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(Chest. 2006;130:681-687.)
© 2006 American College of Chest Physicians

How Frequently Is Venous Thromboembolism in Heparin-Treated Patients Associated With Heparin-Induced Thrombocytopenia?

Robert L. Levine, MD, FCCP; David McCollum, MS and Marcie J. Hursting, PhD

* From the Departments of Neurosurgery and Emergency Medicine (Dr. Levine), The University of Texas School of Medicine at Houston, Houston, TX; Statistics and Data Management (Mr. McCollum), CTI Clinical Trial and Consulting Services, Blue Ash, OH; and Thrombosis and Hemostasis (Dr. Hursting), Clinical Science Consulting, Austin, TX.

Correspondence to: Robert L. Levine, MD, FCCP, The University of Texas School of Medicine at Houston, 6431 Fannin, MSB 7.142, Houston, TX 77030; e-mail: rlevine{at}uth.tmc.edu

Abstract

Background: Patients receiving heparin for thromboprophylaxis or treatment may have new or recurrent venous thromboembolism (VTE) if immune-mediated heparin-induced thrombocytopenia (HIT) occurs or for other reasons, eg, if anticoagulation fails. We estimated from the literature how frequently a patient presenting with VTE during or following heparin therapy has HIT-associated VTE.

Methods: A comprehensive, systematic literature search was conducted to identify studies using unfractionated or low-molecular-weight heparin (LMWH) for thromboprophylaxis or treatment in which new or recurrent VTE and serologically confirmed HIT were reported. From extracted study data, the proportion of patients with HIT-associated VTE relative to any VTE was calculated by heparin type and mode of administration.

Results: We identified 10 studies, some with multiple arms, that used unfractionated heparin (IV administration, 5 studies; subcutaneous administration, 3 studies) or subcutaneous LMWH (5 studies) and met analysis criteria. Across these studies, 386 of 6,219 heparin-treated patients had VTE, including 32 patients who also had HIT. The frequency of HIT-associated VTE among heparin-treated patients with VTE was comparable between IV and subcutaneous unfractionated heparin therapy (13.2% [17 of 129 patients] vs 12.4% [14 of 113 patients]; odds ratio, 1.07; 95% confidence interval, 0.50 to 2.3; p > 0.99) yet significantly different between unfractionated heparin and LMWH therapy (12.8% [31 of 242 patients] vs 0.7% [1 of 144 patients]; odds ratio, 21.0; 95% confidence interval, 2.8 to 156; p < 0.001).

Conclusions: VTE is associated with HIT infrequently (< 1%) in LMWH-treated patients, yet often (approximately one in eight cases) in unfractionated heparin-treated patients. Physicians should suspect the possibility of HIT if VTE develops during or soon after unfractionated heparin use; if thrombocytopenia is present, alternative anticoagulation should be used until HIT is excluded.

Key Words: adverse effects • anticoagulant drugs • heparin • thrombocytopenia • thrombosis • venous thrombosis

Unfractionated heparin and low-molecular-weight heparins (LMWHs) are routinely used for thromboprophylaxis or treatment.1 Despite heparin therapy, patients sometimes have new or recurrent thrombosis if anticoagulation fails or heparin-induced thrombocytopenia (HIT) occurs. HIT is a serious, immune-mediated condition in which 38 to 76% of patients acquire thrombotic complications, typically venous thromboembolism (VTE), in the days to weeks after its onset.2 In patients with HIT or the reactive antibodies that cause HIT, continued exposure or re-exposure to heparins can result in catastrophic outcomes.3 Treatment strategies for VTE differ: if VTE is not associated with HIT, heparins are recommended1; if VTE is associated with HIT, heparins are contraindicated and alternative anticoagulation is recommended.4

Although VTE as a complication of HIT is well described,45678 the recognition of HIT (or HIT-associated thrombosis) can be challenging. Patients with HIT often have relative rather than absolute thrombocytopenia (a decrease of 50% in the platelet count yet a nadir > 150 x 109/L). Platelet counts in HIT typically normalize within days of discontinuing heparin even though the thrombotic risk persists for weeks. It is possible for heparin-treated patients to be discharged from the hospital before their HIT manifests and then return with HIT-associated thrombosis.56 Physicians are encouraged to be vigilant in suspecting HIT in anyone presenting with thrombosis following recent (or current) heparin therapy or recent hospitalization; however, the likelihood that a new or recurrent VTE in a heparin-treated patient is associated with HIT remains unclear. Its clarification is important for facilitating HIT risk assessment and treatment decision making in the heparin-treated patient presenting with VTE.

