Could my patient with acute dysuria and less than 10,000 E. coli/ml on urine culture still have a urinary tract infection (UTI)?

Absolutely! Although historically ≥100,000 bacteria/ml has been used as a criterion for UTI based on studies of women with pyelonephritis in the 1950s,1 several studies have since found that this criterion may not be met in up to 50% of symptomatic patients with UTI. 2-6 A lower criterion of 100-1,000 bacteria/ml of urine increases the sensitivity of urine culture to ~90% or more for diagnosis of UTI (albeit with lower specificity). 2-5

A 1982 NEJM study involving UTIs due to coliforms in acutely dysuric women found that the traditional count of ≥100,000 bacteria/ml in midstream urine missed ~50% of cases based on positive bladder cultures. 2 Similarly a 2013 NEJM study reported that 40% of women with symptomatic UTI would be missed if the ≥100,000 bacteria/ml criterion for midstream urine is used. 3

Among symptomatic men, 32% have been found to have <100,000 bacteria/ml in their midstream urine 4 and a single urine specimen by urethral catheterization growing ≥ 100 bacteria/ml is consistent with bacteriuria for both men and women. 5

Since most of these studies have involved UTI caused by E. coli or other coliforms, more data are needed to find out if the same findings apply to non-coliform urinary pathogens.

Bonus Pearl: Did you know that because quantitative urine culture results are concentration dependent (ie, “per ml”), a dilute urine—as may be found in patients experiencing diuresis—will result in lower numbers of bacteria/ ml. 5

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 References

  1. Kass EH. Asymptomatic infections of the urinary tract. Trans Assoc Am Physicians 1958;69:56-74. https://pubmed.ncbi.nlm.nih.gov/13380946/
  2. Stamm WE, Counts GW, Running KR, et al. Diagnosis of coliform infection in acutely dysuric women. N Engl J Med 1982;307:463-8. https://pubmed.ncbi.nlm.nih.gov/7099208/
  3. Hooten TM, Roberts PL, Cox ME, et al. Voided midstream urine culture and acute cystitis in premenopausal women. N Engl J Med 2013;369:1883-91. https://www.nejm.org/doi/full/10.1056/NEJMoa1302186
  4. Lipsky BA, Ireton RC, Fihn SD, et al. Diagnosis of bacteriuria in men: specimen collection and culture interpretation. J Infect Dis 1987;155:847-54. https://pubmed.ncbi.nlm.nih.gov/3559288/
  5. Nicolle LE, Bradley S, Colgan R, et al. Infectious Diseases Society of America Guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults. Clin Infect Dis 2005;40:643-54. https://pubmed.ncbi.nlm.nih.gov/15714408/
  6. Roberts KB, Wald ER. The diagnosis of UTI: colony count criteria revisited. Pediatrics 2018;141:e20173239. https://doi.org/10.1542/peds.2017-3239

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Could my patient with acute dysuria and less than 10,000 E. coli/ml on urine culture still have a urinary tract infection (UTI)?

How long should I treat my patient with urinary tract infection and E. Coli bacteremia?

Although traditionally 7 to 14 days of antibiotic therapy has been recommended for Gram-negative bacteremia, more recent studies suggest that shorter antibiotic treatment courses are as effective as longer treatments for a variety of infections, particuarly those due to Enterobacteriaceae (eg, E. Coli, Klebsiella sp) in patients with low severity illness (1). 

Keep in mind that short course therapy may not apply to all patients with UTI and bacteremia, such as those with prostatitis (not included in the most recent study [1,2]), which requires longer course of antibiotics (3)

 
A 2019 randomized-controlled study involving primarily patients with bacteremia caused by E. Coli or Klebsiella sp. (~75%) with most cases associated with UTI (~70%) found that 7 days was as effective as 14 days of treatment in hemodynamically stable patients who are afebrile for at least 48 hours without an ongoing focus of infection (1). More specifically, there was no significant difference between the 2 groups in the rates of relapse of bacteremia or mortality at 14 or 28 days.

 
An accompanying editorial concluded that “7 days of treatment may be sufficient for hospitalized, non-critically ill patients with Gram-negative bacteremia and with signs of early response to treatment” (4)  Again, the accent should be on hemodynamically stable patients who respond rapidly to treatment. 

