The results of this study demonstrate that many geriatric elective surgical patients do poorly on cognitive screening tests preoperatively. Specifically, 28.61% of patients ≥65 years old scored in a range that suggests probable cognitive impairment.
Preexisting cognitive impairment preoperatively
The prevalence of cognitive impairment among older patients is high, while frequently undiagnosed before admission. Of the 374 patients included, 107 (28.61%) were identified as having cognitive impairment in this study, lower than previous literature reported. Studies have shown that the prevalence of cognitive impairment is as high as 35–50% in community-dwelling older persons, including mild cognitive impairment (MCI) as well as dementia [
6,
18]. The prevalence in elderly patients in surgical wards varies with the disease. A study including 152 subjects 60 yr of age and older who were scheduled for total hip joint replacement surgery and undergone preoperative assessment found that 22% were classified as having MCI [
21]. The remarkably high prevalence of preoperative MCI in 70% of vascular surgery patients is a cause for concern, among which 88% were undiagnosed before admission [
8]. These studies confirm that preoperative mild cognitive deficits are common in older individuals undergoing major surgery.
Nevertheless, routine preoperative evaluation of cognition continues to be overlooked in clinical practice today. Numerous clinical studies have confirmed that preoperative cognitive impairment in older patients undergoing elective surgery has significant impact on postoperative recovery. Lee et al. investigated 129 patients undergoing lumbar spine surgery and found a high prevalence of undiagnosed cognitive impairment (38%), which was associated with a higher rate of POD and prolonged hospital stays [
22]. In another retrospective study of 82 older patients undergoing elective spinal surgery, Owoicho et al. found that patients with cognitive impairment were more likely to require an additional stay at a skilled nursing or acute rehabilitation facility [
23]. In an observational retrospective study of 1258 patients aged older than 69 years undergoing hip surgery, the severity of cognitive impairment was a prognostic factor for mortality and functional recovery [
24]. Greater mortality risk was consistently associated with cognitive impairment before cardiac surgery in a study of 5407 patients with 11 year follow-up [
9].
In addition, from June to November 2018, similar papers were published in six well-known journals, suggesting that perioperative neurocognitive disorders (PND) were used to describe the decline or change of cognitive function during the perioperative period to replace postoperative cognitive dysfunction (POCD), which not only extends the timeline of perioperative cognitive follow-up but also emphasizes the importance of preoperative cognitive assessment [
25‐
30].
Clinical risk factors for preoperative cognitive impairment
The size and function of the brain decrease with age, causing cognitive decline [
31]. Our multivariable logistic regression analysis showed that venerable age was an independent risk factor for cognitive impairment (OR = 1.089,
P < 0.001), in accordance with those reported in the previous papers [
31,
32]. In a prospective study of 215 patients undergoing elective surgery of all types, Smith et al. found that the effect of aging on cognitive impairment was apparent. The prevalence of MCI increased with aging, with 42% of patients in the 65–69 years age group increasing to 80% of patients aged 80 years and above [
32]. Currently, increasing numbers of elderly patients choose surgery to treat surgical disease [
1,
33]. One or more cardiovascular and cerebrovascular diseases as well as other systemic diseases are often combined in the elderly [
34]. Moreover, the coexistences of multiple preoperative medications, frailty, anxiety and depression further increase the prevalence rates of cognitive impairment and perioperative complications [
35]. Univariate analysis from our data also showed higher ASA grade (
P = 0.004) and CCI score (
P = 0.048) in the cognitive impairment group when compared with the normal group.
There are studies which support mild cognitive impairment is related to the genetics [
36]. Those who have a parent, brother or sister with Alzheimer’s are more likely to develop the disease. The risk increases if more than one family member has the illness. Therefore, it is important to investigate the family history of patients at high risk for cognitive impairment. The way of oral inquiry was used to obtain a family history of the nervous system, nevertheless, the results were almost negative. It is not possible according to its epidemiological investigation. The reason, we supposed, was a large number of patients with undiagnosed and unrecognized [
8]. Therefore, we did not analyze the family history of neurological disease in these elderly.
The impact of gender on cognitive dysfunction has been a concern, while the results have varied in different studies. Lee et al. found a gender disparity in cognitive function in India. Compared with male, Indian women have poor cognitive function in their later years [
37]. In contrast, the cognitive function status of women in developed countries is not significantly different from that of men, and females often have better status [
38]. Evidence-based analysis indicates that gender has an impact on cognitive impairment in elderly patients, which, might be interfered by differences in BMI, tobacco and alcohol use, social and economic activity in different regions, educational attainment, and discrimination against women [
37,
39]. The role of gender in cognitive function requires a multicentered study with a larger sample to confirm because of the large clinical heterogeneity.
