Acute lung injury (ALI) is a clinical condition occurs due to severe systemic inflammatory response for clinical stimulus like pneumonia, sepsis, trauma, aspiration, inhalation of toxic gases, and pancreatitis. Disruption of alveolar barriers, activation of macrophages, infiltration of neutrophils, and proinflammatory cytokines are the vital events occurs during ALI. The drugs which inhibit these inflammatory response can protect lungs from inflammatory insults. In this study, we examined the potency of phytochemical coronarin, a diterpene which have been proven to possess anti-inflammatory, antioxidant, antiangiogenic, and antitumor activities. Healthy BALB/c mice were induced to acute lung injury with intra-tracheal administration of LPS and then treated with 5 and 10 mg/kg concentration of coronarin. The wet/dry lung weight of mice were estimated to assess the induction of pulmonary edema. BALF fluid was analyzed for protein concentrations and immune cells count. Myeloperoxidase activity and levels of chemokines MCP-2 and MIP-2, iNOS, COX-2, and PGE-2 were quantified to assess the immunomodulatory effect of coronarin against LPS-induced ALI. The levels of proinflammatory cytokines was measured to examine the anti-inflammatory property of coronarin, and it was confirmed with histopathological analysis of the lung tissue. Murine RAW 264.7 cells were utilized for the in vitro analysis. Cell cytoxicity and cytoprotective property of coronarin was assessed with MTT assay in LPS-treated Murine RAW 264.7. The anti-inflammatory property of coronarin was further confirmed in in vitro condition by estimating the levels of pro-inflammatory cytokines in coronarin-treated and untreated LPS-induced cells. Overall, our in vivo and in vitro results confirm coronarin significantly inhibited the infiltration of neutrophils prevented immunodulatory activity and synthesis of proinflammatory cytokines and alleviated the acute lung injury induced by LPS. Coronarin is a potent anti-inflammatory drug which can be subjected to further research to be prescribed as drug for ALI.

Coronavirus disease 2019 (COVID-19) typically presents with fever and respiratory symptoms in children. Most children develop an asymptomatic and mild illness, with a minority requiring specialist medical care. Gastrointestinal manifestations and liver injury can also occur in children following infection. The mechanisms of liver injury may include infection following direct viral hepatic tissue invasion, immune response, or medication effects. Affected children might develop mild liver dysfunction which has a benign course in most children with no pre-existing liver disease. However, the presence of non-alcoholic fatty liver disease or other pre-existing chronic liver disorders is associated with a higher risk of developing severe COVID-19 illness with poor outcomes. On the other hand, the presence of liver manifestations is associated with the severity of COVID-19 disease and is considered an independent prognostic factor. Respiratory, hemodynamic, and nutritional supportive therapies are the mainstay of management. Vaccination of children at increased risk of developing severe COVID-19 disease is indicated. This review describes the liver manifestations in children with COVID-19, detailing its epidemiology, basic mechanisms, clinical expression, management, and prognosis in those with and without pre-existing liver disease and also children who have had earlier liver transplantation.

Morbidity and mortality from COVID-19 is due to severe inflammation and end-organ damage caused by a hyperinflammatory response. Multiple immunomodulatory agents to attenuate this response have been studied. Corticosteroids, specifically dexamethasone, have been shown to reduce mortality in hospitalized patients who require supplemental oxygen. Interleukin-6 antagonist, tocilizimab, and Janus kinase inhibitors have also been shown to reduce mortality. However, patients who have severe pulmonary end-organ damage requiring mechanical ventilation or extracorporeal membrane oxygenation appear not to benefit from immunomodulatory therapies. This highlights the importance of appropriate timing to initiate immunomodulatory therapies in the management of severe COVID-19 disease.

Coronavirus disease (COVID-19) is an infectious airborne viral pneumonia caused by a novel virus belonging to the family coronaviridae. On February 11, 2019, the Internal Committee on Taxonomy of Virus (ICTV) announced the name of the novel virus as "severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). One of the proteins present on its membrane i.e. the Spike protein is responsible for the attachment of the virus to the host. It spreads through the salivary droplets released when an infected person sneezes or coughs. The best way to slow down the disease is by protecting self by washing hands and using the disinfectant. Most of the infected people experience mild to moderate breathing issues. Serious illness might develop in people with underlying cardiovascular problems, diabetes and other immuno-compromised diseases. To date, there is no effective medicine available in the market which is effective in COVID-19. However, healthcare professionals are using ritonavir, flavipiravir, lopinavir, hydroxychloroquine and remdesivir. Along with the medicines, some countries are using convalescent plasma and mesenchymal stem cells for treatment. Till date, it has claimed millions of death worldwide. In this detailed review, we have discussed the structure of SARS-CoV-2, essential proteins, its lifecycle, transmission, symptoms, pathology, clinical features, diagnosis, prevention, treatment and epidemiology of the disease.

People across the world are affected by the "coronavirus disease 2019 (COVID-19)", brought on by the "SARS-CoV type-2 coronavirus". Due to its high incidence in individuals with diabetes, metabolic syndrome, and metabolic-associated fatty liver disease (MAFLD), COVID-19 has gained much attention. The metabolic syndrome's hepatic manifestation, MAFLD, carries a significant risk of type-2-diabetes. The link between the above two conditions has also drawn increasing consideration since MAFLD is intricately linked to the obesity epidemic. Independent of the metabolic syndrome, MAFLD may impact the severity of the viral infections, including COVID-19 or may even be a risk factor. An important question is whether the present COVID-19 pandemic has been fueled by the obesity and MAFLD epidemics. Many liver markers are seen elevated in COVID-19. MAFLD patients with associated comorbid conditions like obesity, cardiovascular disease, renal disease, malignancy, hypertension, and old age are prone to develop severe disease. There is an urgent need for more studies to determine the link between the two conditions and whether it might account for racial differences in the mortality and morbidity rates linked to COVID-19. The role of innate and adaptive immunity alterations in MAFLD patients may influence the severity of COVID-19. This review investigates the implications of COVID-19 on liver injury and disease severity and vice-versa. We also addressed the severity of COVID-19 in patients with prior MAFLD and its potential implications and therapeutic administration in the clinical setting.

The study aimed to assess the level of dyspnoea during the COVID-19 pandemic in Poland.

