Thromboelastography for Monitoring Prolonged

Hypercoagulability After Major Abdominal Surgery

Elisabeth Mahla, MD*, Thomas Lang, MD, Martin N. Vicenzi, MD*, Georg Werkgartner,
Robert Maier, MD, Claudia Probst, MD*, and Helfried Metzler, MD*

MD,

Departments of *Anesthesiology and Intensive Care Medicine, Clinical Chemical and Laboratory Medicine, Surgery,
and Cardiology, University of Graz, Graz, Austria

Despite clinical and laboratory evidence of perioperative hypercoagulability, there are no consistent data
evaluating the extent, duration, and specific contribution of platelets and procoagulatory proteins by in vitro
testing. We tested the hypothesis that the parallel use of
standard and abciximab-cytochalasin D-modified
thromboelastography (TEG) can assess 7 days postoperative hypercoagulability and can estimate the independent contribution of procoagulatory proteins and
platelets. Thromboelastograms were performed before
surgery, at the end of surgery, 6 h after surgery, and on
postoperative days 1, 2, 3, and 7; they were analyzed for
the reaction time and the maximal amplitude (MA). We

rterial and venous thrombotic events are the clinical manifestation of postoperative hypercoagulability (13). Although thrombotic events may be
attenuated by anticoagulatory substances (3), the in vitro
verification of the underlying imbalance has been only
incompletely evaluated. This may, in part, be because of
the complex coagulation system, which involves coagulatory proteins and platelets, as well as the lack of appropriate coagulation tests, reflecting both the dynamic
fibrin-platelet interaction and the individual activity of
coagulatory proteins and platelets. Although several
studies have shown a postoperative increase of procoagulatory proteins and parallel reductions of anticoagulatory and fibrinolytic factors relative to the extent of
tissue trauma, data on platelet function are controversial
(2,4 9).
Thromboelastography (TEG) has been established as
a sensitive test for the global assessment of hemostatic
function in several clinical settings (10 13). Standard
thromboelastography, however, cannot distinguish
between the quantitative contribution of plasmatic

Accepted for publication October 11, 2000.

Address correspondence and reprint requests to Elisabeth Mahla,
MD, Department of Anesthesiology and Intensive Care Medicine,
University of Graz, Auenbruggerplatz 29, A-8036 Graz, Austria.
Address e-mail to elisabeth.mahla@kfunigraz.ac.at.

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Anesth Analg 2001;92:5727

calculated the elastic shear modulus of standard MA

(Gt) and modified MA (Gc), which reflect total clot
strength and procoagulatory protein component, respectively. The difference was an estimate of the platelet component (Gp). There was a 10% perioperative increase of standard MA, corresponding to a 50% increase
of Gt (P 0.0001) and an 86%90% contribution of the
calculated Gp to Gt. We conclude that serial standard
and modified thromboelastography may reveal prolonged postoperative hypercoagulability and the independent contribution of platelets and procoagulatory
proteins to clot strength.
(Anesth Analg 2001;92:5727)

procoagulatory proteins and platelets to postoperative hypercoagulability. Recently introduced modified

thromboelastography with substances inhibiting platelet
fibrin interaction (abciximab) (14 16) and platelet actin
polymerization (cytochalasin D) (17,18) may provide a
more specific, though indirect, estimate of the independent contribution of plasmatic proaggregatory proteins
and platelets to perioperative hypercoagulability.
In this investigation, we tested the hypothesis that
the parallel use of standard and modified thromboelastography can assess hypercoagulability and the
independent contribution of plasma proteins and
platelets to this hypercoagulability for 7 days after
elective major abdominal surgery. Furthermore, we
evaluated the association of thromboelastographic
variables to standard coagulation tests and platelet
count and the impact of standard thrombosis prophylaxis on thromboelastographic variables.

