Case Presentation:
A 53 year-old male with history of HTN, DMII, HLD presented with typical chest pain and dyspnea. EKG revealed diffuse ST depressions and troponin returned elevated, consistent with diagnosis of NSTEMI. Therapeutic heparin & aspirin were administered for management of ACS. Cardiac catheterization demonstrated critical left main disease and diffuse non-obstructive disease in other vessels. The patient subsequently underwent urgent three-vessel coronary bypass. He recovered well in his initial post-operative days. However, on post-operative day 8, he was found pulseless with initial rhythm of ventricular fibrillation. ROSC was achieved following ACLS protocol. Bedside echo revealed bi-ventricular failure. Patient underwent repeat cardiac catheterization showing new 100% thrombosis of all native vessels and venous grafts. LIMA-LAD graft was the only graft that was patent. Emergent PCI was performed on affected native vessels and he was initiated on mechanical support by VA-ECMO. Labs demonstrated a 50% drop in platelets in the 24 hours prior to the code, which prompted initiation of bivalirudin for empiric management of HITT. Heparin antibody was sent and was positive (2.44, nl <0.4) and serotonin release assay returned positive confirming diagnosis of heparin-induced thrombocytopenia and thrombosis. The patient remained on VA-ECMO for 4 days. After further evaluation, he was deemed neurologically devastated and family decision was to withdraw cardiorespiratory support. The patient passed away soon after.
Discussion:
Heparin induced thrombocytopenia and thrombosis (HITT) is an immune-mediated, pro-thrombotic condition that occurs in 2-3% of patients exposed to any dosage of unfractionated heparin (UFH). UFH is commonly used in the treatment of acute coronary syndrome (ACS) and is the anticoagulant of choice during coronary artery bypass graft surgery (CABG) elevating risk of HITT in post-CABG patients. Cardiorespiratory collapse secondary to thrombosis has been reported following re-exposure to heparin in patients who were later found to have the diagnosis of HITT. There should be a high degree of suspicion if platelet counts drop by 50% in 4-10 days after exposure to heparin and/or evidence of any venous or arterial thrombosis.
Conclusions:
HITT is a rare but potentially life-threatening condition following heparin administration, especially following coronary bypass surgery. If there is a high index of suspicion, early initiation of empiric therapy should be initiated as confirmatory testing may take up to a week to return. It is also important to be aware of prior heparin exposure, as future adverse thrombotic outcomes may be secondary to undiagnosed HITT.