Heparin-Induced Thrombocytopenia with Thrombosis

2017 ◽  
Author(s):  
Young Kim ◽  
Brent T Xia ◽  
Christopher A Droege ◽  
Kristen E Carter ◽  
Timothy A Pritts
Keyword(s):  
Adverse Drug Reaction ◽  
Clinical Suspicion ◽  
Type Ii ◽  
Significant Morbidity ◽  
Heparin Induced Thrombocytopenia ◽  
Functional Assays ◽  
High Clinical Suspicion ◽  
Immune Mediated ◽  
Laboratory Confirmation ◽  
Key Words Heparin

Heparin-induced thrombocytopenia type II (HIT II) is an immune-mediated adverse drug reaction to heparin and heparinoid compounds. Unlike other etiologies of thrombocytopenia, HIT II frequently manifests with arterial or venous thromboemboli, leading to significant morbidity and mortality. Diagnosis of HIT II requires a high clinical suspicion, pretest probability scoring, and laboratory confirmation through immunologic and functional assays. Moderate probability for HIT II should be met with discontinuation of the offending agent and initiation of an alternative anticoagulant. Key words: heparin-induced thrombocytopenia, heparin-induced thrombocytopenia with thrombosis, HIT II, HITT

scholarly journals Heparin-induced thrombocytopenia: An Update

1970 ◽  
Vol 3 (2) ◽  
pp. 187-199
Author(s):  
LA Sayami ◽  
M Ullah
Keyword(s):  
Morbidity And Mortality ◽  
Diagnosis And Treatment ◽  
Significant Morbidity ◽  
Drug Induced ◽  
Heparin Induced Thrombocytopenia ◽  
Recent Advances ◽  
Immune Mediated

Heparin-induced thrombocytopenia (HIT) is the most important and most frequent drug-induced, immune-mediated type of thrombocytopenia. It is associated with significant morbidity and mortality if unrecognized. In this review, we briefly discuss the main features of heparin-induced thrombocytopenia, particularly analyzing the most recent advances in the pathophysiology, diagnosis and treatment of this syndrome. Keywords: Heparin; Thrombocytopenia DOI: http://dx.doi.org/10.3329/cardio.v3i2.9189 Cardiovasc. J. 2011; 3(2): 187-199

Heparin-Induced Thrombocytopenia in Neonates

2005 ◽  
Vol 24 (5) ◽  
pp. 33-37 ◽  
Author(s):  
Julie Martchenke ◽  
Lynn Boshkov
Keyword(s):  
Heart Surgery ◽  
Heparin Therapy ◽  
Thrombin Inhibitors ◽  
Direct Thrombin Inhibitors ◽  
Type I ◽  
Type Ii ◽  
Heparin Induced Thrombocytopenia ◽  
Heparin Administration ◽  
Immune Mediated ◽  
Limiting Condition

Heparin-induced thrombocytopenia (HIT), an immune-mediated response to heparin administration, has been recognized in adults for some time, but only recently recognized in neonates and children. HIT Type I is a mild, self-limiting condition. HIT type II is a severe immune reaction to heparin that leads to thrombocytopenia and often thromboembolic complications. The incidence of HIT Type II is 2–5 percent in adults on heparin products and may be as high in neonates and children. The mortality rate from HIT in adults is 7–30 percent and is unknown but potentially high in newborns as well. The cardinal sign of HIT is a drop in platelet count by 50 percent or platelet counts below 70,000–100,000/mm3. This drop usually occurs five to ten days after the first exposure to heparin. Treatment is immediate cessation of all heparin therapy and initiation of alternative anticoagulants, especially the direct thrombin inhibitors lepirudin and argatroban. This article reviews the literature on HIT and presents a case of neonatal HIT following heart surgery.

scholarly journals Improved Laboratory Confirmation of Heparin-Induced Thrombocytopenia Type II

2001 ◽  
Vol 115 (3) ◽  
pp. 432-438 ◽  
Author(s):  
Job Harenberg ◽  
Lianchun Wang ◽  
Ursula Hoffmann ◽  
Günter Huhle ◽  
Martin Feuring
Keyword(s):  
Type Ii ◽  
Heparin Induced Thrombocytopenia ◽  
Laboratory Confirmation

Have You Been HIT?