The degree of education has a great impact on cognitive function. Studies have shown that good education and cultural background have a positive effect on the ability of concept formation, vocabulary expression, spatial structure perception and memory, while cultural restriction may contribute to a negative effect [
40]. Highly educated people often have a high reserve of neurons [
41]. The more people receive education, the better subjective initiative and ability to adapt to the external environment, which may stimulate brain cells [
42]. The numbers of nerve connections (neurons) and information hubs (synapses) are likely to be greater in people who are highly educated. Alternatively, even if the quantity of neurons and synapses is no different, the synapses are likely to be more efficient and/or alternative circuitry is likely to be operating in those who are highly educated. Cognitive reserve is an emerging dynamic concept and is thought to be modifiable in keeping with the concept of brain plasticity [
10]. A recent clinical study demonstrated that preoperative cognitive reserve might have protective effects on long-term cognitive function after surgery [
43].
Atherosclerosis was an independent risk factor for cognitive impairment in our study. Most epidemiological studies have shown that vascular risk factors such as diabetes as well as increased blood glucose level, hypertension and hyperlipidemia are closely related to cognitive impairment [
44,
45]. Nevertheless, the results of the present study showed that there were no differences in diabetes, hypertension and hyperlipidemia between patients with and without cognitive impairment (
P > 0.05). There is a possibility that disease severity and the interventions subjects received are not the same. Whether nonpharmacological treatment or pharmacological therapy, the justification for treatment and the targets of management depend upon severity of the disease and the degree of organ damage [
46,
47]; while not all patients would get treatment goals. Future clinical research design should filter the enrolled subjects strictly, expand the sample size, and use subgroup analysis to explore the effects of these comorbidities and their intervention on cognitive function.
A high ASA physical status is associated with substantive functional limitations in the elderly. Our study demonstrated that higher ASA score was not independent risk factors for cognitive impairment in all participants after adjusted for cofounders such as age, diabetes, therosclerosis. The explanation could be that the higher ASA score is a result of one or more moderate to severe diseases people have suffered, such as poorly controlled diabetes or hypertension, history of transient ischemic attack or coronary artery disease /stents.
Growing preclinical and clinical studies have reported associations between elevated plasma homocysteine and brain degeneration, including subtle age-related cognitive decline, cerebrovascular disease, vascular dementia, and Alzheimer disease [
48]. A review by Esther et al. revealed a positive trend between cognitive decline and increased plasma Hcy concentrations in the general population and in patients with cognitive impairment [
49]. Homocysteine is produced in all cells, and mechanisms of homocysteine-induced cognitive impairment include neurotoxicity and vascular injury. Some studies have suggested that protein homocysteinylation contributes to neurotoxicity, while others have shown that homocysteine induces cellular damage via oxidative stress, as well as disrupts astrocytic end-feet [
48,
50]. Animal models have shown that high plasma levels of homocysteine contribute to changes in the ultrastructure of cerebral capillaries, endothelial injury, pericyte swelling, basement membrane thickening and fibrosis [
51]. In keeping with the literature, patients in the cognitive impairment group had a higher level of homocysteine, even though a multivariable regression model did not find the difference.
Sleep disorders are quite common in the elderly and are mostly associated with neurodegenerative processes [
52]. Moreover, sleep disorders and cognitive impairment often coexist and interact with one another in the early stages of Alzheimer’s disease [
53,
54]. Sleep disorders in patients with MCI are associated with changes in memory and execution, suggesting that sleep dysfunction may be a precursor to cognitive changes [
53]. The structure of sleep and EEG findings may also be abnormal, even in the early stage of MCI [
53,
54]. In our study, the elderly often complained of sleep disruption due to frequent nocturia, or easy or early awakening. Electroencephalo-graph (EEG) studies also show that such patients have reduced nighttime slow wave sleep, a weakened sleep promotion process and an enhanced wakefulness process [
55]. Altered sleep seriously affects normal sleep patterns: patients frequently recounted that they were sleepy in the daytime, and several rapid-eye-movement sleep episodes were exhibited in EEG during their naps [
56]. In this study, compared with the normal group, the subjective sleep quality of the impairment group was poorer.