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.

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Autonomic innervation of heart is abnormal in diabetes and produces altered cardiovascular parameters. Cerebrolysin is a neurotrophic factor that improves the dendritic tree and synapses in the central nerve system after brain damage. The aim of this study was to evaluate if cerebrolysin can improve the cardiac neuropathy generated in diabetic rats. Male Sprague-Dawley rats two months old were injected with streptozotocin (70 mg/Kg/, ip). Hyperglycemia and altered cardiac rate were confirmed after eight weeks of STZ injection, and cerebrolysin treatment was started in control and diabetic rats for two months (1 ml/kg/day, ip). Body weight, heart rate, heart rate variability, arterial blood pressure, and blood glucose levels were measured. Also heart weight and levels of nitrites, NGF and VEGF were measured in left ventricle homogenates. The results show that body weight was reduced and blood glucose levels were increased significantly in diabetic rats. Cerebrolysin treatment produced no significant changes in body weight either in blood glucose level in control and diabetic rats. Cerebrolysin treatment in diabetic rats shows an improvement in the altered basal cardiac rate (306 ± 6.5 lat/min) compared to diabetic saline group (272 ± 8.9 lat/min: P < 0.05), without changes in control rats. Levels of nitrites, VEGF, and NGF in the left ventricle increased in diabetic cerebrolysin treated rats. In conclusion, the results show that cerebrolysin improves some abnormalities observed in the diabetic cardiac neuropathy in rats and suggest that could be considered an additional treatment to prevent or reduce the cardiac autonomic alterations generated in diabetes.

In this study was evaluated the effect of chronic hyperglycemia in the vascular response of thoracic aorta and pulmonary trunk in two strain rats. Chronic hyperglycemia was induced in male Wistar Kyoto (WK) and Sprague Dawley (SD) rats for single injection of streptozotocin (60 mg/kg, ip.). After 8 weeks, body weight, glucose, systemic arterial blood pressure (SABP) and right ventricular systolic pressure (RVSP) were measured. Thoracic aorta and pulmonary trunks were removed for vascular reactivity studies. Cumulative concentration‐response curves with phenylephrine (Phe) and Acetylcholine (ACh) were made in aorta and pulmonary rings. Glucose blood levels (mg/dl) were similar in both groups, 525±2 vs. 502±3. SABP in mmHg was increased in hyperglycemic SD compared to WK rats 160±2 vs. 140±2, while RVSP was higher in WK than SD rats 41±2.6 vs. 22±1.5 (P<0.001). Maximal tension contraction (g) response with Phe was higher in hyperglycemic SD against hyperglycemic WK aortic rings (2.1±0.1 vs. 1.2±0.1, P</a><0.001), with similar response in the pulmonary rings in both groups. ACh‐induced relaxation (%) response was reduced in SD aorta and pulmonary rings, 58±3 vs 66±4, and this response was attenuated inaorta 78±3, and pronounced in pulmonary rings, 49±3, from WK rats (P<0.001). The results shown that chronic hyperglycemia induce vascular damage predominantly in pulmonary artery in WK rats as consequence pulmonary hypertension, whereas in SD rats, systemic hypertension consecutive to aorta damage is mainly developed suggesting that a genetic factor determine the vascular damage induced by chronic hyperglycemia.