בשל "הגנת זכויות יוצרים", מובא להלן קישור למאמר בלבד. לקריאתו בטקסט מלא, אנא פנה/י לספרייה הרפואית הזמינה לך.
Although postoperative delirium afflicts as many as half of cardiac surgery patients and is associated with prolonged hospitalization, long-term cognitive decline, and mortality, we know little of the pathophysiologic mechanisms that subtend this common neurobehavioral syndrome.
Delirium is an acute confusional state, generally viewed as a marker of increased brain vulnerability and an aberrant response to stress. As such, its neuropathogenesis depends on complex interrelationships between predisposing and precipitating factors, with a number of overlapping mechanistic theories involving neuronal aging, neuroinflammation, oxidative stress, neurotransmitter deficiency, neuroendocrine activation, circadian dysregulation, and breakdown in brain network connectivity.
While anesthesia/surgery are clearly inciting factors for delirium, intraoperative strategies to reduce it are sorely lacking. This is in part because prevailing theories have focused on preoperative (older age, frailty, medical comorbidities, and preexisting cognitive impairment) and postoperative recovery factors (disrupted sleep, altered sensorium, pain, and sedating medication use/polypharmacy) as drivers of postoperative delirium.