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Objective This systematic review and meta-analysis were conducted to study the prevalence and pattern of sleep disturbances in children and adolescents during the COVID-19 pandemic. Methods MEDLINE, EMBASE, and Web of Science were searched for original studies describing sleep abnormalities in children and adolescents with or without pre-existing neurobehavioral disorders during the COVID-19 pandemic. The pooled estimates for various sleep abnormalities were calculated using a random-effect model. Results Of 371 articles screened, 16 studies were included. Among these, five studies were in preschool children, two were in children with pre-existing neurobehavioral disorders and the remaining were in school going children and adolescents. The outcome measures used for sleep were markedly heterogeneous across the studies. The pooled prevalence of any sleep disturbance in children during the pandemic was 54%(95%CI:50–57%). Interestingly, the prevalence in pre-school children was lower than pre-pandemic times (RR = 0.87; 95% CI:0.58–1.30) but this was not statistically significant. The pooled prevalence of children not meeting sleep recommendation was 49% (95%CI: 39–58%). Conclusion The prevalence of sleep problems in children and adolescents during the COVID-19 pandemic is alarming. Pre-school children had a trend towards relatively fewer sleep disturbances due to home confinement measures in comparison with pre-pandemic times. Sleep duration recommendations were not met in nearly half of healthy children. However, these conclusions need to be seen in light of limited literature on the topic, few included studies done in heterogenous populations, and dubious quality of inferences drawn from these studies which were predominantly online surveys. Prospero registration id CRD42020213788.

Chronic obstructive pulmonary disease (COPD) has a profound impact on people living with the disease and has a high global economic and social burden. Often, people with COPD are undiagnosed, while those diagnosed are undertreated and undereducated on different aspects of COPD care. Although there are many published evidence-based treatment guidelines from different expert groups and societies, they are frequently not adhered to, which results in significant gaps in care. In particular, ‘flare-ups’ (known as exacerbations of COPD), which accelerate disease progression, are often under-reported, despite guidelines recommending an escalation of maintenance treatment to prevent subsequent flare-ups. Management of COPD should be proactive to prevent worsening of symptoms and to reduce the risk of future flare-ups and premature death, rather than a secondary reaction to a worsening health status. Key to this is patient access to accurate diagnosis, effective treatment and specialist care, which can vary widely due to socioeconomic differences, geographical locations and poor guideline implementation. In addition, the stigma associated with COPD can act as a barrier, which can result in people being reluctant to access treatment or clinicians being nihilistic. As global patient advocates, we have co-developed this patient charter to set a standard of care that people living with COPD should expect, raising awareness and understanding of the causes and consequences of COPD as well as the potential to improve patient care. Patients with COPD should be empowered to live the highest quality of life possible with the least number of flare-ups. We set out six principles in line with current COPD guideline recommendations, that should be implemented by governments, healthcare providers, policymakers, lung health industry partners and patients/caregivers to drive meaningful change in COPD care.

Background Chronic obstructive pulmonary disease (COPD) is one of the most common causes of mortality and morbidity in high-income countries. In addition to the high costs of initial hospitalization, COPD patients frequently return to the emergency department (ED) and are readmitted to hospital within 30 days of discharge. A COPD acute care discharge care bundle focused on optimizing care for patients with an acute exacerbation of COPD has been shown to reduce ED revisits and hospital readmissions. The aim of this study was to explore and understand factors influencing implementation and uptake of COPD discharge care bundle items in acute care facilities from the perspective of health care providers and patients. Methods Qualitative methodology was adopted. Nine focus groups were conducted using a semi-structured guide: seven with acute and primary/community health care providers and two with patients/family members. Focus groups were audiotaped, transcribed verbatim, and coded and analyzed using a thematic approach. Results Forty-six health care providers and 14 patients/family members participated in the focus groups. Health care providers and patients identified four factors that can challenge the implementation of COPD discharge care bundles: process of care complexities, human capacity in care settings, communication and engagement, and attitudes and perceptions towards change. Both health care providers and patients recognized process of care complexity as the most important determinant of the COPD discharge bundle uptake. Processes of care complexity include patient activities in seeking and receiving care, as well as practitioner activities in making a diagnosis and recommending or implementing treatment. Important issues linked to human capacity in care settings included time constraints, high patient volume, and limited staffing. Communication during transitions in care across settings and patient engagement were also broadly discussed. Other important issues were linked to patients’, providers’, and system attitudes towards change and level of involvement in COPD discharge bundle implementation. Conclusions Complexities in the process of care were perceived as the most important determinant of COPD discharge bundle implementation. Early engagement of health providers and patients in the uptake of COPD discharge bundle items as well as clear communication between acute and post-acute settings can contribute positively to bundle uptake and implementation success.

