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Persistent fibrinogen deficiency after snake bite: A case report
BACKGROUND: Venom-induced consumption coagulopathy (VICC) is characterized by coagulation dysfunction accompanied by decreased coagulation factor activity and fibrinogen (FBG) concentrations. We report a patient with VICC caused by snake bite who manifested persistent FBG deficiency without abnormal...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8638048/ https://www.ncbi.nlm.nih.gov/pubmed/34904110 http://dx.doi.org/10.12998/wjcc.v9.i33.10355 |
Sumario: | BACKGROUND: Venom-induced consumption coagulopathy (VICC) is characterized by coagulation dysfunction accompanied by decreased coagulation factor activity and fibrinogen (FBG) concentrations. We report a patient with VICC caused by snake bite who manifested persistent FBG deficiency without abnormal coagulation factor activity. This information may be helpful in diagnosing and treating VICC. CASE SUMMARY: A 49-year-old man who had been bitten by a snake 13 h previously was admitted to the Emergency Department of our hospital with visible swelling of a finger and a bleeding puncture site. The provisional diagnosis was VICC, this being made based on persistent bleeding from the puncture site and subcutaneous hemorrhage. Laboratory evidence of coagulation abnormalities, including fibrinolysis, and findings on thromboelastography confirmed VICC. He had persistent afibrinogenemia requiring intravenous infusions of cryoprecipitate and fresh frozen plasma, together with continuous large doses of human FBG. After this treatment, the patient’s right upper limb swelling improved significantly and his subcutaneous hemorrhage resolved. All of his abnormal laboratory findings returned to normal by day 25. During 6 months’ of follow-up, the patient had no further hemorrhagic events. CONCLUSION: Hemorrhagic snake venom can result in coagulation dysfunction characterized by persistent FBG deficiency without abnormal coagulation factor activity. |
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