A Scottish physician and metabolism researcher named Dr David Cuthbertson first reported on the metabolic consequences of surgery in 1932 when he coined the term “ebbs and flows” when studying the effects of lower limb injury. Since that time scientific study has added a great deal more to what we know about the physiological response to surgery, and understanding this response lends itself to more effective management, including mitigating risks of the surgical patient.
This chapter outlines the primary physiologic responses to surgery, and their impact on the management of the postoperative patient, including the typical surgical stress response, effects on fluids and electrolytes, and common organ-specific effects.
The surgical stress response has three key physiologic components:
Sympathetic nervous system activation
Immunologic activation with the production of cytokines and acute phase reactants, and resultant neutrophil release and demargination, and lymphocyte proliferation
SYMPATHETIC NERVOUS SYSTEM ACTIVATION
Surgical stress stimulates the hypothalamic-pituitary-adrenal (HPA) axis and leads to sympathetic nerve activation, which triggers the release of catecholamines. In addition to their cardiovascular affects (tachycardia, hypertension), these hormones also affect the liver, kidneys, and pancreas.
Surgical stress results in a variety of changes in serum levels of endocrinologic hormones (Table 42-1).
TABLE 42-1Principal Hormonal Responses to Surgery |Favorite Table|Download (.pdf) TABLE 42-1 Principal Hormonal Responses to Surgery
|Endocrine Gland ||Hormone ||Change in Secretion |
|Anterior pituitary ||ACTH ||Increases |
| ||Growth hormone ||Increases |
| ||TSH ||May increase or decrease |
| ||FSH and LH ||May increase or decrease |
|Posterior pituitary ||AVP ||Increases |
|Adrenal cortex ||Cortisol ||Increases |
| ||Aldosterone ||Increases |
|Pancreas ||Insulin ||Often decreases |
| ||Glucagon ||Usually small increases |
|Thyroid ||Thyroxine ||Decrease |
These endocrine responses are normal after surgery, but can sometimes result in clinically significant complications. For example, increased cortisol can lead to hyperglycemia, which is associated with surgical complications and poorer outcomes. Cortisol also stimulates protein catabolism, whereby both skeletal and visceral muscle are broken down to release amino acids for energy or to be used by the liver to form new protein including the acute phase reactants. This process can result in weight loss, muscle wasting, and impaired healing. Arginine vasopressin can result in free water retention, which can result in hypervolemia and hyponatremia.
Surgical stress also results in a variety of immunological changes. Such activation is essential for recovery and wound healing, but can also have untoward physiologic effects (such as fever). White blood cells and endothelial cells produce interleukins and interferons, which contribute to an inflammatory cascade. Interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), and IL-6 are the primary cytokines released after surgery. Increased IL-6 production after surgery activates acute phase ...