Lower Urinary Tract Infection (male)

Jump to navigation Jump to search

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor-In-Chief: Joseph Nasr, M.D.[2]

Lead

Lower urinary tract symptoms (LUTS) in men are a group of urinary symptoms related to abnormal storage, voiding, or post-micturition function of the bladder and urethra. Common symptoms include urinary urgency, frequency, nocturia, weak urinary stream, hesitancy, intermittency, straining, and a sensation of incomplete bladder emptying.[1][2]

The prevalence of LUTS in men increases with advancing age and the condition is most commonly associated with benign prostatic hyperplasia (BPH) and overactive bladder (OAB), which frequently coexist in the same individual.[3][4]

In men, LUTS may significantly impair quality of life and, in advanced or untreated cases, may be associated with urinary retention, recurrent urinary tract infections, bladder stones, hematuria, hydronephrosis, and renal dysfunction.[5][6]

Terminology and classification

Lower urinary tract symptoms are commonly classified into voiding (obstructive) and storage (irritative) symptoms.[1][2]

Voiding symptoms include urinary hesitancy, weak or slow stream, intermittency, straining to void, and incomplete bladder emptying. These symptoms are most often related to bladder outlet obstruction.[4]

Storage symptoms include urinary urgency, increased daytime frequency, nocturia, urge urinary incontinence, dysuria, and bladder pain. These symptoms are frequently associated with detrusor overactivity and altered bladder sensory signaling.[3][7]

Symptom severity and quality-of-life impact are commonly assessed using validated instruments such as the International Prostate Symptom Score.[8]

Epidemiology

Lower urinary tract symptoms are highly prevalent worldwide and increase progressively with age.[9][10]

Autopsy and histologic studies demonstrate that benign prostatic hyperplasia is present in approximately half of men aged 50–60 years and in up to 90 percent of men older than 80 years, although many remain asymptomatic.[11].

Population-based surveys suggest that moderate to severe LUTS affect approximately 25–30 percent of men older than 65 years[12]. Overactive bladder symptoms occur in approximately 15–20 percent of men, depending on diagnostic criteria and population studied.[9][13]

Etiology and pathophysiology

Normal lower urinary tract function

Normal urinary storage and voiding require coordinated activity between the detrusor muscle, urethral sphincters, and central and peripheral nervous systems. During bladder filling, sympathetic activity promotes detrusor relaxation and sphincter contraction, while voiding involves parasympathetic detrusor contraction and sphincter relaxation.[5]

Disruption of these mechanisms can result in lower urinary tract symptoms.

Benign prostatic hyperplasia–associated LUTS

Pathophysiology

Benign prostatic hyperplasia is characterized by androgen-dependent hyperplasia of glandular and stromal tissue within the prostate. [11][14].

BPH contributes to LUTS through two principal mechanisms. Static obstruction results from enlargement of the prostate encroaching on the prostatic urethra. Dynamic obstruction results from increased smooth muscle tone mediated by α1-adrenergic receptors in the prostate and bladder neck.[15][16]

Chronic bladder outlet obstruction may lead to bladder wall thickening, reduced compliance, impaired detrusor contractility, and formation of diverticula. Over time, these changes may result in urinary retention, hydronephrosis, bladder stones, recurrent urinary tract infections, and renal impairment.[5][6]

Symptom severity does not consistently correlate with prostate size or degree of obstruction.[1]

Overactive bladder–associated LUTS

Pathophysiology

Overactive bladder is defined by urinary urgency, usually accompanied by frequency and nocturia, with or without urge urinary incontinence, in the absence of urinary tract infection or other identifiable pathology[7].

OAB symptoms are attributed to detrusor overactivity, characterized by involuntary bladder contractions during the filling phase. Proposed mechanisms include altered parasympathetic muscarinic signaling, impaired β3-adrenergic mediated relaxation, abnormal afferent sensory signaling, and urothelial mediator release such as adenosine triphosphate.[3][17]

Increasing age and bladder outlet obstruction are recognized risk factors for the development of detrusor overactivity in men[9].

Risk factors

Risk factors for LUTS in men include increasing age[18], family history and genetic susceptibility[19], metabolic syndrome and obesity,[20][21] and the presence of bladder outlet obstruction. [9]

Evaluation and diagnosis

Initial evaluation of LUTS focuses on symptom characterization, severity assessment, and exclusion of reversible or serious underlying pathology.

