PURPOSE: One of the major causes of flap failure in reconstructive microsurgery is venous thrombosis. When recurrent flap failure occurs, uncommon causes of flap failure should be investigated. We report a case of Heparin Induced Thrombocytopenia (HIT) as a cause of flap failure, and temporary rescue with an anticoagulant secreted by Hirudo Medicinalis (leeches) which was inadvertently treating HIT.
METHOD: case report
RESULTS:
44 year-old male motorcyclist struck by a car sustained a left lower extremity Gustilo grade 3C fracture. His only other injury was a right clavicle fracture. The patient was healthy, had a normal hematological profile on presentation, and went for immediate limb salvage: external fixation, revascularization, and four compartment fasciotomy were performed. He had excellent limb perfusion as demonstrated by clinical exam and angiography, and he was placed on aspirin for the graft and lovenox for chemoprophylaxis. On post-injury day 9, he underwent soft tissue reconstruction for exposed tibia and hardware in the proximal third of the leg. He was treated with open reduction internal fixation and reconstructed with a soleus flap and skin graft. Post-operatively, the soleus flap was non-viable and required operative debridement surprisingly with an intact doppler signal throughout the pedicle of the soleus. Ultimately, a microvascular gracilis reconstruction was performed, heparin bolus was given intraoperatively, and continued as a drip post-operatively with a target goal PTT of twice normal. However, in the immediate post-operative course, the flap became congested and operative exploration demonstrated a patent vein and artery. Heparin therapy was discontinued, but the flap remained congested and leeches were started. There was considerable improvement in the appearance of the flap with leeches despite excellent doppler flow in both artery and vein past the microvascular anastomosis. Of note the patient never became thrombocytopenic during his hospitalization; however, he was found to have thrombosis of the right basilic vein. Leech therapy was discontinued after 7 days since the flap appeared viable and continued to have excellent venous and arterial signal. However, shortly after discontinuation of leeches, the muscle became necrotic. With no clear etiology for flap loss, we initiated a hypercoagulable workup and HIT was diagnosed. He was treated with argatroban, underwent a successful cross-leg flap and skin graft reconstruction, and discharged home on coumadin.
CONCLUSION:
HIT was recently reported cause of flap failure. To our knowledge, this is the second case reported in the literature. HIT is typically treated with a discontinuation of heparin and initiation with an alternative such as argatroban. Hirudin is also a potential treatment as it is an anticoagulant unrelated to heparin. We observed two flap losses on our patient that we are attributing to HIT: the flaps had intact pedicles throughout despite muscle necrosis. With the free gracilis, we experienced improvement of the flap with initiation of leech therapy, and originally attributed this to a “congested appearance” which consisted of darkened muscle despite good flow in the artery and vein. We feel that what we were observing was likely microvascular thrombosis and muscle necrosis secondary to HIT, which improved with inadvertent local administration of the hirudin secreted by the leeches. Unfortunately we did not recognize this and when the leeches were discontinued, the patient thrombosed and flap necrosis ensued. Retrospectively, we had two chances to potentially diagnose the condition and potentially prevent flap loss. The first sign of hypercoagulability was basilic venous thrombosis. Secondly, he had improvement of the flap with leech therapy despite good venous signal in the pedicle. In unexplained flap loss, and maintenance of flap viability with leeches, the reconstructive microsurgeon needs to consider HIT as a possible cause of flap failure.