Micturition is controlled by parasympathetic, sympathetic, somatic, and central nervous mechanisms.[1] Bladder dysfunction after pelvic surgery has been attributed to damage to the sacral splanchnic (parasympathetic) nerves, the hypogastric (sympathetic) nerves, and the pelvic autonomic nerve plexus with overall rates of dysfunction reported to range from 10% to 70%. Permanent neurogenic bladder dysfunction can be seen in up to 10% of cases.[2],[3],[4] This wide variability in incidence may be influenced by preoperative symptomatology, patient factors, assessment instruments, length of follow-up, and technical considerations.

Surgical technical factors including the nature of the total mesorectal excision (TME) of large and low-lying lesions, high vascular ligation, width of lateral node dissection, and nerve preservation techniques strongly influence urinary functional outcomes postoperatively.[5] The nerves innervating the bladder sit in close anatomic proximity to the rectum and its fascia propria and can be traumatized, damaged, or divided as a consequence of surgery. The ligation of the inferior mesenteric artery and TME dissection can cause damage to the superior hypogastric plexus resulting in reduced bladder capacity and urge incontinence. Anterolateral dissection of the lateral ligaments and near Denonvilliers’ fascia can damage the inferior hypogastric plexus resulting in urinary incontinence, voiding dysfunction, and bladder irritation. Perineal dissection can indirectly damage the pudendal nerves.[6] The incidence of major urinary dysfunction has decreased from 26% to 4% with the introduction of nerve-sparing mesorectal excision.[7] The inclusion of pelvic radiation in the treatment course can influence urinary function although data on its impact is variable. Varying dosages, duration of therapy, and timing with relation to surgical intervention make it difficult to clearly delineate the impact of radiation therapy alone on urinary function.

In the immediate postoperative period, patients may suffer from transient bladder dysfunction as a result of inflammatory changes in the paravesical tissues or anatomic displacement of the bladder. This is typically managed with urethral catheter drainage/decompression. Typically, the urinary catheter can be removed around 72 hours post-operatively without resulting urinary retention. Approximately 40% of patients will develop transient urinary retention and often requiring urethral catheter reinsertion or clean intermittent catheterization.[8],[9] A majority of patients will regain the ability to empty the bladder, however, this sometimes takes up to 6 months.[10] Prolonged retention can be managed by intermittent catheterization of the bladder. Should urinary retention be left unmanaged, deleterious effects such as hydronephrosis, urinary reflux, pyelonephritis, and declining renal function can occur. The use of urodynamics allows for objective measurements to identify those patients at risk. Treatment is highly individualized.[11]

Various treatment options exist in the management of postoperative urinary dysfunction. Indwelling catheters in the immediate post-operative period address symptoms of incontinence and voiding dysfunction. Clean intermittent catheterization provides an alternative to prolonged indwelling catheter placement and its sequelae which include local irritation, impacted quality of life, and risk of bladder infection. When catheters cannot be placed through the urethra, a suprapubic tube can be placed. If symptoms fail to improve, urology consultation and formal urodynamic testing is encouraged and allows a specific diagnosis that informs a tailored treatment plan.[10]

Medical management of urinary dysfunction can include alpha blockers which relieve mechanical prostatic obstruction by relaxing the smooth muscle at the bladder neck and the prostatic capsule and 5-alpha-reductase inhibitors which result in gradual reduction of prostatic size. If an enlarged prostate is the cause of retention, surgical approaches may be considered if conservative medical management fails. Severe, persisting postoperative bladder dysfunction can be treated with sacral neuromodulation at the S3 nerve root. In severe, recalcitrant cases urinary diversion with a neobladder or urostomy should be considered.[11]