scholarly journals Recidivne tromboze arterij spodnjega uda pri bolniku s trombocitopenijo, povzročeno s heparinom – Prikaz primera

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.

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.


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


Author(s):  
Wan Nuraisyah Azzahrah Wan Zuki

Phlegmasia cerulea dolens (PCD) is a rare syndrome caused by venous thrombosis and characterised by a triad of limb oedema, cyanosis and pain. It requires early recognition as delay of treatment can cause gangrene, limb amputation and in extreme cases, death. A 67- year-old Chinese lady, with underlying hypertension, diabetes mellitus and dyslipidaemia presented to the emergency department with a 2 days history of pain, oedema and bluish discoloration over the entire left leg. She had a history of fall 6 months prior and since then she used a walking stick for mobilization. This patient underwent ultrasound doppler left lower limb , which showed features suggestive of long-segment left lower limb deep vein thrombosis. A diagnosis of PCD was made. Subsequently, she went for a CT angiogram and venography of the left lower limb which confirmed thrombosis of the left calf vein extending to the long segment of the left common iliac vein. She was commenced on intravenous heparin infusion and then underwent inferior vena cava filter insertion and catheter directed thrombolysis. Repeat venogram showed successful catheter directed thrombolysis of the left lower limb deep venous thrombosis (DVT). Treatment should be initiated as soon as the diagnosis of PCD is suspected. Currently, guidelines for treatment are lacking however 3 therapeutic options are advocated alone or in combination: anticoagulants, thrombolytic therapy, and venous thrombectomy. An early recognition of PCD and appropriate decision regarding the treatment is essential to preserve the limb.International Journal of Human and Health Sciences Supplementary Issue-2: 2021 Page: S16


Blood ◽  
1991 ◽  
Vol 78 (9) ◽  
pp. 2194-2197
Author(s):  
C Demers ◽  
JS Ginsberg ◽  
P Brill-Edwards ◽  
A Panju ◽  
TE Warkentin ◽  
...  

In order to determine the efficacy and safety of ancrod, a rapid acting defibrinogenating drug, for patients with heparin-induced thrombocytopenia, 11 consecutive patients who required anticoagulant therapy because of venous thromboembolism and who developed acute heparin-induced thrombocytopenia or had a history of heparin-induced thrombocytopenia were treated with ancrod. Heparin therapy was discontinued (in patients receiving heparin) and ancrod started at a dose of 1 to 2 U/kg every 24 hours with subsequent daily doses adjusted to maintain fibrinogen levels between 0.5 and 1.0 g/L. Ancrod was continued until warfarin had become effective. The platelet count increased to more than 150 x 10(9)/L within 2 to 10 days in all thrombocytopenic patients. Two patients with a history of heparin- induced thrombocytopenia maintained normal platelet counts while receiving ancrod. Two patients had recurrent venous thrombosis while receiving warfarin, 10 days after ancrod was discontinued: one of these patients had metastatic pancreatic carcinoma and developed phlegmasia cerulea dolens and the other patient developed a venographically proven extension of her deep venous thrombosis. One patient suffered a bleeding episode into the thigh with a 16-g/L decrease in her hemoglobin level while receiving ancrod therapy. No other side effects were noted. Our experience indicates that ancrod therapy is a reasonable approach for patients with heparin-induced thrombocytopenia who require anticoagulant therapy.


Blood ◽  
1991 ◽  
Vol 78 (9) ◽  
pp. 2194-2197 ◽  
Author(s):  
C Demers ◽  
JS Ginsberg ◽  
P Brill-Edwards ◽  
A Panju ◽  
TE Warkentin ◽  
...  

