Due to the patient’s size and weight, local changes in muscle metabolism can also be substantial in the recumbent horse under general anesthesia. Physical compression of muscle groups is associated with restricted local blood perfusion and an increased demand for energy through anaerobic metabolism in the muscle [42]. This can lead to use of adenosine triphosphate and creatinine phosphate as energy sources and production of lactate, which can extend into the recovery period [43, 44]. Because of decreased venous drainage from the muscle, increased muscle lactate is not paralleled by the lower plasma lactate during anesthesia and increases in plasma lactate and potassium extend into the recovery period [42, 44–46]. These metabolic changes can be apparent in healthy horses, especially in the heavy patient and prolonged anesthesia, but changes are more pronounced and commonly recognized in prolonged anesthetics and ill horses such as colic cases [43, 46].
Nutritional supplementation will reverse catabolic processes during simple starvation; however, it will not completely reverse those during metabolic stress, which will remain as long as tissue injury persists. Nutritional support of the critically ill patient aims to minimize the severity of protein loss and morbidity associated with the disease. The goal should be to re‐institute food intake as soon as possible and if that is not possible, consider nutritional support. Nutritional support can be provided in the form of enteral or parenteral nutrition. The enteral route is always preferred as it provides a trophic stimulus for the gastrointestinal tract and has a protective effect against bacterial translocation across the intestinal wall [47]. Early enteral nutrition (initiated within 48 h after surgery) significantly decreased morbidity and length in critically ill human patients [48], and lessened the hypermetabolic and catabolic responses to injury in human and animals [49]. When the enteral route is not available, parenteral nutrition can be used in the form of partial (most commonly) or total parenteral nutrition. Although there is a paucity of published studies, there are some reports of clinical application of enteral and parenteral nutrition in foals and adult horses, from which some guidelines can be obtained [35, 47, 48, 50–55]. Parenteral nutrition is not exempt of complications and, therefore, close monitoring of patients receiving it is required [52, 55, 56]. A clinical nutrition counselling service has recently been pioneered at a referral equine hospital [57].
Neuroendocrine
Surgical patients undergo a sympathetic nervous system response with activation of adrenocortical axis and release of catecholamines, cortisol and glucagon. The degree of surgical trauma will determine the magnitude of this endocrine response, with redistribution of blood flow to preserve important organs, splenic contraction to increase blood volume, mobilization of resources to provide substrates such as glucose and fatty acids, and activation of the immune system in more severe cases [58, 59].
General anesthesia itself is associated with a stress response characterized by sympathetic output in healthy horses [45]. Inhalation anesthesia increased adrenocorticotropic hormone and cortisol release in healthy horses [60, 61], and even in glycerol and non‐esterified fatty acids in prolonged anesthesia in healthy horses [45]. On the contrary, total intravenous anesthesia seemed to cause a lesser stress response than gas anesthesia, although duration of anesthesia and other factors have important effects [62]. Fasting, re‐feeding and anesthetic drugs (i.e. α2‐agonists) affect insulin regulation and therefore different drug combinations, and induction and anesthetic protocols contribute to large variability of the hyperglycemic response and circulating levels of these stress markers in the equine patient [63–65].
Laparoscopic surgery under standing sedation and local anesthesia produced increased cortisol and non‐esterified fatty acids plasma levels in horses [66]. Minor elective surgery under general anesthesia (skin sarcoid removal or laryngeal surgery) produced minor changes in blood glucose, lactate or plasma non‐esterified fatty acid (NEFA) values, beyond those caused by anesthesia [63]. Equine patients undergoing elective arthroscopic surgery showed transient hyperglycemia and increased beta‐endorphin and cortisol [67]. Cortisol response in people undergoing surgery correlates with surgical trauma and is higher in abdominal than other minor surgeries [68, 69]. Similarly, a 1.6‐fold [67] versus a 10‐fold [70] increase in plasma cortisol was observed in horses undergoing arthroscopy or abdominal surgery, respectively. Horses with acute colic showed only a mild increase in plasma cortisol intraoperatively, but already had much higher preoperative cortisol levels, which indicates that the stress response in these patients may be already nearing or at maximum level before undergoing surgery [71]. Postoperative return to baseline of cortisol levels correlates with surgical trauma, being faster after elective arthroscopy than elective abdominal surgery [64]. This return was longest in colic cases (~60 h) compared with 24 hours in the non‐colic group [71]. Sustained increased levels of cortisol in the postoperative period may also reflect response to pain or further trauma in this time period [70].
Surveillance of metabolic and endocrine changes in perioperative equine patients is limited. A recent report investigating the metabolic and hepatic changes in 32 surgical adult colic patients, revealed that hepatic dysfunction, hepatobiliary disease and alterations in metabolism are common in equine colic patients [72]. Surgical colic patients showed increased levels of bile acids, bilirubin, triglyceride and glucose concentrations and activities of liver enzymes such as GGT, AST, AP and SDH, whereas plasma ammonia was expected to remain within normal limits [72–74]. This may indicate hepatocellular injury in equine colic patients but could otherwise be associated with underlying diseases, transient bile duct obstruction, vascular compromise of the liver, or ascending infection from intestinal contents into the liver [72, 74, 75]. Increased TG values have the potential to progress organ damage [76], and were in fact negatively associated with survival [72]; however, a return of TG to normal values was observed at the time of re‐feeding in most horses [72]. Elevated bile acid concentrations at admission were associated with decreased survival in colic patients, although increased bile acid can also be the result of prolonged fasting (>3 days) [72].
Hypothermia is another factor that occurs during surgery, which in humans has been associated with an adrenergic response [77]. A decrease in the mean core body temperature occurs in horses during standing laparoscopy and horses under general anesthesia with or without surgery [45, 78, 79], but the effects of hypothermia on the stress response in horses are unknown.
In conclusion, the stress response to anesthesia and surgery is multifactorial, with pain, tissue perfusion and energy availability being important determinants of stress. Differences in fasting period, anesthetic protocol, length of anesthesia, anesthetic protocol, surgical procedure, surgical trauma, and systemic condition of the patient will have definite effects on the type and magnitude of stress markers such as glycaemia, and plasma insulin, cortisol and NEFA in horses [67], as has been shown in humans.
Systemic Inflammatory Response
All surgery leads to systemic inflammatory response syndrome (SIRS). The majority of information is found in the human literature. It is assumed that similar effects can be found in the equine patient. The inflammatory response consists of hormonal, metabolic and immunological components. The more severe the surgical insult, the more severe the inflammatory response [80]. The hormonal response is characterized by various stress hormones. In people, adrenaline and cortisol levels are increased in the face of surgery, as are glucagon, growth hormone, aldosterone and antidiuretic hormone. The extent of surgical trauma correlates well with the levels of ACTH and cortisol [81]. If patients develop postoperative complications, other abnormalities can occur. In people, critically ill patients can have a cortisol deficiency. High dose therapy with glucocorticosteroids has been associated with increased mortality, while low doses may have beneficial effects by increasing their response to noradrenaline [82]. The metabolism is decreased in the first few hours after surgery. However, this is soon followed by a catabolic and hypermetabolic phase. This phase is characterized by break down of skeletal muscle and fat [83]. Oxygen delivery to the tissues is important during this hypermetabolic