Procedure-specific Risk Factors

Every procedure elicits a stress-response (i.e., “surgical stress”) characterized by physiological (i.e., autocrine, endocrine, and paracrine) changes accompanied by psychological reactions (e.g., fear, anxiety, tension, malaise, or fatigue).1-3 The stress-response or “alarm reaction” likely evolved in more primitive times as a survival mechanism to limit tissue injury, to allow catabolism of stored nutrients, and to activate the healing process.

In the head and neck area, surgical stress is initiated by afferent somatic and autonomic neuronal input from the site of tissue injury through the trigeminal ganglia/dorsal root complex of the spinal cord to the reticular activating system, the limbic system (the hypothalamus and pituitary gland), and the neocortex. Normal negative feedback mechanisms appear to fail and lead to increased secretion of catabolic and decreased secretion of anabolic hormones (Table 1).1-3

Table 1. Hormonal Responses to Tissue Injury.
Endocrine Gland Hormone Change in Secretion
Adrenal Epinephrine Increased
Cortisol Increased
Aldosterone Increased
Anterior pituitary ACTH Increased
Growth hormone Increased
Thyroid stimulating hormone (TSH) Unchanged
Pancreas Insulin Decreased
Glucagon Increased
Thyroid Thyroxin (T4) and tri-iodothyronine (T3) Decreased

Perioperative surgical stress-induced autocrine, endocrine, and paracrine effects include cardio-pulmonary stimulation, hyperglycemia, hyperadrenocorticism, decreased synthesis of thyroid hormones, and modulation of the inflammatory response. The magnitude of these responses is proportional to the severity of tissue trauma, duration of the procedure, volume of blood loss, fluid shifts in the body, and changes in core body temperature.4