Disseminated intravascular coagulation and its immune mechanisms

Clinical Manifestations ◽

Regulatory Control ◽

Contact Pathway ◽

Molecular Patterns ◽

Endothelial Homeostasis ◽

Damage Associated Molecular Patterns ◽

New Strategies

Disseminated intravascular coagulation (DIC) is a syndrome triggered by infectious and non-infectious pathologies characterized by excessive generation of thrombin within the vasculature and widespread proteolytic conversion of fibrinogen. Despite diverse clinical manifestations ranging from thrombo-occlusive damage to bleeding diathesis, DIC etiology commonly involves excessive activation of blood coagulation and overlapping dysregulation of anticoagulants and fibrinolysis. Initiation of blood coagulation follows intravascular expression of tissue factor or activation of contact pathway in response to pathogen-associated or host derived damage-associated molecular patterns. The process is further amplified through inflammatory and immuno-thrombotic mechanisms. Consumption of anticoagulants and disruption of endothelial homeostasis lower the regulatory control and disseminate microvascular thrombosis. Clinical DIC development in patients associates with worsening morbidities and increased mortality regardless of the underlying pathology, therefore timely recognition of DIC is critical to reduce the pathologic burden. Due to diversity of triggers and pathogenic mechanisms leading to DIC, diagnosis is based on algorithms that quantify hemostatic imbalance, thrombocytopenia and fibrin/ogen conversion. Since current diagnosis primarily assesses overt consumptive coagulopathies, there is a critical need for better recognition of non-overt DIC and/or pre-DIC states. Therapeutic strategies for DIC patients involve resolution of the eliciting triggers and supportive care for the hemostatic imbalance. Despite medical care, mortality in DIC patients remains high and new strategies, tailored to the underlying pathologic mechanisms, are needed.

Disseminated intravascular coagulation syndrome

Vrač skoroj pomoŝi (Emergency Doctor) ◽

10.33920/med-02-2004-01 ◽

2020 ◽

pp. 22-40

Author(s):

A. Kulikov

Keyword(s):

Clinical Practice ◽

Blood Cells ◽

Physical State ◽

Clinical Manifestations ◽

Vascular Wall ◽

Stages Of Development ◽

Hemostatic Disorder

Presented material reveals main links in the pathogenesis of hemostatic disorder. In particular, attention is paid to the role of the lungs, liver and other organs in the development of this process. Role of vascular wall and blood cells in regulation of the physical state of blood is described in detail. The most frequent factors leading to hypercoagulation are indicated. Difference between hypercoagulation and thrombophilia is shown. The latter is found in clinical practice quite often, but at the same time, it is poorly diagnosed. Such a terrible complication of hemostatic disorder as disseminated intravascular coagulation is described. Its classification, stages of development, clinical manifestations are offered to the readers.

Detection of disseminated intravascular coagulation with the help of the conception of constant intravascular microcoagulation

Srpski arhiv za celokupno lekarstvo ◽

10.2298/sarh10s1053b ◽

2010 ◽

Vol 138 (suppl. 1) ◽

pp. 53-58

Author(s):

Igor Bokarev ◽

Ludmila Popova

Keyword(s):

Blood Coagulation ◽

19Th Century ◽

High Mortality ◽

Number Of Patients ◽

Arteries And Veins ◽

Exact Diagnosis

The possibility of intravascular blood coagulation existence in the microvascular vessels and capillaries without the presence of a large thrombus in the arteries and veins has been known from the middle of 19th century. It is impossible to know exactly about the prevalence of this pathology, because there is a jumble in terminology that does not help statistics to be exact. One of the reasons of so high mortality from disseminated intravascular coagulation (DIC) is due to the impossibility to always make exact diagnosis, and as ?. Levi thinks it is provoked in the absence of generally accepted idea of DIC syndrome. We investigated these markers and the intensity of intravascular blood coagulation in a number of patients. Our understanding of the problems of DIC was formulated on the grounds of a thirty-year study of the problem involving over 1,500 patients. Thereby, the conception of constant intravascular microcoagulation (CIMC) was developed with the following aims: to report the existing material and bring to researchers and doctors in practice information about the presence of the phenomenon of CIMC and to resolve debatable questions of definitions and practical usage of up-to-date information about DIC with the help of CIMC conception.

