Anticholinergics (including tricyclic antidepressants-TCAs), selective serotonin reuptake inhibitors (SSRIs), benzodiazepines, opioids, alpha-adrenergics, and non-steroidal anti-inflammatory drugs (NSAIDs) are among the most common agents associated with urinary retention1. This adverse reaction is particularly observed in patients with pre-existing hypoactive bladder, including those with spinal cord injury (SCI). Unfortunately, patients with SCI also often require pharmacologic management of neuropathic pain with one or more of these agents (eg, TCAs, opioids, and NSAIDs).
The mechanism of urinary retention may vary depending on the agent. Anticholinergics (eg, TCAs, diphenhydramine) decrease detrusor muscle contraction via blockade of the parasympathetic pathway.1 Opiates may increase the sphincter tone of bladder via sympathetic stimulation, as well as decrease the sensation of bladder fullness by partial inhibition of the parasympathetic nerves that innervate the bladder.2 SSRIs increase external sphincter tone by inhibiting serotonin reuptake.3 Alpha-adrenergics (e.g. ephedrine) can lead to detrusor relaxation and sphincter contraction.3 NSAIDs are thought to inhibit prostaglandin-mediated detrusor contraction.5
Although most patients with SCI have urinary incontinence due to detrusor hyperactivity, some will have urinary retention due to detrusor hyporeflexia.6
Final Fun Fact: Did you know that medications may account for up to 10% of urinary retention episodes?
- Verhamme KM, Sturkenboom MC, Stricker BH, Bosch R. Drug-induced urinary retention. Drug Saf 2008;31(5):373-88. https://www.ncbi.nlm.nih.gov/pubmed/18422378
- Elsamra SE, Ellsworth P. Effects of analgesic and anesthetic medications on lower urinary tract function. Urologic Nursing 2012;32: 60-68. https://www.suna.org/download/education/2014/article320260067.pdf
- Thor KB. Serotonin and norepinephrine involvement in efferent pathways to the urethral rhabdosphincter: implications for treating stress urinary incontinence. Urology 2003; 62:3-9. https://www.ncbi.nlm.nih.gov/pubmed/14550831
- Glidden RS, DiBona FJ. Urinary retention associated with ephedrine. J Pediatr 1977; 90:1013-4. https://www.ncbi.nlm.nih.gov/pubmed/859049
- Verhamme KM, Dieleman JP, Van Wijk MA, et al. Nonsteroidal anti-inflammatory drugs and increased risk of acute urinary retention. Arch Intern Med. 2005;165:1547–1551. https://www.ncbi.nlm.nih.gov/pubmed/16009872
- Fowler CJ, O’Malley KJ. Investigation and management of neurogenic bladder dysfunction. J Neurol Neurosurg Psychiatry 2003;74(Suppl IV):iv27–iv31. http://jnnp.bmj.com/content/jnnp/74/suppl_4/iv27.full.pdf
Contributed by Alice Choi, Medical Student, Harvard Medical School, Boston, MA.
For continuous urethral catheterization (CUC), the estimated daily risk of acquisition of bacteriuria is 3% to 8%1-3. For intermittent urethral catheterization (IUC), the incidence of bacteriuria is 1% to 3% per insertion4. The Infectious Diseases Society of America recommends that IUC should be considered as an alternative to short-term CUC to reduce catheter-associated bacteriuria or UTI based on “poor evidence” (Category C) and, as relates to symptomatic UTIs, without properly designed randomized-controlled studies2.
A Cochrane systematic review of CUC vs IUC in hospitalized patients failed to find any significant differences between the 2 interventions as relates to the rates of symptomatic UTI and asymptomatic bacteriuria in hospitalized patients requiring short-term catheterization5. Of interest, nearly 3 times as many people developed acute urinary retention with IUC compared to CUC in this study (16% vs 45%, respectively, RR 0.45, 95% CI 0.22-0.91).
In short, despite its theoretical advantage in reducing the risk of UTIs due to lack of a constant presence of a catheter, solid data to support preference of IUC over CUC in short-term management of urinary retention in hospitalized patients is still lacking.
