Anticoagulation management and cardiac surgery in patients with heparin-induced thrombocytopenia

Unfractionated heparin (UFH) is the gold standard for anticoagulation during cardiopulmonary bypass (CPB). Of patients undergoing CPB operations, 25% to 50% develop heparin-dependent antibodies during the postoperative period, typically between day 5 and 10, if UFH is continued during the postoperative course. In 1% to 3% of all patients undergoing CPB operation with UFH anticoagulation, these antibodies activate platelets causing a prothrombotic disorder, known as heparin-induced thrombocytopenia (HIT), which can lead to life-threatening thromboembolic complications. If urgent cardiac operation with the use of CPB in patients with positive antibody titer is required, different anticoagulatory approaches are available, such as lepirudin, bivalirudin, and danaparoid or UFH in combination with platelet antagonists, such as epoprostenol or tirofiban. In patients with previous HIT but no detectable antibodies, UFH alone can be used only during CPB, but alternative anticoagulation has to be used pre- and postoperatively.     

In vitro cross-reactivity of danaparoid sodium in patients with heparin-induced thrombocytopenia type II undergoing cardiovascular surgery

STUDY OBJECTIVES: To assess the cross-reactivity of danaparoid sodium in patients undergoing cardiovascular surgery. DESIGN: Prospective investigation. SETTING: A major European heart center and university hospital. PATIENTS: 81 patients who underwent cardiovascular surgery during the period between January 1998 and April 1999 and were diagnosed with heparin-induced thrombocytopenia (HIT) II. INTERVENTIONS: Testing was performed in patients who revealed a decrease in the platelet count >30% or a platelet count <100,000/microL during heparin therapy. Testing for HIT was performed by the use of the heparin-induced platelet-aggregation assay. Patients were evaluated as positive if an agglutination occurred in two of four of the 0.2 IU/mL heparin chambers. Patients were judged to be cross-reactive with danaparoid sodium when an agglutination occurred in two of four chambers that contained 0.2 IU/mL Orgaran. MEASUREMENTS AND MAIN RESULTS: 281 patients (5.4% of the patients who underwent surgery during the period of the investigation) were tested for HIT II. Of these, 81 (1.5% of the total) gave a positive heparin-induced platelet-aggregation assay and 23 (28%) revealed a cross-reactivity with danaparoid sodium. CONCLUSION: Cross-reactivity with heparin-induced platelet antibodies occurred in 28% of the patients who tested positive for heparin-platelet antibodies. In these patients, Orgaran would not have been a safe option. In patients with HIT II undergoing cardiac surgery, cross-reactivity with danaparoid sodium must be excluded before initiation of therapy with Orgaran, otherwise, or in cases of cross-reactivity, other options such as r-hirudin are preferred.     

Heparin-induced thrombocytopenia type II on hemodialysis: switch to danaparoid

We report two pediatric patients with end-stage renal failure who developed heparin-induced thrombocytopenia type II (HIT II) on hemodialysis (HD). Both developed acute respiratory distress and chest pain within 30 min of initiating the 5th HD session. The platelets dropped during HD from 168 to 38×10⁹/l and from 248 to 109×10⁹/l, respectively. Marked clots were observed in the dialyzers. Substitution of heparin with the low molecular weight heparin dalteparin had no effect. Switching from anticoagulation to the heparinoid danaparoid resulted in immediate disappearance of all adverse effects, and further long-term HD was uneventful. HIT II was diagnosed clinically; heparin-induced platelet activation test (HIPA) and serum IgG, IgA, and IgM to heparin-platelet factor 4 complexes (HPF4) were both negative. We conclude that HIT II may occur in children on HD. HIT II is essentially a clinical diagnosis, as HIPA and antibodies to HPF4 are not always positive. Once HIT II is suspected, heparin (and low-molecular-weight heparins) should be stopped immediately. Long-term anticoagulation with danaparoid is a valuable option for patients on HD. Received: 22 July 1999 / Revised: 29 November 1999 / Accepted: 13 December 1999     

Sulodexide for hemodialysis anticoagulation in heparin-induced thrombocytopenia type II

