Background: Meniscal root tears and ramp lesions have been rigorously characterized in recent literature. However, one of the most common lateral meniscal injuries identified with an acute anterior cruciate ligament (ACL) disruption, a posterior horn lateral meniscal oblique radial tear (LMORT), has not been thoroughly described. Purpose: To determine the incidence of all meniscal tears and, more specifically, the incidence of posterior horn LMORTs in a multicenter cohort of consecutive, acute ACL reconstructions. Additionally, the authors aimed to develop a new classification system to help guide treatment of posterior horn LMORTs. Study Design: Cross-sectional study; Level of evidence, 3. Methods: A multicenter retrospective cohort design was used to analyze 200 consecutive cases of acute ACL reconstruction from each of 3 different surgeons, for a total of 600 patients. The operative notes and intraoperative photos were analyzed to determine the incidence and laterality of all meniscal tears. A classification system based on tear characterization was then used to categorize tear patterns into similar groups. Results: A total of 396 (66%) of the 600 patients with acute ACL disruption had concomitant meniscal tears. Specifically, 187 (31%) had a lateral meniscal injury, 89 (15%) had a medial meniscal injury, and 122 (20%) had both medial and lateral meniscal injuries. The most common lateral meniscal tear was an LMORT; 71 (18%) patients with meniscal tears had a posterior horn LMORT. Overall, the incidence of ACL injury with a concomitant posterior horn LMORT was 12%. A classification was developed, which included type 1 tear (partial thickness <10 mm from the root attachment), type 2 tear (complete radial oblique tear that extended <10 mm from root), type 3 tear (incomplete LMORT that extended >10 mm from root), and type 4 tear (complete LMORT >10 mm from root). Conclusion: In 600 consecutive acute ACL reconstructions, the incidence of concomitant ACL injury with meniscal injury was 66%, and posterior horn LMORTs represented a large proportion of all meniscal tears (12%). A classification scheme was developed for posterior horn LMORTs to aid reporting and clinical decision making for these common tears.
Background: While a large volume of literature has focused on risk factors for anterior shoulder instability, the rates of recurrence are inconsistent and require additional population-based epidemiologic data. Purpose/Hypothesis: The purpose was to report the effect of patient age on the number of instability events before physician consultation, rate of surgical stabilization, recurrent instability, and progression to osteoarthritis in patients <40 years old with anterior shoulder instability, utilizing an established US geographic population. We hypothesized that younger patients would be more likely to experience multiple episodes of instability before evaluation, undergo surgery, and experience recurrent instability after surgical intervention. Study Design: Descriptive epidemiologic study. Methods: An established geographic database of more than 500,000 patients was used to identify patients <40 years of age with anterior shoulder instability between 1994 and 2016. Medical records were reviewed to obtain patient characteristics, history, imaging, surgical details, and outcomes. Patients were divided into 5 groups based on age (≤15, 16-20, 21-25, 26-30, and 31-40 years) at initial instability. Comparative analysis was performed to identify differences between groups. Results: The study population consisted of 654 patients with a mean follow-up of 11.1 years (range, 2.0-25.2 years). This resulted in 118 patients (18%) ≤15 years of age at initial instability; 250 (38%), 16 to 20 years; 110 (17%), 21 to 25 years; 80 (12%), 26 to 30 years; and 96 (15%), 31 to 40 years. Of patients ≤15 years old at initial instability 47% had 3+ instability events, compared with 12% of patients aged 31 to 40 years ( P < .001). At 10 years of follow-up, patients ≤15 and 16 to 20 years old demonstrated the highest recurrent instability rates of 38.8% and 47.1% after nonoperative management, respectively. Patients 16 to 20 years old demonstrated the highest rates of both surgical intervention (40.4%) and recurrence after surgery (24.8%). Patients 31 to 40 years of age were significantly more likely to develop clinically symptomatic osteoarthritis (15.6%) than all other age groups. Conclusion: In a US epidemiologic population of patients <40 years old, the rate of recurrent anterior shoulder instability was roughly one-third after initial physician consultation. Younger patients, particularly those ≤15 and 16 to 20 years of age, were more likely to have experienced multiple instability events at the time of initial evaluation, require surgery, and experience recurrent instability compared with older patients. For every year of decrease in age at initial instability, the risk of recurrent instability or surgical intervention after physician consultation increased by 4.1% and 2.8%, respectively.