COPD patients have increased central arterial stiffness and muscle sympathetic nervous activity (MSNA), both of which contribute to cardiovascular (CV) dysfunction and increased CV risk. Previous work suggests that COPD patients have elevated carotid chemoreceptor (CC) activity/sensitivity, which may contribute to the elevated MSNA and arterial stiffness. Accordingly, the effect of CC inhibition on central arterial stiffness, MSNA and CV function at rest in COPD patients was examined in a randomized placebo-controlled study. Thirteen mild-moderate COPD patients (FEV1 predicted ± SD: 83 ± 19%) and 13 age- and risk-matched controls completed resting CV function measurements with either intravenous saline or I.V. dopamine (2 μg kg min−1) while breathing normoxia or hyperoxia (100% O2). On a separate day, a subset of COPD patients and controls completed MSNA measurements while breathing normoxia or hyperoxia. Arterial stiffness was determined by pulse-wave velocity (PWV) and MSNA was measured by microneurography. Brachial blood flow was determined using Doppler ultrasound, cardiac output was estimated by impedance cardiography, and vascular conductance was calculated as flow/mean arterial pressure (MAP). CC inhibition with dopamine decreased central and peripheral PWV, and MAP (P

Heightened arterial stiffness is a marker of cardiovascular risk and is elevated in chronic obstructive pulmonary disease (COPD). Physical activity has been shown to reduce arterial stiffness, and our previous work has shown that arterial stiffness is related to physical activity and exercise tolerance in COPD. The purpose of this study was to evaluate whether baseline physical activity and exercise tolerance influence the cardiovascular benefits associated with standard COPD outpatient pulmonary rehabilitation (PR).A total of 66 patients with COPD were recruited from the G.F. MacDonald Centre for Lung Health, Edmonton, Alberta, prior to entering PR. Another 23 COPD patients not attending the PR program were recruited as time controls (TC). Arterial stiffness (carotid-radial pulse wave velocity, PWV), physical activity (steps taken over three days), and 6-min walk distance (6MWD) were assessed before and after PR, or before and after six weeks of standard care.Thirty-nine PR and 11 TC completed all parts of the study. Following PR, there was no overall change in PWV. However, changes in arterial stiffness with PR were dependent on baseline exercise tolerance, with those patients with a 6MWD350 m showing a significant reduction in PWV following PR (6MWD350 m: 8.2 ± 1.6 to 8.5 ± 1.7 versus 6MWD350 m: 9.2 ± 0.6 to 7.3 ± 2.0 m/s, p 0.05). The PWV response to PR was not influenced by baseline physical activity levels.COPD patients with low exercise tolerance appear to derive the greatest cardiovascular benefits from PR.

RATIONALE: Since the last published Canadian Thoracic Society (CTS) COPD guideline in 2007 and the 2008 update – highlights for primary care, many new clinical trials have challenged COPD treatment...

