Heparin Induced Thrombocytopenia (HIT)


Article Author:
Diala Nicolas


Article Editor:
Mirembe Reed


Editors In Chief:
Wanda Wright
Cynthia Oster


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
5/4/2019 2:59:36 PM

Introduction

Heparin-induced thrombocytopenia (HIT) is a severe complication that can occur in patients exposed to any form or amount of heparin products. A fall in platelet counts and a hypercoagulable state characterize HIT. Patients who experience HIT may also develop thromboembolic complications that are associated with morbidity and mortality. This is a significant burden since heparin is widely used for treatment and prophylaxis of thromboembolism, for line flushes, and in heparin-coated catheters. This review will discuss the pathophysiology, diagnosis, and management of patients with HIT.

Etiology

Types of Thrombocytopenia (occur secondary to heparin use)

Type I HIT, also known as Heparin-associated thrombocytopenia (HAT), is a non-immune mediated reaction. Type I HIT is much more common than type II and can occur as early as day 1 of therapy. This is a mild reaction, it is not associated with any complications, and platelet counts will spontaneously normalize even if heparin is continued.

Type II HIT is an immune, antibody-mediated reaction. Because it takes time for the antibodies to form, this reaction usually occurs after 5 to 14 days of receiving heparin. However, if a patient has been exposed to heparin within the last 100 days, antibodies may remain in the system, causing this reaction to manifest as soon as day one of heparin therapy. This is a very serious reaction that causes a hypercoagulable state and can lead to life-threatening complications. The rest of this review will focus on type II HIT and its management.

Epidemiology

A HIT can occur in up to 5% of patients exposed to heparin products. HIT causes an extremely hypercoagulable state, where up to 50% of patients develop thromboembolic complications, associated with a mortality rate up to 30%.

There are several medication-related as well as patient-related factors that can increase the risk of a HIT. Because of the difference in structure and function, HIT is more likely to occur with unfractionated heparin (UFH) than with low molecular weight heparin (LMWH). Fondaparinux is a heparin-like drug that does not cause HIT. UFH is a heterogeneous product that consists of long saccharide chains of varying lengths and molecular weights; the average UFH molecule is 45 saccharide units long. LMWH is also a heterogeneous product; however, LMWH is, on average, 15 saccharide units long. Fondaparinux is a synthetic pentasaccharide, consisting of only the 5 sugars. The shorter the saccharide chain and the smaller the molecular weight, the less likely the drug is to bind to plasma proteins and cells. Therefore, there is a reduced risk of a HIT with LMWH compared to UFH, whereas fondaparinux does not cause HIT, and can be safely utilized in patients with a history of HIT and potentially in the treatment of acute HIT.

Although no amount of heparin is too small to cause this reaction, HIT is more likely to occur in patients exposed to higher doses of the drug; and the longer the duration of therapy, the higher the risk. Furthermore, females and elderly patients appear to be at an increased risk. The incidence of HIT is also higher among surgical patients, and this may be due to increased platelet activation and PF4 activity due to mechanical intervention and injury.

Pathophysiology

Under normal physiological conditions, PF4 is stored in alpha-granules of the platelets and is released upon platelet activation. PF4 is positively charged and can, therefore, bind to the negatively charged heparan (a heparin-like substance normally present on the endothelial cell surface); PF4 can also bind to exogenous heparin with much higher affinity than heparin.

PF4 binding to heparin may trigger the formation of IgG, IgA, or IgM antibodies specific to the heparin-PF4 complex. A HIT can only occur if IgG, while attached to the heparin-PF4 complex, binds to the FC receptor on the platelet surface and leads to platelet activation. Activated platelets then release pro-thrombotic substances (such as thrombin) and PF4. As IgG activates more platelets, more PF4 is released forming more complexes with heparin, thus activating more platelets. This creates a severely hypercoagulable state and a continuous cycle that can only be broken when heparin is discontinued, and appropriate treatment is initiated.

