Up to One-Half of Runners Return to Running One Year After Arthroscopic Partial Meniscectomy.

Purpose: To determine whether, and at which frequency, runners return to running after undergoing arthroscopic partial meniscectomy (APM). Methods: We identified patients who underwent surgery between August 2012 and December 2019 who were classified as runners (defined as running 2+ times per week according to Marx Activity Rating Scale Q1) and completed the 1-year follow-up to assess outcomes. Patients were followed using the Marx Activity Rating Scale, Knee Injury and Osteoarthritis Outcome Score (KOOS), Veterans RAND 12-item Health Survey mental and physical components, and visual analog pain scale scores preoperatively and 1 and 2 years postoperatively. The association between baseline characteristics and return to running was assessed using the unpaired t test or Wilcoxon rank sum test for continuous predictors and a χ2 test for categorical predictors, using the 1-year postoperative follow-up data. Results: A total of 185 patients were included in this study. One year after APM, 41% of runners returned to running at the same frequency or more frequently than before. Further, 50% of runners returned to running at least twice weekly. Return to running according to those definitions was similar at 2 years (38% and 47%, respectively). At both 1 and 2 years, runners exhibited significant improvements in KOOS (Pain), KOOS (Function in Sport and Recreation), visual analog pain scale, and Veterans RAND 12-item Health Survey physical component scores. Lower body mass index (P = .0248) and greater baseline running frequency (P = .0300) predicted return to running at least twice weekly at 1 year postoperatively. Medial versus lateral compartment partial meniscectomy and Outerbridge grade were not significant predictors of return to running. Conclusions: Roughly 1 in 2 runners return to their preoperative running frequency after undergoing APM. Obesity and lower baseline running frequency were significantly associated with inability to return to running. Level of Evidence: III, retrospective cohort study.

The aging athlete.

Aging athletes, those 60 years and older, are a growing population of mature, active individuals who value sports and exercise participation throughout their lifespan. Although recommendations for younger and masters athletes have been extrapolated to this population, there remains a paucity of specific guidelines, treatment algorithms, and considerations for aging athletes. The benefits of living an active lifestyle must be weighed against the risks for unique cardiovascular, metabolic, and musculoskeletal injuries requiring diagnostic and therapeutic interventions. In this article, we review the unique cardiovascular and muscular physiology of aging athletes and how it influences the risk of specific medical conditions. We also discuss general prevention and treatment strategies. Finally, we identify areas of future research priorities and emerging treatments.

Exertional Heat Stroke at the Boston Marathon: Demographics and the Environment.

PURPOSE: This study aimed to assess associations between exertional heat stroke (EHS) and sex, age, prior performance, and environmental conditions, and report on resources needed for EHS cases at the Boston Marathon. METHODS: We analyzed participant characteristics, environmental data, and EHS medical encounters during the 2015-2019 Boston Marathon races. RESULTS: Among 136,161 starters, there was an incidence of 3.7 EHS cases per 10,000 starters (95% confidence interval, 2.8-4.9), representing 0.5% of all medical encounters. There were significant associations between sex and age (P < 0.0001), sex and start wave (P < 0.0001), and age group and start wave (P < 0.0001). Sex was not significantly associated with increased EHS incidence; however, age younger than 30 yr and assignment to the first two start waves were. All cases occurred at races with average wet bulb globe temperatures of 17°C-20°C. There was a linear correlation between EHS incidence and greater increases in wet bulb globe temperature from start to peak (R2 = 0.7688). A majority of cases (37; 72.5%) were race finishers; nonfinishers all presented after mile 18. Most were triaged 3-4 h after starting, and all were treated with ice water immersion. Treatment times were prolonged (mean (SD), 78.1 (47.5) min; range, 15-190 min); 29.4% (15 cases) developed posttreatment hypothermia, and 35.3% (18 cases) were given intravenous fluids. Most (31 cases; 64.6%) were discharged directly, although 16 cases (33.3%) required hospital transport. There were no fatalities. CONCLUSIONS: Younger and faster runners are at higher risk for EHS at the Boston Marathon. Greater increases in heat stress from start to peak during a marathon may exacerbate risk. EHS encounters comprise a small percentage of race-day medical encounters but require extensive resources and warrant risk mitigation efforts.

