# Viscoelastic Testing for Coagulation Management in Vascular Surgery—A Narrative Review

**Authors:** Alexandru Munteanu, Elena Bax

PMC · DOI: 10.1002/hsr2.71836 · Health Science Reports · 2026-02-22

## TL;DR

This review explores how viscoelastic testing can help manage coagulation in vascular surgery, despite limited evidence.

## Contribution

The paper reviews the potential translational benefits of viscoelastic testing in vascular surgery, highlighting areas for future research.

## Key findings

- Viscoelastic testing allows rapid assessment of coagulation, guiding pre-operative and intra-operative decisions.
- Using viscoelastic testing can reduce transfusion volumes and associated adverse effects in vascular surgery.
- There is a need for large randomized controlled trials to establish standardized guidelines for viscoelastic testing in vascular surgery.

## Abstract

Viscoelastic testing (VET) has been increasingly used in cardiac, trauma, and hepatic surgery where it helps tackle the development of complex coagulopathies. Despite this, data on using VETs in vascular surgery remains limited to small and non‐randomised control studies. Although the improvement in vascular techniques has decreased the rate of massive haemorrhages, there remain situations where they are a serious risk, and the associated coagulopathies pose a challenge to manage.

The aim of this paper is to review the current approved uses of VET and its potential translational benefit in vascular surgery.

An initial PUBMED search provided the foundation for chain sampling to identify relevant papers.

With VET, clinicians can rapidly assess a patient's global haemostatic function thus allowing the timely, or pre‐emptive, correction of coagulopathies. Using the platelet analysis functions pre‐operatively helps guide anaesthetic technique as well as temporary discontinuation of anti‐platelet therapy, an almost ubiquitous drug among vascular patients. Intra‐operatively, the use of this point‐of‐care test, along with goal‐directed algorithms, reduces the volumes of platelets, fibrinogen, and plasma that are transfused. During recovery, using VET can help distinguish a coagulopathic bleed from one requiring surgical re‐exploration. Besides reducing the well‐established adverse effects of transfusions, from electrolyte disturbances to the more rare but severe graft‐vs‐host disease, there is a significant cost‐reducing effect.

Although there is limited evidence of VET in vascular surgery, there seems to be a clear benefit from its use warranting further large randomised controlled trials from which standardised guidelines can be produced.

## Full-text entities

- **Genes:** PLAT (plasminogen activator, tissue type) [NCBI Gene 5327] {aka T-PA, TPA}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}, SERPINE1 (serpin family E member 1) [NCBI Gene 5054] {aka PAI, PAI-1, PAI1, PLANH1}, F3 (coagulation factor III, tissue factor) [NCBI Gene 2152] {aka CD142, TF, TFA}, SERPINF2 (serpin family F member 2) [NCBI Gene 5345] {aka A2AP, AAP, ALPHA-2-PI, API, PLI, alpha2AP}, BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581] {aka BCL2L4}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, WDTC1 (WD and tetratricopeptide repeats 1) [NCBI Gene 23038] {aka ADP, DCAF9}
- **Diseases:** coronary artery thrombosis (MESH:D003324), thromboembolic (MESH:D013923), haemophilia (MESH:D006467), death (MESH:D003643), SLT (MESH:D007757), Thrombosis (MESH:D013927), hypothermia (MESH:D007035), abdominal aortic aneurysm (MESH:D017544), venous graft occlusion (MESH:D006083), coagulation factor dysfunction (MESH:D020147), acidosis (MESH:D000138), toxicity (MESH:D064420), Thrombocytopenia (MESH:D013921), myocardial infarctions (MESH:D009203), cardiovascular disease (MESH:D002318), coagulopathies (MESH:D001778), hypercoagulability (MESH:D019851), stroke (MESH:D020521), VET (MESH:D013736), von Willebrands disease (MESH:D014842), ROTEM (MESH:D009759), Bleeding (MESH:D006470), febrile (MESH:D000071072), thoraco (MESH:C564773), Damage (MESH:D020263), clotting factor dysfunction (MESH:C564885), haemostasis (MESH:D020141), platelet aggregation (MESH:D001791), trauma (MESH:D014947), inflammation (MESH:D007249), blood loss (MESH:D016063), graft-versus-host-disease (MESH:D006086), aortic aneurysm (MESH:D001014), circulatory overload (MESH:D065227), traumatic brain injury (MESH:D000070642), acute lung injury (MESH:D055371), induced (MESH:D000092582), thoracoabdominal aneurysm (MESH:D000094624), pulmonary (MESH:D008171)
- **Chemicals:** citrate (MESH:D019343), Rivaroxaban (MESH:D000069552), Ca (MESH:D002118), heparin (MESH:D006493), warfarin (MESH:D014859), ticagrelor (MESH:D000077486), CKH (-), clopidogrel (MESH:D000077144), Dabigatran (MESH:D000069604), TXA (MESH:D014148), MEA (MESH:D003543), aspirin (MESH:D001241), prasugrel (MESH:D000068799), epsilon-aminocaproic acid (MESH:D015119)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12928011/full.md

## References

56 references — full list in the complete paper: https://tomesphere.com/paper/PMC12928011/full.md

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Source: https://tomesphere.com/paper/PMC12928011