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Eur J Cardiothorac Surg 2007;32:544-546. doi:10.1016/j.ejcts.2007.05.026
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Case reports

Can thromboelastography predict which patients with heparin-induced thrombocytopenia may suffer thrombotic complications of type II?

Ilias A. Kouerinisa,*, Mahmoud El-Alib, Nikolaos Theakosa, Panagiotis Dedeiliasa

a Department of Cardiac Surgery, Evangelismos Hospital, Athens, Greece
b Hematology Laboratory, Evangelismos Hospital, Athens, Greece

Received 27 February 2007; received in revised form 9 May 2007; accepted 31 May 2007.

* Corresponding author. Address: Doukissis Plakentias 46, Melissia, Athens, Greece. Tel.: +30 6932 71 31 71; fax: +30 210 7224449. (Email: ikouerinis{at}hotmail.com).


   Abstract
Top
 Abstract
1. Introduction
 2. Case report
 3. Discussion
 References
 
Despite the existence of several sensitive functional and antigen assays used for the diagnosis of heparin-induced thrombocytopenia (HIT), an additional assessment of the patient's hemostatic status, in order to predict the thrombotic complications of the malevolent HIT type II, has become necessary. Herein below, we present the findings of thromboelastography (TEG) in a post-cardiac-surgery patient with the clinical diagnosis of HIT type II and false negative tests for heparin antibodies. We have reached the conclusion that TEG may prove to be a useful supplementary method to predict those HIT patients who may suffer complications of HIT type II.

Key Words: Heparin-induced thrombocytopenia • Thromboelastography • CPB complications • ELISA


   1. Introduction
Top
 Abstract
 1. Introduction
2. Case report
 3. Discussion
 References
 
Heparin-induced thrombocytopenia is a life- and limb-threatening prothrombotic complication resulting from a platelet-activating immune response triggered by the interaction of negatively charged heparin with a positively charged platelet protein, platelet factor 4 (PF4) [1].

Despite the progress in the detection of anti-heparin antibodies, no test can predict which of those HIT patients will present with thrombotic or hemorrhagic complications of HIT type II [1,2].

Several authors have studied the role of thromboelastography (TEG) to evaluate the effect of platelets and rFVIIa on the kinetics of clot formation and clot firmness [3–5]. Our purpose was to explore the potency of TEG to predict those HIT patients (5%) who are subject to develop thrombotic complications of type II. To the best of our knowledge, this is the first report that investigates the role of TEG in HIT subjects.


   2. Case report
Top
 Abstract
 1. Introduction
 2. Case report
3. Discussion
 References
 
A 77-year-old woman with a previous history of rectal bleeding due to angiodysplasia underwent combined mitral valve replacement and double coronary bypass grafting with complete success. Her immediate postoperative course progressed uneventfully and she was started on per os coumarin as soon as she received oral nutrition.

During the fourth postoperative day, she presented cyanosis at six fingernail phalanxes on both hands despite her perfect hemodynamic condition and the complete lack of vasoconstriction or any other inotropic support.

This striking clinical feature was combined with the significant platelet count reduction (78,000/µl), which was observed from the first postoperative day; so, the most probable diagnosis was heparin-induced thrombocytopenia with thrombosis (HIT type II). As a result, all forms of heparin and coumarin therapy were discontinued.

Despite our strong clinical suspicion for HIT type II; we did not decide to start therapy with a direct thrombin inhibitor due to her high probability for intestinal bleeding. Moreover, the results of ELISA concerning the detection of anti-heparin antibodies in the serum were negative on two occasions.

The significant clinical improvement of the patient's condition during the next 3 days in concordance with the rise in platelet count to 131,000/µl justified initially our ‘watchful waiting’ policy.

However, an accidental catheter flush with heparin on the eighth postoperative day perpetuated the syndrome and the patient showed acute respiratory distress and sharp deterioration of her peripheral cyanosis with extensive skin blistering and signs of gangrene (Fig. 1 ). As the situation had dramatically worsened, the administration of lepirudin was completely indicated.


Figure 1
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  		Fig. 1. The patient of our presentation.

 
The same postoperative day (eighth), just before the administration of lepirudin, we explored, in parallel, the potency of thromboelastography to prevent such catastrophic events obtaining the exact profile of the patient's coagulation status. The performed test revealed abnormal values in all coagulation parameters (R = 1.6 min, K = 0.8 min, {alpha} = 81.2°, MA = 74.5 mm, G = 14.6 dyn/s (k), CI = 6.1, LY30 = 5.7%), confirming the strong thrombotic diathesis of our HIT patient.

Nevertheless, the established signs of gangrene were never reversed, despite the partial improvement observed in the borders of vital-cyanotic zones. A rectal bleeding on the ninth postoperative day was clinically insignificant and the patient was discharged 4 days later with the suggestion of scheduled amputations.


