15 research outputs found

    Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

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    Funder: European Society of Intensive Care Medicine; doi: http://dx.doi.org/10.13039/501100013347Funder: Flemish Society for Critical Care NursesAbstract: Purpose: Intensive care unit (ICU) patients are particularly susceptible to developing pressure injuries. Epidemiologic data is however unavailable. We aimed to provide an international picture of the extent of pressure injuries and factors associated with ICU-acquired pressure injuries in adult ICU patients. Methods: International 1-day point-prevalence study; follow-up for outcome assessment until hospital discharge (maximum 12 weeks). Factors associated with ICU-acquired pressure injury and hospital mortality were assessed by generalised linear mixed-effects regression analysis. Results: Data from 13,254 patients in 1117 ICUs (90 countries) revealed 6747 pressure injuries; 3997 (59.2%) were ICU-acquired. Overall prevalence was 26.6% (95% confidence interval [CI] 25.9–27.3). ICU-acquired prevalence was 16.2% (95% CI 15.6–16.8). Sacrum (37%) and heels (19.5%) were most affected. Factors independently associated with ICU-acquired pressure injuries were older age, male sex, being underweight, emergency surgery, higher Simplified Acute Physiology Score II, Braden score 3 days, comorbidities (chronic obstructive pulmonary disease, immunodeficiency), organ support (renal replacement, mechanical ventilation on ICU admission), and being in a low or lower-middle income-economy. Gradually increasing associations with mortality were identified for increasing severity of pressure injury: stage I (odds ratio [OR] 1.5; 95% CI 1.2–1.8), stage II (OR 1.6; 95% CI 1.4–1.9), and stage III or worse (OR 2.8; 95% CI 2.3–3.3). Conclusion: Pressure injuries are common in adult ICU patients. ICU-acquired pressure injuries are associated with mainly intrinsic factors and mortality. Optimal care standards, increased awareness, appropriate resource allocation, and further research into optimal prevention are pivotal to tackle this important patient safety threat

    Irradiation and contractions evoked by carbachol, ATP and K<sup>+</sup>.

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    <p>(A) Representative carbachol (1μM) contractions in non-irradiated (blue) and 20Gy-irradiated (red), intact or mucosa-free bladder strips. Summary bar chart (mean ± SD) of force integral (AUC) showing that radiation did not affect carbachol-contractions in intact or mucosa-free strips. Interestingly, in irradiated strips, the mucosal layer apparently suppressed carbachol-contractions. * denotes P<0.05, unpaired <i>t</i>-test. Intact: non-irradiated, N = 17, n = 25; irradiated, N = 17, n = 23. Mucosa-free: non-irradiated, N = 7, n = 13; irradiated, N = 7, n = 13. (B) Representative ATP (5mM) contractions. Summary AUC bar chart shows ATP-contractions were unaffected by irradiation in intact or mucosa-free bladder strips. In irradiated strips, the mucosal layer apparently suppressed contractions (P<0.001). ***denotes P<0.001. Unpaired <i>t</i>-test. Intact: non-irradiated, N = 13, n = 19; irradiated, N = 13, n = 17. Mucosa-free: non-irradiated, N = 6, n = 12; irradiated, N = 6, n = 12. (C) Representative 60mM K<sup>+</sup> contractions. Summary AUC bar chart shows these contractions were unaffected by irradiation in intact or mucosa-free strips. In contrast to carbachol and ATP, the mucosal layer had no impact on 60mM K<sup>+</sup> contractions. Intact: non-irradiated, N = 12, n = 15; irradiated, N = 12, n = 15. Mucosa-free: non-irradiated, N = 5, n = 9; irradiated, N = 5, n = 9.</p

    Comparison of cholinergic, purinergic and residual neurogenic contractions in non-irradiated and irradiated bladder strips.

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    <p>(A) Traces of neurogenic contractions (16Hz) on an expanded timescale from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0193923#pone.0193923.g001" target="_blank">Fig 1</a> showing cholinergic, purinergic and residual components. Control (Con), atropine (Atr), Atr/PPADs (atropine and PPADs present). (B) Cholinergic, purinergic and residual components of neurogenic contractions were calculated from atropine-sensitive, PPADs-sensitive and atropine/PPADs-resistant neurogenic contractions in irradiated and non-irradiated, intact and mucosa-free bladder strips. The purinergic component of neurogenic contractions was reduced in irradiated intact strips, compared to non-irradiated (P<0.05). * denotes P<0.05. (C) Bar charts from data in Figs <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0193923#pone.0193923.g001" target="_blank">1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0193923#pone.0193923.g002" target="_blank">2</a> showing that absence of the mucosal layer <i>per se</i> had no significant effect on the amplitude of neurogenic contractions in control tissues (P = 0.54, 2-way ANOVA with Bonferroni post-hoc test). Similar findings were obtained with irradiated tissues (P = 0.59).</p

    Neurogenic contractions in mucosa-free strips are not affected by irradiation.

