Introduction
As with any new disease, the importance of identifying the various manifestations and sequelae become paramount in not only the treatment but improving clinical outcomes in those affected by the disease. Considering that COVID-19 is not only new, but its extensive spread to the point of a worldwide pandemic makes identifying the various sequelae of this pathogen even more important. ITP is an acquired condition that has been linked to several viral diseases. In this case report, we present a 47-year-old with an otherwise benign medical history who develops what was suspected to be ITP, secondary to a severe COVID-19 infection. The objective of this report is to add evidence to the ever-growing body of information on COVID-19 and its various clinical manifestations and complications.
Case Presentation
A 47-year-old male with an otherwise unremarkable medical history, presented with primary complaints of worsening shortness of breath. The patient had been diagnosed with COVID-19 two days prior to presentation. At the time of presentation, the patient was hypoxic with an oxygen saturation of 85% on room air, tachycardic with a regular rhythm, and tachypneic. He demonstrated dry oral mucosa and bilateral crackles were noted on lung auscultation. The remainder of the physical exam was unremarkable. The patient was placed on 4L nasal cannula and started on convalescent plasma, dexamethasone, lovenox, and azithromycin as per hospital protocol at the time. On the night of admission, the patient oxygen requirements rapidly increased and on the following day was moved to the intensive care unit on bilevel positive pressure ventilation. Remdesivir was initiated when he was transitioned to the ICU. On day 6, the patient was noted to have a 50% reduction of his platelets and he became febrile. The patient was taken off lovenox and started on fondaparinux as well as broad spectrum antibiotics, after cultures were drawn. The following day, the patient’s platelets dropped to 17,000. The patient was given one apheresis unit of platelets with subsequent drop in count to 13,000. The patient was started on intravenous immunoglobulins (IVIG) at 400mg/kg and prednisone at 1mg/kg. Work-up including a heparin induced thrombocytopenia (HIT) panel which was negative and peripheral smear which showed no schistocytes and only thrombocytopenia. The patient’s INR and fibrinogen showed mild elevations. With the initiation of IVIG, the patient’s platelets began to increase. He completed a 5-day course of IVIG without complication. The blood cultures came back negative and antibiotics where de-escalated. The patient was continued on high dose steroids for 2-weeks and then was started on a 7-week taper. The patient completed a 10-day course of both dexamethasone and remdesivir. His oxygen requirement was eventually de-escalated to nasal cannula, and he was transferred to the floor. Throughout his hospital course, the patient did not experience any purpura, thrombosis, petechiae, gingival bleeding, epistaxis and/or significant bleeding event. He had no notable alterations in neurological function. After continued improvement, he was discharged home on nasal cannula with home oxygen. On outpatient follow up, the patient platelet count continued to recover and he no longer required supplemental oxygen.
Discussion/Conclusion
ITP is an autoimmune disorder that can be categorized as either primary or secondary in nature. In this case, we describe secondary ITP due to the novel COVID-19 virus. Prior to this, the annual incidence of ITP in the US, calculated in in a retrospective cohort study between 2010-2016 was approximately 6.1 per 100,000 persons, with estimates of about 20,000 new cases a year.1 Viral vectors have been described in the medical literature as causing secondary ITP. Given a negative evaluation for other causes of ITP and the patient’s recent diagnosis of COVID, this case report likely demonstrates a case of ITP secondary to COVID-19 infection.
In this case, we see an otherwise healthy male who presented with severe COVID-19 infection requiring ICU level care who developed ITP, suspected to be secondary to his severe COVID-19 infection. Drug induced ITP was ruled out by tailoring anticoagulation and antibiotics to medications which were not associated with ITP. Adding to the evidence for ITP, the patient had a reduction in his platelet count shortly after apheresis transfusion, giving support to an immune mediated pathology. The use of IVIG and high dose steroids which achieved good clinical response leading to the diagnosis of ITP. Confirmatory testing resulted as treatment continued which showed a negative HIT panel and no evidence of schistocytes on peripheral smear.
Since this case was in the earlier phase of the pandemic, the amount of information regarding COVID-19 induced ITP was extremely limited. There were no documented cases at the time in Mississippi, and therefore the presumptive diagnosis was made and confirmed by treatment response. The purpose of this case report is to document ITP as a confirmed complication of COVID-19, which had not previously been seen in Mississippi. Over the course of the pandemic, other reportable cases of COVID-19 associated ITP have been demonstrated.2–4 Similar to other published cases, our patient responded well to IVIG, and high dose glucocorticoids, which is consistent with the treatment of secondary ITP.