 
Bonus Pearl: While on the subject of shorter course antibiotic therapy, a 2016 “mantra” article nicely summarizes more recent suggestions for common infectious disease conditions (5). Obviously, clinical judgment should be exercised in all cases.
• Community-acquired pneumonia                               3-5 days (vs 7-10 days)
• Nosocomial pneumonia                                                 8 days or less (vs 10-15 days)
• Pyelonephritis                                                                  5-7 days (vs 10-14 days)
• Intraabdominal infection                                             4 days (vs 10 days)
• COPD acute exacerbation                                             5 days or less (vs >6 days)
• Acute bacterial sinusitis                                               5 days (vs 10 days)
• Cellulitis                                                                            5-6 days (vs 10 days)

 

 

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References
1. Yahav D, Franceschini E, Koppel F, et al. Seven versus 14 days of antibiotic therapy for uncomplicated Gram-negative bacteremia: A noninferiority randomized controlled trial. Clin Infect Dis 2019; 69:1091-8. https://academic.oup.com/cid/article/69/7/1091/5237874       2. Yahav D, Mussini C, Leibovici L, et al. Reply to “Should we treat bacteremic prostatitis for 7 days”.  Clin Infect Dis 2010;70:751-3. DOI:10:1093/cid/ciz393.

3.  De Greef J, Doyen L, Hnrard S, et al. Should we treat bacteremic prostatitis for 7 days? Clin Infect Dis 2020;70:351https://academic.oup.com/cid/article-abstract/70/2/351/5488067?redirectedFrom=fulltext
4. Daneman D, Fowler RA. Shortening antibiotic treatment durations for bacteremia. Clin Infect Dis 2019;69:1099-1100. https://academic.oup.com/cid/article-abstract/69/7/1099/5237877?redirectedFrom=fulltext
5. Spellberg B. The new antibiotic mantra: “ Shorter is better”. JAMA Intern Med 2016;176:1254-55. https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2536180

How long should I treat my patient with urinary tract infection and E. Coli bacteremia?

My 70 year old male patient is admitted with 1 day of fever, dysuria, and urinary frequency and urgency, but has a negative urine dipstick test for nitrites and leukocyte esterase. Could he still have acute bacterial prostatitis?

Short answer: Yes! In fact, no routine clinical imaging test can adequately rule out prostatic involvement in men with urinary tract infection (UTI) symptoms (1)! 

Although the presence of nitrites and leukocyte esterase (LE) may have a high positive predictive value for acute bacterial prostatitis (ABP) (~95%), their combined absence has a negative predictive value of only ~70%; ie, we may miss about one-third of patients with UTI symptoms if we relied solely on the results of nitrite and LE urine dipstick (2,3). Negative nitrites alone has a negative predictive value of only ~ 45%, while a negative LE has a negative predictive value of ~60% (3).

To evaluate for ABP, our patient should undergo rectal exam for prostatic tenderness, as should all men with UTI symptoms. The finding of a tender prostate in this setting is supportive of ABP, although its absence will still not rule out this diagnosis because the reported sensitivity of rectal exam may vary from 9% to 100% in ABP (1). 
Although there may not be a general agreement on the definition of ABP, 2 studies utilizing indium-labeled leukocyte scintigraphy or a combination of PSA levels and transrectal ultrasound have provided evidence for frequent prostatic involvement in men with UTI symptoms (4,5).  In these studies, an inflammatory reaction within the prostate was seen in the majority of cases, even when the digital rectal examination was not painful or when clinicians diagnosed pyelonephritis without prostatitis.
Bonus pearl: Did you know that the lifetime probability of a man receiving a diagnosis of prostatitis is >25% (1)? 

Also see a related P4P pearl: https://pearls4peers.com/2017/07/27/should-male-patients-with-suspected-urinary-tract-infection-routinely-undergo-a-prostate-exam/

 

