Depicting occupational trauma concepts impacting nurse well-being during the COVID-19 pandemic.

PURPOSE: The purpose of this concept delineation was to differentiate similar concepts impacting nurse well-being during the COVID-19 pandemic, including: compassion fatigue, burnout, moral injury, secondary traumatic stress, and second victim. METHODS: A total of 63 articles were reviewed for concept delineation. Morse's (1995) approach to concept delineation was utilized to analyse the articles. RESULTS: Concepts were described interchangeably but were found to present themselves in a sequence. A nurse may experience moral injury, leading to a second victim experience, synonymous with secondary traumatic stress, then compassion fatigue and/or burnout that can be acute or chronic in nature. An Occupational Trauma Conceptual Model was created to depict how these concepts interact based on concept delineation findings. CONCLUSION: Nurses are experiencing long-lasting occupational trauma and future intervention research should centre on optimizing nurse well-being to ensure the sustainability of nursing profession.

Matrix Metalloproteinase 9 and Osteopontin Interact to Support Synaptogenesis in the Olfactory Bulb after Mild Traumatic Brain Injury.

Olfactory receptor axons reinnervate the olfactory bulb (OB) after chemical or transection lesion. Diffuse brain injury damages the same axons, but the time course and regulators of OB reinnervation are unknown. Gelatinases (matrix metalloproteinase [MMP]2, MMP9) and their substrate osteopontin (OPN) are candidate mediators of synaptogenesis after central nervous system (CNS) insult, including olfactory axon damage. Here, we examined the time course of MMP9, OPN, and OPN receptor CD44 response to diffuse OB injury. FVBV/NJ mice received mild midline fluid percussion insult (mFPI), after which MMP9 activity and both OPN and CD44 protein expression were measured. Diffuse mFPI induced time-dependent increase in OB MMP9 activity and elevated the cell signaling 48-kD OPN fragment. This response was bimodal at 1 and 7 days post-injury. MMP9 activity was also correlated with 7-day reduction in a second 32-kD OPN peptide. CD44 increase peaked at 3 days, delayed relative to MMP9/OPN response. MMP9 and OPN immunohistochemistry suggested that deafferented tufted and mitral neurons were the principal sites for these molecular interactions. Analysis of injured MMP9 knockout (KO) mice showed that 48-kD OPN production was dependent on OB MMP9 activity, but with no KO effect on CD44 induction. Olfactory marker protein (OMP), used to identify injured olfactory axons, revealed persistent axon damage in the absence of MMP9. MMP9 KO ultrastructure at 21 days post-injury indicated that persistent OMP reduction was paired with delayed removal of degenerated axons. These results provide evidence that diffuse, concussive brain trauma induces a post-injury interaction between MMP9, OPN, and CD44, which mediates synaptic plasticity and reinnervation within the OB.

Mild Fluid Percussion Injury Induces Diffuse Axonal Damage and Reactive Synaptic Plasticity in the Mouse Olfactory Bulb.

Despite the regenerative capacity of the olfactory bulb (OB), head trauma causes olfactory disturbances in up to 30% of patients. While models of olfactory nerve transection, olfactory receptor neuron (ORN) ablation, or direct OB impact have been used to examine OB recovery, these models are severe and not ideal for study of OB synaptic repair. We posited that a mild fluid percussion brain injury (mFPI), delivered over mid-dorsal cortex, would produce diffuse OB deafferentation without confounding pathology. Wild type FVB/NJ mice were subjected to mFPI and OB probed for ORN axon degeneration and onset of reactive synaptogenesis. OB extracts revealed 3 d postinjury elevation of calpain-cleaved 150-kDa αII-spectrin, an indicator of axon damage, in tandem with reduced olfactory marker protein (OMP), a protein specific to intact ORN axons. Moreover, mFPI also produced a 3-d peak in GFAP+ astrocyte and IBA1+ microglial reactivity, consistent with postinjury inflammation. OB glomeruli showed disorganized ORN axons, presynaptic degeneration, and glial phagocytosis at 3 and 7 d postinjury, all indicative of deafferentation. At 21 d after mFPI, normal synaptic structure re-emerged along with OMP recovery, supporting ORN afferent reinnervation. Robust 21 d postinjury upregulation of GAP-43 was consistent with the time course of ORN axon sprouting and synapse regeneration reported after more severe olfactory insult. Together, these findings define a cycle of synaptic degeneration and recovery at a site remote to non-contusive brain injury. We show that mFPI models diffuse ORN axon damage, useful for the study of time-dependent reactive synaptogenesis in the deafferented OB.

A two institution experience with 226 endoscopically placed jejunal feeding tubes in critically ill surgical patients.

BACKGROUND: Early jejunal feeding after surgery or trauma reduces infectious complications. Although not ideal gastric and postpyloric feedings are often used, however, because of difficulty in placing feeding tubes distal to the ligament of Treitz (LOT). Our hypothesis was that feeding tube placement distal to the LOT can be accomplished using a bedside transendoscopic technique. METHODS: Transendoscopic jejunal (TEJ) tube placement and TEJ tubes inserted simultaneously through percutaneous gastrostomy (PEG) tubes (PEG/TEJ) were attempted to be placed distal to the LOT. RESULTS: In all, 226 feeding tubes (185 TEJ, 41 PEG/TEJ) were placed in 179 trauma and 47 nontrauma patients over 3 years (August 20, 1998 to July 15, 2001). Tube location was jejunal in 93.8% of trauma patients, 76.6% of nontrauma patients, and 90.3% of all patients. (Confidence intervals were 89.3% to 96.5%, 62.8% to 86.4%, and 85.7% to 93.5%). Days of total parenteral nutrition were reduced 71.3% in trauma patients, 22.8% in nontrauma patients, and 45% overall at one institution. CONCLUSIONS: Bedside TEJ and PEG/TEJ placement is safe and successful in placing feeding tubes distal to the LOT in more than 90% of critically ill surgical patients.