Background Patients with chronic obstructive pulmonary disease (COPD) have an exaggerated ventilatory response to exercise, contributing to exertional dyspnea and exercise intolerance. We recently demonstrated enhanced activity and sensitivity of the carotid chemoreceptor (CC) in COPD which may alter ventilatory and cardiovascular regulation and negatively affect exercise tolerance. We sought to determine whether CC inhibition improves ventilatory and cardiovascular regulation, dyspnea and exercise tolerance in COPD. Methods Twelve mild-moderate COPD patients (FEV1 83 ± 15 %predicted) and twelve age- and sex-matched healthy controls completed two time-to-symptom limitation (TLIM) constant load exercise tests at 75% peak power output with either intravenous saline or low-dose dopamine (2 μg·kg−1·min−1, order randomized) to inhibit the CC. Ventilatory responses were evaluated using expired gas data and dyspnea was evaluated using a modified Borg scale. Inspiratory capacity maneuvers were performed to determine operating lung volumes. Cardiac output was estimated using impedance cardiography and vascular conductance was calculated as cardiac output/mean arterial pressure (MAP). Results At a standardized exercise time of 4-min and at TLIM; ventilation, operating volumes and dyspnea were unaffected by dopamine in COPD patients and controls. In COPD, dopamine decreased MAP and increased vascular conductance at all time points. In controls, dopamine increased vascular conductance at TLIM, while MAP was unaffected. Conclusion There was no change in time to exhaustion in either group with dopamine. These data suggest that the CC plays a role in cardiovascular regulation during exercise in COPD; however, ventilation, dyspnea and exercise tolerance were unaffected by CC inhibition in COPD patients.

Background Asthma is a complex disease with variable course. Efforts to identify biomarkers to predict asthma severity, the course of disease and response to treatment have not been very successful so far. We have previous suggested that PAR-2 and CRTh2 expression on specific peripheral blood cell subtypes may be biomarkers of asthma severity. We reasoned that parameters that remain stable when asthma symptoms are controlled would be the most appropriate to evaluate for their utility to predict loss of asthma control and/or severity of the disease. Methods Nineteen stable asthmatics were recruited from the University of Alberta Asthma clinic and followed in clinic every 3 months for a total of 4 visits. Patients had spirometry and completed the ACQ questionnaire in every visit. Blood was drawn in every visit and analyzed for a number of immune parameters by flow cytometry. These parameters included PAR-2 and CRTh2 expression on monocyte subgroups and T lymphocytes respectively, as well as numbers of eosinophils, innate lymphoid type-2 cells (ILC2) and dendritic cells. Within person stability of immune and physiological parameters was calculated using the intraclass correlation (ICC) using R version 3.4.0. Results FEV1 (% predicted), FEV1/FVC ratio, ACQ5 and ACQ7 did not differ significantly over the 4 visits, as would be expected for patients with stable asthma. Peripheral blood eosinophil numbers by Kimura stain and by flow cytometry showed ICC scores of 0.44 and 0.52 respectively, indicating moderate stability. The % of ILC2 cells in peripheral blood also showed moderate stability [ICC score of 0.45 (0.14–0.67)]. The stability for all other immune parameters was poor. Conclusion Among the peripheral blood immune parameters we studied, only numbers of eosinophils and ILC2 in peripheral blood were moderately stable over a year in stable asthmatics. Further studies are required to understand the reasons for the variability of the other cell types.

Background Previous work suggests that mild chronic obstructive pulmonary disease (COPD) patients have greater lung dysfunction than previously appreciated from spirometry alone. There is evidence of pulmonary microvascular dysfunction in mild COPD, which may reduce diffusing capacity (DLCO) and increase ventilatory inefficiency during exercise. The purpose of this study was to determine if DLCO, pulmonary capillary blood volume (Vc), and membrane diffusing capacity (Dm) are diminished during exercise in mild COPD, and whether this is related to ventilatory inefficiency and dyspnea. Methods Seventeen mild COPD patients (FEV1/FVC: 64 ± 4%, FEV1 = 94 ± 11%pred) and 17 age- and sex-matched controls were recruited. Ten moderate COPD patients were also tested for comparison (FEV1 = 66 ± 7%pred). DLCO, Vc, and Dm were determined using the multiple-fraction of inspired oxygen (FIO2) DLCO method at baseline and during steady-state cycle exercise at 40W, 50%, and 80% of V ˙ O 2 peak . Using expired gas data, ventilatory inefficiency was assessed by V ˙ E / V ˙ CO 2 . Results Compared to controls, mild COPD had lower DLCO at baseline and during exercise secondary to diminished Vc (P V ˙ E / V ˙ CO 2 (i.e. ≥34) had lower Vc and greater dyspnea ratings compared to control at 40W. Moderate COPD patients were unable to increase Vc with increasing exercise intensity, suggesting further pulmonary vascular impairment with increased obstruction severity. Conclusion Despite relatively minor airflow obstruction, mild COPD patients exhibit a diminished DLCO and capillary blood volume response to exercise, which appears to contribute to ventilatory inefficiency and greater dyspnea.

