Don't forget arterial thrombosis in patients with COVID-19: A case series

Abstract

Introduction The acute disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS COV-2) is accompanied by a hypercoagulable state. Multiple publications have described the venous thromboembolic events associated with coronavirus disease 2019 (COVID-19) but arterial thromboembolic events have yet to be described. Cases description We describe five COVID-19 patients that developed severe morbidity as a result of occlusive arterial thromboembolic events occurring despite treatment with low molecular weight heparin. All cases presented with an acute confusional state and were accompanied by rapid elevations of lactate and D-dimers and leukocytes. The end organs involved were the kidneys, spleen, liver, lungs, central nervous system, intestines and limbs. Only one of the five patients survived. Conclusion COVID-19 is associated with not only venous but also arterial thromboembolic events. Further research is required to clarify the incidence, causes and possible modes of prevention of this potentially lethal disease complication.

Splenic Artery Infarct Requiring Surgery: A Rare Complication of COVID-19 Infection

“…The most common causes of arterial obstruction are neoplasms, cardioembolic events, and hematological diseases; however, this event has also been linked to acute viral infections, which often trigger states of hypercoagulability [16][17][18][19]. SARS-CoV-2 infection is also associated with a prothrombotic state and an increased risk of venous and arterial thromboembolism [8,11,20].…”

“…In the case of a SARS-CoV-2 infection, endothelial integrity and normal venous blood flow may be dysregulated due to endothelial or vascular injury, resulting in venous stasis [8,[21][22][23]. Additionally, the cytokine storm that accompanies the response to coronavirus infection may activate the coagulation system, causing systemic inflammation, endothelial cell activation, and the release of tissue factors, predisposing the tissue to thrombosis [2,6,17,20,22]. Also, there is an abnormal increase in the levels of coagulation parameters, such as D-dimers, fibrin degradation products (FDP), thromboelastographic (TEG) values, and prolonged coagulation times (like activated partial-thromboplastin time, aPTT), which may be associated with coronavirus infection [11,16,[24][25][26][27].…”

“…Also, there is an abnormal increase in the levels of coagulation parameters, such as D-dimers, fibrin degradation products (FDP), thromboelastographic (TEG) values, and prolonged coagulation times (like activated partial-thromboplastin time, aPTT), which may be associated with coronavirus infection [11,16,[24][25][26][27]. Platelet function is also known to be affected by COVID-19 disease, i.e., abnormal platelet function may explain arterial thrombosis resulting from an increase in platelet activation at suboptimal thresholds and an increase in platelet aggregation in COVID-19 patients [20,25]. Despite these hypotheses, the exact mechanism underlying coronavirus-induced coagulopathy remains undetermined [16,28,29].…”

“…We found that the treatment and prevention strategies for such thrombotic events in the presence of COVID-19 infection were debatable [ 11 , 31 ]. The standard of care is antithrombotic treatment using medicines such as heparin, LMWH, ASA, apixaban, rivaroxaban, and antiplatelet agents such as clopidogrel and ticagrelor [ 20 , 45 ]. However, controversy arises as to whether hospital patients with COVID-19 infection without signs of thromboembolism should receive prophylactic or therapeutic anticoagulation [ 11 , 24 ].…”

Accelerated LVAD Pump Thrombosis in COVID-19 Patient: Case report and Mini review

“…Respiratory rate >30 bpm, arterial oxygen saturation less than 93% at rest, development of acute respiratory distress syndrome, septic shock, metabolic acidosis, and coagulopathy, including disseminated intravascular coagulation, are characteristics of severe cases. [2] In addition, patients infected with the COVID-19 virus have an increased risk of developing both venous and arterial thrombosis [3][4][5][6] Thrombocytopenia and an increase in D-dimer are the hemostatic changes caused by COVID-19 that are most frequently observed, and they are linked to a greater need for mechanical ventilation, admission to intensive care, and death. It has been noticed that patients who are older and have comorbid conditions are more likely to have a high mortality rate, [7] which is believed to be greatly influenced by blood vessel dysfunction and clot formation, as indicated by elevated D-dimer levels brought on by blood clots.…”