EQUINE VETERINARY EDUCATION
Equine vet. Educ. (2011) •• (••) ••-••
doi: 10.1111/j.2042-3292.2011.00338.x
Review Article
Thromboelastography in equine medicine: Technique and
use in clinical research
J. L. Mendez-Angulo*, M. C. Mudge and C. G. Couto
Department of Veterinary Clinical Sciences and Veterinary Medical Center, The Ohio State University,
Columbus, Ohio, USA.
Keywords: horse; thrombelastography; haemostasis; hypocoagulation; hypercoagulation; point-of-care
Summary
Thromboelastography (TEG) is a viscoelastic, whole
blood-based assay that integrates information from both
the cellular and soluble components of coagulation,
providing a global evaluation of the haemostatic system.
This contrasts with the conventional coagulation assays (i.e.
platelet count, prothrombin time [PT], activated partial
thromboplastin time [aPTT] and fibrinogen concentration
[FIB]), which only provide information about one
component (e.g. clotting factors in the case of PT and aPTT)
of the haemostatic process, requiring the combination of
several assays for a complete evaluation of haemostasis.
Thromboelastography is an old technology that has been
used in human medicine for over 50 years. However, it is
relatively new in veterinary medicine and has only been
applied to horses in the last 5 years. Clinical applications in
human medicine include diagnosis and monitoring of
coagulopathies. Currently, extensive research is being
carried out to expand the use of TEG in dogs and cats.
Therefore, it is expected that the use of this technique will
also further expand in horses in the near future. To date, the
available studies in the equine species have evaluated TEG
in healthy horses, horses with gastrointestinal disease, septic
foals, horses with exercise-induced pulmonary
haemorrhage (EIPH) and a filly with Glanzmann’s
thrombasthenia. The main objective of this review is to
introduce the TEG technique to equine clinicians, providing
information on how the TEG functions, blood sample
collection and processing, variables measured and their
interpretations, normal reference values and areas of
potential clinical application.
Introduction
Haemostasis is an intricate physiological process in which
blood vessels, blood cells and soluble plasma factors
interact synergistically to control haemorrhage and
*Corresponding author email: v12meanj@uco.es
1
prevent pathological thrombosis. This delicate balance
is often disrupted in horses afflicted by hereditary
haemorrhagic disorders (e.g. Glanzmann’s
thrombasthenia), gastrointestinal diseases (e.g. colic or
colitis), sepsis, trauma or other acquired disorders (e.g.
purpura haemorrhagica) leading to pathological states of
hypo- or hypercoagulability (Monreal et al. 2000; Dolente
et al. 2002; Pusterla et al. 2003; Macieira et al. 2007; Bentz
et al. 2009). These disruptions of haemostasis can lead to
severe complications such as disseminated intravascular
coagulation (DIC), laminitis and thrombophlebitis (Welch
et al. 1992; Weiss et al. 1997; Dolente et al. 2005), among
others.
Typically, a complete equine haemostasis profile
includes a platelet count, fibrinogen concentration (FIB),
prothrombin and activated partial thromboplastin times (PT
and APTT, respectively), antithrombin activity (AT) and
fibrinogen/fibrin degradation products (FDPs) or D-dimers
concentrations (Dallap Schaer and Epstein 2009). Other
plasma-based assays (thrombin time, thrombin-anti-
thrombin [TAT] and soluble fibrin monomer complexes,
activity and concentration of protein C, and plasminogen,
tissue plasminogen activator [TPA], alpha-2 antiplasmin,
and plasminogen activator inhibitor [PAI] activities) have
also been evaluated in horses (experimentally and/or
clinically) to identify coagulopathies and correlate those
with diagnosis and prognosis (Bernard et al. 1987; Barton
et al. 1995; Collatos et al. 1995; Stokol et al. 2005; Armengou
et al. 2008). One limitation to using these plasma-based
coagulation assays is that each assay only provides
information about one component (e.g. clotting factors in
the case of PT and aPTT) of the haemostatic process,
requiring the combination of several assays for a complete
evaluation of haemostasis. Further limitations of
conventional testing include the absence of commercial
assays testing platelet function, inability to assess
contribution of other cellular elements to clot formation and
the difficulties in interpreting the significance of changes in
several parameters relative to each other.
Thromboelastography (TEG), in contrast, is a
viscoelastic whole blood-based assay that provides
© 2011 EVJ Ltd
2 Thromboelastography (TEG) in horses

information from both the cellular and soluble components

of coagulation, providing a more global evaluation of the
equine haemostatic system. Thromboelastography uses
detection of changes in the viscoelastic properties of
whole blood while it clots and subsequently lyses. The
changes are represented on a graph suitable for visual
interpretation of coagulation and provide measured and
calculated parameters for analysis. Another potential
advantage of TEG compared to clotting times (designed
mainly to detect hypocoagulability) is its ability to detect
hypercoagulability, although this is controversial since
there is not a ‘gold standard’ test to compare it with.
Currently, 4 commercial viscoelastic analysers are
available, the TEG (Thromboelastograph)1, the TEM-A
(Automated thromboelastometer)2, the ROTEM (Rotation
Thromboelastometer)3 and the Sonoclot (Sonoclot
Coagulation and Platelet Function Analyser)4 which in
addition provides information about platelet function. This
review focuses on the TEG1, although findings from equine Fig 1: Illustration of thromboelastography testing. Calcium chloride
ROTEM and Sonoclot studies are also discussed. (20 ml) and citrated blood (340 ml) have been placed in a
Thromboelastrography is an old technology utilised in preheated cup (b), then the torsion wire (a) covered by a pin (c) is
immediately immersed in blood and the cup begins to oscillates at
man and animals for more than 50 years but, in the last
4°45⬘. The clot (d) starts forming around the torsion wire (covered
decade, its popularity has dramatically increased in human by the pin) within min. The tension applied on the wire is translated
and veterinary medicine (Kol and Borjesson 2010; Wiinberg to an electrical signal that produces a trace suitable for
and Kristensen 2010). In man, TEG is commonly used in interpretation (Fig 2).
clinical settings to predict bleeding and prevent
pathological thrombosis, assess the need for a blood
product transfusion, monitor patients undergoing surgery
(i.e. cardiac surgery, liver transplantation) and guide
administration of blood products and anticoagulants
(Kashuk et al. 2009; Sivula et al. 2009; Wasowicz et al. 2009,
2010; Leemann et al. 2010; Preisman et al. 2010). In small
animal medicine, the use of TEG has become more popular
in recent years leading to a marked increase in its clinical
research (Otto et al. 2000; Kristensen et al. 2008; Wiinberg
et al. 2008; Sinnott and Otto 2009; Fenty et al. 2011;
Goodwin et al. 2011; Vilar Saavedra et al. 2011). The main
objective of this review is to introduce the TEG technique to
equine clinicians, providing information on how the TEG
functions, blood sample collection and processing, Fig 2: Representative TEG tracing with the following variables
variables measured and their interpretations, normal represented: R-Time (R), K-Time (K), angle (a), and maximum
amplitude (MA).
reference values and areas of potential clinical
application.
analysers is that with the TEG1 and TEM-A, the cup oscillates
around the fixed tension wire; in ROTEM3, the tension wire
TEG function and instrumentation oscillates in the fixed cup and the Sonoclot4 consists of a
probe that oscillates up and down within a blood sample.
The TEG1 is a point-of-care coagulation analyser. It has 2 A complete TEG tracing is typically obtained after 120 min
channels that can run 2 samples simultaneously. Each of running time (this is the time necessary to obtain all
channel consists of a torsion wire covered by a disposable variables that are relevant to horses) at 37°C. A TEG
pin, which is introduced into a preheated disposable maintenance test (i.e. calibration) should be performed
reaction cup (at 37°C) containing a 360 ml aliquot of blood daily before any sample analysis occurs, according to the
(Fig 1). Subsequently, the TEG analysis begins with the manufacturer’s recommendations (TEG 5000 User’s
oscillation of the cup (4°45′). The clot starts forming and the Manual Haemoscope, 1995–2005), as generation of
force applied to the tension wire is translated into an erroneous results is a problem encountered when this test is
electrical signal producing a characteristic trace (Fig 2). not performed. In horses, the TEG1 has been shown to be
The main difference between the available viscoelastic very precise (low intra-assay variability when the same

