Heparin-induced thrombocytopenia after percutaneous coronary intervention complicated by hemothorax and pulmonary thromboembolism: The scylla and charybdis of hematology Free

Introduction: Heparin-induced thrombocytopenia (HIT) is an immune-mediated reaction to heparin caused by antibodies directed against heparin and platelet factor 4 (PF4) complexes. Despite thrombocytopenia, HIT causes a paradoxical prothrombotic state with risk of both venous and arterial thrombosis, most commonly deep venous thrombosis (DVT) and pulmonary embolism (PE). Rare instances of bleeding due to HIT have been reported, such as bilateral adrenal hemorrhage due to adrenal vein thrombosis or intraparenchymal hemorrhage due to cerebral venous thrombosis. Here, we report a case of HIT complicated by spontaneous hemothorax. To the best of our knowledge, no such case has been reported in the literature.

Case presentation: A 74-year-old male with a history of hypothyroidism, hypertension, diabetes mellitus, and chronic kidney disease presented with chest pain and was diagnosed with ST elevation acute MI (STEMI). He had emergent percutaneous coronary intervention (PCI), where he received 8000 IU of unfractionated heparin (UFH). On day 3 of hospitalization, a repeat staged PCI was done when he received 10,000 IU of UFH. On day 10, he was found to have a drop in platelets to 7000 /cu.mm (on day 6 - 160,000 /cu.mm). Peripheral blood smear showed decreased platelets and no schistocytes. Hematology was consulted, and due to high bleeding risk, antiplatelets were stopped. Antibodies to PF4/Heparin complex and serotonin release assay (SRA) were both tested positive, confirming the diagnosis of HIT. On day 12, he had worsening shortness of breath. A chest x-ray showed a new left pleural effusion, and a left-sided chest drain revealed hemothorax, draining 1.8 L of blood. He continued to have worsening hypoxia and breathlessness. A CT angiogram of the chest showed acute PE in the right upper, middle, and lower lobe segmental and subsegmental pulmonary arteries without right heart strain. Ultrasound venous doppler showed acute superficial venous thrombosis in the left cephalic and bilateral basilic veins and acute DVT in the right mid femoral vein. He continued to have severe thrombocytopenia and anemia requiring frequent transfusions of packed red cells and platelets. His condition precluded him from receiving any antiplatelet and anticoagulation therapy. On day 18, he developed new chest pain and hemodynamic decompensation. EKG showed recurrent STEMI in the inferior leads. The patient declined all further treatment, choosing comfort care, and succumbed to his illness.

Discussion: In HIT, a decrease in the platelet counts of more than 50% or thrombosis starting 5 to 10 days after exposure to heparin is the hallmark, as in our patient. Rarely, when platelet fall below 20,000 /cu.mm, which is unique to our case, other causes of thrombocytopenia, like consumptive coagulopathy, need to be ruled out. The incidence of HIT is up to 10 times higher with UFH compared to low-molecular-weight heparin. The risk is more following surgical intervention rather than medical therapy alone. The first step in a patient with thrombocytopenia and suspicion of HIT is to assess the pretest probability with the 4T scoring system (scores 0-8). Patients with intermediate (score 4-5) or high (score 6-8) probability, as in our patient (score 8), should be tested with Anti–PF4–heparin enzyme immunoassays. This test has excellent negative predictive value (98-99%). A positive test should be followed by a functional assay like SRA, which confirms the diagnosis. Our patient had a positive PF4/Heparin antibody (optical density 2.524, £ 0.3 negative) and a positive SRA. Those with a confirmed diagnosis need to be started on therapeutic-dose anticoagulation with argatroban, danaparoid, bivalirudin, or fondaparinux. Since the risk of bleeding is very low, platelet transfusions should be avoided as they increase the risk of thrombosis. However, in our case, a platelet nadir of 7000 /cu.mm with hemothorax necessitated multiple platelet transfusions and precluded initiation of argatroban, predisposing him to a highly prothrombotic state. This, along with his recent PCI and failure to continue antiplatelet therapy, led to a recurrent STEMI and ultimately his death.

Conclusion: Our case highlights a unique case of HIT with both thrombosis and life-threatening bleeding post-PCI that precluded the use of both anticoagulation and antiplatelets, underscoring the complexity of care, need for a multidisciplinary approach, and individualization of treatment in such cases.