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.

Serum 25-(OH)D is a negative acute phase reactant, which has implications for acute and chronic inflammatory diseases. Serum 25-(OH)D is an unreliable biomarker of vitamin D status after acute inflammatory insult. Hypovitaminosis D may be the consequence rather than cause of chronic inflammatory diseases.

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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chemical pathologist and honorary professor of laboratory medicine, Jenna L Waldron senior clinical scientist, Helen L Ashby specialist registrar in chemical pathology and metabolic medicine, Michael P Cornes senior clinical scientist, Julia Bechervaise academic FY2, Cyrus Razavi academic FY2, Osmond L Thomas consultant orthopaedic surgeon, Sanjiv Chugh consultant orthopaedic surgeon, Shreeram Deshpande consultant orthopaedic surgeon, Clare Ford consultant clinical scientist New Cross Hospital, Wolverhampton WV10 0QP, UKIn their editorial calling for vitamin D to be put into perspective Harvey and Cooper do not consider the possibility, supportive to their view, that hypovitaminosis D is the consequence rather than the cause of disease. 1 We recently completed a study showing unequivocally that serum 25-hydroxyvitamin D is a negative acute phase reactant.We measured serum C reactive protein and 25-hydroxyvitamin D concentrations before and two days after elective knee or hip surgery in 30 patients. After surgery the mean serum concentration of C reactive protein increased (5.0 (SD 5.5) v 116.0 (81.2) mg/L; P <0.0001), whereas serum 25-hydroxyvitamin D decreased (56.2 (30.3) v 46.0 (27.6) nmol/L; P <0.0006).These results are consistent with those of two other studies reporting a rapid and noticeable fall in serum 25-hydroxyvitamin D concentration during a systemic inflammatory response. 2 3 They seem, however, to contradict the results of two other studies reporting no change in serum 25-hydroxyvitamin D concentration for up to 90 days after an inflammatory insult. 4 5 The initial serum samples in these last two studies were, however, all collected after the inflammatory insult, 4 5 when serum 25-hydroxyvitamin D is already likely to be at a nadir. 2 3 A unifying explanation for the apparently conflicting results of these four studies is that serum 25-hydroxyvitamin D concentration decreases rapidly and dramatically after an inflammatory insult and persists for at least three months.That serum 25-hydroxyvitamin D is a negative acute phase reactant has implications for acute and chronic diseases. Firstly, serum 25-hydroxyvitamin D is an unreliable biomarker of vitamin D status after an acute inflammatory insult. Secondly, hypovitaminosis D may be the consequence rather than the widely purported cause of a myriad of chronic diseases. 1 et al. The relation between acute changes in the systemic inflammatory response and plasma 25-hydroxyvitamin D concentrations after elective knee arthroplasty. Am J Clin Nutr 2011;93:1006-11. 3 Louw JA, Werbeck A, Louw ME, Kotze TJ, Cooper R, Labadarios D. Blood vitamin concentrations during the acute-phase response. Crit Care Med 1992;20:934-41. 4 Newens K, Filteau S, Tomkins A. Plasma 25-hydroxyvitamin D does not vary over the course of a malarial infection. Trans Roy Soc Trop Med Hyg 2006;100:41-4. 5 Barth JH, Field HP, Mather AN, Plein S. Serum 25 hydroxy-vitamin D does not exhibit an acute phase reaction after acute myocardial infarction. Ann Clin Biochem 2012;49:399-401.