Euglobulin Lysis Test

Euglobulin clot lysis time is one of the tests used for fibrinolysis assessment using
the euglobulin fraction of plasma which is obtained by acidification of platelet-poor
plasma resulting in a significant depletion of fibrinolysis inhibitors with relatively
preserved levels of plasminogen activators [37,41].

From: Thrombosis Research, 2019

Related terms:

Coagulation, Fibrinolysis, Tissue Plasminogen Activator, Prothrombin Time, Throm-

bolytic Drug, Plasminogen Activator Inhibitor-1, Aminocaproic Acid, Thrombin,
Fibrin, Fibrinogen

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Laboratory Assessment of Fibrinolysis

Thomas C. Abshire MD, in Transfusion Medicine and Hemostasis, 2009

Euglobulin Lysis Time:

The euglobulin lysis time (ELT) is the standard screening test for hyperfibrinolysis.
The euglobulin fraction of plasma contains: fibrinogen, plasminogen, plasminogen
activators and plasmin, and is formed as a precipitate. The precipitate is lacking
fibrinolytic inhibitors. The ELT is performed by isolating the euglobulin fraction from
patient plasma, suspending it in buffer to which thrombin is added, allowing a clot
to form, and then measuring clot lysis. A positive test is evident with a shortened ELT
(usually < 60 minutes). This indicates that increased fibrinolysis is present, although
the exact cause of the excessive fibrinolysis is not determined by this methodology.
It is important to note that the ELT can be shortened in consumptive coagulopathies
(e.g. DIC); thus, primary hyperfibrinolysis would consist of a shortened ELT in the
absence of other labs that indicate consumptive processes (e.g. schistocytes on
peripheral smear).

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Laboratory Techniques in Fibrinolysis
Testing
Wayne L. Chandler MD, in Transfusion Medicine and Hemostasis (Third Edition),
2019

Euglobulin Lysis Time

The euglobulin lysis time (ELT) is a historical screening test for hyperfibrinolysis.
Newer, more specific tests for individual fibrinolytic factors and more rapid tests,
such as thromboelastometry, have supplanted ELT. To measure ELT, the euglobulin
fraction of the plasma-containing plasminogen, plasminogen activators, and f-
ibrinogen is acid-precipitated then clotted with thrombin. Time to clot disappearance
is determined. A positive test is premature clot disappearance in 60–120 minutes,
suggesting increased fibrinolysis, although the specific cause of the excessive fibri-
nolysis is not determined by this methodology.

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Laboratory Techniques in Fibrinolysis

Testing
Mikhail Roshal MD, PhD, in Transfusion Medicine and Hemostasis (Second Edi-
tion), 2013

Euglobulin Lysis Time

The euglobulin lysis time (ELT) is a historical test for screening for hyperfibrinolysis.
Newer, more specific, and in some cases more rapid tests (such as thromboelastom-
etry and assays for specific fibrinolysis-associated factors) have in many instances
supplanted ELT. Nonetheless some laboratories continue to perform the test as a
primary hyperfibrinolysis screen. In order to perform the test, the euglobulin fraction
of the plasma containing plasminogen, plasminogen activators (t-PA and u-PA)
and fibrinogen is first isolated from most of the other plasma components. This is
typically done by cold (4°C) precipitation of the euglobulin fraction in the plasma
diluted with acetic acid. The precipitate is then separated from the supernatant by
centrifugation in a refrigerated centrifuge, resuspended in buffer and clotted with
thrombin. The presence of the clot is then checked visually, with wood sticks or via
electromechanical detection every 15 minutes. Positive test is evident when a clot is
dissolved prematurely (usually before 60–120 minutes). This finding indicates that
increased fibrinolysis is present, although the exact cause of the excessive fibrinolysis
is not determined by this methodology.

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Coagulation Disorders in Congenital

Heart Disease
Scott R. Schulman MD, ... William R. Greeley MD, MBA, in Critical Heart Disease in
Infants and Children (Second Edition), 2006

Fibrinolysis
Evidence for fibrinolysis (i.e., shortened euglobulin clot lysis time, hypofibrinogen-
emia, elevated fibrin degradation products, and prolonged prothrombin and partial
thromboplastin times) has been noted after sternotomy and initiation of CPB.6,26
Endothelial cells secrete tissue plasminogen activator (TPA) during extracorporeal
circulation.39 TPA converts plasminogen to plasmin, which degrades fibrin. How-
ever, critics of fibrinolysis as a major offender in the pathogenesis of bleeding
after CPB contend that the presence of fibrin degradation products, low levels of
fibrinogen, and shortened euglobulin clot lysis times are merely a reflection of non-
specific factors such as hemodilution, inadequate heparin anticoagulation, and local
consumption of platelets and fibrinogen.

