The interplay of inflammation and coagulation in COVID-19 Patients receiving extracorporeal membrane oxygenation support

Abstract

Objective: Bleeding and thrombosis are common complications during Extracorporeal Membrane Oxygenation (ECMO) support for COVID-19 patients. We sought to examine the relationship between inflammatory status, coagulation effects, and observed bleeding and thrombosis in patients receiving venovenous (VV) ECMO for COVID-19 respiratory failure. Study Design: Cross-sectional cohort study Settings: Quaternary care institution. Patients: The study period from April 1, 2020, to January 1, 2021, we included all patients with confirmed COVID-19 who received VV ECMO support. Intervention: None. Measurements and Main Results: Thirty-two patients were supported with VV ECMO during the study period, and 17 patients (53%) survived to hospital discharge. The ECMO nonsurvivors mean lactate dehydrogenase (LDH) levels were markedly elevated in comparison to survivors (1046 u/L [IQR = 509, 1305] vs 489 u/L [385 658], p = 0.003). Platelet/fibrinogen dysfunction, as reflected by the low Maximum Amplitude (MA) on viscoelastic testing, was worse in nonsurvivors (65.25 mm [60.68, 67.67] vs 74.80 mm [73.10, 78.40], p = 0.01). Time-group interaction for the first seven days of ECMO support, showed significantly lower platelet count in the nonsurvivors (140 k/ul [103, 170] vs 189.5 k/ul [146, 315], p < 0.001) and higher D-dimer in (21 μg/mL [13, 21] vs 14 μg/mL [3, 21], p < 0.001) in comparison to the survivors. Finally, we found profound statistically significant correlations between the clinical markers of inflammation and markers of coagulation in the nonsurvivors group. The ECMO nonsurvivors experienced higher rate of bleeding (73.3% vs 35.3%, p = 0.03), digital ischemia (46.7% vs 11.8%, p = 0.02), acute renal failure (60% vs 11.8%, p = 0.01) and bloodstream infection (60% vs 23.5%, p = 0.03). Conclusion: The correlation between inflammation and coagulation in the nonsurvivors supported with VV ECMO could indicate dysregulated inflammatory response and worse clinical outcomes.