in 2008 the World Health Organization (WHO) instituted the Surgical Safety Checklist (SSC) as a global initiative to improve surgical safety of human patients. Since then, SSCs have become standard practice in human hospitals and are slowly being implemented in veterinary hospitals. These checklists cover introduction of surgical and anesthetic teams, identification of patient, consent, procedure to be performed, anatomical location, estimated duration of surgery, availability of equipment, and potential complications among others. Use of SSCs has assisted in prevention of potential safety hazards and errors in the operating room, and improved safety and communication among operating staff [22–24]. Their implementation has been associated with reduced morbidity, length of in‐hospital stay and mortality [25]. Sustained use of SSCs seems to be discipline‐specific and is more successful when physicians are actively engaged and leading implementation [26]. In addition, implementation of SSCs did not negatively impact the operating room efficiency, whilst reducing overall disposable costs, in a large multispecialty tertiary care human hospital [27].
Perioperative Consequences to Surgical Trauma
Any surgical procedure is associated with some degree of tissue trauma, which results in a stress response by the patient’s body. This stress response follows the same pathways as that after accidental trauma or disease; however, the magnitude of the stress response will vary with the severity of the stimulus. The patient’s condition, severity of disease, anesthesia and surgical procedure will all contribute to the stimulus of a stress response. Healthy patients undergoing elective minor surgery may not sustain any significant effects, but patients with severe trauma or critical illness can enter prolonged catabolic states with notable consequences to morbidity and mortality.
The stress response is multifactorial and governed by inflammatory, metabolic, neurohormonal and immunologic pathways. As a consequence, it is difficult to categorize the degree of stress response as there is no single variable or combination thereof that define stress in a consistent manner. A combination of variables encompassing all involved pathways, and even variables related to other body systems susceptible to stress‐related consequences such as the reproductive system, should be included to define the short‐ and long‐term effects of stress [28]. The pathways involved are totally interrelated and difficult to separate, but for the purpose of this review the stress response in the surgical patient will be divided into four sections: metabolic/nutritional effects, neuroendocrine consequences, inflammatory response, and pain.
Metabolic and Nutritional Effects
In the 1930s, Cuthbertson described the body’s post‐traumatic response as an immediate “ebb” or shock phase followed by the flow phase [29]. The short‐lived (24–48 h) ebb phase is characterized by reductions in blood pressure, cardiac output, body temperature and oxygen consumption, and when associated with hemorrhage, hypoperfusion and lactic acidosis, depending on the severity. The latter flow phase is characterized by hypermetabolism, increased cardiac outputs, increased urinary nitrogen losses, altered glucose metabolism and accelerated tissue catabolism.
The nutritional status of the human surgical patient is well recognized as a factor associated with morbidity and mortality [30, 31]. Malnourished patients show a reduction in survival, immune function, wound healing and gastrointestinal functions, and associated prolonged hospitalization and increased infection [32, 33]. Preoperative fasting, anesthesia, surgery and disease all contribute to the stress hypermetabolic response. Stimulation of the sympathetic nervous system causes release of catecholamines, an increase in oxygen delivery and consumption at the tissue level, and a rise in body temperature. As a consequence, the resting energy expenditure increases. Individual assessment of resting energy expenditure has become an integral part of the management of the human surgical patient. Providing adequate perioperative nutritional support is standard of care in humans, as malnutrition or overfeeding are associated with poorer outcome [34]. Horses undergoing surgery are subject to variable preoperative fasting times, and colic patients may undergo prolonged food and even water restriction perioperatively. However, standard assessment of the nutritional status of the equine patient is not common, and nutritional support is often limited to intravenous and/or oral fluids with electrolytes. Other nutrients such as glucose, aminoacids and lipids are less frequently incorporated in the form of either enteral or parenteral nutrition.[35].
The healthy adult horse can tolerate food deprivation, commonly referred to as simple starvation or pure protein or calorie malnutrition (PPCM), for 24–72 hours with minimal systemic consequences [36]. In this situation, healthy humans sustain neuroendocrine changes leading to a lower metabolic rate and resting energy expenditure. This is associated with decreased blood glucose, insulin, increased glucagon and down‐regulation of catecholamines. Initial hepatic glycogenolysis and gluconeogenesis followed by use of fat stores maintain normal blood glucose values and survival, while lean tissue (protein) is spared.
Energy demands are increased in patients with a prior history of malnutrition, increased metabolic rate (i.e. young growing animals), underlying metabolic abnormalities, sepsis, severe trauma, or underweight animals at higher risk of stress response. The effect of fasting on stressed catabolic patients is a hypermetabolic state with increased resting energy expenditure. This is the result of the catecholamine release by the stimulated sympathetic nervous system and the inflammatory cytokines released at the site of injury, inflammation, disease or surgery [37, 38]. The magnitude of this hypermetabolic state relates to the severity of the disease or trauma. Stimulation and/or release of corticotrophin, cortisol, epinephrine, growth hormone and glucagon result in an increased resting metabolic rate characterized by insulin resistance, increased glucocorticoid secretion, gluconeogenesis, dysregulation of glycemia, lipolysis, proteolysis, nitrogen loss and rapid malnutrition [39]. Blood triglycerides should be monitored, and appropriate nutritional support instituted in horses at risk of developing hyperlipemia such as obese animals (especially miniature horses and donkeys), lactating mares, and horses suffering from Cushing’s syndrome or equine metabolic syndrome.
The response to an elective surgical procedure will be more limited in a healthy than in a critically ill patient or a patient with severe trauma. However, an increase in metabolic rate occurs postoperatively in humans after simple elective surgery [40]. Anesthesia and midline abdominal exploratory laparotomy increased the postoperative caloric demand in healthy horses by 10% in experimental conditions [41]. Increased demands in critically ill equine patients are expected to be higher but have not been quantified to the editors’ knowledge.
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