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References
1. Etienne M, Chavanet P, Sibert L, et al. Acute bacterial prostatitis: heterogeneity in diagnostic criteria and management. Retrospective multicentric analysis of 371 patients diagnosed with acute prostatitis. BMC Infect Dis 2008, 8:12 doi:10.1186/1471-2334-8-12. https://bmcinfectdis.biomedcentral.com/articles/10.1186/1471-2334-8-12
2. Lipsky BA, Byren I, Hoey CT. Treatment of bacterial prostatitis. Clin Infect Dis 2010;50:1641-1652. https://academic.oup.com/cid/article/50/12/1641/305217
3. Etienne M, Pestel-Caron M, Chavanet P, et al. Performance of the urine leukocyte esterase and nitrite dipstick test for the diagnosis of acute prostatitis. Clin Infect Dis 2008; 46:951-53. https://academic.oup.com/cid/article/46/6/951/351423
4. Velasco M, Mateos JJ, Martinez JA, et al. Accurate topographical diagnosis of urinary tract infection in male patients with (111)indium-labelled leukocyte scintigraphy. Eur J Intern Med 2004;15:157-61. https://www.ncbi.nlm.nih.gov/pubmed/15245717
5. Ulleryd P, Zackrisson B, Aus G, et al. Prostatic involvement in men with febrie urinary tract infection as measured by serum prostate-specific antigen and transrectal ultrasonography. BJU Int 1999;84:470-74. https://onlinelibrary.wiley.com/doi/full/10.1046/j.1464-410x.1999.00164.x

 

My 70 year old male patient is admitted with 1 day of fever, dysuria, and urinary frequency and urgency, but has a negative urine dipstick test for nitrites and leukocyte esterase. Could he still have acute bacterial prostatitis?

Of the commonly used drugs for benign prostatic hypertrophy (BPH), which ones may be the least likely to cause hypotension in my hospitalized patient with borderline systolic blood pressures?

5-alpha-reductase inhibitors (RIs) (eg, finasteride and dutasteride) are less likely to cause hypotension than alpha-1-adrenergic antagonists (AAs) (eg, tamsulosin, doxazocin, terazocin, and alfuzocin), the other major class of drugs commonly used for treatment of signs and symptoms of benign prostatic hypertrophy (BPH).

A Cochrane systematic review found that finasteride, an RI, has a lower risk of postural hypotension compared to doxazosin, an AA. 1 In fact, there’s no solid evidence that RIs exacerbate hypotension on their own. 2,3 Unfortunately, RIs take longer to achieve benefit because they work by reducing prostate size over time, while AAs work much faster by reducing prostate smooth muscle tone.4 So, while it’s reasonable to choose an RI over an AA in our patient with soft pressures, it’s also reasonable to expect it won’t work quite as well during his hospital stay and you may still be forced to choose an AA.  

Among AAs, tamsulosin is the least likely to be associated with hypotension when compared to others in the same class (eg, doxazocin and terazocin) which are also sometimes used for treatment of hypertension. Thus, tamsulosin may be the best choice for patients at risk of  hypotension.5 However, even tamsulosin is not totally safe in this regard, especially in the first 4 weeks after starting or re-starting treatment when its risk of hospital admission for hypotension is about double that of RIs.6

Bonus pearl: Did you know that prazocin was the first promising selective AA investigated for BPH but likely because of its availability in generic form and the general notion at the time that medical therapy of BPH would not be widely accepted by urologists, larger randomized-controlled trials were never pursued!7

References

  1. Tacklind J, Fink HA, MacDonald R, et al. Finasteride for benign prostatic hyperplasia. Cochrane Database of Systematic Reviews, 2010 Oct 6. https://www.ncbi.nlm.nih.gov/pubmed/20927745
  2. Finasteride prescribing information: https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/020180s037lbl.pdf
  3. Dutasteride prescribing information: https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/021319s014lbl.pdf
  4. Rigatti P, Brausi M, Scarpa RM, et al. A comparison of the efficacy and tolerability of tamsulosin and finasteride in patients with lower urinary tract symptoms suggestive of benign prostatic hyperplasia. Prostate Cancer and Prostatic Diseases 2003; 6:315–323. https://www.ncbi.nlm.nih.gov/pubmed/14663474
  5. Tewari A and Narayan P. Alpha-adrenergic blocking drugs in the management of benign prostatic hyperplasia: interactions with antihypertensive therapy. Urology 1999 Mar;53:14-20. https://www.ncbi.nlm.nih.gov/pubmed/10094096
  6. Bird ST, Delaney JAC, Brophy JM, et al. Tamsulosin treatment for benign prostatic hyperplasia and risk of severe hypotension in men aged 40-85 years in the United States: risk window analyses using between and within patient methodology. BMJ 2013; 347 :f6320. https://www.ncbi.nlm.nih.gov/pubmed/24192967
  7. Lepor H. Alpha blockers for the treatment of benign prostatic hyperplasia. Rev Urol 2007;9:181-90.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2213889/

Contributed by Nick Bodnar, Harvard medical student, Boston, MA.

