Clinical Characteristics of Deceased Patients With COVID-19

BMJ : British Medical Journal

Abstract

OBJECTIVE

To delineate the clinical characteristics of patients with coronavirus disease 2019 (covid-19) who died.

DESIGN

Retrospective case series.

SETTING

Tongji Hospital in Wuhan, China.

PARTICIPANTS

Among a cohort of 799 patients, 113 who died and 161 who recovered with a diagnosis of covid-19 were analysed. Data were collected until 28 February 2020.

MAIN OUTCOME MEASURES

Clinical characteristics and laboratory findings were obtained from electronic medical records with data collection forms.

RESULTS

The median age of deceased patients (68 years) was significantly older than recovered patients (51 years). Male sex was more predominant in deceased patients (83; 73%) than in recovered patients (88; 55%). Chronic hypertension and other cardiovascular comorbidities were more frequent among deceased patients (54 (48%) and 16 (14%)) than recovered patients (39 (24%) and 7 (4%)). Dyspnoea, chest tightness, and disorder of consciousness were more common in deceased patients (70 (62%), 55 (49%), and 25 (22%)) than in recovered patients (50 (31%), 48 (30%), and 1 (1%)). The median time from disease onset to death in deceased patients was 16 (interquartile range 12.0-20.0) days. Leukocytosis was present in 56 (50%) patients who died and 6 (4%) who recovered, and lymphopenia was present in 103 (91%) and 76 (47%) respectively. Concentrations of alanine aminotransferase, aspartate aminotransferase, creatinine, creatine kinase, lactate dehydrogenase, cardiac troponin I, N-terminal pro-brain natriuretic peptide, and D-dimer were markedly higher in deceased patients than in recovered patients. Common complications observed more frequently in deceased patients included acute respiratory distress syndrome (113; 100%), type I respiratory failure (18/35; 51%), sepsis (113; 100%), acute cardiac injury (72/94; 77%), heart failure (41/83; 49%), alkalosis (14/35; 40%), hyperkalaemia (42; 37%), acute kidney injury (28; 25%), and hypoxic encephalopathy (23; 20%). Patients with cardiovascular comorbidity were more likely to develop cardiac complications. Regardless of history of cardiovascular disease, acute cardiac injury and heart failure were more common in deceased patients.

CONCLUSION

Severe acute respiratory syndrome coronavirus 2 infection can cause both pulmonary and systemic inflammation, leading to multi-organ dysfunction in patients at high risk. Acute respiratory distress syndrome and respiratory failure, sepsis, acute cardiac injury, and heart failure were the most common critical complications during exacerbation of covid-19.

TAKE-HOME MESSAGE

• As of 28 February, 2020, more than 2858 people had died of COVID-19, with the highest mortality rate of 4.5% in Wuhan, China. Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) infection causes clusters of severe and even fatal pneumonia. Clinical characteristics of patients with COVID-19 who died have not been fully elucidated yet. Certain patients with COVID-19, particularly those of advanced age and with hypertension, were in a critical condition on admission and progressed rapidly to death within 2 to 3 weeks from disease onset.

• SARS-Cov-2 infection can cause both pulmonary and systemic inflammation, leading to multiorgan dysfunction in high-risk populations. In addition to acute respiratory distress syndrome and type I respiratory failure, acute cardiac injury and heart failure may also contribute to the critical illness state associated with high mortality risk.

- Michael Allen, MD

Written by



Peter Lin MD, CCFP

Can we Identify Who Will Die From COVID-19?

With this pandemic, we have become numb to the numbers. Every day, the numbers go up and even when the death count goes up, it does not seem to faze us anymore. It's as if it is to be expected. But these numbers are real people. Someone's father or mother or husband or wife. Their death is tragic, but how can we learn from them so that their deaths would not be in vain.

The first place to start is to see if there were any differences between the patients that died and the patients that recovered. From there, we can begin to understand what leads to a bad outcome and what leads to a good outcome. With that knowledge, we can hopefully figure out treatments or strategies that can alter that path.

This paper is the first step where they compared 113 patients who died to 161 patients who recovered in order to figure out what were the differences between these two groups.

For the group that died, they were older (68 years vs 51 years) and were more likely to be males. They were more likely to have hypertension (48% vs 24%) and other cardiovascular comorbidities (14% vs 4%).

For symptoms, they were more likely to have dyspnea (62% vs 31%), chest tightness (49% vs 30%), and disorder of consciousness (22% vs 1%). This last one might reflect the fact that the ACE2 receptor, which is the doorway that the virus uses to get into the lung cells, is also on neurons, and hence, a change in the level of consciousness could indicate that the virus has infected the brain.

On the laboratory side, the group that died was more likely to have leukocytosis (50% vs 4%) and lymphopenia (91% vs 47%). In fact, a whole host of other tests were also increased, which included alanine aminotransferase, aspartate aminotransferase, creatinine, creatine kinase, lactate dehydrogenase, cardiac troponin I, N-terminal pro-brain natriuretic peptide, and D-dimer. All of those tests were higher in patients that died compared with the patients that recovered.

The median time from onset to death was 16 days (interquartile range 12.0-20.0 days). This means that if we had antibodies from the serum of recovered patients, then we could have a window where we could use that type of therapy.

In addition, the following complications were much higher for the group that died compared to the recovered group: acute respiratory distress syndrome (100% vs 52%), type I respiratory failure, which is hypoxia failure (51% vs 0), sepsis (100% vs 41%), acute cardiac injury (77% vs 17%), heart failure (49% vs 3%), shock (41% vs 0), acute kidney injury (25% vs 1%), and hypoxic encephalopathy (20% vs 1%).

These data paint a picture of patients that had both pulmonary and systemic failure. Their lungs failed and then the rest of their body followed. Depressing as that might sound, this paper gave us valuable information that allows us to identify patients that are headed towards a bad outcome. This first step of patient identification will help us treat those patients more aggressively, and perhaps we can put these patients into clinical trials that offer them some of the promising antivirals or immunoglobulin therapies.

So let's look beyond the numbers and figure out how to protect and treat our sickest during this unprecedented pandemic.

BMJ : British Medical Journal

Clinical Characteristics of 113 Deceased Patients With Coronavirus Disease 2019: Retrospective Study

BMJ 2020 Mar 26;368(xx)m1091, T Chen, D Wu, H Chen, W Yan, D Yang, G Chen, K Ma, D Xu, H Yu, H Wang, T Wang, W Guo, J Chen, C Ding, X Zhang, J Huang, M Han, S Li, X Luo, J Zhao, Q Ning