Peer-review started: October 6, 2021
First decision: January 12, 2022
Revised: January 24, 2022
Accepted: February 27, 2022
Article in press: February 27, 2022
Published online: April 25, 2022
Processing time: 195 Days and 4.5 Hours
Although it is well established that coronavirus disease 2019 (COVID-19) is associated with inflammation and a prothrombotic state leading to stroke and venous thromboembolism (VTE), the nuances of this association are yet to be uncovered[1]. Many studies link elevations in inflammatory markers to cases of thromboembolism. Most reports of thromboembolism associated with COVID-19 occur in the venous circulation during or just after the initial hospitalization due to COVID-19[2]. It is unclear how long the hypercoagulable effect of COVID-19 lasts.
We present a unique case of a 65-year-old-female who presented to her primary care doctor with a sore throat, cough, fatigue, congestion, diarrhea, headache, and anosmia. She tested positive for severe acute respiratory syndrome coronavirus 2 and received a bamlanivimab infusion 9 days later. After recovering from the acute illness, she received the Pfizer-BioNTech COVID-19 vaccine. Months later, she presented to the Emergency Department (ED) complaining of right sided shoulder pain and motor weakness in her left hand while trying to type on a keyboard. On presentation to the ED, her calculated Padua prediction score for risk of VTE was two and inflammatory markers were not elevated. She was found to have a brachiocephalic artery occlusion as well as an ischemic stroke which was treated with heparin.
This case suggests hypercoagulability due to COVID-19 may extend further than current literature suggests, to at least six months.
Core Tip: Acute severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with hypercoagulability. However, in this unique case, a patient suffered two separate thromboembolisms, one in the brachiocephalic artery and an ischemic stroke. With only two risk factors at baseline and no corresponding elevation in inflammatory markers, we hypothesize that the clots grew slowly over time which would not cause acutely elevated inflammatory markers. Although her SARS-CoV-2 infection occurred six months prior to her Emergency Department presentation, we hypothesize the hypercoagulable state caused by coronavirus disease 2019 was contributory. Additionally, it is unlikely the vaccination alone caused her thrombosis, yet it is still possible it had a contributory effect.