Malignant Cerebral Ischemia in A COVID-19 Infected Patient: Case Review and Histopathological Findings

Abstract

Severe acute respiratory syndrome coronavirus (SARS-CoV-2) is responsible for an unprecedented worldwide pandemic that has severely impacted the United States. As the pandemic continues, a growing body of evidence suggests that infected patients may develop significant coagulopathy with resultant thromboembolic complications including deep vein thrombosis, pulmonary embolism, myocardial infarction, and ischemic stroke. However, this data is limited and comes from recent small case series and observational studies on stroke types, mechanisms, and outcomes.^1-14 Furthermore, evidence on the role of therapeutic anticoagulation in SARS-CoV-2 infected patients with elevated inflammatory markers, such as D-dimer, is also limited. We report the case of a middle-aged patient who presented with a large vessel ischemic stroke likely resulting from an underlying inflammatory response in the setting of known novel coronavirus infection (COVID-19). Histopathologic analysis of the patient's ischemic brain tissue revealed hypoxic neurons, significant edema from the underlying ischemic insult, fibrin thrombi in small vessels, and fibroid necrosis of the vascular wall without any signs of vasculature inflammation. Brain biopsy was negative for the presence of SARS-CoV-2 RNA (RT-PCR assay). Along with a growing body of literature, our case suggests that cerebrovascular thromboembolic events in COVID-19 infection may be related to acquired hypercoagulability and coagulation cascade activation due to the release of inflammatory markers and cytokines, rather than virus-induced vasculitis. Further studies to investigate the mechanism of cerebrovascular thromboembolic events and their prevention is warranted.

Keywords: COVID-19; Corona virus; Inflammatory conditions; Ischemic stroke; SARS-CoV-2 RNA; anticoagulation; cerebral sinus thrombosis; cerebrovascular disease; hemorrhagic stroke; thromboembolic conditions; thrombotic conditions; vasculitis.

Figure 1

CT of the thorax with findings suggestive of viral pneumonia with superimposed edema.

Figure 2

Non-contrast CT scans of the head pre- and post-operatively. The image on the left demonstrates RMCA territorial infarct with midline shift and ventricular effacement prior to surgical intervention. The image on the right demonstrates infarcted brain parenchyma with herniation beyond the skull defect following right-sided decompressive hemicraniectomy.

Figure 3

Contrast CT Angiogram of the head did not show RICA or RM1 segment occlusion. RMCA proximal segment was narrower compared to the contralateral side.

Figure 4

Histopathologic specimens of right temporal lobe necrotic tissue. A) Intermediate power microscopy (H&E 100x) demonstrates acute encephalitis (arrows) and microvascular thrombi (arrow heads) within the acutely infarcted area with background parenchymal edema. B) A thrombosed vessel away from the inflamed areas (arrow) (H&E 100x). C) A small vessel away from the inflamed area demonstrating marked endothelial reactive atypia (arrow) (H&E 400x).