The exact role of fibrinolysis in the pathogenesis of post-CPB bleeding awaits further
clarification. Nonetheless, inhibitors of fibrinolysis such as epsilon aminocaproic
acid (EACA) and tranexamic acid have been used after open-heart surgery to decrease
bleeding. Aprotinin, a serine protease inhibitor that functions at many points in
the coagulation cascade including the inhibition of fibrinolysis, produces laboratory
evidence of inhibition of fibrinolysis and decreased blood loss.11

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Bleeding Risks with Cardiac Disease

Thomas C. Abshire MD, in Transfusion Medicine and Hemostasis, 2009

Antifibrinolytic Therapy:
Treatment with an antifibrinolytic, such as aminocaproic acid or tranexemic acid,
may be helpful if the ELT is short (a third antifibrinolytic, aprotinin, is currently not
available in the US). These agents may be utilized empirically if prompt ELT testing is
not possible, or if ongoing bleeding dictates more urgent therapy. The potential side
effects of thrombosis must be weighed. Aminocaproic acid or tranexemic acid are
similar in structure to lysine, and competitively inhibit the binding of plasminogen
and TPA to the lysine binding sites on fibrin. Antifibrinolytic therapy may also reduce
platelet dysfunction, since the agents may decrease fibrin degradation products and
their effect on platelet–platelet interaction. Since use of an antifibrinolytic agent may
also cause thrombosis, careful monitoring is encouraged.

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A
Carl P. Weiner MD, MBA, FACOG, Clifford Mason PhD, in Drugs for Pregnant and
Lactating Women (Third Edition), 2019

Aminocaproic acid — (Amicar; Capracid; Epsikapron)

International Brand Names

Log on to ExpertConsult.com for a list of all international brand names.

Amicar (Canada, Mexico, South Africa); Capramol (France); Caproamin (Spain,

Venezuela); Caprolisin (Italy); Epsicaprom (Portugal); Epsilonaminocapronsav (Hun-
gary); Hemocaprol (Spain); Ipsilon (Argentina, Brazil, Japan, Paraguay, Uruguay);
Resplamin (Japan)

Drug Class Hemostatics

Indications Hemorrhage associated with excess fibrinolysis
(protamine test negative, euglobulin lysis test
positive, and platelet count normal): for exam-
ple, placental abruption, missed abortion, cardiac
surgery or cirrhosis, treatment of a megakaryocy-
tosis, ITP, agranulocytosis, and hereditary hem-
orrhagic telangiectasia
Mechanism Inhibition of plasminogen activator
Dosage With Qualifiers Hemorrhage—typically 4–5 g IV or PO over first
hour, followed by 1 g/h IV; max 30 g/d•Con-
traindications—hypersensitivity to drug
or class, DIC unassociated with prima-
ry fibrinolysis, hemorrhage of unknown
 etiology•Caution—renal or hepatic dys-
function, CAD
Maternal Considerations There are no adequate reports or well-controlled
studies of aminocaproic acid in pregnant
women. It has been used in a variety of hemor-
rhagic circumstances. The literature consists pre-
dominantly of case reports.Side effects include
seizures, acute renal failure, cardiac arrhythmias,
dizziness, myopathy, myositis, rhabdomyolysis,
confusion, and clotting disorders.
Fetal Considerations There are no adequate reports or well-controlled
studies in human fetuses. It is unknown whether
aminocaproic acid crosses the human pla-
centa. Aminocaproic acid decreases implan-
tation in a variety of animal models. Rodent ter-
atogenicity studies have not been reported.
Breastfeeding Safety There are no adequate reports or well-controlled
studies in nursing women. It is unknown whether
aminocaproic acid enters human breast milk.
Drug Interactions No drug-drug interaction studies in human sub-
jects have been conducted. Homeostatic agents
can increase the effects of antiinhibitor coagulant
complex in addition to factor IX and fibrinogen
concentrate in humans. Tretinoin may increase
the effect of homeostatic agents.
References Landers DF, Newland M, Penney LL. J Reprod
Med 1989; 34:988-93.Neubert AG, Golden MA,
Rose NC. Obstet Gynecol 1995; 85:831-3.Peng
TC, Kickler TS, Bell WR, Haller E. Am J Obstet
Gynecol 1991; 165:425-6.
Summary Pregnancy Category: CLactation Cate-
gory: U•Aminocaproic acid should be
used during pregnancy and lactation only
if the benefit justifies the potential peri-
natal risk.•Consideration should be given
to the availability of alternative therapies
when possible.

