Use of argatroban as a substitute for heparin in a patient with suspected HIT type II undergoing carotid endarterectomy

Heparin-induced thrombocytopenia (HIT) type II is characterized by a decrease in platelet count and thrombosis following heparin administration. We anesthetized a 67-year-old woman with suspected HIT type II undergoing carotid endarterectomy (CEA). Preoperatively, the patient had received anticoagulation therapy with heparin for cerebral infarction due to thrombosis and she developed thrombocytopenia with deterioration of cerebral infarction. Platelet level recovered by discontinuation of heparin and platelet infusion. During the surgical procedure, a substitution for heparin as an anticoagulant was necessary and we used argatroban, a direct thrombin inhibitor, with monitoring activated coagulation time (ACT). The ACT values were maintained above 200 sec during endoarterectomy and the operation was successfully carried out. We believe that argatroban is one of the choices for anticoagulants in a patient with HIT type II.     

Anesthesia for a hemodialysis patient with HIT undergoing CABG using argatroban

Anesthetic Management of CABG in a Hemodialysis patient complicated by heparin-induced thrombocytopenia (HIT) type II is one of the different procedures in hemodialysis patients using heparin. An 81-year-old man receiving hemodialysis complicated by HIT type II was scheduled for coronary artery bypass grafting (CABG). Anesthesia was induced and maintained with propofol, remifentanil and rocuronium. During artificial cardiopulmonary bypass, activated clotting time (ACT) was maintained above 300 sec by in initial 0.1 mg x kg(-1) and subsequent 2.0-7.0 microg x kg(-1) x min(-1) doses of argatroban; a direct thrombin inhibitor. Immediately after the completion of the external cardiopulmonary circulation, continuous infusion of argatroban was discontinued. Seven hours later ACT was restored to the preoperative level. Both intra and postoperative courses were uneventful.     

Heparin-induced thrombocytopenia in patients administered heparin solely for hemodialysis

BACKGROUND: Heparin, universally used in patients on dialysis, is the cause for immune-mediated heparin-induced thrombocytopenia (HIT). METHODS: From an HIT registry, six patients were identified who received recent heparin solely for dialysis, developed HIT, and were treated with argatroban. Platelets counts, aPTTs, argatroban dosing, and outcomes were assessed. RESULTS: Before HIT was diagnosed, unfractionated heparin was used in doses of 2,000-12,000 units. The mean platelet count fell from 122 +/- 62 x 10(9)/L to 35 +/- 22 x 10(9)/L, and one patient experienced thrombosis. After HIT was diagnosed, heparin was discontinued, and argatroban therapy (mean dose, 1.7 +/- 0.9 microg/kg/min) was administered for 6.5 +/- 4.5 days (mean aPTT, 66.1 +/- 12.4 s). Patients continued on renal replacement therapy. Platelet counts increased during argatroban therapy. A 37-day composite endpoint of death, amputation, or new thrombosis occurred in four (66.7%) patients: three patients died from causes unrelated to thrombosis, and one patient developed new thrombosis after argatroban was discontinued. One patient experienced a hematocrit drop during treatment without overt bleeding or a need for transfusion. CONCLUSIONS: HIT can occur in patients administered heparin solely for hemodialysis. When HIT is suspected, heparin should be discontinued and an alternative anticoagulation initiated. Argatroban, which is not renally cleared, supports continued renal replacement therapy in HIT patients.     

Heparininduzierte Thrombozytopenie

Heparin-induced thrombocytopenia (HIT) represents a serious side effect caused by an atypical immune response to platelet factor 4 leading to platelet activation and thrombin formation. These patients are at high risk of thromboembolism, with a rapid drop in platelet count between days 5 and 14 after the initiation of heparin treatment. In single cases, especially after major surgery, platelet count reduction might be absent or hidden by preceding thrombocytosis. Different clinical manifestations of HIT include unspecific skin reactions with potential necrosis at the site of heparin injection, mostly after the application of unfractionated heparin but also with low molecular weight heparin. In heparin-induced skin necrosis, administration of unfractionated or low molecular weight heparin is contraindicated and heparin therapy should be stopped immediately. Instead, an alternative anticoagulant in the form of a direct thrombin inhibitor such as argatroban, and respectively lepirudin, or danaparoid sodium must be administered. Due to frequent misinterpretations of heparin-induced unspecific skin reactions, especially in the absence of thrombocytopenia, we present two case reports which should increase the awareness of HIT’s various clinical pictures.     