The online questionnaire was conducted among 204 Polish adult respondents with a positive SARS-CoV-2 test result. The level of dyspnoea was assessed by the modified Medical Research Council (MRC) Dyspnoea Scale in Polish.

Dyspnoea is most common in patients with severe COVID-19, and the prevalence of dyspnoea in the study population of patients with COVID-19 was low (34% respondents presented with dyspnoea with a score of 1 or higher).

There is a need for further investigation and close monitoring of the extent of dyspnoea in different social groups, especially in the event of a prolonged pandemic and the emergence of further waves of COVID-19.

The worldwide COVID-19 pandemic caused by SARS-CoV-2 has resulted in an extraordinary increase in the number of patients who are severely critically ill. For many of these patients, cardiovascular risk factors are key contributors to the development of severe illness. Laboratory markers for cardiac damage and failure, such as natriuretic peptides, are reported to be elevated in patients with severe COVID-19.

We conducted a systematic review and meta-analysis to compare natriuretic peptide levels in patients with severe COVID-19 vs those with nonsevere COVID-19. PubMed and medRxiv were searched through April 7, 2020. The outcome of interest was the difference in B-type natriuretic peptide (BNP) or N-terminal-proBNP levels in patients with severe vs nonsevere COVID-19.

We identified 9 retrospective cohort studies that had a total of 1,575 patients with COVID-19 who had their natriuretic peptides measured and were classified by disease severity. All studies were conducted in China. Patients with severe COVID-19 had significantly higher BNP levels than patients with nonsevere COVID-19 (mean difference, 69.56 pg/mL; 95% CI, 1.77-137.35 pg/mL; P = .04, I2 = 83%). Similarly, patients with severe COVID-19 had significantly higher N-terminal-proBNP levels than patients with nonsevere COVID-19 (mean difference, 518.65 pg/mL; 95% CI, 152.40-884.90 pg/mL; P = .006, I2 = 86%).

In this study, Chinese patients with severe COVID-19 had higher natriuretic peptide levels than those with nonsevere COVID-19. Studies from all countries affected by the virus will help to further delineate whether the cause is directly or indirectly of cardiac origin and whether preexisting heart failure has an influence on this disparity.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induced the new coronavirus disease 2019 (COVID-19) pandemic worldwide. SARS-CoV-2 vaccines are designed to control the transmission of the disease. However, post-vaccination subacute thyroiditis (SAT) also appears with increase vaccination rate. Three cases of SAT after SARS-CoV-2 vaccines are described in this study. We have reported the patients' clinical symptoms, laboratory tests, and thyroid imaging. Tests for COVID-19 were all negative, and the patients did not report thyroid-related diseases, autoimmune diseases, or preceding upper respiratory system infections in their medical history. Three female patients showed neck pain on physical examination. The laboratory test results and imaging findings were consistent with the diagnostic criteria of SAT. The patients were carried out a standardized treatment according to their symptoms, and we closely followed up their response to the treatment. Clinicians must be aware of the possibility of SAT after receiving the vaccines and make timely therapy.

With potential antiviral and anti-inflammatory properties, Janus kinase (JAK) inhibitors represent a potential treatment for symptomatic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. They may modulate the exuberant immune response to SARS-CoV-2 infection. Furthermore, a direct antiviral effect has been described. An understanding of the current evidence regarding the efficacy and safety of JAK inhibitors as a treatment for coronavirus disease 2019 (COVID-19) is required.

To assess the effects of systemic JAK inhibitors plus standard of care compared to standard of care alone (plus/minus placebo) on clinical outcomes in individuals (outpatient or in-hospital) with any severity of COVID-19, and to maintain the currency of the evidence using a living systematic review approach.

We searched the Cochrane COVID-19 Study Register (comprising MEDLINE, Embase, ClinicalTrials.gov, World Health Organization (WHO) International Clinical Trials Registry Platform, medRxiv, and Cochrane Central Register of Controlled Trials), Web of Science, WHO COVID-19 Global literature on coronavirus disease, and the US Department of Veterans Affairs Evidence Synthesis Program (VA ESP) Covid-19 Evidence Reviews to identify studies up to February 2022. We monitor newly published randomised controlled trials (RCTs) weekly using the Cochrane COVID-19 Study Register, and have incorporated all new trials from this source until the first week of April 2022.

We included RCTs that compared systemic JAK inhibitors plus standard of care to standard of care alone (plus/minus placebo) for the treatment of individuals with COVID-19. We used the WHO definitions of illness severity for COVID-19.

We assessed risk of bias of primary outcomes using Cochrane's Risk of Bias 2 (RoB 2) tool. We used GRADE to rate the certainty of evidence for the following primary outcomes: all-cause mortality (up to day 28), all-cause mortality (up to day 60), improvement in clinical status: alive and without need for in-hospital medical care (up to day 28), worsening of clinical status: new need for invasive mechanical ventilation or death (up to day 28), adverse events (any grade), serious adverse events, secondary infections.