Common components of evaluation include symptom quantification using validated questionnaires such as the International Prostate Symptom Score, urinalysis to assess for infection or hematuria, and measurement of post-void residual volume to evaluate for urinary retention.[8][22][4][6]

Voiding diaries are often used to assess fluid intake patterns, nocturia, and frequency.[22] Prostate-specific antigen testing may be performed in selected patients for prostate cancer risk assessment or as a surrogate marker of prostate volume.[23]

Further diagnostic testing, including cystoscopy or imaging, may be indicated in men with hematuria, recurrent urinary tract infections, bladder stones, high residual volumes, or evidence of renal dysfunction.[2]

Management

Conservative and behavioral management

Lifestyle and behavioral interventions may reduce LUTS severity and are often used as first-line management. These include fluid management, avoidance of bladder irritants such as caffeine and alcohol, bladder training, timed voiding, and pelvic floor muscle therapy.[24][25]

Randomized trials and systematic reviews indicate that structured self-management programs can improve LUTS and may provide symptom relief comparable to pharmacologic therapy in selected patients.[26][27]

Pharmacologic management

Alpha-adrenergic blockers

Alpha-1 adrenergic antagonists reduce smooth muscle tone in the prostate and bladder neck, improving urinary flow and reducing voiding symptoms.[28]

Common adverse effects include dizziness, orthostatic hypotension, and ejaculatory dysfunction (premature or delayed). Use of alpha-blockers has been associated with intraoperative floppy iris syndrome during cataract surgery.[29]

5-alpha reductase inhibitors

5-alpha reductase inhibitors reduce intraprostatic dihydrotestosterone levels, leading to prostate volume reduction and decreased risk of disease progression, acute urinary retention, and need for surgery in men with larger prostates.[30][31]

Phosphodiesterase-5 inhibitors

Phosphodiesterase-5 inhibitors, particularly tadalafil, have been shown to improve LUTS with or without concomitant erectile dysfunction, likely through smooth muscle relaxation in the lower urinary tract.[32][33]

Anticholinergic agents

Anticholinergic medications reduce detrusor overactivity and are effective for storage symptoms such as urgency and urge urinary incontinence.[34]

Observational studies and meta-analyses have reported associations between long-term anticholinergic use and increased risk of cognitive decline or dementia, although findings are inconsistent and causality has not been established.[35][36][37]

Beta-3 adrenergic agonists

Beta-3 adrenergic agonists promote detrusor relaxation and are effective for overactive bladder symptoms, with a lower reported risk of cognitive adverse effects compared with anticholinergic agents.[38][39]

Combination therapy

Combination pharmacologic therapy, such as alpha-blockers combined with 5-alpha reductase inhibitors or bladder-directed agents, has been shown to provide greater symptom improvement and reduce disease progression compared with monotherapy.[11][40]

Procedural and surgical management

Procedural intervention is generally reserved for men with persistent symptoms despite medical therapy or those who develop complications such as urinary retention, recurrent infection, bladder stones, or renal impairment.[2]

Established and emerging procedures include transurethral resection of the prostate, holmium laser enucleation, water vapor thermal therapy, prostatic urethral lift, and prostatic artery embolization.[41][42][43][44]

Prognosis

Lower urinary tract symptoms associated with benign prostatic hyperplasia may progress over time, with increasing risk of symptom worsening, urinary retention, and need for surgical intervention. Long-term studies demonstrate that combination medical therapy reduces the risk of progression compared with monotherapy or watchful waiting.[45][11]


