Severe acute respiratory syndrome coronavirus 2 (SARS-CoV–2), which is genetically similar to the severe acute respiratory syndrome (SARS) coronavirus that resulted in the SARS outbreak in 2002, is responsible for a global pandemic of COVID–19.14 The outbreak began in China but has since spread around the world.15–17 The hospitals and clinics were initially overwhelmed, and both patients and healthcare providers became severely ill and died soon after. However, as the healthcare system response ramped up, more designated and newly built hospitals and better equipment became available, the situation was under control within a short period in China. As usual, different countries have different ways of resolving the conundrum. Although the COVID–19 pandemic is still ongoing, the good news is that in China and South Korea, the number of new cases per day has dropped off, largely due to aggressive public health measures, such as quarantining, aggressive testing, sufficient manpower, and the most importantly, everyone’s efforts.18
In our study, there were 94 confirmed cases of COVID–19 in the ICU of Huoshenshan Hospital, and the 42 deaths resulted in a fatality rate of 45%, which is close to the data reported by the Chinese Centers for Disease Control and Prevention.19 As mentioned in the previous literature19, approximately 80% of patients with COVID–19 have mild symptoms, and few people do not develop any symptoms or signs at all. For the remaining 20%, as our study shows, these patients can range from mild symptoms, such as fever and dry cough, all the way to severe conditions, such as ARDS and even sepsis. Based on our data, the rate of critically ill patients is relatively low below the age of 60, but the rate starts to increase for the elderly. Similarly, both the rate of critical illness and the fatality rate are higher for patients with underlying health problems than for those without any of these conditions. In addition, many elderly patients typically have one or more of these conditions, so it is not surprising that these factors go hand in hand. Unlike seasonal flu, vaccines for SARS-CoV–2 have not yet been well established, although both are respiratory viruses.20 Therefore, elderly patients with underlying health problems are truly the ones at highest risk.
The inflammation caused by SARS-CoV–2 builds up much fluid within and around the lung and results in acute respiratory distress syndrome (ARDS) and even subsequent multiple organ dysfunction syndrome, which means that the whole body starts shutting down.21 ARDS is a common complication during the clinical course and is the main cause of death. Among the nonsurvivors, all patients were diagnosed with ARDS and sepsis, which is often caused by severe infection. Our experience revealed that ARDS always had sudden onset and rapid development, so few patients died soon. So far, not many treatment options exist for coronavirus, so the only option is offering supportive treatment, such as maintaining respiratory function with oxygen and ventilatory support, while the patient’s immune system fights off the virus. In addition, multiple antiviral drugs have been tested, including arbidol hydrochloride, Lianhua Qingwen capsules and broad-spectrum antiviral agents. Some antivirals, such as remdesivir, Actemra, hydroxychloroquine and self-developed vaccines for SARS-CoV–2, are undergoing clinical trials as well, and early data showed that these may be helpful.22However, there are still debates about when and how to use glucocorticoids and whether patients should be incubated. In addition, it can be seen from table 2 that the greatest need is a risk prediction model based on basic data at admission if the sample size is sufficient, since many laboratory indexes are significantly different between survivors and nonsurvivors.
The dynamic changes in these biomarkers raise intriguing questions regarding the nature and extent of targeting of SARS-CoV–2. For example, patients with acute liver injury (26[28%]) always have obviously increased ALT/AST and TBIL, whereas other hepatic function indexes, such as alkaline phosphatase and gamma-glutamyl transferase, do not change significantly.23 Nonetheless, we have reasons to believe that COVID–19-associated liver injury may be affected by various elements, such as hepatotoxic agents and a body-wide inflammatory reaction.13 Moreover, other statistically significant biomarkers are a compelling reminder for a poor prognosis.
Temperature trajectories reflect the potential dynamic changing patterns of temperature during the clinical course. This observation provides new insights into COVID–19-associated temperature changes and indicates that critical patients with a high temperature should be particularly paid attention to by health care providers, especially those with high temperature on admission.
The strengths of this study include that it is a large retrospective cohort study of critical patients in the ICU with information on COVID–19 and its associated outcomes. It is worth mentioning that early in the disease, a high temperature should receive extra care. On the other hand, our study has several limitations. First, the results of the arterial blood gas analysis, which we believe are quite valuable for prognosis, were incomplete, and some of these data were missing; hence, we did not perform a thorough analysis. Another potential limitation is that we did not analyze the findings of pulmonary imaging, such as chest X-rays and computed tomography. Further studies that take these flaws and unanswered questions into account will need to be undertaken.24