We included six RCTs with 11,145 participants investigating systemic JAK inhibitors plus standard of care compared to standard of care alone (plus/minus placebo). Standard of care followed local protocols and included the application of glucocorticoids (five studies reported their use in a range of 70% to 95% of their participants; one study restricted glucocorticoid use to non-COVID-19 specific indications), antibiotic agents, anticoagulants, and antiviral agents, as well as non-pharmaceutical procedures. At study entry, about 65% of participants required low-flow oxygen, about 23% required high-flow oxygen or non-invasive ventilation, about 8% did not need any respiratory support, and only about 4% were intubated. We also identified 13 ongoing studies, and 9 studies that are completed or terminated and where classification is pending. Individuals with moderate to severe disease Four studies investigated the single agent baricitinib (10,815 participants), one tofacitinib (289 participants), and one ruxolitinib (41 participants). Systemic JAK inhibitors probably decrease all-cause mortality at up to day 28 (95 of 1000 participants in the intervention group versus 131 of 1000 participants in the control group; risk ratio (RR) 0.72, 95% confidence interval (CI) 0.57 to 0.91; 6 studies, 11,145 participants; moderate-certainty evidence), and decrease all-cause mortality at up to day 60 (125 of 1000 participants in the intervention group versus 181 of 1000 participants in the control group; RR 0.69, 95% CI 0.56 to 0.86; 2 studies, 1626 participants; high-certainty evidence). Systemic JAK inhibitors probably make little or no difference in improvement in clinical status (discharged alive or hospitalised, but no longer requiring ongoing medical care) (801 of 1000 participants in the intervention group versus 778 of 1000 participants in the control group; RR 1.03, 95% CI 1.00 to 1.06; 4 studies, 10,802 participants; moderate-certainty evidence). They probably decrease the risk of worsening of clinical status (new need for invasive mechanical ventilation or death at day 28) (154 of 1000 participants in the intervention group versus 172 of 1000 participants in the control group; RR 0.90, 95% CI 0.82 to 0.98; 2 studies, 9417 participants; moderate-certainty evidence). Systemic JAK inhibitors probably make little or no difference in the rate of adverse events (any grade) (427 of 1000 participants in the intervention group versus 441 of 1000 participants in the control group; RR 0.97, 95% CI 0.88 to 1.08; 3 studies, 1885 participants; moderate-certainty evidence), and probably decrease the occurrence of serious adverse events (160 of 1000 participants in the intervention group versus 202 of 1000 participants in the control group; RR 0.79, 95% CI 0.68 to 0.92; 4 studies, 2901 participants; moderate-certainty evidence). JAK inhibitors may make little or no difference to the rate of secondary infection (111 of 1000 participants in the intervention group versus 113 of 1000 participants in the control group; RR 0.98, 95% CI 0.89 to 1.09; 4 studies, 10,041 participants; low-certainty evidence). Subgroup analysis by severity of COVID-19 disease or type of JAK inhibitor did not identify specific subgroups which benefit more or less from systemic JAK inhibitors. Individuals with asymptomatic or mild disease We did not identify any trial for this population.

In hospitalised individuals with moderate to severe COVID-19, moderate-certainty evidence shows that systemic JAK inhibitors probably decrease all-cause mortality. Baricitinib was the most often evaluated JAK inhibitor. Moderate-certainty evidence suggests that they probably make little or no difference in improvement in clinical status. Moderate-certainty evidence indicates that systemic JAK inhibitors probably decrease the risk of worsening of clinical status and make little or no difference in the rate of adverse events of any grade, whilst they probably decrease the occurrence of serious adverse events. Based on low-certainty evidence, JAK inhibitors may make little or no difference in the rate of secondary infection. Subgroup analysis by severity of COVID-19 or type of agent failed to identify specific subgroups which benefit more or less from systemic JAK inhibitors. Currently, there is no evidence on the efficacy and safety of systemic JAK inhibitors for individuals with asymptomatic or mild disease (non-hospitalised individuals).

Patients with novel coronavirus disease 2019 (COVID-19) worsen into critical illness suddenly is a matter of great concern. Early identification and effective triaging of patients with a high risk of developing critical illness COVID-19 upon admission can aid in improving patient care, increasing the cure rate, and mitigating the burden on the medical care system. This study proposed and extended classical least absolute shrinkage and selection operator (LASSO) logistic regression to objectively identify clinical determination and risk factors for the early identification of patients at high risk of progression to critical illness at the time of hospital admission.

In this retrospective multicenter study, data of 1,929 patients with COVID-19 were assessed. The association between laboratory characteristics measured at admission and critical illness was screened with logistic regression. LASSO logistic regression was utilized to construct predictive models for estimating the risk that a patient with COVID-19 will develop a critical illness.

The development cohort consisted of 1,363 patients with COVID-19 with 133 (9.7%) patients developing the critical illness. Univariate logistic regression analysis revealed 28 variables were prognosis factors for critical illness COVID-19 (p < 0.05). Elevated CK-MB, neutrophils, PCT, α-HBDH, D-dimer, LDH, glucose, PT, APTT, RDW (SD and CV), fibrinogen, and AST were predictors for the early identification of patients at high risk of progression to critical illness. Lymphopenia, a low rate of basophils, eosinophils, thrombopenia, red blood cell, hematocrit, hemoglobin concentration, blood platelet count, and decreased levels of K, Na, albumin, albumin to globulin ratio, and uric acid were clinical determinations associated with the development of critical illness at the time of hospital admission. The risk score accurately predicted critical illness in the development cohort [area under the curve (AUC) = 0.83, 95% CI: 0.78-0.86], also in the external validation cohort (n = 566, AUC = 0.84).

A risk prediction model based on laboratory findings of patients with COVID-19 was developed for the early identification of patients at high risk of progression to critical illness. This cohort study identified 28 indicators associated with critical illness of patients with COVID-19. The risk model might contribute to the treatment of critical illness disease as early as possible and allow for optimized use of medical resources.

The ongoing pandemic coronavirus disease (COVID-19) caused by a novel corona virus, namely, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has had a major impact on global public health. COVID-19 cases continue to increase across the globe with high mortality rates in immunocompromised patients. There is still a pressing demand for drug discovery and vaccine development against this highly contagious disease. To design and develop antiviral drugs against COVID-19, the main protease (M^pro) has emerged as one of the important drug targets. In this context, the present work explored Jadwar (Delphinium denudatum)-derived natural alkaloids as potential inhibitors against M^pro of SARS-CoV-2 by employing a combination of molecular docking and molecular dynamic simulation-based methods. Molecular docking and interaction profile analysis revealed strong binding on the M^pro functional domain with four natural alkaloids viz. panicutine (-7.4 kcal/mol), vilmorrianone (-7.0 kcal/mol), denudatine (-6.0 kcal/mol), and condelphine (-5.9 kcal/mol). The molecular docking results evaluated by using the MD simulations on 200 nanoseconds confirmed highly stable interactions of these compounds with the M^pro. Additionally, mechanics/generalized Born/Poisson-Boltzmann surface area (MM/G/P/BSA) free energy calculations also affirmed the docking results. Natural alkaloids explored in the present study possess the essential drug-likeness properties, namely, absorption, distribution, metabolism, and excretion (ADME), and are in accordance with Lipinski's rule of five. The results of this study suggest that these four bioactive molecules, namely, condelphine, denudatine, panicutine, and vilmorrianone, might be effective candidates against COVID-19 and can be further investigated using a number of experimental methods.