Dyspnea has been reported to be a main contributor to exercise avoidance in asthma. While traditional markers of ventilation do not explain the heightened dyspnea during exercise in patients with asthma, this study proposed that exertional dyspnea in asthma was due to high-operating lung volumes, which may be improved with a short-acting β2-agonist. On two separate days, 16 patients with asthma and 16 controls completed a lung function test and incremental exercise tests to exhaustion. On one of the days (order randomized), 400 µg salbutamol was administered before exercise. Inspiratory capacity (IC), inspiratory reserve volume (IRV), and dyspnea (modified Borg scale) were evaluated throughout exercise. Compared with controls, patients with asthma reported greater dyspnea at the same absolute submaximal workloads. Furthermore, patients with asthma demonstrated altered breathing responses to exercise, characterized by reduced IC and IRV throughout exercise compared with controls. The reduced IRV was associated with increased dyspnea in patients with asthma. Salbutamol did not affect dyspnea or operating lung volumes in either group. The increased perception of dyspnea during incremental exercise in patients with asthma appears to be secondary to a reduction in IRV, which is unaffected by an inhaled β2-agonist. NEW & NOTEWORTHY Increased exertional dyspnea in asthma appears to be due to high operating lung volumes and is not affected by salbutamol.

Background Variation in hospital management of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) may prolong length of stay, increasing the risk of hospital-acquired complications and worsening quality of life. We sought to determine whether an evidence-based computerized AECOPD admission order set could improve quality and reduce length of stay. Methods The order set was designed by a provincial COPD working group and implemented voluntarily among three physician groups in a Canadian tertiary-care teaching hospital. The primary outcome was length of stay for patients admitted during order set implementation period, compared to the previous 12 months. Secondary outcomes included length of stay of patients admitted with and without order set after implementation, all-cause readmissions, and emergency department visits. Results There were 556 admissions prior to and 857 admissions after order set implementation, for which the order set was used in 47%. There was no difference in overall length of stay after implementation (median 6.37 days (95% confidence interval 5.94, 6.81) pre-implementation vs. 6.02 days (95% confidence interval 5.59, 6.46) post-implementation, p = 0.26). In the post-implementation period, order set use was associated with a 1.15-day reduction in length of stay (95% confidence interval − 0.5, − 1.81, p = 0.001) compared to patients admitted without the order set. There was no difference in readmissions. Conclusions Use of a computerized guidelines-based admission order set for COPD exacerbations reduced hospital length of stay without increasing readmissions. Interventions to increase order set use could lead to greater improvements in length of stay and quality of care. Electronic supplementary material The online version of this article (10.1186/s12890-018-0657-x) contains supplementary material, which is available to authorized users.

To be considered bioequivalent to their branded counterparts, generic drugs must meet the standards for bioequivalence (BE) described by the regulatory agencies. While BE of generic inhalational drugs can be evaluated using a similar approach as that for oral dosage from products or drugs that are delivered systemically, the approach is insufficient to address the complexities of inhalational products (e.g., localized site of action, device–patient interface). Therefore, more considerations are needed and caution should be applied when evaluating BE of inhaled compounds. The purpose of this review is to highlight the considerations and challenges in establishing BE of inhaled compounds by (1) outlining the current regulatory approaches (from Health Canada, the U.S. Food and Drug Administration, and the European Medicines Agency) to assess BE for subsequent entry inhaled products (SEIPs) and (2) reviewing the literature pertaining to testing considerations of SEIPs to establish BE.