© 2011 EVJ Ltd

J. L. Mendez-Angulo et al. 3

sample is run on 2 channels) (Mendez-Angulo et al. 2010,

2011). However, Epstein et al. (2009) found significant
differences in TEG results when thromboelastic analyses
performed by 4 different operators were compared.

Blood sample collection and processing

Thromboelastrography was initially designed to be used in

human hospitals as a bedside point of care analyser that
utilised fresh whole blood (without the addition of
anticoagulants). However, the use of citrated whole blood
is preferred in equine medicine because it allows the
possibility of being run in a diagnostic laboratory (Wiinberg
and Kristensen 2010). At the authors’ institution, the cost of
a thromboelastic analysis in clinical cases is $75
(approximately £46.50), which is similar to a conventional
haemostasis panel. The use of viscoelastic analysers is likely
to be restricted to the hospital setting, based on a lack of
portability and the need for a consistent testing
environment.
Equine blood is collected into sodium citrate (3.2 or
3.8%) tubes, the anticoagulant of choice for most
coagulation assays including TEG analysis (Stokol et al.
2000). Sodium citrate works as an anticoagulant due to its
calcium-chelating properties, thus samples must always be
recalcified prior to TEG analysis in order for coagulation to
begin.
Blood can be drawn from a catheter or by venipuncture
(either with a Vacutainer needle, or using a needle and Fig 3: An aliquot of 340 ml of citrated blood is carefully being
syringe technique); however, it is essential that the operator placed on a preheated cup at 37°C.
ensures a consistent technique is used. Glass and plastic
tubes can be utilised, although all samples should be
parameters (R, K and angle) are significantly affected by
obtained using the same material and anti-coagulant
storage time (suggesting an incomplete inhibition of
concentrations within a laboratory because normal values
coagulation in citrated blood); therefore in horses, a fixed
vary with different containers (Roche et al. 2006; Dunkel
storage (resting) time of 30 min has been recommended
et al. 2009; D’Angelo and Villa 2011).
to decrease variability (Leclere et al. 2009). While the
Thromboelastrography assays can be performed with
sample is being rested, a reaction cup is placed in one of
or without (native citrated TEG) the use of an activator
the TEG1 channels to be heated at 37°C in preparation for
such as kaolin, which stimulates the intrinsic pathway or
the test. Once the sample has been stored for long
human recombinant tissue factor (rhTF-TEG), which
enough, 20 ml of CaCl2 is added to the cup, followed by
stimulates the extrinsic pathway. Both activators have
340 ml of citrated blood summing to a total volume of 360 ml
been tested in canine (Wiinberg et al. 2005; Bauer et al.
(Fig 3). An activator (kaolin or rhTF) can be added at this
2009) and equine blood (Macieira et al. 2007; Epstein et al.
time if desired. Special care should be taken when the
2009). Native TEG offers an ex vivo evaluation of the
pipette is introduced in to the cup that the blood is
haemostatic system without alteration from an exogenous
released slowly on to the cup wall to avoid production of
substance, although it has the disadvantage of a high
air bubbles and thus activation of the coagulation. Some
variability and a prolonged time (~10 min in horses) from
laboratories use the pipette to mix the CaCl2 and blood
initiation of the test until the start of clot formation, which
prior to starting the test. Finally, the cup is pushed up,
delays test results (Epstein et al. 2009; Leclere et al. 2009). In
locked and the test begins.
contrast, the use of an activator minimises analytical and
user variation and reduces the time to receiving final results
(Epstein et al. 2009). TEG variables and their interpretation
Independent of the methodology used, the citrated
blood tube should be rested at a fixed temperature for a The TEG variables commonly measured or calculated in
period of time before TEG analysis to allow blood horses are the R-Time, K-Time, angle, maximum amplitude,
stabilisation and to avoid false hypocoagulation G-value, LY30 and LY60. R-Time, or ‘R’, is the time (in min)
(Camenzind et al. 2000). Thromboelastrography from the beginning of the test until the clot starts forming. It

