Abstract
Multi-organ failure is one of the common causes of fatal outcome in COVID-19 patients. However, the pathogenetic association of the SARS-CoV-2 viral load (VL) level with fatal dysfunctions of the lungs, liver, kidneys, heart, spleen and brain, as well as with the risk of death in COVID-19 patients remains poorly understood. SARS-CoV-2 VL in the lungs, heart, liver, kidneys, brain, spleen and lymph nodes have been measured by RT qPCR using the following formula: NSARS-CoV−2/NABL1 × 100. Dissemination of SARS-CoV-2 in 30.5% of cases was mono-organ, and in 63.9% of cases, it was multi-organ. The average SARS-CoV-2 VL in the exudative phase of diffuse alveolar damage (DAD) was 60 times higher than in the proliferative phase. The SARS-CoV-2 VL in the lungs ranged from 0 to 250,281 copies. The “pulmonary factors” of SARS-CoV-2 multi-organ dissemination are the high level of SARS-CoV-2 VL (≥4909) and the exudative phase of DAD. The frequency of SARS-CoV-2 dissemination to lymph nodes was 86.9%, heart–56.5%, spleen–52.2%, liver–47.8%, kidney–26%, and brain–13%. We found no link between the SARS-CoV-2 VL level in the liver, kidneys, and heart and the serum level of CPK, LDH, ALP, ALT, AST and Cr of COVID-19 patients. Isolated detection of SARS-CoV-2 RNA in the myocardium of COVID-19 patients who died from heart failure is possible. The pathogenesis of COVID-19-associated multi-organ failure requires further research in a larger cohort of patients.
Highlights
Introduction iationsCOVID-19, as a multisystemic pathology, has led to more than 5 million deaths worldwide to date [1]
Several questions regarding the “pulmonary mechanisms” of multiorgan spread, dissemination patterns, and the SARS-CoV-2 viral load (VL) level in the vital organ tissues of patients who died from COVID-19 remain open
General characteristics of the 36 patients (21 men, 15 women) with a clinical diagnosis of COVID-19, the number of bed days spent in an intensive care unit (ICU) until fatal outcome, histopathology of lungs, the mean value of SARS-CoV-2 VL in the lungs, tracheobronchial lymph nodes, heart, spleen, liver, kidneys, and brain are presented in
Summary
COVID-19, as a multisystemic pathology, has led to more than 5 million deaths worldwide to date [1]. A severe course and fatal outcomes of the disease are commonly associated with the severe acute respiratory syndrome (ARDS) and multi-organ failure [2–5]. The end-organ failure in COVID-19 patients is generally represented by hepatic lesions in 14–29% of cases, renal injury in 19–29%, heart failure in 33% [6,7], cerebral lesions in. The pathogenesis of multi-organ failure in COVID-19 patients may be associated with cytokine storm [2,12], activation of the adaptive immune system [2], dysregulation of the renin–angiotensin–aldosterone system (RAAS) as a result of virus-mediated suppression of ACE2 expression [13], damage to endothelial cells and vascular inflammation [14], and Licensee MDPI, Basel, Switzerland. The multi-organ tropism of SARS-CoV-2 is considered one of the potential mechanisms of multiple organ failure [16,17]
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