Heparin-Induced Thrombocytopenia

1981 ◽  
Author(s):  
J A Caprini ◽  
A J Sholder ◽  
J P Vagher ◽  
J Mitchell

Review of 6,000 patient records from our laboratory showed 609 individuals who received continuous intravenous infusion heparin therapy for thromboembolic disease. 40/609 (6.5%) of these patients were found to have a platelet count of less than 150,000 cell/mm . Of this group, 34/40 (85%) exhibited thrombocytopenia prior to heparin therapy that was attributable to consumptive coagulopathy in 21/40 (52.5%), sepsis or malignancy in 11/40 (27.5%), and cimetidine or sulfisoxazole in 2/40 (5%). Heparin therapy had no adverse effect on the platelet count in these individuals, and the count returned to normal in surviving individuals if the underlying cause was successfully treated or the offending drug removed.Only 6/40 (15%) of the patients developed low platelet counts during the course of heparin therapy; this represents 6/609 (0.98%) of the population receiving heparin. The etiology of thrombocytopenia in 5/6 (83%) of the cases was traced to metastatic cancer (3), burn wound sepsis (1), and septic shock (1). Only 1/609 (0.16%) of these patients developed low platelet count that could be attributed to heparin. Thus, the incidence of heparin-induced thrombocytopenia is extremely rare in our hospital population.

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Barbara Steinlechner ◽  
Gabriele Kargl ◽  
Christine Schlömmer ◽  
Caroline Holaubek ◽  
Georg Scheriau ◽  
...  

Extracorporeal membrane oxygenation (ECMO) is often used in the management of COVID-19-related severe respiratory failure. We report the first case of a patient with COVID-19-related ARDS on ECMO support who developed symptoms of heparin-induced thrombocytopenia (HIT) in the absence of heparin therapy. A low platelet count of 61 G/L was accompanied by the presence of circulating HIT antibodies 12 days after ECMO initiation. Replacement of the ECMO system including cannulas resulted in the normalization of the platelet count. However, the clinical situation did not improve, and the patient died 9 days later. Careful consideration of anticoagulant therapy and ECMO circuit, as well as routine HIT antibody testing, may prevent a fatal course in ECMO-supported COVID-19 patients.


Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 225-232 ◽  
Author(s):  
Thomas L. Ortel

Abstract Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder caused by the development of antibodies to platelet factor 4 (PF4) and heparin. The thrombocytopenia is typically moderate, with a median platelet count nadir of ~50 to 60 × 109 platelets/L. Severe thrombocytopenia has been described in patients with HIT, and in these patients antibody levels are high and severe clinical outcomes have been reported (eg, disseminated intravascular coagulation with microvascular thrombosis). The timing of the thrombocytopenia in relation to the initiation of heparin therapy is critically important, with the platelet count beginning to drop within 5 to 10 days of starting heparin. A more rapid drop in the platelet count can occur in patients who have been recently exposed to heparin (within the preceding 3 months), due to preformed anti-heparin/PF4 antibodies. A delayed form of HIT has also been described that develops within days or weeks after the heparin has been discontinued. In contrast to other drug-induced thrombocytopenias, HIT is characterized by an increased risk for thromboembolic complications, primarily venous thromboembolism. Heparin and all heparin-containing products should be discontinued and an alternative, non-heparin anticoagulant initiated. Alternative agents that have been used effectively in patients with HIT include lepirudin, argatroban, bivalirudin, and danaparoid, although the last agent is not available in North America. Fondaparinux has been used in a small number of patients with HIT and generally appears to be safe. Warfarin therapy should not be initiated until the platelet count has recovered and the patient is systemically anticoagulated, and vitamin K should be administered to patients receiving warfarin at the time of diagnosis of HIT.


Author(s):  
Vickie McDonald ◽  
Marie Scully

Coagulation is best thought of using the cell-based model of coagulation. Patients commenced on heparin therapy should have their platelet count monitored early because of the risk of heparin-induced thrombocytopenia, which can occur on any type or dose of heparin. Emergency reversal of warfarin should be with prothrombin complex concentrate (containing factors II, VII, IX, and X) and not fresh frozen plasma. New oral anticoagulants have the advantage of predictable pharmacokinetics and do not require routine monitoring, but optimal reversal strategies for these agents are not clear. Thrombolytic agents lead to variable degrees of systemic lysis, which may cause haemorrhage, including intracerebral haemorrhage


2017 ◽  
Vol 86 ◽  
Author(s):  
Blanka Mahne ◽  
Mladen Gasparini ◽  
Matija Kozak