The most characteristic clinical feature of HIT is the thrombocytopenia. Platelet counts fall because macrophages consume the IgG-coated platelets and the removed by the reticuloendothelial system removes them. Simultaneously, as platelets become activated, they aggregate, and the platelet count drops as thrombus forms.

Because HIT causes a hypercoagulable state, venous and/or arterial thrombosis can occur. The most common complications are DVT, PE or skin necrosis. The latter is particularly a risk if warfarin is administered in the acute phase. The risk of these complications is highest within the first 10 days, but the pro-thrombotic state persists up to 30 days after stopping heparin.

Evaluation

HIT should be suspected when there is an unexplained drop in platelet counts in a patient currently on heparin or recently exposed to heparin products. HIT typically presents as a steady drop in platelet counts (no fluctuations), while hemoglobin and hematocrit counts remain relatively stable.

The first step in the diagnosis of HIT is the calculation of the 4T score. This is a scoring system used to determine the likelihood of a patient having HIT based on the presence or absence of certain parameters. The score may be calculated using the following table.

A 4T score of 0 to 3 points means a HIT is unlikely, and heparin therapy may continue while the clinician looks for other causes of thrombocytopenia. A score of 4 to 5 corresponds to intermediate probability and a score of 6 to 8 means high probability. All forms of heparin, including line flushes, should be immediately discontinued and treatment with an alternative anticoagulant should be pursued in any patient who scores 4 or more. In addition, the clinical diagnosis with the 4T score should be confirmed with the PF4 ELISA and the Serotonin Release Assay (SRA).

The PF4 ELISA detects the presence of antibodies. This test is highly sensitive and has a high negative predictive value; HIT can be ruled out if this test is negative. However, if the PF4 ELISA is positive, the result should be confirmed with the SRA, a more specific test that is also more costly and takes several days for the result to be reported. The PF4 ELISA detects not only IgG but also IgA and/or IgM, leading to false positives.

The SRA is the gold standard test for confirming HIT with high sensitivity and specificity. Unlike ELISA, which detects the presence of antibodies, the SRA is a functional test, which detects the activation of platelets in the presence of antibodies. A donor platelet that becomes activated in the presence of heparin and a sample of the patient’s blood (containing IgG) will release serotonin. A positive SRA confirms the diagnosis of HIT, and a negative SRA rules out HIT, even in the setting of a positive ELISA. 

Treatment / Management

The treatment of HIT should start as soon as a 4T score of 4 or more is calculated. The first step in the treatment is the discontinuation of all forms of heparin. Next, an alternative anticoagulant must be initiated to prevent or treat any HIT-induced thrombosis. In patients recently started on warfarin, warfarin should be held, and phytonadione (vitamin K) should be administered to replete protein C and S stores. The PF4 ELISA an SRA should be sent to confirm the diagnosis.

The anticoagulant of choice in an acute HIT is argatroban. Argatroban is a direct thrombin inhibitor that does not interact with PF4 or heparin-induced antibodies. Argatroban has a short half-life of about 50 minutes; it is given as a continuous infusion and requires aPTT monitoring, similar to heparin. This drug is hepatically metabolized and requires adjustment to the starting rate in patients with hepatic dysfunction, heart failure and/or multi-organ failure. Argatroban can profoundly increase INR; however, no therapeutic range for INR has been established for patients on argatroban. Argatroban’s effect on the INR must be considered when bridging a patient to warfarin.

Bivalirudin is another direct thrombin inhibitor that may safely be used in this patient population; however, this agent is usually reserved for use during cardiac catheterization procedures as an alternative to heparin. It is FDA approved for patients undergoing percutaneous coronary intervention with or without a HIT. It is more expensive than argatroban.

Another anticoagulant that may be used in a HIT is fondaparinux, although not FDA-approved for this indication. Fondaparinux is given as a once-daily subcutaneous injection. Unlike UFH and LMWH, fondaparinux does not interact with PF4 or heparin-induced antibodies.

Differential Diagnosis

Other conditions to be considered on the differential when diagnosing HIT include, but are not limited to: type I HIT (HAT), disseminated intravascular coagulation (DIC), liver disease, bleeding, hemodilution, Immune thrombocytopenia (ITP), myelosuppression, as well as other drug-induced causes.

