In this cross-sectional study, we investigated a sample of 306 patients with AECOPD between the ages of 60 and 88 years to evaluate the role of SI in predicting clinical outcomes among elderly patients with AECOPD. We also reported stratified results according to the AECOPD phenotype.
Our results showed that, regardless of group (total, frequent exacerbation group, or non-frequent exacerbation group), the incidence of respiratory failure was negatively associated with SI values. After adjustment for potential confounding factors, binary logistic regression analyses showed that a higher SI was also independently associated with a lower risk of respiratory failure, suggesting that the SI is a stable indicator predicting the risk of respiratory failure among patients with AECOPD. The SI is a simple and low-cost indicator that has been recommended as a novel screening tool for sarcopenia [12]. Poor nutritional status can contribute to decreased muscle mass and strength; therefore, nutritional status plays an important role in the development of sarcopenia [16, 17]. Owing to limited caloric intake and increased energy expenditure, patients with COPD complicated by respiratory failure often have protein-calorie malnutrition [18]. When the patient is having an acute episode of COPD, skeletal muscle dysfunction can be caused by hypoxia and/or hypercapnia, malnutrition, a strong inflammatory response, and the use of corticosteroids [19]. Therefore, sarcopenia is highly prevalent among patients with AECOPD complicated by respiratory failure. Furthermore, studies have shown that sarcopenia can have an impact on diaphragm muscle fatigue and can reduce respiratory muscle strength, including maximum inspiratory muscle pressure and maximum expiratory pressure [20–22]. These findings suggest that sarcopenia can increase the risk of respiratory failure in patients with AECOPD. Hence, we believe that the SI may predict respiratory failure among patients with AECOPD. Respiratory failure is a common complication in these patients. In severe cases, patients may be agitated, combative, or delirious, or they may lose consciousness and fall into a coma, thereby endangering their lives [23, 24]. Previous studies have shown that respiratory failure can increase the frequency of admissions to the emergency department or intensive care unit and is associated with significant mortality among patients with AECOPD [25, 26]. Therefore, routinely assessing the SI in the management of patients with AECOPD would facilitate more accurate early intervention, resulting in a reduced respiratory failure-related burden of the disease.
A systematic review and meta-analysis showed that sarcopenia and heart failure often co-exist, and the prevalence estimates of sarcopenia vary between 10% and 69% in patients with heart failure [27]. Both sarcopenia and heart failure share common pathophysiological pathways involving muscle dysfunction, which include alterations in mitochondrial density and activity, fiber distribution, and oxidative stress [28]. However, previous studies have focused on primary heart disease associated with heart failure [29]. In our study, we did not find an association between SI and heart failure among older patients with AECOPD. The possible reason is that heart failure in our study was mainly caused by chronic pulmonary heart diseases. It is well known that strong respiratory muscles can generate effective coughing that clears the airways and prevents pneumonia; in turn, if respiratory muscles are weak, this results in an increased propensity for pneumonia development. Sarcopenia is reported as a risk factor for the development of pneumonia in elderly people; several reports have also revealed the association between pneumonia and sarcopenia [13, 30, 31]. However, in our study, we detected no correlation between SI and severe pneumonia in patients overall, the group with frequent exacerbation, or the group without frequent exacerbation. Other studies have reported that sarcopenia is associated with mechanical ventilation and mortality among patients in the intensive care unit [32, 33], but there is no correlation between the SI and invasive mechanical ventilation or mortality among patients with AECOPD. It may be that the incidence of severe pneumonia, invasive mechanical ventilation, and mortality in our study was very low. More in-depth research with a larger sample size is needed.
Although as far as we know, this was the first study to evaluate the role of the SI in predicting clinical outcomes among patients with AECOPD, our study has certain limitations. First, this study was carried out at a single institution and included a small sample size. Additionally, most participants were men, which would lead to sex bias. Second, we did not have information for certain confounders, such as education level, income status, or medication complexity; these factors may confound the relationship between the SI and clinical outcomes among patients with AECOPD. Third, we did not use BIA or DXA to assess actual residual muscle mass in our patients. Finally, the inpatients in our study are not representative of patients with AECOPD in the general population or other clinical settings. Our sample is only representative of elderly patients with AECOPD in the Department of Respiratory and Critical Care Medicine and the Department of Geriatrics.
Our study showed that the SI, based on serum Cr and CysC, can predict respiratory failure in patients with AECOPD who have either frequent or infrequent exacerbations, but not other clinical outcomes. Clinicians should consider use of the SI in routine management of AECOPD. Future larger-scale studies are needed to confirm the present findings and define the physiologic range of the SI.