The Role of Alveolar Edema in COVID-19

Abstract

The coronavirus disease 2019 (COVID-19) has spread over the world for more than one year. COVID-19 often develops life-threateninghypoxemia. Endothelial injury caused by the viral infection leads to intravascular coagulation and ventilation–perfusion mismatch. However, besides above pathogenic mechanisms, the role of alveolar edema in the disease progression has not been discussed comprehensively. Since the exudation of pulmonary edema fluid was extremely serious in COVID-19 patients, we bring out a hypothesis that severity of alveolar edema may determine the size of poorly-ventilated area and the blood oxygen content. Treatments to pulmonary edema (conservative fluid management, exogenous surfactant replacementsand ethanol–oxygen vapor therapyhypothetically) may be greatly helpful for reducingthe occurrences of severe cases. Given that late mechanical ventilation may causemucus (edema fluid) to be blown deep intothe small airways,oxygentherapy should be given at the early stages. Theoptimaltimeand blood oxygen saturation (SpO2) thresholdforoxygentherapy are also discussed.

An updated overview of recent advances, challenges, and clinical considerations of IL-6 signaling blockade in severe coronavirus disease 2019 (COVID-19)

“…This causes cytotoxic effects to the host cell and the production of local cytokines and chemokines. Secretion of these cytokines from damaged cells eventually leads to the activation of the immune response to inhibit the viral infection [9] , [10] . Studies have shown that dysregulation of the immune response and disruption of the auto-regulatory immune mechanisms play an important role in the worsening of pulmonary damage in COVID-19 (11) .…”

OM-85 Broncho-Vaxom®, a Bacterial Lysate, Reduces SARS-CoV-2 Binding Proteins on Human Bronchial Epithelial Cells

“…Epithelial cells of the oral cavity, nasal duct, and upper airway are the primary targets for SARS-CoV-2 [ 1 , 2 , 3 ], by the interaction of the viral spike protein (S-protein) with the human angiotensin converting enzyme 2 (ACE2) and other host proteins and glycosaminoglycans [ 4 , 5 ]. Moreover, a recent study defined the susceptibility to SARS-CoV-2 infection as the result of a combination between the genetic variations of SARS-CoV-2 and the genetics of the host [ 6 ].…”

Pre-Dialytic SpO2 Measured with a Wearable Device as a Predictor of Mortality in Patients with OSA and Chronic Kidney Disease

“…Emerging evidence indicates a link between silent hypoxemia and the thrombi formation within the CV system and pulmonary vasculature [20]. Increased thrombogenesis and vascular inflammation could lead to severe hypoxemia and subsequent CAD and CV deaths in various populations [5,14,[21][22][23]. A recent study specifically states that the lectin-like oxidized lowdensity lipoprotein receptor-1 (LOX-1) and the potent vasoconstrictor endothelin-1 (ET-1) are intricately involved in atherosclerotic plaques formation and assisting in detecting the CV risk in OSA subjects, respectively [24].…”