Preoperative systematic staging by EBUS-TBNA of early lung cancer can reduce postoperative upstaging. Sensitivity for detection of radiologically occult mediastinal metastases seems lower than selective sampling of pathologic lymph nodes. Verification of negative results by mediastinoscopy in selected cases remains of value.

Tumour type is an important determinant of pleural fluid cytology diagnostic yield. Cytology has good sensitivity and specificity for the diagnosis of adenocarcinoma, but if another tumour type is suspected, particularly mesothelioma, clinicians should be aware of the limitations.

Aims  Myocardial infarction (MI) accelerates atherosclerosis and greatly increases the risk of recurrent cardiovascular events for many years, in particular, strokes and MIs. Because B cell-derived autoantibodies produced in response to MI also persist for years, we investigated the role of B cells in adaptive immune responses to MI. Methods and results  We used an apolipoprotein-E-deficient (ApoE−/−) mouse model of MI-accelerated atherosclerosis to assess the importance of B cells. One week after inducing MI in atherosclerotic mice, we depleted B cells using an anti-CD20 antibody. This treatment prevented subsequent immunoglobulin G accumulation in plaques and MI-induced accelerated atherosclerosis. In gain of function experiments, we purified spleen B cells from mice 1 week after inducing MI and transferred these cells into atherosclerotic ApoE−/− mice, which greatly increased immunoglobulin G (IgG) accumulation in plaque and accelerated atherosclerosis. These B cells expressed many cytokines that promote humoural immunity and in addition, they formed germinal centres within the spleen where they differentiated into antibody-producing plasma cells. Specifically deleting Blimp-1 in B cells, the transcriptional regulator that drives their terminal differentiation into antibody-producing plasma cells prevented MI-accelerated atherosclerosis. Alarmins released from infarcted hearts were responsible for activating B cells via toll-like receptors and deleting MyD88, the canonical adaptor protein for inflammatory signalling downstream of toll-like receptors, prevented B-cell activation and MI-accelerated atherosclerosis. Conclusion  Our data implicate early B-cell activation and autoantibodies as a central cause for accelerated atherosclerosis post-MI and identifies novel therapeutic strategies towards preventing recurrent cardiovascular events such as MI and stroke.

BackgroundVenous leg ulceration is a common and costly problem that is expected to worsen as the population ages. Current treatment is compression therapy; however, up to 50 % of ulcers remain unhealed after 2 years, and ulcer recurrence is common. New treatments are needed to address those wounds that are more challenging to heal. Targeting the inflammatory processes present in venous ulcers is a possible strategy. Limited evidence suggests that a daily dose of aspirin may be an effective adjunct to aid ulcer healing and reduce recurrence. The Aspirin in Venous Leg Ulcer study (ASPiVLU) will investigate whether 300-mg oral doses of aspirin improve time to healing.Methods/designThis randomised, double-blinded, multicentre, placebo-controlled, clinical trial will recruit participants with venous leg ulcers from community settings and hospital outpatient wound clinics across Australia. Two hundred sixty-eight participants with venous leg ulcers will be randomised to receive either aspirin or placebo, in addition to compression therapy, for 24 weeks. The primary outcome is time to healing within 12 weeks. Secondary outcomes are ulcer recurrence, wound pain, quality of life and wellbeing, adherence to study medication, adherence to compression therapy, serum inflammatory markers, hospitalisations, and adverse events at 24 weeks.DiscussionThe ASPiVLU trial will investigate the efficacy and safety of aspirin as an adjunct to compression therapy to treat venous leg ulcers. Study completion is anticipated to occur in December 2018.Trial registrationAustralian New Zealand Clinical Trials Registry, ACTRN12614000293662

Quality of life See comment Not measured in any studies Adverse events See comment Not reported in any studies Pain See comment Not measured in any studies *The risk in the intervention group (and its 95% confidence interval) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI).