The data on the predictors and prognosis of acute liver injury (ALI) among patients in coronavirus disease 2019 (COVID-19) patients are limited. The aim of this study was to determine the prevalence, predictors and outcomes of ALI among patients with COVID-19. A systematic review was conducted up to 10 June 2021. The relevant papers were searched from PubMed, Embase, Cochrane and Web of Science, and the data were analysed using a Z test. A total of 1331 papers were identified and 16 papers consisting of 1254 COVID-19 with ALI and 4999 COVID-19 without ALI were analysed. The cumulative prevalence of ALI among patients with COVID-19 was 22.8%. Male and having low lymphocyte levels were more likely to be associated with ALI compared with female and having higher lymphocyte level, odds ratio (OR): 2.70; 95% confidence interval (CI): 2.03, 3.60 and mean difference (MD) -125; 95% CI: -207, -43, respectively. COVID-19 patients with ALI had higher risk of developing severe COVID-19 compared with those without ALI (OR: 3.61; 95% CI: 2.60, 5.02). Our findings may serve as the additional evaluation for the management of ALI in COVID-19 patients.

The advent of the novel coronavirus disease 2019 (COVID-19) has caused millions of deaths worldwide. As of December 2021, there is inadequate data on the outcome of hospitalized patients suffering from COVID-19 in Africa. This study aimed at identifying factors associated with hospital mortality in patients who suffered from COVID-19 at Gulu Regional Referral Hospital in Northern Uganda from March 2020 to October 2021.

This was a single-center, retrospective cohort study in patients hospitalized with confirmed SARS-CoV-2 at Gulu Regional Referral Hospital in Northern Uganda. Socio-demographic characteristics, clinical presentations, co-morbidities, duration of hospital stay, and treatments were analyzed, and factors associated with the odds of mortality were determined.

Of the 664 patients treated, 661 (99.5%) were unvaccinated, 632 (95.2%) recovered and 32 (4.8%) died. Mortality was highest in diabetics 11 (34.4%), cardiovascular diseases 12 (37.5%), hypertensives 10 (31.3%), females 18 (56.3%), ≥50-year-olds 19 (59.4%), no formal education 14 (43.8%), peasant farmers 12 (37.5%) and those who presented with difficulty in breathing/shortness of breath and chest pain 32 (100.0%), oxygen saturation (SpO2) at admission <80 4 (12.5%), general body aches and pains 31 (96.9%), tiredness 30 (93.8%) and loss of speech and movements 11 (34.4%). The independent factors associated with mortality among the COVID-19 patients were females AOR = 0.220, 95%CI: 0.059-0.827; p = 0.030; Diabetes mellitus AOR = 9.014, 95%CI: 1.726-47.067; p = 0.010; Ages of 50 years and above AOR = 2.725, 95%CI: 1.187-6.258; p = 0.018; tiredness AOR = 0.059, 95%CI: 0.009-0.371; p < 0.001; general body aches and pains AOR = 0.066, 95%CI: 0.007-0.605; p = 0.020; loss of speech and movement AOR = 0.134, 95%CI: 0.270-0.660; p = 0.010 and other co-morbidities AOR = 6.860, 95%CI: 1.309-35.957; p = 0.020.

The overall Gulu Regional Hospital mortality was 32/664 (4.8%). Older age, people with diabetics, females, other comorbidities, severe forms of the disease, and those admitted to HDU were significant risk factors associated with hospital mortality. More efforts should be made to provide "additional social protection" to the most vulnerable population to avoid preventable morbidity and mortality of COVID-19 in Northern Uganda.

Coronavirus disease 2019 (COVID-19) is, at present, one of the most relevant global health problems. In the literature hepatic alterations have been described in COVID-19 patients, and they are mainly represented by worsening of underlying chronic liver disease leading to hepatic decompensation and liver failure with higher mortality. Several potential mechanisms used by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to cause liver damage have been hypothesized. COVID-19 primary liver injury is less common than secondary liver injury. Most of the available data demonstrate how liver damage in SARS-CoV-2 infection is likely due to systemic inflammation, and it is less likely mediated by a cytopathic effect directed on liver cells. Moreover, liver alterations could be caused by hypoxic injury and drugs (antibiotics and non-steroidal anti-inflammatory drugs, remdesivir, tocilizumab, tofacitinib and dexamethasone). SARS-CoV-2 infection can induce multiple vascular district atherothrombosis by affecting simultaneously cerebral, coronary and peripheral vascular beds. Data in the literature highlight how the virus triggers an exaggerated immune response, which added to the cytopathic effect of the virus can induce endothelial damage and a prothrombotic dysregulation of hemostasis. This leads to a higher incidence of symptomatic and confirmed venous thrombosis and of pulmonary embolisms, especially in central, lobar or segmental pulmonary arteries, in COVID-19. There are currently fewer data for arterial thrombosis, while myocardial injury was identified in 7%-17% of patients hospitalized with SARS-CoV-2 infection and 22%-31% in the intensive care unit setting. Available data also revealed a higher occurrence of stroke and more serious forms of peripheral arterial disease in COVID-19 patients. Hemostasis dysregulation is observed during the COVID-19 course. Lower platelet count, mildly increased prothrombin time and increased D-dimer are typical laboratory features of patients with severe SARS-CoV-2 infection, described as "COVID-19 associated coagulopathy." These alterations are correlated to poor outcomes. Moreover, patients with severe SARS-CoV-2 infection are characterized by high levels of von Willebrand factor with subsequent ADAMTS13 deficiency and impaired fibrinolysis. Platelet hyperreactivity, hypercoagulability and hypofibrinolysis during SARS-CoV-2 infection induce a pathological state named as "immuno-thromboinflammation." Finally, liver dysfunction and coagulopathy are often observed at the same time in patients with COVID-19. The hypothesis that liver dysfunction could be mediated by microvascular thrombosis has been supported by post-mortem findings and extensive vascular portal and sinusoidal thrombosis observation. Other evidence has shown a correlation between coagulation and liver damage in COVID-19, underlined by the transaminase association with coagulopathy, identified through laboratory markers such as prothrombin time, international normalized ratio, fibrinogen, D-dimer, fibrin/fibrinogen degradation products and platelet count. Other possible mechanisms like immunogenesis of COVID-19 damage or massive pericyte activation with consequent vessel wall fibrosis have been suggested.

