This retrospective study described the epidemiological and clinical characteristics of 83 deaths with COVID–19 pneumonia. To my knowledge, our study is the first epidemiological investigation, whose subjects were all patients with COVID–19 pneumonia who died.
In this study, the median of the onset-to-admission interval was longer than that of patients in the previous two studies[11, 14]. Most patients were hospitalized more than 6 days after the onset of the disease, and the longest was 43 days. Two factors likely contributed to the interval. Fisrt,some patients have no severe symptoms in the early stage and it took more for home isolation and community treatment. Second, due to the COVID–19 outbreak, the isolation ward of the hospital may have been under capacity in the initial. Most of the patients who died in the 15–21days after the onset of the disease, both male and female. This result indicate that the third week may be a period of high risk of death for critically ill patients with COVID–19.
Most of the deaths with COVID–19 pneumonia were elderly patients especially those over 70 years of age, and male patients. These are consistent with a recent study[10]. The cases of COVID–19 in pregnant women have been mentioned in previous studiy[15]. Of 29 pregnant women with COVID–19 in the hospital, there are no deaths so far.
The proportion of patients with comorbidities was higher than previous studies in patients with COVID–19[10, 11, 14, 16]. The most common comorbidities were hypertension in our study, which was diabetes in two previous cohort studies of Middle Eastern respiratory syndrome coronavirus (MRSE-Cov) infection and severe acute respiratory syndrome coronavirus(SARS-CoV) infection[17, 18]. We observed that the majority of patients who died were also geriatric patients and those suffering from chronic comorbidities. However, some healthy people(22%) died without complications, which were an indication of the high pathogenicity of COVID–19. The initial clinical symptoms of patients infected with COVID–19 were nonspecific. There were no significant differences in the types of initial symptoms between the deaths in our study and the recently published studies[[11, 14, 16, 19]. However, the first three symptoms in our study were shortness of breath, fever, Myalgia or fatigue. A small number of patients initially presented with gastrointestinal symptoms, such as anorexia, nausea, vomiting, and diarrhoea, which were mentioned in previous studies[14, 16].
Most of the patients in our study developed acute respiratory failure including ARDS, fatal infection, abnormal coagulation and eventually multiple organ failure, except for six who died of acute myocardial infarction. As a newly identified disease, litter is known about the pathogenic mechanism of COVID–19. Most of the patients who died had abnormal coagulation. Increased inflammatory markers such as procalcitonin and C-reactive, lymphopenia were a common characteristic in the patients. This series of changes is a manifestation of the immune response and maybe be a factor in poor prognosis[11, 14, 18]. In a recent fatal case report, typical features of inflammation were observed in the pulmonary pathology of the patient, whose pathological section showed interstitial mononuclear inflammatory infiltrates, dominated by lymphocytes[20]. These pathological characteristics greatly resemble those of MRSE-Cov infection and SARS-CoV infection[20–22].
Until now, no drugs have been found to be specifically effective against coronaviruses. Of the 83 patients in our study, each patient received abidol, and some patients were treated with oseltamivir, ganciclovir, lopinavir and ritonavir, but none of them had a definite therapeutic effect. In addition, radcivir is an unlisted nucleotide drug whose broad-spectrum antiviral activity has been confirmed in animal models[23, 24]. It may be a potential effective drug for patients with COVID–19.[25] Two randomized controlled clinical trials (NCT04252664; NCT04257656) to assess the safety and efficacy of radcivir are is currently underway in patients hospitalized with COVID–19 pneumonia.
The patients in this study were generally had associated with a secondary bacterial infection, followed by sepsis and septic shock. 97.6% of the patients were treated with antibiotics based on abnormal inflammatory markers and bacterial culture results. In patients with SARS and MERS, the effect of glucocorticoid therapy on prognosis is Controversial[26, 27]. However, severe patients with COVID–19 may be beneficial from glucocorticoid therapy to prevent ARDS development, based on recent studies[16, 20]. 65.1% of the patients in this study received glucocorticoid therapy. In the study, 63 patients did not receive invasive mechanical ventilation, 41 of them declined invasive mechanical ventilation, and the other 22 for unknown reasons.
Our study has several limitations. First of all, the study had a limited number of cases, with only 83 deaths. However, to our knowledge, very few case series of deaths have been reported, the data is a valuable demonstration of characteristics of deaths with COVID–19 pneumonia in the early period of exponential growth. Secondly, some data such as cytokines (eg, IL2, IL4, IL6, IL10, TNF, IFN γ) were absent in patients admitted early, which were related to lung injury in previous studies SARS-CoV and MERS-CoV[28, 29]. We will routinely observe the changes of cytokines of patients in further study. Thirdly, data on all patients with COVID–19 pneumonia in the hospital during the same period were not fully available at the time of our analysis. However, this is a series of study designs and the patients will continue to be followed up.