Prognostic factors in patients admitted to an urban teaching hospital with COVID-19 infection

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Abstract

Background

Severe COVID-19 infection results in a systemic inflammatory response (SIRS). This SIRS response shares similarities to the changes observed during the peri-operative period that are recognised to be associated with the development of multiple organ failure.

Methods

Electronic patient records for patients who were admitted to an urban teaching hospital during the initial 7-week period of the COVID-19 pandemic in Glasgow, U.K. (17th March 2020—1st May 2020) were examined for routine clinical, laboratory and clinical outcome data. Age, sex, BMI and documented evidence of COVID-19 infection at time of discharge or death certification were considered minimal criteria for inclusion.

Results

Of the 224 patients who fulfilled the criteria for inclusion, 52 (23%) had died at 30-days following admission. COVID-19 related respiratory failure (75%) and multiorgan failure (12%) were the commonest causes of death recorded. Age ≥ 70 years (p < 0.001), past medical history of cognitive impairment (p ≤ 0.001), previous delirium (p < 0.001), clinical frailty score > 3 (p < 0.001), hypertension (p < 0.05), heart failure (p < 0.01), national early warning score (NEWS) > 4 (p < 0.01), positive CXR (p < 0.01), and subsequent positive COVID-19 swab (p ≤ 0.001) were associated with 30-day mortality. CRP > 80 mg/L (p < 0.05), albumin < 35 g/L (p < 0.05), peri-operative Glasgow Prognostic Score (poGPS) (p < 0.05), lymphocytes < 1.5 10 ⁹/l (p < 0.05), neutrophil lymphocyte ratio (p ≤ 0.001), haematocrit (< 0.40 L/L (male)/ < 0.37 L/L (female)) (p ≤ 0.01), urea > 7.5 mmol/L (p < 0.001), creatinine > 130 mmol/L (p < 0.05) and elevated urea: albumin ratio (< 0.001) were also associated with 30-day mortality.

On multivariate analysis, age ≥ 70 years (O.R. 3.9, 95% C.I. 1.4–8.2, p < 0.001), past medical history of heart failure (O.R. 3.3, 95% C.I. 1.2–19.3, p < 0.05), NEWS > 4 (O.R. 2.4, 95% C.I. 1.1–4.4, p < 0.05), positive initial CXR (O.R. 0.4, 95% C.I. 0.2–0.9, p < 0.05) and poGPS (O.R. 2.3, 95% C.I. 1.1–4.4, p < 0.05) remained independently associated with 30-day mortality.

Among those patients who tested PCR COVID-19 positive (n = 122), age ≥ 70 years (O.R. 4.7, 95% C.I. 2.0—11.3, p < 0.001), past medical history of heart failure (O.R. 4.4, 95% C.I. 1.2–20.5, p < 0.05) and poGPS (O.R. 2.4, 95% C.I. 1.1–5.1, p < 0.05) remained independently associated with 30-days mortality.

Conclusion

Age ≥ 70 years and severe systemic inflammation as measured by the peri-operative Glasgow Prognostic Score are independently associated with 30-day mortality among patients admitted to hospital with COVID-19 infection.

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Most cited references 19

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Dexamethasone in Hospitalized Patients with Covid-19 — Preliminary Report

Mark Peters (2020)

Abstract Background Coronavirus disease 2019 (Covid-19) is associated with diffuse lung damage. Glucocorticoids may modulate inflammation-mediated lung injury and thereby reduce progression to respiratory failure and death. Methods In this controlled, open-label trial comparing a range of possible treatments in patients who were hospitalized with Covid-19, we randomly assigned patients to receive oral or intravenous dexamethasone (at a dose of 6 mg once daily) for up to 10 days or to receive usual care alone. The primary outcome was 28-day mortality. Here, we report the preliminary results of this comparison. Results A total of 2104 patients were assigned to receive dexamethasone and 4321 to receive usual care. Overall, 482 patients (22.9%) in the dexamethasone group and 1110 patients (25.7%) in the usual care group died within 28 days after randomization (age-adjusted rate ratio, 0.83; 95% confidence interval [CI], 0.75 to 0.93; P<0.001). The proportional and absolute between-group differences in mortality varied considerably according to the level of respiratory support that the patients were receiving at the time of randomization. In the dexamethasone group, the incidence of death was lower than that in the usual care group among patients receiving invasive mechanical ventilation (29.3% vs. 41.4%; rate ratio, 0.64; 95% CI, 0.51 to 0.81) and among those receiving oxygen without invasive mechanical ventilation (23.3% vs. 26.2%; rate ratio, 0.82; 95% CI, 0.72 to 0.94) but not among those who were receiving no respiratory support at randomization (17.8% vs. 14.0%; rate ratio, 1.19; 95% CI, 0.91 to 1.55). Conclusions In patients hospitalized with Covid-19, the use of dexamethasone resulted in lower 28-day mortality among those who were receiving either invasive mechanical ventilation or oxygen alone at randomization but not among those receiving no respiratory support. (Funded by the Medical Research Council and National Institute for Health Research and others; RECOVERY ClinicalTrials.gov number, NCT04381936; ISRCTN number, 50189673.)

