Peri-operative SARS-CoV-2 infection increases postoperative mortality. The aim of this study was to determine the optimal duration of planned delay before surgery in patients who have had SARS-CoV-2 infection. This international, multicentre, prospective cohort study included patients undergoing elective or emergency surgery during October 2020. Surgical patients with pre-operative SARS-CoV-2 infection were compared with those without previous SARS-CoV-2 infection. The primary outcome measure was 30-day postoperative mortality. Logistic regression models were used to calculate adjusted 30-day mortality rates stratified by time from diagnosis of SARS-CoV-2 infection to surgery. Among 140,231 patients (116 countries), 3127 patients (2.2%) had a pre-operative SARS-CoV-2 diagnosis. Adjusted 30-day mortality in patients without SARS-CoV-2 infection was 1.5% (95%CI 1.4-1.5). In patients with a pre-operative SARS-CoV-2 diagnosis, mortality was increased in patients having surgery within 0-2 weeks, 3-4 weeks and 5-6 weeks of the diagnosis (odds ratio (95%CI) 4.1 (3.3-4.8), 3.9 (2.6-5.1) and 3.6 (2.0-5.2), respectively). Surgery performed ≥ 7 weeks after SARS-CoV-2 diagnosis was associated with a similar mortality risk to baseline (odds ratio (95%CI) 1.5 (0.9-2.1)). After a ≥ 7 week delay in undertaking surgery following SARS-CoV-2 infection, patients with ongoing symptoms had a higher mortality than patients whose symptoms had resolved or who had been asymptomatic (6.0% (95%CI 3.2-8.7) vs. 2.4% (95%CI 1.4-3.4) vs. 1.3% (95%CI 0.6-2.0), respectively). Where possible, surgery should be delayed for at least 7 weeks following SARS-CoV-2 infection. Patients with ongoing symptoms ≥ 7 weeks from diagnosis may benefit from further delay.

SARS-CoV-2 has been associated with an increased rate of venous thromboembolism in critically ill patients. Since surgical patients are already at higher risk of venous thromboembolism than general populations, this study aimed to determine if patients with peri-operative or prior SARS-CoV-2 were at further increased risk of venous thromboembolism. We conducted a planned sub-study and analysis from an international, multicentre, prospective cohort study of elective and emergency patients undergoing surgery during October 2020. Patients from all surgical specialties were included. The primary outcome measure was venous thromboembolism (pulmonary embolism or deep vein thrombosis) within 30 days of surgery. SARS-CoV-2 diagnosis was defined as peri-operative (7 days before to 30 days after surgery); recent (1-6 weeks before surgery); previous (≥7 weeks before surgery); or none. Information on prophylaxis regimens or pre-operative anti-coagulation for baseline comorbidities was not available. Postoperative venous thromboembolism rate was 0.5% (666/123,591) in patients without SARS-CoV-2; 2.2% (50/2317) in patients with peri-operative SARS-CoV-2; 1.6% (15/953) in patients with recent SARS-CoV-2; and 1.0% (11/1148) in patients with previous SARS-CoV-2. After adjustment for confounding factors, patients with peri-operative (adjusted odds ratio 1.5 (95%CI 1.1-2.0)) and recent SARS-CoV-2 (1.9 (95%CI 1.2-3.3)) remained at higher risk of venous thromboembolism, with a borderline finding in previous SARS-CoV-2 (1.7 (95%CI 0.9-3.0)). Overall, venous thromboembolism was independently associated with 30-day mortality ). In patients with SARS-CoV-2, mortality without venous thromboembolism was 7.4% (319/4342) and with venous thromboembolism was 40.8% (31/76). Patients undergoing surgery with peri-operative or recent SARS-CoV-2 appear to be at increased risk of postoperative venous thromboembolism compared with patients with no history of SARS-CoV-2 infection. Optimal venous thromboembolism prophylaxis and treatment are unknown in this cohort of patients, and these data should be interpreted accordingly.