Pearls and Other Issues

Absolute contraindications during the acute period include the use of UFH, LMWH, warfarin and platelet transfusions.

When warfarin is first initiated, the natural anticoagulants, protein C and S, whose synthesis is vitamin K-dependent, will be depleted first, while the vitamin-K dependent clotting factors remain in circulation, leading to a hypercoagulable state. If warfarin is administered at the onset of a HIT, protein C and S depletion can severely worsen coagulation and increase the risk of thromboembolic complications, particularly skin necrosis. If recently started, warfarin must be stopped and reversed with phytonadione to replete protein C and S stores.

Warfarin can be started once 2 criteria have been met. First, the platelet count has made a substantial resolution and reached a stable plateau, ideally a platelet count of at least 150 or the patient’s baseline, if baseline was below 150. Second, the patient must be therapeutically anticoagulated with argatroban or fondaparinux before the initiation of warfarin and the two agents must overlap for at least 5 days before monotherapy with warfarin.

Platelet transfusions are contraindicated during this acute phase, as transfused platelets can bind to IgG, become activated and release PF4, thus worsening the hypercoagulable state.

The risk of thromboembolic complications persists for up to 30 days after stopping heparin. Therefore, in patients with HIT and no thrombosis, anticoagulation for 1 month should be considered. Warfarin may be used for that purpose once the 2 criteria mentioned above are met.

Following an episode of HIT, IgG antibodies may remain in the system for up to 100 days; if the patient receives any amount of UFH or LMWH during this period, platelet counts can drop in as little as 12 hours. If this 100-day period has passed, heparin products can be used with caution if necessary, at the lowest dose and for the least amount of time possible. Ideally, and if time permits, an SRA should be obtained before using heparin to confirm the absence of IgG in the patient’s blood. If unable to obtain the SRA, then the use of a direct thrombin inhibitor or fondaparinux should be considered.


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Heparin Induced Thrombocytopenia (HIT) - Questions

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In a patient treated with heparin the platelet count is 50,000. A clot develops in the femoral artery. What is the best therapy?



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A patient being treated with heparin for a deep vein thrombosis has a platelet count of 50,000 and is absent pulses in his left leg. Ultrasound reveals a blood clot at the junction of the common femoral and profunda artery. What is the best treatment?



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In the presence of a femoral artery blood clot and heparin-induced thrombocytopenia, which drug is most appropriate for treatment?



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Which of the following is appropriate initial therapy for a patient who has been diagnosed with heparin-induced thrombocytopenia?



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Prophylactic heparin is given to a patient to prevent deep venous thrombosis. The patient develops significant hematuria, ecchymosis, and cold extremities. Which of the following is not true about this condition?



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In a patient with heparin-induced thrombocytopenia associated with bleeding, which of the following is the most appropriate treatment?



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In a patient with heparin-induced thrombocytopenia and thrombosis of arteries, which of the following is not appropriate treatment?



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A patient is found to have a DVT. However, she has been told that she has heparin induced thrombocytopenia. What is the next step in her management?



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Which of the following medications is NOT appropriate for the initial treatment of patients diagnosed with heparin-induced thrombocytopenia (HIT)?



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Which medication is appropriate for acute treatment of deep vein thrombosis in a patient with heparin-induced thrombocytopenia?



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Which of the following medications may cause thrombocytopenia?



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Which of the following regarding heparin-induced thrombocytopenia is false?



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What is the cause of heparin-induced thrombocytopenia?



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Which of the following methods is considered the gold standard for diagnosing heparin-induced thrombocytopenia?



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Which of the following is a serious side effect of heparin?



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An elderly female is admitted for pneumonia from which she is extremely debilitated. She is placed on intravenous vancomycin and low molecular weight heparin subcutaneously as deep vein thrombosis prophylaxis. On day six of her admission, she complains of deep right-sided calf pain. The exam and a subsequent Doppler confirm the presence of deep vein thrombosis. Of note, her platelet count, formerly stable, has plunged to 40,000/mm3. Which of the following would be prudent management of this patient?



