Fibrinogen and D-dimer were also elevated to 708 mg/dL and 1

Fibrinogen and D-dimer were also elevated to 708 mg/dL and 1.44 fibrinogen equivalent units, respectively. heparin, enoxaparin, heparin-induced thrombocytopenia, COVID-19 Introduction An outbreak of novel coronavirus (2019-nCoV) that began in Wuhan, China, is now a major public health concern worldwide. After the first reported case in the state of Washington, the number of cases in the United States has rapidly increased to over 2?000?000 with more than 100?000 deaths.1 In addition to the typical presentation of respiratory symptoms, hematologic complications have been a significant concern in these patients. Thrombocytopenia has been reported in up to 55% of patients with COVID-19.2 A meta-analysis of 9 studies has shown that platelet counts were significantly lower in those with more severe COVID-19 infection, and thrombocytopenia predicts mortality.2 Heparin-induced thrombocytopenia (HIT) is a differential for thrombocytopenia, especially in the intensive care setting. In one review, the authors suggested that clinicians routinely evaluate all COVID-19 patients on heparin for indices of HIT by performing the 4T score.3 We report a case of HIT in a patient with critical COVID-19 infection. Also, we briefly describe 4 other cases that were initially managed as HIT, until proven later not to be true HIT, based on the functional assay. Case Description A 63-year-old male without comorbidities presented with 1 week of dry cough, myalgias, and Vancomycin hydrochloride diarrhea. On examination, he was afebrile but appeared to be in distress, saturating at 89% on room air. Chest X-ray showed bilateral interstitial opacities. Initial laboratory tests revealed an elevated C-reactive protein of 24.49 mg/dL and a high interleukin-6 level of 58 pg/mL. Fibrinogen and D-dimer were also elevated to 708 mg/dL and 1.44 fibrinogen equivalent units, respectively. The platelet count and liver function tests were within normal limits. He was diagnosed with COVID-19 by nasopharyngeal reverse-transcriptaseCpolymerase chain reaction. Low-molecular-weight heparin was started for thromboprophylaxis. On day 2 of admission, he developed progressive worsening of dyspnea and was transferred to the intensive care unit (ICU). On ITGB2 day 7, his right lower extremity was noted to be swollen. Ultrasound duplex Vancomycin hydrochloride revealed a nonocclusive thrombus within the right common femoral vein. He was started on therapeutic anticoagulation for deep vein thrombosis with enoxaparin, which was switched to unfractionated heparin (UFH) later, due to worsening renal function. On the same day, due to worsening respiratory failure, he was intubated and mechanically ventilated. Between days 11 and 12 of hospitalization, platelet count dropped from 304?000 to Vancomycin hydrochloride 96?000 cells/L. He had a high pretest probability for HIT with a 4T score of 6. HIT antibody testing (anti-PF4/heparin antibody, by enzyme-linked immunosorbent assay) was sent, which returned positive with an optical density (OD) of 1 1.243 units. Heparin drip was discontinued and was switched to argatroban. Unfortunately, he died a day later, following a cardiac arrest. Serotonin release assay (SRA) eventually returned positive, with 49% serotonin release at low UFH dose (0.1 IU/mL) with a reduction to 0% release at high UFH dose (100 IU/mL). This confirmed the diagnosis of HIT. Other Patients With COVID and Possible HIT We encountered 4 additional patients admitted to our ICU with a diagnosis of acute respiratory distress syndrome secondary to COVID-19 infection with thrombocytopenia, and an intermediate to high pretest probability for HIT. Due to a positive platelet factor 4 (PF4) antibody, they were started on an argatroban, pending send out results of Vancomycin hydrochloride OD levels and functional assay. However, the SRA was negative. Interestingly, their clinical characteristics (reported in Table 1) were similar to those of our patients with true HIT. Two of these patients had a confirmed Vancomycin hydrochloride deep vein thrombosis, and.