Bone fractures create five problems that must be resolved: bleeding, risk of infection, hypoxia, disproportionate strain, and inability to bear weight. There have been enormous advancements in our understanding of the molecular mechanisms that resolve these problems after fractures, and in best clinical practices of repairing fractures. We put forth a modern, comprehensive model of fracture repair that synthesizes the literature on the biology and biomechanics of fracture repair to address the primary problems of fractures. This updated model is a framework for both fracture management and future studies aimed at understanding and treating this complex process. This model is based upon the fracture acute phase response (APR), which encompasses the molecular mechanisms that respond to injury. The APR is divided into sequential stages of “survival” and “repair.” Early in convalescence, during “survival,” bleeding and infection are resolved by collaborative efforts of the hemostatic and inflammatory pathways. Later, in “repair,” avascular and biomechanically insufficient bone is replaced by a variable combination of intramembranous and endochondral ossification. Progression to repair cannot occur until survival has been ensured. A disproportionate APR—either insufficient or exuberant—leads to complications of survival (hemorrhage, thrombosis, systemic inflammatory response syndrome, infection, death) and/or repair (delayed- or non-union). The type of ossification utilized for fracture repair is dependent on the relative amounts of strain and vascularity in the fracture microenvironment, but any failure along this process can disrupt or delay fracture healing and result in a similar non-union. Therefore, incomplete understanding of the principles herein can result in mismanagement of fracture care or application of hardware that interferes with fracture repair. This unifying model of fracture repair not only informs clinicians how their interventions fit within the framework of normal biological healing but also instructs investigators about the critical variables and outputs to assess during a study of fracture repair.

➤ Necrotizing fasciitis hijacks the acute phase response, increasing the risk of developing pathophysiologic states commonly associated with death: sepsis-induced coagulopathy (SIC), systemic inflammatory response syndrome (SIRS), and adrenal insufficiency, referred to as critical illness-related corticosteroid insufficiency (CIRCI).➤ Dynamic monitoring of SIC, SIRS, and CIRCI may be informative when assessing infection severity and when directing treatment to manage these conditions as soon as they begin to develop.➤ To reduce the risk of oropharyngeal colonization, N95 respirators should be worn by health-care professionals who are operating on patients with necrotizing fasciitis.

Objectives: To explore the effect of intramedullary pin size on the biology of a healing fracture, specifically endochondral angiogenesis. We hypothesized that fracture fixation with a smaller pin would permit greater interfragmentary strain resulting in increased total amount of vascular endothelial growth factor within the callus and greater angiogenesis compared to fixation with a larger pin. Methods: Transverse mid-shaft femur fractures in 8-week-old mice were fixed with either a 23-gauge (G) or 30-G pin. Differences in interfragmentary strain at the fracture site were estimated between cohorts. A combination of histology, gene expression, serial radiography, and microcomputed tomography with and without vascular contrast agent were used to assess fracture healing and vascularity for each cohort. Results: Larger soft-tissue callus formation increased vascular endothelial growth factor—A expression, and a corresponding increase in vascular volume was observed in the higher strain, 30-G cohort. Radiographic analysis demonstrated earlier hard callus formation with greater initial interfragmentary strain, similar rates of union between pin size cohorts, yet delayed callus remodeling in mice with the larger pin size. Conclusions: These findings suggest that the stability conferred by an intramedullary nail influences endochondral angiogenesis at the fracture.

Objectives: To ascertain the incidence of hip fractures in Ecuador in 2016, to determine whether there were variations according to geographic region, residence or season of the year. Materials and methods: Epidemiological, descriptive and retrospective study. The Hospital Discharges Yearbook of Ecuador was used to determine the number of people aged 60 or more hospitalized for hip fracture from January 1 to December 31, 2016. To calculate the incidence per 100,000 inhabitants/year, the Ecuadorian population projection of the Economic Commission for Latin America and the Caribbean (CEPAL) was used as a denominator for the year 2016. The incidence standardized by age was calculated by the direct method using 2 reference populations: 1) the one of 60 or more years for America Latina made by the Latin American and Caribbean Demographic Center (CELADE) in 2016; 2) with the population of Ecuador in 2010. Results: In total, 2,054 people were hospitalized with hip fracture diagnosis (1,470 women and 584 men) in 2016. The crude annual incidence was 123 cases per 100,000 inhabitants/year (74.6 per 100,000 men/year and 165.8 per 100,000 women/year). The age-adjusted incidence increased exponentially with age in both sexes. It was greater in women. The standardized incidence with with the population of Latin America was 165.4 and 80.1 per 100,000/year, in women and men respectively. In-hospital mortality was 5.1% and 3.8% in women and men, respectively. Conclusions: The incidence of hip fractures is greater in women than in men, there being an exponential increase with age, more evident after 80 years. There were no differences by geographical region. In comparison with developed countries and other Latin America countries, incidence of hip fractures was lowest in Ecuador.