COVID-19, a novel coronavirus disease, has provoked a variety of health and safety concerns, and socioeconomic challenges around the globe. The laboratory diagnosis of SARS-CoV-2 was quickly established utilizing nucleic acid amplification techniques (NAAT) after the disease causing virus has been identified, and its genetic sequence has been determined. In addition to NAAT, serological tests based on antibodies testing against SARS-CoV-2 were introduced for diagnostic and epidemiologic studies. Other biochemical investigations include monitoring of peripheral blood cells count, platelets/lymphocyte ratio, coagulation profile, cardiac, and inflammatory markers such as cytokines storm are also crucial in combating COVID-19 pandemic. Further, accurate and reliable laboratory results for SARS-CoV-2 play very important role in the initiation of early treatment and timely management of COVID-19 patients, provide support in clinical decision-making process to control infection, and detection of asymptomatic cases. The Task Force on Coronavirus-19 constituted by International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) has recognized informational framework for epidemiology, pathogenesis, and recommended the PCR-based analysis, serological and biochemical assays for analysis, monitoring, and management of disease. This literature review provides an overview of the currently used diagnostic techniques in clinical laboratories for the diagnosis, treatment monitoring, and management of COVID-19 patients. We concluded that each assays differ in their performance characteristics and the utilization of multiple techniques is necessary for the accurate diagnosis and management of SARS-CoV-2 infection.

Background: Coronavirus disease 2019 (COVID-19) is a severe infectious illness. It has been reported that COVID-19 has an effect on thyroid function. However, the association between thyroid function and prognosis of COVID-19 is still unclear.Methods: This retrospective study included patients with COVID-19 admitted to Tongji Hospital in Wuhan from January 28 to April 4, 2020. Demographic, epidemiological, clinical, laboratory, treatment, and outcome data were collected from patients with laboratory-confirmed COVID-19. Patients without history of thyroid disease who had a thyroid function test at admission were enrolled in the final analysis. Risk factors of in-hospital death were explored using univariable and multivariable Cox regression analyses. Survival differences were assessed with Kaplan-Meier curves and log-rank test.Results: A total of 127 patients were included in this study, with 116 survivors and 11 non-survivors. The serum levels of thyroid stimulating hormone (TSH) [0.8 (0.5-1.7) vs. 1.9 (1.0-3.1) μIU/mL, P = .031] and free triiodothyronine (FT₃) [2.9 (2.8-3.1) vs. 4.2 (3.5-4.7) pmol/L, P < .001] were lower in non-survivors than in survivors, and a low FT₃ state (defined as FT₃ < 3.1 pmol/L) at admission accounted for a higher proportion in non-survivors than in survivors (72.7% vs. 11.2%, P < .001). Univariate Cox regression analysis showed that FT₃ level (HR 0.213, 95% CI: 0.101-0.451, P < .001) and the low FT₃ state (HR 14.607, 95% CI: 3.873-55.081, P < .001) were negatively and positively associated with the risk of in-hospital death, respectively. Furthermore, multivariate Cox regression analysis revealed that a low FT₃ state was associated with an increased risk of in-hospital death after adjusting for confounding factors (HR 13.288, 95% CI: 1.089-162.110, P = .043). Moreover, Kaplan-Meier curves indicated a lower survival probability in COVID-19 patients with a low FT₃ status.Conclusion: Serum FT₃ level is lower in non-survivors among moderate-to-critical patients with COVID-19, and the low FT₃ state is associated with an increased risk of in-hospital mortality of COVID-19.

At present, the pathogenesis of the novel coronavirus disease 2019 (COVID-19) has not been fully elucidated. Clinical and experimental findings from studies investigating COVID-19 have suggested that the immune-inflammatory response has a crucial role in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The present article aimed to systematically review the available literature on the pathogenesis of COVID-19. Severe COVID-19 is characterized by organ dysfunction, hypercytokinemia and lymphopenia. It is assumed that the direct cytopathological damage of host cells and the dysregulated immune response caused by SARS-CoV-2 may be the primary underlying mechanisms of COVID-19. Based on the published literature, this review attempts to provide an integrated view of the immunological mechanisms and the potential pathogenesis of COVID-19, providing an in-depth summary of the host-pathogen interaction and host immune responses. It is of great importance to elucidate the possible pathogenesis of COVID-19 to determine the direction of future research.

2019 novel coronavirus disease (COVID-19) is caused by the infection of severe acute respiratory syndrome novel coronavirus (SARS-CoV-2). It is characterized by substantial respiratory symptoms and complicated with widespread other organ injuries. Cardiovascular impairment is one of the notable extrapulmonary manifestations, in terms of the deterioration of pre-existing cardiovascular diseases and newly onset acute events. We hereby review the high-quality reports about cardiovascular involvement in COVID-19 and summarize the main clinical characteristics of cardiac relevance for the all the first line clinical physicians. Additionally, the possible underlying mechanisms and the rationale for the application of specific medications, such as renin-angiotensin-aldosterone system inhibitors and hydroxychloroquine are also discussed.

Purpose: This study aimed to describe the clinical and laboratory characteristics and the parameters of the respiratory mechanics of mechanically ventilated patients with confirmed COVID-19 pneumonia and to clarify the risk or protective factors for weaning failure. Methods: Patients diagnosed with COVID-19 pneumonia were selected from the special intensive care unit (ICU) of the Sino-French New City Branch of Tong Ji Hospital, Wuhan, and treated by the National Medical Team Work. They were divided into successful weaning (SW) group (N = 15) and unsuccessful weaning (USW) group (N = 18) according to the prognosis. Information of these patients was analyzed. Results: There were 33 patients included in this study. Patients in the USW group were associated with a poor outcome; the 28-day mortality rate was higher than in the SW group (86.7 vs. 16.7% p < 0.001). By comparison, we found that the initial plateau pressure (Pplat) and driving pressure (DP) of the USW group were higher and that compliance was lower than that of the SW group, but there was no difference between positive end-expiratory pressure (PEEP), partial pressure of carbon dioxide (PCO2), and the ratio of partial pressure arterial oxygen and fraction of inspired oxygen (P/F ratio). Comparing the worst respiratory mechanics parameters of the two groups, the results of the Pplat, DP, compliance, and PEEP were the same as the initial data. The PCO2 of the USW group was higher, while the P/F ratio was lower. A logistic regression analysis suggested that higher Pplat might be an independent risk factor and that higher compliance and lower DP might be protective factors for weaning failure of invasive mechanically ventilated patients with COVID-19 pneumonia. Conclusions: Patients with USW were associated with a poor outcome, higher Pplat might be a risk factor, and a higher compliance and a lower DP might be protective factors for the weaning failure of ventilated COVID-19 patients. Mechanical ventilation settings will affect the patient's prognosis.

