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Background: When injuring the anterior cruciate ligament (ACL), simultaneous meniscal tears often occur. However, little data describe ACL reconstruction (ACLR) and the subsequent risk of revision ACLR, as well as cartilaginous and meniscal damage after primary ACLR with different treatments for injury of the lateral meniscus (LM). Purpose: To investigate (1) how different LM treatments during primary ACLR affect the odds of revision ACLR and the cartilaginous and meniscal status at revision in a long-term follow-up and (2) whether the increased risk of subsequent meniscal and cartilaginous injuries seen with meniscal resection in the short term would continue in the long term, and (3) the increased risk with subsequent meniscal injuries with meniscal repair. Study Design: Cohort study; Level of evidence, 3. Methods: Data from the Swedish National Knee Ligament Registry were used. The study compared 2 groups: patients with isolated ACLR and patients with ACLR and concomitant LM injury, further subdividing the latter into 4 treatment types: repair, resection, both, and left in situ. Patients with medial meniscal injuries were excluded. The main outcomes studied were the odds for revision ACLR and the cartilaginous and meniscal status at revision 5 and 10 years after primary surgery. Results: Data for 5 years were available for 22,208 patients and data for 10 years were available for 11,058 patients. Compared with isolated ACLR, patients with concomitant LM injury left in situ had higher odds of revision ACLR at both 5 years (odds ratio [OR], 1.49; 95% CI, 1.14-1.95; P = .004) and 10 years (OR, 1.55; 95% CI, 1.09-2.19; P = .01), while those with LM repair had higher odds at 5 years (OR, 1.73; 95% CI, 1.23-2.43; P = .002). LM repair also increased the odds of subsequent meniscal injuries at 5 years (OR, 3.52; 95% CI, 1.76-7.03; P = .0004) and 10 years (OR, 7.26; 95% CI, 1.67-31.52; P = .008). Partial meniscectomy did not show an increased risk of cartilage injury, subsequent meniscal injury, or revision ACLR at long-term follow-up compared with the control group. Conclusion: This demonstrates that over 5 and 10 years, LM repair during primary ACLR is associated with an increased risk of revision ACLR and subsequent meniscal injuries. The higher risk of revision ACLR when the LM is left in situ emphasizes the need for careful consideration of treatment methods. Conversely, partial meniscectomy did not show an associated increased risk of cartilaginous injury in the long term and is associated with a lower risk of subsequent meniscal injury and revision ACLR than other treatment options, raising questions about whether preserving the meniscus at all costs is always the best approach.

ABSTRACT The Team Physician Consensus Statement delineates qualifications, duties, and responsibilities of the team physician and provides guidelines to individuals and organizations in selecting team physicians. These delineations and guidelines provide a foundation for best practices in the medical care of athletes and teams. The team physician’s education, training, and experience uniquely qualify them to provide the best medical care for the athlete. This document is not intended as a standard of care and should not be interpreted as such. It is only a guide and, as such, is of a general nature, consistent with the reasonable, objective practice of the healthcare profession. Adequate insurance should be in place to help protect the physician, the athlete, and the sponsoring organization. This document was originally developed as the first in the team physician consensus series, representing an ongoing project-based alliance of the major professional associations concerned about clinical sports medicine issues. The organizations are as follows: American Academy of Family Physicians, American Academy of Orthopedic Surgeons, American College of Sports Medicine, American Medical Society for Sports Medicine, American Orthopedic Society for Sports Medicine, and the American Osteopathic Academy of Sports Medicine.

OBJECTIVE Chiari malformation type 1 (CM1) is the most common neurological disorder of the craniocervical junction. CM1 is characterized by cerebellar tonsillar herniation below the foramen magnum, causing CSF obstruction and neural compression. Patients with CM1 suffer from highly variable symptoms, progression, comorbidities, and outcomes, partly due to poor understanding of CM1 pathogenesis. In this paper, the authors present the only familial CM1 cohort study to statistically assess intrafamilial clinical phenotypes to date. METHODS Comprehensive medical, surgical, and family histories and neuroimaging were collected from families with multiple CM1-affected family members. Univariate analysis was performed for each symptom, comorbidity, or surgery to compare observed versus expected frequencies of affected patients with another CM1-affected family member with the same clinical characteristic. RESULTS Twenty-four new familial CM1 cases (totaling 57 patients with CM1) are presented. Intrafamilial similarities were identified for age of onset, symptoms such as headaches (p = 0.007) and neck pain (p = 0.018), neurological comorbidities such as syringomyelia (p = 0.003) and hydrocephalus (p = 0.0001), neurodevelopmental conditions such as dyslexia (p < 0.0001), and connective tissue disorders (CTDs) such as Ehlers-Danlos syndrome (p < 0.0001). CONCLUSIONS These results suggest that CM1 and its associated clinical phenotypes, including age of onset, clinical symptoms, neurological comorbidities, neurodevelopmental conditions, and CTDs, are genetically influenced. Whole-exome sequencing of CM1 patient-parent trios has the potential to identify the genetic determinants of CM1, with implications for neurosurgical management.

