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Spontaneous (Unexplained) Thrombosis: The Inherited Basis for the Thrombohemorrhagic Balance
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
Furthermore, plasmin has its specific inhibitor, a2-antiplasmin (a2AP) (see Reference 38 and 40). Homozygous deficiency of this inhibitor leads to a serious bleeding disorder, like severe hemophilia, indicating its pivotal role in counteracting hyperfibrinolysis.41 It therefore appears that the fibrinolytic mechanism represents in itself a tightly controlled biological mechanism, ideally designed to challenge thrombotic incidents.
Hyperfibrinolysis in Liver Transplantation
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Excessive bleeding can be due to surgical causes and/or derangement of hemostasis.7 It is recognized that during certain stages of OLT generalized oozing, which cannot be attributed to demonstrable bleeding vessels in the surgical field, may occur. Serious “surgical” bleeding may complicate the removal of the native liver (stage I). Some patients have had previous surgery and there are often problems with adhesions, large collateral blood vessels, and portal hypertension. Once the liver is removed (stage II) bleeding from previously dry surgical fields, not clearly related to the surgical trauma, may occur. It is this type of bleeding that is thought to be due to hemostatic disorders, especially hyperfibrinolysis. Reperfusion of the graft liver and the first hour of the third stage are also associated with bleeding from nonsurgical origin. Once the new liver starts functioning, blood loss becomes easier to control, as the hemostatic function is gradually restored.
Transfusion medicine
Published in Ian Greaves, Military Medicine in Iraq and Afghanistan, 2018
As transfusion developed, there was an increasing effort from 2008 onwards to individualise transfusion support after the initial pre-designated sequence. The challenge was whether to use standard laboratory diagnostic testing or to re-explore visco-elastic methodology. These old whole blood techniques promised to give a more dynamic interpretation of whole blood clotting and diagnose specific issues such as hyperfibrinolysis.31 One of the drivers for introduction was that the bespoke treatment would minimise unnecessary use of blood components, thereby reducing donor exposure and preserving blood stocks. Rotational thromboelastometry (ROTEM™) was deployed to Afghanistan as a field trial in 2009 to determine its usefulness and reliability.32 The investigators concluded that the machine was robust enough to be used in a field environment and was useful in detecting coagulopathy and improving outcomes.33 The field trials demonstrated that the early A5 and A10 values were able to predict hypocoagulation, with sensitivities and specificities of 0.98/0.69 (A5) and 0.97/0.78.34 Ironically, the introduction of ROTEM™ increased rather than reduced the demand for platelets and cryoprecipitate.
Apolipoprotein A-I, elevated in trauma patients, inhibits platelet activation and decreases clot strength
Published in Platelets, 2022
Wilbert L. Jones, Christopher R. Ramos, Anirban Banerjee, Ernest E. Moore, Kirk C. Hansen, Julia R. Coleman, Marguerite Kelher, Keith B. Neeves, Christopher C. Silliman, Jorge Di Paola, Brian Branchford
Citrated kaolin-TEGs (CK-TEG) were completed as described, with the addition of apoA-I [50–300 µg/dl] or normal saline (NS) prior to activation [34,35]. The TEG parameters measured included the activated clotting time (ACT) (min), angle (degrees), maximum amplitude (MA, mm), clot strength (G, derived from the MA) and clot lysis at 30 min following the MA (LY30, percent) [34,35]. The maximum amplitude (MA) is the maximum width of the TEG tracing and corresponds with maximum clot strength. G (dynes/cm2) is a measure of shear elastic modulus strength derived according to the formula G = (5000*MA)/(100-MA) [36,37]. Citrated Functional Fibrinogen was evaluated with abciximab (a GPIIb/IIIa monoclonal blocking antibody) to eliminate platelet function and examine fibrin-based clot formation [38,39]. This assay has been previously demonstrated to closely correlate with von Clauss and Clauss fibrinogen assays. [38] Platelet mapping studies were completed employing reptilase and factor XIII to activate fibrin with arachidonic acid (AA) and adenosine diphosphate (ADP) to activate platelets ± pre-incubation with apoA-I [300 µg/ml] or vehicle control [32]. ApoA-I levels were measured in four consecutive severely injured patients with systemic hyperfibrinolysis because of their clot instability using a commercial enzyme-linked immunosorbent assay (ELISA).
Tranexamic acid in gynecologic surgery
Published in Current Medical Research and Opinion, 2020
Andrew Zakhari, Ari Paul Sanders, Meir Jonathon Solnik
Discovered in the search for a hemostatic molecule to treat postpartum hemorrhage, TXA was patented by Dr. S. Okamoto in 1957, who later published on its use in collaboration with her research partner and husband.9,10 TXA was found to be significantly more potent than a precursor molecule known as epsilon-amino-caproic acid (EACA). Both work in a similar fashion; as lysine-analogues, they reversibly bind to plasminogen, preventing its activation to plasmin and subsequent degradation of the fibrin clot complex.11 For this reason, TXA is commonly referred to as an anti-fibrinolytic, or clot-stabilizer. It has also been shown to decrease inflammatory markers and mitigate hyperfibrinolysis-driven coagulopathy.9,12
Prehospital trauma care evolution, practice and controversies: need for a review
Published in International Journal of Injury Control and Safety Promotion, 2020
Tranexamic acid, a very old drug recently, has found use as an effective drug to control bleeding. This was started after a major multicentric trial (CRASH 2 trial) of the drug (Collaborators, 2011; Roberts et al., 2013). It is increasingly being used in ambulances around the world (Strosberg, Nguyen, Mostafavifar, Mell, & Evans, 2016). It is given as a 1 gm bolus dose, recommended as a bolus en route to definitive care in high-risk patients and withholding subsequent doses until hyperfibrinolysis is confirmed by thromboelastography (Huebner, Dorlac, & Cribari, 2017). Available data support the efficacy and the safety of TXA. High-level evidence supports its use in trauma and strongly suggests that its implementation in the prehospital setting offers a survival advantage to many patients, particularly when evacuation to surgical care may be delayed (Ausset et al., 2015). It is also recommended by the ATLS tenth edition.