Introduction: Heparin induced thrombocytopenia (HIT) appears after exposure to unfractioned heparin (2-5%), and rarely (0.7%) after exposure to low-molecular-weight heparin. It associates arterial and venous thrombosis with major clinical implications, requiring an early diagnosis.
Case presentation: A 60 year old caucasian women with no significant past medical history presented for a swollen, painful left calf for the past 2 weeks, after tra-uma with fracture of the ischio-pubian arch and aceta-bular joint. The edema gradually increased and within 2 days before the admission extended to the left thigh, associating erythema. Doppler venous ultrasonogra-phy revealed ilio-femoro-popliteal deep vein thrombo-sis (DVT). Computed tomography pulmonary angio-graphy (CT pulmonary angiography) excluded a pul-monary embolism (PE).
The patient was admitted to the hospital. She recei-ved treatment with enoxaparin in therapeutic dose, and antibiotherapy for suspected cellulitis. Two days after admission, the calf became cyanotic, very painful, and with ischemic cutaneous lesions. We diagnosed phleg-masia cerulea dolens. Meanwhile the platelet number decreased from 146.000/uL on admission to 53.000/ uL, more than 50%. This was initially considered autoimmune thrombocytopenia and the patient received dexamethasone treatment. Subsequently, on the third day of admission, she became tachycardic and hypo-xemic with an O₂ spontaneous saturation of 89%. Re-peated CT pulmonary angiography revealed massive bilateral pulmonary thromboembolism and DVT ex-tension to the inferior vena cava with partial occlusi-on. She was transfered to Cardiology. Since the platelet number continued to decrease, a diagnosis of HIT was made. Enoxaparin administration was stopped and an-ticoagulant treatment was switched to rivaroxaban 15 mg twice daily. The subsequent clinical course was fa-vorable, with normalization of the platelet number on the 13^th day of treatment, reperfusion of the DVT, and resolution of the calf and thigh edema as well as of the cutaneous lesions.
Particularities of this case are HIT after exposure to LMWH in a patient with extensive DVT, complicated with phlegmasia cerulea dolens and massive pulmo-nary thromboembolism with favorable response to ri-varoxaban.
In conclusion, HIT is a clinical entity, still incompletely known, that must be considered in every patient that develops rapid onset thrombocytopenia with unfracti-oned heparin or LMWH administration. Late diagno-sis exposes the patient to potentially life threatening complications.