"Don't Let Your Flap Get HITT": A Case Report and Systematic Review of Heparin Induced Thrombocytopenia and Thrombosis

BACKGROUND:

Heparin induced thrombocytopenia and thrombosis (HITT) is an under-recognized prothrombic disorder that may compromise the successful outcome of microsurgical procedures.  In October 2009, the Plastic Surgery team at the Montreal General Hospital was presented with a patient suffering from a chronic 8x9cm wound of the right medial malleolus. The wound was treated with a left anterolateral thigh perforator free flap complicated by multiple thrombotic events. Despite multiple salvage attempts, including thrombolysis with closed loop TPA administration, a popliteal AV loop and a second free flap procedure, all microvascular attempts at correction of the defect failed. HITT was diagnosed six days postoperatively upon laboratory detection of heparin-PF4 antibodies. Due to the significant impact of HITT on this flap, we reviewed the literature and found very few reports describing HITT in microsurgical procedures.  We present here a comprehensive review of HITT related to microsurgery and how HITT might be identified earlier to promote improved flap viability.

METHODS:

We performed a literature review and analysis using various databases (PUBMED, MEDLINE, Cochrane Reviews) to determine how HITT affects flap viability.

RESULTS:

HITT is estimated to occur in as many as 5% and 1% of patients treated with unfractionated heparin and LMWH, respectively. HITT might be under-diagnosed due to the ‘iceberg’ theory, highlighting the importance of rapid recognition of HITT in plastic surgery.  The onset of HITT varies between 10.5 hours to 14 days.  Suspicion of HITT should prompt the immediate cessation of heparin and implementation of non-heparin anti-coagulants such as argatroban or lepirudin.   Of the 7 diagnosed cases of HITT in free-flaps we identified in the literature, only one reported flap salvage, likely due to immediate substitution of heparin with agatroban therapy in response to thrombocytopenia.

CONCLUSIONS:

HITT is a significant and possibly under-reported threat to free-flap survival.  In patients with thrombotic events, previous heparin exposure, and post-operative decline of platelets, HITT should be considered as the source of coagulopathy in failing flaps.  We recommend using the “4T” algorithm to assess pre-test probability of HITT, and to measure CBC counts daily after flap placement to follow platelet levels.  On suspicion of HITT, heparin treatment should be discontinued and replaced with an alternative anti-coagulant such as agatroban or lepirudin to enhance flap viability and reduce patient mortality.