Two surgical case reports showing atypical heparin-induced thrombocytopenia]

Heparin-induced thrombocytopenia (HIT) represents a serious side effect caused by an atypical immune response to platelet factor 4 leading to platelet activation and thrombin formation. These patients are at high risk of thromboembolism, with a rapid drop in platelet count between days 5 and 14 after the initiation of heparin treatment. In single cases, especially after major surgery, platelet count reduction might be absent or hidden by preceding thrombocytosis. Different clinical manifestations of HIT include unspecific skin reactions with potential necrosis at the site of heparin injection, mostly after the application of unfractionated heparin but also with low molecular weight heparin. In heparin-induced skin necrosis, administration of unfractionated or low molecular weight heparin is contraindicated and heparin therapy should be stopped immediately. Instead, an alternative anticoagulant in the form of a direct thrombin inhibitor such as argatroban, and respectively lepirudin, or danaparoid sodium must be administered. Due to frequent misinterpretations of heparin-induced unspecific skin reactions, especially in the absence of thrombocytopenia, we present two case reports which should increase the awareness of HIT's various clinical pictures.     

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.     

维持性血液透析患者肝素诱导的血小板减少症的临床观察

目的探讨维持性血液透析患者肝素诱导的血小板减少症（heparin-inducedthrombo—cytopenia,HIT）及其治疗。方法选择我院2012年1月至2014年1月期间首次行血液透析的尿毒症患者115例,所有入选患者均于使用肝素前常规进行血小板计数监测。分别记录首次血液透析前患者血小板计数;首次血液透析后每周3次随访血小板计数,于每次透析结束后采静脉血行血小板计数。监测肝素抗凝前、后血小板数目变化,对出现血小板减少的患者进行“4Ts”评分,评分为6～8分的患者临床诊断为HIT。观察HIT患者肝素抗凝前、后外周血血小板计数变化、血小板减少的最低值、HIT发生时间,同时观察患者除血小板减少外的其他临床表现如超声检查深静脉有无新发血栓形成、全身出血倾向（牙龈出血、局部皮肤瘀斑、黑便、肉眼血尿）等。HIT患者停用肝素,换用阿加曲班抗凝,观察HIT患者血小板恢复时间及恢复后血小板计数。结果115例患者中有11例发生HIT,11例HIT患者有2例发展为HITIS（占18．2％）。HIT患者肝素抗凝后血小板数目降至（68±21）×10^9／L,与肝素抗凝前的（179±57）×10^9／L比较,差异有统计学意义（P〈0．01）;停用肝素改为阿加曲班抗凝后血小板计数上升至（166±53）×10^9／L,与阿加曲班抗凝前的（68±21）×10^9／L比较,差异有统计学意义（P〈0．01）。阿加曲班抗凝后血小板计数为（166±53）×10^9／L,与肝素抗凝前的（179±57）×10^9／L比较,差异无统计学意义（P〉0．05）。结论HIT是维持性血液透析患者应用肝素抗凝后的常见并发症,阿加曲班可作为HIT患者的有效抗凝剂。     

A case of heparin-induced thrombocytopenia associated with unexpected excessive argatroban anticoagulation after abdominal aortic aneurysm resection

