Catatonia, a severe neuropsychiatric syndrome, has few studies of sufficient scale to clarify its epidemiology or pathophysiology. We aimed to characterise demographic associations, peripheral inflammatory markers and outcome of catatonia.

Electronic healthcare records were searched for validated clinical diagnoses of catatonia. In a case–control study, demographics and inflammatory markers were compared in psychiatric inpatients with and without catatonia. In a cohort study, the two groups were compared in terms of their duration of admission and mortality.

We identified 1456 patients with catatonia (of whom 25.1% had two or more episodes) and 24 956 psychiatric inpatients without catatonia. Incidence was 10.6 episodes of catatonia per 100 000 person-years. Patients with and without catatonia were similar in sex, younger and more likely to be of Black ethnicity. Serum iron was reduced in patients with catatonia [11.6 v. 14.2 μmol/L, odds ratio (OR) 0.65 (95% confidence interval (CI) 0.45–0.95), p = 0.03] and creatine kinase was raised [2545 v. 459 IU/L, OR 1.53 (95% CI 1.29–1.81), p < 0.001], but there was no difference in C-reactive protein or white cell count. N-Methyl-d-aspartate receptor antibodies were significantly associated with catatonia, but there were small numbers of positive results. Duration of hospitalisation was greater in the catatonia group (median: 43 v. 25 days), but there was no difference in mortality after adjustment.

In the largest clinical study of catatonia, we found catatonia occurred in approximately 1 per 10 000 person-years. Evidence for a proinflammatory state was mixed. Catatonia was associated with prolonged inpatient admission but not with increased mortality.

The objectives of this study were to develop and refine EMPOWER (Enhancing and Mobilizing the POtential for Wellness and Resilience), a brief manualized cognitive-behavioral, acceptance-based intervention for surrogate decision-makers of critically ill patients and to evaluate its preliminary feasibility, acceptability, and promise in improving surrogates’ mental health and patient outcomes.

Part 1 involved obtaining qualitative stakeholder feedback from 5 bereaved surrogates and 10 critical care and mental health clinicians. Stakeholders were provided with the manual and prompted for feedback on its content, format, and language. Feedback was organized and incorporated into the manual, which was then re-circulated until consensus. In Part 2, surrogates of critically ill patients admitted to an intensive care unit (ICU) reporting moderate anxiety or close attachment were enrolled in an open trial of EMPOWER. Surrogates completed six, 15–20 min modules, totaling 1.5–2 h. Surrogates were administered measures of peritraumatic distress, experiential avoidance, prolonged grief, distress tolerance, anxiety, and depression at pre-intervention, post-intervention, and at 1-month and 3-month follow-up assessments.

Part 1 resulted in changes to the EMPOWER manual, including reducing jargon, improving navigability, making EMPOWER applicable for a range of illness scenarios, rearranging the modules, and adding further instructions and psychoeducation. Part 2 findings suggested that EMPOWER is feasible, with 100% of participants completing all modules. The acceptability of EMPOWER appeared strong, with high ratings of effectiveness and helpfulness (M = 8/10). Results showed immediate post-intervention improvements in anxiety (d = −0.41), peritraumatic distress (d = −0.24), and experiential avoidance (d = −0.23). At the 3-month follow-up assessments, surrogates exhibited improvements in prolonged grief symptoms (d = −0.94), depression (d = −0.23), anxiety (d = −0.29), and experiential avoidance (d = −0.30).

Preliminary data suggest that EMPOWER is feasible, acceptable, and associated with notable improvements in psychological symptoms among surrogates. Future research should examine EMPOWER with a larger sample in a randomized controlled trial.

The number of people over the age of 65 attending Emergency Departments (ED) in the United Kingdom (UK) is increasing. Those who attend with a mental health related problem may be referred to liaison psychiatry for assessment. Improving responsiveness and integration of liaison psychiatry in general hospital settings is a national priority. To do this psychiatry teams must be adequately resourced and organised. However, it is unknown how trends in the number of referrals of older people to liaison psychiatry teams by EDs are changing, making this difficult.

We performed a national multi-centre retrospective service evaluation, analysing existing psychiatry referral data from EDs of people over 65. Sites were selected from a convenience sample of older peoples liaison psychiatry departments. Departments from all regions of the UK were invited to participate via the RCPsych liaison and older peoples faculty email distribution lists. From departments who returned data, we combined the date and described trends in the number and rate of referrals over a 7 year period.