 

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Of the commonly used drugs for benign prostatic hypertrophy (BPH), which ones may be the least likely to cause hypotension in my hospitalized patient with borderline systolic blood pressures?

Should I consider fosfomycin in the treatment of urinary tract infection in my male patient with suspected prostatitis?

Although fosfomycin (FM) has been approved by the FDA only for the treatment of uncomplicated urinary tract infection (UTI) in women, it may also have a role in the treatment of acute and chronic prostatitis among males given its favorable levels in the prostate tissue. 1-5

Despite lack of studies comparing the efficacy of FM with that of commonly used antibiotics for treatment of prostatitis, the potential utility of FM is supported by several reports of its efficacy in the treatment of prostatitis, including those caused by extended-spectrum beta-lactamase (ESBL)-producing gram-negative rods. 1,4-5

When considering FM for treatment of prostatitis, a higher dose than customary may be needed (3 g once daily, not every 48-72 h) . 4 Although the optimal duration of therapy with FM is unclear in this setting, 12-16 weeks of therapy was used in 2 patients with recurrent UTIs and prostatitis due to multi-drug resistant ESBL-positive E. coli. 4

Given its pharmacokinetics and lack of proven efficacy, avoid FM in pyelonephritis, perinephric abscess or UTI with bacteremia. 2

References

  1. Falagas ME, Vouloumanou EK, Samonis G, et al. Fosfomycin. Clin Microbiol Rev 2016;29:321-347. https://www.ncbi.nlm.nih.gov/pubmed/26960938
  2. Wankum M, Koutsari C, Gens K. Fosfomycin use. Pharmacy Times. November 30, 2017. https://www.pharmacytimes.com/publications/health-system-edition/2017/november2017/fosfomycin-use
  3. Cunha BA, Gran A, Raza M. Persistent extended-spectrum β-lactamase-positive Escherechia coli chronic prostatitis successfully treated with a combination of fosfomycin and doxycycline. International J Antimicrob Agents 2015;45:427-29. https://www.ncbi.nlm.nih.gov/pubmed/25662814
  4. Grayson ML, Macesic N, Trevillyan J, et al. Fosfomycin for treatment of prostatitis: new tricks for old dogs. Clin Infect Dis 2015;61:1141-3. https://www.ncbi.nlm.nih.gov/pubmed/26063723
  5. Falagas ME, Rafailidis PI. Fosfomycin: the current status of the drug. Clin Infect Dis 2015;61:1144-6. https://www.ncbi.nlm.nih.gov/pubmed/26063717
Should I consider fosfomycin in the treatment of urinary tract infection in my male patient with suspected prostatitis?

Should Aerococcus urinae growth from the urine of my elderly patient be considered a pathogen?

Although for many years Aerococcus urinae was considered a urinary contaminant, increasingly it is recognized as an emerging pathogen capable of causing not only urinary tract infection (UTI) but also secondary bacteremia and endocarditis, among others.1   

The proportion of patients with aerococcal bacteriuria with symptoms suggestive of UTI ranges from 55-98%.1 So A. urinae can no longer be assumed to be a contaminant, particularly in the presence of symptoms suggestive of UTI.

A. urinae UTI often affects the elderly (median age 79 y) and those with pre-existing urinary tract pathologies, such as prostatic hyperplasia, urethral stricture, renal calculi, and prior urinary tract surgery.2,3 Many patients also have underlying comorbidities such as diabetes, heart disease, dementia, and chronic renal failure.3

One clue to the presence of A. urinae in the urine is its particularly pungent odor reminiscent of that of patients with trimethylaminuria (fish odor syndrome).4

Once you decide you should treat A. urinae, keep in mind that it is NOT predictably susceptible to trimethoprim-sulfamethoxazole, fluoroquinolones, or fosfomycin!  Instead, consider penicillin, ampicillin, cephalosporin, or nitrofurantoin to which most strains are susceptible.5,6.