Heparin-induced thrombocytopenia type II (HIT II) is an immune-mediated prothrombotic state. It requires cessation of all forms of heparin exposure. In maintenance hemodialysis (HD) patients, alternative anticoagulants (i.e. bivalirudin, danaparoid, fondaparinux) may be tried for HD procedure anticoagulation. Sulodexide (SLX) - a purified glycosaminoglycan preparation (80% heparan sulfate and 20% dermatan sulfate) - is not neutralized by platelet factor 4 and may be useful in HIT II. A 32-year-old man on continuous ambulatory peritoneal dilaysis (CAPD) and with protracted atrial fibrillation was given enoxaparin prophylaxis. On day 4, his platelets dropped from 119,000/micronL to 27,000/micronL and HIT II was diagnosed by positive heparin-induced platelet aggregation. While enoxaparin was withdrawn, the platelet count increased and remained stable. In the meantime, atrial fibrillation subsided but the patient developed pseudomonal peritonitis; the catheter was removed and the patient was switched to HD with SLX as an anticoagulant (bolus of 30 mg at HD onset). He was uneventfully treated with HD for 6 weeks and then reverted to CAPD. The widely available and inexpensive SLX may be a new, effective and potentially promising alternative anticoagulant in HD patients with HIT II.     

Anticoagulation during cardiopulmonary bypass in patients with heparin-induced thrombocytopenia type II and renal impairment using heparin and the platelet glycoprotein IIb-IIIa antagonist tirofiban

BACKGROUND: Patients with heparin-induced thrombocytopenia type II require an alternative to standard heparin anticoagulation. However, in patients with renal impairment, anticoagulation during cardiopulmonary bypass with agents such as danaparoid sodium or r-hirudin are associated with hemorrhage. Anticoagulation with unfractionated heparins combined with prostacyclin, a potent platelet aggregation inhibitor, is associated with severe hypotension. The authors investigated a new concept using unfractionated heparins after platelet inhibition with the short-acting platelet glycoprotein IIb-IIIa antagonist tirofiban. METHODS: Ten patients with heparin-induced thrombocytopenia type II and renal impairment were enrolled in the investigation. All had heparin-induced thrombocytopenia type II antibodies present as proved by the heparin-induced platelet aggregation assay, the heparin-platelet factor 4 enzyme-linked immunosorbent assay, or both. In all patients, preoperative anticoagulation to an activated partial thromboplastin time of 40-60 s was performed with r-hirudin. Anticoagulation during cardiopulmonary bypass was achieved with a bolus of 400 IU/kg unfractionated heparins after a bolus of tirofiban 10 microg/kg followed by an infusion of tirofiban at a rate of 0.15 microg x kg(-1) x min(-1) until 1 h before conclusion of cardiopulmonary bypass. Additional unfractionated heparins were only administered if activated clotting time decreased below 480 s. Coagulation was monitored by a abciximab-modified TEG and the adenosine diphosphate-stimulated (20 microm) platelet aggregometry. D-dimer concentrations, as a marker of venous thromboembolism, were measured before and 12, 24, and 48 h after surgery. Postoperative antithrombotic therapy was started immediately with r-hirudin to anticoagulation to an activated partial thromboplastin time of 40-60 s. RESULTS: The postoperative blood loss ranged from 110 to 520 ml. No patient needed reexploration. In no patient was there clinical evidence of thrombosis or embolism in the postoperative period or of a critical increase of the D-dimer concentrations, suggesting venous thromboembolism. Transfusion of platelets was necessary in only two patients. CONCLUSIONS: The protocol is easy to perform and no increased postoperative bleeding and no thromboembolic complications occurred. The combination of unfractionated heparins and tirofiban may be an alternative to other anticoagulation strategies in patients with heparin-induced thrombocytopenia.     

Intraoperative infusion of epoprostenol sodium for patients with heparin-induced thrombocytopenia undergoing cardiac surgery

Prevention of catastrophic thromboembolic complications during surgery in patients with heparin-induced thrombocytopenia (HIT) remains a challenging problem during cardiac surgery. We infused an increasing dose of epoprostenol sodium, which is one of three anti-HIT regimens available in Japan, ahead of administration of heparin and performed a mitral valve operation for a patient with type II HIT. The absence of thromboembolic events and platelet consumption during cardiopulmonary bypass, together with considerable reduction of platelet adhesion to the fibers of the membrane oxygenator, support the efficacy and safety of our strategy.     