We conducted a systematic literature analysis to address the question, "how frequently is new or recurrent VTE in a heparin-treated patient associated with HIT?" Because unfractionated heparin is more likely than LMWH to cause HIT,4 we considered the question separately for these heparin types.

Materials and Methods

Literature Search
Articles were to be included in this analysis if they met the following criteria: the study design was a randomized control trial or a prospective or retrospective cohort study that evaluated consecutive patients (or data reanalysis of such studies); unfractionated heparin or LMWH was administered for prophylaxis or treatment of thrombosis; the definition of HIT was clearly stated, with confirmatory laboratory testing for HIT conducted; objectively documented new or recurrent VTE, including deep venous thrombosis, pulmonary embolism, or both, were reported for patients with HIT as well as all patients; and at least one VTE occurred in the relevant study arm(s).

To identify potentially relevant articles, a search was performed using the Medline database (November 1984 to November 2004) and the Cochrane Library (The Cochrane Library 2004, issue 4) and the search terms "heparin-induced thrombocytopenia" or "heparin-associated thrombocytopenia" together with "thrombosis" or "thromboembolism." A search was also performed using the Medline database (November 1984 to November 2004) and the terms "heparin" and "thrombosis" and "thrombocytopenia." The searches were limited to English-language publications and human studies, and for the latter search, randomized clinical trials. A total of 673 unique citations were identified. The titles and abstracts of the citations, when available, were reviewed and coded as "irrelevant" or "possibly relevant" to our research question and associated criteria. Articles that were considered possibly relevant (n = 41) were retrieved in full for in-depth review. Additional search strategies used to find potentially relevant articles included scanning the text and bibliographies of summary articles, books, and other publications related to VTE or HIT and reviewing personal files. Possibly relevant articles were screened with respect to our inclusion criteria by one investigator and included in the analysis on independent review and consensus agreement of its eligibility by another investigator.

Data Analysis
From eligible articles, the numbers of patients who received heparin, who acquired VTE, and who acquired HIT and VTE were extracted and tabulated. We defined HIT-associated VTE as an event that occurred in a patient with HIT. For VTE occurring in a patient lacking HIT, the event was considered "not associated with HIT" and no further attribution of cause was attempted. The proportion of patients with HIT-associated VTE compared with patients with any VTE (and the exact 95% confidence interval) was calculated for each study and across the studies according to the type of heparin administered (unfractionated or low-molecular-weight), accounting for its method of administration (IV or subcutaneous). For the across-study values, the odds ratio (and associated 95% confidence interval) was determined for IV vs subcutaneous unfractionated heparin therapy and for unfractionated vs LMWH therapy; a Fisher Exact Test was used for assessing significance. In heparin-treated patients with VTE, the frequency of HIT was compared between surgical and medical patients using a Fisher Exact Test. Statistical analyses were conducted using statistical software (GraphPad Statistical Software; GraphPad Software; San Diego, CA), and significance was declared at p < 0.05.

Results

Data Set
From 41 possibly relevant articles identified from the literature database search, we found 9 articles involving eight clinical studies that met inclusion criteria for our analysis.91011121314151617 The remaining 32 articles failed to meet one or more inclusion criteria, most often (n = 23) lacking reported outcomes for patients with HIT and/or a prospective definition of HIT or confirmatory testing. The nine eligible articles included both an analysis17 and reanalysis12 of HIT occurring in a single clinical study.18 In the initial analysis, HIT was defined as a platelet count < 150 x 109/L and in the reanalysis as a ≥ 50% fall in the platelet count from the postoperative peak. The investigators considered the latter definition to be improved because it provided greater sensitivity and similar high specificity for detecting HIT. Hence we extracted data from the reanalysis12 and, where needed, the original study report18; and the initial analysis17 is not presented separately herein. From our supplemental search strategies, which included scanning bibliographies of related articles and reviews, we identified 2 more articles that also met our criteria,1920 yielding a total of 10 studies for our analysis.

