My hospitalized patient with pneumonia has now suffered an acute myocardial infarction (MI). Can acute infection and MI be related?

Yes! Ample epidemiological studies implicate infection as an important risk factor for MI.1 The increased risk of MI has been observed during the days, weeks, months or even years following an infection.

A 2018 paper reported a several-fold risk of MI during the week after laboratory-confirmed infection caused by a variety of respiratory pathogens such as influenza virus (6-fold), respiratory syncytial virus (4-fold), and other respiratory viruses (3-fold). 2 Among patients hospitalized for pneumococcal pneumonia, 7-8% may suffer an MI.3,4 One study found a 48-fold increase in the risk of MI during the first 15 days after hospitalization for acute bacterial pneumonia.5 Similarly, an increase in the short-term risk of MI has been observed in patients with urinary tract infection and bacteremia.6

The risk of MI appears to be the highest at the onset of infection and correlates with the severity of illness, with the risk being the highest in patients with pneumonia complicated by sepsis, followed by pneumonia and upper respiratory tract infection. Among patients with pneumonia, the risk exceeds the baseline risk for up to 10 years after the event, particularly with more severe infections.1

Potential mechanisms of MI following infections include release of inflammatory cytokines (eg, interleukins 1, 6, tumor necrosis factor alpha) causing activation of inflammatory cells in atherosclerotic plaques, in turn resulting in destabilization of the plaques. In addition, the thrombogenic state of acute infections, platelet and endothelial dysfunction may increase the risk of coronary thrombosis at sites of plaque disruption beyond clinical resolution of the acute infection. 1

References

  1. Musher DM, Abers MS, Corrales-Medina VF. Acute infection and myocardial infarction. N Engl J Med 2019;380:171-6. https://www.ncbi.nlm.nih.gov/pubmed/30625066
  2. Kwong JC, Schwartz KL, Campitelli MA, et al. Acute myocardial infarction after laboratory-confirmed influenza infection. N Engl J Med 2018;378:345-53. https://www.nejm.org/doi/full/10.1056/NEJMoa1702090
  3. Musher DM, Alexandraki I, Graviss EA, et al. Bacteremic and nonbacteremic pneumococcal pneumonia: a prospective study. Medicine (Baltimore) 2000;79:210-21. https://www.ncbi.nlm.nih.gov/pubmed/10941350
  4. Musher DM, Rueda Am, Kaka As, Mapara SM. The association between pneumococcal pneumonia and acute cardiac events. Clin Infect Dis 2007;45:158-65. https://www.ncbi.nlm.nih.gov/pubmed/17578773
  5. Corrales-Medina VF, Serpa J, Rueda AM, et al. Acute bacterial pneumonia is associated with the occurrence of acute coronary syndromes. Medicine (Baltimore) 2009;88:154-9. https://www.ncbi.nlm.nih.gov/pubmed/19440118
  6. Dalager-Pedersen M, Sogaard M, Schonheyder HC, et al. Risk for myocardial infarction and stroke after community-acquired bacteremia: a 20-year population-based cohort study. Circulation 2014;129:1387-96. https://www.ncbi.nlm.nih.gov/pubmed/24523433

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My hospitalized patient with pneumonia has now suffered an acute myocardial infarction (MI). Can acute infection and MI be related?

My previously healthy patient is admitted with a multi-drug resistant E. coli urinary tract infection. Could her urinary tract infection (UTI) be foodborne?

Yes! Although foodborne infections are often thought to cause infections limited to the GI tract, an increasing number of studies have linked foodborne E.coli to extraintestinal infections in humans, including UTIs.1

Supportive data include frequent genetic similarly between antimicrobial-resistant E. coli from humans and poultry-associated E. coli. 2 In fact, antimicrobial-resistant E. coli isolates from humans may be  genetically more similar to poultry isolates than susceptible commensal E. coli strains in the human GI tract.3

A U.S. study found that 14% of chicken meat products were contaminated with E. coli strains capable of causing extraintestinal disease, 1/3 of which were mutli-drug resistant.4  Another study found that 94% of retail chicken meat samples contained E. coli with ESBL-genes,  of which nearly 40% contained isolates present in humans.5

Among women, UTI caused by antimicrobial-resistant extraintestinal pathogenic E. coli has been linked to high levels of self-reported chicken consumption.6

The plausibility of foodborne transmission of antimicrobial-resistant E. coli to humans is further supported by the finding that drug resistant E coli from chicken carcasses widely contaminate the kitchen during meal preparation and can appear in the intestinal tract of those who prepare such food.2

