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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood dose not normally coagulate in the blood vessels covered with endothelial cells, because these cells contain some substances responsible for antithrombotic action such as thrombomodulin, heparin-like substance, prostacyclin, nitric oxide and tissue plasminogen activator. Most important role of blood coagulation is hemostasis. Blood can coagulate in two ways: intrinsic coagulation pathway and extrinsic coagulation pathway that is activated by negatively charged substances and FVIIa-tissue-factor (TF) complex, respectively. Prothrombin time(PT) can represent extrinsic pathway, while activated partial thromboplastin time (APTT) can represent intrinsic pathway. PT is prolonged in such diseases as vitamin K deficiency, hepatic failure and warfarin intake, while APTT is prolonged such diseases as hemophilia A & B, von Willebrand disease and lupus anticoagulant. Cross mixing test is very useful to assess prolonged clotting time. FDP means fibrin/fibrinogen degradation products and D-dimer is the smallest products of fibrin degradation. These markers are often used to diagnose disseminated intravascular coagulation (DIC) and deep vein thrombosis (DVT). Thrombin-antithrombin complex (TAT) and plasmin-alpha2 plasmin inhibitor (PIC) can be used to evaluate the extent of coagulation and fibrinolysis activation, respectively. These two markers is essential for classify the pathophysiology of DIC: DIC with suppressed fibrinolysis, enhanced fibrinolysis or balanced fibrinolysis. In conclusion, exact interpretation of hemostatic and fibrinolytic markers is one of the most important abilities in clinical situation.
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PMID:[Interpretation of hemostatic and fibrinolytic markers]. 2218 80

A bleeding child is a cause of great concern and often, panic, for parents and pediatricians alike. Causes of bleeding could be trivial or secondary to an underlying bleeding disorder or a potentially serious systemic illness. Based on etiology, they can be categorized into disorders affecting platelets or the coagulation cascade and can be inherited or acquired. A systematic approach with relevant clinical history and examination along with appropriate laboratory investigations aid in reaching the diagnosis promptly. Indication and administration of blood products including fresh frozen plasma, cryoprecipitate, random donor and single donor apheresis platelets is elaborated. Management of hemophilia, Von Willebrand disease, disseminated intravascular coagulation and bleeding in cyanotic congenital heart disease, among other causes is outlined. Role of antifibrinolytic therapy, desmopressin and recombinant factor VIIa is briefly described. The review outlines the approach to a bleeding child in the emergency room. Practical points in history, examination, investigations and management are discussed. Management in resource constraint setting of developing countries is addressed.
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PMID:Approach to a child with bleeding in the emergency room. 2326 40

Thrombocytopenia-associated multiple organ failure (TAMOF) is a clinical phenotype that encompasses a spectrum of syndromes associated with disseminated microvascular thromboses, such as the thrombotic microangiopathies thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS) and disseminated intravascular coagulation (DIC). Autopsies findings in TTP, HUS, or DIC reveal specific findings that can differentiate these 3 entities. Von Willebrand factor and ADAMTS-13 play a central role in TTP. Shiga toxins and the complement pathway are vital in the development of HUS. Tissue factor is the major protease that drives the pathology of DIC. Acute kidney injury (AKI) is a common feature in patients with TAMOF.
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PMID:Thrombocytopenia-Associated Multiple Organ Failure and Acute Kidney Injury. 2641 Jan 36

The neonatal hemostatic system is continuously developing with rapidly changing concentrations of many coagulation proteins. Thus, determining the etiology of bleeding in a newborn has additional challenges beyond those seen in older children or adults. Bleeding can be seen in both well and sick newborns due to congenital causes, such as hemophilia or von Willebrand disease, and acquired causes, such as liver failure or disseminated intravascular coagulation. Traditional coagulation testing should be interpreted with caution and with the help of a hematologist, if possible, due to the greatly different normal ranges between neonates as compared with older children and adults. However, despite these challenges, both clinical and laboratory clues can guide physicians appropriately to diagnose and treat the bleeding newborn.
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PMID:The bleeding newborn: A review of presentation, diagnosis, and management. 2677 26