References

  1. ↑ 1.0 1.1 1.2 Sarma AV, Wei JT. Clinical practice: Benign prostatic hyperplasia and lower urinary tract symptoms. New England Journal of Medicine. 2012;367(3):248–257. doi:10.1056/NEJMcp1106637.
  2. ↑ 2.0 2.1 2.2 2.3 Gravas S, Cornu JN, Drake MJ, et al. Summary paper on the 2023 European Association of Urology guidelines on the management of non-neurogenic male lower urinary tract symptoms. European Urology. 2023;84(2):207–222. doi:10.1016/j.eururo.2023.04.008.
  3. ↑ 3.0 3.1 3.2 Peyronnet B, Mironska E, Chapple C, et al. A comprehensive review of overactive bladder pathophysiology: On the way to tailored treatment. European Urology. 2019;75(6):988–1000. doi:10.1016/j.eururo.2019.02.038.
  4. ↑ 4.0 4.1 4.2 Lerner LB, McVary KT, Barry MJ, et al. Management of lower urinary tract symptoms attributed to benign prostatic hyperplasia: AUA guideline, Part I—Initial work-up and medical management. Journal of Urology. 2021;206(4):806–817. doi:10.1097/JU.0000000000002183.
  5. ↑ 5.0 5.1 5.2 Washington and Shinohara, 2020: Washington SL III, Shinohara K. Disorders of the bladder, prostate, and seminal vesicles. In: McAninch JW, Lue TF, eds. Smith & Tanagho’s General Urology. 19th ed. McGraw Hill; 2020:chap 38. Accessed February 24, 2024. https://accessmedicine.mhmedical.com/content.aspx?bookid=2840&sectionid=241663907
  6. ↑ 6.0 6.1 6.2 Stoffel JT, Peterson AC, Sandhu JS, Suskind AM, Wei JT, Lightner DJ. AUA white paper on nonneurogenic chronic urinary retention: consensus definition, treatment algorithm, and outcome end points. J Urol. 2017;198(1):153-160. doi:10.1016/j.juro.2017.01.075 33. Bradley CS, Erickson BA,Messersmith
  7. ↑ 7.0 7.1 Lightner DJ, Gomelsky A, Souter L, Vasavada SP. Diagnosis and treatment of overactive bladder (non-neurogenic) in adults: AUA/SUFU guideline amendment 2019. J Urol. 2019;202(3):558-563. doi: 10.1097/JU.0000000000000309
  8. ↑ 8.0 8.1 BarryMJ, Fowler FJ Jr, O’LearyMP, et al; The Measurement Committee of the American Urological Association. The American Urological Association symptom index for benign prostatic hyperplasia. J Urol. 1992;148(5):1549-1557. doi:10. 1016/S0022-5347(17)36966-5
  9. ↑ 9.0 9.1 9.2 9.3 Irwin DE, Milsom I, Hunskaar S, et al. Population-based survey of urinary incontinence, overactive bladder, and other lower urinary tract symptoms in five countries: results of the EPIC study. Eur Urol. 2006;50(6):1306-1314. doi:10. 1016/j.eururo.2006.09.019
  10. ↑ Przydacz M, Golabek T, Dudek P, Lipinski M, Chlosta P. Prevalence and bother of lower urinary tract symptoms and overactive bladder in Poland: an Eastern European study. Sci Rep. 2020;10(1):19819. doi:10.1038/s41598-020-76846-0
  11. ↑ 11.0 11.1 11.2 11.3 McConnell JD, Roehrborn CG, Bautista OM, et al; Medical Therapy of Prostatic Symptoms (MTOPS) Research Group. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Engl J Med. 2003;349(25):2387-2398. doi:10.1056/NEJMoa030656
  12. ↑ Zhang AY, Xu X. Prevalence, burden, and treatment of lower urinary tract symptoms in men aged 50 and older: a systematic review of the literature. SAGE Open Nurs. 2018;4: 2377960818811773. doi:10.1177/2377960818811773
  13. ↑ Coyne KS, Sexton CC, Vats V, Thompson C, Kopp ZS, Milsom I. National community prevalence of overactive bladder in the United States stratified by sex and age. Urology. 2011;77(5):1081-1087. doi: 10.1016/j.urology.2010.08.039
  14. ↑ Madersbacher S, Sampson N, Culig Z. Pathophysiology of benign prostatic hyperplasia and benign prostatic enlargement: a mini-review. Gerontology. 2019;65(5):458-464. doi:10.1159/ 000496289
  15. ↑ Langan RC. Benign prostatic hyperplasia. Prim Care. 2019;46(2):223-232. doi:10.1016/j.pop.2019. 02.003
