Emboli, inflammation, and CNS impairment: an overview.

Perioperative stroke occurs in 2-3% of adult cardiac surgery patients, and significant cognitive dysfunction is experienced by 40-60% of patients in the first postoperative week. Perioperative neurocognitive abnormalities are associated with a greatly increased risk of perioperative mortality, lengthy intensive care and hospital stay, and more intensive rehabilitative care. Long-term cognitive dysfunction, ranging from months to years, occurs in 25-40% of adult cardiac surgery patients, resulting in a decreased quality of life. Cerebral emboli are an important cause of perioperative neurocognitive abnormalities. Aortic cannulation, clamping, and manipulation during surgery may dislodge atheromatous materials into the cerebral circulation, leading to perioperative or postoperative stroke. Nevertheless, acute and chronic neurocognitive dysfunction frequently occurs in non-cardiac surgery patients as well, suggesting that some element of surgery and/or anesthesia itself causes or contributes to this phenomenon. One possible cause may be central nervous system (CNS) responses to peripheral tissue injury or inflammation. The CNS is sensitive to systemic pro-inflammatory mediators such as endotoxin and the cytokines interleukin-6 and interleukin- 8, which are activated by surgical trauma. This article discusses the behavior and effects of these inflammatory agents and their intensification in combination with postoperative hyperthermia. The potential beneficial role of pharmacological agents such as heparin, lidocaine, and aprotinin is also examined.