General anesthetics cause decreased bladder contractility by acting as smooth muscle relaxants. They also interfere with autonomic regulation of detrusor tone (Darrah et al., 2009). Some anesthetics substantially increase bladder capacity (Darrah et al., 2009; Doyle & Briscoe, 1976). In vitro work with isolated human bladder strips demonstrated that clinical doses of halothane (Fluothane®) and thiopentone (Trapanal®) decrease the response of the bladder to cholinergic stimulation (Doyle & Briscoe, 1976). Petros, Rimm, Robillard, and Argy (1991) noted that patients undergoing inguinal herniorrhaphy under general anesthesia with halothane, a potent smooth muscle relaxant, had a significantly higher rate of urinary retention compared with similar cases performed via a lidocaine (Lidoderm®) spinal anesthetic. Furthermore, sedative-hypnotics and volatile anesthetics inhibit the PMC and voluntary cortical control of the bladder, suppressing detrusor contraction and the micturition reflex (Combrisson, Robain, & Cotard, 1993; Darrah et al., 2009; Matsuura & Downie, 2000).
The urodynamic effect of volatile anesthetics and sedative-hypnotics, when combined with other agents commonly used for general anesthesia (pre-medication or reversal of neuromuscular blockade) on the LUT, has been evaluated. Glycopyrrolate (Robinul®) and atropine, two agents used for preventing bradycardia, do not appear to affect the incidence of urinary retention (Orko & Rosenberg, 1984). Sympathomimetic agents used to treat intraoperative hypotension can increase the risk of urinary retention as a result of their effects on beta-adrenergic receptors in the bladder and alpha-adrenergic receptors in the bladder neck and proximal urethra. In patients treated with ephedrine, a statistically significant increase in retention to 43.8% was noted (Darrah et al., 2009; Olsen & Nielsen, 2007).
Urol Nurs. 2012;32(2):60-67. © 2012 Society of Urologic Nurses and Associates