Burden of Injury and Illness in the Road Race Medical Tent: A Narrative Review.

OBJECTIVE: To summarize the literature relating to prehospital care at 5 km through marathon distance road races and present the epidemiology of common medical encounters, significant medical complications, and medical outcomes. DATA SOURCES: We searched PubMed and Google Scholar for the published literature pertaining to road race medical tent encounters at 5 km through marathon distance road races from 2000 to 2018. We included English-language, original articles reporting on injury and illness incidence. MAIN RESULTS: Standard medical encounter definitions have recently been formulated in response to the previous lack of uniform definitions. The incidence of medical complications at road races may be influenced by environmental conditions and race distance. Minor and moderate medical encounters, such as dermatologic injuries, musculoskeletal injuries, and exercise-associated collapse, are common. Serious and life-threatening medical complications, including exertional heat stroke, exercise-associated hyponatremia, and cardiac arrest, are less frequent. Fatalities are also rare, with rates of 0.3 to 5 per 100 000 participants reported at marathons. The ratio of hospital transports to medical encounters is low. CONCLUSIONS: On-site medical services play a key role in the safety of both runners and the community. Future research and care initiatives in this field should focus on optimizing treatment protocols, promoting injury prevention efforts and reducing host community costs.

Medical Tent Utilization at 10-km Road Races: Injury, Illness, and Influencing Factors.

PURPOSE: To increase awareness of the need for coordinated medical care at 10-km races and to help direct future medical planning for these events. METHODS: We related medical encounter data from nineteen 10-km road races to runner, race, and environmental characteristics. We quantified the most commonly used resources and described the disposition of runners in these encounters. RESULTS: Across the 19 races and 90,265 finishers, there were 562 medical events for a cumulative incidence of 6.2 events per 1000 finishers (95% confidence interval, 5.7-6.8). Race size was associated with an increased incidence of medical events. Overall, the most common diagnosis was heat-related illness (1.6 per 1000 finishers), followed by musculoskeletal complaints (1.3 per 1000 finishers) and fluid-electrolyte imbalances (1.2 per 1000 finishers). For all diagnoses, runners with finishing times in the first performance quintile and in the fifth performance quintile had greater representation in the medical tent than mid-pack runners. Most runners were treated with supportive care, basic first aid, and oral rehydration. Ninety-four runners (1.0 per 1000 finishers) required ice water immersion for exertional heat stroke. There were low rates of hospital transport (0.2 per 1000 finishers), and no fatalities. CONCLUSIONS: In 10-km road races, injury rates are low compared with longer races in similar weather conditions. Common medical issues can be managed with basic resources in the on-site medical tent. Green flag start race conditions may not predict race safety with regard to exertional heat stroke risk. There were no deaths in nearly 100,000 finishers.

Downregulation of key early events in the mobilization of antigen-bearing dendritic cells by leukocyte immunoglobulin-like Receptor B4 in a mouse model of allergic pulmonary inflammation.

Leukocyte Immunoglobulin-like Receptor B4 (LILRB4) null mice have an exacerbated T helper cell type 2 (Th2) immune response and pulmonary inflammation compared with Lilrb4(+/+) animals when sensitized intranasally with ovalbumin (OVA) and low-dose lipopolysaccharide (LPS) followed by challenge with OVA. Moreover, OVA-challenged Lilrb4(-/-) mice exhibit greater migration of antigen (Ag)-bearing dendritic cells (DCs) to lymph nodes and accumulation of interleukin 4- and interleukin 5-producing lymph node lymphocytes. The main objective of this study was to determine how the absence of LILRB4 leads to a greater number of DCs in the lymph nodes of Ag-challenged mice and increased lung Th2 inflammation. Mice were sensitized intranasally with PBS alone or containing OVA and LPS; additional cohorts were subsequently challenged with OVA. Expression of chemokine (C-C motif) ligand 21 (CCL21) in the lung was assessed immunohistologically. OVA ingestion and expression of LILRB4 and chemokine (C-C motif) receptor 7 (CCR7) were quantified by flow cytometry. Inhalation of OVA and LPS induced upregulation of LILRB4 selectively on lung Ag-bearing DCs. After sensitization and challenge, the lung lymphatic vessels of Lilrb4(-/-) mice expressed more CCL21, a chemokine that directs the migration of DCs from peripheral tissue to draining lymph nodes, compared with Lilrb4(+/+) mice. In addition, lung DCs of challenged Lilrb4(-/-) mice expressed more CCR7, the CCL21 receptor. The lungs of challenged Lilrb4(-/-) mice also contained significantly greater numbers of CD4+ cells expressing interleukin-4 or interleukin-5, consistent with the greater number of Ag-bearing DCs and Th2 cells in lymph nodes and the attendant exacerbated Th2 lung pathology. Our data establish a new mechanism by which LILRB4 can downregulate the development of pathologic allergic inflammation: reduced upregulation of key molecules needed for DC migration leading to decreases in Th2 cells in lymph nodes and their target tissue.

