Thromboelastography (TEG) is a method of testing the efficiency of blood coagulation. It is a test mainly used in surgery and anesthesiology, although increasingly used in resuscitations in Emergency Departments, intensive care units, and labor and delivery suites. More common tests of blood coagulation include prothrombin time (PT,INR) and partial thromboplastin time (aPTT) which measure coagulation factor function, but TEG also can assess platelet function, clot strength, and fibrinolysis which these other tests cannot.
Thromboelastometry (TEM), previously named rotational thromboelastography (ROTEG) or rotational thromboelastometry (ROTEM), is another version of TEG in which it is the sensor shaft, rather than the cup, that rotates.
A small sample of blood is taken from the selected person and rotated gently through 4º 45', six times a minute, to imitate sluggish venous flow and activate coagulation. A thin wire probe is used to measure, which the clot forms around. The speed and strength of clot formation is measured in various ways, typically by computer. The speed at which the sample coagulates depends on the activity of the plasma coagulation system, platelet function, fibrinolysis and other factors which can be affected by genetics, illness, environment and medications. The patterns of changes in strength and elasticity in the clot provide information about how well the blood can perform hemostasis, and how well or poorly different factors are contributing to clot formation.[ citation needed ]
Four values that represent clot formation are determined by this test: the reaction time (R value), the K value, the angle and the maximum amplitude (MA). The R value represents the time until the first evidence of a clot is detected. The K value is the time from the end of R until the clot reaches 20mm and this represents the speed of clot formation. The angle is the tangent of the curve made as the K is reached and offers similar information to K. The MA is a reflection of clot strength. A mathematical formula determined by the manufacturer can be used to determine a Coagulation Index (CI) (or overall assessment of coagulability) which takes into account the relative contribution of each of these 4 values into 1 equation. The G-value is a log-derivation of the MA and is meant to also represent the clot strength using dynes/sec as its units. There are some studies which suggest that an elevated G-value is associated with a hypercoagulable state and therefore increases the risk for venous thromboembolic disease. However, there are no studies dosing of prophylactic heparin products based on the G-value. TEG also measures clot lysis which is reported as both the estimated percent lysis (EPL) and the percentage of clot which has actually lysed after 30 minutes (LY 30,%). Although a normal EPL can be as high as 15% and a normal LY 30 can be as high as 8%, some studies in the trauma population suggest that a LY30 greater than 3% is associated with risk of hemorrhage.
Thromboelastometry (TEM), previously named rotational thromboelastography (ROTEG) or rotational thromboelastometry (ROTEM), is another version of TEG in which it is the sensor shaft, rather than the cup, that rotates. Blood (300 µl, anticoagulated with citrate) is placed into the disposable cuvette using an electronic pipette. A disposable pin is attached to a shaft which is connected with a thin spring (the equivalent to Hartert's torsion wire in thrombelastography) and slowly oscillates back and forth. The signal of the pin suspended in the blood sample is transmitted via an optical detector system. The test is started by adding appropriate reagents. The instrument measures and graphically displays the changes in elasticity at all stages of the developing and resolving clot. The typical test temperature is 37 °C, but different temperatures can be selected, e.g. for patients with hypothermia.
Sonoclot is the latest version of Thromboelastography which takes into account the initial viscosity changes (which typically happens before Fibrin polymerization) and later the elastic changes of the developed clot.
This section does not cite any sources . (September 2017) (Learn how and when to remove this template message)
There are several types of assays that can be run using TEG: Standard (kaolin), RapidTEG, heparinase, Functional Fibrinogen and PlateletMapping. A standard TEG is the most commonly ordered test and includes the parameters noted above. A RapidTEG uses tissue factor in addition to kaolin thereby further speeding up the reaction. In this assay, the R-value is replaced by the TEG-ACT value which is measured in seconds rather than in minutes. The remainder of the TEG parameters do not differ between a standard and RapidTEG. A heparinase TEG is used to assess for heparin-associated anticoagulation as the cause of hemorrhage. It is used most commonly following cardiopulmonary bypass procedures where heparin is reversed using protamine intraoperatively. In instances where a patient develops bleeding due to recurrent coagulopathy (usually shortly after arrival to the ICU), the heparinase TEG can help quickly discern patients who can be treated with additional dosing of protamine versus those who need to be taken back to the operating room for re-exploration. In this assay, a standard TEG is run twice – once using the patient's blood only and another time using the patient's blood plus added heparinase. If the two graphs are nearly the same, the cause of bleeding is not related to heparin rebound. However, if the R-time associated with the heparinase-added specimen is significantly shorter than the R-time of the patient's blood without added heparinase, the bleeding is likely due to heparin rebound and should respond to administration of protamine. Lastly, the platelet map TEG aims to determine to what degree platelet function may be inhibited due to pharmacologic inhibition of either the arachidonic acid (AA) or adenosine diphosphate (ADP) pathways. Aspirin inhibits platelet function via the AA pathway while clopidogrel inhibits platelet function via the ADP pathway; thus, this test can be used to determine the degree to which a patient is anticoagulated due to either medication. In this assay, a standard TEG is run using patient's whole blood. Then, separate assays are run using the patient's blood with added AA or ADP. The contribution of fibrin to the MA is subtracted using a mathematical formula. This allows determination of the MA (AA) and MA (ADP), respectively. The difference between the patient's whole blood result and AA/ADP added results are used to calculate the percent inhibition.