Referral data from up to 28 EDs across England and Scotland over a 7 year period were analysed (n = 18828 referrals). There is a general trend towards increasing numbers of older people referred to liaison psychiatry year on year. Rates rose year on year from 1.4 referrals per 1000 ED attenders (>65 years) in 2011 to 4.5 in 2019 . There is inter and intra site variability in referral numbers per 1000 ED attendances between different departments, ranging from 0.1 - 24.3.

To plan an effective healthcare system we need to understand the population it serves, and have appropriate structures and processes within it. The overarching message of this study is clear; older peoples mental health emergencies presenting in ED are common and appear to be increasingly so. Without appropriate investment either in EDs or community mental health services, this is unlikely to improve.

The data also suggest very variable inter-departmental referral rates. It is not possible to establish why rates from one department to another are so different, or whether outcomes for the population they serve are better or worse. The data does however highlight the importance of asking further questions about why the departments are different, and what impact that has on the patients they serve.

The purpose of this study was to look longitudinally at ECT practice in England over the past 7 years: namely over the following key time periods; 2012/13, 2014/15, 2016/17, 2017/18, and 2018/19. A previous study by Chaplin et al, published in 2016, found that there had been a striking decline observed in the number of courses of ECT prescribed to patients from 2006 to two time points i.e. 2012/13 and 2014/15.

In this study we investigated whether or not this trend had continued. Hence we looked at the change in frequency of ECT use, the length of ECT courses, patient demographics and clinical outcomes; between 2012/13 and 2018/19.

Electroconvulsive therapy (ECT) is an effective treatment for Major Depression, Treatment-Resistant Depression, Catatonia, and Clozapine-resistant psychosis. There have been regular improvements in the administration of ECT, over the past two decades. Increases in the volume of the hippocampus and the amygdala have consistently been observed in ECT studies. Stigma has been the major barrier to patients receiving ECT in a timely fashion. The Royal College of Psychiatrists (RCPsych) Centre for Quality Improvement (CCQI) established the ECT Accreditation Service (ECTAS) back in 2006. ECTAS had the aim of standardising ECT practice through the production of evidence-based standards that all member ECT Clinics could use to support their practice.

We looked at the minimum dataset of information collected from ECTAS Members within England for the following years; 2012/13, 2014/15, 2016/17, 2017/18, 2018/19. In 2012/13, 2325 adjusted courses of ECT treatment were given to patients in England. In 2014/15 it was 2302.

Between 2012/13 and 2018/19; two thirds of ECT patients continue to be female. The modal age of patients has also remained the same at 70 years. The number of patients detained under the Mental Health Act 1983 receiving ECT has gone up by 12%; suggesting that the patients receiving ECT were more clinically unwell. After treatment, CGI scale scores (i.e. the very much improved and much improved scores) slightly reduced by 6% from 2012/3 to 2018/19.

The use of ECT in England notably declined from 2006 to 2012/13 and 2014/15. However, from 2012/13 to 2018/19, ECT use has remained relatively stable; suggesting that it is currently being used appropriately on patients, who are amongst the most severely unwell. The clinical effectiveness of ECT remains high however, it has slightly dipped by 6%.

Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver disease that accompanies obesity and the metabolic syndrome. Excess fructose consumption can initiate or exacerbate NAFLD in part due to a consequence of impaired hepatic fructose metabolism. Preclinical data emphasized that fructose-induced altered gut microbiome, increased gut permeability, and endotoxemia play an important role in NAFLD, but human studies are sparse. The present study aimed to determine if two weeks of excess fructose consumption significantly alters gut microbiota or permeability in humans.

We performed a pilot double-blind, cross-over, metabolic unit study in 10 subjects with obesity (body mass index [BMI] 30–40 mg/kg/m2). Each arm provided 75 grams of either fructose or glucose added to subjects’ individual diets for 14 days, substituted isocalorically for complex carbohydrates, with a 19-day wash-out period between arms. Total fructose intake provided in the fructose arm of the study totaled a mean of 20.1% of calories. Outcome measures included fecal microbiota distribution, fecal metabolites, intestinal permeability, markers of endotoxemia, and plasma metabolites.

Routine blood, uric acid, liver function, and lipid measurements were unaffected by the fructose intervention. The fecal microbiome (including Akkermansia muciniphilia), fecal metabolites, gut permeability, indices of endotoxemia, gut damage or inflammation, and plasma metabolites were essentially unchanged by either intervention.

In contrast to rodent preclinical findings, excess fructose did not cause changes in the gut microbiome, metabolome, and permeability as well as endotoxemia in humans with obesity fed fructose for 14 days in amounts known to enhance NAFLD.

To examine associations between diet and risk of developing gastro-oesophageal reflux disease (GERD).