  16. ↑ Lepor H, Shapiro E. Characterization of alpha1 adrenergic receptors in human benign prostatic hyperplasia. J Urol. 1984;132(6):1226-1229. doi:10. 1016/S0022-5347(17)50110-X
  17. ↑ Chess-Williams R, Sellers DJ. Pathophysiological mechanisms involved in overactive bladder/detrusor overactivity. Curr Bladder Dysfunct Rep. 2023;18(2):79-88. doi:10.1007/ s11884-023-00690-x
  18. ↑ Chute CG, Panser LA, Girman CJ, et al. The prevalence of prostatism: a population-based survey of urinary symptoms. J Urol. 1993;150(1):85- 89. doi:10.1016/S0022-5347(17)35405-8
  19. ↑ Rohrmann S, Fallin MD, PageWF, et al. Concordance rates and modifiable risk factors for lower urinary tract symptoms in twins. Epidemiology. 2006;17(4):419-427. doi:10.1097/01.ede. 0000219723.14476.28
  20. ↑ Vignozzi L, Gacci M, MaggiM. Lower urinary tract symptoms, benign prostatic hyperplasia and metabolic syndrome. Nat Rev Urol. 2016;13(2):108- 119. doi:10.1038/nrurol.2015.301
  21. ↑ Kristal AR, Arnold KB, Schenk JM, et al. Race/ethnicity, obesity, health related behaviors and the risk of symptomatic benign prostatic hyperplasia: results from the Prostate Cancer Prevention Trial. J Urol. 2007;177(4):1395-1400. doi:10.1016/j.juro.2006.11.065
  22. ↑ 22.0 22.1 Bradley CS, Erickson BA,Messersmith EE, et al; Symptoms of Lower Urinary Tract Dysfunction Research Network (LURN). Evidence of the impact of diet, fluid intake, caffeine, alcohol and tobacco on lower urinary tract symptoms: a systematic review. J Urol. 2017;198(5):1010-1020. doi:10.1016/j. juro.2017.04.097
  23. ↑ Sandhu JS, Bixler BR, Dahm P, et al. Management of lower urinary tract symptoms attributed to benign prostatic hyperplasia (BPH): AUA guideline amendment 2023. J Urol. 2024;211 (1):11-19. doi:10.1097/JU.0000000000003698
  24. ↑ Brown CT, Yap T, Cromwell DA, et al. Self management for men with lower urinary tract symptoms: randomised controlled trial. BMJ. 2007; 334(7583):25. doi:10.1136/bmj.39010.551319.AE
  25. ↑ Albarqouni L, Sanders S, Clark J, Tikkinen KAO, Glasziou P. Self-management for men with lower urinary tract symptoms: a systematic review and meta-analysis. Ann FamMed. 2021;19(2):157-167. doi:10.1370/afm.2609
  26. ↑ Burgio KL, Goode PS, Johnson TM, et al. Behavioral versus drug treatment for overactive bladder in men: the Male Overactive Bladder Treatment in Veterans (MOTIVE) trial. J AmGeriatr Soc. 2011;59(12):2209-2216. doi:10.1111/j.1532-5415. 2011.03724.x
  27. ↑ Kumar A, Ashraf H, Lal PK, et al. Self-management interventions for men with lower urinary tract symptoms: a systematic review and meta-analysis of randomized controlled trials. Arch Gerontol Geriatr. 2025;131:105742. doi:10.1016/j. archger.2024.105742
  28. ↑ Fusco F, Creta M, De Nunzio C, Gacci M, Li Marzi V, Finazzi Agrò E. Alpha-1 adrenergic antagonists, 5-alpha reductase inhibitors, phosphodiesterase type 5 inhibitors, and phytotherapic compounds in men with lower urinary tract symptoms suggestive of benign prostatic obstruction: a systematic review and meta-analysis of urodynamic studies. Neurourol Urodyn. 2018;37(6):1865-1874. doi:10.1002/nau. 23554
  29. ↑ Kim A, Hak AJ, ChoiWS, Paick SH, Kim HG, Park H. Comparison of long-term effect and complications between holmium laser enucleation and transurethral resection of prostate: Nations-Wide Health Insurance study. Urology. 2021;154:300-307. doi:10.1016/j.urology.2021.04. 019
  30. ↑ Kaplan SA. 5Alpha-reductase inhibitors: what role should they play? Urology. 2001;58(6)(suppl 1): 65-70. doi:10.1016/S0090-4295(01)01347-4
  31. ↑ Roehrborn CG, Boyle P, Bergner D, et al; PLESS Study Group. Serum prostate-specific antigen and prostate volume predict long-term changes in symptoms and flow rate: results of a four-year, randomized trial comparing finasteride versus placebo. Urology. 1999;54(4):662-669. doi:10. 1016/S0090-4295(99)00232-0
