Micturition is controlled by parasympathetic, sympathetic, somatic, and central nervous system mechanisms.[1] Bladder dysfunction after pelvic surgery has been attributed to damage to the hypogastric (sympathetic) nerves and the pelvic inferior hypogastric plexus (sympathetic and parasympathetic) 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. The spectrum of urinary dysfunction after surgery includes incomplete voiding, tenesmus, urgency, frequency, nocturia and incontinence. The severity of these symptoms may be evaluated by several validated quantitative scoring systems: the International Prostate Symptom Score (IPSS) for men and the Urinary Symptom Profile (USP) and International Consultation on Incontinence (ICIQ) for women.

Contributing surgical technical factors that influence postoperative functional urinary outcomes include total mesorectal excision (TME) of large and low-lying cancers near or invading circumferential margins, high vascular ligation, wide lateral lymph node dissection, and nerve preservation techniques.[5] Nerves innervating the bladder are in close anatomic proximity to the rectum and its fascia propria, and can be injured or divided during rectal resection. High ligation of the inferior mesenteric artery during TME dissection can cause injury to the superior hypogastric plexus (sympathetic fibers) resulting in reduced bladder capacity and urge incontinence. Anterolateral dissection of the lateral ligaments and Denonvilliers’ fascia may injure nerves associated with the inferior hypogastric plexus (sympathetic and parasympathetic fibers) resulting in urinary incontinence, voiding dysfunction, and bladder irritation. Perineal dissection can indirectly damage the pudendal nerves.[6] Technical recommendations to avoid nerve injury include ligating the IMA at least 1 cm from its origin, identifying the superior hypogastric plexus nerves near the IMA and carefully dissecting them away, preserving the left and right hypogastric nerves as they course down the sacral concavity, and preserving the neurovascular bundles located at 2 and 10 o’clock anterior to Denonvilliers’ fascia in the male and posterior to the rectovaginal septum in the female.[7] The incidence of major urinary dysfunction has decreased from 26% to 4% with the introduction of nerve-sparing mesorectal excision.[8]Identification of the pelvic autonomic nerves decreases urinary complications in multiple comparative studies.[7]

Neoadjuvant radiation may impair urinary function though data are inconsistent. Varying radiation 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. The urinary catheter can then be removed around 72 hours post-operatively often without resulting urinary retention. For prolonged urinary retention, clean intermittent catheterization provides an alternative to long-term indwelling urinary catheters and the sequelae that include local irritation, urinary tract infection, and decreased quality of life. When catheters cannot be placed through the urethra, a suprapubic tube is an option. If symptoms fail to improve, urology consultation and formal urodynamic testing is encouraged and allows a specific diagnosis that informs a tailored treatment plan.[9]

Medical management of urinary dysfunction may include alpha blockers that relieve mechanical prostatic obstruction by relaxing smooth muscle at the bladder neck and prostatic capsule, and 5-alpha-reductase inhibitors that result in gradual reduction in prostate size. If an enlarged prostate is the cause of retention, surgical approaches may be considered if conservative medical management fails. Urinary incontinence may respond to pelvic physiotherapy.[7] Severe, persisting postoperative bladder dysfunction may be treated with sacral neuromodulation at the S3 nerve root. In severe, rare recalcitrant cases, urinary diversion with a neobladder or urostomy may be considered.[10]