Anticoagulation during Cardiopulmonary Bypass in Patients with Heparin-induced Thrombocytopenia Type II and Renal Impairment Using Heparin and the Platelet Glycoprotein IIb-IIIa Antagonist Tirofiban

Background: Patients with heparin-induced thrombocytopenia type II require an alternative to standard heparin anticoagulation. However, in patients with renal impairment, anticoagulation during cardiopulmonary bypass with agents such as danaparoid sodium or r-hirudin are associated with hemorrhage. Anticoagulation with unfractionated heparins combined with prostacyclin, a potent platelet aggregation inhibitor, is associated with severe hypotension. The authors investigated a new concept using unfractionated heparins after platelet inhibition with the short-acting platelet glycoprotein IIb-IIIa antagonist tirofiban.

Methods: Ten patients with heparin-induced thrombocytopenia type II and renal impairment were enrolled in the investigation. All had heparin-induced thrombocytopenia type II antibodies present as proved by the heparin-induced platelet aggregation assay, the heparin-platelet factor 4 enzyme-linked immunosorbent assay, or both. In all patients, preoperative anticoagulation to an activated partial thromboplastin time of 40-60 s was performed with r-hirudin. Anticoagulation during cardiopulmonary bypass was achieved with a bolus of 400 IU/kg unfractionated heparins after a bolus of tirofiban 10 [mu]g/kg followed by an infusion of tirofiban at a rate of 0.15 [mu]g [middle dot] kg-1 [middle dot] min-1 until 1 h before conclusion of cardiopulmonary bypass. Additional unfractionated heparins were only administered if activated clotting time decreased below 480 s. Coagulation was monitored by a abciximab-modified TEG(R) and the adenosine diphosphate-stimulated (20 [mu]m) platelet aggregometry. D-dimer concentrations, as a marker of venous thromboembolism, were measured before and 12, 24, and 48 h after surgery. Postoperative antithrombotic therapy was started immediately with r-hirudin to anticoagulation to an activated partial thromboplastin time of 40-60 s.

Results: The postoperative blood loss ranged from 110 to 520 ml. No patient needed reexploration. In no patient was there clinical evidence of thrombosis or embolism in the postoperative period or of a critical increase of the D-dimer concentrations, suggesting venous thromboembolism. Transfusion of platelets was necessary in only two patients.     

Recombinant hirudin as an alternative for anticoagulation during cardiopulmonary bypass in patients with heparin-induced thrombocytopenia type II: a 1-year experience in 57 patients

OBJECTIVE: To explore the possible use of recombinant hirudin (r-hirudin) as an alternative to heparin for anticoagulation during cardiovascular surgery. DESIGN: Retrospective analysis. SETTING: Two university hospitals. PARTICIPANTS: Fifty-seven patients with heparin-induced thrombocytopenia type II (HIT II) in whom r-hirudin was used during cardiovascular surgery with cardiopulmonary bypass (CPB). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The r-hirudin concentration was monitored on-line, at the point of the patient's care using the ecarin clotting time and maintained in the range of 3 to 4 microg/mL. The r-hirudin elimination at the conclusion of CPB was augmented through modified zero-balanced ultrafiltration and forced diuresis. The duration of CPB was 63 to 246 minutes. The r-hirudin requirement per minute of CPB was 0.016 to 0.035 microg/kg/min, and the 24-hour blood drainage was 50 to 2,200 mL. Of the 57 patients, 54 fully recovered, including 9 patients who did not require any allogenic products. Four patients, all with impaired renal function, showed prolonged r-hirudin elimination and excessive bleeding and required surgical reexploration. Three patients died as a result of complications unrelated to the perioperative management. CONCLUSION: This study provides evidence that r-hirudin can be used safely and effectively for routine anticoagulation during CPB in patients diagnosed with HIT II. Almost 95% of the patients in whom it was used were discharged uneventfully. Patients with perioperative renal failure, however, showed increased bleeding.     

White-clot-Syndrom bei Heparin-induzierter Thrombozytopenie Typ II mit Kreuzreaktion gegen Danaparoid-Na (Orgaran)

The case of a 71-year-old patient is discussed in whom early occlusions of an implanted bypass and peripheral arteries developed after implantation of a femoropopliteal PTFE bypass and several reoperations. Heparin-induced thrombocytopenia (HIT) type II was suspected because of the intraoperative aspect of white clots and when platelet counts fell below 50% of initial levels. A platelet aggregation test confirmed the diagnosis. After discontinuing the heparin therapy and using danaparoid, the platelet count continued to fall, so cross-reactivity to this heparinoid was assumed and confirmed in a second laboratory test. We switched to an anticoagulation regimen with phenprocoumon and used hirudin for the perioperative prophylaxis when another reoperation was required. Problems confirming the diagnosis of HIT type II and difficulties in patients with cross-reactivity to other heparinoids are discussed.     

