative dementias. Astrocytes respond to both the neurofibrillary tangles and plaques of Alzheimer's disease, to hyperphosphorylated tau and Aß, eliciting an effect which may be neuroprotective or deleterious. Not only astrocyte hypertrophy, in the form of gliosis, occurs, but also astrocyte injury and atrophy. Loss of normal astrocyte functions may contribute to reduced support for neurones and dysfunction of the NVU. Understanding how astrocytes contribute to dementia requires an understanding of the underlying heterogeneity of astrocyte populations, and the complexity of their responses to pathology. Enhancing the supportive and neuroprotective components of the astrocyte response has potential translational applications in therapeutic approaches to dementia.

Characterizing the Diagnosis and Treatment of Allergic Contact Dermatitis to 2-Octyl Cyanoacrylate Used for Skin Closure in Elective Orthopedic Surgery.

BACKGROUND: While studies have shown that postoperative wound complications can predispose to deep infection following orthopedic surgery, the best form of skin closure has not been elucidated. Furthermore, the unique risks and benefits of each type of wound closure have not been studied. The goal of this study is to present the diagnosis and treatment of patients with allergic contact dermatitis (ACD) from 2-octyl cyanoacrylate, a skin adhesive commonly used in wound closure. METHODS: Twenty-nine patients with ACD to 2-octyl cyanoacrylate (Prineo, Ethicon, NJ) following elective orthopedic surgeries from 2013 to 2016 were retrospectively reviewed; this occurred in 29 of 6088 units of Prineo used at our institution, for an estimated incidence of 0.5%. Nineteen patients (66%) had knee operations. Mean age was 55 years (range, 15-92 years). We classified patients by symptom severity and treatment requirements into mild, moderate, and severe reactions. RESULTS: Most reactions were moderate (48%) or severe (38%) reactions. Mean time from surgery to diagnosis was 11.8 days (range, 2-42 days). All patients underwent removal of the Prineo dressing and daily dressing changes with a specific protocol. Twenty patients (69%) received oral antihistamines, 16 patients (55%) required topical corticosteroids, and 5 patients (17%) required oral corticosteroids. All cases of ACD ultimately resolved at a mean of 22 days (range, 13-56 days) postoperatively. CONCLUSION: 2-Octyl cyanoacrylate skin adhesive occurs in an estimated 0.5% of cases and can lead to severe postoperative ACD when used following orthopedic operations. However, with early recognition and appropriate treatment, patients' symptoms resolve without a significant impact on wound healing.