SAFCS SymposiumHeparin-induced thrombocytopenia and thrombosis syndrome after cardiac surgery☆
Introduction
A 51-year-old man with chronic stable angina and a murmur underwent outpatient cardiac catheterization, which demonstrated 3-vessel coronary artery disease amenable to coronary artery bypass grafting (CABG). Echocardiography revealed critical aortic stenosis with an aortic valve area of 0.7 cm2 and an ejection fraction of 30%.
Before scheduled elective CABG and aortic valve replacement (AVR), the patient presented emergently to our facility after experiencing a myocardial infarction and sudden death episode. After stabilization, he was admitted to the intensive care unit with initiation of a continuous heparin (Wyeth-Ayerst, Philadelphia, Pennsylvania) infusion. While awaiting elective CABG and valve replacement, the patient was transitioned from heparin to low-molecular-weight heparin (LMWH) use in the form of subcutaneous lovenox (Aventis Pharmaceuticals, Bridgewater, New Jersey). Having already received heparin-related compounds during his initial cardiac catheterization and again during his readmission, the patient received the additional large exposure to heparin associated with his on-pump CABG/AVR.
The patient tolerated his surgical procedure well, and his initial postoperative course was uneventful. On the third postoperative day, coumadin (Bristol-Myers Squibb, Princeton, New Jersey) therapy was initiated for aortic valve prophylaxis. Lovenox was added on the fifth postoperative day for additional valve prophylaxis because of initial difficulty attaining an adequate INR with early coumadin dosing. After receiving 2 doses of lovenox, the patient's platelet count dropped from a postoperative value of 168,000 to 89,000. Lovenox was immediately discontinued because of concerns for possible development of heparin-induced thrombocytopenia (HIT). A careful review of the patient's plan of care was undertaken, ensuring no practice of heparin catheter flushes by any member of the health care team, presence of heparin bonded catheters, or other source of ongoing heparin or heparin-related compound exposure.
Two days later, the patient's platelet count reached a nadir of 40,000, and he was found to have a cool left lower extremity with absent distal pulses. Within 1 hour, the patient developed a pulseless left lower extremity below the knee and associated cyanotic changes were observed. Vascular studies confirmed arterial insufficiency of the left lower extremity consistent with acute thrombosis that was not amenable to surgical intervention. The patient also developed worsening azotemia and renal insufficiency with abdominal distension and peritoneal signs. In addition, the patient developed pulmonary failure caused by suspected pulmonary embolism, although no significant deep vein thrombosis was identified via ultrasound.
The patient underwent below-the-knee guillotine amputation of his ischemic left lower limb, which revealed white thrombus in the posterior tibial, anterior tibial, and peroneal arteries. Exploratory laparotomy was also performed and revealed an ischemic cecum, which necessitated right hemicolectomy with primary anastamosis and diverting loop ileostomy. Laboratory investigation performed at the time of the acute event would reveal a positive heparin-induced platelet aggregation screen with no identification of specific antiplatelet antibodies. A gradual increase in platelet count would follow the initial decline, with normalization to 227,000 on the seventh day after the discontinuation of the heparin and heparin-related compounds.
Anticoagulation was reinstituted after operation with recombinant hirudin, Refludin (Aventis Pharmaceuticals). Therapy was initiated with a bolus of 0.4 mg/kg over 15 to 20 minutes followed by 0.15 mg/kg/hour. Refludin was continued, with compensatory dosing adjustments for renal insufficiency, as coumadin reached therapeutic levels. During his prolonged intensive care unit course, his renal failure and azotemia resolved after initial use of intermittent hemodialysis. His respiratory failure ultimately proved to require tracheostomy to facilitate extended ventilator support, but he ultimately tolerated complete independence from ventilatory support in the third week postoperative. After a 29-day intensive care unit course and a 36-hospital-day course, the patient met criteria for discharge. At 2.5 years of follow-up, the patient was found normal bowel function after reversal of his loop ileostomy, normal renal and pulmonary function, and was ambulating adequately on and playing golf with the use of prosthesis.
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Comment
The HIT syndrome is subclassified into 2 distinct types based on differences in etiology and clinical features. Heparin-induced thrombocytopenia type I is thought to be caused by direct activation of platelets by unfractionated heparin (UFH) or LMWH in a nonimmune mediated fashion. It characteristically occurs within the first 4 days of therapy and typically resolves without treatment or complication, even with continued heparin use.
Heparin-induced thrombocytopenia type II, caused by
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2011, Turk Kardiyoloji Dernegi ArsiviThe pharmacotherapy of heparin-induced thrombocytopenia (HIT): A review of contemporary therapeutic challenges in clinical practice
2008, Malaysian Journal of Medical SciencesHeparin-induced thrombocytopenia and recent advances in its therapy
2007, Journal of Clinical Pharmacy and Therapeutics
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