Strategies to reduce waiting times in outpatient rehabilitation services for adults with physical disabilities : a systematic literature review

Objective: Identifying effective strategies to reduce waiting times is a crucial issue in many areas of health services. Long waiting times for rehabilitation services have been associated with numerous adverse effects in people with disabilities. The main objective of this study was to conduct a systematic literature review to assess the effectiveness of service redesign strategies to reduce waiting times in outpatient rehabilitation services for adults with physical disabilities. Methods: We conducted a systematic review, searching three databases (MEDLINE, CINAHL and EMBASE) from their inception until May 2021. We identified studies with comparative data evaluating the effect of rehabilitation services redesign strategies on reducing waiting times. The Mixed Methods Appraisal Tool was used to assess the methodological quality of the studies. A narrative synthesis was conducted. Results: Nineteen articles including various settings and populations met the selection criteria. They covered physiotherapy (n = 11), occupational therapy (n = 2), prosthetics (n = 1), exercise physiology (n = 1) and multidisciplinary (n = 4) services. The methodological quality varied (n = 10 high quality, n = 6 medium, n = 3 low); common flaws being missing information on the pre-redesign setting and characteristics of the populations. Seven articles assessed access processes or referral management strategies (e.g. self-referral), four focused on extending/modifying the roles of service providers (e.g. to triage) and eight changed the model of care delivery (e.g. mode of intervention). The different redesign strategies had positive effects on waiting times in outpatient rehabilitation services. Conclusions: This review highlights the positive effects of many service redesign strategies. These findings suggest that there are several effective strategies to choose from to reduce waiting times and help better respond to the needs of persons experiencing physical disabilities

Constitutive Overexpression of Muscarinic Receptors Leads to Vagal Hyperreactivity

BACKGROUND: Alterations in muscarinic receptor expression and acetylcholinesterase (AchE) activity have been observed in tissues from Sudden Infant Death Syndrome (SIDS). Vagal overactivity has been proposed as a possible cause of SIDS as well as of vasovagal syncopes. The aim of the present study was to seek whether muscarinic receptor overexpression may be the underlying mechanism of vagal hyperreactivity. Rabbits with marked vagal pauses following injection of phenylephrine were selected and crossed to obtain a vagal hyperreactive strain. The density of cardiac muscarinic receptors and acetylcholinesterase (AchE) gene expression were assessed. Blood markers of the observed cardiac abnormalities were also sought. METHODOLOGY/PRINCIPAL FINDINGS: Cardiac muscarinic M(2) and M(3) receptors were overexpressed in hyperreactive rabbits compared to control animals (2.3-fold and 2.5-fold, respectively) and the severity of the phenylephrine-induced bradycardia was correlated with their densities. A similar overexpression of M(2) receptors was observed in peripheral mononuclear white blood cells, suggesting that cardiac M(2) receptor expression can be inferred with high confidence from measurements in blood cells. Sequencing of the coding fragment of the M(2) receptor gene revealed a single nucleotide mutation in 83% of hyperreactive animals, possibly contributing for the transcript overexpression. Significant increases in AchE expression and activity were also assessed (AchE mRNA amplification ratio of 3.6 versus normal rabbits). This phenomenon might represent a compensatory consequence of muscarinic receptors overexpression. Alterations in M(2) receptor and AchE expression occurred between the 5th and the 7th week of age, a critical period also characterized by a higher mortality rate of hyperreactive rabbits (52% in H rabbits versus 13% in normal rabbits) and preceeded the appearance of functional disorders. CONCLUSIONS/SIGNIFICANCE: The results suggest that cardiac muscarinic receptor overexpression plays a critical role in the development of vagal hyperreactivity, whereas AchE hyperactivity appears as a compensatory consequence of it. Since similar vagal disorders were observed recently by us in SIDS, muscarinic receptor overexpression could become a marker of risk of vasovagal syncopes and SIDS

M₂ muscarinic receptor gene expression in peripheral mononuclear white blood cells from normal (N) and vagal hyperreactive (H) rabbits.

<p>R-R intervals were measured in conscious rabbits challenged with PNE 500 µg kg⁻¹ following the procedure described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0015618#s2" target="_blank">Material and Methods</a>. M<b>₂</b> muscarinic gene expression was assessed in peripheral mononuclear white blood cells by quantitative RT-PCR and normalized to the rabbit 18S housekeeping gene. Values in (<b>a</b>) show amplification ratio calculated according to the 2^{−ΔΔ<i>C</i>t} method of 9 (N) and 16 (H) experiments. In (<b>b</b>), each symbol represents one animal; ΔCt M<b>₂</b>-18S corresponds to the number of amplification cycles needed to detect M<b>₂</b> fluorescence standardized to 18S; thus, the lower the ΔCt M₂-18S, the greater M<b>₂</b> mRNA initial quantity. *: <i>P</i><0.0001 <i>versus</i> N.</p

Effect of AchE enzyme blockade in normal (N) and vagal hyperreactive (H) rabbits.

<p>R-R intervals were measured in conscious rabbits challenged with PNE 250 µg kg^-1 before (control) and after administration of neostigmine 25 µg kg⁻¹. Values are means ± SD of 4 N and 4 H experiments. *: <i>P</i> = 0.02 <i>versus</i> N control; **: <i>P</i> = 0.03 <i>versus</i> H control.</p