Case Presentation: 55 year old man with history of diabetes, hypertension and remote history of testicular cancer treated with chemotherapy and orchiectomy in 1993 and currently with no active malignancy presents with fever and malaise which began about a week ago. On admission, his laboratory results were notable for leukocytosis with a white blood cell count of 12.5, lactic acidosis of 2.5 and platelet count of 453. His chest radiograph demonstrated diffuse bilateral reticulonodular opacities and more confluent nodular opacities at the lung bases. He initially required oxygen via nasal cannula for oxygen desaturations in the 80s, initially and gradually required high flow oxygen within 48 hours of hospitalization. The patient was treated with 5 days of remdesevir and dexamethasone based on available clinical guideline at the time. He was also initiated on enoxaparin per VTE prophylaxis. He was given empiric antibiotics with piperacillin-tazobactam given concerns for pneumonia based on above radiographic findings and clinical symptoms, especially with respect to worsening hypoxia and persistent fevers. Despite clinical treatment, patient continued to become more hypoxic, a d-dimer level was found to exceed 20, our maximal measurable value. A chest CT showed no central pulmonary embolism, extensive Ground glass opacities in the lower lobes. The patient’s enoxaparin dose was modified to give full dose anticoagulation. Of note, the patient gradually required less oxygen on high flow and eventually three days later, he was transitioned back to nasal cannula. However, he was persistently requiring up to 5L via nasal cannula despite our interventions and his platelets were noted to be rising up to 900s. He was thus initiated on aspirin and evaluated for genetic testing and found to lack Jak-2/STAT and MPL mutations, thus supporting the etiology of thrombosis as a consequence of an inflammatory process related to COVID-19. Patient clinically improved and was discharged with aspirin. During follow-up, his platelets were noted to have normalized to 396.
Discussion: Analysis of data in COVID-19 patients have so far revealed a strong association with hypercoagulable state that is still being studied. The patient’s thrombocytosis is a result of reactive process secondary to underlying COVID-19 infection. The patient had no symptoms suggestive of autonomous causes of thrombocytosis. He has a history of prior chemotherapy, dated more than 25 years ago, which he was unable to recall, if treated with cisplatin or etoposide, there is a potential risk of secondary myeloid malignancy. However, there was no evidence of this in his blood cell counts. Further more, his platelet count continued to rise despite antibiotic treatment as his hypoxia worsened. The work up of diagnostic molecular pathology to evaluate for myeloproliferative neoplasm panel for JAK2 mutation, BCR-ABL and MPL mutations were negative.
Conclusions: This case highlights the importance of recognizing thrombosis as an important contributor in the severity of covid illness. His treatment required careful attention to his pneumonia, coagulopathy and thrombosis which persisted with hypoxia and did not improve until it was adequately addressed with aspirin. Preliminary review of the literature indicate that thrombocytosis is not as common as thrombocytopenia in covid. However, there are observed cases where thrombocytosis could be a marker for worsening severity and may support the idea that these patients may benefit from short-term antiplatelet therapy.