Background This study aimed to determine the impact of pulmonary complications on death after surgery both before and during the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic. Methods This was a patient-level, comparative analysis of two, international prospective cohort studies: one before the pandemic (January–October 2019) and the second during the SARS-CoV-2 pandemic (local emergence of COVID-19 up to 19 April 2020). Both included patients undergoing elective resection of an intra-abdominal cancer with curative intent across five surgical oncology disciplines. Patient selection and rates of 30-day postoperative pulmonary complications were compared. The primary outcome was 30-day postoperative mortality. Mediation analysis using a natural-effects model was used to estimate the proportion of deaths during the pandemic attributable to SARS-CoV-2 infection. Results This study included 7402 patients from 50 countries; 3031 (40.9 per cent) underwent surgery before and 4371 (59.1 per cent) during the pandemic. Overall, 4.3 per cent (187 of 4371) developed postoperative SARS-CoV-2 in the pandemic cohort. The pulmonary complication rate was similar (7.1 per cent (216 of 3031) versus 6.3 per cent (274 of 4371); P = 0.158) but the mortality rate was significantly higher (0.7 per cent (20 of 3031) versus 2.0 per cent (87 of 4371); P < 0.001) among patients who had surgery during the pandemic. The adjusted odds of death were higher during than before the pandemic (odds ratio (OR) 2.72, 95 per cent c.i. 1.58 to 4.67; P < 0.001). In mediation analysis, 54.8 per cent of excess postoperative deaths during the pandemic were estimated to be attributable to SARS-CoV-2 (OR 1.73, 1.40 to 2.13; P < 0.001). Conclusion Although providers may have selected patients with a lower risk profile for surgery during the pandemic, this did not mitigate the likelihood of death through SARS-CoV-2 infection. Care providers must act urgently to protect surgical patients from SARS-CoV-2 infection.

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The demonstration of viraemia in experimental poliomyelitis of the monkey1, 7, 2a, and in human poliomyelitis a, s, 9, 11 has shifted the attention from the neural to the haematogenous spread of the virus as an event in the pathogenesis of the disease. Whether or not viraemia plays a primary and essential part in the pathogenesis of the paralytic attack, is still an unsolved problem. Faber and his associates ~, 5 observed early invasion of peripheral ganglia connected with the alimentary tract in eynomolgus monkeys which had been fed type I poliomyelitis Virus. These ganglia are considered as the site of the initial infection, and the presence of virus in the blood, the alimentary tract and other extraneural tissues is considered as secondary to a primary neural infection, and as a result of centrifugal migration of the virus from the central nervous system to peripheral ganglia and nerves. Bodian and Pa]/enberger a, on the contrary, consider viraemia as a frequent and possibly regular event, in which infection of the central nervous system depends on the resistance of the blood-CNS barrier. 0versfxain and injury, such as tonsillectomy and certain intramuscular vaccination procedures known as factors precipitating paralysis, would advance a break-through of this balTier.In earlier experiments in this laboratory is, a straio~ of type 2 poliomyelitis virus could be recovered regularly from the sciatic nerve of monkeys, which had been infected by intramuscular inoculation of the * Aided by a grant from the National Health l~eseareh CounciI T. N. O. ** On leave of absence from the University of Berne, Switzerland. Since viraemia has been demonstrated, another explanation would be more satisfactory. The centripetal neural spread following intramuscular inoculation of the virus does not exclude a simultaneous haematogenous spread by which the virus may be transported to various tissues. At the time of this experiment, the tissue culture technique was not yet introduced in our laboratory, and we failed to recover the virus from the blood by inoculation of monkeys. The injurious action of the intramuscularly introduced pertussis vaccine may have facilitated the invasion of virus from the blood into nerve fibres, as a result of which a secondary neural spread may have occurred. Bodian and Howe ~' indeed succeeded in producing paralysis in monkeys by dipping the central stump of the intersected sciatic nerve in a virus suspension.The initiation of bulbar poliomyelitis following tonsillectomy might be explained by a similar mechanism, with the exception that viraemia is not essential. A direct neural migration of the virus from the damaged tonsillar region through the glossopharyngeal nerve could be assumed 21, 2~.The present paper is a report of an experimental investigation, in which we have tried to prove or to disprove both hypotheses. The significance of both viraemia and neural spread of the virus in the pathogenesis of poliomyelitis following oral administration of virus, and following tonsillectomy and intramuscular...

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