© 2011 EVJ Ltd

4 Thromboelastography (TEG) in horses
Fig 4: Superimposed tracings from a healthy and a hypocoagulable horse.
is correlated with the activity of the plasma coagulation
factors. K-Time, or ‘K’, is the time (in min) from R (clot
initiation) until an amplitude of 20 mm is reached, and it is
related to the clot kinetics. Angle, or ‘a’ (in degrees), is the
angle between baseline and a line tangent to the
elasticity curve, and is correlated to the fibrinogen
concentration (representing the rapidity of fibrin build-up
and cross-linking). Maximum amplitude, or ‘MA’ (expressed
in mm), corresponds to the ultimate strength of the clot
and depends on the contribution of platelet aggregation
and fibrinogen activation. G-value, or ‘G’ (expressed in
dyn/cm2), represents the viscoelastic shear/strength of the
clot and it is calculated using the MA. Finally, LY30 and LY60
represent the percentage of clot lysis present at 30 and
60 min, respectively, once the MA is reached. R, K, angle
and MA are represented in Figure 2.
In general, hypocoagulation (measured by TEG) is
characterised by prolonged R and K times and a decrease
in the angle and MA values compared to normal.
Inversely, hypercoagulability is characterised by
decreased R and K times and increased angle and MA
compared to normal. Calculation of the coagulation
index (CI = 0.1227R + 0.0092 K + 0.1655MA - 0.0241a-5.022)
may also aid in the diagnosis of hypo- or hypercoagulation
(Donahue and Otto 2005). Visual interpretation of TEG
requires minor training of clinicians (Fig 4) and the most
relevant variables to horses (R and K times, angle, MA and
G) are available within the first 30 min of testing.
To better understand the value of the equine
thromboelastogram and facilitate its interpretation, it is
necessary to understand the correlations found between
TEG variables and standard clotting tests in man and
animals. For example, the R-Time has been correlated with
clotting times (PT and aPTT) (Zuckerman et al. 1981; Epstein
et al. 2009; Wagg et al. 2009; Mendez-Angulo et al. 2010),
whereas K-time and angle have both been associated
with the concentration and function of platelets and
fibrinogen, as well as clotting factor activity (Zuckerman
et al. 1981; Mendez-Angulo et al. 2011). Furthermore, a
correlation has been observed between MA and G-value
(which is calculated from MA) and the concentration and
function of platelets and fibrinogen (Zuckerman et al. 1981;
© 2011 EVJ Ltd
Normal
Hypocoagulable
Nielsen et al. 2000; Epstein et al. 2009; Wagg et al. 2009;
Mendez-Angulo et al. 2010, 2011).
TEG values in healthy horses
A limited number of research groups have evaluated
TEG variables in native or activated (tissue factor)
citrated whole blood from healthy horses. The currently
reported native citrated TEG values for horses in the
equine literature (6 TEG1 studies and 1 ROTEM study) have
been summarised in Table 1 (healthy adult horses) and
Table 2 (healthy neonatal foals). The reported rhTF-TEG
values in healthy adult horses are presented in Table 3.
Sonoclot values for healthy adult horses and healthy
neonatal foals have been also reported and are
presented in Table 4.
Some of the hypotheses that could explain the
different reported TEG values among equine researchers
are a high interindividual variability, different storage
times used, operators, blood collection technique, blood
tubes (glass vs. plastic) or differences in TEG technique
(such as mixing the blood and CaCl2 prior to starting
TEG), since they all have been shown to affect TEG
variables (Roche et al. 2006; McDonnell et al. 2007;
Dunkel et al. 2009; Epstein et al. 2009; Leclere et al. 2009;
Mendez-Angulo et al. 2010). Our research group
observed a high interindividual variability in 45 healthy
adults horses for R, K, a, G and LY60. Maximum amplitude
was the value with the lowest variability, only 9.3%
(coefficient of variation, CV), suggesting that MA could
be the most reliable of the TEG variables in horses
(Mendez-Angulo et al. 2010). In addition, Leclere et al.
(2009) showed a significant effect of storage time on R, K
and a but not MA after 30, 60 and 120 min of storage of
equine blood. Results from an international TEG study
performed in 9 human laboratories showed a significant
inter-laboratory variance with CVs greater than 10%
(Chitlur et al. 2011).
One of the reports on rhTF-TEG in healthy horses showed
that the addition of tissue factor consistently decreased R
and K times, increased angle and reduced variability (for
R, K, a, CL60 and LY60) in the equine thromboelastogram
J. L. Mendez-Angulo et al. 5

TABLE 1: Reference values of citrate native thromboelastography in healthy adult horses expressed as mean (⫾ s.d.)

R-Time K-Time Angle MA LY30

(min) (min) (degree) (mm) (%) LY60 (%)

Paltrinieri et al. (2008) 8.1 ⫾ 4.7 3.0 ⫾ 1.4 59.8 ⫾ 10.9 50.0 ⫾ 8.1 ND ND
n = 30 ROTEM
Epstein et al. (2009) 17.0 ⫾ 3.0 5.8 ⫾ 2.3 42 ⫾ 14 60.3 ⫾ 5.7 0.8 ⫾ 0.6 3.2 ⫾ 2.5
n = 26 TEG
Leclere et al. (2009) 16.6 ⫾ NA 6.05 ⫾ NA 30.5 ⫾ NA 42.35 ⫾ NA ND ND
n = 20 TEG
Mendez-Angulo et al. (2010) 10.4 ⫾ 3.1 3.5 ⫾ 1.2 55.6 ⫾ 11.0 55.6 ⫾ 5.1 ND 6.1 ⫾ 3.1
n = 45 TEG
Dunkel et al. (2010) 22.8 ⫾ 12 13.0 ⫾ 19.5 30.6 ⫾ 17.0 57.3 ⫾ 14.0 1.0 ⫾ 0.8 3.4 ⫾ 2.3
N = 30 TEG
Epstein et al. (2011) 16.2 ⫾ 5.8 5.7 ⫾ 3.7 42.5 ⫾ 13.2 61.7 ⫾ 8.4 0.7 ⫾ 0.7 3.8 ⫾ 1.7
n = 20 TEG

No data = ND; Not available = NA.

TABLE 2: Reference values of citrate native thromboelastography in healthy neonatal foals expressed as mean (⫾ s.d.)

R-Time K-Time Angle MA LY30 LY60

(min) (min) (degree) (mm) (%) (%)

Mendez-Angulo et al. (2011) n = 18 TEG 11.8 ⫾ 5.3 3.0 ⫾ 1.3 51.1 ⫾ 12.7 55.0 ⫾ 6.7 ND ND

No data = ND.

TABLE 3: Reference values of tissue factor activated citrate thromboelastography (rhTF-TEG) in healthy horses expressed as mean (⫾ s.d.)

R-Time K-Time Angle MA LY30

(min) (min) (degree) (mm) (%) LY60 (%)

Epstein et al. (2009) 6.6 ⫾ 1.4 3.1 ⫾ 1.0 50.9 ⫾ 9 62.3 ⫾ 5.1 0.6 ⫾ 0.5 3.6 ⫾ 1.9
n = 26 TEG
Leclere et al. (2009) 5.0 ⫾ NA 3.55 ⫾ NA 43.6 ⫾ NA 53.1 ⫾ NA ND ND
n = 20 TEG
Epstein et al. (2011) 6.9 ⫾ 1.3 3.2 ⫾ 1.1 52.8 ⫾ 7.5 62.9 ⫾ 5.2 0.5 ⫾ 0.5 3.0 ⫾ 1.5
n = 20 TEG

No data = ND; Not available = NA.

TABLE 4: Reference Sonoclot values in healthy adult horses and neonatal foals expressed as median (25–75% percentile)

ACT CR PCS TP
(s) (Dsignal/min) PF (Clot signal) (min)

Dallap Schaer et al. (2009b) Healthy adult horses 242.0 18.5 4.1 ND 14.8
n = 13 Sonoclot (205–279) (8.0–27.2) (1.1–4.9) (13.2–19.2)
Dallap Schaer et al. (2009b) Healthy neonatal foals 346.0 21.0 4.6 113 14.3
n = 10 Sonoclot (231.5–421) (13.6–26.1) (3.9–5.0) (90–125) (12.1–19.4)

No data = ND. ACT = time to initial clot formation; CR = clot rate; PF = platelet function; PCS = peak clot strength; TP = time to peak.