Anticoagulation for patients with heparin-induced thrombocytopenia using recombinant hirudin during cardiopulmonary bypass

Heparin-induced thrombocytopenia (HIT) is a common complication of heparin therapy. There are three types of HIT. In the majority of patients, thrombocytopenia is modest and resolves without sequelae (HIT I). In a smaller number of patients, the thrombocytopenia is severe (HIT II), and in still others, the thrombocytopenia is also associated with thrombosis (HITT). Administration of heparin to this latter group of patients causes platelet aggregation, thromboembolism, and thrombocytopenia. It is advisable that heparin not be administered in any form to patients with documented or suspected HIT II or HITT. This situation, of course, poses a problem for those patients requiring cardiopulmonary bypass (CPB) surgery. In this report, we summarize our experience with Lepirudin (Hoechst, Frankfurt Ammain, Germany), which is a recombinant hirudin (r-hirudin), as an alternative to heparin for systemic anticoagulation, as well as the use of the ecarine clotting time (ECT) for monitoring anticoagulation status during CPB.     

Heparin-induced thrombocytopenia and cardiopulmonary bypass: perioperative argatroban use

Heparin-induced thrombocytopenia (HIT), a serious complication of heparin therapy, mandates heparin cessation and alternative anticoagulation. We report a patient with a history of HIT who successfully underwent cardiopulmonary bypass (CPB) using short-term reexposure to heparin and perioperative therapy with argatroban. No bleeding complications or HIT-related problems occurred. The pharmacokinetics of argatroban, especially its hepatic rather than renal elimination, makes it the drug of choice for some HIT patients in whom other alternative anticoagulants (eg, danaparoid and hirudin) are less well suited. Because of interference with the international normalized ratio (INR), switching from argatroban to oral anticoagulants is not straightforward.     

Direkte Thrombininhibitoren

Over the past few decades, numerous improvements in several components of the heart–lung machine have been made. However, unfractionated heparin is still the state-of-the-art anticoagulant during extracorporeal circulation. If a preoperative cardiosurgical patient suffers from heparin-induced thrombocytopenia (HIT) type II, alternative anticoagulatory agents are necessary. However, reviewing the existing studies, particularly with regard to criteria for evidence-based medicine, platelet aggregation inhibitors and danaparoid cannot be recommended. On the contrary, direct thrombin inhibitors are promising substances. Especially bivalirudin, which has favorable pharmacokinetic properties, seems to be an appropriate anticoagulant for patients with HIT type II. In order to determine whether bivalirudin could become a standard agent for intraoperative anticoagulation even in patients without blood coagulation disorders, further evidence-based trials are necessary.     

Successful use of Argatroban as a heparin substitute during cardiopulmonary bypass: heparin-induced thrombocytopenia in a high-risk cardiac surgical patient

Whereas heparin is the most widely used intravenous anticoagulant in the US for the treatment of thromboembolic disease and is a seminal adjunct to many clinical procedures, its use can cause serious adverse events. Heparin-induced thrombocytopenia (HIT) has emerged as one of the most frequently seen complications of heparin therapy and can be a life-threatening immunohematological challenge for patients requiring cardiopulmonary bypass (CPB) with obligatory heparin exposure. Unfortunately, lack of convenient monitoring techniques and the presence of HIT and other comorbidities in the complex patient frequently limits or precludes the use of most alternatives to heparin anticoagulation during CPB. This case report describes the successful use of the celite activated clotting time and high-dose thrombin time, while using the direct thrombin inhibitor Argatroban as an alternative to heparin anticoagulation during CPB in a high-risk patient presenting with type II HIT, end-stage renal failure, and ischemic cardiomyopathy with ventricular fibrillatory arrest.     

