Abstract
Compared with other deadly diseases, the coronavirus disease 2019 (COVID-19) is highly infectious with a relatively low mortality rate. Although critical cases account for only 5% of cases, the mortality rate for the same is nearly 50%. Therefore, the key to the COVID-19 treatment is to effectively treat severe patients and reduce the transition from severe to critical cases. A retrospective study was carried out to evaluate outcomes of treatment in patients with severe and critical COVID-19 admitted to a COVID-19 special hospital in Wuhan, China. A total of 75 severe and critical COVID-19 patients were admitted and treated with immunomodulation as the main strategy combined with anti-inflammatory therapy and appropriate anticoagulation. Leukocyte levels in patients with 7-14 days of onset to diagnosis were significantly lower than in those with >14 days. Higher levels of globulin and D-dimer and lower lymphocyte levels were found in the older age group (>65 years) than in the middle-aged group (50-64 years). Patients with comorbidity had higher levels of inflammatory indicators. After treatment, 65 (86.67%) patients were cured, 7 (9.33%) had improved, and 3 (4.00%) had died. Median hospitalization duration was 23 days. Fatal cases showed continuously increased levels of globulin, dehydrogenase (LDH), hypersensitive C-reactive protein (hs-CRP), D-dimer, and cytokines during treatment. Time from onset to diagnosis, age, and comorbidity are important influencing factors on treatment effects. The occurrence of immunosuppression, “cytokine storm,” and thrombosis may be an important cause of death in severely infected cases. In conclusion, high cure rate and low mortality suggested that immunomodulation combined with anti-inflammatory therapy and appropriate anticoagulant therapy is a good strategy for treatment of patients with severe and critical COVID-19.
Highlights
Coronavirus is a common cause of the human cold but has led to serious respiratory infectious diseases, such as the Middle East respiratory syndrome (MERS) and severe acute respiratory syndrome (SARS) [1]
Improving the treatment of severe or critical cases and controlling the transition from severe to critical are the key to improving the clinical cure rate and reducing the mortality rate of COVID-19
Cytokine analysis showed that proinflammatory factors such as IL-1β, IL-6, GM-CSF, tumor necrosis factor α (TNF-α), and IFN-γ were abnormally elevated in severe COVID-19 patients, which is consistent with the clinical results [8, 9]
Summary
Coronavirus is a common cause of the human cold but has led to serious respiratory infectious diseases, such as the Middle East respiratory syndrome (MERS) and severe acute respiratory syndrome (SARS) [1]. As of May 20, 2020, the emerging coronavirus infection has caused over 4.9 million cases in more than 200 countries and over 320 thousand of death. Cytokine analysis showed that proinflammatory factors such as IL-1β, IL-6, GM-CSF, TNF-α, and IFN-γ were abnormally elevated in severe COVID-19 patients, which is consistent with the clinical results [8, 9]. Clinical studies have found that cytokine storm is emerging as one of the mechanisms leading to severe COVID-19 infection, which is associated with organ injury and poor prognosis [10]. Patients with severe symptoms show high fever, headache, fatigue, disseminated intravascular coagulation (DIC), shock, multiple organ failure (MOF), and even death [11,12,13]. Suppression of cytokine storm is an important way to effectively prevent disease progression and reduce the mortality rate
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