Case Presentation: A 73-year-old female with a history of ascending aortic aneurysm repaired by ascending aortic replacement with hemi-arch replacement in June presented in July for symptomatic low home blood pressure readings. Her workup incidentally revealed an absolute eosinophil count (AEC) of 1800/µL with thrombocytosis (726 x1000/µL) and mild leukocytosis (11.5×1000/µL). Repeat testing demonstrated a continued rise in AEC, prompting a workup for her hypereosinophilia (HE). The patient denied recent travel, her review of systems was unremarkable, and her medication list did not reveal an offending agent. A complete hematologic, infectious, and rheumatologic workup was unrevealing (Table 1). As there was no history, imaging, or lab evidence of end-organ damage, she was discharged to follow up with hematology given improvement in her chief concern. Follow-up later revealed spontaneous resolution of HE after her AEC peaked at 4500/µL. Since her diagnostic workup was unrevealing, her recent surgery was carefully reviewed. During the surgery, she received TachoSil, a topical fibrin sealant patch consisting of human fibrinogen and thrombin (1). Through evaluation of post-marketing analysis, it was discovered that TachoSil has been associated with eosinophilia. Given this association and the chronicity of the patient’s abnormal AEC (Fig. 1), her TachoSil was determined to be the cause of her HE.
Discussion: HE (AEC ≥1500/µL) is not an uncommon clinical finding that warrants evaluation, since eosinophilic infiltration of tissues can lead to irreversible, life-threatening organ damage. It is caused by numerous conditions such as allergic, infectious, inflammatory, and neoplastic disorders. Workup begins with a clinical history focusing on medication history, travel, and risk factors for malignancy (2). Initial laboratory evaluation should assess hematological status, organ function, inflammation, and immune status (3). If a comprehensive evaluation is unrevealing, clinicians should consider drug-induced HE as a diagnosis of exclusion. It can be challenging to determine whether HE is caused by therapeutic compounds given the diversity of agents associated with the condition and the inconsistent time it takes to develop a reaction after exposure. As in our case, clinicians can try to elucidate the sequence of events from introduction of a new treatment to discovery of HE and/or symptoms to help with diagnosis (2,3). While clinical guidelines recommend reviewing patient’s medications/supplements during the evaluation, we highlight the importance of including etiologies from surgical grafts/implants in the differential diagnosis.
Conclusions: HE is potentially harmful regardless of etiology and requires careful evaluation. Our case highlights the TachoSil patch as a rare cause of HE, while emphasizing the importance of recognizing possible adverse effects of surgical grafts/implants when caring for patients.