We experienced excessive anticoagulation induced by argatroban for the treatment of heparin-induced thrombocytopenia (HIT). A 74-year-old man was scheduled for elective abdominal aortic aneurysm resection. During the surgery, both femoral arteries were found non-pulsatile requiring thrombectomy. The next day, second laparotomy was needed because of superior mesenteric artery occlusion. After the surgery, acute renal failure and hypoxemia continued with progressive thrombocytopenia necessitating frequent administration of platelet concentrates. Considering possibility of HIT, we stopped heparin and began argatroban. Due to his mild liver dysfunction, we initiated argatroban at 0.5 microg x kg(-1) x min(-1) one-fourth of standard initial dose, according to its drug information approved by FDA. Although expected APTT level was from 50 to 60 sec, it increased immediately up to 93 sec. Excessive anticoagulation continued more than 24 hours after cessation of argatroban and bleeding occurred from the tracheostomy site. When APTT decreased to the target range, we restarted argatroban and found the adequate dosage at 0.08 microg x kg(-1) x min(-1). After argatroban treatment, platelet count recovered immediately and no thromboembolism was observed. We recommend that argatroban should be initiated at a lower dosage than the dose shown in its drug information for HIT patients after cardiovascular surgery with frequent monitoring of APTT.     

Combined treatment with nafamostat mesilate and aspirin prevents heparin-induced thrombocytopenia in a hemodialysis patient

We report on the management of a 36-year-old hemodialysis patient with heparin-induced thrombocytopenia (HIT, type II) and clot formation in extracorporeal circulation. Platelet aggregation test and measurement of anti-platelet factor 4/heparin complex antibody by enzyme-linked immunosorbent assay revealed to us that our patient had developed HIT. Instead of heparin, we used nafamostat mesilate (NM) as an anticoagulant during hemodialysis, but could not completely prevent HIT-induced thrombocytopenia or clot formation in the extracorporeal circuit. Combined use of NM and aspirin completely inhibited platelet aggregation, decrease in platelet count and clot formation in the extracorporeal circuit.     

Heparin-Induced Thrombocytopenia in Patients Administered Heparin Solely for Hemodialysis

Background. Heparin, universally used in patients on dialysis, is the cause for immune-mediated heparin-induced thrombocytopenia (HIT). Methods. From an HIT registry, six patients were identified who received recent heparin solely for dialysis, developed HIT, and were treated with argatroban. Platelets counts, aPTTs, argatroban dosing, and outcomes were assessed. Results. Before HIT was diagnosed, unfractionated heparin was used in doses of 2,000–12,000 units. The mean platelet count fell from 122 ± 62 × 10⁹/L to 35 ± 22 × 10⁹/L, and one patient experienced thrombosis. After HIT was diagnosed, heparin was discontinued, and argatroban therapy (mean dose, 1.7 ± 0.9 μg/kg/min) was administered for 6.5 ± 4.5 days (mean aPTT, 66.1 ± 12.4 s). Patients continued on renal replacement therapy. Platelet counts increased during argatroban therapy. A 37-day composite endpoint of death, amputation, or new thrombosis occurred in four (66.7%) patients: three patients died from causes unrelated to thrombosis, and one patient developed new thrombosis after argatroban was discontinued. One patient experienced a hematocrit drop during treatment without overt bleeding or a need for transfusion. Conclusions. HIT can occur in patients administered heparin solely for hemodialysis. When HIT is suspected, heparin should be discontinued and an alternative anticoagulation initiated. Argatroban, which is not renally cleared, supports continued renal replacement therapy in HIT patients.     

Heparin-induced thrombocytopenia: diagnosis and management

Heparin is the predominant anticoagulant used in cardiac and vascular surgery. Heparin-induced thrombocytopenia (HIT) is one of the most serious and life-threatening adverse drug reactions associated with heparin use. In addition to the development of thrombocytopenia, HIT is associated with a high risk (40-50%) of thrombotic complications. The pathophysiology of HIT is now well understood and results from the formation of platelet-activating antibodies against the heparin-platelet factor 4 complex (H-PF4) on the platelet surface. The risk of HIT varies significantly depending on the type of heparin (unfractionated heparin greater than low-molecular-weight heparin), duration of heparin use, and patient population (surgery greater than medical). Readily available serologic assays for serum antibodies against H-PF4 allow for rapid confirmation of a clinical diagnosis of HIT. Owing to the high risk of thrombosis associated with HIT, antithrombotic therapy with direct thrombin inhibitors (lepirudin or argatroban) should be started when serologic assays confirm clinical suspicion.     