Methods
After ethics committee approval and informed consent, 20 consecutive patients (16 men, 4 women, ages
58.6 11.7 yr [mean sd]) scheduled for major
abdominal surgery under general anesthesia were included in this study. Exclusion criteria were a history
2001 by the International Anesthesia Research Society
0003-2999/01

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or clinical signs of coronary artery disease, anticipated

large intraoperative transfusion requirements, preexisting coagulation disorders, preoperative anticoagulation, use of nonsteroidal antiinflammatory drugs or
aspirin within 1 wk before surgery, renal dysfunction
(creatinine 120 mol/L), and surgery under regional
anesthesia. Four patients were treated for hypertension (-blocker, n 2; angiotensin-converting enzyme
inhibitor, n 2), 12 patients were hypercholesterolemic (lipid-lowering therapy with statins, n 4),
and five patients were active smokers. The patients
underwent gastrectomy (n 6), colonic resection (n
6), or Whipple procedure (n 8) under general anesthesia. The mean ( sd) duration of surgery was 303
146 min. Sixteen of the 20 patients suffered from
cancer.
Anesthesia and perioperative care were at the discretion of the attending anesthesiologist. Postoperative analgesia with piritramide IV or subcutaneously
was administered on demand. Perioperative hematocrit was maintained close to 30%. A total of 20 packed
red blood cells (range 0 7) was administered during
the entire study period. Neither platelets nor fresh
frozen plasma nor other coagulation factors were
used. Patients received the recommended thrombosis
prophylaxis of 40 mg enoxaparin subcutaneously once
daily (19), starting before surgery (n 13) or on the
evening of surgery (n 7), according to the surgeons
preference. No patient suffered from perioperative
cardiac morbidity, pneumonia, or renal insufficiency.
Four patients sustained late surgical complications, all
of which occurred after the study period.
Two 4.5-mL blood samples were drawn from a central venous line into siliconized Vacutainer tubes (Becton Dickinson, Meylan, France) containing 0.5 mL sodium citrate (0.129M), and the initial 3 mL of blood
was discarded. Blood samples were collected after the
induction of anesthesia, after surgery on arrival at the
intensive care unit, 6 h after surgery, on the morning
of postoperative day (POD) 1, on the morning of POD
2, on the morning of POD 3, and on the morning of
POD 7.
Prothrombin time, thrombin clotting time, partial
thromboplastin time, fibrinogen (Clauss method), and
antithrombin III were measured with the Behring Coagulation System (Dade-Behring Marburg GmBH,
Marburg, Germany). Platelet count, red blood cells,
and hematocrit were determined by using the Coulter
STKS (Coulter Electronics Inc, Hialeah, FL).
Three different thromboelastographic assays were
performed within 1 to 2 h of blood sampling (20) on a
computerized thromboelastographic coagulation analyzer (roTEG Coagulation Analyzer; Dynabite
GmbH, Munich, Germany). Clot formation was triggered by recalcification of 300 L whole blood with 20
L 0.2M calcium chloride (StartTEG; Fa Nobis, Endingen, Germany) and 20 L of an intrinsic activator

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573

(InTEG-LS Aktivator; Fa Nobis) in all three assays.

The thromboelastographic trace was analyzed for the
reaction time (r-time), which reflects the rate of initial
fibrin formation, and for the maximal amplitude
(MA), which reflects the absolute strength of the clot
(21,22).
The assays were the following:
Activated whole-blood thromboelastogram. The
reference levels (mean sd) in our laboratory are
r-time (176.2 27.2 s) and MA (62.2 3.3 mm).
Abciximab-cytochalasin D-modified thromboelastogram. To assess the independent contributions of
platelets and fibrinogen to clot strength, thromboelastography was performed after inhibiting
platelets with 10 L of 2 mg/mL abciximab (Reopro; Centocor B.V., CB Leiden, Netherlands) together with 10 L of 0.2 mg/mL cytochalasin D
(Sigma Chemical Co, St Louis, MO). The reference
levels (mean sd) in our laboratory are r-time
(166.0 22.8 s) and MA (14.1 3.5 mm).
Activated whole-blood thromboelastography
with heparinase (heparinase-modified thromboelastography). To eliminate trace amounts of
heparin, thromboelastography was performed
with 20 L heparinase (Dade Hepzyme, 5.5IU/
mL; Dade-Behring Marburg GmbH, Marburg,
Germany).
Accounting for the exponential increase of the elastic
shear modulus in relation to the MA (17), we calculated
the elastic shear modulus (G) of the activated wholeblood MA, reflecting total clot strength (Gt) and the
elastic shear modulus of the abciximab-cytochalasin D
MA, reflecting the contribution of procoagulatory proteins to clot strength (Gc). The difference of Gt and Gc
was calculated as an estimation of the platelet contribution to clot strength (Gp) (15,18). We further calculated
the percentage contribution of Gc and Gp to Gt. The
elastic shear modulus was calculated as follows: G
(5000 MA)/(100 MA) in dynes/cm2.
Considering the perioperative change of the platelet
count, we created a platelet index, defined as Gp per
1000 platelets, as a calculated measure of the platelet
contribution to clot strength.
All data were tested for normal distribution and are
expressed as mean sd. Effects over time were analyzed by a one-way repeated measures analysis of
variance model. The correlation between fibrinogen
and the MA of the activated whole blood and the
abciximab-cytochalasin D-modified thromboelastography, as well as the correlation between the platelet
count and the MA of activated whole blood and the
Gp, was performed by simple linear regression analysis (Stat View 4.5; Abacus Concepts, Berkeley, CA).
The intercept was not removed. P 0.05 was used to
indicate statistical significance.