Inhibition of Th2 adaptive immune responses and pulmonary inflammation by leukocyte Ig-like receptor B4 on dendritic cells.

We previously established that the inhibitory receptor LILRB4 mitigates LPS-induced, neutrophil-dependent pathologic effector mechanisms in inflammation. We now report that LILRB4 on dendritic cells (DCs) counterregulates development of an adaptive Th2 immune response and ensuing inflammation in a model of allergic pulmonary inflammation, initiated by inhalation sensitization with OVA and LPS followed by airway challenge with OVA. We found that Lilrb4(-/-) mice had significantly exacerbated eosinophilic pulmonary inflammation, as assessed in bronchoalveolar lavage and lung tissue, as well as elevated levels of OVA-specific IgE and Th2 cytokines produced by OVA-restimulated lymph node cells. LILRB4 was preferentially expressed on MHC class II(high)CD86(high) OVA-bearing DCs in lung-draining lymph nodes after sensitization or challenge. Moreover, the lymph nodes of Lilrb4(-/-) mice had significantly more of these mature DCs after challenge with OVA, which was accompanied by significantly more IL-4-producing lymphocytes, compared with Lilrb4(+/+) mice. Sensitization of naive Lilrb4(+/+) mice by transfer of OVA-LPS-pulsed Lilrb4(-/-) bone marrow-derived DCs was sufficient to confer exacerbated allergic lung pathology upon challenge with OVA, compared with mice that received Lilrb4(+/+) bone marrow-derived DCs. Our findings establish that maturation and migration of pulmonary DCs to lymph nodes in response to Ag and an innate immune stimulus is associated with upregulated expression of LILRB4. In addition, this receptor attenuates the number of these mature DCs and attendant IL-4-producing lymphocytes in the lymph nodes, and accordingly, the ability of DCs to elicit pathologic Th2 pulmonary inflammation.

Acetylsalicylic acid and montelukast block mast cell mediator-related symptoms during rapid desensitization.

BACKGROUND: Rapid desensitization is a process in which drug-allergic patients receive their target dose in incremental steps, resulting in a state of temporary tolerization. In this manner, first-line therapy can be delivered safely, even in patients who present with severe hypersensitivity reactions (HSRs) to the given agent. A small subset of patients has persistent HSRs during rapid desensitization that can be refractory to antihistamines and corticosteroids. OBJECTIVE: To increase the safety and tolerability of rapid desensitization by prostaglandin and leukotriene blockade in patients with refractory mast cell mediator-related symptoms. METHODS: Fourteen adult patients developed HSRs to platinum chemotherapy that persisted during rapid desensitization. All patients had cutaneous symptoms (flushing, pruritus, or urticaria), many with associated systemic reactions. These patients were then pretreated with acetylsalicylic acid, 325 mg orally, and montelukast, 10 mg orally, 2 days before and on the day of desensitization. Response to subsequent desensitizations was assessed by medical record review and was compared with a group of matched historic control patients who received methylprednisolone for HSRs during desensitization. RESULTS: Seventy-eight desensitizations in 14 patients were performed. Using acetylsalicylic acid and montelukast, 86% of patients (12/14) experienced substantial improvement in symptoms (grade 0.5 vs grade 2.14, P < .0001). Reduction in symptoms during desensitization was also significantly greater than that experienced by historic control patients who received methylprednisolone pretreatment (grade 0.5 vs grade 1.75, P = .0008). All patients received their target dose of chemotherapy, and there were no severe systemic HSRs. CONCLUSIONS: Pretreatment with acetylsalicylic acid and montelukast lessens the severity of HSRs during rapid desensitization.