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. 2012 Jan;9(1):35–41.

TABLE 2.

Possible pathogenic mechanism of postoperative cognitive decline13,20,21,26,31,33,34

ETIOLOGY PROPOSED MECHANISM
Neuroinflammation Activation of the systemic inflammatory response is a feature of several acute medical or surgical disorders, particularly when involving tissue destruction and/or infection. In such cases, pro-inflammatory cytokines circulating in the bloodstream elicit a cascade of functional and structural changes within the neurovascular unit leading to the activation of microglial cells and astrocytes. The acute neuroinflammatory reaction affects physiological processes implicated in neuronal and synaptic function with consequent neurochemical disturbances and functional disconnection between different anatomical structures.
General anesthesia In-vitro studies have shown that inhaled anesthetics result in amyloid aggregates and neurofibrillary tangles, which are known to result in neurodegenerative changes. Such findings appear to support the hypothesis that general anesthesia is neurotoxic yet no significant difference in postsurgical cognition has been observed between general and regional anesthetics in humans.
Surgery type, specifically cardiac surgery (e.g., coronary artery bypass graft [CABG] and left ventricular assist devices [LVAD]) This has been attributed to the use of cardiopulmonary bypass (CPB), which is used during the implantation of certain LVADs (as in our patient) and CABG. CPB can also produce a systemic inflammatory response, making the blood-brain barrier more permeable, and can produce microemboli. Postmortem exams of patients who had cardiac procedures with CPB have revealed multiple small capillary arteriolar dilatations in the brain, which are caused by microemboli.
Metabolic syndrome Lack of cognitive reserve is accelerated by aging-induced frontal-subcortical syndrome. Many of the diagnostic characteristics that define metabolic syndrome are individually related to cognitive impairment; hypertension, obesity, elevated serum triglyceride concentrations, and hyperglycemia are all known risk factors for postoperative cognitive dysfunction.