The rapid global spread of the novel coronavirus SARS–CoV–2 has caused societal, economic, and medical upheaval not seen since the 1918 influenza pandemic. As of May 9th, cases were confirmed in 203 countries, areas or territories, with over 3.9 million confirmed cases and over 275,000 deaths. Further, many experts believe these numbers to be a gross underestimate for a variety of reasons, including inadequate testing capacity and suboptimal reporting of cases. Despite extensive modeling by epidemiologists all over the world, it is not possible to accurately predict the course and duration of this pandemic. It is important that we continue to obtain objective data on which we base recommendations. A calm and rational approach from both society and individuals is necessary during these uncertain times.
The higher burden and mortality may be attributed to the fact that SARS–CoV–2 is a “newly emerged” virus, and consequently, there is very little innate immunity to it among humans, unlike with influenza where both prior infection and annual vaccination can provide protection. Overall, however, the sheer contagiousness of this new virus has led to the high morbidity and mortality seen globally – simply put, healthcare systems have been unable to cope with the number of infected persons seeking care. Indeed, a proportion of the reported deaths are due to overwhelmed medical systems rather than the virulence of COVID-19. This is a crucial factor explaining the “flatten the curve” strategy adopted by many countries.
Now that more scientific data are available on COVID-19, the Global Sepsis Alliance can more definitively state that COVID-19 does indeed cause sepsis.
Sepsis is “a life-threatening organ dysfunction caused by a dysregulated host response to infection.” In the case of COVID-19, the effects on the respiratory system are well-known, with most people requiring hospital admission developing pneumonia of varying severity; however, virtually all other organ systems can be affected. This is consistent with a combination of direct viral invasion and sepsis.
For example, in a recently published case series of severe COVID-19 cases from the Seattle area in the United States, over 30% had evidence of liver injury and 75% had evidence of a depressed immune response1; another series from the same region reported acute kidney failure in almost 20% of affected patients requiring ICU care 2, and both series reported septic shock severe enough to require drugs to support the heart and circulation in almost 70% of patients.
A recent study from China reported that in patients hospitalized with COVID-19, 28% had evidence of significant heart damage (potentially from direct invasion of cardiac muscle by the virus), resulting in heart failure and abnormal heart rhythms – this damage was associated with a five-fold increase in the risk of death3.
In a paper just published on The Lancet the authors speculate that in clinical practice, many severe or critically ill COVID-19 patients developed typical clinical manifestations of shock, including cold extremities and weak peripheral pulses, even in the absence of overt hypotension.
Understanding the mechanism of viral sepsis in COVID-19 is warranted for exploring better clinical care for these patients. With evidence collected from autopsy studies on COVID-19 and basic science research on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and SARS-CoV, the authors hypothesise that a process called viral sepsis is crucial to the disease mechanism of COVID-19.
1 (Bhatraju PK, et al. NEJM 2020)
2 (Arentz M, et al. JAMA 2020)
3 (Guo T, et al. JAMA 2020)