Disseminated intravascular coagulation in paediatrics

Archives of Disease in Childhood ◽

10.1136/archdischild-2016-311053 ◽

2016 ◽

Vol 102 (2) ◽

pp. 187-193 ◽

Cited By ~ 12

Author(s):

Revathi Rajagopal ◽

Jecko Thachil ◽

Paul Monagle

Keyword(s):

Diagnostic Tests ◽

Early Life ◽

Clinical Manifestations ◽

Review Article ◽

Morbidity And Mortality ◽

Significant Morbidity ◽

Management Algorithm ◽

Recent Advances

Disseminated intravascular coagulation (DIC) in paediatrics is associated with significant morbidity and mortality. Although there have been several recent advances in the pathophysiology of DIC, most of these studies were done in adults. Since the haemostatic system is very different in early life and changes dramatically with age, creating a variety of challenges for the clinician, delay in the diagnosis of DIC can happen until overt DIC is evident. In this review article, we report the aetiology, pathophysiology, clinical manifestations, diagnostic tests and a management algorithm to guide paediatricians when treating patients with DIC.

Diagnosis and treatment of disseminated intravascular coagulation syndrome

Kazan medical journal ◽

10.17816/kmj2337 ◽

2012 ◽

Vol 93 (2) ◽

pp. 364-366

Author(s):

S V Kemerov

Keyword(s):

Blood Coagulation ◽

Treatment Strategy ◽

Diagnostic Algorithm ◽

Diagnosis And Treatment ◽

Disseminated intravascular blood coagulation syndrome is a rather complex pathology, accompanied by multi-directional shifts in the overall haemostasis. This article presents the diagnostic algorithm and treatment strategy, depending on the stage of disseminated intravascular blood coagulation syndrome.

Recombinant Thrombomodulin and Activated Protein C in the Treatment of Disseminated Intravascular Coagulation

Thrombosis and Haemostasis ◽

10.1055/s-0037-1615902 ◽

1999 ◽

Vol 82 (08) ◽

pp. 718-721 ◽

Cited By ~ 84

Author(s):

Ikuro Maruyama

Keyword(s):

Endothelial Cells ◽

Tissue Factor ◽

Blood Coagulation ◽

Protein C ◽

Activated Protein C ◽

Coagulation Cascade ◽

Regulation System ◽

Luminal Surface ◽

IntroductionThe blood coagulation cascade is regulated by the luminal surface of the endothelial cell lining.1 Endothelial cells synthesize tissue factor pathway inhibitor (TFPI), which, in part, binds to the cell surface glycosaminoglycans and inhibits factors Xa, VIIa, and tissue factor.2 Endothelial cells also produce and exhibit thrombomodulin (TM) on their luminal surface.3 TM is a kind of thrombin receptor that forms a 1:1 complex with thrombin. In this complex, thrombin activates protein C (PC) more than 1,000-fold more than thrombin alone. TM then loses its procoagulant activities, which include fibrinogen clotting, activation of factors V and VIII, and platelet activation. Thus, TM converts thrombin from a procoagulant protease to an anticoagulant. Pathologic states, such as an endothelial injury or perturbation or continuous rapid coagulation cascade activation, overcomes the endothelial regulating activity, resulting in the development of intravascular coagulation and the induction of disseminated intravascular coagulation (DIC). Theoretically, then, supplementing soluble TM or activated PC (APC) to reconstitute the endothelial coagulation regulation system in the circulation and regulate pathologically-activated blood coagulation could be beneficial. In this chapter, application of soluble TM and APC in the treatment of DIC is reviewed.

The effects of FUT-175 (nafamostat mesilate) on blood coagulation and experimental disseminated intravascular coagulation (DIC)

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)59528-2 ◽

1986 ◽

Vol 40 ◽

pp. 261

Author(s):

Yoshiko Koshiyama ◽

Akemi Motoyoshi ◽

Madoka Ogihara ◽

Yasuki Yokomoto ◽

Kyoko Otani ◽

...

