Drug-Induced Thrombocytopenia: A Critical Condition in Hospitalized Cancer Patients

Drug-induced thrombocytopenia (DIT) is a critical condition that is rarely encountered in hospitalized patients. In DIT, medications drive the destruction or consumption of platelets through immune or non-immune-related mechanisms. One common example of DIT is heparin-induced thrombocytopenia (HIT type 2), which is an immune-mediated condition where the combination of heparin and platelet factor 4 (PF4) results in an immunogenic complex that triggers a humoral immune response against the PF4 antigen. Another well-studied mechanism involves the generation of antibodies that bind to drugs covalently linked to platelet surface proteins, resulting in platelet destruction. This mechanism is often observed with small-molecule drugs like penicillins and cephalosporins.

DIT is typically detected 24-48 hours after the drug is administered, and platelet counts usually recover after the drug is discontinued. During the early stages of DIT, it can be challenging to differentiate between primary and secondary thrombocytopenia. In such cases, a trial of glucocorticoids may be warranted. In cases of severe thrombocytopenia or high risk of bleeding, intravenous immunoglobulin (IVIG) is frequently administered to expedite the recovery of platelet counts.

Here, we present a case of a 62-year-old female with stage III clear-cell carcinoma of the left ovary who was admitted for planned surgical resection and tumor debulking, which was complicated by severe postoperative thrombocytopenia. Of note, the patient has an extensive list of pharmacological and non-pharmacological allergies, including chlorhexidine, latex, lavender, chamomile, and calamine. On admission, the patient had a platelet count of 126 x 10(9)/L and hemoglobin of 9.4 g/dL. The patient received cefazolin for surgical prophylaxis. Cefazolin was continued, as this was not initially thought to be the etiology of thrombocytopenia. Despite platelet transfusions and administration of dexamethasone on postoperative days (POD), platelet counts continued to drop, with a nadir of less than 10x10(9)/L on POD 3. Hemoglobin, however, remained stable. Clinically, the patient did not exhibit any signs of active bleeding, such as petechiae, purpura, hematuria, or hematochezia. Due to refractory severe thrombocytopenia and a high risk of bleeding postoperatively, the patient was admitted to the intensive care unit and received IVIG, which led to a rapid increase in platelet counts to 49x10(9)/L by POD 7.

This case highlights how DIT can be a critical condition that can be difficult to identify and is often complicated by simultaneous high-risk factors, especially in hospitalized surgical cancer patients. Postoperative patients are prone to thrombocytopenia secondary to platelet consumption, which can lead to high-risk bleeding episodes resulting in severe anemia and shock. Furthermore, DIT can worsen bleeding in cancer patients who are already predisposed to bone marrow suppression and malignancy-related disseminated intravascular coagulopathy. Considering the combination of these two risk factors in surgical cancer patients, it is important to have a high suspicion for DIT should thrombocytopenia arise.

No relevant conflicts of interest to declare.