  32. ↑ Porst H, McVary KT, Montorsi F, et al. Effects of once-daily tadalafil on erectile function in men with erectile dysfunction and signs and symptoms of benign prostatic hyperplasia. Eur Urol. 2009;56(4):727-735. doi:10.1016/j.eururo.2009.04.033
  33. ↑ Roehrborn CG, McVary KT, Elion-Mboussa A, Viktrup L. Tadalafil administered once daily for lower urinary tract symptoms secondary to benign prostatic hyperplasia: a dose finding study. J Urol. 2008;180(4):1228-1234. doi:10.1016/j.juro.2008.06. 079
  34. ↑ Filson CP, Hollingsworth JM, Clemens JQ, Wei JT. The efficacy and safety of combined therapy with α-blockers and anticholinergics for men with benign prostatic hyperplasia: ameta-analysis. J Urol. 2013;190(6):2153-2160. doi: 10.1016/j.juro.2013.05.058
  35. ↑ Coupland CAC, Hill T, Dening T, Morriss R, Moore M, Hippisley-Cox J. Anticholinergic drug exposure and the risk of dementia: a nested case-control study. JAMA Intern Med. 2019;179(8): 1084-1093. doi:10.1001/jamainternmed.2019.0677
  36. ↑ Pieper NT, Grossi CM, ChanWY, et al. Anticholinergic drugs and incident dementia, mild cognitive impairment and cognitive decline: ameta-analysis. Age Ageing. 2020;49(6):939-947. doi:10.1093/ageing/afaa090
  37. ↑ Zillioux J,Welk B, Suskind AM, Gormley EA, Goldman HB. SUFU white paper on overactive bladder anticholinergic medications and dementia risk. Neurourol Urodyn. 2022;41(8):1928-1933. doi: 10.1002/nau.25037
  38. ↑ Shin DG, Kim HW, Yoon SJ, et al. Mirabegron as a treatment for overactive bladder symptoms in men (MIRACLE study): efficacy and safety results from a multicenter, randomized, double-blind, placebo-controlled, parallel comparison phase IV study. Neurourol Urodyn. 2019;38(1):295-304. doi: 10.1002/nau.23852
  39. ↑ Welk B, McArthur E. Increased risk of dementia among patients with overactive bladder treated with an anticholinergic medication compared to a beta-3 agonist: a population-based cohort study. BJU Int. 2020;126(1):183-190. doi:10.1111/bju.15040
  40. ↑ Roehrborn CG, Siami P, Barkin J, et al; CombAT Study Group. The effects of combination therapy with dutasteride and tamsulosin on clinical outcomes in men with symptomatic benign prostatic hyperplasia: 4-year results from the CombAT study. Eur Urol. 2010;57(1):123-131. doi:10. 1016/j.eururo.2009.09.035
  41. ↑ Ahyai SA, Gilling P, Kaplan SA, et al. Meta-analysis of functional outcomes and complications following transurethral procedures for lower urinary tract symptoms resulting from benign prostatic enlargement. Eur Urol. 2010;58(3): 384-397. doi:10.1016/j.eururo.2010.06.005
  42. ↑ McVary KT, Rogers T, Roehrborn CG. Rezūm water vapor thermal therapy for lower urinary tract symptoms associated with benign prostatic hyperplasia: 4-year results from randomized controlled study. Urology. 2019;126:171-179. doi:10. 1016/j.urology.2018.12.041
  43. ↑ Xiang P,WangM, Guan D, et al. A systematic review and meta-analysis of prostatic urethral lift for male lower urinary tract symptoms secondary to benign prostatic hyperplasia. Eur Urol Open Sci. 2020;19:3-15. doi:10.1016/j.euros.2020.05.001
  44. ↑ Altman R, Ferreira R, Barragan C, et al. Comparing prostatic artery embolization to surgical and minimally invasive procedures for the treatment of benign prostatic hyperplasia: a systematic review and meta-analysis. BMC Urol. 2024;24(1):22. doi:10.1186/s12894-023-01397-1
  45. ↑ Jacobsen SJ, Girman CJ, Lieber MM. Natural history of benign prostatic hyperplasia. Urology. 2001;58(6)(suppl 1):5-16. doi:10.1016/S0090-4295 (01)01298-5
Retrieved from "https://www.wikidoc.org/index.php?title=Lower_Urinary_Tract_Infection_(male)&oldid=1742243"