Delayed Onset Heparin Induced Thrombocytopenia (HIT) Resulting in Common Carotid Artery (CCA) Occlusion (P3.193)

Objective: We report a case of delayed onset HIT in a patient previously exposed to heparin with no adverse effects. Two weeks after his last heparin exposure the patient developed delayed HIT resulting in acute right CCA occlusion and other thrombotic events. Background: Delayed onset HIT is an immune-mediated disorder where antibodies against heparin/platelet factor 4 complex formed after heparin exposure persist for several days despite absence of circulating heparin resulting in thrombocytopenia and a hypercoagulable state. Heparin exposure may predispose to HIT antibody formation but does not always lead to immediate clinical manifestations. Design/Methods: A 42 year old man recently discharged from the hospital presented with left hemiparesis due to an embolic right MCA stroke secondary to right CCA occlusion. Heparin drip was initiated on admission for suspected acute carotid embolic occlusion or dissection. During the patient’s recent admission he had a normal platelet count and CT angiography head/neck at that time was unremarkable. Heparin was replaced with Argatroban after a 40[percnt] decline in platelets was noted. While on Argatroban, the patient developed a painful cold upper extremity requiring emergent thrombectomy. Results: MRI brain revealed right MCA stroke. CT angiography head/neck/chest revealed complete occlusion of the right CCA just above its origin and multiple pulmonary emboli. Platelet count rapidly declined from 101,000/mm3 to 60,000/mm3 prompting initiation of Argatroban for suspected HIT. Arterial Doppler confirmed left radial and ulnar artery occlusion. HIT and serotonin release assay were positive confirming the diagnosis. Conclusion: Delayed onset HIT can be a diagnostic challenge because prior heparin exposure may result in antibody formation without immediate clinical symptoms. The diagnosis should be considered in stroke patients with recent hospitalization and lack of trauma or vascular risk factors. The high morbidity and mortality associated with HIT requires early recognition to initiate treatment and prevent further complications. Disclosure: Dr. Pednekar has nothing to disclose. Dr. Sahni has nothing to disclose. Dr. Ahluwalia-Singh has nothing to disclose. Dr. Thomas has nothing to disclose.