Urinary Retention
Three nerves provide primary control ofthe bladder, namely the hypogastric nerve (sympathetic nervous system), the pelvic nerve (parasympathetic nervous system) and the pudendal nerve (somatic nervous system). The storage phase of micturition is mainly mediated through stimulation of β3-adrenergic receptors (sympathetic) causing bladder relaxation, the a-adrenergic receptors of the internal sphincter (sympathetic) and the external sphincter (somatic nervous system). The external sphincter striated muscle is controlled by the neurons in Onuf s nucleus, located within the S2-4 sacral segments of the spinal cord. The neurons from Onuf's send axons into the pudendal nerve causing contraction of external sphincter. (2)
PREVALENCE
Two large population-based studies in the US found an overall incidence in men of 4.5-6.8 per 1000 person years. (3,4) In men w/ BPH, research has suggested this is much higher at 3.7 up to 130 per 1000 person-years. (5) In female this is much less, common and most commonly occurs after childbirth with the cumulative incidence of postpartum urinary retention ranges from 0.2% to 17.9% of all deliveries. (6,7)
DRUG INDUCED RETENTION
A review of 27 publications identified two case reports, three pooled analyses, two observational studies and one randomized controlled trial. Two of the observational studies and a pooled analysis of randomized controlled trials reported a significant increase in the risk of acute urinary retention (UR) with inhaled anticholinergics. (1)
Observational studies have shown up to 10% of UR is drug induced. UR has been described from use of anticholinergic, antipsychotics, antidepressants, opiods, aneashetics, a-adrenoceptor agonists, benzodiazepines, NSAIDs, detrusor relaxants and calcium channel antagonists and antihistamines. (2) One study of a general male population aged >45 years and found that the use of calcium channel antagonists and anticholinergic drugs doubled and tripled the risk of acute urinary retention, respectively. (4) One interesting meta-analysis looking at NSAID use rather than opioids found that NSAID's reduced the incidence of nausea and vomiting, but did not reduce pruritus, urinary retention or respiratory depression. (10) In fact one study showed despite a reduction in opiate use of 35%, there was no reduction in urinary retention. (9) T
A systemic review found four randomized controlled trials published in peer-reviewed journals that showed the incidence of acute urinary retention was not significantly more for patients treated with an antichoiinergic agent in combination with an α-blocker than in the control group of patients, who were treated with an α-blocker or placebo. (12) A RCT of 879 patients w/ OAB and BPH showed no difference in UR between placebo, tolterodine and tolterodine + tamsulosin. (11) The authors of the systemic review explained the safety of the anticholinergic agents in patients with overactive bladder is due to these drugs acting mostly during the storage phase by blocking the afferent activity, resulting in decreased urge feelings and an increased biadder capacity. Furthermore, during voiding, the action of these antichoiinergic agents is reduced by a massive release of acetylcholine. (12)
DRUG TREATMENT FOR RETENTION
A systemic review showed cholinergic agents (bethanechol or carbachol) or cholinesterase inhibitors for the treatment of urinary bladder underactivity had little evidence to support the use of these drugs for this medical condition. (8)
INFLAMMATION ROLE IN URINARY RETENTION
Inflammation may impact risk of retention: MTOPS study found 5.6% of patients with inflammation on pathology progressed to urinary retention whereas 0 patients lacking inflammation had susequent progression to AUR. Analysis of CD-8 inflammatory marker showed the highest tertile had a 3.64 risk of AUR despite no increased I-PSS. (13)
NSAIDS
Retrospective studies have shown conflicting data of the effect of NSAIDS on BPH/LUTS. 2 RCT did show I-PSS improvement and flow rate improvement and a meta-analysis found NSAIDs improved symptoms by 2.9 I-PSS points and flow by 0.89ml/sec. (14,15,16)
PREVALENCE
Two large population-based studies in the US found an overall incidence in men of 4.5-6.8 per 1000 person years. (3,4) In men w/ BPH, research has suggested this is much higher at 3.7 up to 130 per 1000 person-years. (5) In female this is much less, common and most commonly occurs after childbirth with the cumulative incidence of postpartum urinary retention ranges from 0.2% to 17.9% of all deliveries. (6,7)
DRUG INDUCED RETENTION
A review of 27 publications identified two case reports, three pooled analyses, two observational studies and one randomized controlled trial. Two of the observational studies and a pooled analysis of randomized controlled trials reported a significant increase in the risk of acute urinary retention (UR) with inhaled anticholinergics. (1)
Observational studies have shown up to 10% of UR is drug induced. UR has been described from use of anticholinergic, antipsychotics, antidepressants, opiods, aneashetics, a-adrenoceptor agonists, benzodiazepines, NSAIDs, detrusor relaxants and calcium channel antagonists and antihistamines. (2) One study of a general male population aged >45 years and found that the use of calcium channel antagonists and anticholinergic drugs doubled and tripled the risk of acute urinary retention, respectively. (4) One interesting meta-analysis looking at NSAID use rather than opioids found that NSAID's reduced the incidence of nausea and vomiting, but did not reduce pruritus, urinary retention or respiratory depression. (10) In fact one study showed despite a reduction in opiate use of 35%, there was no reduction in urinary retention. (9) T
