In our research, 107 death patients confirmed with COVID-19 had been included. The average age of all dead patients is 71.2 ± 12.1 years, male accounted for 66.4%. As it had been reported that the older and male patients are more likely to be infected with SARS-CoV-2, and the male and older patients with viral pneumonia are also prone to develop ARDS, which is the main cause of death in our research. Some research found that X chromosome and sex hormones could protect females from viral infections. All above may explain why age and gender were associated with death.
Chronic diseases had been treated as important risk factors for poor outcome of COVID-19 as well. In a research about critically ill patients with SARS-CoV-2 pneumonia, 50% of non-survivors have chronic diseases, while 25% for survivors. As for our research, 76.6% of dead cases had chronic underlying diseases, the most common one was hypertension, followed by cardiovascular diseases. At the same time, cardiac injuries were most common cause of death behind respiratory failure (Fig. 2), followed by the injury of kidney and liver. As mentioned above, we guess that SARS-CoV-2 may worsen the injury of heart, exacerbating the death of patients. So, for critically ill patients, more attention should be focus on the injury of heart.
Most patients with SARS-CoV-2 infection had fever,[8, 12] which is in accordance with our studies. But research found that 11·5% of patients did not have fever at the onset of illness and thought this make the early identification more difficult. There are also 11(12.5%) out of 88 patients with fever in our research who did not manifest fever at the onset of symptoms. At the same time, the median duration from onset of symptoms to ICU admission was 5 (3–7) days, while the median duration from onset of symptoms to admission to hospital in our study is 7 (IQR,4–11) days. So the delay manifestation of fever and delay reception of medical care may exacerbate the death of patients with SARS-CoV-2 pneumonia.
It has been reported that the mortality rate in critically ill patients with SARS-CoV-2 infection can reach to 61.5%, higher than that of SARS-CoV and Middle Eastern respiratory syndrome (MERS)-CoV. Although many drugs are under clinical trial, there is no specific treatment for coronavirus infection at this time apart from supportive care. 93 (86.9%) patients in our research received mechanical ventilation, except for some patients whose relatives refused mechanical ventilation. 83 (77.6%) dead cases were given oseltamivir or others and almost half of patients received methylprednisolone. Although the use of glucocorticoids for patients with COVID-19 is controversial and no antiviral agents treating SARS and MERS have been found effective for SARS-CoV-2, more researches are need.
As for laboratory findings, lymphocytopenia is a common feature of patients with SARS-CoV-2 infection. Similar to those with SARS-CoV and MERS infection, targeted invasion by the virus may results in the apoptosis of lymphocytes in patients with SARS-CoV-2 infection.[17, 18] In one research, 35% of non-critical patients with SARS-CoV-2 infection had mild lymphocytopenia. While another research found that more than 80% of critically ill patients had lymphocytopenia and thought that the severity of lymphocytopenia reflects the severity of SARS-CoV-2 infection. In our study, 83.5% of dead patients in our study have lymphocytopenia on admission. Comparing with first value after admission, the absolute value of lymphocytes before death were decreased in 43 (54.4%) of patients. Lymphocytopenia is good to diagnosis of SARS-CoV-2 infection, but whether the severity of lymphocytopenia can predict the prognosis of SARS-CoV-2 infection is unclear. It has been reported the presence of secondary infection and elevated inflammatory indicators is predictor of poor prognosis in COVID-19 by comparing laboratory parameters between survivors and non-survivors. By comparing with first value after admission, the absolute value of white blood cells and Neutrophils before death were elevated in 55 (69.6%) and 56 (70.1%) of patients during the process of the disease. At the same time, PCT, an effective indicator of bacterial infection, was elevated in 67 (91.8%) patients on admission and 38 (71.7%) of patients experienced the elevation of PCT before death. Besides, 9 patients with hospital-acquired pneumonia, 4 with urinary tract infection and 2 with bacteraemia had been found. The results of our research furtherly suggest that coinfections and inflammation do exacerbate the death of patients.
As for organ dysfunction, cardiac damage is the most common one except for lung. Fulminant myocarditis is related to the rapid progress and a critically ill state of illness. Concerning the laboratory parameters of heart, cardiac troponin and myoglobin of non-survivors is higher than survivors. In our study, the elevations of myoglobin, CKMB, Pro-BNP, BNP and Troponin I is found in about 70% of patients, the elevation of lactate dehydrogenase and troponin T were found more than 90% of patients, during the process of disease. Myoglobin, Creatine Kinase-MB Form, BNP may predict the prognosis. But the other biomarker of cardiac function has been repeated in few patients, more researches are needed. On the other aspects, 68 (76.4%) and 64 (71.9%) patients had abnormal liver function and renal function damage on admission, which is higher than that of previous study. we also found near 50% of patients experienced the elevation of alanine aminotransferase and aspartate aminotransferase. while the rate of elevated blood urea nitrogen (71.2%) and cystatin C (68.8%) is higher than Serum creatinine (58.9%). The damage of kidney and liver maybe sever on the admission and during the process of COVID-19. Blood urea nitrogen and cystatin C maybe sensitive to predict the change of renal function
In addition, 56 (61.5%) patients’ Hb levels and 34 (37.4%) patients’ PLT levels were below the normal range after admission. Comparing with the first one, 58 (73.4%) patients’ Hb and 64 (81.0%) patients’ PLT levels of last test before death were decreased. In terms of coagulation function, the first levels of PT increased in 36 (52.9%) patients, the levels of APTT increased in 19 (24.7%) patients. As for change of coagulation function, longer PT was found in 42 (68.9%) patients, longer APTT was found in 38 (58.5%) patients. At the same time, 36 patients have hematuria and 9 patients had gastrointestinal haemorrhage. We also should pay more attention to the change of coagulation function of critically ill patients. But whether hematuria and gastrointestinal haemorrhage are associated with change of coagulation function is unclear. At last, 86 (96.6%) patients’ albumin levels were below the normal range at first test. What is more, the last level of albumin is decreased in 55 (78.6%) patients, comparing with the first test. it indicates that most of severe patients may have malnutrition.
This study has several limitations. First, only dead patients with confirmed SARS-CoV-2 infection were included. It would be better to have discharged patients included in our research and compare the difference between them. Second, some dead patients did not have the repeated measurements of some laboratory findings, so the sample size of some part of this research is small. Third, some important laboratory results were not tested by the same way in three hospital, which may impact the research negatively. Finally, this is a retrospective study. The data in this study permit a preliminary assessment of the clinical course of critically ill patients with SARS-CoV-2 pneumonia. More researches are still needed.