Clinical meaning
Surgery triggers a complex neuroendocrine stress response that begins with tissue injury and anesthesia. The hypothalamic-pituitary-adrenal (HPA) axis activates within minutes of surgical incision, releasing cortisol and catecholamines (epinephrine and norepinephrine) from the adrenal glands. Cortisol promotes gluconeogenesis, protein catabolism, and anti-inflammatory effects, while catecholamines increase heart rate, blood pressure, and cardiac output to maintain perfusion to vital organs. The sympathetic nervous system activation causes peripheral vasoconstriction, which redirects blood flow away from the skin and gastrointestinal tract toward the heart, brain, and kidneys. This explains why postoperative patients often present with cool extremities, decreased bowel sounds, and urinary retention. The inflammatory cascade releases cytokines (interleukin-1, interleukin-6, tumor necrosis factor-alpha) from damaged tissue, producing the systemic inflammatory response that manifests as fever, tachycardia, leukocytosis, and increased metabolic rate in the first 24 to 72 hours after surgery. Anesthetic agents depress the central nervous system, respiratory center, and cardiovascular reflexes. General anesthesia suppresses the cough reflex, impairs mucociliary clearance, and reduces functional residual capacity of the lungs, predisposing patients to atelectasis (alveolar collapse) and pneumonia. Opioid analgesics further depress respiratory drive...