(Epstein et al. 2009). The same author, in a different study,
also mentioned that rhTF-TEG reduced the variability of
most of the TEG variables in horses with gastrointestinal
diseases although they did not publish any supportive data
(Epstein et al. 2011). Similarly, another equine study
showed decreased R and K times but increased angle and
MA values when using tissue factor compared to native
citrated TEG (Leclere et al. 2009).
Reported TEG values in healthy newborn foals are
similar to those from healthy horses although a higher
interindividual variability has been observed in this age
(Mendez-Angulo et al. 2011). Our group also performed
TEG analysis in 5 neonatal foals over time (at 12 , 24 h and
7 days after birth) and found changes in TEG variables
(consistent with a trend toward hypercoagulation) during
the first week of life. These findings may represent the
changes in coagulation that occur in foals during the first
month of life (Barton et al. 1995).
In summary, the range of normal values published in the
equine literature undoubtedly emphasises the

© 2011 EVJ Ltd

6 Thromboelastography (TEG) in horses
recommendation that each laboratory must establish a
consistent technique and its own reference intervals for
healthy horses. In addition, cut-off values for clinical hypo-
and hypercoagulability are difficult to define because a
large overlap exists between healthy and sick horses,
which limits the clinical usefulness of the TEG technique in
the equine species.
Areas for potential clinical application
Despite the extensive experimental and clinical research
of TEG in human medicine for many years, clinical research
in veterinary medicine is scarce in the literature. The dog is
possibly the veterinary species where TEG has been studied
the most in clinical cases, followed by the horse. Currently,
the number of TEG studies involving clinical patients in the
equine literature is very limited (only 6 reports published in
the last 5 years). These studies have focused mainly on the
evaluation of coagulopathies in horses affected with
gastrointestinal disorders (Mendez-Angulo et al. 2010;
Dunkel et al. 2010; Epstein et al. 2011), sepsis in foals
(Mendez-Angulo et al. 2010), racehorses with EIPH
(Giordano et al. 2010) and hereditary haemorrhagic
disorders (Macieira et al. 2007). Two recent studies have
also evaluated the coagulation system of sick neonatal
foals using Sonoclot (Dallap Schaer et al. 2009a,b).
Hypercoagulability
Hypercoagulation is a state characterised by an increase
in procoagulant activity or a reduction of natural
anticoagulant factors and/or fibrinolysis, leading to a more
rapid and stronger clot formation. This coagulopathy is due
to a disruption of the highly regulated haemostatic system
and occurs as a result of hereditary defects in one or more
clotting factors, or some acquired conditions. Historically,
this state has been suspected in horses with early stages of
inflammatory or ischaemic gastrointestinal disorders or
sepsis. In these cases if the disease progresses, fibrin and
thrombus formation occurs within the vasculature (DIC)
causing deposition of fibrin in different tissues which may
consequently lead to multiple organ dysfunction (MODS)
(Dallap Schaer and Epstein 2009; Monreal and Cesarini
2009).
An early diagnosis of hypercoagulation is believed to
be vital in order to be able to implement treatment and
thus impede the progression of the coagulopathy.
Unfortunately, to date, clinicians do not have a ‘gold
standard’ test to diagnose hypercoagulation accurately.
Traditional coagulation assays (i.e. PT and aPTT) are not
reliable predictors of hypercoagulation in man (Park et al.
2009) and, although other markers such as decreased
activity and concentration of protein C, AT and
plasminogen activities and increased TAT, and D-dimers
concentrations have been evaluated for this purpose in
horses, they are indirect and not specific (Darien et al.
1991; Topper et al. 1996; Monreal et al. 2000). At post
© 2011 EVJ Ltd
mortem examination, the identification of intravascular
fibrin deposits within different tissues likely provides the best
evidence of hypercoagulation (Cotovio et al. 2007, 2008).
Thromboelastrography has been proposed as an
alternative to detect hypercoagulability in man and dogs,
with an increase in MA and G-value being the most
reliable indicators by many authors (Otto et al. 2000;
Wiinberg et al. 2008; Park et al. 2009; Sinnott and Otto 2009;
Wagg et al. 2009). In human medicine, Park et al. (2009)
demonstrated that thromboelastographic analysis of
whole blood was a better indicator of a hypercoagulable
state than plasma PT or aPTT in patients admitted to the
surgical or burn care unit. Kashuk et al. (2009) also reported
the ability of TEG to predict thromboembolic events in
surgical patients. In that study, researchers established a
presumptive diagnosis of hypercoagulopathy based only
on an increased G-value (G>12.4 dynes/cm2). In addition,
other studies have provided evidence that a
hypercoagulable state diagnosed by TEG may be
predictive of thrombosis post operatively (McCrath et al.
2005; Dai et al. 2009).
Thromboelastrography has also been successfully
employed to detect hypercoagulability in canine patients.
An initial study of puppies with gastrointestinal disease
(parvoviral enteritis) showed hypercoagulability in all of
them, as evidenced by increased MA. Four of these dogs
developed catheter associated thrombophlebitis (Otto
et al. 2000) during hospitalisation. More recently, a number
of clinical studies have also identified hypercoagulation by
means of TEG in dogs with neoplasia, DIC and
immune-mediated haemolytic anaemia (Kristensen et al.
2008; Sinnott and Otto 2009; Fenty et al. 2011; Goggs et al.
2011). Wiinberg et al. (2008) evaluated a group of 50 dogs
diagnosed with DIC, finding hypercoagulation (based on
an increase in K, angle and MA) in 44% of the patients. Vilar
Saavedra et al. (2011) described a thromboelastographic
characterisation of hypercoagulation in dogs with
carcinoma and showed that TEG is a valid parameter to
detect this coagulopathy.
Hypocoagulability
Hypocoagulability is a coagulopathy frequently suspected
(by means of prolonged PT and aPTT) in horses with severe
gastrointestinal disease, sepsis, liver disease and other
acquired or inherited haemorrhagic disorders (e.g. purpura
haemorrhagica, vitamin K deficiency, Glanzmann’s
thrombasthenia) (McGorum et al. 1999, 2009; Pusterla et al.
2003; Livesey et al. 2005; Johns and Sweeney 2008; Monreal