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COVID-19: consider cytokine storm syndromes and immunosuppression

Puja Mehta, Daniel McAuley, Michael Brown … (2020)

As of March 12, 2020, coronavirus disease 2019 (COVID-19) has been confirmed in 125 048 people worldwide, carrying a mortality of approximately 3·7%, 1 compared with a mortality rate of less than 1% from influenza. There is an urgent need for effective treatment. Current focus has been on the development of novel therapeutics, including antivirals and vaccines. Accumulating evidence suggests that a subgroup of patients with severe COVID-19 might have a cytokine storm syndrome. We recommend identification and treatment of hyperinflammation using existing, approved therapies with proven safety profiles to address the immediate need to reduce the rising mortality. Current management of COVID-19 is supportive, and respiratory failure from acute respiratory distress syndrome (ARDS) is the leading cause of mortality. 2 Secondary haemophagocytic lymphohistiocytosis (sHLH) is an under-recognised, hyperinflammatory syndrome characterised by a fulminant and fatal hypercytokinaemia with multiorgan failure. In adults, sHLH is most commonly triggered by viral infections 3 and occurs in 3·7–4·3% of sepsis cases. 4 Cardinal features of sHLH include unremitting fever, cytopenias, and hyperferritinaemia; pulmonary involvement (including ARDS) occurs in approximately 50% of patients. 5 A cytokine profile resembling sHLH is associated with COVID-19 disease severity, characterised by increased interleukin (IL)-2, IL-7, granulocyte-colony stimulating factor, interferon-γ inducible protein 10, monocyte chemoattractant protein 1, macrophage inflammatory protein 1-α, and tumour necrosis factor-α. 6 Predictors of fatality from a recent retrospective, multicentre study of 150 confirmed COVID-19 cases in Wuhan, China, included elevated ferritin (mean 1297·6 ng/ml in non-survivors vs 614·0 ng/ml in survivors; p 39·4°C 49 Organomegaly None 0 Hepatomegaly or splenomegaly 23 Hepatomegaly and splenomegaly 38 Number of cytopenias * One lineage 0 Two lineages 24 Three lineages 34 Triglycerides (mmol/L) 4·0 mmol/L 64 Fibrinogen (g/L) >2·5 g/L 0 ≤2·5 g/L 30 Ferritin ng/ml 6000 ng/ml 50 Serum aspartate aminotransferase <30 IU/L 0 ≥30 IU/L 19 Haemophagocytosis on bone marrow aspirate No 0 Yes 35 Known immunosuppression † No 0 Yes 18 The Hscore 11 generates a probability for the presence of secondary HLH. HScores greater than 169 are 93% sensitive and 86% specific for HLH. Note that bone marrow haemophagocytosis is not mandatory for a diagnosis of HLH. HScores can be calculated using an online HScore calculator. 11 HLH=haemophagocytic lymphohistiocytosis. * Defined as either haemoglobin concentration of 9·2 g/dL or less (≤5·71 mmol/L), a white blood cell count of 5000 white blood cells per mm3 or less, or platelet count of 110 000 platelets per mm3 or less, or all of these criteria combined. † HIV positive or receiving longterm immunosuppressive therapy (ie, glucocorticoids, cyclosporine, azathioprine).

