ABSTRACT
SESSION TITLE: Pathologies of the Post-COVID-19 World SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: SARS-CoV-2 related autoimmune and thrombotic complications due to vigorous immune system stimulation and induction of hypercoagulable state are not uncommon. Two hypotheses have been proposed for thrombotic microangiopathy associated with low ADAMTS13 levels in patients with COVID-19 disease. First underscores a significant increase in von Willebrand factor (vWF), likely due to endothelial activation, that overwhelms ADAMTS13. It is observed in the absence of thrombocytopenia or ADAMTS13 inhibitor. The second highlights the formation of autoantibodies against ADAMTS13 because of an immunological trigger (SARS-CoV-2), resulting in the diagnosis of TTP. CASE PRESENTATION: This is a case of a 72-year-old Caucasian man with a history of hypertension, diabetes, chronic obstructive lung disease, and asymptomatic SARS-CoV-2 infection three weeks ago who was transferred to our institution to initiate plasmapheresis for suspected TTP due to new-onset confusion, anemia and worsening renal function. Patient had presented with confusion a day before transfer. Vital signs were remarkable for tachycardia (heart rate of 105 beats/min). Labs were significant for anemia (hemoglobin:6.7 g/dL), thrombocytopenia (platelet count:13 K/µL), acute kidney injury (creatinine:1.8 mg/dL), elevated lactate dehydrogenase (1983 IU/L), high bilirubin (2.3 mg/dL), low haptoglobin (<4 mg/dL), and demonstration of schistocytes on peripheral smear. The coagulation profile was normal. On arrival, he required emergent intubation due to multiple seizures. Computed tomography scan of the head was normal. SARS-CoV-2 molecular testing was negative. Given a PLASMIC score of six, urgent plasmapheresis and high-dose methylprednisolone were started. Screening for human immunodeficiency virus, hepatitis viruses, Epstein-Barr virus, and Cytomegalovirus were negative. Subsequently, his ADAMTS13 activity resulted as being ≤5% with an elevated inhibitor Bethesda titer of 0.9 (normal < 0.4). The patient completed six sessions of plasmapheresis. He was discharged on steroid taper and weekly rituximab. DISCUSSION: COVID-19 associated de-novo TTP has been mostly reported with typical COVID-19 symptoms within a few days of a positive test. One report described presentation with only neurological symptoms 19 days after a positive test with low autoantibody titers, favoring the hypothesis of consumption of ADAMTS13. To the best of our knowledge, this is the first case of new, late-onset immune TTP developing three weeks after asymptomatic COVID-19 infection with a robust positive inhibitor screen and infinitesimal ADATMS13 levels. The temporal sequence of events and lack of other plausible causes aided in the diagnosis of COVID-19 induced TTP. CONCLUSIONS: Our report aims to make clinicians aware of ruling out TTP as a cause of thrombocytopenia and/or altered mental status in patients with past COVID-19 infection, aiding in early management. Reference #1: 1. Mancini I, Baronciani L, Artoni A, Colpani P, Biganzoli M, Cozzi G, Novembrino C, Boscolo Anzoletti M, De Zan V, Pagliari MT, Gualtierotti R, Aliberti S, Panigada M, Grasselli G, Blasi F, Peyvandi F. The ADAMTS13-von Willebrand factor axis in COVID-19 patients. J Thromb Haemost. 2021 Feb;19(2):513-521. doi: 10.1111/jth.15191. Epub 2020 Dec 18. PMID: 33230904;PMCID: PMC7753796. Reference #2: 2. Tehrani HA, Darnahal M, Vaezi M, Haghighi S. COVID-19 associated thrombotic thrombocytopenic purpura (TTP);A case series and mini-review. Int Immunopharmacol. 2021;93:107397. doi:10.1016/j.intimp.2021.107397 Reference #3: 3. Beaulieu, M.-C., Mettelus, D.S., Rioux-Massé, B. and Mahone, M. (2021), Thrombotic thrombocytopenic purpura as the initial presentation of COVID-19. J. Thromb. Haemost., 19: 1132-1134. https://doi-org.libproxy.uams.edu/10.1111/jth.15231 DISCLOSURES: No relevant relationships by Harmeen Goraya No relevant relationships by PRACHI SALUJA