and Cesarini 2009). Traditional coagulation assays are
performed in clinical settings to attempt to predict bleeding
in equine patients, although an abnormal coagulation
profile is not reliably associated with haemorrhage after
invasive procedures in man and horses (Segal et al. 2005;
Johns and Sweeney 2008). Therefore, whole-blood based
analysers such as TEG have been evaluated for this purpose
in people and dogs, showing better sensitivity and
J. L. Mendez-Angulo et al.
specificity than conventional coagulation tests (Wiinberg
et al. 2009; Sharma and Saxena 2010).
In man, hypocoagulability as evaluated by TEG was
frequently diagnosed at admission in general ICU patients
and associated with a higher rate of ventilator treatment,
higher rate of renal replacement therapy and higher use of
blood products. It was also found to be an independent risk
factor associated with a more than 3 times increased risk of
death within 30 days in these patients (Johansson et al.
2010). Windeløv et al. (2011) showed that neurosurgical
patients with hypocoagulation detected by TEG have a
worse prognosis and thus TEG has a predictive value in this
group of patients. Another recent human study reported a
sensitivity of 95.2% and a specificity of 81% for a novel
thromboelastographic score to identify overt DIC resulting
in a hypocoagulable state (Sharma and Saxena 2010).
In small animals, there is also scientific evidence that
TEG may predict bleeding more accurately than
conventional coagulation tests. Wiinberg et al. (2009)
evaluated coagulation from 27 hypocoagulable, 27
normocoagulable and 27 hypercoagulable dogs by
TF-TEG and routine haemostasis assays. Based on G-value
alone, TF-TEG identified dogs with clinical signs of bleeding
more accurately than the combination of platelet
concentration, PT and aPTT results, D-dimers and FIB.
However, another recent study has showed that TEG may
be too sensitive for monitoring heparin therapy in dogs
(Pittman et al. 2010).
TEG in equine clinical cases
The first publication on the use of TEG to assess haemostasis
in an equine patient was by Macieira et al. (2007) where
the authors diagnosed a hereditary haemorrhagic disorder
(Glanzmann’s thrombasthenia) in an 18-month-old filly with
the aid of TEG and other laboratory coagulation assays.
Thromboelastrography was performed with both kaolin
and TF in the patient and in a control healthy horse.
Thromboelastrography results showed similar R and K times
between both; however, MA was decreased in the patient
with both kaolin (43.7 mm; control, 63.9 mm) and tissue
factor (37.7 mm; control, 57.8 mm).
Aside from that case report, TEG researchers have
mainly focused their interest on horses with gastrointestinal
disease, a population known to be at increased risk for
coagulopathy. In 2010, our group published TEG profiles
from 45 healthy horses and 12 horses with gastrointestinal
disorders (colitis) and preidentified coagulopathies
(hypocoagulation). Sick horses were selected based on a
clinical diagnosis of colitis and prolonged clotting times
(PT>12.5 s and/or aPTT>62.5 s). TEG results from this group
were compared to those from healthy controls in order to
ascertain whether TEG was able to distinguish between
physiological and abnormal haemostasis. TEG tracings
showed changes consistent with hypocoagulability
(prolonged R and K times, narrower angle, decreased MA
and smaller G-value) in horses with colitis and prolonged
7
clotting times, when compared to controls. One of the
horses with acute severe colitis evaluated in this study was
monitored over time with TEG and the sequential tracings
(a, b, c and d) are presented in Figure 5. Trace a (obtained
on admission) demonstrates hypocoagulation according
to the equine reference values of our laboratory. Trace b
(6 h after admission and the administration of 20 l of
lactated Ringer’s and 6 l plasma) demonstrates a slight
improvement compared to trace a. Trace c (24 h after
admission) demonstrates the worsening of the
hypocoagulability. Finally, trace d (36 h after admission
and just before humane euthanasia) demonstrates the
absence of coagulation. Bilateral epixtasis was also noted
at that time.
Dunkel et al. (2010) also assessed haemostasis by TEG
and a conventional coagulation profile (PT, aPTT and
D-dimers concentration) on admission to a referral hospital
and 48 h later in 30 horses with ischaemic or inflammatory
gastrointestinal disease, 30 horses with nonischaemic or
noninflammatory gastrointestinal disease and 30 healthy
horses. Results showed a shorter R time in horses with
ischaemic or inflammatory disease compared to the other
2 groups; a change indicative of hypercoagulation.
However, in general, TEG profiles did not reflect the
changes associated with hypercoagulability in other
species (i.e. higher MA and G-value) (Otto et al. 2000;
Kristensen et al. 2008; Wiinberg et al. 2008).
Epstein et al. (2011) evaluated coagulation by TEG,
rhTF-TEG and traditional coagulation panels in a larger
group of horses (n = 101) with acute gastrointestinal
disease. For comparison purposes, investigators included
20 healthy controls and grouped sick horses into 1 of 4
lesion categories: nonstrangulating medical,
nonstrangulating surgical, strangulating, and
inflammatory. Based on TEG and rhTF-TEG results, they
grouped horses as having a coagulopathy of ⱖ1, 2 or 3
TEG or rhTF-TEG variables. A coagulopathy of a TEG or
rhTF-TEG variable was defined as at least 2 standard
deviations (s.d.) above or below the mean for all variables.
Horses with coagulopathies were compared for lesion
type, presence of systemic inflammatory response
syndrome (SIRS), complications and survival. Based on the
statistical analysis results, the investigators concluded that
TEG performed at admission identified abnormalities
associated with inflammatory lesions, SIRS, diarrhoea,
thrombophlebitis, laminitis and fatality. In general, changes
detected on the TEG variables in sick horses were
consistent with hypocoagulation and hypofibrinolysis.
These 3 TEG studies of horses with colic and colitis add
relevant data to the equine literature and contribute to the
understanding of the coagulopathies that occur in the
horse with gastrointestinal disease. The dissimilar reported
thromboelastographic values amongst authors may be
due to the TEG idiosyncrasy (e.g. inter-laboratory
variability), treatments received prior to hospital admission
and/or blood sample collection, inclusion criteria of horses
with different pathologies (e.g. strangulating lesions vs.
© 2011 EVJ Ltd
 8

