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Abstract Background Blunt cerebrovascular injuries (BCVI) are generally associated with high-energy injury mechanisms. Less is known regarding lower-energy injuries in elderly patients. We sought to determine the incidence of BCVI and characterize current BCVI screening practices and associated complications in elderly ground-level fall patients (EGLF, ≥ 65 years). We hypothesized that BCVI in EGLF patients would be clinically significant and screening would be less common. Methods A retrospective study was performed utilizing the National Trauma Data Bank (NTDB, 2007–2014) and single institutional data. BCVI risk factors and diagnosis were determined by ICD-9 codes. Presenting patient characteristics and clinical course were obtained by chart review. The NTDB dataset was used to determine the incidence of BCVI, risk factors for BCVI, and outcomes in the EGLF cohort. Local chart review focused on screening rates and complications. Results The incidence of BCVI in EGLF patients was 0.15% overall and 0.86% in those with at least one BCVI risk factor in the NTDB. Upper cervical spine fractures were the most common risk factor for BCVI in EGLF patients. In EGLF patients, the diagnosis of BCVI was an independent risk factor for mortality (OR1.8, 95% C.I. 1.5–2.1). The local institutional data (2007–2014) had a BCVI incidence of 0.37% (n = 6487) and 1.47% in those with at least one risk factor (n = 1429). EGLF patients with a risk factor for BCVI had a very low rate of screening (44%). Only 8% of EGLF patients not screened had documented contraindications. The incidence of renal injury was 9% irrespective of BCVI screening. Conclusions The incidence of BCVI is clinically significant in EGLF patients and an independent predictor of mortality. Screening is less common in EGLF patients despite few contraindications. This data suggests that using age and injury mechanism to omit BCVI screening in EGLF patients may exclude an at-risk population. Trial registration IRB approval number: PRO15020269. Retrospective trial not registered

Alterations in genes encoding for proteins that control fucosylation are known to play causative roles in several developmental disorders, such as Dowling-Degos disease 2 and congenital disorder of glycosylation type IIc (CDGIIc). Recent studies have provided evidence that changes in fucosylation can contribute to the development and progression of several different types of cancers. It is therefore important to gain a detailed understanding of how fucosylation is altered in disease states so that interventions may be developed for therapeutic purposes. In this report, we find that fucosylation occurs on many intracellular proteins. This is an interesting finding, as the fucosylation machinery is restricted to the secretory pathway and is thought to predominately affect cell-membrane-bound and secreted proteins. We find that Ribosomal protein S3 (RPS3) is fucosylated in normal tissues and in cancer cells, and that the extent of its fucosylation appears to respond to stress, including MAPK inhibitors, suggesting a new role in posttranslational protein function. Our data identify a new ribosome-independent species of fucosylated RPS3 that interacts with proteins involved in posttranscriptional regulation of RNA, such as Heterogeneous nuclear ribonucleoprotein U (HNRNPU), as well as with a predominance of non-coding RNAs. These data highlight a novel role for RPS3, which, given previously reported oncogenic roles for RPS3, might represent functions that are perturbed in pathologies such as cancer. Together, our findings suggest a previously unrecognized role for fucosylation in directly influencing intracellular protein functions.