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Figure 1. Perioperative change of the reaction time (r-time) in the

activated whole-blood thromboelastography (black bars) and the
heparinase-modified thromboelastography (hatched bars). The x
axis represents the observation points, and the y axis, the r-time in
seconds (mean sd). P 0.0001 for the effect time. PREOP after
the induction of anesthesia; OP 6 6 h after surgery; POD
postoperative day.

Results
The perioperative trend of the r-time in the activated
whole-blood thromboelastography as compared with
the heparinase thromboelastography is depicted in
Figure 1. There was a significant and parallel perioperative change of the r-time in both thromboelastographic traces, with an initial r-time decrease at the
end of surgery and a return to the preoperative baseline on POD 7 (P 0.0001).
The perioperative trend of the MA in the activated
whole-blood thromboelastography as compared with
the heparinase thromboelastography is depicted in
Figure 2. There was an equal and continuous perioperative increase of the MA in both thromboelastographic traces until POD 7 (P 0.0001). This 10%
perioperative increase of the MA corresponded to a
50% increase of the calculated elastic shear modulus.
Prothrombin time, partial thromboplastin time,
thrombin clotting time, and antithrombin III, respectively, changed slightly over time but remained within
the reference limits (Table 1). Fibrinogen increased
substantially on POD 2 and had a peak on POD 3,
exceeding the preoperative baseline by 90%. Platelet
count remained stable until an increase on POD 7.
After an initial decrease of the abciximab-cytochalasin
D-modified MA on the day of surgery, the MA increased
until POD 3 and exceeded the preoperative baseline by
40% (Fig. 3). This increase persisted until POD 7 (P
0.0001). The biphasic change of the MA coincided with a
parallel change of fibrinogen levels (Table 1).
There was a weak correlation between fibrinogen
and the activated whole-blood MA (adjusted r2
0.442; P 0.0001) and a strong correlation between
fibrinogen and the abciximab-cytochalasin D MA (adjusted r2 0.767) (Fig. 4). Small levels of fibrinogen

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Figure 2. Perioperative change of the maximal amplitude (MA) in

the activated whole-blood thromboelastography (black bars) and
the heparinase-modified thromboelastography (hatched bars). The x
axis represents the observation points, and the y axis, the MA (mean
sd). P 0.0001 for the effect time. PREOP after the induction
of anesthesia; OP 6 6 h after surgery; POD postoperative day.

were associated with a small MA, and increased levels

of fibrinogen corresponded to a large MA.
The platelet count did not correlate with the activated whole-blood MA (adjusted r2 0.165), and
there was a weak correlation with Gp (adjusted r2
0.371). The relative contribution of Gp to Gt varied
over time but remained between 86% and 90%.
Figure 5 depicts the perioperative trend of the platelet index. There was an immediate increase after surgery that reached its peak on POD 3 and exceeded the
preoperative baseline on POD 7 by 25% (P 0.0001).