Malnutrition, defined as deficiency, excess, or imbalance of nutrients, is a common complication in patients with liver disease, especially those with cirrhosis. Malnutrition may present as an isolated micronutrient deficiency, such as zinc deficiency, and it commonly presents as frailty and/or sarcopenia in patients with advanced liver disease. Patients with cirrhosis and/or alcohol-associated hepatitis should be assessed for malnutrition because it adversely affects patient outcomes including mortality, as well as waitlist and posttransplant outcomes among liver transplant candidates. The prevalence of malnutrition varies based on the method of assessment and disease severity, being higher in those with advanced liver disease. Among stable outpatients with cirrhosis, counseling should be done to eat small frequent meals, a night-time snack between 7 PM and 10 PM, and 2 or more cups of coffee daily. In selected patients with metabolic dysfunction-associated steatohepatitis, vitamin E 800 IU/d should be provided. Among hospitalized patients with cirrhosis, nutritional supplementation preferably by enteral route should be implemented in those with poor oral intake of daily requirements of proteins and/or calories. Protein intake should not be restricted including patients with decompensated cirrhosis and hepatic encephalopathy. A vegetable source of protein seems to be better tolerated than an animal source of protein in patients with hepatic encephalopathy. Branched chain amino acids augment the efficacy of lactulose and rifaximin in the treatment of hepatic encephalopathy. Level of evidence and strength of recommendations were evaluated using the Grading of Recommendations, Assessment, Development, and Evaluations system. This guideline was developed under the auspices of the American College of Gastroenterology Practice Parameters Committee.

PURPOSE The combination of the Bruton tyrosine kinase inhibitor ibrutinib with bendamustine-rituximab for first-line treatment of mantle cell lymphoma (MCL) prolonged progression-free survival (PFS), but without improvement in overall survival (OS), likely because of toxicity. Acalabrutinib was shown to be efficacious and less toxic than ibrutinib in a head-to-head trial in chronic lymphocytic leukemia and therefore might lead to better outcomes in MCL. METHODS Patients 65 years and older with previously untreated MCL received acalabrutinib (100 mg twice daily) or placebo (until disease progression or unacceptable toxicity), plus six cycles of bendamustine (90 mg/m 2 once daily; days 1 and 2) and rituximab (375 mg/m 2 as a single dose; day 1) followed by rituximab maintenance in responding patients for 2 years. Crossover to acalabrutinib at disease progression was permitted. The primary end point was PFS per the independent review committee; overall response rate and OS were secondary end points. RESULTS In total, 598 patients were randomly assigned, with 299 in each arm. At a median follow-up of 49.8 months using the reverse Kaplan-Meier method, the median PFS was 66.4 months in the acalabrutinib arm and 49.6 months in the placebo arm (hazard ratio [HR], 0.73 [95% CI, 0.57 to 0.94]; P = .0160). Benefit was seen across all subgroups, including those with high-risk features. Overall response/complete response rates were 91.0%/66.6% and 88.0%/53.5% in the acalabrutinib and placebo arms, respectively. OS was not significantly different (HR, 0.86 [95% CI, 0.65 to 1.13]; P = .27). Grade 3 or greater adverse events were reported in 88.9% and 88.2% in the acalabrutinib and placebo arms, respectively. CONCLUSION The combination of acalabrutinib with bendamustine-rituximab significantly improved PFS. Clinical benefit of acalabrutinib with bendamustine-rituximab was achieved with manageable toxicity.

Abstract Objective In utero fetal spina bifida repair decreases the risk for cerebrospinal fluid (CSF) diversion including ventriculoperitoneal (VP) shunt placement, reverses hindbrain herniation, and improves motor function with a higher likelihood of independent ambulation. Unfortunately, in utero surgery can be complicated by preterm delivery. The goal of this study was to compare pregnancy and neonatal outcomes between individuals who delivered very preterm, and those who delivered later in gestation following in utero spina bifida repair. Methods Data from the North American Fetal Therapy Network Fetal Myelomeningocele Consortium Registry collected from 2011 to 2024 were analyzed. Three cohorts of patients were categorized by gestational age at delivery and compared: <30 weeks, 30–34 weeks, and >34 weeks. Comparisons between groups for maternal and delivery outcomes were completed for the entire cohort and then analyzed for those with available CSF diversion data up to 1 year of life. Chi‐square or Fisher's exact tests were used to compare categorical variables, and Kruskal–Wallis tests were used to determine if there are significant differences between the distributions of the three groups. A p ‐value <0.05 was considered significant. Results A total of 1213 patients were analyzed (<30 weeks, n = 111 [9.2%]; 30–34 weeks, n = 323 [26.6%]; >34 weeks, n = 779 [64.2%]). Overall fetal and neonatal mortality was 2.2%, 85% of which occurred in the <30‐week cohort, where perinatal mortality was 21%. Latency from fetal surgery to delivery averaged 2.1 weeks for the <30‐week group. Rates of abruption, chorioamnionitis, and spontaneous labor were higher in the <30‐week group compared to later gestational age cohorts. Neonatal morbidity was also significantly higher in the <30‐week cohort for sepsis, apnea, respiratory distress, patent ductus arteriosus, intraventricular hemorrhage, and periventricular leukomalacia in the <30‐week cohort. CSF diversion data were available for 677 neonates (<30 weeks, n = 53; 30–34 weeks, n = 186; >34 weeks, n = 438). There was no significant difference in VP shunt placement between the different gestational age groups. Conclusion Very preterm birth following in utero spina bifida repair results in significant perinatal mortality and neonatal morbidity. Delivery prior to 30 weeks of gestation occurs in 9% of patients after in utero spina bifida repair, resulting in a 21% perinatal mortality rate. However, even among those who delivered very preterm, a reduction in VP shunt rates, a benefit of in utero repair, appears to be preserved. Further data are warranted to assess the impact of prematurity following in utero surgery on ambulation and developmental outcomes.