Incidence of heparin-induced thrombocytopenia type II and postoperative recovery of platelet count in liver graft recipients: a retrospective cohort analysis

Background

Thrombocytopenia in patients with end-stage liver disease is a common disorder caused mainly by portal hypertension, low levels of thrombopoetin, and endotoxemia. The impact of immune-mediated heparin-induced thrombocytopenia type II (HIT type II) as a cause of thrombocytopenia after liver transplantation is not yet understood, with few literature citations reporting contradictory results. The aim of our study was to demonstrate the perioperative course of thrombocytopenia after liver transplantation and determine the occurrence of clinical HIT type II.

Method

We retrospectively evaluated the medical records of 205 consecutive adult patients who underwent full-size liver transplantation between January 2006 and December 2010 due to end-stage or malignant liver disease. Preoperative platelet count, postoperative course of platelets, and clinical signs of HIT type II were analyzed.

Results

A total of 155 (75.6%) of 205 patients had thrombocytopenia before transplantation, significantly influenced by Model of End-Stage Liver Disease score and liver cirrhosis. The platelet count exceeded 100,000/μL in most of the patients (n = 193) at a medium of 7 d. Regarding HIT II, there were four (1.95%) patients with a background of HIT type II.

Conclusions

The incidence of HIT in patients with end-stage hepatic failure is, with about 1.95%, rare. For further reduction of HIT type II, the use of intravenous heparin should be avoided and the prophylactic anticoagulation should be performed with low-molecular-weight heparin after normalization of platelet count.     

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: a common complication in cardiac transplant recipients

BACKGROUND: Heparin-induced thrombocytopenia (HIT) is an idiosyncratic complication of heparin therapy triggered by the development of immunoglobulin G (IgG) antibodies to platelet factor 4 heparin. It typically results in a 50% decrease in platelet count. Paradoxically, although bleeding is rare, there is a high risk of venous or arterial thrombotic events. Given that many patients awaiting transplantation are exposed to heparin for prolonged periods, we sought to determine the frequency of HIT and its consequences among patients before and after cardiac transplantation. METHODS: We reviewed retrospectively the clinical, pathologic, and laboratory databases for all patients who underwent heart transplantation at our institution between January 1, 1998, and December 31, 2000. An enzyme-linked immunoabsorption assay (ELISA) that detected IgG, IgA, and IgM antibodies directed against platelet factor 4 heparin complex confirmed the diagnosis of HIT. We analyzed bleeding and thrombotic complications and determined the influence of HIT on post-transplant outcomes. RESULTS: An assay for HIT antibody was performed before or after transplantation in 26 of 46 patients (46% of the entire cohort). In all cases, the clinical indication for testing was thrombocytopenia. Among patients screened, HIT antibody was detected in 11 patients (39%); HIT developed in 10 of 11 patients before transplantation. The mean platelet count at diagnosis was 88,000 +/- 22,000/mm(3). Heparin-induced thrombocytopenia with thrombosis syndrome developed in 5 of 11 patients (45%). Manifestations included splenic and renal infarctions, renal artery occlusion, coronary artery embolism with myocardial infarction, pulmonary embolism, and femoral and jugular venous occlusions. Alternative pre-operative anti-coagulation included lepirudin (n = 7), argatroban (n = 1), dalteparin (n = 1), and abciximab (n = 1). Two deaths occurred in the HIT-positive group; neither bleeding nor thrombosis caused either death. Actuarial 36-month survival did not differ between HIT-positive and HIT-negative cohorts (78% and 79%, respectively). CONCLUSION: Heparin-induced thrombocytopenia is a frequent complication among patients hospitalized for heart failure who are awaiting heart transplantation. Timely HIT-antibody screening and the use of alternative forms of systemic anti-coagulation may permit successful transplantation with intermediate survival rates comparable to those of HIT-negative recipients.     