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TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: Several studies have observed thrombotic complications in COVID-19 patients with rates as high as 30%. We present two COVID-19 cases of arterial and venous thrombotic complications. CASE PRESENTATION: A 64-year-old African American female was admitted for worsening respiratory failure due to COVID-19. HIT panel was obtained due to worsening thrombocytopenia, as the patient was on heparin for venous thrombosis prophylaxis, which was negative. Duplex of the lower extremities performed on hospital day 12 showed an acute non-occlusive deep vein thrombosis of the left common femoral vein, for which therapeutic heparin was initiated. On hospital day 25, the patient was found to have right digit ischemia with no flow to the right ulnar artery secondary to an occlusive arterial thrombus. Hematology was consulted for severe thrombocytopenia and considered to treat empirically for ITP with IVIG;however, the patient continued to decompensate and the family elected for comfort care measures. The patient expired on hospital day 30.Our second case report is a 64-year-old African American male presented from a local prison with worsening shortness of breath and was found to have COVID-19. Shortly after arrival from the ED to ICU, the patient went into cardiac arrest, ACLS was initiated and ROSC was achieved. The patient was in torsades and Vfib rhythm. He underwent left heart catheterization on hospital day 1 and was found to have 100% occlusion of obtuse marginal and underwent successful percutaneous coronary intervention with a drug-eluting stent to OM2. On hospital day 8, the patient was found to have digit ischemia of the right first through third digits. Arterial and venous duplex showed thrombotic occlusion of the right radial artery from the mid-forearm to the wrist and an acute deep vein thrombus of the left subclavian and axillary veins. DISCUSSION: COVID-19 can be associated with arterial and venous thrombosis as highlighted by our two cases. Even though the pathophysiology of thromboembolic complications in COVID-19 is not reported in the literature, it is implicated due to inflammation, hypoxia, immobilization, and DIC. In a study done by Klok et al in COVID-19 ICU patients, 27% of the study population had CTPE/Ultrasonography confirmed venous thromboembolism and 3.7% had arterial thrombosis compared to 12% of venous thrombosis in the ICU. The mechanism for hyper-coagulability in COVID infection is not known, it has been linked to the inflammatory response rather than specific properties of the virus. This association of excess inflammation and COVID-19 with subsequent activation of coagulation has been implicated in the pathogenesis of thrombosis. CONCLUSIONS: Intermediate to therapeutic anticoagulation may be necessary to prevent venous and arterial thromboembolic events in ICU patients admitted with COVID-19 given their excessive inflammatory state. REFERENCE #1: Connors JM, Levy JH. COVID-19 and its implications for thrombosis and anticoagulation. Blood, The Journal of the American Society of Hematology. 2020 Jun 4;135(23):2033-40. REFERENCE #2: Leisman DE, Deutschman CS, Legrand M. Facing COVID-19 in the ICU: vascular dysfunction, thrombosis, and dysregulated inflammation. Intensive Care Medicine. 2020 Apr 28:1-4. REFERENCE #3: Middeldorp S, Coppens M, van Haaps TF, Foppen M, Vlaar AP, Müller MC, Bouman CC, Beenen LF, Kootte RS, Heijmans J, Smits LP. Incidence of venous thromboembolism in hospitalized patients with COVID-19. Journal of Thrombosis and Haemostasis. 2020 May 5. DISCLOSURES: No relevant relationships by Sarenthia Epps, source=Web Response No relevant relationships by Harmeen Goraya, source=Web Response No relevant relationships by Raga Deepak Reddy Palagiri, source=Web Response