Anticoagulative management of patients requiring left ventricular assist device implantation and suffering from heparin-induced thrombocytopenia type II

BACKGROUND: Heparin-induced thrombocytopenia type II (HIT II) is a rare but life-threatening side effect of heparin therapy. We describe the perioperative anticoagulative management of patients tested positive for HIT II and requiring implantation of a left ventricular assist device (LVAD). METHODS: We report on 3 patients with a different perioperative anticoagulative management (preoperative, intraoperative, and postoperative anticoagulation with danaparoid-sodium; preoperative anticoagulation with recombinant hirudin, anticoagulation with danaparoid-sodium intraoperatively and postoperatively; preoperative anticoagulation with recombinant hirudin, intraoperative anticoagulation with heparin, and postoperative anticoagulation with danaparoid-sodium) and discuss the difficulties of the treatment. RESULTS: Anticoagulation with alternative drugs such as recombinant hirudin and danaparoid-sodium led to serious and life-threatening bleeding complications as well as to thromboembolic events in the first 2 patients. Therefore the third patient underwent LVAD implantation using heparin for intraoperative anticoagulation to avoid administration of high doses of recombinant hirudin or danaparoid-sodium. Despite very low anti-factor Xa activities, when using danaparoid-sodium postoperatively, the patient suffered from a bleeding complication on the 4th day after LVAD implantation requiring reexploration. CONCLUSIONS: In selected cases (negative heparin-induced platelet aggregation (HIPA) test at the time of LVAD implantation and continuation of postoperative anticoagulation with recombinant hirudin or danaparoid-sodium), heparin may be used for LVAD implantation in HIT II patients to reduce bleeding complications.     

Deep hypothermic circulatory arrest and bivalirudin use in a patient with heparin-induced thrombocytopenia and antiphospholipid syndrome

BACKGROUND: Patients with heparin-induced thrombocytopenia II (HIT II) need an alternative nonheparin-based method of anticoagulation for cardiopulmonary bypass (CPB) to prevent thrombosis and thrombosis related complications. METHODS: Bivalirudin was used during CPB and deep hypothermic circulatory arrest (DHCA) for resection of multiple right atrial masses in a patient with HIT II and antiphospholipid antibodies syndrome (APS). Anticoagulation was monitored with the activated clotting time (ACT) and a target ACT of 450 seconds or greater was maintained. RESULTS: Surgical removal of multiple right atrial masses was successful and there was no evidence of thromboembolic events. Clot was noticed in the cardiotomy and venous reservoir after CPB was discontinued and the system flushed. The postoperative course was uneventful. CONCLUSIONS: Anticoagulation was successfully managed with bivalirudin, a new short-acting, and direct thrombin inhibitor. Further studies are necessary to evaluate the safety of bivalirudin during DHCA.     

Thrombosis of a cardiopulmonary bypass circuit despite recommended hypocoagulation with danaparoid during the acute phase of type II heparin-induced thrombocytopenia

A 36-year-old patient was admitted to our hospital with ischaemic stroke. The initial assessment allowed the diagnosis of an antiphospholipid syndrome (APS) and an intracardiac mass suggestive of a heart tumour. The patient was treated with unfractionated heparin. Type II heparin-induced thrombopenia (HIT) was diagnosed on the 18th day of therapy. Given the risk of stroke recurrence it was decided to remove the cardiac tumour surgically. Cardiopulmonary bypass (CPB) was performed using danaparoid in a state of deep hypothermia, in accordance with the well-established protocol in use in our department. As the CPB and surgical procedure came to an end a massive thrombus began forming in the circuit, requiring immediate displacement of the CPB cannulae. The anti-Xa activity level obtained had been considered effective at an estimated 1.20 IU/ml, although, the level recommended by Magnani is between 1.50 and 2.0 IU/ml. There was no clinical consequence and postoperative recovery was uneventful. The discrepancy between the satisfactory level of anti-Xa activity and the thrombus formation in the CPB circuit raises the issue of the diversity of published anticoagulation protocols, the difficulty to extrapolate within a surgical team, the need for intensive laboratory monitoring within a narrow therapeutic range, as well as the patient profiles variability with concurrent disorders complicating their clinical management.     

National survey of heparin-induced thrombocytopenia in the haemodialysis population of the UK population.