Discussion
Clinical evidence of postoperative hypercoagulability
has been incompletely evaluated by in vitro coagulation monitoring. The results of the present investigation clearly demonstrate a substantial postoperative
hypercoagulability lasting for at least seven days after
major uneventful abdominal surgery under general
anesthesia. This hypercoagulability comprised an accelerated clot formation, as evidenced by an early
decrease of the r-time, and an increase of the clot
strength, as evidenced by a continuous postoperative
increase of the MA. It is unclear when coagulation
returned to preoperative baseline values, but the
present data suggest that hypercoagulability after major abdominal surgery persists beyond the known duration of surgical stress response after similar procedures (23,24).
The principles and the methods of the thromboelastogram, reflecting the dynamic interaction between
platelets and the protein coagulation cascade, are well
described in the literature (20 22). Thromboelastography is being increasingly used to guide therapeutic

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Table 1. Perioperative Hematologic Data

Variable

Preop

End of
surgery

OP 6

POD 1

POD 2

POD 3

Hematocrit (%)
Platelet count
(1000 per mm3)
PTa (%)
PTTb (s)
TCTc (s)
Fibrinogend (g/L)
Antithrombin IIIe (%)

31.3 4.0
221.6 75.5

30.2 3.2
222.9 99.2

29.9 2.5
231.1 95.0

28.5 4.1
220.2 100.9

27.4 4.3
208.2 107.4

27.5 3.4
206.7 105.4

89.4 17.0
34.3 3.8
18.5 1.5
3.58 0.90
88.7 16.6

85.2 14.2
31.7 3.1
19.8 1.7
3.04 0.91
74.1 16.0

86.9 14.5
32.8 5.2
19.2 1.4
3.19 0.80
81.1 10.9

82.2 15.6
37.3 5.0
17.3 1.2
3.93 0.83
82.6 11.6

93.3 20.2
35.6 5.1
16.4 1.7
5.46 1.61
81.0 13.1

100.0 16.0
34.5 4.5
16.3 1.7
6.7 2.12
81.4 15.1

POD 7

29.2 3.0
0.0001
276.3 119.9 0.0001
91.4 20.1
33.1 3.6
16.9 1.1
6.3 2.4
90.0 17.9

0.0005
0.0001
0.0001
0.0001
0.0002

Values are expressed as mean sd.

Preop after the induction of anesthesia; OP 6 6 h after surgery; POD postoperative day; PT prothrombin time; PTT partial thromboplastin time;
TCT thrombin clotting time.
a
Reference limits 70%130%.
b
Reference limits 26 36 s.
c
Reference limits 16 21 s.
d
Reference limits 1.8 3.5 g/L.
e
Reference limits 75%125%.

Figure 3. Perioperative changes of the maximal amplitude (MA) in

the abciximab-cytochalasin D-modified thromboelastography. The x
axis represents the observation points, and the y axis represents the
MA (mean sd). P 0.0001 for the effect time. PREOP after the
induction of anesthesia; OP 6 6 h after surgery; POD
postoperative day.

decisions during liver transplantation and cardiac surgery and in preeclamptic and eclamptic parturients
(10 13). Data on perioperative changes of thromboelastographic variables in noncardiac surgery are
rare and limited to a short postoperative period
(1,2527).
Our study differs from previous work in several
regards. We included only patients without a history
or clinical signs of coronary artery disease. All of our
patients underwent major abdominal surgery, which
is known to trigger a substantial stress response and
activation of the coagulation cascade (4,7,23,24). Most
importantly, we evaluated our patients until the seventh POD.
Because of the exponential increase of the elastic
shear modulus, the perioperatively observed 10% increase of the MA corresponds to a 50% perioperative
increase of the clot strength. This is in accordance with

Figure 4. Correlation between fibrinogen and the maximal amplitude (MA) of the abciximab-cytochalasin D-modified thromboelastography; adjusted r2 0.767. The x axis represents the fibrinogen
level, and the y axis, the MA. Values are mean sd. The solid line
represents the regression line; the dotted lines represent the 95%
confidence limits.

the findings of Khurana et al. (17), who showed a

similar increase of the elastic shear modulus after
maximally triggering coagulation with tissue factor.
Comparing conventional with laparoscopic cholecystectomy, Caprini et al. (25) demonstrated thromboelastographic signs of hypercoagulability on the
first POD in the laparoscopic group.
In morbidly obese patients, Pivalizza et al. (27) demonstrated an already preoperatively accelerated coagulability and clot strength without additional changes
of the thromboelastographic variable after minor surgical procedures. In contrast to patients undergoing
major vascular surgery under epidural anesthesia,
Tuman et al. (1) demonstrated thromboelastographic
evidence of hypercoagulability on the first POD after
comparable procedures under general anesthesia. This
early postoperative hypercoagulability was associated
with the occurrence of arterial thrombotic events (1).