Bonus pearl: Did you know that compared to indwelling urinary catheters, suprapubic catheters are associated with lower incidence of asymptomatic bacteriuria, but not necessarily symptomatic UTIs? 5
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- Lo, Nicolle LE, Coffin SE, et al. Strategies to prevent catheter-associated urinary tract infections in acute care hospitals: 2014 update. Infect Control Hosp Epidemiol 2014;35:464-78. https://www.ncbi.nlm.nih.gov/pubmed/25376068
- Hooton TM, Bradley SF, Cardenas DD, et al. Diagnosis, prevention, and treatment of catheter-associated urinary tract infection in adults: 2009 International Clinical Practice Guidelines from the Infectious Diseases Society of America. Clin Infect Dis 2010;50:625-663. https://academic.oup.com/cid/article/50/5/625/324341
- Kunin CM, McCormack RC. Prevention of catheter-induced urinary-tract infections by sterile closed drainage. N Engl J Med 1966;274:1155-61. https://www.ncbi.nlm.nih.gov/pubmed/5934951
- Saint S, Lipsky BA. Preventing catheter-related bacteriuria: Should we? Can we? How? Arch Intern Med 1999;159:800-808. https://reference.medscape.com/medline/abstract/10219925
- Kidd EA, Stewart F, Kassis NC, et al. Urethral (indwelling or intermittent) or suprapubic routes for short-term catheterization in hospitalized adults (review). Cochrane Database of Systematic Reviews 2015; Issue 12. Art No. :CD004203. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD004203.pub3/full
Patients admitted with AECOPD are commonly on maintenance tiotropium and are frequently treated with additional inhaled anticholinergic agents (eg, ipratropium) during hospitalization. However, the scientific evidence justifying IDAT in patients with AECOPD is lacking, and is quite limited even in patients with stable COPD1-3. Two small, randomized double-blind studies compared the impact of tiotropium combined with either ipratropium or placebo in outpatients with stable COPD. Both studies selected FEV1 alone as their primary end-point and found only a marginal benefit with IDAT2,3.
A population-based study of acute urinary retention in persons with COPD aged ≥66 years found a significantly higher odds of acute urinary retention among those on IDAT vs monotherapy or no anticholinergics (odds ratios 1.4 and 2.7, respectively)4.
In short, routine use of IDAT in patients with AECOPD lacks firm evidence in its clinical efficacy and may be associated with acute urinary retention.
- Cole JM, Sheehan AH, Jordan JK. Concomitant use of ipratropium and tiotropium in chronic obstructive pulmonary disease. Ann Pharmacother 2012;46:1717-21.
- Kerstjens HA, Bantje TA, Luursema PB, Sinninghe Damste HE, de Jong JW. Effects of short-acting bronchodilators added to maintenance tiotropium therapy. Chest 2007;132:1493-9.
- Cazzola M, Santus P, D’Adda A, et al. Acute effects of higher than standard doses of salbutamol and ipratropium on tiotropium-induced bronchodilation in patients with stable COPD. Pulm Pharmacol Ther 2009; 22:177-82.
- Singh S, Furbergt CD. Inhaled anticholinergic drug therapy and the risk of acute urinary retention in chronic obstructive pulmonary disease. Arch Intern Med 2011;171:920-2.
Contributed by Josh Ziperstein, MD, Massachusetts General Hospital, Boston.
Although measurement of PVR is a common everyday occurrence in hospitalized patients, the threshold of what constitutes an abnormal value is often poorly defined and not standardized. However, most urologists consider volumes of 50 ml to 100 ml to constitute the lower threshold of abnormal PVR (1).
Large PVRs are associated with urinary tract infections, especially in persons at risk (e.g. diabetes, spinal cord injury), while very large PVRs (>300 ml) may be associated with an increased risk of upper urinary tract dilatation and renal insufficiency.
Chronic urinary retention is often defined as a PVR > 300 ml (2).
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1. Kelly CE. Evaluation of voiding dysfunction and measurement of bladder volume. Rev Urol 2004;6 (suppl 1):S32-S37. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472847
2. Kaplan SA, Wein AJ, Staskin DR, Roehrborn CG, Steers WD. Urinary retention and post-void residual urine in men: separating truth from tradition. J Urology 2008;180:47–54. https://www.ncbi.nlm.nih.gov/pubmed/18485378
The association between constipation and urinary retention is well known (1,2).
Several mechanisms may explain this relationship, including sharing of the innervations of the internal anal and urinary sphincters via S2-S4 nerve roots, and the presence of impacted stool in the rectum leading to invaginations in the posterior wall of the bladder and urethral obstruction (1,2).
Interestingly, in laboratory experiments involving rats, rectal distention with a balloon diminished bladder contractility (3). So, along with many other factors, constipation should routinely be considered a potential cause of acute urinary retention.
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1. Selius BA, Subedi R. Urinary retention in adults: diagnosis and initial management. Am Fam Physician 2008;77:643-650. https://www.aafp.org/afp/2008/0301/p643.html
2. Ariza Traslavina, Del Ciampo LA, Ferraz IS. Acute urinary retention in a pre-school girl with constipation. Rev Paul Pediatr 2015;33:488-492. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4685571/
3. Miyazato M, Sugaya K, Nishijima S, et al. Rectal distention inhibits the spinal micturition reflex via glycinergic or GABAergic mechanisms in rats with spinal cord injury. Urol Int 2005;74:160-65. https://www.ncbi.nlm.nih.gov/pubmed/15756069