Heparin-induced Thrombocytopenia with Associated Thrombosis Causing Multiple Thromboses with Aortic Occlusion: Report of a Case

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• Abstract
• Case Presentation
• Discussion
• References
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A 44-year-old woman with deep vein thrombosis caused by intrapelvic peritonitis associated with adenomyosis uteri was administered unfractionated heparin. The platelet count gradually decreased, and computed tomography scan revealed abdominal aortic occlusion from the origin of the left renal artery to the intrapelvic arteries, left renal infarction, pulmonary embolism, and deep vein thrombosis. Heparin was replaced by argatroban and a successful aortobifemoral bypass was performed.

Keywords: Heparin induced thrombocytopenia, Multiple thromboses

Heparin-induced thrombocytopenia (HIT) is an idiosyncratic autoimmune disorder that occurs in 1% to 3% of patients receiving heparin.¹, ², ³ HIT occasionally causes severe thrombosis; heparin-induced thrombocytopenia with associated thrombosis (HITT). We describe a case of HITT with abdominal aortic occlusion after HIT.

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Case Presentation 

A 44-year-old woman was referred to our hospital for evaluation and treatment of multiple thromboses of the abdominal aorta, deep vein thrombosis, and pulmomary embolism. She was suffering from abdominal pain and fever caused by intrapelvic peritonitis from adenomyosis uteri for 1 month. Computed tomography (CT) had revealed deep vein thrombosis (DVT) and anticoagulation with unfractionated heparin (UFH) infusion was initiated. Ten days after initiating heparin, her platelet count decreased (from 36.8×10⁴/mm³ to 4.8×10⁴/mm³) and she complained of slight dyspnea. Twenty days after initiation of heparin infusion, CT revealed pulmonary embolism (PE), DVT, abdominal aortic occlusion from the origin of the left renal artery to both external and internal iliac arteries, and left renal infarction (Fig. 1, Fig. 2). She was transferred to our hospital and HIT with a suspected thrombosis syndrome (HITTS). Heparin was discontinued and anticoagulant therapy with continuous infusion of argatroban (100 to 140mg/d) was initiated. The thrombocytopenia improved rapidly, and anticoagulation therapy with warfarin was begun.

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• Fig. 1 

  A through D, Series of representative axial images illustrating multiple clots in the right pulmonary artery (indicated by arrows in A). Axial images at a lower level demonstrate clots in the abdominal aorta with complete occlusion of the vessel lumen (B, C). Bilateral femoral arteries were enhanced (D).

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• Fig. 2 

  This 3-dimensional image rendered from original data in the coronal view depicts complete thrombotic obstruction from the origin of the left renal artery and collateral vessel. The presence of the collateral vessel suggested a subacute event.

After insertion of a temporary filter into the supra-renal inferior vena cava (IVC), we performed two staged operations. First, an abdominal total hysterectomy (ATH) was performed for the treatment of adenomyosis uteri. Then, after we placed a permanent IVC filter in the infra-renal IVC, we performed aortobifemoral bypass grafting with a Hemashield graft (16×9mm). At first, we intended to perform thrombectomies, but thromboses were very stiff and occupied long arterial segments. Therfore we performed an aortobifemoral bypass. The proximal aortic anastomosis was in the infra-renal aorta and the distal anasomoses were on the common femoral arteries. The internal mesenteric artery (IMA) was re-implanted in the graft.

The patient's post operative course was favorable. The post operative CT revealed no recurrence of thrombosis and no problem with aortobifemoral bypass grafting. On postoperative day 20 she was discharged home.

A diagnosis of HIT was subsequently confirmed by enzyme-linked immunosorbent assay (ELISA), using the PF4-heparin antibody. Anti-heparin PF4 antibodies were found to be strongly positive in the plasma at the time of admission to our hospital.

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Discussion 

HIT presents in two forms. The more common type I occurs 2 to 3 days after initiation of heparin therapy. The thrombocytopenia is transient, and its sequelae are clinically insignificant. This condition is thought to be caused by the direct platelet-aggregating effect of heparin. Type IIHIT is an immune mediated reaction that typically occurs 5 to 10 days after the initial heparin exposure.⁴, ⁵ HIT is caused by the binding of antibodies (most frequently IgG) to a complex of heparin and platelet factor 4. Type IIHIT is frequently associated with life-threatening or limb-threatening thromboembolic complications.² The patient described in this report had type IIHIT. Thromboembolic events are most frequently venous, but arterial thromboses also occur. Arterial thromboses are more commonly peripheral thromboses compared to central thromboses.¹ In the our case, the initial deep vein thrombosis was caused by abdominal peritonitis. However, it is possible that the subsequent pulmonary embolism was caused by HITT because the amount of venous thrombus increased after using heparin.

Early diagnosis is very important in preventing this life-threatening side effect of heparin therapy. In diagnosing HIT, serologic examinations are useful. Two types of assays for HIT: washed platelet activation assays and commercial PF4/polyanion enzyme immunoassays (EIAs), are sensitive for detecting clinically relevant HIT antibodies. However, for early detection, careful platelet count monitoring and a clinical suspicion of HIT are important. When HIT is suspected, all forms of heparin should be discontinued. In the present case, we successfully treated the patient without recurrence of life-threatening multiple thromboses by discontinuing heparin, using argatroban as the anticoagulant therapy, and performing two staged operations.

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References 

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