key: cord-0806445-8cu3a29x
authors: Kewan, Tariq; Saleem, Talha; daw, hamed; Abdelghaffar, Bahaa
title: COVID-19 COAGULOPATHY SECONDARY TO ACTIVATING PLATELET ANTIBODIES
date: 2021-10-31
journal: Chest
DOI: 10.1016/j.chest.2021.07.410
sha: 1bab76e7e46c0d31674066974ef26b710112bfa0
doc_id: 806445
cord_uid: 8cu3a29x

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Coagulopathies have been extensively reported in COVID-19 patients (1). CASE PRESENTATION: A 58-year old female presented to the emergency department (ED) with 2-weeks history of shortness of breath. A nasopharyngeal swab was positive for SARS-CoV-2. She was treated and discharged on room air. D-dimer (DD) and platelet (plt) count at the time of discharge were within normal. Six days after discharge she presented to the ED with severe abdominal and right leg pain. Lower extremity pulses were present by doppler but hard to palpate. Laboratory tests showed elevated DD (27,820 ng/ml) and elevated plt (530 x109/L), table-1. Computed tomography scan (fig-1) of the abdomen and pelvis showed multiple wedge-shape infarcts in the liver, spleen, and right kidney and acute thrombosis of the right common iliac artery. Acute deep vein thrombosis in the lower and upper extremities were excluded by US. Duplex US of the right lower extremity showed ankle brachial index of 0.2. The patient was admitted and started on heparin therapy. On day 2, plt count dropped to 127 x 109/L. The 4T score was 5, heparin was stopped and argatroban was started. Serotonin release assay was sent and showed no inhibition with high dose heparin. However, non-heparin dependent anti-platelet activating antibodies (class I HLA antibodies) were detected. Anti-platelet factor-4 was negative and patient was restarted back on heparin. Thrombophilia and autoimmune work up were negative. Patient was discharged on low-molecular weight heparin. Plt count was 179 x109/L before discharge. DISCUSSION: Recent study published by Bilaloglu showed that 533 (16.0%) COVID-19 patients had at least one thrombotic evet during hospitalization. Of all 3334 patients, only 32 (1.0%) had acute limb ischemia, upper extremity arterial thrombosis, renal, and splenic infarcts, and portal vein thrombosis (2). In another case series, 4 of the reported 7 cases developed progressive irreversible lower limb ischemia. Two patients presented with lower limb ischemia and the other two developed severe thrombosis after 4 and 15 days respectively. Of the reported lab values, two patients had D-dimer levels more than 20,000 ng/ml and the same two were thrombocytopenic (1). Interestingly, our patient had reversible limb ischemia as shown by the repeated duplex US done after discharge. Nicolai and colleagues reported that plts hyperactivation and possible immuno-thrombosis may play a role in the pathogenesis of coagulopathy among severe COVID-19 patients (3). In our case, patient had hypercoagulability secondary to activating anti-platelets antibodies, a novel finding that can help understanding the pathogenesis of COVID-19 induced hypercoagulability. CONCLUSIONS: COVID-19 associated coagulopathy can be un-predictable. Activating anti-plt antibodies may play a role in the pathogenesis of COVID-19 coagulopathy. REFERENCE #1: Kashi M, Jacquin A, Dakhil B, et al. Severe arterial thrombosis associated with Covid-19 infection. Thromb Res 2020;192:75-7. REFERENCE #2: Bilaloglu S, Aphinyanaphongs Y, Jones S, Iturrate E, Hochman J, Berger JS. Thrombosis in Hospitalized Patients With COVID-19 in a New York City Health System. JAMA 2020. REFERENCE #3: Nicolai L, Leunig A, Brambs S, et al. Immunothrombotic Dysregulation in COVID-19 Pneumonia is Associated with Respiratory Failure and Coagulopathy. Circulation 2020. DISCLOSURES: No relevant relationships by Bahaa Abdelghaffar, source=Web Response No relevant relationships by hamed daw, source=Web Response No relevant relationships by Tariq Kewan, source=Web Response No relevant relationships by Talha Saleem, source=Web Response

A 58-year old female presented to the emergency department (ED) with 2-weeks history of shortness of breath. A nasopharyngeal swab was positive for SARS-CoV-2. She was treated and discharged on room air. D-dimer (DD) and platelet (plt) count at the time of discharge were within normal. Six days after discharge she presented to the ED with severe abdominal and right leg pain. Lower extremity pulses were present by doppler but hard to palpate. Laboratory tests showed elevated DD (27,820 ng/ml) and elevated plt (530 x109/L), table-1. Computed tomography scan (fig-1) of the abdomen and pelvis showed multiple wedge-shape infarcts in the liver, spleen, and right kidney and acute thrombosis of the right common iliac artery. Acute deep vein thrombosis in the lower and upper extremities were excluded by US. Duplex US of the right lower extremity showed ankle brachial index of 0.2. The patient was admitted and started on heparin therapy. On day 2, plt count dropped to 127 x 109/L. The 4T score was 5, heparin was stopped and argatroban was started. Serotonin release assay was sent and showed no inhibition with high dose heparin. However, non-heparin dependent anti-platelet activating antibodies (class I HLA antibodies) were detected. Anti-platelet factor-4 was negative and patient was restarted back on heparin. Thrombophilia and autoimmune work up were negative. Patient was discharged on low-molecular weight heparin. Plt count was 179 x109/L before discharge.

DISCUSSION: Recent study published by Bilaloglu showed that 533 (16.0%) COVID-19 patients had at least one thrombotic evet during hospitalization. Of all 3334 patients, only 32 (1.0%) had acute limb ischemia, upper extremity arterial thrombosis, renal, and splenic infarcts, and portal vein thrombosis (2). In another case series, 4 of the reported 7 cases developed progressive irreversible lower limb ischemia. Two patients presented with lower limb ischemia and the other two developed severe thrombosis after 4 and 15 days respectively. Of the reported lab values, two patients had D-dimer levels more than 20,000 ng/ml and the same two were thrombocytopenic (1). Interestingly, our patient had reversible limb ischemia as shown by the repeated duplex US done after discharge. Nicolai and colleagues reported that plts hyperactivation and possible immuno-thrombosis may play a role in the pathogenesis of coagulopathy among severe COVID-19 patients (3). In our case, patient had hypercoagulability secondary to activating anti-platelets antibodies, a novel finding that can help understanding the pathogenesis of COVID-19 induced hypercoagulability.

CONCLUSIONS: COVID-19 associated coagulopathy can be un-predictable . Activating anti-plt antibodies may play a role in the pathogenesis of COVID-19 coagulopathy.

Severe arterial thrombosis associated with Covid-19 infection

Thrombosis in Hospitalized Patients With COVID-19 in a New York City Health System