 

References

  1. Rasmussen M. Aerococcus: an increasingly acknowledged human pathogen. Clin Microbiol Infect 2016;22:22-27. https://www.ncbi.nlm.nih.gov/pubmed/26454061
  2. Tathireddy H, Settypalli S, Farrell JJ. A rare case of aerococcus urinae infective endocarditis. J Community Hosp Intern Med Perspectives 2017; 7:126-129. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5473194/
  3. Higgins A, Garg T. Aerococcus urinae: An emerging cause of urinary tract infection in older adults with multimordidity and urologic cancer. Urology Case Reports 2017;24-25. https://www.ncbi.nlm.nih.gov/pubmed/28435789
  4. Lenherr N, Berndt A, Ritz N, et al. Aerococcus urinae: a possible reason for malodorus urine in otherwise healthy children. Eur J Pediatr. 2014;173:1115-7 https://www.ncbi.nlm.nih.gov/pubmed/24913181
  5. Christensen JJ, Nielsen XC. Aerococcus urinae. Antimicrobe @ http://www.antimicrobe.orgb75.asp , accessed June 14, 2018.
  6. Dimitriadi D, Charitidou C, Pittaras T, et al. A case of urinary tract infection caused by Aerococcus urinae. J Bacteriol Mycol 2016; 2: 00041. https://pdfs.semanticscholar.org/a1cf/048d8444ce054ca9a332f7c2b4a218325ff6.pdf

 

Should Aerococcus urinae growth from the urine of my elderly patient be considered a pathogen?

Can I rely on the physical exam to rule out symptomatic urinary tract infection (UTI) in my hospitalized patient?

Suprapubic tenderness, costovertebral angle tenderness (CVAT) and fever seem to be more helpful in ruling in than ruling out infection. And, before you hang your hat on the available data, remember that most of the studies involve women with uncomplicated UTI in primary care or emergency department settings, not our older hospitalized patients at risk of complicated infections.  With these caveats in mind….

Suprapubic tenderness has been reported in only about 15-20% of women with acute cystitis. 1

CVAT has been associated with symptomatic UTI but with only a weakly positive LR (1.7, 1.1-2.5), and an insignificant negative LR. 2  In a single center study involving hospitalized patients (mean age 53 y), CVAT was either absent or “obscure” in about 10% of patients with acute pyelonephritis on CT.3

Fever was associated with a positive likelihood ratio (1.6, 1.0-2.6) by 1 systematic study 2 but not another, 4 with insignificant negative LR in both. Fever was also absent in about 10% of hospitalized patients with pyelonephritis in the single center study above.3

So, when evaluating a patient with possible symptomatic UTI (particularly cystitis), the presence of physical exam findings  may be more helpful than their absence.

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References

  1. Kurowski K. The woman with dysuria. Am Fam Physician 1998, 57:2155-2164. https://www.aafp.org/afp/1998/0501/p2155.html
  2. Bent S, Nallamothu BK, Simel DL, et al. Does this woman have an acute uncomplicated urinary tract infection? JAMA 2002;287:2701-2710. https://www.ncbi.nlm.nih.gov/pubmed/12020306
  3. Lee Y-J, Cho S, Kim SR. Unilateral and bilateral acute pyelonephritis: differences in clinical presentation, progress and outcome. Postgrad Med 2014;90:80-85. https://www.ncbi.nlm.nih.gov/pubmed/24255118
  4. Median-Bombardo D, Jover-Palmer A. Does clinical examination aid in the diagnosis of urinary tract infections in women? A systematic review and meta-analysis. BMC Family Practice 2011;12:111. https://bmcfampract.biomedcentral.com/articles/10.1186/1471-2296-12-111

 

Can I rely on the physical exam to rule out symptomatic urinary tract infection (UTI) in my hospitalized patient?

What common drugs may exacerbate urinary retention in my patient with spinal cord injury?

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? 

 

References

  1. 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
  2. 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
  3. 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
  4. Glidden RS, DiBona FJ. Urinary retention associated with ephedrine. J Pediatr 1977; 90:1013-4. https://www.ncbi.nlm.nih.gov/pubmed/859049
  5. 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
  6. 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.

 

What common drugs may exacerbate urinary retention in my patient with spinal cord injury?

Should male patients with suspected urinary tract infection routinely undergo a prostate exam?

Yes! That’s because any urinary tract infection (UTI) in men has the potential for prostatic involvement1 —-as high as 83% by one report. 2  

To make the matters more confusing, patients with acute bacterial prostatitis (ABP) often present with symptoms just like those of UTI,  such as urinary frequency, dysuria, malaise, fever, and myalgias. 3  In the elderly, atypical presentation is not uncommon (eg, confusion, incontinence, fall). 4  Under these circumstances, bacteriuria and pyuria may also be related to ABP and the prostate exam should be an important part of your evaluation.

