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Surgical Stress (Veterinary)
The stress response to surgery is a combination of the physiological, metabolic and endocrine changes which accompany the trauma of surgery. Its centered around the physiological and metabolic effects that can induce inflammatory, hormonal and genomic changes. It is crucial that the veterinary industry work to address surgical stress as it can often have deleterious affects on outcomes, if not properly considered.

Physical/Behavioral Response to Surgery
Many surgeries are traumatic in nature. Tissues are being crushed, cut, sewn, cauterized or otherwise harmed in order to mend wounds or correct malformations. Animals, who cannot comprehend why the damage is being done to them, will naturally try to flee or otherwise react if under anesthesia, to the negative stimuli. To do so the body typically mounts an internalized endocrine response, yet outward signs are still evident in the post-surgery period. Animals will often guard specific body areas which have been afflicted by trauma or pain. Some prey species may avoid weight bearing on affected limbs or in ways which cause pain in a clinical setting, as they do in nature, to prevent perceived predators from sensing their weakness. Common prey species worked on in veterinary surgery include cattle, cats and horses. Across species, the stress afflicted on surgical patients can also cause decreased appetite, sleep cycle changes, lethargy, and repeated bouts of standing and laying. These are all associated with the cortisol being released as a result of Hypothalamic Pituitary Adrenal (HPA) axis activation as well as the entire systemic response to pain. In 2000, Roughan and Fleckness performed laparotomy surgery on mice and found they had reduced active and attentive behaviors regardless of pain medication given. In cattle who were dehorned, head shaking, tail flicking, restlessness and refusal to lay down can all be noted. These are all indicative of the bodies response to surgery.

Hypothalamic-Pituitary Axis Response
Endocrinologically, surgical stress strongly activates the generalized stress response. Often, there is a surge in pituitary hormone secretion in response to surgical stress. The HPA axis response to surgery first occurs when the surgically damaged nerves send impulses to the hypothalamus. Hypothalamic releasing factors stimulate the synthesis of CRH (corticotropin-releasing hormones) which stimulates the production of ACTH           (andrenocorticotropic releasing hormone) from the anterior pituitary. The ACTH stimulates the release of cortisol from the adrenal glands above the kidneys. Normally, cortisol has negative feedback mechanism with ACTH in which the secretion of cortisol inhibits itself by inhibiting CRH and ACTH secretion. However, this is not the case in surgery patients, as they appear to lack this inhibition of CRH and ACTH during and post -surgery; as the stress on the body is too great. Because of this there is net breakdown of protein in the body and this creates condition perfect for hypermetabolism/catabolism, which can results in muscle wasting, impaired immune function and wound healing, organ failure and death with enough severity.

Consequences from the release of CRH, and cortisol in response to surgery also ensue. CRH has been found to inhibit reproductive hormones like GnRH (gonadotropin releasing hormone) in monkeys and humans. In rats, CRH has also been found to inhibit the release of LH (lutenizing hormone). This in turn can affect the gonads, estrus cycling in females, and the overall fertility of production animals. CRH also has a direct impact on appetence. It decreases the neuropeptide Y levels, which is a hormone associated with hunger stimulation. The release of cortisol can also have many deleterious effects on the body. It is the main promoter the catabolic effect seen in HPA axis activation and it results in a over production of sugars in the body, hyperglycemia. It is this hyperglycemia that results in decreased wound healing after surgery. The effects of cortisol is generally acute, resolving themselves within a few hours post surgery, as the bodies homeostasis reinstates itself.

Activation of sympathoadrenal System
Another consideration in surgical stress is the activation of the adrenal medulla to produce epinephrine via sympathetic nerves. When a stressor is perceived, the body releases CRH and vasopressin hormones which act on the adrenal medulla to release catecholamines. These work to increase blood pressure, heart rate, blood glucose levels and respiratory rate through their various pathways. Surgery can have a major stimulatory effect on the sympathetic adrenal axis. Sylvester et al., in 2008 found that castrated cattle had elevated heart rates and respiration rates for 7-9 hours post surgery. In dehorning procedures in cattle, there was also found to be significant heart rate and respiratory rate elevations post surgery. Bantel and Trapp in 2011 cited several animal studies which found exposure to catecolamines increased sensitization to certain inflammatory injuries, such as burns. It is believed that some scenarios can exacerbate the pain response. For instance, sympathetic nerve fibers are common along the vagus nerve, which branches out into the viscera of the abdomen. Hence a common procedure, like an abdominal surgery, could cause intense amounts of pain. In rats it was found that the lumbar spinal chord has afferent branches to the vagus nerve s. When stimulated with noxious stimuli these same nerves can cause an increased pain perception in the abdomen. A perfect examples of this is the increase in catecholamines produced during feline and canine ovariohysterectomy surgeries.

Immunological response to surgery
One of the major effects surgery is its affect on the immune system. But these effects are not entirely obvious. Local production of inflammatory cytokines appear to consistently increase at the site of surgery during and post-operatively Post-operatively there should also be a massive production of inflammatory cytokines. Other studies, however, suggest a prolonged increase of immune suppression as a result of some anti-inflammatory compounds being released. Some studies even go as far as saying that major surgical trauma is almost always associated with increases in immune suppression Routine procedures in cattle, such as castration, have been found to decrease neutrophil counts, leukocyte counts and suppress cytokines like lesser tumor necrosis alpha, and interferon Y. As a result of surgery animals are usually subject to increased chances of infection. One that is suggested to explain this effect is that surgery which uses regional anesthesia, such as a lidocaine pain blocker, may modify the innate humoral immunity and learned cell mediated immunity by interfering with cellular processes in that specific area. However, more general forms of surgical anesthesia such as a spinal epidural administration of may help boost immunity by blocking the cortisol release from the HPA axis and allowing the release of inflammatory cytokines (in the absence of cortisol . Overall, more research is needed in this field to found out what the effects of surgery are on the immune systems of all species specifically.