In the first part of the medical education article on haemostatic disorders in ENT patients the basic physiology of haemostasis and main diagnostic tools were presented and discussed.The second part presents disorders of the coagulation system,thrombocyte function and blood vessels with special emphasis on clinical practice in ENT surgery. In this context, haemophilia A and B, von Willebrand disease and different forms of thrombocytopenia are of main clinical importance. Some underlying diseases such as malignomas, renal and hepatic insufficiency in combination with drug therapy (e.g.anticoagulants and thrombocyte function inhibitors) play an important role in clinical practice as well.Sepsis and haemorrhage may lead to disseminated intravascular coagulation (DIC).Beside a systematic review, important haemostatic disorders are illustrated with case reports.
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PMID:[Haemostatic disorders in ENT patients.Part 2: Pathophysiology, diagnostics, clinical feature and therapy]. 2827 Dec 45

Hemostasis is a complicated biological system, where the balance between procoagulation and anticoagulation processes maintains fluidity of blood through intact blood vessels and creates thrombi when it is needed to prevent bleeding from the impaired vessels. The modern model of hemostasis is divided into 2 principal phases, the first being defined as primary hemostasis which involves the platelet-vessel interplay, while the second, defined as secondary hemostasis, mainly involves coagulation factors and surfaces of activated cells. The activation and amplification of the coagulation cascade is regulated by natural inhibitors of coagulation. The blood clots which arise to prevent loss of blood must subsequently be broken down and the compact blood vessel wall must be restored. This process is called fibrinolysis. Bleeding and thromboses are manifestations of the impaired hemostatic balance. Detection of its cause is important for efficient treatment and prevention of the condition. This requires a combined evaluation of the family and personal history, a clinical anamnesis along with the evaluation of laboratory results. It is not reasonable or economical to perform all the available tests of hemostasis at the same time. It is recommendable to proceed from the global to the screening and then special tests and, through the process of elimination, obtain an explanation of the bleeding or prothrombotic phenotypes. The purpose of this report is to provide a brief overview of the principal causes of the hemostatic disorders and the practices which facilitate their diagnosis. Key words: diagnosis of hemorrhagic manifestations - diagnostics of thrombophilias - DIC diagnostics - hemophilia A - thrombopathy - von Willebrand disease.
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PMID:Diagnostic strategies in disorders of hemostasis. 3019 24

Thrombocytopenia-associated multiple organ failure is a clinical phenotype encompassing a spectrum of syndromes associated with disseminated microvascular thromboses. Autopsies performed in patients that died with thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, or disseminated intravascular coagulation reveal specific findings that can differentiate these 3 entities. Significant advancements have been made in our understanding of the pathologic mechanisms of these syndromes. Von Willebrand factor and ADAMTS-13 play a central role in thrombotic thrombocytopenic purpura. Shiga toxins and the complement pathway drive the hemolytic uremic syndrome pathology. Tissue factor activity is vital in the development of disseminated intravascular coagulation.
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PMID:Thrombocytopenia-Associated Multiple Organ Failure. 3217 19

The process of fibrin clot formation is a series of complex and well-regulated reactions involving blood vessels, platelets, procoagulant plasma proteins, natural inhibitors, and fibrinolytic enzymes. Vasculitis can be caused by a variety of different agents as bacteria, viruses, protozoal, rickettsial organisms, toxic, drugs, medications, and neoplasms. The most common cause of vasculitis is the purpura hemorrhagica, which is associated with exposure to Streptococcus equi ssp. equi or less commonly, equine influenza. Deficiencies or defects of the hemostatic components may result in bleeding and/or thrombosis. Inherited alterations of primary hemostasis (von Willebrand disease: vWD and Glanzmann's thrombasthenia: GT) and of secondary hemostasis (hemophilia A and prekallikrein: PK deficiency) are scarcely reported in equine clinic. On the contrary, acquired alterations of primary and secondary hemostasis are commonly found. They include thrombocytopenia, platelet dysfunction due to the administration of some drugs and targeted antiplatelet agents, decreased factor synthesis (liver disease or deficiency of vitamin K), release of inactive factors, inhibition of factor activity, or excessive consumption and depletion of factors (platelets, coagulation factors, and anticoagulants factors as antithrombin (AT) and protein C). Disseminated intravascular coagulation (DIC) is the most common and complex hemostatic disorder in horses and appears to be associated with sepsis, inflammatory and ischemic gastrointestinal tract disorders and other systemic severe diseases. These alterations are commonly found in patients in intensive care units.
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PMID:Clinical and laboratorial description of the differential diagnoses of hemostatic disorders in the horse. 3236 18


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