A 61-year-old healthy male presented with one-hour of chest pain and exertional dyspnea. He had no surgical history, exposure to heparin, or family history of thrombophilic disease. Upon presentation, BP was 96/68, HR 109, and RR 20. He had JVD and pericardial friction rub but no lower extremity edema or calf tenderness. He was diagnosed with cardiac tamponade due to acute S. pneumoniae pericarditis and started on ceftriaxone. Labs were notable for a WBC of 24,800/µL and a platelet count of 800,000/µL, attributed to the underlying infection. The patient received subcutaneous heparin prophylactically. The patient’s condition improved, and platelets reduced to 369,000/µL by day ten. An echocardiogram four days later revealed a prolapsing elongated mass in the right atrium originating from the IVC, concerning for thrombus. The patient was offered an emergent AngioVac to aspirate the mass, but he declined. Unfortunately, the patient then suffered PEA arrest, likely due to massive PE caused by the atrial mass. Emergently, an Alteplase bolus was given, and heparin infusion was started with achievement of ROSC. The following day the platelet count rapidly declined to 39,000/µL. Nine apheresis platelet units were transfused over seven days (including cross-matched platelets) to maintain a platelet count above 10,000/µL. The patient had no petechiae or bleeding. Analyses revealed low fibrinogen, and peripheral smear with large platelets and occasional schistocytes. Ultrasound was negative for hepatosplenomegaly. Heparin-induced thrombocytopenia (HIT) was suspected with a 4T score of 6 (platelet fall >50%, platelet fall <1 day, new thrombosis). PF4 (antiplatelet factor 4) EIA was twice negative, but the serotonin release assay (SRA) was positive, confirming HIT. Heparin was discontinued, and the patient was started on fondaparinux. At twenty days post-arrest, he was discharged on coumadin with a platelet count of 647,000/µL.
Discussion: HIT is a prothrombotic drug reaction: thrombosis is the presenting symptom in 25% of individuals. Diagnosis is guided by the 4Ts pretest clinical scoring system, followed by PF4 EIA. We overlooked the platelet trend initially since the patient presented with thrombocytosis. We also doubted our clinical judgement due to the discordant PF4 EIA results. However, with high suspicion, heparin should be discontinued until confirmation. Moreover, PF4 EIA can be falsely-negative, despite having high negative predictive values (90-99%). Possible causes are involvement of antigens other than PF4/heparin complexes, dilutional effects of transfusions, or undetectable titers in early HIT. We suggest simultaneous SRA testing in cases with high pretest probability.
Conclusions: High clinical suspicion for HIT may trump PF4-EIA results. Although massive PE’s are rare in HIT, this case emphasizes the importance of trending platelet counts in patients exposed to heparin before thrombocytopenia and catastrophic events ensue.