Angiology ◽  
2011 ◽  
Vol 62 (8) ◽  
pp. 641-644 ◽  
Author(s):  
Jane Cross ◽  
Mary Weisters ◽  
Robina Aslam ◽  
David Keeling ◽  
Ashok Handa
Keyword(s):  
Platelet Count ◽  
Rare Complication ◽  
Major Complication ◽  
Clinical Suspicion ◽  
Enzyme Linked Immunosorbent Assay ◽  
Significant Morbidity ◽  
Vascular Surgeon ◽  
Heparin Induced Thrombocytopenia ◽  
Heparin Administration ◽  
Alternative Anticoagulation

This review is specifically designed to aid the vascular surgeon in the management of heparin-induced thrombocytopenia (HIT). Heparin-induced thrombocytopenia is a rare complication of heparin administration, which poses significant morbidity and mortality. Its onset is usually 5 to 10 days after the heparin administration and should be suspected if platelet counts drop by at least 50%. Confirmation is given by the presence of HIT antibodies on an enzyme-linked immunosorbent assay (ELISA) or in functional platelet activation assays. The major complication is thrombosis and surprisingly bleeding is rare. Heparin must be stopped immediately if there is a clinical suspicion of HIT and alternative anticoagulation must be started. Anticoagulation is required for at least 2 to 3 months to prevent recurrence of thrombosis. Oral anticoagulation with warfarin should not be initiated until the platelet count has been recovered and there should be an overlap of at least 5 days between starting warfarin and stopping the alternative anticoagulant.

An Overview of Heparin-Induced Thrombocytopenia

2010 ◽  
Vol 23 (3) ◽  
pp. 226-234 ◽  
Author(s):  
Jennifer L. Donovan ◽  
Maichi T. Tran ◽  
Abir O. Kanaan
Keyword(s):  
Adverse Drug Reaction ◽  
Drug Reaction ◽  
Limb Amputation ◽  
Prothrombotic State ◽  
Heparin Induced Thrombocytopenia ◽  
Arterial Thromboembolism ◽  
Immune Mediated

Heparin-induced thrombocytopenia (HIT) is an immune-mediated adverse drug reaction to heparin products leading to a prothrombotic state. Devastating clinical sequelae may result, including venous or arterial thromboembolism, limb amputation, and death. Heparin cessation alone is insufficient to manage HIT. Pharmacotherapy with argatroban or lepirudin is essential. This article reviews the pathogenesis, diagnosis, and pharmacotherapy of HIT.

scholarly journals Heparin-induced thrombocytopenia

Medicina ◽  
2008 ◽  
Vol 44 (9) ◽  
pp. 723
Author(s):  
Dagmara Reingardienė
Keyword(s):  
Platelet Count ◽  
Oral Anticoagulants ◽  
Thrombin Inhibitors ◽  
Direct Thrombin Inhibitors ◽  
Heparin Induced Thrombocytopenia ◽  
Immune Mediated ◽  
Laboratory Confirmation ◽  
Blood Clots ◽  
Life Threatening ◽  
Low Platelet Count

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.

scholarly journals Heparin-induced thrombocytopenia diagnosis: a retrospective study comparing heparin-induced platelet activation test to 14C-serotonin release assay

TH Open ◽  
2021 ◽  
Author(s):  
Marie-Caroline Gonthier ◽  
Nicolas Gendron ◽  
philippine Eloy ◽  
Marie-Charlotte Bourrienne ◽  
martine alhenc-gelas ◽  
...  
Keyword(s):  
Retrospective Study ◽  
Platelet Activation ◽  
Serotonin Release ◽  
Functional Assay ◽  
Heparin Induced Thrombocytopenia ◽  
Functional Assays ◽  
Laboratory Confirmation ◽  
Activation Assay ◽  
Circulation Circuit ◽  
Release Assay

