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Review
. 2024 Jun 17:19:1067-1078.
doi: 10.2147/CIA.S462471. eCollection 2024.

The Association of Cerebral Oxygen Desaturation with Postoperative Cognitive Dysfunction in Older Patients: A Review

Chun-Yan Zhang  1 , Yu-Shen Yang  1 , Meng-Qin Pei  1 , Xin-Li Chen  1 , Wei-Can Chen  1 , He-Fan He  1
Affiliations
Review

The Association of Cerebral Oxygen Desaturation with Postoperative Cognitive Dysfunction in Older Patients: A Review

Chun-Yan Zhang et al. Clin Interv Aging. .

Abstract

Postoperative cognitive dysfunction (POCD) is a neurological complication associated with surgery and anesthesia that is commonly observed in older patients, and it can significantly affect patient prognosis and survival. Therefore, predicting and preventing POCD is important. Regional cerebral oxygen saturation (rSO2) reflects cerebral perfusion and oxygenation, and decreased intraoperative cerebral oxygen saturation has been reported to increase the risk of POCD. In this review, we elucidated the important relationship between the decline in rSO2 and risk of POCD in older patients. We also emphasized the importance of monitoring rSO2 during surgery to predict and prevent adverse perioperative cognitive outcomes. The findings reveal that incorporating intraoperative rSO2 monitoring into clinical practice has potential benefits, such as protecting cognitive function, reducing perioperative adverse outcomes, and ultimately improving the overall quality of life of older adults.

Keywords: anesthesia; cognitive function; perioperative adverse outcome; prognosis; surgery.

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Conflict of interest statement

The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
Mechanisms of cerebral hypoxia impairment of cognitive function. Cerebral hypoxai impairs cognitive function via a combination of multiple mechanisms. (1) The S100 calcium-binding protein A8 (S100A8) secreted from neurons under hypoxia induces neuronal apoptosis through several pathways. S100A8 activates ERK, JNK, and the priming signals of the NLRP3 inflammasome through TLR4 receptors in microglial cells. This, in turn, promotes the secretion of TNF-α, IL-6, and IL-1β. In addition, microglial S100A8 expression can activate COX-2 expression and PGE2 secretion. (2) Hypoxia reduces the release of presynaptic membrane acetylcholine and stimulates the release of dopamine and glutamate, ultimately leading to excitotoxic neuronal death and subsequent impairment of cognitive function. (3) Hypoxia reduces Cirbp expression, resulting in reduced ATP production, ROS accumulation, and mitochondrial damage, which leads to damage to the hippocampus and impaired cognitive and memory functions. (4) Cerebral hypoxia deactivates the brain’s DMN, causing cognitive impairment. (5) Brain hypoxia damages the blood–brain barrier, which allows for the accumulation of Aβ in the brain and leads to cognitive impairment and dementia.
Figure 2
Figure 2
Methods of improving cerebral hypoxia.
See this image and copyright information in PMC

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