Coronavirus disease 2019 (COVID-19) has become a challenging public health catastrophe worldwide. The newly emerged disease spread in almost all countries and infected 100 million persons worldwide. The infection is not limited to the respiratory system but involves various body systems and may lead to multiple organ failure. Tissue degenerative changes result from direct viral invasion, indirect consequences, or through an uncontrolled immune response. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spreads to the brain via hematogenous and neural routes accompanied with dysfunction of the blood-brain barrier. The involvement of the central nervous system is now suspected to be among the main causes of death. The present review discusses the historical background of coronaviruses, their role in previous and ongoing pandemics, the way they escape the immune system, why they are able to spread despite all undertaken measures, in addition to the neurological manifestations, long-term consequences of the disease, and various routes of viral introduction to the CNS.

Objectives: The aim of this review is to summarize the most relevant scientific discoveries regarding SARS- CoV-2 virus infection, with the special emphasis put on its pathophysiology and way of treatment. Methods: In November 2020, the research articles have been collected and examined manually to pick the most relevant. In case of fresh topics, e.g. vaccines, we have performed searching using adequate keywords. Preliminary analysis was conducted on 200 manuscripts. Results: Among them 59 papers were out-of-scope, and thus were rejected from the further elaboration. Another 25 papers were rebuffed because they presented topics, that have been extensively described in the already included papers. Basing on the 29 papers we have estimated ratio of observed SARS-CoV-2 infection clinical manifestations and comorbidities among hospitalized patients. 12 papers let us evaluate frequencies of deviations within laboratory markers concentrations, as well as weighted average of the laboratory tests results. Conclusion: Due to the significant infectivity of the virus and its harmfulness towards organism further studies are required to find accurate way of the disease treatment and suspending its spreading.

The spectrum of health complications instigated by coronavirus disease 2019 (COVID-19, caused by the novel severe acute respiratory syndrome coronavirus 2 or SARS-CoV-2) pandemic has been diverse and complex. Besides the evident pulmonary and cardiovascular threats, accumulating clinical data points to several neurological complications, which are more common in elderly COVID-19 patients. Recent pieces of evidence have marked events of neuro infection and neuroinvasion, producing several neurological complications in COVID-19 patients; however, a systematic understanding of neuro-pathophysiology and manifested neurological complications, more specifically in elderly COVID-19 patients is largely elusive. Since the elderly population gradually develops neurological disorders with aging, COVID-19 inevitably poses a higher risk of neurological manifestations to the aged patients. In this report, we reviewed SARS-CoV-2 infection and its role in neurological manifestations with an emphasis on the elderly population. We reviewed neuropathological events including neuroinfection, neuroinvasion, and their underlying mechanisms affecting neuromuscular, central- and peripheral- nervous systems. We further assessed the imminent neurological challenges in the COVID-19 exposed population, post-SARS-CoV-2-infection. Given the present state of clinical preparedness, the emerging role of AI and machine learning was also discussed concerning COVID-19 diagnostics and its management. Taken together, the present review summarizes neurological outcomes of SARS-CoV-2 infection and associated complications, specifically in elderly patients, and underlines the need for their clinical management in advance.

We herein seek to expound on up-to-the-minute information regarding cardiovascular disease in the era of coronavirus disease 2019 (COVID-19) by highlighting acute myocardial injury caused by COVID-19 and probing into its pathophysiology, clinical signs, diagnostic tests, and treatment modalities. We aim to share the latest research findings vis-à-vis cardiovascular disease patients with confirmed or suspected COVID-19 on the association between hypertension and this infectious disease along with the relevant recommendations; describe the mechanism of coronary artery disease in such patients together with the necessary measures in the setting of non-ST-segment elevation acute coronary syndrome, ST-segment elevation myocardial infarction, and chronic coronary syndrome; discuss tachy- and bradyarrhythmias in the COVID-19 setting alongside their treatments; elucidate coagulopathies, venous thromboembolism, and its prophylactic measures in the context of this infection; set out the cardiopulmonary resuscitation protocol as well as the pertinent safety concerns during the current pandemic; and, finally, explicate drug-drug interactions between COVID-19 and cardiovascular medication in hypertension, acute coronary syndrome, heart failure, venous thromboembolism, and arrhythmias.

As elective surgery slowly reopens across the country, it is paramount that surgeons recognize and take responsibility for their roles in protecting patient safety during the coronavirus disease 2019 pandemic. Namely, these include (1) to prevent further spread of the severe acute respiratory syndrome-CoV-2 virus, (2) to understand the shift in injuries that has occurred as a result of altered lifestyles led by our patients, and (3) to leverage our platforms to disseminate information regarding how individuals can maintain musculoskeletal health during the pandemic. Efforts taken to reduce the spread of severe acute respiratory syndrome-CoV-2 virus can be focused on 3 broad categories of provider-patient interaction: preoperative and clinic visits, surgical encounters, and postoperative care.

The pandemic of coronavirus disease (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has involved more than one hundred million individuals, including more than two million deaths. Diabetes represents one of the most prevalent chronic conditions worldwide and significantly increases the risk of hospitalization and death in COVID-19 patients. In this review, we discuss the prevalence, the pathophysiological mechanisms, and the outcomes of COVID-19 infection in people with diabetes. We propose a rationale for using drugs prescribed in patients with diabetes and some pragmatic clinical recommendations to deal with COVID-19 in this kind of patient.

Despite an overall reduction in the number of stroke cases presenting to hospitals during the COVID-19 pandemic, a remarkably high incidence of acute cerebrovascular disease associated with the infection has been reported. In this systematic review, we assess the neurological outcomes and complications of endovascular thrombectomy (EVT) for large vessel occlusions (LVO) in COVID-19 patients.

A literature search was performed in PubMed from December 1, 2019 through September 1st, 2020 using different combinations of suitable keywords. Ten studies reporting EVT outcomes and complications were identified. Two studies that included non-LVO pathologies and COVID-19 negative patients with the outcomes analysis were excluded. Patient demographics, comorbidities, anatomic thrombus location, neurological and angiographic outcomes were assessed.

