Purpose of review: Indications for ureterorenoscopy are expanding without hard scientific evidence to support its efficacy. Therefore, it is extremely important to focus on potential harmful effects of the procedure itself. This review explores how physiology of the upper urinary tract reacts to ureterorenoscopy, potentially translating into harmful effects, and how such pathophysiological processes may be minimized.
Recent findings: Complications to ureterorenoscopy and postoperative pain seem to be related to intrarenal pressure and/or access. Mean intrarenal pressures in the range of 60-100 mmHg during ureterorenoscopy without access sheaths have been measured, thus by far exceeding the threshold for intrarenal backflow, potentially resulting in septic complications. Intrarenal pressure may be reduced by use of ureteral access sheaths, which, however, may cause ureteral damage due to the limited size of the ureter and strain-induced ureteral contractions (peristalsis). Different receptor types modulate this peristaltic activity. β-receptor agonists have been investigated in animal and human trials for the purpose of relaxing the ureter. In randomized, placebo-controlled trials in pigs and humans, usage of the β-receptor agonist isoproterenol in the irrigation fluid has shown a potential for reducing both intrarenal pressure and ureteral tone during ureterorenoscopy.
Summary: Upper urinary tract physiology has unique features that may be pushed into pathophysiological processes by the unique elements of ureterorenoscopy: access and irrigation. Pharmacological ureteral relaxation during ureterorenoscopy deserves further attention with regard to reducing complications and postoperative pain.