Acute stress response in perioperal period

Akutni stresni odgovor obuhvaća niz metaboličkih i hormonalnih promjena, zajedničkih svim pacijentima tijekom i nakon operacije, što dovodi do promjena u funkciji organa. Te su promjene slične onima koje nalazimo u drugim stresnim stanjima kao što su krvarenje, opekotine, porođaj i napor. Iako je kirurški odgovor na stres evolucijski obrambeni mehanizam, promjene u funkciji organa uzrokovane stresom mogu također biti uključene u razvoj postoperativnih komplikacija i odgođen oporavak. Aferentni unos neurona s mjesta kirurškog zahvata aktivira hipotalamopituitarnu hormonsku sekreciju i simpatički živčani sustav. Početak operacije povezan je s brzim izlučivanjem hormona hipofize, zajedno s aktivacijom simpatičkog živčanog sustava i oslobađanjem noradrenalina i adrenalina. Nakon toga pomno slijedi porast vrijednosti kortizola, aldosterona i renina u cirkulaciji. Pojačana simpatička aktivnost i razina noradrenalina uzrokovana kirurškim stresom dovode do smanjenog izlučivanja inzulina, potrošnje glukoze kao i povećanja glukoneogeneze, što rezultira hiperglikemijom, povećavajući tako postoperativnu infekciju i smrtnost zbog supresije imunološkog sustava. Ove hemodinamičke promjene dovode do oštećenja neurona, bubrega i kardiovaskularnog sustava što produžuje hospitalizaciju pacijenta. Uravnotežena reakcija na stres može se postići različitim metodama ovisno o težini i vrsti operacije, ali i stanju bolesnika. One uključuju neuronsku blokadu epiduralnom ili spinalnom anestezijom, koja inhibira prijenos impulsa s mjesta traume, intravenozno davanje velike doze jakih opioidnih analgetika koji blokiraju hipotalamopituitarnu os, te infuzija anaboličkih hormona poput inzulina koji uzrokuje promjene u hormonalnom statusu bolesnika.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