Abstract
BackgroundThe infection caused by SARS CoV-2 has been postulated to induce a cytokine storm syndrome that results in organ failure and even death in a considerable number of patients. However, the inflammatory response in Corona virus disease-19 (Covid-19) and its potential to cause collateral organ damage has not been fully elucidated to date. This study aims to characterize the acute cytokine response in a cohort of critically ill Covid-19 patients. Method24 adults with PCR-confirmed Covid-19 were included at time of admission to intensive care a median of eleven days after initial symptoms. Eleven adult patients admitted for elective abdominal surgery with preoperative plasma samples served as controls. All patients were included after informed consent was obtained. 27 cytokines were quantified in plasma. The expression of inflammatory mediators was then related to routine inflammatory markers, SAPS3, SOFA score, organ failure and 30-day mortality. ResultsA general increase in cytokine expression was observed in all Covid-19 patients. A strong correlation between respiratory failure and IL-1ra, IL-4, IL-6, IL-8 and IP-10 expression was observed. Acute kidney injury development correlated well with increased levels of IL-1ra, IL-6, IL-8, IL-17a, IP-10 and MCP-1. Generally, the cohort demonstrated weaker correlations between cytokine expression and 30-day mortality out of which IL-8 showed the strongest signal in terms of mortality. ConclusionThe present study found that respiratory failure, acute kidney injury and 30-day mortality in critically ill Covid-19 patients are associated with moderate increases of a broad range of inflammatory mediators at time of admission.
Highlights
Corona virus disease – 2019 (Covid-19) is an acute viral infection caused by severe acute respiratory syndrome virus 2 (SARS CoV-2), a novel β-coronavirus
The present study found that respiratory failure, acute kidney injury and 30-day mortality in critically ill Covid-19 patients are associated with moderate increases of a broad range of inflammatory mediators at time of admission
During the first seven days of intensive care 18 (75%) patients required mechanical ventilation and 16 (67%) patients were treated with norepinephrine, no other vasopressor was administered. 24 (100%) patients developed acute kidney injury (AKI) based on increased creatinine and/or loss of urine production. 17 (71%) developed AKI grade 2 and three (13%) patients progressed to grade 3
Summary
Corona virus disease – 2019 (Covid-19) is an acute viral infection caused by severe acute respiratory syndrome virus 2 (SARS CoV-2), a novel β-coronavirus. Clinical presentation ranges from mild to severe illness associated with acute respiratory failure requiring intensive care and considerable mortality. Induced acute respiratory distress syndrome (ARDS) and systemic hyperinflammation appear common features of critically ill Covid-19 patients [2]. The infection caused by SARS CoV-2 has been postulated to induce a cytokine storm syndrome that results in organ failure and even death in a considerable number of patients. This study aims to characterize the acute cytokine response in a cohort of critically ill Covid-19 patients. Results: A general increase in cytokine expression was observed in all Covid-19 patients. Conclusion: The present study found that respiratory failure, acute kidney injury and 30-day mortality in critically ill Covid-19 patients are associated with moderate increases of a broad range of inflammatory mediators at time of admission
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