© 2011 EVJ Ltd

a) b)

R K Angle MA G LY60 aPTT PT HCT PLT R K Angle MA G LY60 aPTT PT

min min deg mm d/sc % sec sec % X 10^9 min min deg mm d/sc % sec sec
^ ^ 27.5 13.8 14.4 37.9 3.0k 0.0 13.4 106.0
29.3 17.0 13.3 30.6 2.2k 0 14.8 130.0 54 85.3

c) d)

R K Angle MA G LY60 aPTT PT R K Angle MA G LY60 aPTT PT

min min deg mm d/sc % sec sec min min deg mm d/sc % sec sec
33.7 N\A 6.7 19.4 1.2k 0.0 13.2 120.0 69.7 N\A 0.7 2.4 0.2k 0.0 13.2 160.0

Fig 5: Sequential TEG tracings and clotting times of a horse with acute severe colitis followed over a 36 h period.
Thromboelastography (TEG) in horses
J. L. Mendez-Angulo et al.
colitis) in the same group or the progression of the
coagulopathies.
Septic foals are another population at risk of
coagulopathies (especially hypercoagulability and DIC),
associated with decreased survival (Armengou et al. 2008;
Cotovio et al. 2008; Dallap Schaer and Epstein 2009).
Hypocoagulation, measured by both conventional testing
and a viscoelastic coagulation and platelet function
analyser (Sonoclot), has also been reported in foals with
sepsis and associated with poor outcome (Dallap Schaer
et al. 2009a,b). Thus, to further characterise the
coagulopathies of this population, we designed a clinical
prospective study to evaluate haemostasis in healthy (n =
18), sick nonseptic (n = 15) and septic (n = 17) neonatal
foals (<7-days-old) by TEG and a conventional haemostasis
profile (PT, aPTT, FIB and AT) (Mendez-Angulo et al. 2011).
Thromboelastrography changes observed in the septic
foals compared to the other 2 groups were consistent with
hypercoagulability (greater angle and MA as identified in
other species). However, aPTT was prolonged in the septic
group suggesting a trend toward hypocoagulation as
reported by other authors (Dallap Schaer et al. 2009a,b).
Although these 2 findings are inconsistent, DIC is
characterised by an early hypercoagulable state leading
to depletion of clotting factors, and therefore, it is possible
that the different techniques were demonstrating an
overlapping of hyper- and hypocoagulation in this septic
population.
A single study has evaluated horses (n = 13) with EIPH
(confirmed by bronchoscopy) by thromboelastometry
(ROTEM) and compared them to healthy (n = 11) negative
controls. Thromboelastometric analyses were performed
before and after the race in all horses. Compared to
controls, ROTEM results showed that EIPH-affected horses
had a trend toward hypercoagulability in both sampling
points (before and after the race), suggesting that
coagulation is possibly preactivated in horses with EIPH due
to previous haemorrhage (Giordano et al. 2010).
Conclusions
The use of TEG has gained popularity in veterinary
medicine in the last decade and several studies in healthy
and sick horses are now available. However, the observed
high inter-individual variability in healthy horses and
substantial overlap found between healthy and sick horses
makes interpretation of results difficult and limits its clinical
use. Additionally, other potential sources of variation are
the blood collection method, storage time and containers
and anticoagulant concentration. Therefore, it is the
general consensus amongst researchers that the TEG
technique should be standardised and reference intervals
for healthy horses obtained independently in each
laboratory because results are not interchangeable.
Finally, more prospective studies, including both
experimental and clinical research, are needed to further
validate the TEG technique in horses and to determine if
9
TEG can be used to detect coagulopathies and/or
monitor blood product transfusion and anticoagulant
therapy in the equine hospitalised patient.
Manufacturers’ addresses
1Haemoscope Corp., Niles, Illinois, USA.
2Framar Biomedica, Rome, Italy.
3Pentapharm GmbH, Munich, Germany.
4Sienco Inc, Arvada, Colorado, USA.
Authors’ declaration of interests
No conflicts of interest have been declared.
References
Armengou, L., Monreal, L., Tarancon, I., Navarro, M., Rios, J. and Segura,
D. (2008) Plasma d-dimer concentration in sick newborn foals. J. vet.
Intern. Med. 22, 411-417.
Barton, M.H., Morris, D.D., Crowe, N., Collatos, C. and Prasse, K.W. (1995)
Hemostatic indices in healthy foals from birth to one month of age.
J. vet. Diagn. Invest. 7, 380-385.
Bauer, N., Eralp, O. and Moritz, A. (2009) Establishment of reference
intervals for kaolin-activated thromboelastography in dogs
including an assessment of the effects of sex and anticoagulant use.
J. vet. Diagn. Invest. 21, 641-648.
Bentz, A.I., Palmer, J.E., Dallap, B.L., Wilkins, P.A. and Boston, R.C. (2009)
Prospective evaluation of coagulation in critically ill neonatal foals.
J. vet. Intern. Med. 23, 161-167.
Bernard, W., Morris, D.D., Divers, T.J. and Ramberg, C. (1987) Plasma
antithrombin-III values in healthy horses: effect of sex and/or breed.
Am. J. vet. Res. 48, 866-868.
Camenzind, V., Bombeli, T., Seifert, B., Jamnicki, M., Popovic, D., Pasch,
T. and Spahn, D. (2000) Citrate storage affects Thrombelastograph
analysis. Anesthesiol. 92, 1242-1249.
Chitlur, M., Sorensen, B., Rivard, G.E., Young, G., Ingerslev, J., Othman,
M., Nugent, D., Kenet, G., Escobar, M. and Lusher, J. (2011)
Standardization of thromboelastography: a report from the
TEG-ROTEM working group. Haemophilia 17, 532-537.
Collatos, C., Barton, M.H. and Moore, J.N. (1995) Fibrinolytic activity in
plasma from horses with gastrointestinal diseases: changes
associated with diagnosis, surgery, and outcome. J. vet. Intern.
Med. 9, 18-23.
Cotovio, M., Monreal, L., Armengou, L., Prada, J., Almeida, J.M. and
Segura, D. (2008) Fibrin deposits and organ failure in newborn foals
with severe septicemia. J. vet. Intern. Med. 22, 1403-1410.
Cotovio, M., Monreal, L., Navarro, M., Segura, D., Prada, J. and Alves, A.
(2007) Detection of fibrin deposits in tissues from horses with severe
gastrointestinal disorders. J. vet. Intern. Med. 21, 308-313.
Dai, Y., Lee, A., Critchley, L.A. and White, P.F. (2009) Does
thromboelastography predict postoperative thromboembolic
events? A systematic review of the literature. Anesth. Analg. 108,
734-742.
Dallap Schaer, B.L. and Epstein, K. (2009) Coagulopathy of the
critically ill equine patient. J. vet. Emerg. Crit. Care (San Antonio) 19,
53-65.