Prospective cohort with a median follow-up of 15·8 years. Baseline diet was measured using a FFQ. GERD was defined as self-reported current or history of daily heartburn or acid regurgitation beginning at least 2 years after baseline. Sex-specific logistic regressions were performed to estimate OR for GERD associated with diet quality scores and intakes of nutrients, food groups and individual foods and beverages. The effect of substituting saturated fat for monounsaturated or polyunsaturated fat on GERD risk was examined.

Melbourne, Australia.

A cohort of 20 926 participants (62 % women) aged 40–59 years at recruitment between 1990 and 1994.

For men, total fat intake was associated with increased risk of GERD (OR 1·05 per 5 g/d; 95 % CI 1·01, 1·09; P = 0·016), whereas total carbohydrate (OR 0·89 per 30 g/d; 95 % CI 0·82, 0·98; P = 0·010) and starch intakes (OR 0·84 per 30 g/d; 95 % CI 0·75, 0·94; P = 0·005) were associated with reduced risk. Nutrients were not associated with risk for women. For both sexes, substituting saturated fat for polyunsaturated or monounsaturated fat did not change risk. For both sexes, fish, chicken, cruciferous vegetables and carbonated beverages were associated with increased risk, whereas total fruit and citrus were associated with reduced risk. No association was observed with diet quality scores.

Diet is a possible risk factor for GERD, but food considered as triggers of GERD symptoms might not necessarily contribute to disease development. Potential differential associations for men and women warrant further investigation.

Air pollution is linked to mortality and morbidity. Since humans spend nearly all their time indoors, improving indoor air quality (IAQ) is a compelling approach to mitigate air pollutant exposure. To assess interventions, relying on clinical outcomes may require prolonged follow-up, which hinders feasibility. Thus, identifying biomarkers that respond to changes in IAQ may be useful to assess the effectiveness of interventions.

We conducted a narrative review by searching several databases to identify studies published over the last decade that measured the response of blood, urine, and/or salivary biomarkers to variations (natural and intervention-induced) of changes in indoor air pollutant exposure.

Numerous studies reported on associations between IAQ exposures and biomarkers with heterogeneity across study designs and methods. This review summarizes the responses of 113 biomarkers described in 30 articles. The biomarkers which most frequently responded to variations in indoor air pollutant exposures were high sensitivity C-reactive protein (hsCRP), von Willebrand Factor (vWF), 8-hydroxy-2′-deoxyguanosine (8-OHdG), and 1-hydroxypyrene (1-OHP).

This review will guide the selection of biomarkers for translational studies evaluating the impact of indoor air pollutants on human health.

The utility and efficacy of bolus dose vasopressors in hemodynamically unstable patients is well-established in the fields of general anesthesia and obstetrics. However, in the prehospital setting, minimal evidence for bolus dose vasopressor use exists and is primarily limited to critical care transport use. Hypotensive episodes, whether traumatic, peri-intubation-related, or septic, increase patient mortality. The purpose of this study is to assess the efficacy and adverse events associated with prehospital bolus dose epinephrine use in non-cardiac arrest, hypotensive patients treated by a single, high-volume, ground-based Emergency Medical Services (EMS) agency.

This is a retrospective, observational study of all non-cardiac arrest EMS patients treated for hypotension using bolus dose epinephrine from September 12, 2018 through September 12, 2019. Inclusion criteria for treatment with bolus dose epinephrine required a systolic blood pressure (SBP) measurement <90mmHg. A dose of 20mcg every two minutes, as needed, was allowed per protocol. The primary data source was the EMS electronic medical record.

Forty-two patients were treated under the protocol with a median (IQR) initial SBP immediately prior to treatment of 78mmHg (65-86) and a median (IQR) initial mean arterial pressure (MAP) of 58mmHg (50-66). The post-bolus SBP and MAP increased to 93mmHg (75-111) and 69mmHg (59-83), respectively. The two most common patient presentations requiring protocol use were altered mental status (55%) and respiratory failure (31%). Over one-half of the patients treated required both advanced airway management (62%) and multiple bolus doses of vasopressor support (55%). A single episode of transient severe hypertension (SBP>180mmHg) occurred, but there were no episodes of unstable tachyarrhythmia or cardiac arrest while en route or upon arrival to the receiving hospitals.

These preliminary data suggest that the administration of bolus dose epinephrine may be effective at rapidly augmenting hypotension in the prehospital setting with a minimal incidence of adverse events. Paramedic use of bolus dose epinephrine successfully increased SBP and MAP without clinically significant side effects. Prospective studies with larger sample sizes are needed to further investigate the effects of prehospital bolus dose epinephrine on patient morbidity and mortality.