ECMO produces very rapid changes in primary hemostasis detected by PFA-200 during lung transplantation: An observational study
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, pozorovací studie
PubMed
39038564
DOI
10.1016/j.healun.2024.07.012
PII: S1053-2498(24)01745-5
Knihovny.cz E-zdroje
- Klíčová slova
- ECMO, ROTEM platelet, VWF, platelet function analyzer, primary hemostasis, shear stress,
- MeSH
- časové faktory MeSH
- dospělí MeSH
- hemostáza * fyziologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- mimotělní membránová oxygenace * metody MeSH
- transplantace plic * MeSH
- von Willebrandův faktor metabolismus analýza MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- pozorovací studie MeSH
- Názvy látek
- von Willebrandův faktor MeSH
BACKGROUND: The pathology of primary hemostasis is a common complication of extracorporeal membrane oxygenation (ECMO) support. Scientific data describing its changes in patients on short-term ECMO support and the ability and speed of the restoration of its functions are limited. AIMS: The aim of this study was to describe the pathology of primary hemostasis induced by short-term ECMO support and its development over time using PFA-200, ROTEM platelet, and von Willebrand factor (vWF) analyses. METHODS: In patients undergoing lung transplantation surgery using intraoperative veno-arterial ECMO support, blood samples were analyzed using the following tests: PFA-200, ROTEM platelet tests, vWF antigen, ristocetin cofactor (RCo), and collagen-binding protein (CB) before, during, and after ECMO support. RESULTS: Blood samples from 32 patients were analyzed. All 3 PFA-200 tests (COL/EPI, COL/ADP, and COL/P2Y) showed significant deterioration during ECMO support with rapid restoration after ECMO cessation (p < 0.05), suggesting an ECMO-induced primary hemostasis disorder. A significant increase of vWF antigen after ECMO cessation (p < 0.05) was found with an increase of RCo and CB levels, although it was not significant (p > 0.05). CONCLUSIONS: Short-term ECMO support induces primary hemostasis pathology. It occurs immediately after initiation but is rapidly restored after ECMO cessation, which is detectable by PFA-200. Despite there being persistent platelet dysfunction after ECMO cessation, as seen with the ROTEM platelet results, the increased levels of vWF antigen might explain the normal results of primary hemostasis detected by PFA-200.
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