Adenoid cystic carcinoma (ACC) accounts for less than 1% of laryngeal tumors. Surgery is the treatment of choice which can be combined with adjuvant radiotherapy. We present a rare case of ACC of glottis and subglottis presented to us with respiratory distress. How to cite this article Verma H, Dass A, Punia RS, Singhal SK, Gupta N, Bhutani M. Adenoid Cystic Carcinoma of Larynx: A Case Report and Rare Experience. Int J Phonosurg Laryngol 2016;6(2):86-88.

BACKGROUND: Although underused, written asthma action plans (AAPs) are associated with reduced numbers of emergency department (ED) visits and hospitalizations.OBJECTIVE: To describe the frequency of use and contents of any AAPs reported by patients presenting with exacerbations to three urban Canadian EDs.METHODS: Prospective data were collected through ED interview and chart review. Descriptive analyses used proportions and medians with interquartile range; multivariable logistic regression was used for the adjusted analyses.RESULTS: Among 176 enrolled patients, the median age was 27 years (interquartile range 23 to 39 years) and 97 (55%) were female. Few (n=42 [24%]) reported having AAPs at ED presentation and only six were written. Most (n=35 [75%]) patients with any AAP took action before the ED visit; none used a valid anti-inflammatory strategy. The first step of 27 plans was to increase asthma medication; no patients appropriately increased inhaled corticosteroids (ICS). In multivariable analyses, only the use of either ICS or ICS/long-acting β-agonist combination agents (31% had AAPs versus 12% did not have AAPs (adjusted OR 3.0 [95% CI 1.14 to 8.07]) and asthma education (47% had AAPs versus 21% did not have AAPs, adjusted OR 3.2 [95% CI 1.13 to 9.19]) were independently associated with AAP possession.CONCLUSION: Possession of AAPs among patients presenting to the ED with acute asthma was low, and only one in 10 AAPs were written. Patients who reported having any AAP used ineffective strategies to abort or mitigate the severity of an ED visit. Increasing frequency of written AAPs and improving their contents holds immediate promise in improving outcomes related to asthma.

Background A COPD discharge bundle is a set of evidence-based practices aimed at improving patient outcomes after discharge from acute care settings following an exacerbation. We conducted a systematic review on the effectiveness of COPD discharge bundles and summarised their individual care elements. Methods Biomedical electronic databases and clinical trial registries were searched from database inception through April 2016 to identify experimental studies evaluating care bundles offered to patients with COPD at discharge. Random-effects meta-analyses of clinical trials data were conducted for hospital readmissions, mortality, and quality of life (QoL). Results The review included 14 studies (5 clinical trials, 7 uncontrolled trials, and 2 interrupted time series). A total of 26 distinct elements of care were included in the bundles of individual studies. Evidence from four clinical trials with moderate-to-high risk of bias showed that COPD discharge bundles reduced hospital readmissions (pooled risk ratio (RR): 0.80; 95% CI 0.65 to 0.99). There was insufficient evidence that care bundles influence long-term mortality (RR: 0.74; 95% CI 0.43 to 1.28; four trials) or QoL (mean difference in St. George9s Respiratory Questionnaire: 1.84; 95% CI −2.13 to 5.8). Conclusions Discharge bundles for patients with COPD led to fewer readmissions but did not significantly improve mortality or QoL. Future studies should employ higher quality research methods, fully report care bundle elements, implementation strategies and intervention fidelity to better evaluate the effectiveness of packaging evidence-based interventions together to improve outcomes of patients with COPD discharged from acute care settings.

