2020
DOI: 10.1053/j.jvca.2020.09.132
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COVID-19 and ECMO: An Unhappy Marriage of Endothelial Dysfunction and Hemostatic Derangements

Abstract: No funding or sponsorship was received for this manuscript, including manuscript design or any process in manuscript creation. Standard Health Insurance Portability and Accountability Act documentation and consent for use of the patient's medical record for research purposes were obtained from the patients in accordance with Mayo Clinic policy.

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Cited by 8 publications
(8 citation statements)
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“…29 However, the rate of severe bleeding, including intracranial hemorrhage, and fatal bleeding on ECMO was particularly high in these studies. The hemostatic changes induced by ECMO support in COVID-19 patients have been yet poorly documented [15][16][17][18][19]30,31 and the optimal anticoagulation scheme remains unknown. The present study aimed to fill this knowledge gap by comprehensively describing the kinetics of coagulation and fibrinolysis markers during vv-ECMO support and their potential contribution to outcomes.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…29 However, the rate of severe bleeding, including intracranial hemorrhage, and fatal bleeding on ECMO was particularly high in these studies. The hemostatic changes induced by ECMO support in COVID-19 patients have been yet poorly documented [15][16][17][18][19]30,31 and the optimal anticoagulation scheme remains unknown. The present study aimed to fill this knowledge gap by comprehensively describing the kinetics of coagulation and fibrinolysis markers during vv-ECMO support and their potential contribution to outcomes.…”
Section: Discussionmentioning
confidence: 99%
“…Positive end-expiratory pressure, cm of water Plateau pressure, cm of water Compliance, ml/cm of water 12 [10][11][12][13][14][15] 30 [28][29][30][31][32][33][34] 20.3 [15.3-30.3] 12 [7][8][9][10][11][12] 29 [19][20][21][22][23][24][25][26][27][28][29][30] 22.5 [21.2-32.9] 14 [10][11][12][13][14][15] 30 [28][29][30][31][32][33][34]…”
Section: Tidal Volume Ml/kgmentioning
confidence: 99%
“… 11 The multi-system involvement can be explained by binding of a surface glycoprotein on SARS COV2 (commonly referred to as the “spike protein”) to angiotensin converting enzyme 2(ACE 2) receptors expressed not only by vascular endothelial cells but also by epithelial cells in the lungs, heart, kidney and intestine. 12 …”
Section: Pathophysiology Of Rv Dysfunction In Covid-19mentioning
confidence: 99%
“…protein") to angiotensin converting enzyme 2(ACE 2) receptors expressed not only by vascular endothelial cells but also by epithelial cells in the lungs, heart, kidney and intestine. 12 The entry of the virus contributes to inflammation and damage of the endothelial cells causing release of plasminogen activator which explains the high D-dimer concentration in severe cases, and prothrombotic mediators primarily factor VIIIc and von Willebrand factor multimers. The latter mediates the consequent deposit of microvascular thrombi, especially in affected pulmonary vessels.…”
mentioning
confidence: 99%
“…ECMO can be lifesaving for patients with profound and refractory hypoxemia in COVID-19 ARDS. Due to extensive hospital resource utilization, availability of equipment and invasive nature of ECMO; it remains to be used as a salvage therapy for patients in which despite optimal mechanical ventilation strategies, adequate oxygenation or ventilation cannot be achieved [38][39][40]. As per the recent ELSO (extracorporeal life-support organization) guidance paper; PaO2:FiO2 less than 80 mm Hg for more than 6 hours or PaO2:FiO2 less than 50 mm Hg for less than 3 hours should prompt an early ECMO consult [41].…”
Section: Discussionmentioning
confidence: 99%