BACKGROUND: Heparin-induced thrombocytopoenia (HIT) type II is an antibody-mediated, drug-induced thrombocytopenia which is associated with significant morbidity and mortality. Several case reports and small series have described the occurrence of HIT type II in the haemodialysis population and the challenges associated with it. Some of these reports raise the possibility of a recent increase in prevalence of this condition. But to date, there has never been a large study to estimate the prevalence, demography or treatment options for this syndrome in the haemodialysis population. METHODS: The renal units in the UK were surveyed to establish the prevalence of HIT type II syndrome in the haemodialysis population. Demographic data for haemodialysis patients with HIT type II syndrome were gathered and current treatments assessed. RESULTS: Fifty responses from the 81 UK renal units surveyed were received. The combined population for these units was 13 682 patients on dialysis of whom 10 564 were on maintenance haemodialysis. The prevalence and incidence of HIT type II syndrome in the UK haemodialysis population were 0.26 and 0.32 per 100 patients, respectively. The mean age of the patients with HIT type II syndrome was 62 years (range 22-86), 52% were females and 92% were Caucasians. Only 17% of patients have had complications of HIT syndrome. Thirty-six percent of renal units use danaparoid as anticoagulant of choice for patients on haemodialysis with HIT type II syndrome. CONCLUSION: This is the largest survey of HIT type II in the haemodialysis population to date. The prevalence is considerably lower (0.26 per 100 patients) than previous estimates, with only a minority of patients developing complications of the condition. Haemodialysis patients with HIT type II in the UK are predominantly treated with danaparoid.     

Heparininduzierte Thrombocytopenie Typ II

Heparin-induced thrombocytopenia type II (HIT type II) is an immunoglobulin-mediated, drug-induced side effect for heparin-treated patients with thromboembolic complications. With an incidence of 1-3 %, mortality of 20 % it and permanent disability for another 20 % is a clinically relevant disorder. With heparin treatment or prophylaxis frequent platelet count monitoring is necessary. With HIT type II the thrombocytopenia is often a harbinger of thromboembolic complications in the venous or arterial system. If HIT type II is suspected, further heparin exposure is to be stopped immediately and another anticoagulant therapy should be started. The two anticoagulant options in Germany are discussed. At the same time the diagnosis should be confirmed by laboratory testing, including testing for cross-reactivity with danaparoid. Further therapy depends on the symptoms. In the case of clinical relevance of this disorder we should think about prophylaxis: strict indications for perioperative prophylaxis only use of low-molecular-weight heparin (LMWH) for routine prophylaxis, use of LMWH for thrombosis treatment and early change to cumarine.     

Significance and incidence of type II heparin-induced thrombocytopenia. A prospective study

AIM: The incidence of heparin-induced thrombocytopenia (HIT type II) as a consequence of postoperative thrombosis prophylaxis after hip or knee prosthesis was investigated in this study. Furthermore the platelets count was postoperatively analysed in patients without HIT II. PATIENTS AND METHODS: Patients with knee and hip prosthesis were included in a prospective study during an 8 months period. All patients received 3 x 5,000 Liquemin (Hoffmann-LaRoche) from the day of the operation until discharge. In cases with a platelet count drop of more than 40% and in patients with clinically manifest thrombosis or embolism a HIT type II test was initiated. RESULTS: 5 of 252 patients included in this study developed a HIT type II. The platelet count drop was on average 65.7% (40.9-81.6). One patient died of a lung embolism (lethality 20%). Four patients were treated with Hirudin and 1 patient with Danaproid-Natrium. There was no drop of the platelet count between the 5th and 7th postoperative day of more than 15% in the other patients without HIT type II. CONCLUSION: In operative departments not enough attention is paid to HIT type II. Knowing the risks with an appropriate monitoring HIT type II can be early detected. Under these conditions the advantages of a heparin prophylaxis outweigh the risk of developing a HIT type II with it's life threatening sequelae.     

Heparin-Induced Thrombocytopenia After Coronary Artery Bypass Grafting with Cardiopulmonary Bypass: Report of a Case

A 79-year-old man was transferred to our hospital with severe chest pain and a suspected diagnosis of acute myocardial infarction. Emergency cardiac catheterization showed triple-vessel coronary artery disease, and we performed coronary artery bypass grafting under cardiopulmonary bypass (CPB). Continuous hemodiafiltration was started for acute renal failure postoperatively, and heparin was given as an anticoagulanting agent. By 9 days after the initiation of heparin therapy, his platelet count had fallen and a deep vein thrombosis had formed in his left leg. We suspected heparin-induced thrombocytopenia (HIT), and immediately discontinued the heparin, implementing danaparoid (Orgaran) instead, following which the platelet count recovered. Heparin-induced thrombocytopenia, which causes thrombosis, is a serious side effect of heparin therapy and few cases of HIT associated with CPB surgery have been reported in Japan.