Background Chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTh2) is a receptor for PGD2 and expressed by T cells, eosinophils, basophils, and ILC2 cells. CRTh2 expression by CD4(+) T cells identifies the Th2 subset, and these cells have been characterized as allergen-specific central memory Th2 cells. Recently, activation of the PGD2 -CRTh2 pathway in the lungs was associated with severe asthma. Objective To assess circulating levels of Th2 cells and related mediators in severe asthma and those who experience asthma exacerbations. Methods Peripheral blood cells expressing CRTh2 were characterized by flow cytometry and qRT-PCR. Serum IL-13 and PGD2 were measured by ELISA and compared with asthma severity and tendency to exacerbate. Results Severe asthmatics had more circulating CD4(+) CRTh2(+) T cells, CRTh2 and GATA3 mRNA, and a higher level of serum IL-13 compared to mild/moderate asthmatics. The proportion of CD4(+) CRTh2(+) T cells was associated with lower lung function and was highest in severe asthmatics that exacerbated in the last year. Circulating CD4(+) CRTh2(+) T cells, unlike eosinophils, were positively correlated with inhaled steroid dose. Conclusions and clinical relevance Elevated levels of circulating CD4(+) CRTh2(+) T cells are a feature of severe asthma, despite high-dose corticosteroids. Tracking the systemic level of these cells may help identify type 2 severe asthmatics at risk of exacerbation.

IntroductionHospital and emergency department discharge for patients with chronic obstructive pulmonary disease (COPD) is often poorly organised. We developed a patient-centred, evidence-based and consensus-based discharge care bundle for patients with acute exacerbations of COPD.MethodsA purposeful sample of clinicians and patients were invited to participate in a two-round Delphi study (July–November 2015). In round 1, participants rated on a seven-point Likert scale (1=not at all important; 7=extremely important) the importance of 29 unique COPD care actions. Round 2 comprised items selected from round 1 based on consensus (>80% endorsement for Likert values 5–7). A list of 18 care items from round 2 was discussed in a face-to-face nominal group meeting.ResultsSeven care items were included in the COPD discharge bundle based on clinician and patient input: (1) ensure adequate inhaler technique is demonstrated; (2) send discharge summary to family physician and arrange follow-up; (3) optimise and reconcile prescription of respiratory medications; (4) provide a written discharge management plan and assess patient’s and caregiver’s comprehension of discharge instructions; (5) refer to pulmonary rehabilitation; (6) screen for frailty and comorbidities; and (7) assess smoking status, provide counselling and refer to smoking cessation programme.ConclusionWe present a seven-item, patient-centred, evidence-based and consensus-based discharge bundle for patients with acute exacerbations of COPD. Alignment with clinical practice guidelines and feasibility of local adaptations of the bundle should be explored to facilitate wide applicability and evaluation of the effectiveness of the COPD discharge bundle.

COPD is associated with elevated cardiovascular risk and a potentiated ventilatory response to exercise. Enhanced carotid chemoreceptor (CC) activity/sensitivity is present in other clinical conditions, has been shown to contribute to sympathetic vasoconstrictor outflow, and is predictive of mortality. CC activity/sensitivity, and the resulting functional significance, has not been well examined in COPD. We hypothesized that CC activity/sensitivity would be elevated in COPD, and related to increased pulse wave velocity (a marker of CV risk) and the ventilatory response to exercise. Methods: 30 COPD patients and 10 healthy age-matched controls were examined. Participants performed baseline cardiopulmonary exercise and pulmonary function testing. CC activity was later evaluated by the drop in ventilation with breathing 100% O2, and CC sensitivity was then assessed by the ventilatory response to hypoxia (ΔVE/ΔSpO2). Peripheral arterial stiffness was subsequently evaluated by measurement of pulse wave velocity (PWV) using applanation tonometry while the subjects were breathing room air, and then following chemoreceptor inhibition by breathing 100% O2 for 2 minutes. Results: CC activity, CC sensitivity, PWV and the ventilatory response to exercise were all increased in COPD relative to controls. CC sensitivity was related to PWV; however, neither CC activity nor CC sensitivity was related to the ventilatory response to exercise in COPD. CC inhibition by breathing 100% O2 normalized PWV in COPD, while no effect was observed in controls. Conclusion: CC activity and sensitivity are elevated in COPD, and appear related to cardiovascular risk; however, CC activity/sensitivity does not contribute to the potentiated ventilatory response to exercise.