Delirium is a common complication after aortic dissection surgery with an incidence of 32.5 to 52.0% , and the results of this study showed that the incidence of delirium was 40.08%, which was consistent with other studies. The area under the curve of the SDBG was greater than the MBG. After adjusting for confounding factors, the SDBG was independently correlated with the risk of delirium.
No matter how the quality of perioperative blood glucose controls in patients who underwent cardiac surgery, blood glucose changes are reported they are related to postoperative complications [20, 21]. Hypoglycemia and hyperglycemia have been identified as risk factors for delirium [22, 23], but there are few reports on the relationship between glucose fluctuation and delirium. Keulen et al.  shows that delirium is positively associated with hypoglycemia in severe patients with diabetes, but not associated with pronounced glycemic variability. And Heymann et al.  found that patients with hyperactive delirium have higher MBG than the non-hyperactive delirium patients. There is no consensus on the relationship between glucose fluctuation and delirium, and this study showed that high glycemic variability increases the risk of postoperative delirium.
Glucose, a simple carbohydrate, is the main source of energy for many cells. Studies have shown that the brain consumes 50% of the total body’s consumption of glucose . Glucose sensory neurons are present in several areas of the brain. The activity of neurons changes with the level of glucose, and the brain function depends on the stable glucose levels, which is why the brain is particularly sensitive to glucose level. Therefore, the blood glucose level needs to be maintained in a narrow physiological range . A study shows that people with diabetes are at least 1.5 times more likely to develop dementia than people without diabetes, further highlighting the effect of glucose changes on brain function and long-term consequences . Both acute and chronic hyperglycemia has been shown to cause oxidative stress, subsequent neuronal damage, and cognitive decline , and the reason is closely related to delirium.
At present, the mechanism of blood glucose volatility promoting the development of critical illness and poor prognosis is not clear. However, blood glucose volatility is the biological basis of the human body . According to the theory of oxidative stress, fluctuating hyperglycemia can easily cause oxidative stress than persistent hyperglycemia . The specific mechanism may be that intermittent hyperglycemia can increase the overexpression of reactive oxygen species in the mitochondrial transport chain, thereby promoting oxidative stress response, increasing the apoptosis rate of endothelial cells, and ultimately causing damage to central nervous function . Meanwhile, it has been reported that the oxidative stress of intermittent hyperglycemia is greater than that of sustained hyperglycemia under experimental conditions, which has been confirmed by clinical studies. Besides, high blood glucose will also cause the release of a large number of pro-inflammatory cytokines, resulting in coagulation dysfunction, vascular reactivity abnormalities, and other injuries. However, patients with acute aortic dissection often present intermittent hyperglycemia due to acute illness, surgical stress, drugs, and other reasons, which are closely involved in a central nervous injury.
Cardiopulmonary bypass is the main technology for acute aortic dissection. Inflammatory mediators are released in large quantities during cardiopulmonary bypass cardiac surgery, and the inflammatory state is another common phenomenon of a stress response. The inflammatory response itself has a protective effect on the body. But when the balance between inflammatory and anti-inflammatory is broken, the body shows an inflammatory state and a large number of inflammatory factors in the peripheral circulation enter the central nervous system through various channels, which can cause inflammation in the central nervous system . A large number of studies have suggested that neuron inflammation may be one of the mechanisms of cognitive impairment. Cibelli et al.  founds that surgical trauma activates the innate immune system, which in turn triggers an IL-1-mediated inflammatory response in the hippocampus, resulting in memory impairment in mice. Besides, the operation itself is a kind of serious trauma, causing the organism to appear stress state. The imbalance of the central nervous system about noradrenaline and acetylcholine decreases the acetylcholine content, resulting in a series of neurological complications.
There are several limitations to this study. First, the sample size was small, and the relevant conclusions need to be further demonstrated with a larger sample. Second, we only evaluated delirium in ICU patients without long-term follow-up. Finally, continuous glucose monitoring was used to continuously measure blood glucose in recent studies, which the frequency of BG tests in our study may not be enough. In future studies, we will use the continuous glucose monitoring for real-time monitoring of patients.