Mortality and pulmonary complications in patients undergoing surgery with perioperative SARS-CoV-2 infection: an international cohort study

Background: The impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on postoperative recovery needs to be understood to inform clinical decision making during and after the COVID-19 pandemic. This study reports 30-day mortality and pulmonary complication rates in patients with perioperative SARS-CoV-2 infection. Methods: This international, multicentre, cohort study at 235 hospitals in 24 countries included all patients undergoing surgery who had SARS-CoV-2 infection confirmed within 7 days before or 30 days after surgery. The primary outcome measure was 30-day postoperative mortality and was assessed in all enrolled patients. The main secondary outcome measure was pulmonary complications, defined as pneumonia, acute respiratory distress syndrome, or unexpected postoperative ventilation. Findings: This analysis includes 1128 patients who had surgery between Jan 1 and March 31, 2020, of whom 835 (74·0%) had emergency surgery and 280 (24·8%) had elective surgery. SARS-CoV-2 infection was confirmed preoperatively in 294 (26·1%) patients. 30-day mortality was 23·8% (268 of 1128). Pulmonary complications occurred in 577 (51·2%) of 1128 patients; 30-day mortality in these patients was 38·0% (219 of 577), accounting for 81·7% (219 of 268) of all deaths. In adjusted analyses, 30-day mortality was associated with male sex (odds ratio 1·75 [95% CI 1·28–2·40], p\textless0·0001), age 70 years or older versus younger than 70 years (2·30 [1·65–3·22], p\textless0·0001), American Society of Anesthesiologists grades 3–5 versus grades 1–2 (2·35 [1·57–3·53], p\textless0·0001), malignant versus benign or obstetric diagnosis (1·55 [1·01–2·39], p=0·046), emergency versus elective surgery (1·67 [1·06–2·63], p=0·026), and major versus minor surgery (1·52 [1·01–2·31], p=0·047). Interpretation: Postoperative pulmonary complications occur in half of patients with perioperative SARS-CoV-2 infection and are associated with high mortality. Thresholds for surgery during the COVID-19 pandemic should be higher than during normal practice, particularly in men aged 70 years and older. Consideration should be given for postponing non-urgent procedures and promoting non-operative treatment to delay or avoid the need for surgery. Funding: National Institute for Health Research (NIHR), Association of Coloproctology of Great Britain and Ireland, Bowel and Cancer Research, Bowel Disease Research Foundation, Association of Upper Gastrointestinal Surgeons, British Association of Surgical Oncology, British Gynaecological Cancer Society, European Society of Coloproctology, NIHR Academy, Sarcoma UK, Vascular Society for Great Britain and Ireland, and Yorkshire Cancer Research

Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp-1

Eptides p31–60, p136–165, and p151–180 were eluted, respectively, at 1.09, 1.31, and 1.29 M NaCl.<p><b>Copyright information:</b></p><p>Taken from "Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp"</p><p>http://www.biomedcentral.com/1471-2180/8/75</p><p>BMC Microbiology 2008;8():75-75.</p><p>Published online 15 May 2008</p><p>PMCID:PMC2409343.</p><p></p

Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp-3

CSY spectrum of the aromatic region. (C) STD-TOCSY of p46–75 (2 mM) in the presence of heparan sulfate (10 μM). Spectra were recorded as in Figure 3.<p><b>Copyright information:</b></p><p>Taken from "Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp"</p><p>http://www.biomedcentral.com/1471-2180/8/75</p><p>BMC Microbiology 2008;8():75-75.</p><p>Published online 15 May 2008</p><p>PMCID:PMC2409343.</p><p></p

Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp-2

�M). (B) STD-TOCSY spectrum. Spectra were recorded in PBS-DO, pH 7.6, 25°C with mixing time of 66 ms, 32 scans per 1 increment. 200 increments were collected in an interlaced mode for on or off pre-saturation.<p><b>Copyright information:</b></p><p>Taken from "Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp"</p><p>http://www.biomedcentral.com/1471-2180/8/75</p><p>BMC Microbiology 2008;8():75-75.</p><p>Published online 15 May 2008</p><p>PMCID:PMC2409343.</p><p></p

Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp-5

Idual 30-mer synthetic peptides covering the entire sequence of Hlp were incubated with biotinylated heparan sulfate in phosphate buffer 10 mM, pH 7.2. Heparan sulfate binding was measured by adding streptavidin peroxidase to the wells and expressed in absorbency units at 490 nm. The data are expressed as mean ± SD of a representative experiment from five independent ones performed in duplicate. (B) Microtiter-plate wells were coated with Hlp or peptides p31–60, p136–165, and p151–180 and biotinylated heparan sulfate was added in the presence of increasing concentrations of NaCl. Heparan sulfate binding was quantified as above.<p><b>Copyright information:</b></p><p>Taken from "Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp"</p><p>http://www.biomedcentral.com/1471-2180/8/75</p><p>BMC Microbiology 2008;8():75-75.</p><p>Published online 15 May 2008</p><p>PMCID:PMC2409343.</p><p></p

Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp-0

Idual 30-mer synthetic peptides covering the entire sequence of Hlp were incubated with biotinylated heparan sulfate in phosphate buffer 10 mM, pH 7.2. Heparan sulfate binding was measured by adding streptavidin peroxidase to the wells and expressed in absorbency units at 490 nm. The data are expressed as mean ± SD of a representative experiment from five independent ones performed in duplicate. (B) Microtiter-plate wells were coated with Hlp or peptides p31–60, p136–165, and p151–180 and biotinylated heparan sulfate was added in the presence of increasing concentrations of NaCl. Heparan sulfate binding was quantified as above.<p><b>Copyright information:</b></p><p>Taken from "Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp"</p><p>http://www.biomedcentral.com/1471-2180/8/75</p><p>BMC Microbiology 2008;8():75-75.</p><p>Published online 15 May 2008</p><p>PMCID:PMC2409343.</p><p></p

Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp-4

D-TOCSY of p151–180 (2 mM) in the presence of heparan sulfate (10 μM). Spectra were recorded as in Figure 3.<p><b>Copyright information:</b></p><p>Taken from "Characterization of two heparan sulphate-binding sites in the mycobacterial adhesin Hlp"</p><p>http://www.biomedcentral.com/1471-2180/8/75</p><p>BMC Microbiology 2008;8():75-75.</p><p>Published online 15 May 2008</p><p>PMCID:PMC2409343.</p><p></p

Initial invasive or conservative strategy for stable coronary disease

BACKGROUND Among patients with stable coronary disease and moderate or severe ischemia, whether clinical outcomes are better in those who receive an invasive intervention plus medical therapy than in those who receive medical therapy alone is uncertain. METHODS We randomly assigned 5179 patients with moderate or severe ischemia to an initial invasive strategy (angiography and revascularization when feasible) and medical therapy or to an initial conservative strategy of medical therapy alone and angiography if medical therapy failed. The primary outcome was a composite of death from cardiovascular causes, myocardial infarction, or hospitalization for unstable angina, heart failure, or resuscitated cardiac arrest. A key secondary outcome was death from cardiovascular causes or myocardial infarction. RESULTS Over a median of 3.2 years, 318 primary outcome events occurred in the invasive-strategy group and 352 occurred in the conservative-strategy group. At 6 months, the cumulative event rate was 5.3% in the invasive-strategy group and 3.4% in the conservative-strategy group (difference, 1.9 percentage points; 95% confidence interval [CI], 0.8 to 3.0); at 5 years, the cumulative event rate was 16.4% and 18.2%, respectively (difference, 121.8 percentage points; 95% CI, 124.7 to 1.0). Results were similar with respect to the key secondary outcome. The incidence of the primary outcome was sensitive to the definition of myocardial infarction; a secondary analysis yielded more procedural myocardial infarctions of uncertain clinical importance. There were 145 deaths in the invasive-strategy group and 144 deaths in the conservative-strategy group (hazard ratio, 1.05; 95% CI, 0.83 to 1.32). CONCLUSIONS Among patients with stable coronary disease and moderate or severe ischemia, we did not find evidence that an initial invasive strategy, as compared with an initial conservative strategy, reduced the risk of ischemic cardiovascular events or death from any cause over a median of 3.2 years. The trial findings were sensitive to the definition of myocardial infarction that was used