Background: Donor site morbidity after anterior cruciate ligament (ACL) reconstruction with a bone–patellar tendon–bone (BTB) autograft is clinically significant, but evidence with contemporary techniques is lacking. Purpose: To (1) evaluate donor site morbidity at a single institution using modern techniques of BTB autograft harvest at 2-year follow-up, (2) develop a 10-question donor site morbidity instrument, and (3) compare this instrument against traditional outcome tools. Study Design: Case series; Level of evidence, 4. Methods: We analyzed the 2-year follow-up outcomes of 200 consecutive patients who underwent ACL reconstruction with a BTB autograft performed by 2 surgeons at a single institution. The surgical technique utilized modern and consistent BTB autograft harvest, including graft sizing, patellar tendon and peritenon closure, and patellar and tibial donor site bone grafting. There were 187 patients included, with 13 patients undergoing revision ACL reconstruction excluded. An original 10-question scoring instrument evaluating donor site morbidity was administered to each patient (score, 0-100) and compared against each patient’s International Knee Documentation Committee (IKDC) and Lysholm scores. Results: Overall, 13.9% of patients were noted to have anterior knee pain with activity at 2-year follow-up. Moreover, 3.7% of patients reported an inability to kneel on hard surfaces but had no problems on soft surfaces; 5.9% of patients reported mild discomfort but were able to kneel on all surfaces. Additionally, 75.4% of patients had a perfect (100/100) donor site morbidity score. The mean donor site morbidity score at 2-year follow-up was 98.3 ± 3.4. There was a very strong correlation between the IKDC and Lysholm scores but only a strong and moderate correlation when the donor site morbidity score was compared with the IKDC and Lysholm scores, respectively. Conclusion: Donor site morbidity after ACL reconstruction with a BTB autograft was less frequent than reported in the existing literature. Some patients developed anterior knee pain; therefore, an informed discussion is advised. IKDC and Lysholm scores may not capture donor site symptoms after surgery. The 10-question donor site morbidity instrument may provide a more accurate assessment.
Introduction Vaccines have demonstrated protection against the morbidity and mortality of COVID-19, but concerns regarding the rare side effect of acute myocarditis have stymied immunization efforts. This review aims to describe the incidence and theorized mechanisms of COVID vaccine-associated myocarditis and review relevant principles for management of vaccine-associated myocarditis Areas covered Epidemiologic studies of myocarditis after COVID vaccination are reviewed, which show an incidence of approximately 20–30 per million patients. The vast majority of these cases are seen with mRNA vaccines especially in male patients under 30 years of age. Mechanisms are largely theoretical, but molecular mimicry and dysregulated innate immune reactions have been proposed. While studies suggest that this subtype of myocarditis is mild and self-limited, long-term evidence is lacking. Principles of myocarditis treatment and surveillance are outlined as they apply to COVID vaccine-associated myocarditis. Expert Opinion COVID vaccine-associated myocarditis is rare but well described in certain at-risk groups. Better understanding of its pathogenesis is key to mitigating this complication and advancing vaccination efforts. Risk-benefit analyses demonstrate that individual- and population-level benefits of vaccination exceed the risks of this rare and mild form of myocarditis.
All muscle contraction occurs due to the cyclical interaction between sarcomeric thin and thick filament proteins within the myocyte. The thin filament consists of the proteins actin, tropomyosin, Troponin C, Troponin I, and Troponin T. Mutations in these proteins can result in various forms of cardiomyopathy, including hypertrophic, restrictive, and dilated phenotypes and account for as many as 30% of all cases of inherited cardiomyopathy. There is significant evidence that thin filament mutations contribute to dysregulation of Ca2+ within the sarcomere and may have a distinct pathomechanism of disease from cardiomyopathy associated with thick filament mutations. A number of distinct clinical findings appear to be correlated with thin-filament mutations: greater degrees of restrictive cardiomyopathy and relatively less left ventricular (LV) hypertrophy and LV outflow tract obstruction than that seen with thick filament mutations, increased morbidity associated with heart failure, increased arrhythmia burden and potentially higher mortality. Most therapies that improve outcomes in heart failure blunt the neurohormonal pathways involved in cardiac remodeling, while most therapies for hypertrophic cardiomyopathy involve use of negative inotropes to reduce LV hypertrophy or septal reduction therapies to reduce LV outflow tract obstruction. None of these therapies directly address the underlying sarcomeric dysfunction associated with thin-filament mutations. With mounting evidence that thin filament cardiomyopathies occur through a distinct mechanism, there is need for therapies targeting the unique, underlying mechanisms tailored for each patient depending on a given mutation.
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