Acute stress response involves a series of metabolic and hormonal changes, common to all patients during and after surgery, leading to changes in organ function. These changes are similar to those found in other stressful conditions such as bleeding, burns, childbirth, and exertion. Although surgical stress response is an evolutionary defense mechanism, changes in organ function caused by stress may also be involved in the development of postoperative complications and delayed recovery. Afferent neuronal input from the site of surgery activates hypothalamopituitary hormonal secretion and the sympathetic nervous system. The onset of surgery is associated with the rapid secretion of the pituitary hormone, along with the activation of the sympathetic nervous system and the release of noradrenaline and adrenaline. This is followed closely by an increase in circulating cortisol, aldosterone and renin. Increased sympathetic activity and the level of norepinephrine caused by surgical stress lead to decreased insulin secretion, glucose consumption as well as increased gluconeogenesis, resulting in hyperglycemia, thereby increasing postoperative infection and mortality due to suppression of the immune system. These hemodynamic changes lead to neuronal, renal, and cardiovascular damage, which prolongs patient hospitalization. A balanced response to stress can be achieved by different methods depending on the severity and type of surgery, as well as the patient's condition. These include neural blockade by epidural or spinal anesthesia, which inhibits impulse transmission from the site of trauma, intravenous administration of a large dose of strong opioid analgesics that block the hypothalamopituitary axis, and infusion of anabolic hormones such as insulin that cause changes in the hormonal status of the patient.