Because the R value on the TEG represents the time it takes for clot formation to start, it is a reflection of coagulation factor activity. Coagulation factors are essentially enzymes that drive clot formation. Thus, a significantly prolonged R time could be treated with frozen plasma. The alpha angle represents the thrombin burst and conversion of fibrinogen to fibrin. Thus, a depressed alpha angle could be treated with cryoprecipitate. 80% of the MA is derived from platelet function whereas the remaining 20% is derived from fibrin. Thus, a significantly depressed MA could be treated with platelet transfusion or medications that improve platelet function, such as DDAVP. An elevated EPL or LY30 suggests fibrinolysis and may be treated with an antifibrinolytic, such as tranexamic acid or aminocaproic acid, in the appropriate clinical setting. A single, modified TEG assay with exogenous tissue plasminogen activator (tPA) demonstrated remarkable efficiency in unmasking patients' impending risk for massive transfusion in trauma patients.
Clinical studies of thromboelastography during elective surgery (cardiac and liver surgery) and emergency resuscitation have shown improvements in clinical outcomes.In elective surgery there was a decreased need for blood products (platelets and plasma) and reduced operating room length of stay as well as duration of intensive care admission and bleeding rates; mortality was not affected. In emergency settings, mortality was reduced with an associated decrease in the need for platelets and plasma.
Additional studies show thromboelastography may be used to characterize COVID-19 associated coagulopathy. TEG with platelet mapping may be used to guide use of anticoagulant and antiplatelet medications. When using a TEG guided strategy hospital length of stay, intensive care unit length of stay, mortality, acute kidney injury, intensive care unit admissions and need for mechanical ventilation may be reduced.
A thrombus, colloquially called a blood clot, is the final product of the blood coagulation step in hemostasis. There are two components to a thrombus: aggregated platelets and red blood cells that form a plug, and a mesh of cross-linked fibrin protein. The substance making up a thrombus is sometimes called cruor. A thrombus is a healthy response to injury intended to prevent bleeding, but can be harmful in thrombosis, when clots obstruct blood flow through healthy blood vessels.
Platelets, also called thrombocytes, are a component of blood whose function is to react to bleeding from blood vessel injury by clumping, thereby initiating a blood clot. Platelets have no cell nucleus; they are fragments of cytoplasm that are derived from the megakaryocytes of the bone marrow, which then enter the circulation. Circulating unactivated platelets are biconvex discoid (lens-shaped) structures, 2–3 µm in greatest diameter. Activated platelets have cell membrane projections covering their surface. Platelets are found only in mammals, whereas in other vertebrates, thrombocytes circulate as intact mononuclear cells.
Coagulation, also known as clotting, is the process by which blood changes from a liquid to a gel, forming a blood clot. It potentially results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion and aggregation of platelets, as well as deposition and maturation of fibrin.
Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. Symptoms may include chest pain, shortness of breath, leg pain, problems speaking, or problems moving parts of the body. As clotting factors and platelets are used up, bleeding may occur. This may include blood in the urine, blood in the stool, or bleeding into the skin. Complications may include organ failure.
Fibrin is a fibrous, non-globular protein involved in the clotting of blood. It is formed by the action of the protease thrombin on fibrinogen, which causes it to polymerize. The polymerized fibrin, together with platelets, forms a hemostatic plug or clot over a wound site.
Fibrinogen is a glycoprotein complex, made in the liver, that circulates in the blood of all vertebrates. During tissue and vascular injury, it is converted enzymatically by thrombin to fibrin and then to a fibrin-based blood clot. Fibrin clots function primarily to occlude blood vessels to stop bleeding. Fibrin also binds and reduces the activity of thrombin. This activity, sometimes referred to as antithrombin I, limits clotting. Fibrin also mediates blood platelet and endothelial cell spreading, tissue fibroblast proliferation, capillary tube formation, and angiogenesis and thereby promotes revascularization and wound healing.
Fibrinolysis is a process that prevents blood clots from growing and becoming problematic. This process has two types: primary fibrinolysis and secondary fibrinolysis. The primary type is a normal body process, whereas secondary fibrinolysis is the breakdown of clots due to a medicine, a medical disorder, or some other cause.