   3. Discussion
Top
 Abstract
 1. Introduction
 2. Case report
 3. Discussion
References
 
Heparin-induced thrombocytopenia is the result of the production of an antibody to the complex that is created between heparin and platelet factor 4 (H-PF4) released from activated platelets. It presents after an interval of 3–15 days of heparin therapy and can be diagnosed in 1–3% of patients following cardiac surgery [6]. The rare malevolent type II accounts for 5% of all cases and is complicated with hemorrhage, thromboembolism and death in 53, 44 and 33% of these patients, respectively [2].

Nevertheless, it has not been clarified which of those post-cardiac-surgery patients diagnosed for HIT are subject to manifest the thrombotic or hemorrhagic complications of type II. Such a selection would be very helpful and would allow us to start an early and aggressive treatment, which aims at eliminating morbidity and mortality. Although there is an obvious trend in hematology to interpret qualitatively and quantitatively complicated coagulation profiles with additional methods [4,5,7,8], their exact role in HIT has not been investigated yet.

According to our report, the role of TEG can prove to be of great significance at this special point (Fig. 2a and b) [9]. Any HIT patient with abnormal TEG parameters should be considered for further evaluation and proper treatment before the establishment of irreversible thrombotic complications [10]. In our case, the interpretation of TEG results revealed platelet and enzymatic hypercoagulability demanding aggressive treatment with a direct thrombin inhibitor (Fig. 2c and d).


Figure 2
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  		Fig. 2. (a, b) TEG tracing parameters and qualitative analysis. (c, d) Qualitative and quantitative TEG analysis of our patient.

 
Nevertheless, it should be noted that TEG results should be considered along with the patient's history, clinical condition and other available laboratory tests [8,10]. ELISA still plays the central role in HIT diagnosis with both high specificity and sensitivity, but in our patient, it proved inadequate to detect the special epitope resulting in two false negative results. This phenomenon is observed in less than 2% of patients tested for heparin antibodies; thus, in the presence of strong clinical suspicion for HIT, ELISA should be followed by platelet aggregation tests.

In conclusion, TEG can help the cardiac surgeon predict which HIT patients may suffer type II complications of HIT and ‘buy some precious time’ by starting early, aggressive treatment from the onset of thrombocytopenia, before the establishment of potentially fatal thrombotic and hemorrhagic complications.


   References
Top
 Abstract
 1. Introduction
 2. Case report
 3. Discussion
 References
 

  1. Francis JL. A critical evaluation of assays for detecting antibodies to the heparin–PF4 complex. Semin Thromb Hemost 2004;30(3):359-368.[CrossRef][Medline]
  2. Dandecar U, Young J, Kalkat M, Satur CMR. Heparin induced thrombocytopenia II complicating coronary artery bypass surgery: a tale of caution. Interact Cardiovasc Thorac Surg 2004;3:121-123.[Abstract/Free Full Text]
  3. Gerotziafas GT, Chakroun T, Depasse F, Arzoglou P, Samama MM, Elalamy I. The role of platelets and recombinant factor VIIa on thrombin generation, platelet activation and clot formation. Thromb Haemost 2004;91:977-985.[Medline]
  4. Vig S, Chitolie A, Bevan DH, Halliday A, Dormandy J. Thromboelastography: a reliable test?. Blood Coagul Fibrinolysis 2001;12:555-561.[CrossRef][Medline]
  5. Oshita K, Az-ma T, Osawa Y, Yuge O. Quantitative measurement of thromboelastography as a function of platelet count. Anesth Analg 1999;89:296-299.[Free Full Text]
  6. Warkentin TE, Greinacher A. Heparin induced thrombocytopenia and cardiac surgery. Ann Thorac Surg 2003;76:638-648.[Abstract/Free Full Text]
  7. Hemker HC, Giesen P, AlDieri R, Regnault V, de Smed E, Wagenvoord R, Lecompte T, Beguin S. The Calibrated Automated Thrombogram (CAT): a universal routine test for hyper- and hypocoagulability. Pathophysiol Haemost Thromb 2002;32:249-253.[CrossRef][Medline]
  8. Collins PW, Macchiavello LI, Lewis SJ, Macartney NJ, Saayman AG, Luddington R, Baglin T, Findlay GP. Global tests of haemostasis in critically ill patients with severe sepsis syndrome compared to controls. Br J Haematol 2006;135:220-227.[CrossRef][Medline]
  9. Mallett SV, Cox DJ. Thromboelastography. Br J Anaesth 1992;69:307-313.[Free Full Text]
  10. Sharma SK, Vera RL, Stegall WC, Whitten CW. Management of postpartum coagulopathy using thromboelastography. J Clin Anesth 1997;9:243-247.[CrossRef][Medline]



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I. A. Kouerinis, A. Kourtesis, M. El-Ali, T. Sergentanis, A. Plagou, M. Argiriou, N. Theakos, and A. Giannakopoulou
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