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Heparin-Induced Thrombocytopenia in a Patient With Extensive Venous Thrombosis and Complex Comorbidities
Mohammed A Kassis1, Mustafa H Adleh2, Adel Mahmah2
1Department of Medicine, Ras Al Khaimah (RAK) Medical & Health Sciences University, Ras Al Khaimah, ARE.
Heparin-induced thrombocytopenia (HIT) type 2 typically presents with thrombosis. Bleeding is uncommon and can obscure diagnosis. We describe a 69-year-old woman with chronic kidney disease who presented with progressive left-leg swelling. Initial evaluation included ultrasonography. However, an abrupt >50% platelet fall after recent heparin exposure raised clinical suspicion for HIT; therefore, serial 4Ts reassessments and an anti-platelet factor 4 (PF4)/heparin immunoassay were performed. Management included open thrombectomy, cautious anticoagulation, and transfusion minimization. Given hemorrhagic risk and renal impairment, apixaban was favored. Duplex ultrasound showed extensive acute deep vein thrombosis (DVT) in the left femoral system (common, profunda, and mid-femoral) and saphenofemoral junction, with chronic thrombi in the femoral and popliteal veins. During hospitalization, the patient developed recurrent severe anemia, large hematomas, and late thrombocytopenia with no bleeding source identified. Multiple erythrocyte alloantibodies were detected. Later during the hospital stay, serial 4Ts evolved to intermediate probability, and the anti-PF4 test was positive. Following appropriate measures, the patient was stabilized and subsequently discharged safely. Bleeding-dominant, alloimmunization-complicated courses can mask HIT. Serial 4Ts reassessment, careful laboratory interpretation, early transfusion-medicine input, and appropriate anticoagulant selection for renal impairment may reduce thrombotic and hemorrhagic risk.
Heparin-induced thrombocytopenia (HIT) type 2 typically presents with thrombosis. Bleeding is uncommon and can obscure diagnosis. We describe a 69-year-old woman with chronic kidney disease who presented with progressive left-leg swelling. Initial evaluation included ultrasonography. However, an abrupt >50% platelet fall after recent heparin exposure raised clinical suspicion for HIT; therefore, serial 4Ts reassessments and an anti-platelet factor 4 (PF4)/heparin immunoassay were performed. Management included open thrombectomy, cautious anticoagulation, and transfusion minimization. Given hemorrhagic risk and renal impairment, apixaban was favored. Duplex ultrasound showed extensive acute deep vein thrombosis (DVT) in the left femoral system (common, profunda, and mid-femoral) and saphenofemoral junction, with chronic thrombi in the femoral and popliteal veins. During hospitalization, the patient developed recurrent severe anemia, large hematomas, and late thrombocytopenia with no bleeding source identified. Multiple erythrocyte alloantibodies were detected. Later during the hospital stay, serial 4Ts evolved to intermediate probability, and the anti-PF4 test was positive. Following appropriate measures, the patient was stabilized and subsequently discharged safely. Bleeding-dominant, alloimmunization-complicated courses can mask HIT. Serial 4Ts reassessment, careful laboratory interpretation, early transfusion-medicine input, and appropriate anticoagulant selection for renal impairment may reduce thrombotic and hemorrhagic risk.
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