Effects of Thoracic Epidural Analgesia and Surgery on Lower Urinary Tract Function: A Randomized, Controlled Study

Background

Acute urinary retention is one of the most common complications after surgery and anesthesia. It can occur in patients of both sexes and all age groups and after all types of surgical procedures. It is linked to several factors including increased intravenous fluids, postoperative pain and type of anaesthesia 1.

Micturition depends on coordinated actions between the detrusor muscle and the external urethral sphincter. Motorneurons of both muscles are located in the sacral spinal cord and coordination between them occurs in the pontine tegmentum of the caudal brain stem. Motorneurons innervating the external urethral sphincter are located in the nucleus of Onuf, extending from segment S1 to S3. The detrusor smooth muscle is innervated by parasympathetic fibers, which reside in the sacral intermediolateral cell group and are located in S2-4. Sympathetic fibers innervating the bladder and urethra play an important role in promoting continence and are located in the intermediolateral cell group of the lumbar cord (L1-L4). Most afferent fibers from the bladder enter the sacral cord through the pelvic nerve at segments L4-S2 and the majority are thin myelinated or unmyelinated.

There are few studies on the urodynamic effects of various anaesthetic agents 2-8, which mainly focused on lumbar epidural anaesthesia. Under the influence of epidural analgesia, patients may not feel the sensation of bladder filling, which can result in urinary retention and bladder overdistension. Overfilling of the bladder can stretch and in some cases permanently damage the detrusor muscle.

Because epidural anesthesia can be performed at various levels of the spinal cord, it is possible to block only a portion of the spinal cord (segmental blockade). Based on knowledge of the bladder innervations, it can be assumed that epidural analgesia within segments T4-6 to T10-12 has no or minimal influences on lower urinary tract function.

In a previous study, we found, against our expectations that thoracic epidural analgesia significantly inhibits the detrusor muscle during voiding, resulting in clinically relevant post void residuals which required monitoring or transurethral catheterisation 9. Because the study adopted a before-after design, we could not definitively identify the mechanisms responsible for bladder dysfunction. In particular, we could not say whether thoracic epidural analgesia per se or surgery was the cause of bladder dysfunction. Furthermore, it remains which ingredients, whether the local anesthetic, the opioid or both are behind changes in voiding function.

Objective

In our previous studies, we found that TEA significantly inhibits the detrusor muscle during voiding, resulting in clinically relevant post-void residuals which required monitoring or catheterization with similar findings 5,30.

Because these studies adopted a before-after design, we could not definitively identify the mechanisms responsible for lower urinary tract dysfunction. In particular, we could not say whether TEA per se or surgery was the cause of lower urinary tract dysfunction. Furthermore, it remains unclear which compounds in the epidural solution, the local anesthetic, the opioid or both are behind the observed changes in lower urinary tract function.

The objectives of this study are to determine if TEA per se or surgery are the cause of bladder dysfunction and which drugs in the epidural solution are responsible for this effect.

Methods

Randomised controlled double-blind study. Patients will be randomly allocated to one of the two groups by a computer-generated randomization list. Randomization will be stratified by gender, in order to reach an equal number of male and females in the two groups. Patients and investigators will be blinded to the epidural solution administrated.