Publication date: Jun 13, 2025
Background and Objectives: Coronavirus disease 2019 (COVID-19) triggers a dysregulated host response that may culminate in refractory hypoxaemic shock. Whether veno-venous ECMO modifies the inflammatory cascade more effectively in COVID-19 than in other septic states, and how it compares with conventional ventilatory support for COVID-19, remains uncertain. We compared three groups: COVID-19 patients supported with ECMO (COVID-ECMO, n = 25), non-COVID-19 septic shock patients on ECMO (SEPSIS-ECMO, n = 19) and critically ill COVID-19 patients managed without ECMO (COVID-CONV, n = 74). Methods: This retrospective study (January 2018-January 2025) extracted demographic, laboratory and clinical data at baseline, 48 h and 72 h. The primary end-point was the 72 h change in SOFA score (ΔSOFA). The secondary end-points included the evolution of interleukin-6 (IL-6), C-reactive protein (CRP), D-dimer and ferritin; haemodynamic variables; and 28 day mortality. A post hoc inverse-probability-of-treatment weighting (IPTW) sensitivity analysis adjusted for between-group severity imbalances. Results: Baseline APACHE II differed significantly (29. 5 +/- 5. 8 COVID-ECMO, 27. 4 +/- 6. 1 SEPSIS-ECMO, 18. 2 +/- 4. 9 COVID-CONV; p < 0. 001). At 48 h, IL-6 fell by 51. 8% in COVID-ECMO (-1 116 +/- 473 pg mL) versus 32. 4% in SEPSIS-ECMO and 18. 7% in COVID-CONV (p < 0. 001). The ΔSOFA values at 72 h were -4. 6 +/- 2. 2, -3. 1 +/- 2. 5 and -1. 4 +/- 1. 9, respectively (p < 0. 001). ECMO groups achieved larger mean arterial pressure rises (+16. 8 and +14. 2 mmHg) and greater norepinephrine reduction than COVID-CONV. The twenty-eight-day mortality was 36. 0% (COVID-ECMO), 42. 1% (SEPSIS-ECMO) and 39. 2% (COVID-CONV) (p = 0. 88). Across all patients, IL-6 clearance correlated with ΔSOFA (ρ = 0. 48, p < 0. 001) and with vasopressor-free days (ρ = 0. 37, p = 0. 002). Conclusions: ECMO, regardless of aetiology, accelerates inflammatory-marker decline and organ failure recovery compared with conventional COVID-19 management, but survival advantage remains elusive. COVID-19 appears to display a steeper cytokine-response curve to ECMO than bacterial sepsis, suggesting phenotype-specific benefits that merit confirmation in prospective trials.
Open Access PDF
| Concepts | Keywords |
|---|---|
| Apache | COVID-19 |
| Coronavirus | cytokines |
| Dysregulated | extracorporeal membrane oxygenation |
| Organ | multiple organ failure |
Semantics
| Type | Source | Name |
|---|---|---|
| disease | MESH | COVID-19 |
| disease | MESH | Sepsis |
| disease | IDO | host |
| disease | MESH | shock |
| disease | MESH | septic shock |
| disease | MESH | critically ill |
| drug | DRUGBANK | Norepinephrine |
| disease | MESH | Respiratory Diseases |
| disease | MESH | Infectious Disease |
| pathway | REACTOME | Infectious disease |
| disease | MESH | multiple organ failure |
| disease | MESH | inflammation |
| disease | MESH | acute respiratory distress syndrome |
| disease | MESH | immunothrombosis |
| pathway | KEGG | Viral replication |
| disease | MESH | comorbidity |
| disease | IDO | blood |
| disease | MESH | respiratory failure |
| disease | MESH | Emergency |
| disease | MESH | hypercapnia |
| disease | MESH | infection |
| drug | DRUGBANK | Methionine |
| drug | DRUGBANK | Trestolone |
| drug | DRUGBANK | Heparin |
| drug | DRUGBANK | Nitric Oxide |
| drug | DRUGBANK | Dexamethasone |
| disease | IDO | symptom |
| drug | DRUGBANK | Tocilizumab |
| drug | DRUGBANK | Oxygen |
| disease | IDO | site |
| disease | MESH | bleeding |
| disease | IDO | intervention |
| drug | DRUGBANK | Isoxaflutole |