Table 1 summarizes the purpose, design, patient population, heparin dosing information, and follow-up period of each of the 10 studies. There were six randomized controlled trials,91011121920 three prospective studies,131415 and one retrospective study.16 The studies may have had multiple study arms. The comparator in two studies1920 was the selective factor Xa inhibitor fondaparinux, and no VTE occurred in the subcutaneous unfractionated heparin arm of another study11; these study arms were not included in our analyses. One study16 was conducted in pediatric patients, and the other studies were in adults. In each study, medical or surgical patients received IV unfractionated heparin (five studies), subcutaneous unfractionated heparin (three studies), or subcutaneous LMWH (five studies) therapy typically for 7 to 10 days. Patients were followed up in the hospital or after discharge at most for 90 days for new or recurrent VTE. Two studies912 were of orthopedic surgical patients, who are at increased risk of HIT compared with cardiac surgery patients.4 Across the studies, four different LMWHs were used: dalteparin,11 enoxaparin,19 fraxiparin,9 and reviparin.10 In each of three studies151617 reporting the animal source of the unfractionated heparin, porcine-derived heparin was used. In each of four studies10131920 of heparin therapy for acute VTE, patients also received longer-term anticoagulation with a vitamin K antagonist typically for up to 90 days. In one study,9 antithrombotic treatment after the 9- to 11-day study period was at the discretion of the investigator, and 88% of patients also received continued therapy for an average of 4 to 6 weeks using unfractionated heparin, LMWH, vitamin K antagonist, aspirin, or a combination of these.


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  		Table 1. Studies in Analysis Data Set*

 
HIT was prospectively defined in the studies, typically as a platelet count < 100 x 109/L or a 40 to 50% decrease in count, with serologic confirmation (Table 2 ). Thrombocytopenia without laboratory confirmation of heparin-dependent antibody was not considered HIT in our analyses. By single exception, confirmatory laboratory testing was not performed in 2 of 11 unfractionated heparin-treated patients with VTE and HIT in one study.12 Their HIT was diagnosed based on the platelet count criteria being met, other causes of thrombocytopenia being excluded, and the platelet count recovering on heparin cessation.


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  		Table 2. Identification of HIT in Heparin-Treated Patients*

 
Frequency Estimates
For each study and overall, we estimated the frequency of VTE, HIT-associated VTE, and their relative proportion, by type of heparin (Table 3 ). In one study,16 only 38 of 57 patients with thrombosis had plasma available for heparin-dependent antibody testing, and we based frequency estimations on the tested patients only. It is possible that some events among the tested patients were arterial rather than venous, and hence the relative proportion of HIT-associated venous events to any "venous" event may be underestimated for this study. Although not reported in Table 3, an additional five patients in the unfractionated heparin arm of one study9 had VTE within 30 to 50 days after the 9- to 11-day study period; it was unclear if they had HIT. In general, frequency estimates of VTE and HIT-associated VTE were fairly comparable across studies of unfractionated heparin and those of LMWH.


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  		Table 3. Frequency of VTE, HIT-Associated VTE, and Their Relative Proportion, by Type of Heparin and Overall*

 
Overall, of 6,219 patients administered unfractionated heparin (n = 3,792) or LMWH (n = 2,427), VTE occurred in 386 patients, 32 of whom had HIT. Of 386 patients with VTE, there were 348 adults, of whom 154 were postoperative orthopedic or craniotomy patients; and 38 pediatric patients, of whom the number of surgical patients could not be determined from available data. In the adults with VTE, 14 of 154 surgical patients (9.1%) and 6 of 194 medical patients (3.1%) had HIT (p = 0.02). Of 12 pediatric patients with VTE and HIT, 10 patients (83.3%) had recent cardiac or abdominal surgery.

Among unfractionated heparin-treated patients with VTE, 17 of 129 IV-treated patients (13.2%) and 14 of 113 subcutaneously treated patients (12.4%) had HIT-associated VTE (odds ratio, 1.07; 95% confidence interval, 0.50 to 2.3; p > 0.99). Among patients with VTE from any cause, the frequency of HIT-associated VTE was 12.8% (31 of 242 patients) with unfractionated heparin therapy and 0.7% (1 of 144 patients) with LMWH therapy (odds ratio, 21.0; 95% confidence interval, 2.8 to 156; p < 0.001).