Background: Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder following heparin therapy presenting with thrombocytopenia and associated arterial or/and venous thrombosis (heparin induced thrombocytopenia with thrombosis–HITT). Unrecognised HIT can lead to severe complications like limb amputation and death.Case report: We report a case of a patient who presented with HIT-associated recurrent lower limb arterial thrombotic occlusions and popliteal venous thrombosis 29 days after coronary bypass graf surgery. The patient underwent urgent thrombectomy of superfcial femoral, popliteal and posterior tibial artery. Because of recurrent thrombotic occlusions of lower limb arteries three surgical revisions were performed. Te platelet count decreased from 124 × 109/l to 53 × 109/l on the fifth day after the first intervention. After clinical suspicion of HIT, heparin was discontinued and fondaparinux was started. Arterial thrombosis did not recur and the patient recovered without consequences.Conclusions: HIT occurs in 1–3 % of patients after cardiac surgery. Strict following of international guidelines regarding the frequency of platelet count monitoring, assessing probability for HIT and laboratory testing is mandatory in order not to miss the diagnosis of HIT. HIT can manifest clinically several days after the first exposure to heparin. If a patient presents with acute thrombosis and thrombocytopenia, HITT should be suspected. Postoperative HIT is associated with higher morbidity and mortality. Early recognition is crucial to prevent severe complications and death.


2020 ◽  
Vol 8 ◽  
pp. 232470962094409 ◽  
Author(s):  
Prasanth Lingamaneni ◽  
Sriram Gonakoti ◽  
Krishna Moturi ◽  
Ishaan Vohra ◽  
Maryam Zia

COVID-19 (coronavirus disease-2019) infection is a highly prothrombotic state, resulting from a dysregulation of the coagulation cascade. Therefore, thromboprophylaxis is strongly recommended in these patients, with some experts even advocating for therapeutic dosing to prevent thromboembolic events. Heparin-induced thrombocytopenia (HIT) is a well-known complication of heparin therapy. In this article, we report a case of HIT in a patient with COVID-19. A 63-year-old male presented with 1 week of dry cough and diarrhea. He had a positive nasopharyngeal COVID-19 reverse-transcriptase–polymerase chain reaction. On admission, the platelet count and liver function tests were within normal limits. During his hospitalization, he developed a right femoral deep venous thrombosis and was started on therapeutic anticoagulation. Due to worsening respiratory failure, he was intubated and mechanically ventilated. Between days 11 and 12 of hospitalization, platelet count dropped from 304 000 to 96 000 cells/µL. He had a high pretest probability for HIT with a 4T score of 6 and a positive anti-PF4/heparin antibody. Heparin drip was discontinued and was switched to argatroban. The serotonin release assay eventually returned positive, which confirmed the diagnosis of HIT. We also discuss potential overdiagnosis of HIT in COVID-19 through 4 cases with false-positive HIT antibodies.


1998 ◽  
Vol 32 (1) ◽  
pp. 55-59 ◽  
Author(s):  
Aditya K Gupta ◽  
Michael J Kovacs ◽  
Daniel N Sauder

