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Review
. 2020 Aug;288(2):192-206.
doi: 10.1111/joim.13091. Epub 2020 May 13.

COVID-19 diagnosis and management: a comprehensive review

Affiliations
Review

COVID-19 diagnosis and management: a comprehensive review

Giuseppe Pascarella et al. J Intern Med. 2020 Aug.

Abstract

Severe acute respiratory syndrome coronavirus (SARS-CoV)-2, a novel coronavirus from the same family as SARS-CoV and Middle East respiratory syndrome coronavirus, has spread worldwide leading the World Health Organization to declare a pandemic. The disease caused by SARS-CoV-2, coronavirus disease 2019 (COVID-19), presents flu-like symptoms which can become serious in high-risk individuals. Here, we provide an overview of the known clinical features and treatment options for COVID-19. We carried out a systematic literature search using the main online databases (PubMed, Google Scholar, MEDLINE, UpToDate, Embase and Web of Science) with the following keywords: 'COVID-19', '2019-nCoV', 'coronavirus' and 'SARS-CoV-2'. We included publications from 1 January 2019 to 3 April 2020 which focused on clinical features and treatments. We found that infection is transmitted from human to human and through contact with contaminated environmental surfaces. Hand hygiene is fundamental to prevent contamination. Wearing personal protective equipment is recommended in specific environments. The main symptoms of COVID-19 are fever, cough, fatigue, slight dyspnoea, sore throat, headache, conjunctivitis and gastrointestinal issues. Real-time PCR is used as a diagnostic tool using nasal swab, tracheal aspirate or bronchoalveolar lavage samples. Computed tomography findings are important for both diagnosis and follow-up. To date, there is no evidence of any effective treatment for COVID-19. The main therapies being used to treat the disease are antiviral drugs, chloroquine/hydroxychloroquine and respiratory therapy. In conclusion, although many therapies have been proposed, quarantine is the only intervention that appears to be effective in decreasing the contagion rate. Specifically designed randomized clinical trials are needed to determine the most appropriate evidence-based treatment modality.

Keywords: COVID-19; COVID-19 diagnosis; COVID-19 management; COVID-19 treatment; SARS-CoV-2; novel coronavirus.

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Conflict of interest statement

The authors declare no affiliations with or involvement in any organization or entity with any financial or nonfinancial interest related to this manuscript.

Figures

Fig. 1
Fig. 1
Typical patterns of COVID‐19 at CT imaging. Ground glass shadows (early stage). Ground‐glass opacities. Ground glass nodules and subpleural consolidation. Focal consolidation. Multifocal consolidation. Multifocal consolidation with honeycomb (end stage).
Fig. 2
Fig. 2
Patterns of COVID‐19 at chest ultrasound. Early bilateral multifocal areas of interstitial syndrome. Interstitial pneumonia characterized by interstitial syndrome with B lines and preserved sliding sign. Advanced, organized pneumonia with interstitial syndrome associated with multiple subpleural consolidations and reduced sliding sign.
Fig. 3
Fig. 3
Virus‐induced inflammation pathway. Immune cells are sequentially activated to limit virus dissemination. Dendritic cells and macrophages act as first‐line antigen‐presenting cells which, following virus antigen recognition, produce cytokines, including interleukin (IL)‐12, IL‐15 and IL‐18. Their interaction determines the chemotaxis and activation of natural killer (NK) cells, the recruitment of Group 1 innate lymphoid cells (ILC1) and the differentiation of T helper (Th) lymphocytes into Type 1 helper (Th1) cells. The latter are associated with an increased expression of cytokines, including interferon (IFN)‐γ, tumour necrosis factor (TNF)‐α, IL‐1 and IL‐2, with consequent activation of NK cells, secreting perforin, granzymes, reactive oxygen species (ROS), nitric oxide (NO) and cytotoxic T lymphocytes in order to kill the virus. Excess neutrophils and persistently activated macrophages cause extensive damage to the lung epithelium and endothelium, resulting in an alveolar capillary barrier. The disruption of this barrier allows protein‐rich fluid to enter the alveoli, causing fluid accumulation in alveolar spaces (noncardiogenic pulmonary oedema) which interferes with gas exchange.

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