Silent COVID-19: what your skin can reveal.
Ontology highlight
ABSTRACT:
SUBMITTER: Guarneri C
PROVIDER: S-EPMC7234773 | biostudies-literature | 2021 Jan
REPOSITORIES: biostudies-literature
Publications
Silent COVID-19: what your skin can reveal.
Guarneri Claudio C Rullo Emmanuele Venanzi EV Pavone Piero P Berretta Massimiliano M Ceccarelli Manuela M Natale Alfonso A Nunnari Giuseppe G
The Lancet. Infectious diseases 20200518 1
Similar Datasets
Project description: Not available
| S-BSST563 | biostudies-other
Project description:Objective This study assesses the impact of coronavirus disease 2019 (COVID-19) on the pattern of neurological emergencies reaching a tertiary care center. Materials and Methods This is a retrospective and single center study involving 295 patients with neurological emergencies mainly including acute stroke, status epilepticus (SE), and tubercular meningitis visiting emergency department (ED) from January 1 to April 30, 2020 and divided into pre- and during lockdown, the latter starting from March 25 onward. The primary outcome was number of neurological emergencies visiting ED per week in both periods. Secondary outcomes included disease severity at admission, need for mechanical ventilation (MV), delay in hospitalization, in-hospital mortality, and reasons for poor compliance to ongoing treatment multivariate binary logistic regression was used to find independent predictors of in-hospital mortality which included variables with p <0.1 on univariate analysis. Structural break in the time series analysis was done by using Chow test. Results There was 53.8% reduction in number of neurological emergencies visiting ED during lockdown (22.1 visits vs. 10.2 visits per week, p = 0.001), significantly affecting rural population ( p = 0.004). Presenting patients had comparatively severe illness with increased requirement of MV ( p < 0.001) and significant delay in hospitalization during lockdown ( p < 0.001). Poor compliance to ongoing therapy increased from 34.4% in pre-lockdown to 64.7% patients during lockdown ( p < 0.001), mostly due to nonavailability of drugs ( p < 0.001). Overall, 35 deaths were recorded, with 20 (8.2%) in pre-lockdown and 15 (29.4%) during lockdown ( p = 0.001). Lockdown, nonavailability of local health care, delay in hospitalization, severity at admission, and need for MV emerged as independent predictors of poor outcome in stroke and delay in hospitalization in SE. Conclusion COVID-19 pandemic and associated lockdown resulted in marked decline in non-COVID neurological emergencies reporting to ED, with more severe presentations and significant delay from onset of symptoms to hospitalization.
| S-EPMC8289548 | biostudies-literature
Project description:IntroductionIt has been hypothesized that silent hypoxemia is the cause of rapid progressive respiratory failure with severe hypoxia that occurs in some COVID-19 patients without warning.Presentation of caseA 60-year-old male presented cough without any breathing difficulty. Vital signs showed blood pressure 130/75 mmHg, pulse 84x/minute, respiratory rate (RR) 21x/minute, body temperature 36.5C, and oxygen saturation (SpO2) 75% on room air. RT-PCR for COVID-19 were positive. On third day, he complained of worsening of breath shortness, but his RR was still normal (22x/minute) with SpO2 of 98% on 3 L/minute oxygen via nasal cannula. On fifth day, he experienced severe shortness of breath with RR 38x/minute. He was then intubated using a synchronized intermittent mandatory ventilation. Blood gas analysis showed pH 7.54, PaO2 58.9 mmHg, PaCO2 31.1 mmHg, HCO3 26.9mEq/L, SaO2 94.7%, FiO2 30%, and P/F ratio 196 mmHg. On eighth day, his condition deteriorated with blood pressure 80/40 mmHg with norepinephrine support, pulse 109x/minute, and SpO2 72% with ventilator. He experienced cardiac arrest and underwent basic life support, then resumed strained breathing with return of spontaneous circulation. Blood gas analysis showed pH 7.07, PaO2 58.1 mmHg, PaCO2 108.9 mmHg, HCO3 32.1mEq/L, SaO2 78.7%, FiO2 90%, and P/F ratio 65 mmHg. Three hours later, he suffered cardiac arrest again and eventually died.DiscussionPossible mechanisms of silent hypoxemia are V/Q mismatch, intrapulmonary shunting, and intravascular microthrombi.ConclusionsSilent hypoxemia might be considered as an early sign of deterioration of COVID-19 patients, thus, physician may be able to intervene early and decrease its morbidity and mortality.
| S-EPMC7685064 | biostudies-literature
Project description:COVID-19, caused by SARS-CoV-2, can result in acute respiratory distress syndrome and multiple-organ failure, but little is known about its pathophysiology. Here, we generated single-cell atlases of 23 lung, 16 kidney, 15 liver and 18 heart COVID-19 autopsy donor tissue samples, and spatial atlases of 14 lung donors. Integrated computational analysis uncovered substantial remodeling in the lung epithelial, immune and stromal compartments, with evidence of multiple paths of failed tissue regeneration, including defective alveolar type 2 differentiation and expansion of myofibroblasts and putative TP63+ intrapulmonary basal-like progenitor cells. Viral RNAs were enriched in mononuclear phagocytic and endothelial lung cells which induced specific host programs. Spatial analysis in lung distinguished inflammatory host responses in lung regions with and without viral RNA. Analysis of the other tissue atlases showed transcriptional alterations in multiple cell types in COVID-19 donor heart tissue, and mapped cell types and genes implicated with disease severity based on COVID-19 GWAS. Our foundational dataset elucidates the biological impact of severe SARS-CoV-2 infection across the body a key step towards new treatments.
