Cardiovascular Journal of Africa: Vol 26 No 3 (May/June 2015)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 26, No 3, May/June 2015 e14 AFRICA
of patients. Although thrombosis may occur in any vascular bed,
venous thrombosis is more common than arterial thrombosis
and often presents as deep-vein thrombosis or pulmonary
embolism. However, arterial thrombosis can be predominant in
cardiac and vascular surgical patients.5 Major complications of
arterial thrombosis are acute limb ischaemia, stroke and acute
myocardial infarction. Arterial thrombi are uncommonly seen in
the renal, mesenteric or spinal arteries.4
The diagnosis of HIT is essentially made on the basis of clinical
grounds and a decrease in platelet count in a patient receiving
heparin, for which there are no obvious causes. Laboratory
assays (frequently with slow turnaround times) play a supportive
role and involve functional and non-functional tests.12 Most
laboratory tests are not readily available in the acute setting.8
HIT should be suspected in the setting of absolute
thrombocytopenia (platelet count < 150 000 cells/μl) as well as
relative thrombocytopenia (fall in platelet count of at least 50%
from baseline value). However, this syndrome should also be
considered in patients with the unexplained development of new
or progressive thrombosis while receiving a heparin product.
To aid in the diagnosis of HIT, a specific scoring system
for clinical diagnosis, called the 4 Ts score was developed
and validated by Lo et al.13 A score is calculated based on the
following four categories: degree of thrombocytopenia, timing
of onset of thrombocytopenia, clinical sequelae such as the
development of venous or arterial thrombosis, and presence of
other aetiologies of thrombocytopenia.5
Functional and immunological tests for HIT involve the
platelet aggregation test (PAT), serotonin release assay (SRA),
heparin-induced platelet aggregation (HIPA) test, the anti-H-
PF4 complex antibody enzyme-linked immunosorbent assays
(ELISA), and flow cytometry studies.8 The sensitive (> 90%)
but less specific (~ 71%) H-PF4 ELISA test is often used as a
screening test, and the SRA (sensitivity and specificity 100 and
97%, respectively) can be performed as a confirmatory test, but
is not universally available and utilised.12
The HIT-associated mortality rate in cardiac surgery patients
is 35–42%.7 About 20% of patients developing HIT syndrome
may require limb amputation because of peripheral arterial
thrombosis. This syndrome is associated with a myriad of
complications, including multiple organ systems: mesenteric
ischaemia, renal insufficiency and stroke.8
Delays in the availability of diagnostic assay results frequently
necessitate initiation of treatment for HIT based on clinical
evaluation alone. When HIT with or without thrombosis is
suspected postoperatively, the first step in treatment is immediate
discontinuation of all heparin exposure, including heparin
flushes and LMWH.12
In addition to heparin discontinuation, patients with either
HIT with thrombosis or isolated HIT (type 2 HIT without
thrombosis) require further treatment with an alternative
anticoagulant agent.Heparindiscontinuationalone is insufficient,
because patients (even type 2 HIT without thrombosis) remain
in a prothrombotic state. In light of the sustained thrombus
propagation that occurs with HIT, current treatment is focused
on reduction of thrombin generation via direct thrombin
inhibition (e.g. bivalirudin, lepirudin, argatroban) or indirect
factor Xa inhibition (e.g. danaparoid, fondaparinux).5
Prophylactic and therapeutic fondaparinux failed to prevent
the development of and to treat HIT in our case, but we used
fondaparinux because it is the only alternative anticoagulant
agent in our country. Although successful results have been
reported in the treatment of HIT with the use of fondaparinux,
it was recommended as grade 2C at the 9th ACCP Conference on
Antithrombotic Therapy and Prevention of Thrombosis.14
There are often plausible alternative explanations in critical
patients with thrombocytopenia. CPB and the use of the IABP
are clearly associated with thrombocytopenia. However, in
our patient, the decreased platelet count was not attributed to
these devices and conditions because there was no drop (> 50%)
in platelet count within the first three postoperative days. It
is also essential to differentiate HIT from other conditions
causing thrombocytopenia, such as haemodilution, disseminated
intravascular coagulation and sepsis. In our patient, these
conditions were excluded by several examinations and laboratory
tests.
Conclusion
HIT is a clinicopathological syndrome in which one or more
clinical events occur, usually thrombocytopenia or thrombosis.
Patients undergoing cardiac surgery can be at risk of HIT in the
early postoperative period, therefore daily platelet counts should
be performed during this period. If signs of HIT develop in a
patient receiving heparin, it must be stopped immediately and
alternative anticoagulant agents started. In our case, we did not
have success with fondaparinux as the alternative anticoagulant.
Despite discontinuation of heparin and initiation of alternative
anticoagulant agents, high morbidity and mortality rates are
associated with HIT.
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