Heparin-induced thrombocytopenia type II as a cause of serial microsurgical failures in oncologic mandibular reconstruction: a case report

Abstract

Introduction. Heparin-induced thrombocytopenia (HIT) type II is an immune-mediated prothrombotic complication driven by anti-PF4/heparin antibodies, uncommon but potentially devastating. In reconstructive microsurgery, repeated flap failure is usually attributed to technical or local factors, and a systemic prothrombotic cause is rarely considered. In oncologic craniofacial reconstruction, serial failure may lead to a non-reconstructible defect and permanent functional disability (mastication, deglutition, phonation, and facial form).

Objective. To describe HIT type II as a reversible cause of serial microsurgical failure in oncologic mandibular reconstruction, and to highlight its timely recognition as a key factor in preventing permanent disability.

Methodology. Case report. A 55-year-old patient with mandibular squamous cell carcinoma underwent staged reconstruction after oncologic resection. Five consecutive flap failures were documented (two free fibula flaps, one DCIA free flap with vascularized iliac crest, and two pedicled pectoralis major flaps), with four thrombotic events across independent vascular territories. Platelets fell 56 % (396→174 ×10⁹/L), with spontaneous recovery within 48 h of heparin discontinuation (174→320 ×10⁹/L). 4T score 7/8. Positive anti-PF4/heparin IgG ELISA. Antiphospholipid syndrome was excluded.

Results. HIT type II was diagnosed. Heparin was discontinued and fondaparinux started as non-heparin anticoagulation. No new thrombotic events occurred under fondaparinux, with sustained platelet recovery. Subsequent surgical procedures under fondaparinux proceeded without thrombotic complications, supporting heparin causality. Anticoagulant management was validated by the Hematology service of the Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, with a planned 3–6 month course of non-heparin anticoagulation. The patient was discharged stable on fondaparinux, with definitive radial forearm flap reconstruction scheduled.

Conclusions. HIT type II should be considered in repeated, unexplained flap failure, particularly with thrombosis across independent vascular territories. Recognizing this reversible systemic cause halts progression toward a non-reconstructible defect and permanent craniofacial disability, and enables definitive reconstruction under non-heparin anticoagulation.