A total of 8 studies, in addition to our institutional case series, were ultimately included in this review. The mean age was 62.2 years, of which 67.6% were males. M1 segment involvement was the most commonly reported (53.8%) thrombus location. The mean NIHSS at presentation was 20.4 with no significant change at 24 h. Successful revascularization (TICI ≥ 2b) was achieved in 89%. Early proximal cerebral re-occlusion was reported in 6 patients (11%) and cerebral hemorrhage in 3 patients (4%). In hospital mortality was reported in 15 patients (28.8%).

Despite angiographically successful EVT of LVOs in the majority of patients, this literature analysis demonstrates overall poor outcomes and high mortality in COVID-19 patients post EVT. An unusual incidence of early intracerebral proximal arterial re-occlusion was notable.

Diabetes, hypertension and cardiovascular disease have been listed as risk factors for severe coronavirus disease 2019 (COVID-19) since the first report of the disease in January 2020. However, this report did not mention chronic kidney disease (CKD) nor did it provide information on the relevance of estimated glomerular filtration rate (eGFR) or albuminuria. As the disease spread across the globe, information on larger populations with greater granularity on risk factors emerged. The recently published OpenSAFELY project analysed factors associated with COVID-19 death in 17 million patients. The picture that arose differs significantly from initial reports. For example, hypertension is not an independent risk factor for COVID-19 death [adjusted hazard ratio (aHR) 0.89], but renal disease very much is. Dialysis (aHR 3.69), organ transplantation (aHR 3.53) and CKD (aHR 2.52 for patients with eGFR <30 mL/min/1.73 m2) represent three of the four comorbidities associated with the highest mortality risk from COVID-19. The risk associated with CKD Stages 4 and 5 is higher than the risk associated with diabetes mellitus (aHR range 1.31-1.95, depending upon glycaemic control) or chronic heart disease (aHR 1.17). In another recent publication, the Global Burden of Disease collaboration identified that worldwide, CKD is the most prevalent risk factor for severe COVID-19. Moreover, the distribution of risk factors for COVID-19 mortality appears to be different in patients with CKD when compared with the general population. The high prevalence of CKD in combination with the elevated risk of mortality from COVID-19 in CKD necessitates urgent action for this group of patients. This article defines essential action points (summarized in Box 1), among which is advocating the inclusion of CKD patients in clinical trials testing the efficacy of drugs and vaccines to prevent severe COVID-19.

Outbreaks of coronavirus disease 2019 (COVID-19) have been reported in nursing homes and assisted living facilities; however, the extent of asymptomatic and presymptomatic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in this high-risk population remains unclear.

We conducted an investigation of the first known outbreak of SARS-CoV-2 at a skilled nursing facility (SNF) in Illinois on 15 March 2020 and followed residents for 30 days. We tested 126/127 residents for SARS-CoV-2 via reverse-transcription polymerase chain reaction and performed symptom assessments. We calculated the point prevalence of SARS-CoV-2 and assessed symptom onset over 30-day follow-up to determine: (1) the proportion of cases who were symptomatic, presymptomatic, and asymptomatic and (2) incidence of symptoms among those who tested negative. We used the Kaplan-Meier method to determine the 30-day probability of death for cases.

Of 126 residents tested, 33 had confirmed SARS-CoV-2 on 15 March. Nineteen (58%) had symptoms at the time of testing, 1 (3%) developed symptoms over follow-up, and 13 (39%) remained asymptomatic. Thirty-five residents who tested negative on 15 March developed symptoms over follow-up; of these, 3 were re-tested and 2 were positive. The 30-day probability of death among cases was 29%.

SNFs are particularly vulnerable to SARS-CoV-2, and residents are at risk of severe outcomes. Attention must be paid to preventing outbreaks in these and other congregate care settings. Widespread testing and infection control are key to help prevent COVID-19 morbidity and mortality in these high-risk populations.

Acute kidney injury (AKI) is a frequent complication in coronavirus disease 2019 (COVID-19). It is often linked to progressive respiratory failure and is associated with increased morbidity and mortality. The AKI is presumably of multifactorial origin, whereby direct viral infestation of the kidneys also seems to be involved. Specific treatment procedures for AKI associated with COVID-19 are currently missing. In addition, the role of extracorporeal procedures in the treatment of COVID-19 could so far not be clarified. Latest data indicate persistent loss of renal function following COVID-19-associated AKI. Therefore, a re-evaluation of renal function following recovery from COVID-19 should be recommended.

Detailed descriptions of the patterns of disease progression of deceased coronavirus disease 2019 (COVID-19) patients have not been well explored.

This study sought to explore disease progression patterns and risk factors associated with mortality of deceased patients with COVID-19.

Epidemiological, clinical, laboratory, and imaging data (from 15 January to 26 March 2020) of laboratory-confirmed COVID-19 patients were collected retrospectively from two hospitals, Hubei province, China. Disease progression patterns of patients were analyzed based on laboratory data, radiological findings, and Sequential Organ Failure Assessment (SOFA) score. Risk factors associated with death were analyzed.

A total of 792 patients were enrolled in this study, of whom 68 died and 724 survived. Complications during hospitalization, such as sepsis, severe acute respiratory distress syndrome, acute cardiac injury, and acute kidney injury, were markedly more frequent in deceased patients than in surviving patients. Deceased patients presented progressive deterioration pattern in laboratory variables, chest computed tomography evaluation, and SOFA score, while surviving patients presented initial deterioration to peak level involvement followed by improvement pattern over time. Days 10 to 14 after illness onset was a critical stage of disease course. Older age, number of preexisting comorbidities ≥2, and SOFA score were independently associated with death for COVID-19.

