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Our study examined whether the early-onset depression phenotype among young adults (probands) is associated with the metabolic syndrome (MetS) and its components, and if MetS characterizes unaffected but high-risk siblings of probands.
We studied three groups of young adults (Mage = 25 years, s.d. = 3.84 years): probands with histories of childhood onset depression – i.e. early-onset phenotype – (n = 293), their unaffected siblings (high-risk siblings, n = 273), and healthy controls (n = 171). Participants completed a full psychiatric interview, physical and laboratory assessments, and self-rating scales. MetS was defined using the criteria of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (2001).
Early-onset depression phenotype and being a high-risk sibling were associated with higher MetS composite scores relative to that of controls, but did not differ from one another. With regard to MetS components: Probands and siblings had similarly larger waist circumference and lower HDL than did controls, while siblings and controls had lower triglyceride levels than did probands but did not differ from one another. Groups did not differ on glucose levels and SBP.
Our study extends the literature on the association between MetS and depression and underscores the importance of depression phenotypes: failure to account for the clinical heterogeneity of depression may partly underlie the inconsistent findings regarding its relation to MetS. The results also suggest that, in depression-prone populations, MetS may predate and possibly function as a risk factor for eventual depression.
A previously healthy 42-year-old male developed a fever and cough shortly after returning to Canada from overseas. Initially, he had mild upper respiratory tract infection symptoms and a cough. He was aware of the coronavirus disease-2019 (COVID-19) and the advisory to self-isolate and did so; however, he developed increasing respiratory distress over several days and called 911. On arrival at the emergency department (ED), his heart rate was 130 beats/min, respiratory rate 32 per/min, and oxygenation saturation 82% on room air. As per emergency medical services (EMS) protocol, they placed him on nasal prongs under a surgical mask at 5 L/min and his oxygen saturation improved to 86%.
Various medications and devices are available for facilitation of emergent endotracheal intubations (EETIs). The objective of this study was to survey which medications and devices are being utilized for intubation by Canadian physicians.
A clinical scenario-based survey was developed to determine which medications physicians would administer to facilitate EETI, their first choice of intubation device, and backup strategy should their first choice fail. The survey was distributed to Canadian emergency medicine (EM) and intensive care unit (ICU) physicians using web-based and postal methods. Physicians were asked questions based on three scenarios (trauma; pneumonia; heart failure) and responded using a 5-point scale ranging from “always” to “never” to capture usual practice.
The survey response rate was 50.2% (882/1,758). Most physicians indicated a Macintosh blade with direct laryngoscopy would “always/often” be their first choice of intubation device in the three scenarios (mean 85% [79%-89%]) followed by video laryngoscopy (mean 37% [30%-49%]). The most common backup device chosen was an extraglottic device (mean 59% [56%-60%]). The medications most physicians would “always/often” administer were fentanyl (mean 45% [42%-51%]) and etomidate (mean 38% [25%-50%]). EM physicians were more likely than ICU physicians to paralyze patients for EETI (adjusted odds ratio 3.40; 95% CI 2.90-4.00).
Most EM and ICU physicians utilize direct laryngoscopy with a Macintosh blade as a primary device for EETI and an extraglottic device as a backup strategy. This survey highlights variation in Canadian practice patterns for some aspects of intubation in critically ill patients.
Because depressive illness is recurrent, recurrence prevention should be a mainstay for reducing its burden on society. One way to reach this goal is to identify malleable risk factors. The ability to attenuate sadness/dysphoria (mood repair) and parasympathetic nervous system functioning, indexed as respiratory sinus arrhythmia (RSA), are impaired during depression and after it has remitted. The present study therefore tested the hypothesis that these two constructs also may mirror risk factors for a recurrent major depressive episode (MDE).
At time 1 (T1), 178 adolescents, whose last MDE had remitted, and their parents, reported on depression and mood repair; youths’ RSA at rest and in response to sad mood induction also were assessed. MDE recurrence was monitored until time 2 (T2) up to 2 years later. Mood repair at T1 (modeled as a latent construct), and resting RSA and RSA response to sadness induction (RSA profile), served to predict onset of first recurrent MDE by T2.
Consistent with expectations, maladaptive mood repair predicted recurrent MDE, above and beyond T1 depression symptoms. Further, atypical RSA profiles at T1 were associated with high levels of maladaptive mood repair, which, in turn, predicted increased risk of recurrent MDE. Thus, maladaptive mood repair mediated the effects of atypical RSA on risk of MDE recurrence.
This study documented that a combination of behavioral and physiological risk factors predicted MDE recurrence in a previously clinically referred sample of adolescents with depression histories. Because mood repair and RSA are malleable, both could be targeted for modification to reduce the risk of recurrent depression in youths.
Clinical depression involves persistent dysphoria, implicating impaired affect regulation or mood repair failure. However, there is comparatively little information about the mood repair repertoires of individuals with histories of clinical depression, how their repertories differ from that of never-depressed people, and whether particular types of mood repair responses differentially contribute to depression risk.
Adult probands who had childhood-onset depressive disorder (n=215) and controls with no history of major mental disorder (n=122) reported which specific (cognitive, behavioral, interpersonal and somatic-sensory) responses they typically deploy when experiencing sad affect, including responses known to appropriately attenuate dysphoria (‘adaptive’ responses) and those known to exacerbate dysphoria in the short or long run (‘maladaptive’ responses). Subjects were longitudinally followed and evaluated.
Remitted probands and probands in depressive episodes both reported a greater number of maladaptive responses and fewer adaptive responses to their own sadness than did controls, although probands did not have an absolute deficiency of adaptive responses. Maladaptive (but not adaptive) mood repair responses predicted future increases in depression symptoms and an increased probability of a recurrent depressive episode among probands (even after controlling for several clinical predictors of course). Post-hoc analyses revealed that maladaptive non-cognitive and maladaptive cognitive mood repair response sets each predicted depression outcomes.
Individuals with past and present episodes of depressive disorder report an array of cognitive and non-cognitive responses to their own sadness that are likely to exacerbate that affect, and this pattern predicts a worse course of the disorder.
To examine the safety of emergency department (ED) procedural sedation and analgesia (PSA) and the patterns of use of pharmacologic agents at a Canadian adult teaching hospital.
Retrospective analysis of the PSA records of 979 patients, treated between Aug. 1, 2004, and July 31, 2005, with descriptive statistical analysis. This represents an inclusive consecutive case series of all PSAs performed during the study period.
Hypotension (systolic blood pressure ≤ 85 mm Hg) was documented during PSA in 13 of 979 patients (1.3%; 95% confidence interval [CI] 0.3%–2.3%), and desaturation (Sao2 ≤ 90) in 14 of 979 (1.4%; CI 0.1%–2.7%). No cases of aspiration, endotracheal intubation or death were recorded. The most common medication used was fentanyl (94.0% of cases), followed by propofol (61.2%), midazolam (42.5%) and then ketamine (2.7%). The most frequently used 2-medication combinations were propofol and fentanyl (P/F) followed by midazolam and fentanyl (M/F), used with similar frequencies 58.1% (569/979) and 41.0% (401/979) respectively. There was no significant difference in the incidence of hypotension or desaturation between the P/F and M/F treated groups. In these patients, 9.1% (90/979) of patients received more than 2 different drugs.
Adverse events during ED PSA are rare and of doubtful clinical significance. Propofol/fentanyl and midazolam/fentanyl are used safely, and at similar frequencies for ED PSA in this tertiary hospital case series. The use of ketamine for adult PSA is unusual in our facility.
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