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Figure 5. Perioperative change of the platelet index as a calculated

measure of platelet function. The x axis represents the observation
points, and the y axis represents the platelet index, which is defined
as Gp per 1000 platelets (in dynes/cm2). Gp difference of the
calculated elastic shear modulus of the activated whole blood maximal amplitude (MA) and abciximab-cytochalasin D-modified MA.
PREOP after the induction of anesthesia; OP 6 6 h after
surgery; POD postoperative day.

Likewise, Gibbs and Bell (28) demonstrated evidence of hypercoagulability on the second POD after abdominal aortic surgery, which was attenuated
by small-dose unfractionated heparin. Their findings are in line with the available literature, which
demonstrates dose-dependent alterations of the
r-time and the MA and their reversibility with heparinase, both in vitro and in vivo (12,28,29). In
contrast to a similar dose-dependent effect of low
molecular weight heparin in vitro, there are no conclusive data in vivo (29). The results of this investigation, however, suggest that thromboelastographic
variables are unable to monitor an in vivo effect of
standard thrombosis prophylaxis with low molecular weight heparin. This is most likely because of the
prophylactic dose and the time window between
subcutaneous administration and thromboelastographic assessment.
Modified thromboelastography, which uses plateletinactivating substances such as abciximab and cytochalasin D, has been introduced to estimate the independent
contribution of procoagulatory proteins and platelets to
clot strength (14 17) to specifically correct coagulation
defects (14,15,30). The difference between the calculated
elastic shear modulus of the whole-blood MA and that of
the modified MA has been suggested to represent the
platelet contribution to clot strength (15,17,18). Whether
these considerations apply to hypercoagulable states is
unknown. The perioperative change of the abciximabcytochalasin D-modified MA in our study coincided
with a parallel change of fibrinogen that peaked on the
third POD, similarly to previously published data (2,4,8).
Despite this substantial 60%90% increase of fibrinogen
concentration, there were only minimal changes of the

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relatively small contribution of the plasmatic component

to the clot strength (10%14%). This small contribution of
the plasma protein component to the clot strength is in
agreement with recent findings (17,18). Similar to the
findings of Khurana et al. (17) and Nielson et al. (18), the
relative perioperative contribution of the platelet component to clot strength ranged from 86% to 90% in this
study. Correction for the perioperative change of the
platelet count revealed an estimated peak platelet reactivity on the second and third PODs. This is in agreement with the findings of Rosenfeld et al. (8), who used
whole-blood aggregometry to demonstrate maximal
platelet reactivity 48 hours after major abdominal surgery. However, because we did not measure platelet
activation variables, the calculated platelet component of
clot strength is only indirect evidence of the possible role
of platelet reactivity in postoperative hypercoagulability.
Our study was designed to evaluate whether major
abdominal surgery induces hypercoagulability, which
may be detected by changes in the thromboelastographic trace and calculated variables. Because of the
seven-day study period and the fluid requirements
associated with major abdominal surgery, we cannot
exclude a potential impact of the administration of
hydroxyethyl starch, saline, or both on thromboelastographic variables, as has been precisely described to
occur after in vitro hemodilution and in healthy volunteers (3133).
This investigation demonstrates thromboelastographic evidence of substantial hypercoagulability
lasting for at least seven days after major and uneventful abdominal surgery. Despite a significant increase
of fibrinogen, this hypercoagulability seems to be predominantly caused by a substantial platelet activity.
Postoperative hypercoagulability is not reflected by
standard coagulation monitoring but can be easily and
quickly determined by serial analyses of standard and
modified thromboelastography. Standard thromboelastography is unable to monitor prophylactic
doses of low molecular weight heparin.

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