2021-04-09 | GSE171668 | GEO
Project description: Not available
| S-BSST416 | biostudies-other
Project description:SARS-CoV-2 mainly invades respiratory epithelial cells by adhesion to angiotensin-converting enzyme 2 (ACE-2) and thus, infected patients may develop mild to severe inflammatory responses and acute lung injury. Afferent impulses that result from the stimulation of pulmonary mechano-chemoreceptors, peripheral and central chemoreceptors by inflammatory cytokines are conducted to the brainstem. Integration and processing of these input signals occur within the central nervous system, especially in the limbic system and sensorimotor cortex, and importantly feedback regulation exists between O2, CO2, and blood pH. Despite the intensity of hypoxemia in COVID-19, the intensity of dyspnea sensation is inappropriate to the degree of hypoxemia in some patients (silent hypoxemia). We hypothesize that SARS-CoV-2 may cause neuronal damage in the corticolimbic network and subsequently alter the perception of dyspnea and the control of respiration. SARS-CoV-2 neuronal infection may change the secretion of numerous endogenous neuropeptides or neurotransmitters that distribute through large areas of the nervous system to produce cellular and perceptual effects. SARS-CoV-2 mainly enter to CNS via direct (neuronal and hematologic route) and indirect route. We theorize that SARS-CoV-2 infection-induced neuronal cell damage and may change the balance of endogenous neuropeptides or neurotransmitters that distribute through large areas of the nervous system to produce cellular and perceptual effects. Thus, SARS-CoV-2-associated neuronal damage may influence the control of respiration by interacting in neuromodulation. This would open up possible lines of study for the progress in the central mechanism of COVID-19-induced hypoxia. Future research is desirable to confirm or disprove such a hypothesis.
| S-EPMC7480672 | biostudies-literature
Project description:Coronavirus-19 (COVID-19), the infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, has wreaked havoc across the globe since its emergence in December 2019. Reports of patients presenting with syncope and pre-syncope, as well as hypoxemia without symptoms of dyspnea ("silent hypoxemia"), have led researchers to speculate whether SARS-CoV-2 can alter autonomic nervous system function. As viral infections are commonly reported triggers of altered autonomic control, we must consider whether SARS-CoV-2 can also interfere with autonomic activity, at least in some patients. As we are still in the early stages of understanding COVID-19, we still do not know whether syncope and silent hypoxemia are more strongly associated with COVID-19 compared to any other viral infections that severely compromise gas exchange. Therefore, in this perspective we discuss these two intriguing clinical presentations, as they relate to autonomic nervous system function. In our discussion, we will explore COVID-specific, as well as non-COVID specific mechanisms that may affect autonomic activity and potential therapeutic targets. As we move forward in our understanding of COVID-19, well-designed prospective studies with appropriate control and comparator groups will be necessary to identify potential unique effects of COVID-19 on autonomic function.
| S-EPMC8258030 | biostudies-literature
Project description:IntroductionSilent hypoxia is an entity that has been described in patients diagnosed with COVID-19. It is typically described as objective hypoxia in the absence of proportional respiratory distress. The physiological basis for this phenomenon is controversial, and its prognostic value is unclear. We present a case below, of a 66-year-old female presenting with severe hypoxia that was managed without mechanical ventilation.Presentation of caseA 66 year old female with multiple comorbidities initially presented with a cough, fever and an oxygen saturation of 70% on room air in the absence of respiratory distress or altered mentation. She subsequently tested positive for COVID-19 and was admitted to the intensive care unit; received oxygen via high flow nasal cannula and continuous positive pressure mask. The patient remained in the intensive care unit for 40 days under close observation and exhibited multiple episodes of silent hypoxia on weaning oxygen. She was discharged on room air with an oxygen saturation >90% after 56 days. The patient was not intubated during her stay.Discussion and conclusionClinicians face a clinical dilemma on whether to intubate a "silently hypoxemic" patient, who displays hypoxia out of proportion to clinical examination. The decision is confounded by a lack of clear evidence on whether the benefits of precautionary intubation outweighs the risks, especially in the current COVID-19 pandemic. A recent paradigm shift that recommends delaying intubation further displays the need for clearer analysis of the situation. Our case demonstrates a favorable outcome of the latter approach, yet emphasizes a case-by-case approach until clearer recommendations are available.
| S-EPMC7640922 | biostudies-literature