Abstract In order to determine the efficacy and safety of ancrod, a rapid acting defibrinogenating drug, for patients with heparin-induced thrombocytopenia, 11 consecutive patients who required anticoagulant therapy because of venous thromboembolism and who developed acute heparin-induced thrombocytopenia or had a history of heparin-induced thrombocytopenia were treated with ancrod. Heparin therapy was discontinued (in patients receiving heparin) and ancrod started at a dose of 1 to 2 U/kg every 24 hours with subsequent daily doses adjusted to maintain fibrinogen levels between 0.5 and 1.0 g/L. Ancrod was continued until warfarin had become effective. The platelet count increased to more than 150 x 10(9)/L within 2 to 10 days in all thrombocytopenic patients. Two patients with a history of heparin- induced thrombocytopenia maintained normal platelet counts while receiving ancrod. Two patients had recurrent venous thrombosis while receiving warfarin, 10 days after ancrod was discontinued: one of these patients had metastatic pancreatic carcinoma and developed phlegmasia cerulea dolens and the other patient developed a venographically proven extension of her deep venous thrombosis. One patient suffered a bleeding episode into the thigh with a 16-g/L decrease in her hemoglobin level while receiving ancrod therapy. No other side effects were noted. Our experience indicates that ancrod therapy is a reasonable approach for patients with heparin-induced thrombocytopenia who require anticoagulant therapy.


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.


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.


2001 ◽  
Vol 35 (7-8) ◽  
pp. 885-890 ◽  
Author(s):  
William E Dager ◽  
Richard H White

OBJECTIVE: To report two cases of successful lepirudin use in two patients with heparin-induced thrombocytopenia (HIT) and renal failure. CASE SUMMARY: Two patients with renal failure requiring hemodialysis developed HIT syndrome during intravenous heparin therapy. Anticoagulation was necessary to prevent recurrent, acute venous thrombosis in one patient and to prevent arterial thrombosis associated with the use of an intraaortic balloon pump in the second. Intravenous lepirudin was initiated at doses of 0.01 mg/kg/h and 0.005 mg/kg/h, respectively, and titrated based on the activated partial thromboplastin time (aPTT). Steady-state doses were 0.015 mg/kg/h to maintain aPTT values of approximately 60 seconds in one patient, and 0.005–0.008 mg/kg/h to achieve an aPTT of approximately 45 seconds in the other patient. DISCUSSION: Lepirudin is one of few anticoagulants that can be safely used in patients with HIT. Because it is eliminated through the kidneys, great care must be taken when administering lepirudin to patients with renal failure; in fact, its use is currently not recommended in patients requiring hemodialysis. Lepirudin effectively prevented acute thrombosis in both of our patients with documented HIT, with no bleeding complications. We describe how we selected the initial doses and report results of aPTT monitoring. CONCLUSIONS: In patients with renal failure who develop HIT, lepirudin is one available alternative to heparin despite its poor renal elimination pattern and subsequently prolonged half-life.


Author(s):  
V.M. Bernhard ◽  
C.V. Hussey ◽  
J.B. Towne

Heparin induced thrombocytopenia and its vascular complications were identified in 25 patients. Aggregation studies performed using ADP and/or heparin in these patients were compared with responses in 18 normal. individuals. The specific aggregating factor was demonstrated in plasma. Other findings of note were normal fibrinogen, minimal elevation of fibrin split products, a normal or slightly prolonged prothrombin time and severe thrombocytopenia. Arterial and venous thrombosis required surgery in seven patients, four of whom required major amputation. Although an antibody has not been identified, the time of development of this phenomenon suggests an immune response. Only those patients who had previous exposure to heparin developed this phenomenon in less than six days. Thrombotic complications occurred with either bovine lung or porcine gut preparations from different manufacturers and appeared following both subcutaneous and intravenous administration. Electron microscopy of clots removed from four patients revealed characteristic platelet fibrin thrombi. Early recognition, prompt discontinuance of heparin and the use of platelet antiaggregants will prevent disastrous consequences. All patients undergoing heparin therapy should be carefully observed for thrombocytopenia with specific platelet aggregation studies when appropriate.


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