The stress response to surgery, critical illness, trauma, and burns encompasses derangements of metabolic and physiological processes that induce perturbations in the inflammatory, acute phase, hormonal, and genomic responses. Hypermetabolism and hypercatabolism result, leading to muscle wasting, impaired immune function and wound healing, organ failure, and death. The surgical stress response is largely similar to that triggered by traumatic injuries; the duration of the stress response, however, varies according to the severity of injury (surgical or traumatic). This spectrum of injuries and insults ranges from small lacerations to severe insults such as large poly-traumatic and burn injuries. Burn injuries provide an extreme model of trauma induced stress responses that can be used to study the long-term effects of a prolonged stress response. Although the stress response to acute trauma evolved to confer improved chances of survival following injury, in modern surgical practice the stress response can be detrimental.
Following surgical or accidental trauma, the nervous system activates the response to stress by sending impulses from the injured site to the hypothalamus. The hypothalamus either removes its inhibitory tone on the pituitary or releases hormones which stimulate the production and/or release of pituitary hormones. Pituitary hormones act on their respective target organ causing the release of hormones such as the stress hormone, cortisol. Elevations of cortisol, glucagon, catecholamines, and a host of inflammatory cytokines, also exacerbate the stress response to surgery. Afferent nerve signals from the injured site and proinflammatory cytokines have the net effect of increasing the secretion of hormones from the pituitary gland. Increased secretion of the anterior pituitary hormones corticotrophin (ACTH) and growth hormone (GH) have particularly significant metabolic consequences. Other anterior pituitary hormones such as thyrotrophin (TSH) and the gonadotropins (follicle stimulating hormone [FSH] and luteinizing hormone [LH]) are not as significantly affected. The HPA axis is regulated by a negative feedback mechanism in which cortisol suppresses the release of both CRH and ACTH. Cortisol is a catabolic glucocorticoid hormone that mobilizes energy stores to prepare the body for the fight or flight response to stressors. It promotes gluconeogenesis in the liver, leading to raised blood glucose levels. Hyperglycemia reduces the rate of wound healing and is associated with an increase in infections and other comorbidities including ischemia, sepsis, and death.
Tight glycaemic control is necessary for rapid wound healing and patient outcome. Researchers have shown that in recent years, the emergence of protocols for tight glycaemic control with intensive insulin administration has reduced complications and improved outcomes in critically ill and severely burned patients. Aggressive glycaemic control in line with these intensive insulin protocols reduces insulin resistance and hyperglycaemia. Although most physicians agree that maintenance of normoglycaemia is beneficial, controversy persists regarding establishment of the target blood glucose levels and protocolization of indications for intensive insulin therapy initiation.
The stress response to surgery, critical illness, trauma, and burns encompasses derangements of metabolic and physiological processes that induce perturbations in the inflammatory, acute phase, hormonal, and genomic responses. Hypermetabolism and hypercatabolism result, leading to muscle wasting, impaired immune function and wound healing, organ failure, and death. Optimal nutrition support is required to insure positive patient outcomes following surgery, trauma, critical illness, and burn injuries. Amelioration of the systemic inflammatory, hormonal, and metabolic responses with nutrition supplementation, pharmacologic interventions, and exercise reduces the impact of the hypermetabolic and surgical stress responses.