Multiorgan dysfunction was common in deceased COVID-19 patients. Deceased patients presented progressive deterioration pattern, while surviving patients presented a relatively stable pattern during disease progression. Older age, number of preexisting comorbidities ≥2, and SOFA score were independent risk factors for death for COVID-19.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) initially most appreciated for its pulmonary symptoms, is now increasingly recognized for causing multi-organ disease and stroke in the setting of a hypercoagulable state. We report a case of 33-year-old African American woman with COVID-19 who developed acute malignant middle cerebral artery infarction due to thromboembolic occlusion of the left terminal internal carotid artery and middle cerebral artery stem. Mechanical thrombectomy was challenging and ultimately unsuccessful resulting in limited reperfusion of <67% of the affected vascular territory, and thrombectomized clot was over 50 mm in length, at least three times the average clot length. The final stroke size was estimated at 224 cubic centimeters. On admission her D-dimer level was 94,589 ng/mL (normal 0-500 ng/ml). Throughout the hospitalization D-dimer decreased but never reached normal values while fibrinogen trended upward. Hypercoagulability panel was remarkable for mildly elevated anticardiolipin IgM of 16.3 MPL/mL (normal: 0-11.0 MPL/mL). With respect to remaining stroke workup, there was no evidence of clinically significant stenosis or dissection in the proximal internal carotid artery or significant cardioembolic source including cardiomyopathy, atrial fibrillation, cardiac thrombus, cardiac tumor, valvular abnormality, aortic arch atheroma, or patent foramen ovale. She developed malignant cytotoxic cerebral edema and succumbed to complications. This case underscores the importance of recognizing hypercoagulability as a cause of severe stroke and poor outcome in young patients with COVID-19 and highlights the need for further studies to define correlation between markers of coagulopathy in patients with COVID-19 infection and outcome post stroke.

This study aimed to analyse the spatial-temporal distribution of COVID-19 mortality in Sergipe, Northeast, Brazil. It was an ecological study utilising spatiotemporal analysis techniques that included all deaths confirmed by COVID-19 in Sergipe, from 2 April to 14 June 2020. Mortality rates were calculated per 100 000 inhabitants and the temporal trends were analysed using a segmented log-linear model. For spatial analysis, the Kernel estimator was used and the crude mortality rates were smoothed by the empirical Bayesian method. The space-time prospective scan statistics applied the Poisson's probability distribution model. There were 391 COVID-19 registered deaths, with the majority among ⩾60 years old (62%) and males (53%). The most prevalent comorbidities were hypertension (40%), diabetes (31%) and cardiovascular disease (15%). An increasing mortality trend across the state was observed, with a higher increase in the countryside. An active spatiotemporal cluster of mortality comprising the metropolitan area and neighbouring cities was identified. The trend of COVID-19 mortality in Sergipe was increasing and the spatial distribution of deaths was heterogeneous with progression towards the countryside. Therefore, the use of spatial analysis techniques may contribute to surveillance and control of COVID-19 pandemic.

COVID-19 caused by severe acute respiratory syndrome coronavirus 2 has developed into a global pandemic. COVID-19 poses a huge threat to health care, and the shortage of medical resources caused by COVID-19 brought serious secondary disasters to elderly cancer patients who are particularly dependent on medical resources. The clinical challenges of cancer management, including aging, immunosuppression, and comorbidities, make cancer patients more vulnerable to COVID-19 with different clinical manifestations, disease severity, and outcomes. The review comprehensively analyzed the characteristics of the cancer patients under the pandemic and concluded that cancer patients were more susceptible to COVID-19, and also concluded that they were more likely to develop poor outcomes and the severe form of the disease. Three basic management strategies have been proposed to protect susceptible elderly cancer patients, find reliable indicators to monitor the course of disease, and implement effective prevention measures.

SARS-CoV-2 (Covid-19) infection has recently become a worldwide challenge with dramatic global economic and health consequences. As the pandemic is still spreading, new data concerning Covid-19 complications and related mechanisms become increasingly available. Accumulating data suggest that the incidence of cardiac arrest and its outcome are adversely affected during the Covid-19 period. This may be further exacerbated by drug-related cardiac toxicity of Covid-19 treatment regimens. Elucidating the underlying mechanisms that lead to Covid-19 associated cardiac arrest is imperative, not only in order to improve its effective management but also to maximize preventive measures. Herein we discuss available epidemiological data on cardiac arrest during the Covid-19 pandemic as well as possible associated causes and pathophysiological mechanisms and highlight gaps in evidence warranting further investigation. The risk of transmission during cardiopulmonary resuscitation (CPR) is also discussed in this review. Finally, we summarize currently recommended guidelines on CPR for Covid-19 patients including CPR in patients with cardiac arrest due to suspected drug-related cardiac toxicity in an effort to underscore the most important common points and discuss discrepancies proposed by established international societies.

The aim of this study was to investigate whether right ventricular longitudinal strain (RVLS) was independently predictive of higher mortality in patients with coronavirus disease-2019 (COVID-19).

RVLS obtained from 2-dimensional speckle-tracking echocardiography has been recently demonstrated to be a more accurate and sensitive tool to estimate right ventricular (RV) function. The prognostic value of RVLS in patients with COVID-19 remains unknown.

One hundred twenty consecutive patients with COVID-19 who underwent echocardiographic examinations were enrolled in our study. Conventional RV functional parameters, including RV fractional area change, tricuspid annular plane systolic excursion, and tricuspid tissue Doppler annular velocity, were obtained. RVLS was determined using 2-dimensional speckle-tracking echocardiography. RV function was categorized in tertiles of RVLS.

Compared with patients in the highest RVLS tertile, those in the lowest tertile were more likely to have higher heart rate; elevated levels of D-dimer and C-reactive protein; more high-flow oxygen and invasive mechanical ventilation therapy; higher incidence of acute heart injury, acute respiratory distress syndrome, and deep vein thrombosis; and higher mortality. After a median follow-up period of 51 days, 18 patients died. Compared with survivors, nonsurvivors displayed enlarged right heart chambers, diminished RV function, and elevated pulmonary artery systolic pressure. Male sex, acute respiratory distress syndrome, RVLS, RV fractional area change, and tricuspid annular plane systolic excursion were significant univariate predictors of higher risk for mortality (p < 0.05 for all). A Cox model using RVLS (hazard ratio: 1.33; 95% confidence interval [CI]: 1.15 to 1.53; p < 0.001; Akaike information criterion = 129; C-index = 0.89) was found to predict higher mortality more accurately than a model with RV fractional area change (Akaike information criterion = 142, C-index = 0.84) and tricuspid annular plane systolic excursion (Akaike information criterion = 144, C-index = 0.83). The best cutoff value of RVLS for prediction of outcome was -23% (AUC: 0.87; p < 0.001; sensitivity, 94.4%; specificity, 64.7%).

RVLS is a powerful predictor of higher mortality in patients with COVID-19. These results support the application of RVLS to identify higher risk patients with COVID-19.