Abstract. Prostaglandins participate in the regulation of important glomerular functions and are involved in the pathogenesis of glomerular diseases. This study investigates the influence of prostaglandins on membrane voltage, ion conductances, cAMP accumulation, and cytosolic calcium activity ([Ca2+]i) in differentiated podocytes. Prostaglandin E2 (PGE2) caused a concentration-dependent depolarization and an increase of the whole cell conductance in podocytes (EC50 ≈ 50 nM). Compared with PGE2, the EP2/EP3/EP4 receptor agonist 11-deoxy-PGE1 caused an equipotent depolarization, whereas the DP receptor agonist BW 245 C, the EP1/EP3 receptor agonist sulprostone, and the IP receptor agonist iloprost were at least 100 to 1000 times less potent than PGE2. The EP2 receptor agonist butaprost did not change membrane voltage of podocytes. The depolarizing effect of PGE2 was increased in an extracellular solution with a reduced Cl- concentration (from 145 to 32 mM). PGE2 and the prostaglandin agonists, but not the IP receptor agonist iloprost and the EP2 receptor agonist butaprost, induced a time- and concentration-dependent cAMP accumulation in podocytes. In fura-2 fluorescence experiments, PGE2, sulprostone, PGF2α, fluprostenol (a potent FP agonist), and U-46619 (a selective thromboxane A2 agonist) induced a biphasic increase of [Ca2+]i in 60 to 80% of podocytes. In reverse transcription-PCR studies, podocyte mRNA for the EP1, EP4, FP, and TP receptor could be amplified. These data indicate that in podocytes, PGE2 regulates distinct cellular functions via the EP1 and EP4 receptor, thereby increasing [Ca2+]i and cAMP, respectively. Furthermore, PGF2α and U-46619 increase [Ca2+]i via their specific receptors.

Background Back pain patients are more likely to suffer from depression, anxiety and reduced quality of life. Pain drawing is a simple, frequently used anamnesis tool that facilitates communication between physicians and patients. This study analysed pain drawings to examine whether pain drawing is suitable as a screening tool for signs of anxiety, depression or reduced quality of life, as the detection of these symptoms is essential for successful treatment. Methods Pain drawings of 219 patients with lower back pain were evaluated retrospectively. Pain drawings are a schematic drawing of a human being. Six variables of the pain drawing were analysed. Subscales of the Hospital Anxiety and Depression Scale (HADS) and the Mental Component Summary (MCS) of the Short Form 12 (SF-12) were used to measure anxiety, depression and quality of life, respectively. Descriptive statistics, uni- and multivariate linear regression analyses and analysis of variance were performed. Logistic regression analyses were conducted for suitable variables. Results We revealed significant positive correlations between the variables "filled body surface" and "number of pain sites" and the anxiety (HADS-A) and depression subscales (HADS-D) of the HADS (p<0.01). The same predictors had significant negative correlations with the MCS (p<0.01). However, the sensitivity and specificity of the variable "number of pain sites" were too low compared to those for existing screening tests to consider it as a screening tool for anxiety, depression and quality of life (HADS-A: sensitivity: 45.2%, specificity: 83.3%; HADS-D: sensitivity: 61.1%, specificity: 51%; MCS: sensitivity: 21.2%, specificity: 85.7%). Conclusions There were significant correlations between the amount of filled body surface and the number of pain sites in the pain drawing and anxiety, depression and quality of life. Although useful in routine clinical practice, pain drawing cannot be used as a screening tool based on our results.

Results: Basal I Ca,L were not changed by the PO 2 (range, 9 -150 mmHg) at 21°or 36°C. The reducing agent 1,4-dithiothreitol (DTT) left I Ca,L unaffected, and the oxidizing agent 5,5=-dithiobis(2-nitrobenzoic acid) (DTNB) irreversibly inhibited I Ca,L . The PO 2 significantly affected the inhibition of I Ca,L by isoflurane (1 minimum alveolar concentration) that decreased I Ca,L by 17 ؎ 2.0% at the high PO 2 but only by 5.8 ؎ 2.9% (P ‫؍‬ 0.037) at the low PO 2 . The inhibition of I Ca,L by isoflurane was also significantly diminished (P ‫؍‬ 0.018) by a low PO 2 when isoflurane effects at both PO 2 conditions were compared in the same cell.Conclusions: In contrast to the situation in guinea pigs, basal I Ca,L in human atrial cardiomyocytes was not sensitive to acute PO 2 changes over a wide range. This might be explained by a lack of oxygen-sensitive splice variants of L-type calcium channel subunits. The PO 2 , however, has a decisive role for the effects of isoflurane on I Ca,L .