Update in hematology: heparin-induced thrombocytopenia and bivalirudin

Heparin-induced thrombocytopenia (HIT) is important because it is common, and it significantly increases mortality after cardiac surgery. Although thrombocytopenia after cardiac surgery is common, it predicts serious adverse outcome when it is severe. Despite the high prevalence of heparin/platelet factor 4 antibodies in cardiac surgical patients, they typically do not indicate a higher perioperative risk. Recent evidence suggests, however, that when these antibodies are in the immunoglobulin M class, there is an increased risk of nonthrombotic adverse outcomes after cardiac surgery. According to the guidelines from the American College of Chest Physicians, patients with HIT require parenteral anticoagulation with a direct thrombin inhibitor such as lepirudin, argatroban, or bivalirudin. The transition to oral anticoagulation must be undertaken cautiously and only after the platelet count has recovered. Patients with a remote history of HIT can have cardiac surgery safely with unfractionated heparin. Patients with clinically active HIT who require cardiac surgery before the resolution of the HIT preferably should be anticoagulated with bivalirudin, dosed according to body weight and the goal-activated coagulation time. Given that bivalirudin is an established alternative to heparin as a thrombin inhibitor for cardiac surgery, it is likely that future trials will investigate which anticoagulant confers better outcomes after cardiac surgery, as is the case in percutaneous coronary intervention.     

Current recommendations for diagnosis and therapy of heparin-induced thrombocytopenia

Thrombosis prophylaxis using heparins is mandatory in most trauma patients. However, heparins can induce heparin-induced thrombocytopenia (HIT), the most common and clinically important immune-mediated drug-dependent thrombocytopenia. Affected patients are at risk of developing new thromboembolic complications. HIT has to be considered if platelet counts decrease >50% between day 5-10 of heparin therapy that cannot be explained alternatively or if new thromboses occur in a sufficiently heparinised patient. Immediately changing the anticoagulant to danaparoid or lepirudin is most important. Proof of anti-platelet-factor-4/heparin antibodies secures the diagnosis, usually retrospectively.Diagnosis and therapy are demonstrated in a typical HIT patient. HIT usually occurs in the second week of heparin administration. Heparin-reexposure within 100 days can lead to HIT before day 5. For early recognition of HIT, platelet counts should be monitored regularly. Because of earlier discharge of patients to rehabilitation or outpatient care, the problem of HIT-diagnosis and therapy gains increasing relevance in these sectors.     

Erfahrungen mit der Heparin-induzierten Thrombozytopenie Typ II bei gefäßchirurgischen Patienten

Heparin-induced or -associated thrombocytopenia type II (HIT II) is the most important clinical side effect of heparin therapy. At the University Hospital of Jena the detection of HIT II antibodies has been done using the heparin-induced platelet activation assay (HIPA) since 1995. During this period, 89 patients of the surgical clinic were examined under a clinical suspicion of HIT II syndrome. Indication for the HIPA was thrombocytopenia or any thrombembolic complication during therapy with heparin. In 21 patients the results were positive. In 15 cases, prior to the diagnosis of HIT II, complications known as white clot syndrome occurred [pulmonary embolism (n = 1), shunt reocclusion (n = 3), arterial thrombosis, embolism or reocclusion of bypass (n = 8), deep vein thrombosis (n = 4)]. 8 patients had a history of similar events during earlier phases of therapy with heparin. Three of the patients died. Therapy with heparin implies frequent control of thrombocyte count. In any case of thrombocytopenia and/or thrombembolic complications testing for HIT II antibodies is necessary. If it is positive and vascular reconstruction is indicated, we recommend hirudin for anticoagulation.     

