When Covid-19 came into this world, we soon realized that the havoc wreaked by such a novel virus is due to the accumulation of inflammatory cytokines of which medical experts describe as " Cytokine Storm". This remains to be the prevailing theory up to this time and our local experience echos what has been observed. The presence of a persistent and unrelenting rise in measurable inflammatory cytokines among Covid-19 infected patients that is responsible for determining the overall clinical outcome.
After having seen quite a few Covid-19 infected patients, my view has changed. I look at “cytokine storm” as a misnomer because it seems to imply a sudden unpredictable surge in inflammatory levels. I prefer to describe Covid-19 infection as "an inflammatory condition associated with a progressive cytokine build-up". Our body compensates very well early on as these cytokines start building up but, it comes to a point when the body’s compensatory
mechanisms start to fail and clinically failure comes in two phases:
1st Phase is Respiratory: As the name implies, this is characterized by a progressive increase in patients' need
for oxygenation along with lung infiltrates on the CXR that could progress and lead to intubation on some select patients. One important observation is that these infiltrates are often inversely proportional to the degree of hypoxemia suggesting that there is more to it that what meets the eye when you look at the chest X-ray. Simply put, the degree of hypoxemia more often than not is disproportionately worst when compared to the degree and extent of pulmonary infiltrates seen on the chest X-ray.
2nd Phase is Autonomic Collapse: This is usually a terminal event associated with hyperinflammatory cytokines with the patient having intractable hypotension with multiorgan failure & eventual death. This is a very common terminal event that we see & call as cytokine storm.
In the most recent randomized clinical trial from Harvard, by John H. Stone et. al. published in the NEJM Oct. 21, 2020 "Efficacy of Tocilizumab in Patients Hospitalized with Covid-19." (https://www.nejm.org/doi/full/10.1056/NEJMoa2028836) on patients with severe respiratory distress syndrome, the use of Tocilizumab did not seem to confer any benefit in terms of preventing intubation. Furthermore patients randomized on that study had a very wide range of baseline inflammatory levels suggesting that patients have different thresholds with regard to when they show signs of clinical decompensation. This observation suggests that if we try to seek the
answer and predict decompensation by looking at levels of inflammatory cytokines, we might not find one. It reenforces my belief that the presence
of known comorbidities like obesity, diabetes, heart disease (CAD and CHF), COPD play a
greater role in determining the overall clinical course and outcome of Covid-19 infected patients. These highly variable inflammatory cytokine levels at baseline on recruited patients is in keeping with my proposition that best describes Covid-19 infection as a condition characterized by
“progressive cytokine build-up” alongside clinical deterioration determined largely by the presence or absence of comorbidities as mentioned earlier.
