Published in:
Open Access
01-12-2020 | Septic Shock | Letter
Therapeutic plasma exchange as a routine therapy in septic shock and as an experimental treatment for COVID-19: we are not sure
Authors:
Patrick M. Honore, Aude Mugisha, Luc Kugener, Sebastien Redant, Rachid Attou, Andrea Gallerani, David De Bels
Published in:
Critical Care
|
Issue 1/2020
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Excerpt
We read with interest the recent editorial by Keith et al. who concluded that their practice has changed based on their experience, and they now often utilize therapeutic plasma exchange (TPE) earlier in the clinical course of septic shock with multiple organ failure (MODS) and acute respiratory distress syndrome (ARDS) rather than using it as a “rescue therapy” [
1]. We would like to make some comments. They quoted several studies, including one from Knaup et al., in order to support their argument [
2]. They assert that TPE is unique by offering benefit on multiple levels by removing inflammatory cytokines, stabilizing endothelial membranes, and resetting the hypercoagulable state [
1]. Knaup et al. stated that a major difference between TPE and modern extracorporeal adsorption strategies is based on the fact that the exchange of septic shock plasma with fresh frozen plasma may not lead to an unselective depletion of pro- and anti-inflammatory cytokines and will rather replenish protective factors (within FFPs) that have been consumed by the sepsis [
2]. It is currently impossible when employing an unselective removal technique to know if we are doing something good by removing an excess of pro-inflammatory mediators or something wrong by removing anti-inflammatory mediators. At this time, we are unable to clearly identify at the bedside which patients are in a pro-inflammatory state that could kill them or an anti-inflammatory state that could help them to survive. The fact that the inflammation is huge during COVID-19 does not justify the non-selective removal of inflammation components, when some elements may be saving patients. TPE also has the potential to cause harm by diluting or attenuating the host’s adaptive response to infection by depletion of immunoglobulins and complement component 3 and 4 in individuals treated with plasmapheresis [
3]. Importantly, in the case of SARS-CoV-2 outbreak, TPE will remove the protective antibodies formed by the patient, which is not desirable. In conclusion, TPE may not restore immune homeostasis but may rather aggravate immunoparalysis [
4]. We agree with the authors that this outbreak should serve as an impetus to investigate therapies targeting the pathways that lead to morbidity and mortality in these syndromes [
1]. This does not mean that we have received a signed blank check to start a therapy without deeply reviewing the rationale and the quality of existing data. …