COVID-19 Associated Large Vessel Thrombosis and Ischemic Stroke: A Case Series

Case Report

Austin J Clin Case Rep. 2020; 7(6): 1187.

COVID-19 Associated Large Vessel Thrombosis and Ischemic Stroke: A Case Series

Ans Alamami1*, Rabee Tawel1, Abdussalam Elgrewi2, Ahmed L M Abdussalam1 and Anam M Elarabi3

¹Medical Intensive Care Department, Hamad General Hospital, Hamad Medical Corporation, Qatar

²Internal Medicine Department, Hamad General Hospital, Hamad Medical Corporation, Qatar

³Pulmonology Department, Hamad General Hospital, Hamad Medical Corporation, Qatar

*Corresponding author: Ans Alamami, Critical Care Department, Hamad General Hospital, Hamad Medical Corporation, Qatar

Received: December 04, 2020; Accepted: December 22, 2020; Published: December 29, 2020


The novel severe acute respiratory syndrome coronavirus (SARS-COV-2) affects different people in different ways. Most infected people will develop mild to moderate respiratory flu-like illness and recover without the need for hospitalization. However, one of the not uncommonly observed extrapulmonary associations with SARS-COV-2 is developing severe large-vessel acute ischemic stroke. Moreover, COVID-19 virus-linked Cerebrovascular Accidents (CVA) were more severe and resulted in a higher risk for severe disability and mortality following acute insult. Although the pathophysiology is not fully understood, the neuro-targeting nature of SARS-COV-2 due to vascular injury and the hyperimmune response were plausible proposed mechanisms. Further research is warranted to have a deep insight into the possible mechanisms. Herein, we review the current literature and describe five patients we have encountered during the SARS-COV-2 viral pandemic.

Keywords: Coronavirus; SARS-COV-2; COVID-19; Stroke; Thrombophilia


ARDS: Adult Respiratory Syndrome; NRBM: Non-Re breather Bag Mask; PCR: Polymerase Chain Reaction; IL: Interleukin; TNF: Tumor Necrotizing Factor


The novel Severe Acute Respiratory Syndrome Coronavirus (SARS-COV-2) is a viral respiratory illness of the coronavirus family. It was first discovered in Wuhan, China, in December 2019 and rapidly became a global pandemic of SARS-COV-2. It is transmitted primarily through respiratory droplets, but airborne transmission concerns have been raised by the World Health Organization (WHO). COVID-19 presents with widely variable clinical manifestations such as cough, fever, shortness of breath, and its complications, like pneumonia with Adult Respiratory Distress Syndrome (ARDS), circulatory shock, severe inflammatory reaction, in addition to coagulopathy and thromboembolism [1].

COVID-19-associated coagulopathy ranges from mild thrombocytopenia to severe coagulopathy, meeting the International Society on Thrombosis and Hemostasis (ISTH) criteria for Disseminated Intravascular Coagulation (DIC). One of the most commonly observed coagulation abnormalities of COVID-19 is the raised D-Dimer and the reduction in serum fibrinogen levels [19], which are considered a marker of disease severity and therefore have been used to monitor disease activity. The underlying pathophysiology of Venous Thromboembolism (VTE) is related to endothelial injury by SARS-COV-2’s direct effect on the vascular endothelium, particularly in those with well-established secondary sepsis, venous stasis [7,13] and coagulopathy, especially in critically-ill patients [12].

Another key role in developing hypercoagulability in COVID-19 patients is the hyper-inflammatory response to SARS-COV-2 (cytokine storm syndrome), resembling the CAR-T associated cytokine release syndrome, mainly a serial cytokine rush particularly IL1, IL6 [1,4,9,14], TNF-alpha and IL8. These inflammatory mediators directly affect the vascular endothelium concurrently with the viral insult. They together activate the coagulation cascade resulting in arterial and venous thrombosis manifested as VTE, pulmonary embolism, arterial events such as ischemic stroke [2,3] and peripheral limb ischemia.

Herein, we report five cases of confirmed COVID-19 who developed an ischemic stroke of varying severity during their COVID-19 disease course.

Patient 1

An 80-year-old man with a past medical history of diabetes mellitus type 2 (Type 2 D.M.), hypertension, and prostate cancer on hormonal therapy, presented to the E.D. complaining of fever, generalized fatigue, cough, and shortness of breath for three days. Upon initial evaluation, he was in respiratory distress with oxygen saturation of 92% on a Non-Rebreather Bag Mask (NRBM). His laboratory investigations were significant for lymphopenia and elevated D-Dimer, C-reactive protein, and ferritin levels. A chest x-ray showed bilateral perihilar infiltrates. His real-time Polymerase Chain Reaction (PCR) from nasopharyngeal swab was positive for COVID-19; therefore, we started him on azithromycin, hydroxychloroquine, ritonavir/lopinavir combination daily, steroids, and anticoagulation. He received tocilizumab for the significant underlying inflammatory process; then, he reported a new leftsided body weakness and tingling 24-hours after hospitalization. His physical exam revealed reduced power in the right upper and lower limbs with increased muscle tone. An urgent C.T. scan of the head ruled out acute intracerebral bleeding. MRI and MRA of the head of T2/FLAIR confirmed hyperintense acute infarct in the right parietal frontal lobe (Figure 1), and smaller multifocal areas of patchy acute infarcts in the left frontoparietal lobe, right more than left insula, bilateral temporooccipital regions, left caudate head, and tiny acute lacunar infarct in the right cerebellar hemisphere in addition to the occluded right Middle Cerebral Artery (MCA) from the origin in the neck (Figure 2).