HYPERCOAGULABLE STATE: AN ENIGMA IN COVID-19 INFECTION

Abstract

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Coronavirus disease 2019 (COVID-19) is associated with a hypercoagulable state predisposing patients to both arterial and venous thrombosis. The pathophysiology is not completely understood as new data continues to emerge. Our case features a patient with multiple causes of hypercoagulability and a similar disease profile as catastrophic antiphospholipid syndrome (CAPS). CASE PRESENTATION: A 28-year-old male with a past medical history of obesity presented with dyspnea on exertion, presyncope, and bilateral lower extremity edema. Physical exam revealed jugular venous distension and 3+ bilateral pitting edema. COVID-19 PCR was positive. CTA chest showed bilateral pulmonary emboli and right lower lobe pulmonary infarcts. During the hospital course, he developed chest pain and elevated troponin. EKG revealed an anterolateral STEMI. Cardiac catheterization showed 100% LAD occlusion that was not amenable to stenting. An echocardiogram showed cardiomyopathy with an ejection fraction of 18%. Other laboratory tests revealed hypoalbuminemia and nephrotic-range proteinuria, confirming nephrotic syndrome. Renal biopsy was a limited sample but showed mild epithelial foot process effacement. Immune-complex disease was ruled out. The patient was discharged on apixaban. Two weeks later, he presented with altered mental status and right-sided weakness. CTA and CTP showed large core infarct in the left middle cerebral artery territory. Due to core infarction volume, he was not a candidate for endovascular intervention. Hypercoagulability workup revealed positive anti-cardiolipin antibody IgG and IgM, suggestive of an acquired antiphospholipid syndrome (APS) secondary to COVID-19. Other causes of hypercoagulability were ruled out. He was transitioned to warfarin outpatient. DISCUSSION: This case represents a multifactorial etiology of hypercoagulable state secondary to COVID-19-infection, antiphospholipid antibodies (APLA), and nephrotic syndrome. One mechanism of COVID-19 hypercoagulability is related to neutrophil activation and unregulated formation of neutrophil extracellular traps (NETS) which can cause platelet activation and thrombin generation. Viral infections have been associated with the production of APLA. A study among hospitalized patients with COVID-19 infection showed that more than 50% were transiently positive for APLA, which are prothrombotic. This case bears resemblance to CAPS, which is a severe form of APS with multi-organ involvement in a short period of time. CONCLUSIONS: This case highlights the need for further investigation on the pathophysiology of COVID-19 hypercoagulability state, the immunological similarities between COVID-19 and CAPS, and the population that should receive thromboprophylaxis as well as the duration of therapy. REFERENCE #1: Zuo Y, Estes S, Ali R et al. Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19. Sci. Transl. OMed. 2020 Nov;12(570):eabd3876 REFERENCE #2: Tung M, Tan B, Cherian R, et al. Anti-phospholipid syndrome and COVID-19 Thrombosis: Connecting the dots. Rheumatology Advances in Practice. 2021 Feb;5(1):rkaa081 REFERENCE #3: Ortega-Paz L, Capodanno D, Montalescot G, et al. Coronavirus Disease 2019– Associated Thrombosis and Coagulopathy: Review of the Pathophysiological Characteristics and Implications for Antithrombotic Management. J Am Heart Assoc. 2021;10:e019650 DISCLOSURES: No relevant relationships by Mohammad Omar Butt, source=Web Response No relevant relationships by Lisa Ezegbu, source=Web Response No relevant relationships by Saima Mili, source=Web Response No relevant relationships by Tamim Naber, source=Web Response No relevant relationships by Azka Sadiq, source=Web Response No relevant relationships by Sivashankar Sivaraman, source=Web Response