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OBJECTIVE: To retrospectively assess the prevalence of secondary overtriage (SO) within a rural regional Appalachian health care system. METHODS: Trauma registry data was extracted for all trauma activation transfer patients from 2017 to 2022. Transferred patients were then stratified into two groups, non-secondary overtriage (non-SO) or SO. Patients were considered SO if they met three criteria following transfer: an Injury Severity Score (ISS) of less than 15, no required operative intervention, and discharge within 48 hours of arrival. Descriptive statistics were compared for age, length of stay (LOS), ICU LOS, and ISS. Surgical subspecialty consultations were compared between the two groups. Patients in the SO group were further assessed by body region of injury and Abbreviated Injury Score (AIS). RESULTS: Among 3,291 trauma activation transfer patients, 43% (1,407) were considered SO transfers. Patients in the SO group were significantly younger, had shorter average hospital and ICU LOS, and lower ISS compared to the non-SO group. Additionally, 25.7% of patients in the SO group had injuries to the head or neck of which 8.96% have an AIS ≥3. 21% of patients had injuries to the face, with 0.14% having an AIS ≥3. CONCLUSIONS: 43% of transfer patients in this study met our definition of SO. Although no optimal rate of SO has been universally established, limiting SO stands to benefit both patients and trauma systems. This study highlights how institutional analysis of transfer patients may help inform transfer protocols to reduce secondary overtriage and overutilization of scarce resources.
RESUMO
BACKGROUND: 1p36 deletion syndrome can predispose to pediatric-onset cardiomyopathy. Deletion breakpoints are variable and may delete the transcription factor PRDM16. Early studies suggest that deletion of PRDM16 may underlie cardiomyopathy in patients with 1p36 deletion; however, the prognostic impact of PRDM16 loss is unknown. METHODS: This retrospective cohort included subjects with 1p36 deletion syndrome from 4 hospitals. Prevalence of cardiomyopathy and freedom from death, cardiac transplantation, or ventricular assist device were analyzed. A systematic review cohort was derived for further analysis. A cardiac-specific Prdm16 knockout mouse (Prdm16 conditional knockout) was generated. Echocardiography was performed at 4 and 6 to 7 months. Histology staining and qPCR were performed at 7 months to assess fibrosis. RESULTS: The retrospective cohort included 71 patients. Among individuals with PRDM16 deleted, 34.5% developed cardiomyopathy versus 7.7% of individuals with PRDM16 not deleted (P=0.1). In the combined retrospective and systematic review cohort (n=134), PRDM16 deletion-associated cardiomyopathy risk was recapitulated and significant (29.1% versus 10.8%, P=0.03). PRDM16 deletion was associated with increased risk of death, cardiac transplant, or ventricular assist device (P=0.04). Among those PRDM16 deleted, 34.5% of females developed cardiomyopathy versus 16.7% of their male counterparts (P=0.2). We find sex-specific differences in the incidence and the severity of contractile dysfunction and fibrosis in female Prdm16 conditional knockout mice. Further, female Prdm16 conditional knockout mice demonstrate significantly elevated risk of mortality (P=0.0003). CONCLUSIONS: PRDM16 deletion is associated with a significantly increased risk of cardiomyopathy and cardiac mortality. Prdm16 conditional knockout mice develop cardiomyopathy in a sex-biased way. Patients with PRDM16 deletion should be assessed for cardiac disease.