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• W2026072014 abstract "Sir: A major cause of flap failure in reconstructive microsurgery is thrombosis.1 Recently, Tremblay et al. reported two cases of flap failure secondary to heparin-induced thrombocytopenia; they also described unexplained improvement of the flaps with leech therapy.2 To prevent potentially life-threatening complications, heparin-induced thrombocytopenia is usually treated with a nonheparin anticoagulant such as argatroban or Coumadin.3Hirudo medicinalis (leeches) were first used to treat flap congestion in 1960.4 Medicinal leeches increase blood flow within congested flaps by active feeding, and indirectly by passive bleeding from leech bite.5 In this article, we report two flap failures in one patient secondary to heparin-induced thrombocytopenia, and that hirudin, a nonheparin anticoagulant secreted by leeches, kept one of the flaps viable because it was treating the heparin-induced thrombocytopenia. A healthy 44-year-old male motorcyclist sustained a left lower extremity Gustilo grade IIIC fracture and a right clavicle fracture. Hematologic profile on presentation was normal. He underwent successful limb salvage and was placed on aspirin and Lovenox (Sanofi-Aventis, Bridgewater, N.J.) (chemoprophylaxis) postoperatively. After serial washouts and vacuum-assisted closure changes, he underwent open reduction internal fixation and reconstruction with a soleus flap and skin graft on postinjury day 18. Four days later, the soleus flap was necrotic and required débridement, surprisingly with an intact Doppler signal throughout the pedicle (Fig. 1). Ultimately, on postinjury day 29, a microvascular gracilis and skin graft reconstruction was performed; heparin was administered as a bolus (5000 units) intraoperatively and continued as a drip. However, in the immediate postoperative course, the gracilis flap became congested and exploration demonstrated a patent vein and artery. Heparin was discontinued; the flap remained congested and so leeches were started. Leech decompression was discontinued after 7 days because the flap appeared viable. However, shortly after discontinuation of leeches, muscle necrosis ensued (Fig. 2). With no clear cause for flap loss, we initiated a hypercoagulable workup and heparin-induced thrombocytopenia was diagnosed; in our patient, heparin-induced thrombocytopenia manifested as a relative reduction in platelet count and right basilic vein thrombosis. He was treated with argatroban, underwent a successful cross-leg flap and skin graft reconstruction, and was discharged to home on Coumadin.Fig. 1.: On postinjury day 22 (postreconstruction day 4), the soleus muscle flap demonstrates muscle necrosis despite arterial Doppler signal out to the distal tip of the muscle; the darkened area represents the area of necrosis.Fig. 2.: Gracilis muscle flap necrosis despite intact arterial and venous Doppler signal prompted a hypercoagulable workup that ultimately led to a diagnosis of heparin-induced thrombocytopenia.To our knowledge, this is the first report in the literature implicating leeches as a potential marker of heparin-induced thrombocytopenia. We observed two flap failures in our patient that we attribute to heparin-induced thrombocytopenia: the flaps had intact pedicles throughout despite muscle necrosis. With the free gracilis, the flap improved with initiation of leech therapy. We feel that this was attributable to inadvertent local administration of the hirudin secreted by the leeches. Hirudin is a potential treatment for heparin-induced thrombocytopenia, as it is an anticoagulant unrelated to heparin. In summary, heparin-induced thrombocytopenia can cause flap failure by venous congestion. Flap salvage in the presence of leeches should alert the reconstructive surgeon to the possibility of heparin-induced thrombocytopenia, as the secretion of hirudin by leeches is essentially treating the thromboembolic complications associated with heparin-induced thrombocytopenia. More research is required to demonstrate and define the role of hirudin in heparin-induced thrombocytopenia patients requiring flaps. DISCLOSURE None of the authors has a financial interest in or commercial affiliation with any of products or drugs mentioned in this article. Nilton D. Medina, M.D. Vineet Mehan, M.D. Scott T. Schmidt, M.D. Division of Plastic and Reconstructive Surgery Alpert Medical School of Brown University Rhode Island Hospital Providence, R.I." @default.
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• W2026072014 date "2010-05-01" @default.
• W2026072014 modified "2023-10-07" @default.
• W2026072014 title "Heparin-Induced Thrombocytopenia Leading to Flap Failure: Hirudo medicinalis and Implications" @default.
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• W2026072014 doi "https://doi.org/10.1097/prs.0b013e3181d51704" @default.
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