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Investigation of a Thrombotic Tenden-

cy
Michael A. Laffan, Richard A. Manning, in Dacie and Lewis Practical Haematology
(Twelfth Edition), 2017

Investigation of fibrinolysis
The ‘fibrinolytic potential’ of plasma is measured as the combined effect of
plasminogen activators and inhibitors. The euglobulin lysis time and fibrin
plate lysis have been used to give a global assessment of fibrinolytic potential,
sometimes augmented by venous occlusion or administration of desmopressin
(1-deamino-8-D-arginine vasopressin). However these tests are laborious, tech-
nically difficult and of uncertain clinical significance. They are now rarely
performed and have been largely supplanted by assays of individual components of
the fibrinolytic system. Instructions for their performance can be found in previous
editions. For rapid assessment of fibrinolytic activity, a viscoelastic test such as
thromboelastography or ROTEM can be performed (www.rotem.de/en).

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Thrombolytic Therapy
Victor J. Marder MD, in Consultative Hemostasis and Thrombosis (Third Edition),
2013

Plasma Proteolytic (Lytic) State

The term lytic state describes the effects of plasmin in the circulation,98 the final
and most clinically notable of which are a shortening of the euglobulin lysis time,
a decrease in plasma fibrinogen level, and a prolongation of the partial throm-
boplastin time (PTT) (absent any other cause of such changes, such as heparin
effects). Plasmin may increase or decrease platelet aggregation,99,100 so a patient may
experience sequential or simultaneous hypercoagulability and hypocoagulability.
Based on the concept that the actions of a PA in the blood and on the thrombus
are separate events,3,4 thrombolysis or bleeding would not necessarily correlate
with the degree of lytic state. However, a recurring assumption is that a PA with
fibrinogen-sparing properties would cause less bleeding, since the induced lytic
state is minimized. For example, UK or SK treatment regularly induces a lytic state,
but changes in fibrinogen concentration, plasminogen level, and euglobulin lysis
time are not significantly different in patients with hemorrhagic complications
and in those without.101,102 Further, SK-treated patients in phase 1 of the TIMI
trial showed significantly lower fibrinogen values than did patients treated with
tPA, but the incidence of bleeding complications was the same in both treatment
groups.103 Also, among patients treated with tPA, those who experienced an ischemic
(thrombotic) cerebrovascular event and those who experienced a hemorrhagic event
had the same nadir concentrations of fibrinogen.104 The only blood value predictive
of hemorrhagic complications during tPA treatment is the plasma tPA concentration
(3.4 µg/mL in bleeders versus 2.2 µg/mL in nonbleeders; P = .002).105 The higher
value noted in those who bled suggests that tPA has a direct effect on susceptible
hemostatic plugs or vascular sites that is greater at higher concentrations and is
independent of changes in fibrinogen concentration—an effect that helps to explain
the higher rate of ICH at higher dosages of tPA.106 A retrospective analysis of data for
more than 40,000 patients in the GUSTO-I study found independent predictors of
hemorrhage to be older age, lighter body weight, female sex, and African ancestry,
rather than the degree of derangement in laboratory values.107

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The Bleeding Child: Congenital and Ac-

quired Disorders
BrianM , Wicklund MD, CM MPH, in Handbook of Pediatric Transfusion Medicine,
2004

Alpha 2-antiplasmin
Severe deficiency of alpha 2-antiplasmin is associated with a severe bleeding dis-
order caused by excessive fibrinolysis. The usual hemostatic screening tests are
normal, and the euglobulin clot lysis time, a measure of fibrinolytic activity, is usually
shortened. Testing for alpha 2-antiplasmin is done with functional and antigenic
assays. The heterozygous presentation of this disorder is asymptomatic or has mild
bleeding with menorrhagia, easy bruising, postdental or postsurgical bleeding. FFP
contains alpha 2-antiplasmin, but most bleeding episodes can be controlled with the
antifibrinolytics epsilon aminocaproic acid or tranexamic acid (Griffin et al. 1993).

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Antiplatelet Therapy for Secondary Pre-

vention of Stroke
Babette B. Weksler, in Stroke (Fourth Edition), 2004

Other Potential Hemostatic Effects of Aspirin

In addition to effects on platelet activation, aspirin has been reported to have effects
on fibrinolysis that may add to its antithrombotic effect.7273 Long-term aspirin
administration is associated with shortening of plasma clot lysis time, likely through
 acetylation of fibrinogen that impedes factor XIII—induced fibrin cross-linking and
so permits fibrinolysis to occur more easily.73 Conversely, large doses of aspirin may
block release of tissue plasminogen activator from venous endothelium without
impeding release of plasminogen activator inhibitor-1.74 This effect would be pre-
dicted to inhibit fibrinolysis, but whether the net effects of aspirin on fibrinolysis are
clinically important has not been clearly established. At very high concentrations,
such as those used to treat rheumatic fever or rheumatoid arthritis, aspirin can
induce hypoprothrombinemia and can inhibit synthesis of vitamin K—dependent
clotting factors. These effects are more likely due to high levels of blood salicylate
and can be reversed with vitamin K. At the usual antiplatelet doses of aspirin, no
significant depression of vitamin K dependent clotting factors is seen.

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