Fibrinolysis in Dogs with Intracavitary Effusion: A Review.
D-dimer
FDPs
ROTEM
ascites
hyperfibrinolysis
pleural effusion
primary hyperfibrinolysis
Journal
Animals : an open access journal from MDPI
ISSN: 2076-2615
Titre abrégé: Animals (Basel)
Pays: Switzerland
ID NLM: 101635614
Informations de publication
Date de publication:
20 Sep 2022
20 Sep 2022
Historique:
received:
09
06
2022
revised:
15
09
2022
accepted:
16
09
2022
entrez:
14
10
2022
pubmed:
15
10
2022
medline:
15
10
2022
Statut:
epublish
Résumé
Physiologic fibrinolysis is a localized process in which stable fibrin strands are broken down by plasmin in response to thrombosis. Plasmin activation can also take place separately from the coagulation process, resulting in pathologic fibrinolysis. When plasmin activation exceeds the neutralizing capacity of plasmin inhibitors, severe bleeding can potentially take place. Although the processes which regulate coagulation and fibrinolysis in the blood are well known, it is less clear as to what extent the same processes take place in the body cavities and whether they influence systemic hemostasis. The results of the studies herein cited demonstrate that coagulation followed by fibrinogenolytic/fibrinolytic activity takes place in all kinds of canine ascitic and pleural fluids. Moreover, systemic clotting abnormalities suggesting primary fibrinolysis/primary hyperfibrinolysis (i.e., elevated plasma fibrin/fibrinogen degradation products [FDPs] and normal D-dimer concentrations with fibrinogen concentrations ≤ 100 mg/dL or above this cut-off, respectively) occur in dogs with intracavitary effusion. Enhanced fibrinolytic activity in dogs with intracavitary effusion can also be detected using rotational thromboelastometry (ROTEM), although the degree of agreement between ROTEM and FDPs, D-dimer and fibrinogen concentrations is poor. Finally, contrary to the thrombotic events commonly documented in some humans and cats with cardiac diseases, bleeding tendencies due to primary fibrinolysis/primary hyperfibrinolysis have been documented in dogs with cardiogenic ascites.
Identifiants
pubmed: 36230236
pii: ani12192487
doi: 10.3390/ani12192487
pmc: PMC9558497
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
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