Disseminated intravascular coagulation
Abstract Background Disseminated intravascular coagulation (DIC) is characterized by systemic coagulation activation, anticoagulation pathway impairment, and persistent fibrinolysis suppression, resulting in widespread microvascular thrombosis, followed by hemorrhagic consumption coagulopathy and mu...
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BMC
2025-06-01
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| Series: | Journal of Intensive Care |
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| Online Access: | https://doi.org/10.1186/s40560-025-00794-y |
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| author | Satoshi Gando Marcel Levi Cheng-Hock Toh |
| author_facet | Satoshi Gando Marcel Levi Cheng-Hock Toh |
| author_sort | Satoshi Gando |
| collection | DOAJ |
| description | Abstract Background Disseminated intravascular coagulation (DIC) is characterized by systemic coagulation activation, anticoagulation pathway impairment, and persistent fibrinolysis suppression, resulting in widespread microvascular thrombosis, followed by hemorrhagic consumption coagulopathy and multiple organ dysfunction syndrome. This article aimed to provide a comprehensive and updated DIC overview. Main body The International Society on Thrombosis and Hemostasis provides definitions, underlying disorders, diagnostic algorithms, and management guidelines for DIC. Two clinical features of DIC are hemorrhagic consumption coagulopathy, characterized by oozing and difficult-to-control bleeding, and microvascular thrombosis, leading to dysfunctions in multiple vital organs. Histones derived from cellular damage play central roles in the innate-immune-based coagulation model, comprising the initiation, amplification, propagation, and reinforcement phases, which, if dysregulated, develop into DIC. Thus, the innate immune-mediated pathogenic pathways in DIC have become clear. Cell death, damage-associated molecular patterns (including histones), crosstalk between hypoxic inflammation and coagulation, and the serine protease network (comprising coagulation and fibrinolysis, the Kallikrein–Kinin system, and complement pathways) play major roles in DIC pathogenesis. Conversely, these pathogenic pathways and DIC synergistically contribute to organ dysfunction, leading to poor prognoses. Effective DIC management requires treating the underlying condition, along with substitution therapies and, in some cases, antifibrinolytics. Anticoagulant use has been extensively debated; however, the selection of optimal target patients could optimize their application and improve patient outcomes in the near future. Conclusions This review provides an updated overview of DIC, aiming to help readers understand various aspects of DIC today. |
| format | Article |
| id | doaj-art-6a2ed80f24e54ee397dde18788e26da7 |
| institution | DOAJ |
| issn | 2052-0492 |
| language | English |
| publishDate | 2025-06-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Intensive Care |
| spelling | doaj-art-6a2ed80f24e54ee397dde18788e26da72025-08-20T03:10:27ZengBMCJournal of Intensive Care2052-04922025-06-0113112410.1186/s40560-025-00794-yDisseminated intravascular coagulationSatoshi Gando0Marcel Levi1Cheng-Hock Toh2Department of Acute and Critical Care Medicine, Sapporo Higashi Tokushukai HospitalDepartment of Vascular Medicine, Amsterdam University Medical CenterDepartment of Clinical Infection, Microbiology and Immunology, University of LiverpoolAbstract Background Disseminated intravascular coagulation (DIC) is characterized by systemic coagulation activation, anticoagulation pathway impairment, and persistent fibrinolysis suppression, resulting in widespread microvascular thrombosis, followed by hemorrhagic consumption coagulopathy and multiple organ dysfunction syndrome. This article aimed to provide a comprehensive and updated DIC overview. Main body The International Society on Thrombosis and Hemostasis provides definitions, underlying disorders, diagnostic algorithms, and management guidelines for DIC. Two clinical features of DIC are hemorrhagic consumption coagulopathy, characterized by oozing and difficult-to-control bleeding, and microvascular thrombosis, leading to dysfunctions in multiple vital organs. Histones derived from cellular damage play central roles in the innate-immune-based coagulation model, comprising the initiation, amplification, propagation, and reinforcement phases, which, if dysregulated, develop into DIC. Thus, the innate immune-mediated pathogenic pathways in DIC have become clear. Cell death, damage-associated molecular patterns (including histones), crosstalk between hypoxic inflammation and coagulation, and the serine protease network (comprising coagulation and fibrinolysis, the Kallikrein–Kinin system, and complement pathways) play major roles in DIC pathogenesis. Conversely, these pathogenic pathways and DIC synergistically contribute to organ dysfunction, leading to poor prognoses. Effective DIC management requires treating the underlying condition, along with substitution therapies and, in some cases, antifibrinolytics. Anticoagulant use has been extensively debated; however, the selection of optimal target patients could optimize their application and improve patient outcomes in the near future. Conclusions This review provides an updated overview of DIC, aiming to help readers understand various aspects of DIC today.https://doi.org/10.1186/s40560-025-00794-yCell deathComplementDisseminated intravascular coagulation (DIC)HistoneHypoxiaHemorrhage |
| spellingShingle | Satoshi Gando Marcel Levi Cheng-Hock Toh Disseminated intravascular coagulation Journal of Intensive Care Cell death Complement Disseminated intravascular coagulation (DIC) Histone Hypoxia Hemorrhage |
| title | Disseminated intravascular coagulation |
| title_full | Disseminated intravascular coagulation |
| title_fullStr | Disseminated intravascular coagulation |
| title_full_unstemmed | Disseminated intravascular coagulation |
| title_short | Disseminated intravascular coagulation |
| title_sort | disseminated intravascular coagulation |
| topic | Cell death Complement Disseminated intravascular coagulation (DIC) Histone Hypoxia Hemorrhage |
| url | https://doi.org/10.1186/s40560-025-00794-y |
| work_keys_str_mv | AT satoshigando disseminatedintravascularcoagulation AT marcellevi disseminatedintravascularcoagulation AT chenghocktoh disseminatedintravascularcoagulation |