OBJECTIVE To highlight the importance of heparin-induced thrombocytopenia (HIT), a potentially fatal adverse effect of heparin therapy. CASE SUMMARY: There are two types of HIT with a distinct etiology. Type 1 HIT is a relatively mild thrombocytopenia of early onset that generally resolves with ongoing heparin therapy. Clinical complications are uncommon. Type 2 HIT, which is more severe, is the main focus of this report. Five patients receiving heparin therapy developed type 2 HIT, which in some cases resulted in complications that required limb amputation, or eventuated in death. DISCUSSION: In a patient receiving heparin therapy, the development of thrombocytopenia should alert the caregiver to the possible development of HIT. Prompt management of HIT can help prevent complications. HIT usually manifests 5–8 days after starting heparin therapy. The platelet count usually decreases to less than 100 times 103/mm3. It generally normalizes within 5–7 days after discontinuing heparin therapy. In spite of the thrombocytopenia, thrombosis or disseminated intravascular coagulation can occur. The management may be subdivided into three clinical situations: mild-to-moderate asymptomatic thrombocytopenia, severe thrombocytopenia with a platelet count of less than 50 times 103/mm3, and thrombosis or embolism complicating HIT. CONCLUSIONS Heparin-induced thrombocytopenia is an uncommon but potentially serious, and sometimes lethal, complication of heparin therapy. Therefore, it is important to be aware of the possibility of the development of HIT with heparin therapy, to recognize it early, and to manage it appropriately before the manifestation of adverse effects. OBJETIVO Establecer la importancia de la trombocitopenia inducido por heparina (TIH), lo cual representa un posible efecto adverso fatal associado con la terapia de este medicamento. RESUMEN DEL CASO Existen dos tipos de TIH con etiologias distintas. TIH del tipo I representa trombocitopenia que es relativamente leve y de occurrencia temprana y que se resuelve generalmente con la terapia continua de heparina. Complicaciones clínicas son infrequentes. TIH del tipo II es más severa y representa el foco principal de este reporte. Se describe cinco pacientes que recibieron terapia con heparina que desarrollaron TIH del tipo II y cuyos casos resultaron en complicaciones que necesitaron amputaciones en las extremidades o que aveces resultaron en condiciones fatales. DISCUSSIÓN En pacientes que reciben terapia con heparina, el desarrollo de trombocitopenia debe alertar el médico al posible desarrollo de TIH. El manejo inmediato de TIH puede prevenir estas complicaciones. Después de la primera exposición a la heparina, TIH se manifiesta 5–8 días después del inicio del tratamiento. En estos casos, el número de plaquetas usualmente se disminuye a menos de 100 times 103/mm3 y generalmente se normalisa dentro de 5–7 días al descontinuarse la heparina. A pesar de la trombocitopenia, trombosis y coagulación intravascular deseminada puede desarrollarse en estos pacientes. El manejo de éstas complicaciones puede ser subdividido en tres situaciones clínicas: trombocitopenia asintomático leve o moderada, trombocitopenia severa con un conteo de plaquetas de menos de 50 times 103/mm3 o complicaciones de trombosis y embolismo debido al TIH. CONCLUSIONES TIH es una complicación infrequente, pero este puede resultar en complicaciones serias y a veces letales debido a la terapia de heparina. Como resultado, es importante estar al tanto del posible desarrollo de TIH asociado con el tratamiento de heparina, reconocer esta complicación lo más pronto posible, y manejarlo apropriadamente antes de las manifestaciones de los efectos adversos. OBJECTIF Souligner l'importance de la thrombocytopénie induite par l'héparine (TIH), un effet indésirable potentiellement fatal de l'héparine. RÉSUMÉ DU CAS Il existe deux types de TIH, présentant des étiologies distinctes. Le type I se définit comme une thrombocytopénie légère, d'apparition précoce et qui se résout généralement malgré la poursuite du traitement à l'héparine. Les complications cliniques de ce premier type sont inhabituelles. Le type II est plus grave et il sera le point de mire du présent article. Cinq patients recevant de l'héparine ont développé une TIH de type II ayant résulté, dans certains cas, en des complications menant à l'amputation d'un membre ou même, à la mort. DISCUSSION Chez un patient recevant de l'héparine, le développement de thrombocytopénie devrait alerter l'équipe soignante à la possibilité de TIH. Le traitement rapide de la TIH peut aider à prévenir les complications. Suivant une première exposition à l'héparine, la TIH se manifeste généralement 5–8 jours après le début du traitement. Le décompte plaquettaire diminue habituellement à moins de 100 times 103/mm3. Par la suite, il se normalise en 5–7 jours après l'arrêt du traitement à l'héparine. Malgré la thrombocytopénie, une thrombose ou de la coagulation intravasculaire disséminée peuvent se produire. Le traitement peut se subdiviser selon trois situations cliniques: thrombocytopénie légère à modérée asymptomatique, thrombocytopénie grave avec un compte de plaquettes moins de 50 times 103/mm3, et TIH compliquée de thromboembolie. CONCLUSIONS La TIH est une complication rare, potentiellement grave, et parfois fatale de l'héparinothérapie. Ainsi, lorsqu'un patient reçoit de l'héparine, le clinicien doit surveiller l'apparition de TIH, afin de la reconnaître de façon précoce et de la traiter adéquatement avant l'apparition de complications graves.


2017 ◽  
Vol 64 (2) ◽  
Author(s):  
Agata Winiarska ◽  
Norbert Kwella ◽  
Tomasz Stompór

Thrombotic thrombocytopenic purpura (TTP) is a rare disorder belonging to thrombotic microangiopathies (TMA) and is caused by functional deficiency of metalloproteinase ADAMTS-13. Plasma exchange (PE) remains the treatment of choice in this disease. Here were describe the case of patient who apparently recovered from TTP following multiple sessions of PE, but remained thrombocytopenic. Careful analysis revealed the development of heparin-induced thrombocytopenia (HIT) that precluded platelet count (PLT) normalization. Full normalization of PLT followed discontinuation of PE and low-molecular weight heparin.


2021 ◽  
Vol 14 (9) ◽  
pp. e245092
Author(s):  
Pujon Purkayastha ◽  
Charlie Mckechnie ◽  
Pallavi Kalkur ◽  
Marie Scully

Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a relatively novel term which describes patients who have developed a low platelet count and prothrombotic tendencies secondary to receiving a vaccine. The concept has been derived from the well-established phenomenon of heparin-induced thrombocytopenia, and several cases of VITT have now been reported in patients who have received the AstraZeneca (ChAdOx1 nCov-19) vaccine. Unfortunately, some of these patients have gone on to develop intracranial venous sinus thrombosis. We present a case of VITT-associated sinus thrombosis secondary to the AstraZeneca (ChAdOx1 nCov-19) vaccine, which was complicated by a large intracerebral haemorrhage.