Keyword(s):

Blood Coagulation ◽

Nafamostat Mesilate ◽

Thrombotic Thrombocytopenic Purpura— Coagulation Parameters in Twelve Patients

Blood ◽

10.1182/blood.v42.4.499.499 ◽

1973 ◽

Vol 42 (4) ◽

pp. 499-507 ◽

Cited By ~ 58

Author(s):

Eric A. Jaffe ◽

Ralph L. Nachman ◽

Clarence Merskey

Keyword(s):

Blood Coagulation ◽

Thrombotic Thrombocytopenic Purpura ◽

Hemolytic Anemia ◽

Temporal Relationship ◽

Primary Factor ◽

Thrombocytopenic Purpura ◽

Coagulation Abnormalities ◽

Heparin Administration

Abstract Twelve patients with thrombotic thrombocytopenic purpura have been studied with emphasis on the changes in blood coagulation and the occurrence of disseminated intravascular coagulation (DIC). No coagulation abnormalities were found in six patients. Minimal abnormalities were present in three patients and major abnormalities compatible with DIC were present in three patients. There was little temporal relationship between the coagulation abnormalities and the clinical pathological course except for the extent of hemolysis. In addition, heparin administration in four patients had no effect on the course of the disease. Intravascular coagulation does not appear to be a primary factor in the pathogenesis of thrombotic thrombocytopenic purpura and the changes suggestive of DIC, when present, may well result from, rather than cause, the hemolytic anemia.

An enhanced fibrinolysis prevents the development of multiple organ failure in disseminated intravascular coagulation in spite of much activation of blood coagulation

Critical Care Medicine ◽

10.1097/00003246-200106000-00015 ◽

2001 ◽

Vol 29 (6) ◽

pp. 1164-1168 ◽

Cited By ~ 51

Author(s):

Hidesaku Asakura ◽

Yasuo Ontachi ◽

Tomoe Mizutani ◽

Minori Kato ◽

Masanori Saito ◽

...

Keyword(s):

Multiple Organ Failure ◽

Organ Failure ◽

Blood Coagulation ◽

Multiple Organ ◽

Mycobacterium tuberculosis inducing disseminated intravascular coagulation

Thrombosis and Haemostasis ◽

10.1160/th04-09-0562 ◽

2005 ◽

Vol 93 (04) ◽

pp. 729-734 ◽

Cited By ~ 21

Author(s):

Jann-Yuan Wang ◽

Po-Ren Hsueh ◽

Yuang-Shuang Liaw ◽

Wen-Yi Shau ◽

Pan-Chyr Yang ◽

...

Keyword(s):

Mortality Rate ◽

Clinical Manifestation ◽

Early Stage ◽

Prognostic Significance ◽

Clinical Manifestations ◽

Clinical Findings ◽

Mediastinal Lymphadenopathy ◽

Disseminated Tuberculosis ◽

SummaryDisseminated intravascular coagulation (DIC) can develop infrequently in patients with tuberculosis and has a very high mortality rate. We conducted a retrospective study to evaluate the incidence of tuberculosis-induced DIC and to investigate the clinical manifestation, outcome, and prognostic factors of such patients. From January 2002 to December 2003, all culture-proven tuberculosis patients who developed DIC before starting anti-tuberculosis treatments were selected for this study. Patients who had other clinical conditions or were infected by other pathogens that may have been responsible for their DIC were excluded. Survival analysis was performed for each variable with possible prognostic significance. Our results showed that 27 (3.2%) out of the 833 patients with culture-proven tuberculosis had tuberculosis-induced DIC with a mortality rate of 63.0%. The most common clinical manifestations were fever (63.0%) and multiple patches of pulmonary consolidation (59.3%). Seven (25.9%) patients had disseminated tuberculosis. Twelve (44.4%) developed acute respiratory distress syndrome and three (11.1%) were associated with hemophagocytosis. Twenty-four (88.9%) patients had findings that were unusual for an acute bacterial infection, such as positive acid-fast smear, miliary pulmonary lesions, lymphocytotic exudative pleural effusion, and mediastinal lymphadenopathy. Early anti-tuberculosis treatment significantly improved survival. In conclusion, tuberculosis can cause DIC. Patients with non-miliary, non-disseminated tuberculosis could also develop the rare clinical manifestation. Since the prognosis was very poor in patients not treated at an early stage, a high index of suspicion is required, especially in those with clinical findings suggestive of tuberculosis.