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Ann Thorac Surg 2003;76:615-617
© 2003 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, New York, NY, USA
b Department of Medicine, New York, NY USA
c and Division of Vascular Surgery, College of Physicians and Surgeons, Columbia University, New York, New York, USA
Accepted for publication January 8, 2003.
* Address reprint requests to Dr Morgan, Columbia University, College of Physicians and Surgeons, 177 Fort Washington Avenue, Milstein 7GN-435, New York, NY 10032 USA
e-mail: jm2240{at}columbia.edu
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A 72-year-old woman with a history of atrial fibrillation presented with recurrent, acute ischemia of her left lower extremity. Three weeks earlier she presented with ischemia due to thromboembolization, which was unresponsive to thrombolytic therapy, requiring a popliteal/tibial artery thrombectomy. The patient underwent repeat thrombectomies with vein patch angioplasties of the popliteal and posterior tibial arteries. Her postoperative course was complicated by heparin-induced thrombocytopenia and restenosis of the popliteal/tibial thrombectomy sites, requiring a femoral-to-distal posterior tibial bypass. Her postoperative course was further complicated by occlusion of her bypass graft requiring amputation, thrombosis of her brachial, axillary, and radial veins, as well as development of a mobile right atrial thrombus, traversing the tricuspid valve into the right ventricle, causing ventricular irritation, and multiple episodes of supraventricular and ventricular tachycardia.
For the intracardiac thrombus, the patient underwent off-pump right atrial thrombectomy. After sternotomy, the superior vena cava and inferior cava were encircled and snared, resulting in total inflow occlusion for a period of 20 seconds, during which point the systolic blood pressure decreased to 30 mm Hg. A small right atriotomy was made within the confines of a pursestring suture, through which a 4.1 x 3.6 cm white, freely mobile thrombus was removed (Fig 1). The pursestring suture was closed and the snares released, restoring inflow to the heart.
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Four basic criteria are used to make the diagnosis of HIT. These include current or recent exposure to heparin, a decrease in the platelet count by at least 50%, laboratory evidence of heparin-dependent antibodies, and resolution of thrombocytopenia after discontinuation of heparin [1, 3].
Approximately 20% of patients with HIT will develop HITT, with a morbidity and mortality of 60% to 80%, and 20% to 30%, respectively [3]. Most thrombotic events are venous and include deep vein thrombosis, pulmonary embolism, and central sinus thrombosis. Possible arterial thrombotic sequelae include limb ischemia, cerebrovascular accident, myocardial infarction, and various end organ thromboses [5].
Medical treatment of HITT
If there is a strong clinical suspicion for HITT, unfractionated and LMWH should be discontinued, as crossreactivity of heparin-dependent antibodies with LMWH may be seen in up to 90% of patients [6]. Alternative antithrombotic medications, which include danaparoid, ancrod, and lepirudin, should be administered [4].
Intraoperative management of HITT
Intraoperative use of alternative antithrombotics is appropriate for patients who require CPB. Although weak crossreactivity between danaparoid and HIT antibodies can be seen in 15% to 20% of patients, it is safer than LMWH. Its use during CPB is limited, however, because of a lack of an accepted dose and method of monitoring its anticoagulant effects, as well as frequent development of clots and prolonged postoperative bleeding [4].
Ancrod prevents the development of clots by selectively depleting fibrinogen. It can be reversed with FFP or cryoprecipitate. However, ancrod is not approved by the Food and Drug Administration and is available for compassionate use only [4].
Lepirudin, a direct inhibitor of thrombin, is a safe and effective anticoagulant, although there is no specific antidote [5, 6]. Three to five times more potent than heparin, it does not crossreact with heparin-induced antibodies. It leads to rapid recovery in platelet count and prevents progression of thrombotic complications. Monitoring the activated partial thromboplastin time (aPTT) is required [4, 5].
Back-up plan if Off-Pump approach not possible
At our institution, patients with HITT who require cardiac surgery are maintained on lepirudin and warfarin preoperatively. If the procedure cannot be performed off-pump, abciximab is given intraoperatively (bolus of 0.25 mcg/kg followed by an infusion of 0.125 mcg/kg per minute). Abciximab inhibits platelet aggregation, the primary etiology of thrombosis in patients with HITT. Abciximab acts by binding to intact glycoprotein IIb/IIIa receptor and preventing binding of fibrinogen, von Willebrand factor, and other adhesive molecules. A standard dose of heparin is given as a bolus. Abciximab is continued until 10 minutes before reversal of heparin, which is accomplished using the usual dose of protamine. Because abciximab disrupts platelet function, platelets are given (12–18 units) immediately after heparin reversal.
Warfarin should be given only after therapeutic levels (PTT of 1.5 to 2.5 the normal) of lepirudin have been achieved. Ideally, warfarin should not be given until there is substantial resolution of thrombocytopenia, as thrombotic complications have been described in patients when alternative anticoagulants were discontinued prior to resolution of thrombocytopenia. Lepirudin can be discontinued when the INR is therapeutic for 48 hours or after 5 days of warfarin therapy, whichever is longer [1, 4].
Prophylactic platelet transfusions are not recommended, as petechiae and other clinical evidence of bleeding are uncommon. In addition, thrombotic events occurring early after transfusion of platelets have been reported. Platelet transfusions should be reserved for patients with serious hemorrhagic complications [5]. Platelet inhibitors, such as aspirin and prostin, should be used to decrease the adhesiveness of platelets, which can limit thrombosis.
Surgical thromboembolectomy may be appropriate for select patients with large vessel or intracardiac thromboembolism. For patients who cannot receive heparin, an off-pump pump approach with total inflow occlusion is preferred. A backup plan should be in place, however, regarding alternative methods of anticoagulation in the event that CPB is required.
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This article has been cited by other articles:
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  A. V Singh, J. T Walsh, and I. S Birdi Right Atrial Thrombus Masquerading as Intracardiac Cyst: a Case Report Asian Cardiovasc Thorac Ann, August 1, 2008; 16(4): e35 - e36. [Abstract] [Full Text] [PDF]
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