Heparin-Induced Thrombocytopenia After Revascularization of Gustilo-Anderson Type IIIC Open Lower Leg Fracture: A Case Report of Subsequent Ischemic Limb Salvage Failure

Gustilo-Anderson IIIC型开放性下肢骨折血管重建术后肝素诱导的血小板减少症:一例后续缺血性肢体挽救失败的病例报告

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Abstract

BACKGROUND Heparin-induced thrombocytopenia (HIT) is a disease in which the immune response elicited by heparin results in a state of hypercoagulability and platelet activation, leading to thrombocytopenia and thromboembolism. Gustilo-Anderson type IIIC open fractures of the extremities are defined as open fractures presenting with arterial injuries that require repair and result in treatment challenges and complications. The diagnosis of HIT can be difficult in patients with severe trauma with consumptive thrombocytopenia associated with heavy bleeding and the use of heparin after vascular anastomosis. CASE REPORT A 48-year-old man was injured in a car accident, pinching his right lower leg and sustaining a Gustilo-Anderson type IIIc open fracture, for which he underwent emergency revascularization surgery. Heparin was administered continuously immediately after the surgery. On postoperative day 9, ischemic changes were observed in the right foot, and we performed suture re-anastomosis; however, the blood circulation in the right lower leg did not resume, and right lower leg amputation was performed due to ischemic necrosis with the onset of HIT. Postoperatively, the patient was switched to edoxaban after the recovery of his platelet count. Thereafter, the patient experienced no new thrombus occlusion or wound trouble, and was able to walk on a prosthetic leg and return to daily life. CONCLUSIONS It is important to consider the possibility of HIT as soon as thrombocytopenia appears in patients with Gustilo-Anderson type IIIC open fracture who are receiving heparin after vascular anastomosis, as a delayed diagnosis of HIT can make it difficult to save the limb.

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