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A 17-year-old female with a pulmonary embolism is started on IV unfractionated heparin. Five days later, her platelet count has dropped to 60,000/microLiter. Her serum is positive for antibodies to heparin-platelet factor 4 complexes. Which of the following is the best initial step in management?



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Which is true regarding patients with heparin induced thrombocytopenia (HIT)?



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Which is a common presenting symptom of heparin induced thrombocytopenia (HIT)?



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Which of the following drugs is most likely to induce thrombocytopenia?



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Heparin-induced thrombocytopenia is caused by antibodies to which one of the following?



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Of the following, which is a serious possible side effect of heparin?



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A 55-year-old female presents to the emergency department with right calf pain. Doppler confirms the presence of deep venous thrombosis. She is started on warfarin and a heparin drip to bridge to goal INR. On day 6 of therapy, the patient has an INR for 1.9. In addition, platelet counts have dropped from her baseline of 265 to 124. Hemoglobin and hematocrit are stable. Her 4T score is 4. The PF4 ELISA and Serotonin Release Assay (SRA) are sent to confirm the diagnosis of heparin-induced thrombocytopenia. What is the next step in the management of this patient?



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Which of the following patients is at the highest risk of developing heparin-induced thrombocytopenia (HIT) during their hospital admission?



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A patient is suspected to have heparin-induced thrombocytopenia (HIT). A 4T score of 5 is calculated. What is the next step in the management of this patient?



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A patient presents to the emergency department with chest pain and is found to have ST-elevation myocardial infarction (STEMI). The patient is taken to the cath lab for primary percutaneous coronary intervention (PCI). Of note, the patient’s allergies in the electronic medical record include thrombocytopenia with heparin, which was documented 2 years ago. Labs from the most recent admission last month include a positive PF4 ELISA and a negative serotonin release assay (SRA). Which of the following is the best option of the adjunctive antithrombotic therapy during PCI?



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What is the difference between type II heparin-induced thrombocytopenia (known HIT) and type I heparin-induced thrombocytopenia (also known as heparin-associated thrombocytopenia or HAT)?



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What is the most likely timing of platelet count decline in heparin-induced thrombocytopenia (HIT) relative to when heparin is started? Assume the patient has not had a prior exposure to heparin products.



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Heparin Induced Thrombocytopenia (HIT) - References

References

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Association Between Hypercoagulable Conditions and Calciphylaxis in Patients With Renal Disease: A Case-Control Study., Dobry AS,Ko LN,St John J,Sloan JM,Nigwekar S,Kroshinsky D,, JAMA dermatology, 2017 Dec 13     [PubMed]
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The intent of StatPearls is to provide practice questions and explanations to assist you in identifying and resolving knowledge deficits. These questions and explanations are not intended to be a source of the knowledge base of all of medicine, nor is it intended to be a board or certification review of CNS-Adult Health. The authors or editors do not warrant the information is complete or accurate. The reader is encouraged to verify each answer and explanation in several references. All drug indications and dosages should be verified before administration.

StatPearls offers the most comprehensive database of free multiple-choice questions with explanations and short review chapters ever developed. This system helps physicians, medical students, dentists, nurses, pharmacists, and allied health professionals identify education deficits and learn new concepts. StatPearls is not a board or certification review system for CNS-Adult Health, it is a learning system that you can use to help improve your knowledge base of medicine for life-long learning. StatPearls will help you identify your weaknesses so that when you are ready to study for a board or certification exam in CNS-Adult Health, you will already be prepared.

Our content is updated continuously through a multi-step peer review process that will help you be prepared and review for a thorough knowledge of CNS-Adult Health. When it is time for the CNS-Adult Health board and certification exam, you will already be ready. Besides online study quizzes, we also publish our peer-reviewed content in eBooks and mobile Apps. We also offer inexpensive CME/CE, so our content can be used to attain education credits while you study CNS-Adult Health.