Dallap Schaer, B.L., Bentz, A.I., Boston, R.C., Palmer, J.E. and Wilkins, P.A.
(2009a) Comparison of viscoelastic coagulation analysis and
standard coagulation profiles in critically ill neonatal foals to
outcome. J. vet. Emerg. Crit. Care (San Antonio) 19, 88-95.
Dallap Schaer, B.L., Wilkins, P.A., Boston, R.C. and Palmer, J.E. (2009b)
Preliminary evaluation of hemostasis in neonatal foals using a
viscoelastic coagulation and platelet function analyzer. J. vet.
Emerg. Crit. Care (San Antonio) 19, 81-87.
© 2011 EVJ Ltd
10
D’Angelo, G. and Villa, C. (2011) Comparison between
siliconized evacuated glass and plastic blood collection tubes for
prothrombin time and activated partial thromboplastin time assay
in normal patients, patients on oral anticoagulant therapy and
patients with unfractioned heparin therapy. Int. J. Lab. Hematol. 33,
219-225.
Darien, B.J., Potempa, J., Moore, J.N. and Travis, J. (1991) Antithrombin
III activity in horses with colic: An analysis of 46 cases. Equine vet. J.
23, 211-214.
Dolente, B.A., Wilkins, P.A. and Boston, R.C. (2002) Clinicopathologic
evidence of disseminated intravascular coagulation in horses with
acute colitis. J. Am. vet. med. Ass. 220, 1034-1038.
Dolente, B.A., Beech, J., Lindborg, S. and Smith, G. (2005) Evaluation of
risk factors for development of catheter-associated jugular
thrombophlebitis in horses: 50 cases (1993-1998). J. Am. vet. med.
Ass. 227, 1134-1141.
Donahue, S.M. and Otto, C.M. (2005) Thromboelastography: A tool for
measuring hypercoagulation, hypocoagulation, and fibrinolysis.
J. vet. Emerg. Crit. Care. 15, 9-16.
Dunkel, B., Chan, D. and Monreal, L. (2009) Influence of citrate
concentration and material of blood tubes on
thromboelastographic parameters in horses. J. vet. Emerg. Crit.
Care 19, A14. [Abstract].
Dunkel, B., Chan, D.L., Boston, R. and Monreal, L. (2010) Association
between hypercoagulability and decreased survival in horses with
ischemic or inflammatory gastrointestinal disease. J. vet. Intern.
Med. 24, 1467-1474.
Epstein, K.L., Brainard, B.M., Lopes, M.A., Barton, M.H. and Moore, J.N.
(2009) Thrombelastography in 26 healthy horses with and without
activation by recombinant human tissue factor. J. vet. Emerg. Crit.
Care (San Antonio) 19, 96-101.
Epstein, K.L., Brainard, B.M., Gomez-Ibanez, S.E., Lopes, M.A.,
Barton, M.H. and Moore, J.N. (2011) Thrombelastography in
horses with acute gastrointestinal disease. J. vet. Intern. Med. 25,
307-314.
Fenty, R.K., Delaforcade, A.M., Shaw, S.E. and O’Toole, T.E. (2011)
Identification of hypercoagulability in dogs with primary
immune-mediated hemolytic anemia by means of
thromboelastography. J. Am. vet. med. Ass. 238, 463-467.
Giordano, A., Meazza, C., Salvadori, M. and Paltrinieri, S. (2010)
Thromboelastometric profiles of horses affected by
exercise-induced pulmonary hemorrhages. Vet. med. Int. 2010,
Article ID 945789 (E-pub); doi: 10.4061/2010/945789.
Goggs, R., Wiinberg, B., Kjelgaard-Hansen, M. and Chan, D.L.
(2011) Serial assessment of the coagulation status of
dogs with immune-mediated haemolytic anaemia using
thromboelastography. Vet. J. April 21. Epub ahead of print; doi:
10.1016/j.tvjl.2011.03.015.
Goodwin, L.V., Goggs, R., Chan, D.L. and Allenspach, K. (2011)
Hypercoagulability in dogs with protein-losing enteropathy. J. vet.
Intern. Med. 25, 273-277.
Johansson, P.I., Stensballe, J., Vindeløv, N., Perner, A. and Espersen, K.
(2010) Hypocoagulability, as evaluated by thrombelastography, at
admission to the ICU is associated with increased 30-day mortality.
Blood Coagul. Fibrinolysis 21, 168-174.
Johns, I.C. and Sweeney, R.W. (2008) Coagulation abnormalities and
complications after percutaneous liver biopsy in horses. J. vet.
Intern. Med. 22, 185-189.
Kashuk, J.L., Moore, E.E., Sabel, A., Barnett, C., Haenel, J., Le, T., Pezold,
M., Lawrence, J., Biffl, W.L., Cothren, C.C. and Johnson, J.L. (2009)
Rapid thrombelastography (r-TEG) identifies hypercoagulability and
predicts thromboembolic events in surgical patients. Surgery 146,
764-774.
Kol, A. and Borjesson, D.L. (2010) Application of thrombelastography/
thromboelastometry to veterinary medicine. Vet. clin. Pathol. 39,
405-416.
Kristensen, A.T., Wiinberg, B., Jessen, L.R., Andreasen, E. and Jensen, A.L.
(2008) Evaluation of human recombinant tissue factor-activated
© 2011 EVJ Ltd
Thromboelastography (TEG) in horses
thromboelastography in 49 dogs with neoplasia. J. vet. Intern. Med.
22, 140-147.
Leclere, M., Lavoie, J.P., Dunn, M. and Bedard, C. (2009) Evaluation of a
modified thrombelastography assay initiated with recombinant
human tissue factor in clinically healthy horses. Vet. clin. Pathol. 38,
462-466.
Leemann, H., Lustenberger, T., Talving, P., Kobayashi, L., Bukur, M.,
Brenni, M., Bruesch, M., Spahn, D.R. and Keel, M.J. (2010) The role of
rotation thromboelastometry in early prediction of massive
transfusion. J. Trauma 69, 1403-1409.
Livesey, L., Christopherson, P., Hammond, A., Perkins, J., Toivio-Kinnucan,
M., Insalaco, T. and Boudreaux, M.K. (2005) Platelet dysfunction
(Glanzmann’s thrombasthenia) in horses. J. vet. Intern. Med. 19,
917-919.
Macieira, S., Rivard, G.E., Champagne, J., Lavoie, J.P. and Bedard, C.
(2007) Glanzmann thrombasthenia in an Oldenbourg filly. Vet. Clin.
Pathol. 36, 204-208.
McCrath, D.J., Cerboni, E., Frumento, R.J., Hirsh, A.L. and
Bennet-Guerrero, E. (2005) Thromboelastography maximum
amplitude predicts postoperative thrombotic complications
including myocardial infarction. Anesth. Analg. 100, 1576-1583.
McDonnell, E., Lyons, G. and Chau, S. (2007) Effects of storing blood in
citrated silicone-coated glass tubes vs. citrated plastic tubes on
thromboelastograph variables. Eur. J. Anaesthesiol. 24, 291-292.
McGorum, B.C., Murphy, D., Love, S. and Milne, E.M. (1999)
Clinicopathological features of equine primary hepatic disease: a
review of 50 cases. Vet. Rec. 145, 134-139.
McGorum, B.C., Henderson, I.S., Stirling, D., Wallace, R., Haggart, C. and
Thomas, A.E. (2009) Vitamin K deficiency bleeding in a
Standardbred colt. J. vet. Intern. Med. 23, 1307-1310.
Mendez-Angulo, J.L., Mudge, M.C., Vilar-Saavedra, P., Stingle, N.
and Couto, C.G. (2010) Thromboelastography in healthy horses
and horses with inflammatory gastrointestinal disorders and
suspected coagulopathies. J. vet. Emerg. Crit. Care (San Antonio)
20, 488-493.