Background In July 2020, a COVID‐19 outbreak was recognised in the geriatric wards at a subacute campus of the Royal Melbourne Hospital affecting patients and staff. Patients were also admitted to this site after diagnosis in residential care. Aims To describe the early symptoms and the outcomes of COVID‐19 in older adults. Methods Patients diagnosed with COVID‐19 at the facility in July or August 2020 were identified and their medical records were examined to identify symptoms present before and after their diagnosis and to determine their outcomes. Results Overall, 106 patients were identified as having COVID‐19, with median age of 84.3 years (range 41–104 years); 64 were diagnosed as hospital inpatients after a median length of stay of 49 days, 31 were transferred from residential aged care facilities with a known diagnosis and 11 were diagnosed after discharge. There were 95 patients included in an analysis of symptom type and timing onset. Overall, 61 (64.2%) were asymptomatic at the time of diagnosis of COVID‐19, having been diagnosed through screening initiated on site. Of these, 88.6% developed symptoms of COVID‐19 within 14 days. The most common initial symptom type was respiratory, but there was wide variation in presentation, including fever, gastrointestinal and neurological symptoms, many initially not recognised as being due to COVID‐19. Of 104 patients, 32 died within 30 days of diagnosis. Conclusions COVID‐19 diagnosis is challenging due to the variance in symptoms. In the context of an outbreak, asymptomatic screening can identify affected patients early in the disease course.

Background The REStORing health of acutely unwell adulTs (RESORT) is an observational longitudinal cohort, including geriatric rehabilitation inpatients aged ≥65 years admitted to a geriatrician‐led rehabilitation service at a tertiary hospital. The aim of this study is to describe a home‐based bed‐substitution rehabilitation model for geriatric inpatients, including patient phenotype, and health outcomes at preadmission, admission, discharge, and three‐month follow‐up. Methods A standardized Comprehensive Geriatric Assessment was performed on admission and discharge, including demographics (home situation, cognitive impairment, medical diagnoses, etc.), frailty (Clinical Frailty Scale (CFS)), mobility (patient‐reported and Functional Ambulation Classification), physical performance (Short Physical Performance Battery (SPPB), handgrip strength), and functional independence (Activities of Daily Living (ADL), Instrumental ADL (IADL)). Service provision data (health care staff visits, length of stay (LOS), and negative events (e.g., falls)) were extracted from medical records. Three‐month outcomes included mobility, ADL and IADL scores, institutionalization, and mortality. Results Ninety‐two patients were included with a mean age of 81.1 ± 7.8 years, 56.5% female. Twenty‐nine (31.5%) patients lived alone, 39 (42.4%) had cognitive impairment and the commonest geriatric rehabilitation admission reason was falls (n = 30, 32.6%). Patients received care from nurses, physicians, and a median of four (interquartile range (IQR) 3–6) allied health disciplines for a median LOS of 13.0 days (IQR 10.0–15.0). On a population level, patient mobility and functional independence worsened from preadmission to admission. CFS, SPPB, ADL, and IADL scores improved from admission to discharge, and seven (7.6%) patients fell. At three‐month follow‐up, patient‐reported mobility was comparable to preadmission baseline, but functional independence (ADL, IADL) scores worsened for 27/69 (39.1%) and 28/63 (44.4%), respectively. Conclusions Hospitalization‐associated decline in mobility and functional independence improved at discharge and three‐months, but was not fully reversed in the multidisciplinary home‐based geriatric rehabilitation bed‐substitution service. Future research should compare outcomes to equivalent hospital‐based geriatric rehabilitation and evaluate patient perspectives.

Malignant pleural effusion (MPE) may be diagnosed by cytologic evaluation of pleural fluid, though false negative results can occur. Pleural effusions may provide a source of tumour material for genotyping in lung cancer patients. Detection of MPE may be improved through use of highly sensitive molecular techniques. We identified five patients with non-small cell lung cancer (NSCLC) with initial pleural fluid samples that were non-malignant on cytology, but were subsequently clinically confirmed to have MPE. Tumour mutation status was confirmed via routine testing of diagnostic clinical specimens. Cytologically negative pleural fluid cell-block specimens were analysed by amplicon-based parallel sequencing (APS) for somatic mutations commonly detected in NSCLC, and selected cases by improved and complete enrichment CO-amplification at lower denaturation temperature PCR (ICECOLD PCR) for known mutations. Mutations were detected in three out of three (sensitivity 100%) cytologically non-malignant pleural fluids from patients with a known mutation: two patients with known Kirsten rat sarcoma (KRAS) mutation demonstrated the same KRAS mutation in their pleural fluids by APS, both at approximately 2% mutant allele frequency. In one patient with a known KRAS mutation, ICECOLD PCR detected the same KRAS variant at 0.7% frequency. No mutations were detected in patients with wild-type findings from reference samples (specificity 100%). Sensitive DNA sequencing methods can detect cancerdriver mutations in cytologically non-malignant pleural fluid specimens from NSCLC patients with MPE. Our findings demonstrate the feasibility of sensitive molecular diagnostic techniques for improvement of diagnostic assessment of pleural effusions in patients with lung cancer.