Hemostasis or haemostasis is a process to prevent and stop bleeding, meaning to keep blood within a damaged blood vessel. It is the first stage of wound healing as well as a process in blood clotting. This involves coagulation, blood changing from a liquid to a gel. Intact blood vessels are central to moderating blood's tendency to form clots. The endothelial cells of intact vessels prevent blood clotting with a heparin-like molecule and thrombomodulin and prevent platelet aggregation with nitric oxide and prostacyclin. When endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor, which initiate the maintenance of hemostasis after injury. Hemostasis has three major steps: 1) vasoconstriction, 2) temporary blockage of a break by a platelet plug, and 3) blood coagulation, or formation of a fibrin clot. These processes seal the hole until tissues are repaired.
Low-molecular-weight heparin (LMWH) is a class of anticoagulant medications. They are used in the prevention of blood clots and treatment of venous thromboembolism and in the treatment of myocardial infarction.
D-dimer is a fibrin degradation product, a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis. It is so named because it contains two D fragments of the fibrin protein joined by a cross-link.
Factor XIII or fibrin stabilizing factor is a zymogen found from the blood of humans and some other animals. It is activated by thrombin to factor XIIIa. XIIIa is an enzyme of the blood coagulation system that crosslinks fibrin. Deficiency of XIII worsens clot stability and increases bleeding tendency.
Dilute Russell's viper venom time (dRVVT) is a laboratory test often used for detection of lupus anticoagulant (LA).
Renal vein thrombosis (RVT) is the formation of a clot in the vein that drains blood from the kidneys, ultimately leading to a reduction in the drainage of one or both kidneys and the possible migration of the clot to other parts of the body. First described by German pathologist Friedrich Daniel von Recklinghausen in 1861, RVT most commonly affects two subpopulations: newly born infants with blood clotting abnormalities or dehydration and adults with nephrotic syndrome.
Antifibrinolytics are a class of medication that are inhibitors of fibrinolysis. Examples include aminocaproic acid and tranexamic acid. These lysine-like drugs interfere with the formation of the fibrinolytic enzyme plasmin from its precursor plasminogen by plasminogen activators which takes place mainly in lysine rich areas on the surface of fibrin. These drugs block the binding sites of the enzymes or plasminogen respectively and thus stop plasmin formation.
The thrombin time (TT), also known as the thrombin clotting time (TCT) is a blood test that measures the time it takes for a clot to form in the plasma of a blood sample containing anticoagulant, after an excess of thrombin has been added. It is used to diagnose blood coagulation disorders and to assess the effectiveness of fibrinolytic therapy. This test is repeated with pooled plasma from normal patients. The difference in time between the test and the 'normal' indicates an abnormality in the conversion of fibrinogen to fibrin, an insoluble protein.
Fibrin degradation products (FDPs), also known as fibrin split products, are components of the blood produced by clot degeneration. Clotting, also called coagulation, at the wound site produces a mass of fibrin threads called a net that remains in place until the cut is healed. As a cut heals, the clotting slows down. Eventually the clot is broken down and dissolved by plasmin. When the clot and fibrin net dissolve, fragments of protein are released into the body. These fragments are fibrin degradation products or FDPs. If your body is unable to dissolve a clot, you may have abnormal levels of FDPs. The most notable subtype of fibrin degradation products is D-dimer.
Quebec Platelet Disorder (QPD) is a rare, autosomal dominant bleeding disorder described in a family from the province of Quebec in Canada. The disorder is characterized by large amounts of the fibrinolytic enzyme urokinase-type plasminogen activator (uPA) in platelets. This causes accelerated fibrinolysis which can result in bleeding.
The fibrinolysis system is responsible for removing blood clots. Hyperfibrinolysis describes a situation with markedly enhanced fibrinolytic activity, resulting in increased, sometimes catastrophic bleeding. Hyperfibrinolysis can be caused by acquired or congenital reasons. Among the congenital conditions for hyperfibrinolysis, deficiency of alpha-2-antiplasmin or plasminogen activator inhibitor type 1 (PAI-1) are very rare. The affected individuals show a hemophilia-like bleeding phenotype. Acquired hyperfibrinolysis is found in liver disease, in patients with severe trauma, during major surgical procedures, and other conditions. A special situation with temporarily enhanced fibrinolysis is thrombolytic therapy with drugs which activate plasminogen, e.g. for use in acute ischemic events or in patients with stroke. In patients with severe trauma, hyperfibrinolysis is associated with poor outcome. Moreover, hyperfibrinolysis may be associated with blood brain barrier impairment, a plasmin-dependent effect due to an increased generation of bradykinin.
Thromboelastometry (TEM), previously named rotational thromboelastography (ROTEG) or rotational thromboelastometry (ROTEM), is an established viscoelastic method for hemostasis testing in whole blood. It is a modification of traditional thromboelastography (TEG). TEM investigates the interaction of coagulation factors, their inhibitors, anticoagulant drugs, blood cells, specifically platelets, during clotting and subsequent fibrinolysis. The rheological conditions mimic the sluggish flow of blood in veins.
Blood clotting tests are the tests used for diagnostics of the hemostasis system. Coagulometer is the medical laboratory analyzer used for testing of the hemostasis system. Modern coagulometers realize different methods of activation and observation of development of blood clots in blood or in blood plasma.