Silent Hypoxia in Coronavirus disease-2019: Is it more dangerous? -A retrospective cohort study

Abstract

Background: Hypoxia in patients with COVID-19 is one of the strongest predictors of mortality. Silent hypoxia is characterised by the presence of hypoxia without dyspnoea. Silent hypoxia has been shown to affect the outcome in previous studies. Methods: This was a retrospective study of a cohort of patients with SARS-CoV-2 infection who were hypoxic at presentation. Clinical, laboratory and treatment parameters in patients with silent hypoxia and dyspnoeic hypoxia were compared. Multivariate logistic regression models were fitted to identify the factors predicting mortality. Results: Among 2080 patients with COVID-19 admitted to our hospital, 811 patients were hypoxic with SpO2 <94% at the time of presentation. Among them, 174 (21.45%) did not have dyspnoea since the onset of COVID-19 symptoms. Further, 5.2% of patients were completely asymptomatic for COVID-19 and were found to be hypoxic only on pulse oximetry. The case fatality rate in patients with silent hypoxia was 45.4% as compared to 40.03% in dyspnoeic hypoxic patients (P = 0.202). The odds ratio of death was 1.1 (95% CI: 0.41–2.97) in the patients with silent hypoxia after adjusting for baseline characteristics, laboratory parameters, treatment and in-hospital complications, which did not reach statistical significance (P = 0.851). Conclusion: Silent hypoxia may be the only presenting feature of COVID-19. As the case fatality rate is comparable between silent and dyspnoeic hypoxia, it should be recognised early and treated as aggressively. Because home isolation is recommended in patients with COVID-19, it is essential to use pulse oximetry in the home setting to identify these patients.

Bioinformatics and systems biology approaches to identify the effects of COVID-19 on neurodegenerative diseases: A review

“…SARS- CoV-2 causes a systemic inflammatory response resulting in elevated plasma cytokine counts in the brain and blood, [58] where chemokines such as IL-6, TNF-α and cytokines such as the acute phase protein CRP, depending on the severity of inflammation, can disrupt the BBB paracellular and transcytosis. [59,60] Another pathological manifestation caused by SARS-CoV-2 -hypoxia, [61] induces BBB destruction, which is thought to be the mechanism by which viral and infected immune cells enter the CNS of the brain. [62] Animal models can indeed more easily illustrate how SARS-CoV-2 enters the brain, but data generated using transgenic ACE2 mice driven by artificial promoter systems should be interpreted when considering the translatability of the results to humans.…”

The Role of Cytokines and Molecular Pathways in Lung Fibrosis Following SARS-CoV-2 Infection: A Physiopathologic (Re)view

“…It is worth mentioning that COVID-19-associated ARDS cases manifest through “happy”/“silent” hypoxemia or the hypoxemia/hypocapnia syndrome, which refers to the presence of hypoxemia in the absence of dyspnea [ 81 ]. Among the possible theories explaining the physiopathology of silent hypoxemia were the alteration of the cortical center of breathing through its inflammation caused by the traveling of SARS-CoV-2 from the nasal cavity to the brain or the reduction in sensitivity of the carotid body when dealing with hypoxia due to the ACE2 receptors present there which connect to the virus [ 82 ]. Another hypothesis implies the cytokine storm that causes pulmonary neovascularization and, further, hypoxia through a right-to-left shunt; hypoxia compensatory ventilation causes hypocapnia, which then hinders the additional ventilation, preventing dyspnea [ 82 ].…”

“…Among the possible theories explaining the physiopathology of silent hypoxemia were the alteration of the cortical center of breathing through its inflammation caused by the traveling of SARS-CoV-2 from the nasal cavity to the brain or the reduction in sensitivity of the carotid body when dealing with hypoxia due to the ACE2 receptors present there which connect to the virus [ 82 ]. Another hypothesis implies the cytokine storm that causes pulmonary neovascularization and, further, hypoxia through a right-to-left shunt; hypoxia compensatory ventilation causes hypocapnia, which then hinders the additional ventilation, preventing dyspnea [ 82 ]. The hypoxemia induced by COVID-19 is responsible for the increase in Gal-1, a lectin proven to be a major factor in pulmonary fibrosis, also considered a “hypoxia-responsive protein” [ 40 ].…”

The impact of the COVID-19 pandemic on the incidence of myocardial infarctions: an overview of current research

“…This condition increases the oxygen demand of the heart muscle, particularly in situations where pre-existing conditions, such as coronary artery disease, limit the heart's ability to meet this demand. Prolonged hypoxia can lead to ischemia and damage to the heart tissue, increasing the risk of a myocardial infarctions, especially in the presence of other risk factors [24,25].…”