Neuroendocrine Response to and Initial Management of Traumatic Injury

Abstract

Traumatic injury often results in hypovolemic shock and is responsible for significant morbidity and mortality in canine and feline patients. Adrenocorticotropic hormone is released from the pituitary gland and acts on the adrenal cortex to begin synthesis and release of glucocorticoids, primarily cortisol. Cortisol plays a major role in facilitating adaptation to trauma. Glucocorticoids inhibit the release of arachidonic acid from cell membranes through inhibition of the enzyme phospholipase A2. The treatment of hypovolemic shock with glucocorticoids has long been a debatable issue. No clinical studies have shown a benefit to the use of glucocorticoids in posttraumatic, hypovolemic animals or humans. The mainstay of treatment for animals following a traumatic event and presenting in hypovolemic shock is IV fluid therapy. Trauma that results in hypovolemic shock causes decreased perfusion to tissues, with subsequent tissue and cellular hypoxia. A clear understanding of the neuroendocrine response to trauma assists the veterinary practitioner’s approach to the posttraumatic patient.