Surgeries for the Heart and Abdominal Aorta in a Patient with Heparin-Induced Thrombocytopenia:
Manifestations Following Initial Heart Surgery 11
month after CABG. Preoperatively, 6 units of autologous
blood were obtained using erythropoietin. In the operat-
ing room, 6 units of autologous fresh blood were taken
by the “switch-back method”. All pressure lines and the
circuit of the autologous blood transfusion device were
replaced with saline containing argatroban or acid-cit-
rate-dextrose solution. Prior to clamping the arteries, 8.5
mg (0.1 mg/kg) of argatroban was administered as a bo-
lus, and maintained at 10 - 15 mg/h to achieve activated
coagulation time (ACT) >200 s. The AAA was success-
fully replaced by a vascular prosthesis. Argatroban was
discontinued after reperfusion, and autologous fresh blood
was given. No bleeding was noted, but as there is no an-
tidote to argatroban, it was necessary to wait for over 90
min until ACT had normalized. Postoperatively, argatro-
ban was resumed and then switched to oral warfarin. The
postoperative course was uneventful and the patient was
discharged on POD14. PAT were repeated and remained
positive with heparin for 3 years.
3. Discussion
In the present case with postoperative manifestations of
HIT after CABG, the patient underwent abdominal aortic
surgery using argatroban instead of heparin. This case
raised the issue of the time between onset of HIT and
treatment. Perioperatively, platelet count may be lower
than 100,000/mm3 after cardiac surgery. Therefore, it is
quite difficult to make a definite diagnosis in patients
with initial manifestations of HIT. IABP may have been
responsible for thrombocytopenia in this case. Therefore,
another day was required for suspicion of HIT, and the
initiation of treatment was delayed. Most patients under-
going cardiovascular surgery have been exposed to hepa-
rin during treatment or examination by the cardiology
service. Postoperative manifestations of HIT tend to oc-
cur in patients referred from institutes other than cardi-
ology services or requiring emergent surgery. In the 3
years since treating this patient, three other patients have
presented with HIT postoperatively in our department;
two of these patients underwent emergent surgery due to
acute mitral regurgitation and dissecting ao rtic aneurysm.
Based on these cases, we have implemented preoperative
PAT using heparin in patients without heparin exposure.
The pf4 antibody test is a simple means of identifying
HIT type II, but does not provide information to exclude
a diagnosis of HIT type I. Even by ELISA, the presence
of pf4 antibodies can be confirmed only with a delay of 2
days or more in approximately 50% of patients in whom
HIT develops [2]. At present, PAT using heparin is much
faster even in cases with HIT type I in our institution, but
no HIT patients have been encountered to date.
Another issue is the initial treatment for HIT. The cur-
rent recommendation is to discontinue heparin in cases of
suspected HIT and begin treatment with direct thrombin
inhibitors, such as hirudin/bivalrudin, danaparoid, and
argatroban [3]. Danaparoid and argatroban are available
in Japan. Argatroban is a derivative of l-arginine, which
binds reversibly to the active site of thrombin, and is ap-
proved for treating HIT by the FDA as well as recombi-
nant hirudin (lepirudin). We chose argatroban because it
has a number of advantages, includi ng speci fi c rapi d onset ,
and is safe in patients with renal impairment. Periopera-
tively, when HIT was suspected, hemodynamic status
was aggravated in this case. As coronary angiography
was not performed, there was no actual evidence of graft
occlusion. However, it was suspected that bypass would
have a risk of thrombotic occlusion. In this patient, car-
diac status settled down after initiation of argatroban
treatment, suggesting thrombolysis in the n ative coronary
arteries and/or bypass grafts. Argatroban would be effec-
tive for HIT not only in this case, but also in the three
HIT patients we encountered previously.
The other issue is the treatment strategy for the AAA.
Over the past decade methods for endovascular repair
(EVAR) of aortic aneurysms have been developed, and
the indications have been expanded from the descending
aorta to other branched aortae, such as the aortic arch,
thoracoabdominal aorta, and abdominal aorta. At the
time of surgery for AAA in the present case, approval for
EVAR in Japan was strictly limited to elderly patients or
those with difficulties in conventional surgical repair,
such as previous abdominal surgery. Therefore, this pa-
tient underwent conventional surgical repair of AAA
with argatroban treatment. There have been no previous
reports of EVA R in patients known to hav e HIT, but two
cases of HIT manifestations following EVAR by graft
occlusion were reported [4,5]. There have been a small
number of reports and reviews regarding EVAR in pa-
tients with preoperatively diagnosed HIT, but many re-
views regarding cardiovascular surgery the principles of
which can be summarized as: 1) wait until pf4 antibody
level subsides, then use heparin; 2) use alternative anti-
coagulation, such as danaproid or hirudin/bivalrudin to
replace heparin. Warkentin and Greinacher included use
of heparin with epoprostenol/tirofiban as an option [1].
As mentioned above, not all cases of HIT are diagnosed
by pf4 antibody, and therefore there are HIT type II pa-
tients negative for pf4 antibody. We encountered a pa-
tient on hemodialysis who underwent surgery to create
an internal shunt when he was found to have HIT. Al-
though pf4 antibody was negative, he developed severe
thrombosis with a trace amount of heparin. In this case,
although pf4 antibody was negative, PAT remained posi-
tive for heparin for at least 3 years. The PAT results
suggested high risk in this case, and we were hesitant to
use heparin. We again chose argatroban bolus and con-
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