Disseminated intravascular coagulation laboratory findings: Difference between revisions
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==Overview== | ==Overview== | ||
==Laboratory findings== | |||
Although numerous [[blood test]]s are often performed on patients prone to DIC, the important measures are: [[full blood count]] (especially the [[platelet]] count), [[fibrin degradation product]]s or [[D-dimer]] tests (markers of [[fibrinolysis]]), [[bleeding time]] and [[fibrinogen]] levels. Decreased platelets, elevated FDPs or D-dimers, prolonged bleeding time and decreased fibrinogen are markers of DIC. In general; | |||
* The diagnosis of DIC is suggested when the appropriate clinical picture (hemorrhage and thrombosis with end-organ dysfunction) is accompanied by lab evidence of procoagulant activation, fibrinolytic activation, and inhibitor consumption. | |||
The peripheral smear will reveal schistocytes and RBC (red blood cell) fragments in ~ 50%, and the absence of schistocytes does not rule out DIC. Most patients will have a mild reticulocytosis and leukocytosis, as well as thrombocytopenia with an increased population of young platelets (due to increased destruction and turnover). | * [[Thrombocytopenia]] is an almost universal finding. | ||
* The peripheral smear will reveal schistocytes and RBC (red blood cell) fragments in ~ 50%, and the absence of schistocytes does not rule out DIC. Most patients will have a mild reticulocytosis and leukocytosis, as well as thrombocytopenia with an increased population of young platelets (due to increased destruction and turnover). | |||
Pathologically, early signs include platelet-rich microthrombi, which are then replaced by fibrin-rich microthrombi. | Pathologically, early signs include platelet-rich microthrombi, which are then replaced by fibrin-rich microthrombi. | ||
* Although one would think that the PT and PTT ([[prothrombin]] time and [[partial thromboplastin time]]) should uniformly be elevated in DIC, this is not the case, with up to 50% of patients having normal values (due to higher circulating levels of clotting factors such as factor Xa and thrombin). | |||
* Fibrin and fibrinogen degradation products, however, are elevated in 80 – 100% of patients. | |||
*:* High FDPs, however, are not specific and can be elevated in any state associated with elevated plasmin levels such as PE/DVT (pulmonary embolism/deep vein thrombosis), liver or renal disease, in patients s/p (status post) surgery, and in women on oral contraceptives. | |||
* The [[D-dimer]], however, is specific for the presence of fibrin degradation, and is thought to be more sensitive and specific for DIC. | |||
* Antithrombin levels have become a key test for diagnosing and monitoring therapy in DIC. | |||
*:* With thrombin activation, antithrombin is also activated, forming thrombin – antithrombin complexes --> reduced AT levels. | |||
* The main differential is TTP-HUS (thrombotic thrombocytopenic purpura-hemolytic uremic syndrome), which is associated primarily with thrombocytopenia, and minimal effects on fibrin degradation. | |||
*:* The PT and PTT in TTP – HUS are therefore usually normal, and there is little evidence of fibrinolysis and inhibitor consumption. | |||
==References== | ==References== | ||
Revision as of 16:45, 28 August 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Laboratory findings
Although numerous blood tests are often performed on patients prone to DIC, the important measures are: full blood count (especially the platelet count), fibrin degradation products or D-dimer tests (markers of fibrinolysis), bleeding time and fibrinogen levels. Decreased platelets, elevated FDPs or D-dimers, prolonged bleeding time and decreased fibrinogen are markers of DIC. In general;
- The diagnosis of DIC is suggested when the appropriate clinical picture (hemorrhage and thrombosis with end-organ dysfunction) is accompanied by lab evidence of procoagulant activation, fibrinolytic activation, and inhibitor consumption.
- Thrombocytopenia is an almost universal finding.
- The peripheral smear will reveal schistocytes and RBC (red blood cell) fragments in ~ 50%, and the absence of schistocytes does not rule out DIC. Most patients will have a mild reticulocytosis and leukocytosis, as well as thrombocytopenia with an increased population of young platelets (due to increased destruction and turnover).
Pathologically, early signs include platelet-rich microthrombi, which are then replaced by fibrin-rich microthrombi.
- Although one would think that the PT and PTT (prothrombin time and partial thromboplastin time) should uniformly be elevated in DIC, this is not the case, with up to 50% of patients having normal values (due to higher circulating levels of clotting factors such as factor Xa and thrombin).
- Fibrin and fibrinogen degradation products, however, are elevated in 80 – 100% of patients.
- High FDPs, however, are not specific and can be elevated in any state associated with elevated plasmin levels such as PE/DVT (pulmonary embolism/deep vein thrombosis), liver or renal disease, in patients s/p (status post) surgery, and in women on oral contraceptives.
- The D-dimer, however, is specific for the presence of fibrin degradation, and is thought to be more sensitive and specific for DIC.
- Antithrombin levels have become a key test for diagnosing and monitoring therapy in DIC.
- With thrombin activation, antithrombin is also activated, forming thrombin – antithrombin complexes --> reduced AT levels.
- The main differential is TTP-HUS (thrombotic thrombocytopenic purpura-hemolytic uremic syndrome), which is associated primarily with thrombocytopenia, and minimal effects on fibrin degradation.
- The PT and PTT in TTP – HUS are therefore usually normal, and there is little evidence of fibrinolysis and inhibitor consumption.