Thromboelastography

Last updated
Thromboelastography
MeSH D013916
LOINC 67790-6. Io

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) 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. [1] [2]

Contents

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.

Mechanics

Thromboelastography mechanics. Thromboelastography mechanics.jpg
Thromboelastography mechanics.

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. The clot forms around a thin wire probe used for measurement. 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. [2]

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. [2] [3]

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. [4]

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.[ citation needed ]

Parameters

Normal thromboelastogram with parameters. Thromboelastography parameters.png
Normal thromboelastogram with parameters.

Parameters derived from thromboelastography are mainly: [5]

Interpretation

Following are examples of thromboelastography patterns and recommended treatments. [6] [7]

ConditionAppearanceMain treatment
Normal Normal thromboelastography.png
Hemodilution or clotting factor deficiency Thromboelastography in hemodilution or clotting factor deficiency.png Fresh frozen plasma
Fibrinogen deficiency Thromboelastography in fibrinogen deficiency.png Cryoprecipitate
Low or dysfunctional platelets Thromboelastography in low or dysfunctional platelets.png Platelets
Thrombosis Thromboelastography in thrombosis.png Anticoagulant
Primary fibrinolysis Thromboelastography in primary fibrinolysis.png Antifibrinolytics or tranexamic acid
Secondary fibrinolysis Thromboelastography in secondary fibrinolysis.png Treating disseminated intravascular coagulation

Assay types

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.

Use in treatment

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. [8]

Clinical studies of thromboelastography during elective surgery (cardiac and liver surgery) and emergency resuscitation have shown improvements in clinical outcomes. [9] 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. [9]

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. [10]

Related Research Articles

Thrombus Blood clot

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.

Platelet Component of blood aiding in coagulation

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 or lung, which then enter the circulation. Circulating inactivated 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 Process by which blood changes from a liquid to a gel, forming a blood clot

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 Medical condition

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

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 Soluble protein complex in blood plasma and involved in clot formation

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. Primary fibrinolysis is a normal body process, while 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. 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.

Heparin-induced thrombocytopenia Low platelet count due to heparin, associated with a risk of thrombosis

Heparin-induced thrombocytopenia (HIT) is the development of thrombocytopenia, due to the administration of various forms of heparin, an anticoagulant. HIT predisposes to thrombosis because platelets release microparticles that activate thrombin, thereby leading to thrombosis. When thrombosis is identified the condition is called heparin-induced thrombocytopenia and thrombosis (HITT). HIT is caused by the formation of abnormal antibodies that activate platelets. If someone receiving heparin develops new or worsening thrombosis, or if the platelet count falls, HIT can be confirmed with specific blood tests.

Schistocyte Fragmented portion of a red blood cell

A schistocyte or schizocyte is a fragmented part of a red blood cell. Schistocytes are typically irregularly shaped, jagged, and have two pointed ends.

An antihemorrhagic (antihæmorrhagic) agent is a substance that promotes hemostasis. It may also be known as a hemostatic agent.

Kasabach–Merritt syndrome Medical condition

Kasabach–Merritt syndrome, also known as hemangioma with thrombocytopenia is a rare disease, usually of infants, in which a vascular tumor leads to decreased platelet counts and sometimes other bleeding problems, which can be life-threatening. It is also known as hemangioma thrombocytopenia syndrome. It is named after Haig Haigouni Kasabach and Katharine Krom Merritt, the two pediatricians who first described the condition in 1940. ==Signs and symptoms== Initially a vascular lesion is usually noted on the skin which can be firm and hard (indurated). Areas of tiny red dots (petechiae) can appear around the lesion or on other parts of the body. If the vascular lesion is internal, these petechiae and bruising can be seen on the skin. Bruising and spontaneous bleeding can also occur. The tumors are not hemangiomas. They usually present in young infants, less than three months of age, but have also been reported in the toddler age group. These tumors occur in the extremities, chest, neck, abdomen and pelvis. They infiltrate across tissue and can be aggravated by interventions, infection and trauma. When the tumors associated with KMP are internal such as in the chest or abdomen, they can cause significant illness and can be life-threatening due to bleeding. Internal lesions can take a longer time to diagnose.

Thrombin time

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 product

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.

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. While traditional thromboelastography is a global assay for blood clotting disorders and drug effects, TEM is primarily used in combination with appropriate differential assays. They allow testing in the presence of therapeutic heparin concentrations and provide differential diagnostic information to support decisions in therapy. In numerous publications the validity of the method is shown. Application of TEM at the point of care (POC) or in emergency laboratories is getting more and more popular. TEM detects both hypo- and hyperfunctional stages of the clotting process and is probably the only reliable rapid test for the diagnosis of hyperfibrinolysis. In contrast to standard clotting tests, the fibrin stabilizing effect of factor XIII contributes to the result. The rapid availability of results helps to discriminate surgical bleeding from a true haemostasis disorder and improves the therapy with blood products, factor concentrates, anticoagulants and protamine, hemostyptic and antifibrinolytic drugs. Several reports confirm that application of TEM is cost effective by reducing the consumption of blood products.

Thrombodynamics test is a method for blood coagulation monitoring and anticoagulant control. This test is based on imitation of coagulation processes occurring in vivo, is sensitive both to pro- and anticoagulant changes in the hemostatic balance. Highly sensitive to thrombosis.

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.

References

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  2. 1 2 3 Hartmann, Jan; Walsh, Mark; Grisoli, Anne; Thomas, Anthony V.; Shariff, Faisal; McCauley, Ross; Vande Lune, Stefani; Zackariya, Nuha; Patel, Shivani; Farrell, Michael S.; Sixta, Sherry; March, Robert; Evans, Edward; Tracy, Rebecca; Campello, Elena; Scărlătescu, Ecaterina; Agostini, Vanessa; Dias, João; Greve, Sarah; Thomas, Scott (March 2020). "Diagnosis and Treatment of Trauma-Induced Coagulopathy by Viscoelastography". Seminars in Thrombosis and Hemostasis. 46 (2): 134–146. doi:10.1055/s-0040-1702171. PMID   32160640. S2CID   212679113.
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  5. Tyler PD, Yang LM, Snider SB, Lerner AB, Aird WC, Shapiro NI (2021). "New Uses for Thromboelastography and Other Forms of Viscoelastic Monitoring in the Emergency Department: A Narrative Review". Ann Emerg Med. 77 (3): 357–366. doi: 10.1016/j.annemergmed.2020.07.026 . PMID   32988649.CS1 maint: multiple names: authors list (link)
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  8. Moore, Hunter B.; Moore, Ernest E.; Chapman, Michael P.; Huebner, Benjamin R.; Einersen, Peter M.; Oushy, Solimon; Silliman, Christopher C.; Banerjee, Anirban; Sauaia, Angela (July 2017). "Viscoelastic Tissue Plasminogen Activator Challenge Predicts Massive Transfusion in 15 Minutes". Journal of the American College of Surgeons. 225 (1): 138–147. doi:10.1016/j.jamcollsurg.2017.02.018. ISSN   1879-1190. PMC   5527680 . PMID   28522144.
  9. 1 2 Dias, João D.; Sauaia, Angela; Achneck, Hardean E.; Hartmann, Jan; Moore, Ernest E. (4 April 2019). "Thromboelastography‐guided therapy improves patient blood management and certain clinical outcomes in elective cardiac and liver surgery and emergency resuscitation: a systematic review and analysis". Journal of Thrombosis and Haemostasis. Online first (6): 984–994. doi: 10.1111/jth.14447 . PMC   6852204 . PMID   30947389.
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