Ivan Mancipe-Ceballos, Yosimar Méndez-Andrade, Gilberto Gómez-GarzaPatient
30 years, male
39 y/o male with RT-PCR test positive for SARS-CoV2 and mild respiratory symptoms treated as an outpatient for seven days was admitted with deterioration on respiratory function and sepsis. Confusion, disorientation, and somnolence added and head CT was performed. The patient's condition has deteriorated, and died the next day.
Chest X-Ray showed bilateral air space infiltrate with basal predilection consistent with atypical pneumonia (not shown). On a non-enhanced CT (NECT) of the head, asymmetric bilateral areas of cortico-subcortical hypodensities in the cerebral hemispheres were found, with loss of the gray-white matter junction suggesting bilateral middle cerebral arteries (MCAs) infarction (Figure 1). Additionally, diffuse hyperdensity of the intracranial circulation was noted, including both MCAs (59-68 H.U.), anterior cerebral arteries (ACAs, 69-73 U.H.), posterior cerebral arteries (72 U.H.), sagital sinus (77 U.H.) and rectus sinus (72 U.H.), simulating a contrast-enhanced CT, making possible to obtain Maximum Intensity Projection reconstruction images showing the affected vessels (Figures 2, 3).
COVID-19 infection carries significant risk as an independent factor for acute cerebral infarction attributable to proinflammatory and prothrombotic state . Even has not yet completely elucidated, direct endothelial lesion could precipitate hypercoagulability-related thrombotic vascular events . Extensive damage to vascular endothelium and activation of platelets by cytokine storm results in coagulation dysfunction, thrombosis and thromboembolism. This meets the criteria for disseminated intravascular coagulation with a higher mortality rate in severe cases [3,4]. Venous and arterial thromboembolic events occur in 10% to 25% in hospitalized patients with COVID-19  and has been postulated that diffuse thrombotic microangiopathy could be indicative of sluggish venous flow seen as hyperdense veins in some studies . Large vessel occlusion with multiple arterial territories infarction leads to a poor prognosis in patients with COVID-19 [3,7]. Pathologic examination of extracted thrombus of COVID patients showed that they are mainly composed of fibrin and platelets .
Other factors related to poorer prognosis like advanced age or pre-existing comorbidities, including diabetes, hypertension, or chronic lung disease, were not present in our patient. Laboratory abnormalities previously reported as indicators for mortality risk, including neutrophilia with lymphopenia, higher LDH, CPR and BUN, and lower albumin levels , were consistently altered in our case. The patient evaluation was incomplete and the D-dimer level was not determined, however, a striking elevation of serum ferritin was observed. This finding has been associated with a nine-fold increase in the odds of death before discharge .
Focal hyperdensity of the cerebral vasculature in NECT above the normal range of 47-61 H.U. (mean 58 H.U.) is often seen in intravascular clots causing acute cerebral infarction, and occasionally, both MCAs can be affected . Venous thrombosis may also demonstrate hyperdensity of the dural sinuses involved [9,10]. While some image artifacts and vascular calcification may show dense intracranial arteries in expected locations , diffuse hyperdensity of the cerebral vasculature must prompt to investigate systemic causes that promotes hemoconcentration such as polycythemia vera or severe dehydration. [9,10,11]
Considering that diffuse hyperdensity of intracranial circulation is not a typical finding in patients with respiratory illness or sepsis and giving that our patient had no obvious comorbidities, we think that this appearance could be directly related to a hypercoagulable state provoked by SARS-CoV2 infection. At our knowledge, this has not been previously reported; therefore further observations must be investigated.
Written informed patient’s relative consent for publication has been obtained.
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