Laboratory confirmation of heparin-induced thrombocytopenia (HIT) is of crucial importance and remains challenging and relies on platelet functional assays highlighting the presence of heparin-dependent platelet-activating antibodies in patient serum or plasma. Platelet functional assays using washed platelets include the 14C-serotonin release assay (SRA), usually described as the gold standard, and the heparin-induced platelet activation assay (HIPA). Since its first comparison with SRA there has been no additional published study regarding HIPA diagnostic performances compared to SRA. Aim of our retrospective study was to compare the concordance between HIPA and SRA in HIT suspected-patients with positive anti-PF4/heparin antibodies between October 2010 and October 2015. Fifty-five HIT-suspected patients who beneficiated from both HIPA and SRA were included. Positive and negative percent agreements were 83.8% (95% CI 68.0–93.8%) and 66.7% (95% CI 41.0–86.7%), respectively. Overall percent agreement was 78.2% (95% CI 65.0–92.2%). Agreement was higher in patients who underwent cardiopulmonary bypass with extracorporeal circulation circuit for cardiac surgery. We also confirm that the use of a minimum of 2 platelet donors to establish positive HIT diagnosis and 4 platelet donors to exclude HIT diagnosis allows obtaining a good agreement with SRA. Although HIPA and SRA were performed with different platelet donors and in different laboratories, HIPA had a good positive agreement with SRA for HIT diagnosis, showing that HIPA is a useful functional assay that does not require radioactivity and could be developed worldwide to improve HIT diagnosis.

scholarly journals The Challenge of Diagnosing Heparin-Induced Thrombocytopenia with Negative Immunologic and Functional Assays

2021 ◽  
Vol 8 (9) ◽  
Author(s):  
Glosser LD ◽  
◽  
Knauss HM ◽  
Jodeh W ◽  
Craig D ◽  
...  
Keyword(s):  
Clinical Course ◽  
Heparin Therapy ◽  
Serotonin Release ◽  
Functional Assay ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Functional Assays ◽  
Complex Patient ◽  
High Clinical Suspicion ◽  
Work Up

Heparin-Induced Thrombocytopenia (HIT) is a prothrombotic and potentially fatal immune complication of heparin therapy. HIT is challenging to diagnose, particularly in critically ill patients where multiple causes of thrombocytopenia must be considered. Diagnostic algorithms for HIT begin with a clinical assessment, followed by laboratory testing when indicated. If Platelet Factor-4 (PF4)/heparin immunoassay and Serotonin Release Assays (SRA) are negative, HIT is deemed unlikely and heparin therapy may be resumed. Current recommendations have excluded the next step in work up for thrombocytopenia after immunoassay and functional assays result negative despite worsening thrombocytopenia following heparin re-initiation. We present the case of an 85-year-old male with multiple comorbidities, found to have a clinical course consistent with HIT despite negative serologic and functional assay results. Our case highlights the challenge in diagnosing heparin-induced thrombocytopenia in a medically complex patient and demonstrates the need for standardized recommendations following negative laboratory results despite high clinical suspicion.

scholarly journals GTH 2021 State of the Art—Cardiac Surgery: The Perioperative Management of Heparin-Induced Thrombocytopenia in Cardiac Surgery

2021 ◽  
Vol 41 (01) ◽  
pp. 059-062
Author(s):  
Laura Ranta ◽  
Emmanuelle Scala
Keyword(s):  
Adverse Drug Reaction ◽  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Multidisciplinary Approach ◽  
Perioperative Management ◽  
State Of The Art ◽  
Short Review ◽  
Prothrombotic State ◽  
Heparin Induced Thrombocytopenia ◽  
Immune Mediated

AbstractHeparin-induced thrombocytopenia (HIT) is a severe, immune-mediated, adverse drug reaction that paradoxically induces a prothrombotic state. Particularly in the setting of cardiac surgery, where full anticoagulation is required during cardiopulmonary bypass, the management of HIT can be highly challenging, and requires a multidisciplinary approach. In this short review, the different perioperative strategies to run cardiopulmonary bypass will be summarized.

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