Total admissions and hospital charges for PE have increased over the past two decades. However, the population-adjusted admission rate has increased disproportionately to the incidence of patients with severe PE. We hypothesize that these findings reflect a concerning national movement toward more admissions of less severe PE.

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Background Although historical trends before 1998 demonstrated improvements in mortality caused by pulmonary embolism (PE), contemporary estimates of mortality trends are unknown. Therefore, our objective is to describe trends in death rates caused by PE in the United States, overall and by sex‐race, regional, and age subgroups. Methods and Results We used nationwide death certificate data from Centers for Disease Control and Prevention Wide‐Ranging Online Data for Epidemiologic Research to calculate age‐adjusted mortality rates for PE as underlying cause of death from 1999 to 2018. We used the Joinpoint regression program to examine statistical trends and average annual percent change. Trends in PE mortality rates reversed after an inflection point in 2008, with an average annual percent change before 2008 of −4.4% (−5.7, −3.0, P <0.001), indicating reduction in age‐adjusted mortality rates of 4.4% per year between 1999 and 2008, versus average annual percent change after 2008 of +0.6% (0.2, 0.9, P <0.001). Black men and women had approximately 2‐fold higher age‐adjusted mortality rates compared with White men and women, respectively, before and after the inflection point. Similar trends were seen in geographical regions. Age‐adjusted mortality rates for younger adults (25–64 years) increased during the study period (average annual percent change 2.1% [1.6, 2.6]) and remained stable for older adults (>65 years). Conclusions Our study findings demonstrate that PE mortality has increased over the past decade and racial and geographic disparities persist. Identifying the underlying drivers of these changing mortality trends and persistently observed disparities is necessary to mitigate the burden of PE‐related mortality, particularly premature preventable PE deaths among younger adults (<65 years).

This study evaluates the structural and biochemical alterations of the elbow capsule after trauma through microscopy and immunohistochemistry. We compared capsules from 37 patients undergoing surgery for elbow contracture with normal capsules from 7 donors. Contracture capsules were significantly thicker than control capsules (P < .05) and exhibited extensive disorganization of collagen fiber bundle arrangement. Levels of specific cytokines involved in connective tissue turnover were measured. The results showed that the levels of cytokines matrix metalloproteinase (MMP) 1, MMP-2, and MMP-3 were greater as compared with control capsules (P < .05). This was associated with collagen disorganization, fibroblast infiltration, and in some specimens, lymphocytic infiltration in the capsular tissue. In contracture specimens, there was a localization of tissue inhibitor of matrix metalloproteinase 2 staining only in the vicinity of the synovial membrane and in blood vessels. Immunohistochemistry for type III collagen showed a greater presence in the control capsules compared with contracture capsules. This study demonstrates pathologic thickening, disorganization of the collagen fiber arrangement, and involvement of cytokines in the pathology of post-traumatic contracture of the elbow.