Pulmonary embolism and heparin-induced thrombocytopenia successfully treated with tissue plasminogen activator and argatroban Zachary Hourmouzis MD, Mary Colleen Bhalla MD, Jennifer A. Frey PhD, Sharhabeel Jwayyed MD, MS PII: DOI: Reference:

S0735-6757(14)00862-6 doi: 10.1016/j.ajem.2014.11.027 YAJEM 54629

To appear in:

American Journal of Emergency Medicine

Received date: Accepted date:

6 October 2014 15 November 2014

Please cite this article as: Hourmouzis Zachary, Bhalla Mary Colleen, Frey Jennifer A., Jwayyed Sharhabeel, Pulmonary embolism and heparin-induced thrombocytopenia successfully treated with tissue plasminogen activator and argatroban, American Journal of Emergency Medicine (2014), doi: 10.1016/j.ajem.2014.11.027

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ACCEPTED MANUSCRIPT Pulmonary embolism and heparin-induced thrombocytopenia successfully treated with tissue plasminogen activator and argatroban

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Corresponding author, requests for reprints Mary Colleen Bhalla, MD Department of Emergency Medicine Summa Akron City Hospital 525 East Market St. Akron, OH 44304-1619 Office 330-375-7530 Fax 330-375-7564 Email [email protected]

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Authors Zachary Hourmouzis, MD1

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Mary Colleen Bhalla, MD 1, 2

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Jennifer A. Frey, PhD 1

Sharhabeel Jwayyed, MD, MS 1, 2 1

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Summa Akron City Hospital, Department of Emergency Medicine, Akron, OH

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Northeast Ohio Medical University, Rootstown, OH

No outside funding used

Previously presented as a poster at the Summa Akron City and St. Thomas Hospitals Annual Postgraduate Day, June, 21014.

Key words: Pulmonary embolism, heparin-induced thrombocytopenia

Short Running Head: PE and HIT treated with argatroban and tPA

ACCEPTED MANUSCRIPT Abstract

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Heparin-induced thrombocytopenia (HIT) is a disorder characterized by antibodies formed against the heparin-platelet factor 4 (PF4) complex that results in thrombosis and platelet consumption. It can lead to extensive thromboembolic disease and coagulopathy. Diagnosis remains a challenge, but there are now assays that can be used for confirmation.

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A 56 year old female presented to the emergency department with a complaint of shortness of breath. She had been hospitalized five weeks prior for a laparatomy, which was complicated by pneumonia requiring intubation, and deep vein thrombosis. Initial platelet level was 63 x 109/L after being 275 upon discharge. Computed tomography angiography revealed massive bilateral saddle pulmonary emboli. She was hemodynamically stable when she was started on a heparin bolus and drip, but it was then revealed that she had received low molecular weight heparin (LMWH) as an outpatient. Her blood pressure dropped and the heparin was discontinued. She was given 100 mg of tissue plasminogen activator (tPA) over one hour rather than two, with symptomatic improvement. She was treated with argatroban and later tested positive for antibodies against the heparin-PF4 complex which confirmed the diagnosis of HIT. She was converted to and discharged on warfarin and has done well.

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This case demonstrates the proper diagnosis and workup for pulmonary embolism caused by HIT, with successful treatment of both the underlying disease and its life-threatening complications. It demonstrates that, though the risk of HIT is less with LMWH than for heparin, it is not zero.

Heparin-induced thrombocytopenia (HIT) is a thrombotic and coagulopathic disorder caused by use of heparin or low molecular weight heparin (LMWH) or fondaprinux, the latter two being less associated with causing the disorder. Typically, platelets will fall to

Pulmonary embolism and heparin-induced thrombocytopenia successfully treated with tissue plasminogen activator and argatroban.

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