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Dysregulation of immune response in patients with COVID-19 in Wuhan, China

Chuan Qin, Luoqi Zhou, Ziwei Hu … (2020)

Abstract Background In December 2019, coronavirus disease 2019 (COVID-19) emerged in Wuhan and rapidly spread throughout China. Methods Demographic and clinical data of all confirmed cases with COVID-19 on admission at Tongji Hospital from January 10 to February 12, 2020, were collected and analyzed. The data of laboratory examinations, including peripheral lymphocyte subsets, were analyzed and compared between severe and non-severe patients. Results Of the 452 patients with COVID-19 recruited, 286 were diagnosed as severe infection. The median age was 58 years and 235 were male. The most common symptoms were fever, shortness of breath, expectoration, fatigue, dry cough and myalgia. Severe cases tend to have lower lymphocytes counts, higher leukocytes counts and neutrophil-lymphocyte-ratio (NLR), as well as lower percentages of monocytes, eosinophils, and basophils. Most of severe cases demonstrated elevated levels of infection-related biomarkers and inflammatory cytokines. The number of T cells significantly decreased, and more hampered in severe cases. Both helper T cells and suppressor T cells in patients with COVID-19 were below normal levels, and lower level of helper T cells in severe group. The percentage of naïve helper T cells increased and memory helper T cells decreased in severe cases. Patients with COVID-19 also have lower level of regulatory T cells, and more obviously damaged in severe cases. Conclusions The novel coronavirus might mainly act on lymphocytes, especially T lymphocytes. Surveillance of NLR and lymphocyte subsets is helpful in the early screening of critical illness, diagnosis and treatment of COVID-19.

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Author and article information

Contributors

Donogh Maguire:

ORCID: http://orcid.org/0000-0002-0317-4079

Donogh.Maguire@glasgow.ac.uk

Journal

Journal ID (nlm-ta): J Transl Med

Journal ID (iso-abbrev): J Transl Med

Title: Journal of Translational Medicine

Publisher: BioMed Central (London )

ISSN (Electronic): 1479-5876

Publication date (Electronic): 15 September 2020

Publication date PMC-release: 15 September 2020

Publication date Collection: 2020

Volume: 18

Electronic Location Identifier: 354

Affiliations

[1 ]GRID grid.411714.6, ISNI 0000 0000 9825 7840, Emergency Medicine Department, , Glasgow Royal Infirmary, ; 84 Castle Street, Glasgow, G4 0SF UK

[2 ]GRID grid.8756.c, ISNI 0000 0001 2193 314X, School of Medicine Veterinary and Life Sciences, Wolfson Medical School Building, , University of Glasgow, ; University Avenue, Glasgow, G12 8QQ UK

[3 ]Academic Unit of Surgery, School of Medicine, University of Glasgow, New Lister Building, Royal Infirmary, Glasgow, G31 2ER UK

[4 ]GRID grid.411714.6, ISNI 0000 0000 9825 7840, Department of Acute Medicine, , Glasgow Royal Infirmary, ; Glasgow, G4 0SF UK

[5 ]GRID grid.4305.2, ISNI 0000 0004 1936 7988, Institute of Genetics and Molecular Medicine, , University of Edinburgh, ; Edinburgh, EH4 2XU UK

[6 ]St Columba’s Hospice, 15 Boswall Rd, Edinburgh, EH5 3RW UK

[7 ]GRID grid.411714.6, ISNI 0000 0000 9825 7840, The Scottish Trace Element and Micronutrient Reference Laboratory, Department of Biochemistry, , Royal Infirmary, ; Glasgow, G31 2ER UK

[8 ]GRID grid.415490.d, ISNI 0000 0001 2177 007X, Department of Clinical Biochemistry, , Queen Elizabeth University Hospital, ; Govan, Glasgow, G51 4TF UK

Author information

Donogh Maguire http://orcid.org/0000-0002-0317-4079

Article

Publisher ID: 2524

DOI: 10.1186/s12967-020-02524-4

PMC ID: 7491021

PubMed ID: 31900168

SO-VID: 032e930e-e716-45d7-b3b6-354f9d8e3fb4

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 6 July 2020

Date accepted : 8 September 2020

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ScienceOpen disciplines: Medicine

Keywords: covid-19,systemic inflammatory response (sirs),c-reactive protein (crp),albumin,peri-operative glasgow prognostic score (pogps),neutrophil lymphocyte ratio (nlr),30-day mortality,host inflammatory response

Data availability:

ScienceOpen disciplines: Medicine

Keywords: covid-19, systemic inflammatory response (sirs), c-reactive protein (crp), albumin, peri-operative glasgow prognostic score (pogps), neutrophil lymphocyte ratio (nlr), 30-day mortality, host inflammatory response

Prognostic factors in patients admitted to an urban teaching hospital with COVID-19 infection

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Abstract

Background

Methods

Results

Conclusion

Related collections

Novel Coronavirus Disease COVID-19

Most cited references 19

Dexamethasone in Hospitalized Patients with Covid-19 — Preliminary Report

COVID-19: consider cytokine storm syndromes and immunosuppression

Dysregulation of immune response in patients with COVID-19 in Wuhan, China

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