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    <p>(A) Original traces of EFS-evoked neurogenic contractions in non-irradiated controls (blue) and 20Gy irradiated mucosa-free strips (red). Atropine (1μM) reduced neurogenic contractions at all frequencies and subsequent addition of PPADs (100μM) caused further reduction. (B) Summary graphs (mean ± SD) showing that neurogenic contractions in irradiated strips (N = 6, n = 12) were not different than non-irradiated controls (N = 6, n = 12) across the force-frequency range (P = 0.59) and at each frequency tested (post-hoc test). Atropine (N = 6, n = 12) and subsequent addition of PPADs (N = 6, n = 12) affected both non-irradiated and irradiated strips similarly 2-way repeated measures ANOVA, Bonferroni post-hoc test. * denotes P<0.05.</p

    Spontaneous activity and <i>ex-vivo</i> irradiation.

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    <p>(A) Representative traces of spontaneous activity from non-irradiated (blue) and irradiated (red) bladder strips which were either intact, or mucosa-free. (B) AUC (mean ± SD) of spontaneous activity (g.min) was unaffected by irradiation (20Gy) (blue vs. red) in intact or mucosa-free bladder strips. The intact mucosal layer enhanced activity in non-irradiated strips (P<0.05, unpaired <i>t</i>-test) however this effect was lost in irradiated strips. * denotes P<0.05. (C) Irradiation did not affect the amplitude (mean ± SD) of spontaneous contractions in intact or mucosa-free bladder strips. The amplitude of contractions was also similar between intact and mucosa-free, non-irradiated and irradiated strips. (D) The frequency (mean ± SD) of spontaneous contractions was similar in all bladder strips. * denotes P<0.05. Intact: non-irradiated, N = 17, n = 25; irradiated, N = 17, n = 25. Mucosa-free: non-irradiated, N = 7, n = 13; irradiated, N = 7, n = 13.</p

    Neurogenic contractions in intact strips are reduced by irradiation.

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    <p>(A) Original traces of EFS-evoked neurogenic contractions in non-irradiated controls (blue) and 20Gy irradiated intact strips (red). Atropine (1μM) reduced neurogenic contractions at all frequencies and subsequent addition of PPADs (100μM) caused further reduction. (B) Summary graphs (mean ± SD) showing that neurogenic contractions in irradiated strips (N = 12, n = 19) were significantly smaller than non-irradiated controls across the force-frequency range (P = 0.02, N = 12, n = 18) and at 8Hz and 16Hz (P<0.05, post-hoc test). Atropine did not affect the radiation-induced significant difference seen between non-irradiated (N = 9, n = 13) and irradiated strips (N = 9, n = 14). PPADs eliminated the radiation-induced effect at 8Hz and 16Hz (N = 9, n = 13; N = 9, n = 14). ** denotes P<0.01 vs. non-irradiated, 2-way repeated measures ANOVA, Bonferroni post-hoc test.</p

    Acute spinal cord injury is associated with mitochondrial dysfunction in mouse urothelium

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    AIM To characterize the effects of acute spinal cord injury (SCI) on mitochondrial morphology and function in bladder urothelium and to test the therapeutic efficacy of early treatment with the mitochondrially targeted antioxidant, MitoTempo. METHODS We used a mouse model of acute SCI by spinal cord transection between the T8-T9 vertebrae with or without MitoTempo delivery at the time of injury followed by tissue processing at 3 days after SCI. Control, SCI, and SCI-MitoTempo-treated mice were compared in all experimental conditions. Assessments included analysis of markers of mitochondrial health including accumulation of reactive oxygen species (ROS), morphological changes in the ultrastructure of mitochondria by transmission electron microscopy, and Western blot analysis to quantify protein levels of markers for autophagy and altered mitochondrial dynamics. RESULTS SCI resulted in an increase in oxidative stress markers and ROS production, confirming mitochondrial dysfunction. Mitochondria from SCI mice developed large electron-dense inclusions and these aberrant mitochondria accumulated throughout the cytoplasm suggesting an inability to clear dysfunctional mitochondria by mitophagy. SCI mice also exhibited elevated levels of dynamin-related protein 1 (DRP1), consistent with a disruption of mitochondrial dynamics. Remarkably, treatment with MitoTempo reversed many of the SCI-induced abnormalities that we observed. CONCLUSIONS Acute SCI negatively and severely affects mitochondrial health of bladder urothelium. Early treatment of SCI with MitoTempo may be a viable therapeutic agent to mitigate these deleterious effects
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