Cervical Collars and Dysphagia Among Geriatric TBIs and Cervical Spine Injuries: A Retrospective Cohort Study.

INTRODUCTION: Dysphagia, a complication of traumatic brain injuries (TBIs), can lead to death. Cervical collar (c-collar) restriction may increase the risk for dysphagia. The objective was to determine how c-collars affect dysphagia rates. METHODS: This retrospective cohort study included geriatric TBIs or cervical spine injuries (January 2016 to December 2018) at a Level 1 trauma center. Outcomes (dysphagia, aspiration, and respiratory failure) were compared by c-collar placement. RESULTS: There were 684 patients: 21.5% had a c-collar and 78.5% did not. Demographics, injury severity score, and Glasgow Coma Scale were comparable. Dysphagia (53.7% vs. 39.3%, p = .002) and respiratory failure (17.0% vs. 6.9%, p = .0002) were more common among patients with c-collars. Aspiration rates ( p = .11) were similar. After adjustment, patients with a c-collar had a significantly higher odds of dysphagia and respiratory failure. Among patients who did not receive swallow therapy, aspiration ( p = .02) and respiratory failure ( p < .0001) were more common for those with c-collars. CONCLUSIONS: C-collar placement increased the risk for dysphagia and respiratory failure. There was evidence that swallow therapy may modify the effect of c-collar placement. For patients who did not receive swallow therapy, aspiration was more common among those with a c-collar. Dysphagia screening among patients with a c-collar may improve patient quality.

Cell death after traumatic brain injury: Detrimental role of anoikis in healing.

Within the first few hours of a traumatic brain injury, the activity of extracellular matrix degradative enzymes increases. As a result, the blood brain barrier becomes disrupted as secondary white matter injury increases. Anoikis, a form of apoptosis, results from cells detaching from the extracellular matrix leading to cell death. This "homelessness" (anoikis) of cells hinders recovery progression, exacerbating brain injury while disrupting synaptic plasticity and other central nervous system functions. Here, we discuss the current knowledge of molecular pathways and proteins involved in both the activation and inhibition of anoikis.