Although the sensitivity of prostate tenderness on digital rectal exam varies widely for ABP (9%-100%), a painful exam should raise suspicion for ABP, and by itself may be an independent predictor for clinical and bacteriologic failure of therapy. 1 Along with tenderness, fluctuance of prostate, particularly in the setting of voiding difficulties and longer duration of symptoms, may also suggest the presence of prostatic abscess. 5,6 

But be gentle when performing a prostate exam and don’t massage it because you could potentially cause bacteremia and worsening of sepsis! 1,7

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References

  1. Etienne M, Chavanet P, Sibert L, et al. Acute bacterial prostatitis: heterogeneity in diagnostic criteria and management. Retrospective multicentric analysis of 371 patients diagnosed with acute prostatitis. BMC Infectious Diseases 2008;8:12. https://bmcinfectdis.biomedcentral.com/track/pdf/10.1186/1471-2334-8-12?site=bmcinfectdis.biomedcentral.com
  2. Ulleryd P, Zackrisson B, Aus G, et al. Prostatic involvement in men with febrile urinary tract infection as measured by serum prostate-specific antigen and transrectal ultrasonography. BJU Int 1999;84:470-4. http://onlinelibrary.wiley.com/doi/10.1046/j.1464-410x.1999.00164.x/pdf
  3. Krieger JN, Nyberg L, Nickel JC. NIH consensus definition and classification. JAMA 1999;282:236-37. http://jamanetwork.com/journals/jama/article-abstract/1030245
  4. Harper M, Fowlis. Management of urinary tract infections in men. Trends in Urology Gynaecology & Sexual Health. January/February 2007. http://onlinelibrary.wiley.com/doi/10.1002/tre.8/pdf
  5. Lee DS, Choe HS, Kim HY, et al. Acute bacterial prostatitis and abscess formation. BMC Urology 2016;16:38. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936164/
  6. Oliveira P, Andrade JA, Porto HC, et al. Diagnosis and treatment of prostatic abscess. International Braz J Urol 2003;29: 30-34. http://www.scielo.br/pdf/ibju/v29n1/v29n1a06.pdf
  7. Lipsky BA, Byren I, Hoey CT. Treatment of bacterial prostatitis. Clin Infect Dis 2010; 50:1641-52. https://academic.oup.com/cid/article/50/12/1641/305217

 

Should male patients with suspected urinary tract infection routinely undergo a prostate exam?

My 35 year old patient with chronic alcoholism blames benign prostatic hypertrophy for his difficulty voiding. Could his bladder dysfunction be related to his alcoholism?

Several case reports in the literature have stressed the association of bladder dysfunction (BD) with chronic alcohol abuse1,2.  Although some cases may be associated with concurrent thiamine deficiency (with its attendant neuropathy), other cases of BD do not appear to be. The mechanism of BD in this setting may be related to the toxic effect of alcohol on peripheral, autonomic and/or central nervous systems2,3.

Binge drinking may also be associated with urinary retention, with spontaneous atraumatic urinary bladder rupture having been reported on several occasions4. Lastly, alcohol withdrawal alone may precipitate urinary retention5.  

Unfortunately, many cases of abdominal pain due to urinary retention in the setting of alcohol abuse or withdrawal may be mistakenly attributed to ascites or other causes5.  High index of suspicion for BD is essential to minimize its complications.

In our patient, given the low prevalence of benign prostatic hypertrophy in men less than 40 years of age, urinary retention due to alcohol-related BD is more likely.

 

References

  1. Yuan R, Carcciolo VJ, Kulaga M. Chronic abdominal distension secondary to urinary retention in a patient with alcoholism. JAMA 2002;287;318-19.
  2. Sheremata WA, Sherwin I. Alcoholic myelopathy with spastic urinary bladder. Dis Nerv Syst 1972;33:136-139.
  3. Mellion M, Gilchrist JM, De La Monte S. Alcohol-related peripheral neuropathy: nutritional, toxic or both? Muscle Nerve 2011;43:309-16.
  4. Muneer M, Abdelrahman H, El-Menyar A, et al. Spontaneous atraumatic urinary bladder rupture secondary to alcohol intoxication: a case report and review of literature. Am J Case Rep 2015;16:778-81.
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My 35 year old patient with chronic alcoholism blames benign prostatic hypertrophy for his difficulty voiding. Could his bladder dysfunction be related to his alcoholism?