Discussion

Each year, an estimated 2 million Americans acquire deep venous thrombosis and 600,000 acquire pulmonary embolism.21 Many of these patients will receive heparin, which is routinely initiated (often in the emergency department) for treatment of VTE, yet is potentially catastrophic if the patient has HIT-associated VTE and/or reactive heparin-dependent antibodies. HIT should be suspected whenever thrombocytopenia and/or thrombosis such as VTE occur during or soon after heparin treatment, with other causes of thrombocytopenia excluded.22 Because heparin-treated patients may also acquire VTE due to other causes, ie, inadequate anticoagulation, we wondered how big the "HIT problem" is in this setting. That is, what is the risk that a patient presenting with VTE during or following heparin therapy has HIT? This question is distinct from questions related to the risk of HIT with heparin therapy, which is well documented to be < 0.1 to 5% depending on the patient population and type of heparin,423 or the risk of thrombosis in patients with HIT, which is well documented to be 38 to 76% in the absence of alternative anticoagulation.2 To address our question, we conducted a literature analysis with the aim of estimating how frequently VTE in heparin-treated patients is associated with HIT.

Our analysis included studies using unfractionated heparin or LMWH for thromboprophylaxis or treatment in which an outcome variable was new or recurrent VTE and in which the occurrence of HIT was reported. Because our study purpose was to determine the likelihood that VTE, when it does develop, is associated with HIT, we analyzed only studies in which an event occurred. Therefore, our estimates of VTE frequency do not, nor were intended to, accurately reflect the overall efficacy of heparin therapies. Although HIT-associated thrombosis most typically occurs in the venous circulation, arterial events including myocardial infarction and stroke are also well-documented complications of HIT.45678 Our analysis focused on venous events, and the likelihood that new or recurrent arterial thrombosis in a heparin-treated patient is associated with HIT remains to be investigated.

Using our selection criteria, we identified 10 studies in which a variety of medical and surgical patients received IV or subcutaneous unfractionated heparin or subcutaneous LMWH and were followed up for VTE while in the hospital or at most 90 days. Our analysis did not apply differential weights to the data based on the design of the source study, which included randomized controlled studies as well as prospective and retrospective cohort studies. There was also heterogeneity across other aspects of the studies. For example, although generally similar working definitions for HIT based on platelet count changes were used in the studies, different confirmatory tests were used that are known to vary in their sensitivity and specificity for HIT.4 Although patients remain at increased risk of thrombosis for at least a month after the onset of HIT5678 and have detectable heparin-dependent antibodies for ≥ 4 months,24 only five studies had follow-up beyond hospitalization. HIT-associated thrombotic events may therefore have been underestimated. Despite these limitations, together the studies described 386 heparin-treated patients with VTE (32 patients also with HIT).

Our findings indicate that VTE is infrequently (< 1%) associated with HIT in patients treated with LMWH. However in unfractionated heparin-treated patients, approximately one of eight cases of VTE is associated with HIT. The likelihood that VTE is associated with HIT is significantly greater with unfractionated heparin than LMWH (odds ratio, 21; p < 0.001). The prevalence of HIT is generally greater in surgical patients than medical patients,423 and we also demonstrated a preponderance of surgical patients among heparin-treated individuals with VTE and HIT. Physicians should therefore have a high degree of suspicion for HIT-associated thrombosis in patients, particularly surgical patients, acquiring VTE during or soon after unfractionated heparin therapy, yet lower suspicion with LMWH therapy.

In a patient presenting with VTE, careful history taking concerning any recent hospitalization, heparin exposure, heparin allergy, or platelet problem is important for risk assessment of HIT before initiating anticoagulant therapy.3 Because of the ubiquitous use of heparins, a high percentage of recently hospitalized patients have had heparin exposure. A recent single-center study25 found that 42% of inpatients received unfractionated heparin therapy; exposure to LMWHs and other heparin sources such as heparin-coated devices was not evaluated. Review of previous platelet counts, if available, is prudent, and determination of the current platelet count is essential. Because tests for heparin-platelet factor 4 antibodies typically take several hours to perform, initiation of appropriate anticoagulant therapy usually cannot wait pending their results. In a patient with VTE and strongly suspected HIT, heparins should be avoided and alternative parenteral anticoagulation (argatroban or lepirudin) should be initiated.4 Warfarin should not be used as sole therapy because it can worsen the thrombosis and cause venous gangrene. Its initiation, if desired for longer-term anticoagulation, should be delayed until adequate alternative anticoagulation is provided and the platelet count is at least 100 to 150 x 109/L.

Footnotes

Abbreviations: HIT = heparin-induced thrombocytopenia; LMWH = low-molecular-weight heparin; VTE = venous thromboembolism

Dr. Levine has received grant support and consultancy fees from GlaxoSmithKline. Mr. McCollum has no conflicts of interest to disclose. Dr. Hursting has received consultancy fees from GlaxoSmithKline.

Received for publication February 27, 2006. Accepted for publication April 12, 2006.

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