AbstractIntroductionActive learning engages learners in constructing knowledge through interactive strategies such as simulation, small‐group discussion, and peer instruction. Although recognized as a superior approach to traditional passive learning, its adoption has been inconsistent. Barriers include reliance on traditional lectures, lack of training, and limited time to develop materials. Simulation educators have a unique skill set that may inform and support active learning initiatives.MethodsFifteen emergency medicine simulation experts convened to define the unique skill set of simulation educators and identify transferable simulation‐based medical education (SBME) skills and concepts to promote effective active learning beyond the simulation lab. Workgroup members are simulation education directors who have undergone specialized training in SBME. During biweekly meetings over 6 months, workgroup members reviewed primary literature in SBME and active learning, along with relevant simulation educator training materials. Objectives were achieved through iterative review, group conceptualization, and expert consensus.Unique treatmentThe increasing prevalence of SBME in medical education, along with the growth of simulation fellowships, has produced a group of education experts with shared competencies. Simulation educators acquire expertise in psychological safety, facilitation, communication, and debriefing, through specialized training and extensive experience. These skills are critical for active learning environments where learners benefit from structured, engaging, and psychologically safe experiences.Implications for educatorsKey transferable SBME topics were identified for use in active learning environments outside of the simulation lab: (1) psychological safety, (2) facilitation strategies, and (3) communication techniques. Transferable tools and concepts were identified to promote efficacy and learner engagement during active learning in diverse environments. Simulation educators’ expertise is an underutilized resource for faculty development initiatives aimed at advancing active learning. This work advocates for leveraging simulation educators’ skills to close the active learning implementation gap, enhance learner outcomes, and meet the evolving needs of contemporary medical education.

OBJECTIVE Despite the known negative physiological impact of repeated mild head trauma events, their multiplicative impact on long-term seizure risk remains unclear. The objective of this study was to evaluate how multiple mild traumatic brain injuries (mTBIs) impact long-term seizure risk by testing 3 distinct machine learning approaches. Baseline and injury-specific characteristics were incorporated to enhance prognostication of individual seizure risk. METHODS Children with at least 1 mTBI event without prior evidence of seizure or antiepileptic drug treatment, from 2003 to 2021, were identified from a nationally sourced administrative claims database. The primary outcome of interest was a seizure event after mTBI, defined by qualifying principal diagnosis codes. Time-varying multivariable Cox regression was used to assess the impact of repeated mTBI. RESULTS A total of 156,118 children (mean age 11.7 ± 4.7 years) were included, with a median follow-up duration of 22.6 months (IQR 9.2–45.4 months). Among patients who experienced seizure after mTBI, the median time to seizure was 306 days. Seizures among those with radiographic findings and/or loss of consciousness occurred earlier (median time to seizure 112.5 days [imaging findings only, IQR 5–526.25 days], 80 days [loss of consciousness only, IQR 7–652 days], 22 days [both, IQR 5–192 days]). Both mTBI without and with short-term loss of consciousness resulted in increasing seizure risk with repeated trauma (HR 1.196, 95% CI 1.082–1.322; HR 2.025, 95% CI 1.828–2.244; respectively). The random survival forest approach achieved fixed-time areas under the receiver operating characteristic curve of 0.780 and 0.777 at 30 and 90 days after mTBI, and children predicted at high risk by the final model experienced a significantly higher burden of early seizure after mTBI (46.7% within the first 30 days vs 17.7% and 19.9% of children at low and medium risk). A simplified model using the top 12 contributing features achieved 95% of the full model’s performance in the validation set. CONCLUSIONS A novel machine learning model was developed and validated for personalized prediction of long-term seizure risk following multiple mTBIs. Model performance remained robust with a limited feature set, suggesting the feasibility of real-time incorporation into clinical workflows for individualized prognostication following each repeat mTBI event. In children predicted to be at high risk, early intervention should be considered.