ABSTRACT
BACKGROUND: Factors influencing the quality of end-of-life communication are relevant to improving end-of-life care. We assessed the quality of end-of-life communication and influencing factors in 2 intensive care unit (ICU) cohorts at high risk of death: patients living in nursing homes and those on extracorporeal membrane oxygenation (ECMO). METHODS: This retrospective cohort study included admissions to 4 ICUs in Winnipeg, Manitoba, from 2000 to 2017. We identified cohorts and influencing factors from the Winnipeg ICU database and by manual chart review. We assessed quality of end-of-life communication using 18 validated, binary quality indicators to calculate a weighted, scaled, composite score (range 0-100). We used median regression to identify factors associated with the composite score. RESULTS: The ECMO cohort (n = 109) was younger than the nursing home cohort (n = 230), with longer hospital stays and higher disease severity. Mean composite scores of end-of-life communication were extremely low in both cohorts (mean 48.5 [standard error of the mean (SEM) 1.7] for the nursing home cohort, 49.1 [SEM 2.5] for the ECMO cohort). Patient characteristics associated with higher median composite scores were older age (5.0 per decade, 95% confidence interval [CI] 2.1-7.8) and lower (worse) Glasgow Coma Scale (GCS) scores (1.8 per GCS point, 95% CI 0.5-3.2). The median composite score rose significantly over time (1.7 per year, 95% CI 0.5-2.8). INTERPRETATION: The quality of end-of-life communication in ICUs is poor, and factors associated with better prognosis are also associated with worse communication. Direct and early communication should occur with all patients in the ICU and their surrogates, not just those who are believed most likely to die.
Subject(s)
Communication Barriers , Critical Illness , Death , Professional-Patient Relations/ethics , Quality of Life , Terminal Care , Truth Disclosure/ethics , Advance Care Planning/ethics , Aged , Canada/epidemiology , Critical Illness/mortality , Critical Illness/psychology , Extracorporeal Membrane Oxygenation/methods , Extracorporeal Membrane Oxygenation/mortality , Extracorporeal Membrane Oxygenation/psychology , Female , Humans , Intensive Care Units/ethics , Intensive Care Units/standards , Intensive Care Units/statistics & numerical data , Male , Middle Aged , Nursing Homes/ethics , Nursing Homes/statistics & numerical data , Prognosis , Quality of Health Care/organization & administration , Quality of Health Care/standards , Risk Assessment , Severity of Illness Index , Terminal Care/methods , Terminal Care/psychologyABSTRACT
Pannexin 1 (Panx1) and Pannexin 3 (Panx3) are single membrane channels recently implicated in myogenic commitment, as well as myoblast proliferation and differentiation in vitro. However, their expression patterns during skeletal muscle development and regeneration had yet to be investigated. Here, we show that Panx1 levels increase during skeletal muscle development becoming highly expressed together with Panx3 in adult skeletal muscle. In adult mice, Panx1 and Panx3 were differentially expressed in fast- and slow-twitch muscles. We also report that Panx1/PANX1 and Panx3/PANX3 are co-expressed in mouse and human satellite cells, which play crucial roles in skeletal muscle regeneration. Interestingly, Panx1 and Panx3 levels were modulated in muscle degeneration/regeneration, similar to the pattern seen during skeletal muscle development. As Duchenne muscular dystrophy is characterized by skeletal muscle degeneration and impaired regeneration, we next used mild and severe mouse models of this disease and found a significant dysregulation of Panx1 and Panx3 levels in dystrophic skeletal muscles. Together, our results are the first demonstration that Panx1 and Panx3 are differentially expressed amongst skeletal muscle types with their levels being highly modulated during skeletal muscle development, regeneration, and dystrophy. These findings suggest that Panx1 and Panx3 channels may play important and distinct roles in healthy and diseased skeletal muscles.