Response to trauma and metabolic changes: posttraumatic metabolism Stress response caused by events such as surgical trauma includes endocrine, metabolic and immunological changes. Stress hormones and cytokines play a role in these reactions. More reactions are induced by greater stress, ultimately leading to greater catabolic effects. Cuthbertson reported the characteristic response that occurs in trauma patients: protein and fat consumption and protection of body fluids and electrolytes because of hypermetabolism in the early period. The oxygen and energy requirement increases in proportion to the severity of trauma. The awareness of alterations in amino acid, lipid, and carbohydrate metabolism changes in surgical patients is important in determining metabolic and nutritional support. The main metabolic change in response to injury that leads to a series of reactions is the reduction of the normal anabolic effect of insulin, i.e. the development of insulin resistance. Free fatty acids are primary sources of energy after trauma. Triglycerides meet 50 to 80 % of the consumed energy after trauma and in critical illness. Surgical stress and trauma result in a reduction in protein synthesis and moderate protein degradation. Severe trauma, burns and sepsis result in increased protein degradation. The aim of glucose administration to surgical patients during fasting is to reduce proteolysis and to prevent loss of muscle mass. In major stress such as sepsis and trauma, it is important both to reduce the catabolic response that is the key to faster healing after surgery and to obtain a balanced metabolism in the shortest possible time with minimum loss. For these reasons, the details of metabolic response to trauma should be known in managing these situations and patients should be treated accordingly.Key Words: Posttraumatic metabolism, stress response, trauma response
INTRODUCTIONResponse to trauma includes various endocrine, metabolic and immunological changes. The severity of these changes is related to the amount of exposed stress. In the activation of central nervous system and hormonal responses against injury, the direct effect of mediators like TNF-α and IL 1, which are released from traumatic tissue, on the hypothalamus has been well-known. However, many new studies refer to nuclear factor kappa B (NF-kB) in this regard. In a burn-rat model study, it was stated that melatonin, which is protective against liver damage, played a role in the suppression of NF-kB that is accepted as a mediator of inflammatory response, and melatonin treatment reduced the significantly increased hepatic NF-kB and TNF-α activity (1).Protein malnutrition affects defense against infection by disrupting inflammatory response. Glutamine, although considered as a non-essential amino acid, has been shown to be essential in cases such as trauma, surgery, or sepsis where cytokine synthesis is modulated. In a study, it was noted that the effect of glutamine on macrophage activation and TNF-α synthesis is dose-dependent, and it effects the N...