COVID-19 and multiorgan failure: A narrative review on potential mechanisms

Abstract

The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) in December 2019 form Wuhan, China leads to coronavirus disease 2019 (COVID-19) pandemic. While the common cold symptoms are observed in mild cases, COVID-19 is accompanied by multiorgan failure in severe patients. The involvement of different organs in severe patients results in lengthening the hospitalization duration and increasing the mortality rate. In this review, we aimed to investigate the involvement of different organs in COVID-19 patients, particularly in severe cases. Also, we tried to define the potential underlying mechanisms of SARS-CoV2 induced multiorgan failure. The multi-organ dysfunction is characterized by acute lung failure, acute liver failure, acute kidney injury, cardiovascular disease, and as well as a wide spectrum of hematological abnormalities and neurological disorders. The most important mechanisms are related to the direct and indirect pathogenic features of SARS-CoV2. Although the presence of angiotensin-converting enzyme 2, a receptor of SARS-CoV2 in the lung, heart, kidney, testis, liver, lymphocytes, and nervous system was confirmed, there are controversial findings to about the observation of SARS-CoV2 RNA in these organs. Moreover, the organ failure may be induced by the cytokine storm, a result of increased levels of inflammatory mediators, endothelial dysfunction, coagulation abnormalities, and infiltration of inflammatory cells into the organs. Therefore, further investigations are needed to detect the exact mechanisms of pathogenesis. Since the involvement of several organs in COVID-19 patients is important for clinicians, increasing their knowledge may help to improve the outcomes and decrease the rate of mortality and morbidity.

Keywords: Angiotensin-converting enzyme-2; COVID-19; Coagulation; Cytokine storm; Multi-organ failure; SARS-CoV2.

Fig. 1

The features of multiorgan failure were summarized due to the laboratory and imaging findings. hs-cTnI sensitive cardiac troponin I, CK creatine cinase, α-HBDH α-hydroxybutyrate dehydrogenase, LV left ventricular, ALT alanine aminotransferase, AST aspartate aminotransferase, TB total bilirubin, GGT gamma-glutamyl transferase, ALP alkaline phosphatase, Cr creatinin, eGFR estimated glomerular filtration rate, BUN blood urea nitrogen, DIC disseminated intravascular coagulation, VTE venous thromboembolism, LDH lactate dehydrogenase, NLR neutrophil/lymphocyte ratio, PLR platelet/lymphocyte ratio, PT prothrombin time, aPTT activated partial thromboplastin time