Medicina ◽  
2008 ◽  
Vol 44 (9) ◽  
pp. 723
Author(s):  
Dagmara Reingardienė

In clinical use for over 50 years, heparin is an important and widely used anticoagulant for the prophylaxis or treatment of thromboembolic disease as well as other numerous clinical situations. Ordinarily, heparin prevents clotting and does not affect the platelets, components of the blood that help to form blood clots. However, heparin can also cause heparin-induced thrombocytopenia. Two distinct types of heparininduced thrombocytopenia can occur: nonimmune and immune mediated. Nonimmune heparin-induced thrombocytopenia, which occurs most frequently, is characterized by a mild decrease in the platelet count and is not harmful. The second type, immune-mediated heparin-induced thrombocytopenia, occurs much less frequently but is dangerous. Immune-mediated heparin-induced thrombocytopenia causes much lower platelet count. Paradoxically, despite a very low platelet count, patients who suffer from heparin-induced thrombocytopenia are at risk for arterial or venous thrombosis. In this review article, there are discussed about pathogenesis of heparin-induced thrombocytopenia, other causes of thrombocytopenia, clinical features, laboratory confirmation of diagnosis, and management of patients (direct thrombin inhibitors, other therapies, duration of therapy, and use of oral anticoagulants). Prognosis and prophylaxis of this life-threatening disorder, which can develop from the use of unfractionated or (less commonly) low-molecular-weight heparin, are also discussed.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 908-908
Author(s):  
Susan M. Begelman ◽  
Marcie J. Hursting ◽  
Richard V. Aghababian ◽  
David McCollum

Abstract Heparin therapy for any indication, including venous thromboembolism (VTE), can be complicated by heparin-induced thrombocytopenia (HIT). The purpose of this retrospective study was to characterize the clinical experience of patients in whom HIT complicated heparin therapy for VTE and who were switched to argatroban therapy. From the previously reported prospective, multicenter, historical-controlled Argatroban-911 and Argatroban-915 studies of argatroban therapy in HIT, we identified all patients who developed HIT while on heparin therapy for pulmonary embolism and/or deep venous thrombosis and in whom heparin was discontinued and argatroban therapy initiated. The primary study end point was a composite of death, amputation, or new thrombosis within 37 days of argatroban initiation; we also evaluated a 37-day composite end point of thrombosis-associated events, including death due to thrombosis, amputation secondary to HIT, or new thrombosis. A total of 145 patients with VTE and HIT were included in our analysis. During heparin therapy before HIT was diagnosed, platelet counts decreased from daily mean values greater than 175x109/L to a mean±SD nadir of 78±67x109/L over the course of 5 days, and new thrombosis developed in 75 (52%) patients. After heparin was discontinued, patients received argatroban (mean dose 2.1±1.2 mcg/kg/min) for 6.8±4.3 days achieving mean activated partial thromboplastin times during therapy of 63±12 s. By day 6 of argatroban therapy, the mean platelet count had risen to >150x109/L. The primary end point occurred in 41 (28.3%) patients, and the thrombotic composite in 23 (15.9%) patients (Table 1). Seventeen (11.7%) patients, including 12 who had also experienced thrombosis while on heparin, developed new thrombosis after argatroban initiation, typically on the day argatroban was discontinued or later (n=10). Death due to thrombosis occurred in only 1 (0.7%) patient. Seven (4.8%) patients experienced major bleeding. We conclude that in heparin-treated patients with VTE, HIT-associated thrombosis often occurs before HIT is recognized, emphasizing the importance of platelet count monitoring and a high degree of suspicion for HIT in this setting. For VTE patients with HIT, argatroban provides effective anticoagulation, with outcomes comparable with those reported for argatroban-treated patients in whom HIT developed following heparin therapy for any indication. New thrombosis occurring after switching to argatroban therapy more typically occurs in patients with existing HIT-associated thrombosis and at/after argatroban discontinuation. Clinical Outcomes n(%) Outcome n=145 Primary (all cause)* Thrombosis-related†,¥ *All-cause death, all-cause amputation, or new thrombosis within 37 days. †Death due to thrombosis, amputation secondary to HIT, or new thrombosis within 37 days. ¥More than 1 outcome may have occurred in a single patient. Composite end point 41 (28.3) 23 (15.9) Individual components Death 19 (13.1) 1 (0.7) Amputation 8 (5.5) 6 (4.1) New thrombosis 17 (11.7) 17 (11.7)


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