Histopathological Signatures of SARS-CoV-2-Induced Microvascular Injury Across Organs

Increasingly, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is being considered a systemic disease with systemic effects on the microvasculature. Though observation and care of respiratory compromise was the starting point of management, the growing evidence indicates that the central tissue pathophysiology factors are endothelial dysfunction and microvascular destruction is the cornerstone of Coronavirus disease 2019 (COVID-19). The article dwells on the pathological alterations of microvascular damage in various organs of patients infected by the SARS-CoV-2 based on a few post-mortems of patients with confirmed COVID-19. The endothelial detector and the inflammatory marker of hematoxylin-eosin stained lung, heart, kidney, brain and liver formalin-fixed, paraffin embedded slices were immunohistochemically stained, where the presence of the ultrastructural changes was through the electron microscope checked. The similarities in histology across organs were the swelling of the endothelium, lymphocytic infiltration around vessels, microthrombi of fibrin in the endothelium and disturbance of the glycocalyx. Capillary congestion and thickening of alveoli walls in pulmonary tissue dominated, and small-vessel microthrombosis with the presence of adjacent myocyte necrosis was common in myocardial samples. Pathologic findings in the renal specimens included inflammation of peritubular capillaries and microthrombin in the glomeruli, which was associated with clinical acute kidney injury. Cerebral microvasculature showed perivascular cuffing and focal microhemorrhages, and their presence initiated the assumption of blood a brain barrier damage. The hepatic changes were sinusoidal congestion and portal microthrombosis. These results justify the hypothesis that there is a diffuse endotheliitis caused by SARS-CoV2, probably through viral infiltration of endothelial cells and an uncontrolled host immune response. Systemic Vascular Injury in COVID-19 The prevalence of the injury indicates that the aspect of the disease is systemic endothelial-mediated and that endothelialprotective/microthrombus-induction-treatment strategies could have cross-organ effects. Being able to identify the histopathologic hallmarks of microvascular damage may be helpful in comprehending its mechanisms and helping manage them or even develop specific interventions to prevent complications later in life when a patient survives.