Mendez-Angulo, J.L., Mudge, M.C., Zaldivar-Lopez, S., Vilar-Saavedra, P.
and Couto, C.G. (2011) Thromboelastography (TEG) in healthy, sick
non-septic, and septic neonatal foals. Aust. vet. J. Epub ahead of
print; doi: 10.1111/j.1751-0813.2011.00854.x.
Monreal, L. and Cesarini, C. (2009) Coagulopathies in horses with colic.
Vet. Clin. N. Am.: Equine Pract. 25, 247-258.
Monreal, L., Angles, A., Espada, Y., Monasterio, J. and Monreal, M.
(2000) Hypercoagulation and hypofibrinolysis in horses with colic
and DIC. Equine vet. J., Suppl. 32, 19-25.
Nielsen, V.G., Geary, B.T. and Baird, M.S. (2000) Evaluation of the
contribution of platelets to clot strength by thromboelastography in
rabbits: the role of tissue factor and cytochalasin D. Anesth. Analg.
91, 35-39.
Otto, C.M., Rieser, T.M., Brooks, M.B. and Russell, M.W. (2000) Evidence of
hypercoagulability in dogs with parvoviral enteritis. J. Am. vet. med.
Ass. 217, 1500-1504.
Paltrinieri, S., Meazza, C., Giordano, A. and Tunesi, C. (2008) Validation
of thromboelastometry in horses. Vet. Clin. Pathol. 37, 277-285.
Park, M.S., Martini, W.Z., Dubick, M.A., Salinas, J., Butenas, S.,
Kheirabadi, B.S., Pusateri, A.E., Vos, J.A., Guymon, C.H., Wolf, S.E.,
Mann, K.G. and Holcomb, J.B. (2009) Thromboelastography as
a better indicator of hypercoagulable state after injury
than prothrombin time or activated partial thromboplastin time.
J. Trauma 67, 266-276.
Pittman, J.R., Koenig, A. and Brainard, B.M. (2010) The effect of
unfractionated heparin on thrombelastographic analysis in healthy
dogs. J. vet. Emerg. Crit. Care (San Antonio) 20, 216-223.
Preisman, S., Kogan, A., Itzkovsky, K., Leikin, G. and Raanani, E. (2010)
Modified thromboelastography evaluation of platelet dysfunction in
patients undergoing coronary artery surgery. Eur. J. Cardiothorac
Surg. 37, 1367-1374.
J. L. Mendez-Angulo et al.
Pusterla, N., Watson, J.L., Affolter, V.K., Magdesian, K.G., Wilson, W.D.
and Carlson, G.P. (2003) Purpura haemorrhagica in 53. Horses Vet.
Rec. 153, 118-121.
Roche, A.M., James, M.F., Grocott, M.P. and Mythen, M.G. (2006) Just
scratching the surface: varied coagulation effects of polymer
containers on TEG variables. Eur. J. Anaesthesiol. 23, 45-49.
Segal, J.B., Dzik, W.H. and Transfusion Medicine/Hemostasis Clinical Trials
Network (2005) Paucity of studies to support that abnormal
coagulation test results predict bleeding in the setting of invasive
procedures: an evidence-based review. Transfusion 45, 1413-1425.
Sharma, P. and Saxena, R. (2010) A novel thromboelastographic score
to identify overt disseminated intravascular coagulation resulting in
a hypocoagulable state. Am. J. clin. Pathol. 134, 97-102.
Sinnott, V.B. and Otto, C.M. (2009) Use of thromboelastography in dogs
with immune-mediated hemolytic anemia: 39 cases (2000-2008).
J. vet. Emerg. Crit. Care (San Antonio) 19, 484-488.
Sivula, M., Pettila, V., Niemi, T.T., Varpula, M. and Kuitunen, A.H.
(2009) Thromboelastometry in patients with severe sepsis and
disseminated intravascular coagulation. Blood Coagul. Fibrinolysis
20, 419-426.
Stokol, T., Brooks, M.B. and Erb, H.N. (2000) Effect of citrate
concentration on coagulation test results in dogs. J. Am. vet. med.
Ass. 217, 1672-1677.
Stokol, T., Erb, H.N., De Wilde, L., Tornquist, S.J. and Brooks, M. (2005)
Evaluation of latex agglutination kits for detection of fibrin(ogen)
degradation products and d-dimer in healthy horses and horses
with severe colic. Vet. clin. Pathol. 34, 375-382.
Topper, M.J., Prasse, K.W., Morris, M.J., Duncan, A. and Crowe, N.A.
(1996) Enzyme-linked immunosorbent assay for
thrombin-antithrombin III complexes in horses. Am. J. vet. Res. 57,
427-431.
Vilar Saavedra, P., Lara García, A., Zaldívar López, S. and Couto, G.
(2011) Hemostatic abnormalities in dogs with carcinoma: A
thromboelastographic characterization of hypercoagulability. Vet.
J. Mar 31. Epub ahead of print; doi:10.1016/j.tvjl.2011.02.025.
Wagg, C.R., Boysen, S.R. and Bedard, C. (2009) Thrombelastography in
dogs admitted to an intensive care unit. Vet. Clin. Pathol. 38,
453-461.
11
Wasowicz, M., Meineri, M., McCluskey, S.M., Mitsakakis, N. and Karkouti,
K. (2009) The utility of thromboelastography for guiding recombinant
activated factor VII therapy for refractory hemorrhage after
cardiac surgery. J. Cardiothorac. Vasc. Anesth. 23, 828-834.
Wasowicz, M., McCluskey, S.A., Wijeysundera, D.N., Yau, T.M., Meinri, M.,
Beattie, W.S. and Karkouti, K. (2010) The incremental value of
thrombelastography for prediction of excessive blood loss after
cardiac surgery: an observational study. Anesth. Analg. 111,
331-338.
Weiss, D.J., Evanson, O.A., McClenahan, D., Fagliari, J.J. and Jenkins, K.
(1997) Evaluation of platelet activation and platelet-neutrophil
aggregates in ponies with alimentary laminitis. Am. J. vet. Res. 58,
1376-1380.
Welch, R.D., Watkins, J.P., Taylor, T.S., Cohen, N.D. and Carter, G.K.
(1992) Disseminated intravascular coagulation associated with colic
in 23 horses (1984-1989). J. vet. Intern. Med. 6, 29-35.
Wiinberg, B. and Kristensen, A.T. (2010) Thromboelastography in
veterinary medicine. Semin. Thromb. Hemost. 36, 747-756.
Wiinberg, B., Jensen, A.L., Rojkjaer, R., Johansson, P., Kjelgaard-Hansen,
M. and Kristensen, A.T. (2005) Validation of human recombinant
tissue factor-activated thromboelastography on citrated whole
blood from clinically healthy dogs. Vet. Clin. Pathol. 34, 389-393.
Wiinberg, B., Jensen, A.L., Johansson, P.I., Rozanski, E., Tranholm, M. and
Kristensen, A.T. (2008) Thromboelastographic evaluation of
hemostatic function in dogs with disseminated intravascular
coagulation. J. vet. Intern. Med. 22, 357-365.
Wiinberg, B., Jensen, A.L., Rozanski, E., Johansson, P.I.,
Kjelgaard-Hansen, M., Tranholm, M. and Kristensen, A.T. (2009) Tissue
factor activated thromboelastography correlates to clinical signs of
bleeding in dogs. Vet. J. 179, 121-129.
Windeløv, N.A., Welling, K.L., Ostrowski, S.R. and Johansson, P.I. (2011)
The prognostic value of thrombelastography in identifying
neurosurgical patients with worse prognosis. Blood Coagul.
Fibrinolysis 22, 416-419.
Zuckerman, L., Cohen, E., Vagher, J.P., Woodward, E. and Caprini, J.A.
(1981) Comparison of thrombelastography with common
coagulation tests. Thromb. Haemost. 46, 752-756.
© 2011 EVJ Ltd