A systemic review found four randomized controlled trials published in peer-reviewed journals that showed the incidence of acute urinary retention was not significantly more for patients treated with an antichoiinergic agent in combination with an α-blocker than in the control group of patients, who were treated with an α-blocker or placebo. (12) A RCT of 879 patients w/ OAB and BPH showed no difference in UR between placebo, tolterodine and tolterodine + tamsulosin. (11) The authors of the systemic review explained the safety of the anticholinergic agents in patients with overactive bladder is due to these drugs acting mostly during the storage phase by blocking the afferent activity, resulting in decreased urge feelings and an increased biadder capacity. Furthermore, during voiding, the action of these antichoiinergic agents is reduced by a massive release of acetylcholine. (12)
DRUG TREATMENT FOR RETENTION
A systemic review showed cholinergic agents (bethanechol or carbachol) or cholinesterase inhibitors for the treatment of urinary bladder underactivity had little evidence to support the use of these drugs for this medical condition. (8)
INFLAMMATION ROLE IN URINARY RETENTION
Inflammation may impact risk of retention: MTOPS study found 5.6% of patients with inflammation on pathology progressed to urinary retention whereas 0 patients lacking inflammation had susequent progression to AUR. Analysis of CD-8 inflammatory marker showed the highest tertile had a 3.64 risk of AUR despite no increased I-PSS. (13)
NSAIDS
Retrospective studies have shown conflicting data of the effect of NSAIDS on BPH/LUTS. 2 RCT did show I-PSS improvement and flow rate improvement and a meta-analysis found NSAIDs improved symptoms by 2.9 I-PSS points and flow by 0.89ml/sec. (14,15,16)
- Loke, Yoon K., and Sonal Singh. "Risk of acute urinary retention associated with inhaled anticholinergics in patients with chronic obstructive lung disease: systematic review." Therapeutic advances in drug safety 4.1 (2013): 19-26.
- Verhamme, Katia MC, et al. "Drug-induced urinary retention." Drug safety 31.5 (2008): 373-388.
- Jacobsen SJ, Jacobson DJ, Girman CJ, et al. Natural history of prostatism: risk factors for acute urinary retention. J Urol 1997 Aug; 158 (2): 481-7
- Meigs JB. Barry MJ, Giovannucci E. ct al. incidence rates and risk factors for acute urinary retention: the health professionals followup study. J Urol 1999 Aug: 162 (2): 376-82.
- Roehitom CG. The epidemiology of acute urinary retention in benign prostatic hyperplasia. Rev Urol 2001 Fail: 3 (4): 187-92.
- Glavind K, Bjork J. Incidence and treatment of urinary retention postpartum. Int Urogynccol J Pelvic Floor Dysfunct 2003 Jun: 14(2): 119-21.
- Teo R. Punier J, Ahrams K, et al. Clinically overt postpartum urinary retention after vaginal delivery: a retrospective casecontrol study. Int Urogynecol J Pelvic Floor Dysfunct 2006 Aug 23: 18(5): 521-4
- Barendrecht MM, Oelke M, Laguna MP. et al. Is the use of parasympathomimetics for treating an underactive urinary bladder evidence-based? BJU Int 2(X)7 Apr; 99 (4): 749-52.
- Romsing J. Mniniche S, Mathiesen O, et al. Reduction of opioid-related adverse events using opioid-sparing analgesia with COX-2 inhibitors lacks documentation: a systematic review, Acta Anaesthesiol Scand 2005 Feb; 49 (2): 133-42.
- Marret E, Kurdi O, Zufferey P, el al. Effects of nonsteroidal anti inflammatory drugs on patient-controlled analgesia morphine side effects: meta-analysis of randomized controlled trials. Anesthesiology 2005 Jun; 102 (6): 1249-60
- Kaplan SA, Roehrborn CG, Rovner ES, et al, Tolterodine and tamsulosin for treatment uf men with lower urinary tract symptoms and mcractive bladder: a randomized controlled trial. JAMA 2006; Nov 15: 296 (19): 2319-28.
- Novara G, Galfano A, Ficarra V, et al, Anticholinergic drugs in patients with bladder outlet obstruction and lower urinary tract symptoms: a systematic review. Eur Urol 2006 Oct: 50 (4): 675-83.
- Torkko, K. C., Wilson, R. S., Smith, E. E., Kusek, J. W., Bokhoven, A. van, & Lucia, M. S. (2015). Prostate Biopsy Markers of Inflammation are Associated with Risk of Clinical Progression of Benign Prostatic Hyperplasia: Findings from the MTOPS Study. The Journal of Urology, 194(2), 454–461.
- Sutcliffe, S., Grubb, R. L., Platz, E. A., Ragard, L. R., Riley, T. L., Kazin, S. S., … Andriole, G. L. (2012). Non-steroidal anti-inflammatory drug use and the risk of benign prostatic hyperplasia-related outcomes and nocturia in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. BJUI, 110(7), 1050–1059.
- Lloyd, G. L., Ricke, W. A., & McVary, K. T. (2019). Inflammation, Voiding and Benign Prostatic Hyperplasia Progression. The Journal of Urology, 201(5), 868–870.
- Kahokehr, A., Vather, R., Nixon, A., & Hill, A. G. (2013). Non‐steroidal anti‐inflammatory drugs for lower urinary tract symptoms in benign prostatic hyperplasia: systematic review and meta‐analysis of randomized controlled trials. BJUI, 111(2), 304–311.