# ECMO decannulation is associated with dynamic changes in coagulation profiles: an exploratory, nested cohort study

**Authors:** Matthias Noitz, Dennis Jenner, Roxane Brooks, Johannes Szasz, Romana Erblich, Bernhard Eichler, Marius Knöll, Niklas Krenner, Tina Tomić-Mahečić, Martin W. Dünser, Andreas Zierer, Jens Meier

PMC · DOI: 10.1186/s12871-026-03641-1 · 2026-01-29

## TL;DR

This study shows that coagulation profiles rapidly change in the 72 hours after ECMO decannulation, indicating a quick recovery of blood clotting and a possible shift toward increased clotting tendency.

## Contribution

The study provides new insights into dynamic coagulation changes following ECMO decannulation, which could inform post-ECMO care strategies.

## Key findings

- Platelet counts, Factor VIII, and Factor XIII activity significantly increased within 72 hours after ECMO decannulation.
- D-Dimer levels significantly declined, suggesting reduced clot breakdown activity.
- ROTEM® analyses showed improved clot formation and firmness, indicating a prothrombotic shift.

## Abstract

ECMO-associated coagulopathy is a common phenomenon in patients undergoing ECMO therapy. However, data on coagulation trajectories in the post ECMO decannulation period are limited. This study aimed to explore changes in coagulatory function within 72 h after weaning of ECMO therapy.

Exploratory, nested cohort study of a prospective, observational, single-centre cohort study investigating haemostatic changes in adult patients undergoing ECMO therapy at a tertiary academic centre and ECMO referral facility in Linz/Austria. Coagulation tests as well as ROTEM® analyses were performed at the time of ECMO decannulation (d0) and three days later (d3). Intra-individual changes in coagulation parameters and viscoelastic test results after weaning of ECMO therapy were determined using paired comparisons (Student’s t-tests or Wilcoxon signed-rank tests) between the two timepoints.

30 adult patients were included into the final analysis. Platelet counts [97 (82–149) vs. 211 (161–346) G/L, p < 0.001)], Factor VIII activity [294 (208–427) vs. 400 (304–450) %, p = 0.03] and Factor XIII activity [63 (52–73) vs. 86 (70–96) %, p < 0.001] increased significantly between d0 and d3. Fibrinogen levels trended upwards after decannulation [601 (419–711) vs. 650 (495–790) mg/dL, p = 0.08]. Antithrombin activity [96 (83–117) vs. 111 (93–130) %, p = 0.001], Protein C [83 (69–99) vs. 93 (90–104) %, p = 0.01] and Protein S activity [78 (60–91) vs. 80 (72–103), p = 0.002] significantly increased between the two timepoints. D-Dimer levels significantly declined between d0 and d3 [13.5 [6–29] vs. 8.1 (3.9–17.3) %, p = 0.019]. ROTEM® analyses showed significant decreases in INTEM® coagulation time and clot formation time, and significant increases in clot amplitude at five and ten minutes, as well as maximum clot firmness in the INTEM® and EXTEM® assays between d0 and d3.

Extensive changes in coagulation profiles were observed within 72 hours following ECMO weaning and decannulation. These changes reflect a rapid restoration of haemostasis and possibly an early shift towards a prothrombotic phenotype.

The online version contains supplementary material available at 10.1186/s12871-026-03641-1.

## Linked entities

- **Proteins:** antithrombin (antithrombin protein)

## Full-text entities

- **Genes:** F13A1 (coagulation factor XIII A chain) [NCBI Gene 2162] {aka F13A}, VWF (von Willebrand factor) [NCBI Gene 7450] {aka F8VWF, VWD}, PROC (protein C, inactivator of coagulation factors Va and VIIIa) [NCBI Gene 5624] {aka APC, PC, PROC1, THPH3, THPH4}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, SERPINC1 (serpin family C member 1) [NCBI Gene 462] {aka AT3, AT3D, ATIII, ATIII-R2, ATIII-T1, ATIII-T2}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, F3 (coagulation factor III, tissue factor) [NCBI Gene 2152] {aka CD142, TF, TFA}, F8 (coagulation factor VIII) [NCBI Gene 2157] {aka AHF, DXS1253E, F8B, F8C, FVIII, HEMA}, PC (pyruvate carboxylase) [NCBI Gene 5091] {aka PCB}
- **Diseases:** fever (MESH:D005334), ARDS (MESH:D012128), hypofibrinogenemia (MESH:D000347), haemolysis (MESH:D006461), bleeding (MESH:D006470), hypercoagulable (MESH:D019851), ROTEM (MESH:D009759), acquired von Willebrand syndrome (MESH:D014842), endothelial dysfunction (MESH:D014652), SIRS (MESH:D018746), lung injury (MESH:D055370), critical illness (MESH:D016638), platelet aggregation (MESH:D001791), inflammation (MESH:D007249), respiratory or circulatory failure (MESH:D012769), PC (MESH:D015324), haemostasis (MESH:D020141), Factor VIII deficiency (MESH:D006467), Factor VIII and XIII deficiencies (MESH:D005177), thromboembolic (MESH:D013923), low cardiac output syndrome (MESH:D002303), Thrombocytopenia (MESH:D013921), coagulation (MESH:D001778), infection (MESH:D007239), venous and arterial thrombosis (MESH:D020246), thrombosis (MESH:D013927), hereditary haemorrhagic or thrombophilic disorders (MESH:D006474), FXIII deficiency (MESH:D007153), blood trauma (MESH:D006402)
- **Chemicals:** epoprostenol (MESH:D011464), AT (MESH:D001246), enoxaparin (MESH:D017984), PS (MESH:D010758), UFH (MESH:D006493), ellagic acid (MESH:D004610), LMWH (MESH:D006495), PC (MESH:C053518), cytochalasin D (MESH:D015638), -molecular-weight-heparin (-), D (MESH:D003903)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12924452/full.md

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Source: https://tomesphere.com/paper/PMC12924452