Heparin-induced thrombocytopenia after liver transplantation

BACKGROUND: Unfractionated heparin sodium (UFH) or low-molecular weight heparin (LMWH) is used in anticoagulant protocols at several institutions to prevent thrombosis after liver transplantation. Heparin-induced thrombocytopenia (HIT) is an adverse immune-mediated reaction to heparin, resulting in platelet count decreases of more than 50%. The frequencies of HIT after liver transplantation and platelet factor 4/heparin-reactive antibody (HIT antibody) positivity in liver transplantation patients, however, are unknown. PATIENTS AND METHODS: The 32 men and 20 women underwent living donor liver transplantation. We started LMWH (25 IU/kg/h) on postoperative day (POD) 1, switching to UFH (5000 U/d) on POD 2 or 3. The dose of UFH was changed according to the activated clotting time level. HIT antibody levels were measured the day before surgery and on POD 7 and 14. Platelet count was measured daily for 3 weeks. RESULTS: The average platelet counts preoperatively, and on POD 7, 14, and 21 were 65, 88, 149, and 169 x 10(9)/L, respectively. Two patients developed hepatic artery thrombosis on POD 11 and 19, respectively, although they were HIT antibody-negative and their platelet counts were stable. In 2 other patients, the platelet count decreased suddenly from 107 x 10(9)/L on POD 4 to 65 x 10(9)/L on POD 6 and from 76 x 10(9)/L on POD 7 to 33 x 10(9)/L on POD 9, respectively. The heparin-induced platelet aggregation test was negative in these patients. The percentage of HIT antibody-positive patients was 0.5% preoperatively, 5.6% on POD 7, and 5.6% on POD 14. None of the subjects/patients developed UFH-related HIT. CONCLUSIONS: In our series, the occurrence of HIT after liver transplantation was uncommon.     

The emergency use of recombinant hirudin in cardiopulmonary bypass

The most common anticoagulant used for cardiopulmonary bypass is heparin. An alternate form of anticoagulant therapy is needed for patients who have immune-mediated heparin-associated thrombocytopenia (HIT). Thrombocytopenia causes bleeding and may lead to serious arterial and venous thrombosis. HIT or heparin-induced thrombocytopenia with thrombosis type II (HITT) are both described as adverse reactions to heparin. They are diagnosed with a platelet count less than a 100,000/mcl for 2 consecutive days. HITT, the severe form, is characterized with the thrombocytopenia in combination with thromboembolic complications, such as strokes, myocardial infarctions, and limb ischemia. Two cases are presented in which r-hirudin was used for anticoagulation for aortocoronary bypass surgery and mitral valve replacement. The activated partial prothrombin time (aPTT) was used to monitor coagulation. In the first case, the aPTT was maintained greater than 100 seconds, and at the termination of cardiopulmonary bypass, some clot was noted in the cardiopulmonary bypass circuit. In the second case, a longer cardiopulmonary bypass run was anticipated, the hirudin bolus and infusion rate were increased, and the aPTT was maintained at greater than 200 sec. Adequate coagulation resulted, and, at the end of bypass, no clot was noted. These case studies seem to suggest a higher dosage of r-hirudin may be required for the use of cardiopulmonary bypass and a need to maintain aPTT values greater than 200 sec to help monitor anticoagulation.     

Delayed onset of heparin induced thrombocytopenia--a case report]

A 64-year-old man underwent CABG. 18000 unit of bovine lung heparin was used during operation for extracorporeal circulation and small amount of heparin was injected until the 5th postoperative day to keep intravenous line patent. His postoperative course was uneventful until the 10th postoperative day when marked ecchymosis developed on his eyelid. Laboratory data showed marked thrombocytopenia (1.3 x 10(4)/microliters) and disseminated intravascular coagulation. The diagnosis of heparin-induced thrombocytopenia (HIT) was confirmed by platelet aggregation test with heparin. Gabexate mesilate and platelet-concentrates were administered and platelet count returned to normal within a week. HIT usually occurs during administration of heparin. In this case, it occurred 5 days after we stopped heparin. Delayed onset of HIT might be related to delayed metabolism of heparin due to postoperative fluid shift.