Bonus Pearl: Did you know that women with multi-drug resistant E. coli UTI are 3.7 times more likely to report frequent consumption of chicken? 6

References

  1. Manges AR. Escherichia coli and urinary tract infections: the role of poultry-meat. Clin Microbiol Infect 2016;22:122-29. https://www.ncbi.nlm.nih.gov/pubmed/26679924
  2. Manges AR, Johnson JR. Reservoirs of extraintestinal pathogenic Escherichia coli. Microbiol Spectrum 2012;3(5):UTI-0006-2012. https://www.ncbi.nlm.nih.gov/pubmed/26542041
  3. Johnson JR, Menard M, Johsnton B, et al. Epidemic clonal groups of Escherichia coli as a cause of antimicrobial-resistant urinary tract infections in Canada, 2002 to 2004. Antimicrob Agents Chemother 53;2733-2739. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2704706/
  4. Johnson JR, Porter SB, Johnston B, et al. Extraintestinal pathogenic and antimicrobial-resistant Escherichia coli, including sequence type 131 (ST131) from retail chicken breasts in the United States in 2013. Apppl Environ Microbiol 83:e02956-16. https://www.ncbi.nlm.nih.gov/pubmed/28062464
  5. Leverstein-van Hall MA, Dierikx CM, Stuart JC, et al. Dutch patients, retail chicken meat and poultry share the same ESBL genes, plasmids and strains. Clin Microbiol Infect 2011;17:873-880. https://www.ncbi.nlm.nih.gov/pubmed/21463397
  6. Manges AR, Smith SP, Lau BJ, et al. Retail meat consumption and the acquisition of antimicrobial resistant Escherichia coli causing urinary tract infections: a case-control study. Foodborne Path Dis 4:419-431. https://www.ncbi.nlm.nih.gov/pubmed/18041952

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My previously healthy patient is admitted with a multi-drug resistant E. coli urinary tract infection. Could her urinary tract infection (UTI) be foodborne?

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?

My patient with pyelonephritis has positive blood cultures for E. coli? Should I order repeat blood cultures to make sure the bacteremia is clearing?

Although a common practice, follow-up blood cultures (FUBCs) may not be necessary in otherwise clinically stable or improving patients with aerobic gram-negative bacteremia. This is probably due to the often-transient nature of gram-negative bloodstream infections  and less propensity of these organisms to cause intravascular infections (eg, endocarditis) compared to gram-positives. 1

A 2017 study addressing the value of FUBCs in gram-negative bacteremia found that repeat positive blood cultures were uncommon with positive results not associated with mortality or higher ICU admissions. 1 Specifically, 17 FUBCs had to be drawn to yield 1 positive result.  Although the numbers of positive FUBCs were too low for in-depth analysis, it was concluded that FUBCs added little value in the management of gram-negative bacteremias.

In contrast, FUBCs are recommended in the following situations: 1-3

  • Staphylocccus aureus bacteremia given the propensity of this organism to cause intravascular (eg, endocarditis) and metastatic infections.
  • Presumed or documented endocarditis or intravascular device infections (eg, intravenous catheters and pacemakers) to document timely clearance of bacteremia
  • Infections involving organisms that may be difficult to clear such as fungemia or multi-drug resistant pathogens.

As with many things in medicine, clinical context is important before ordering tests and blood cultures are no different. The urge to order FUBCs should also be balanced with the possibility of having to deal with  contaminants. 

References

  1. Canzoneri CN, Akhavan BJ, Tosur Z et al. Follow-up blood cultures in gram-negative bacteremia: Are they needed? Clin Infect Dis 2017;65:1776-9. https://www.ncbi.nlm.nih.gov/pubmed/29020307
  2. Tabriz MS, Riederer K, Baran J, et al. Repeating blood cultures during hospital stay: Practice pattern at a teaching hospital and a proposal for guidelines. Clin Microbiol Infect 2004;10:624-27. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1469-0691.2004.00893.x
  3. Mylotte JM, Tayara A. Blood cultures: Clinical aspects and controversies. Eur J Clin Microbiol Infect Dis 200;19:157-63. https://www.ncbi.nlm.nih.gov/pubmed/10795587

 

 

My patient with pyelonephritis has positive blood cultures for E. coli? Should I order repeat blood cultures to make sure the bacteremia is clearing?

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?

My diabetic patient complains of new onset tingling, burning, and numbness in her feet and ankles while taking levofloxacin for sinusitis. Could it be the antibiotic?

Although there are numerous culprits in peripheral neuropathy (PN), fluoroquinolones (FQs) are increasing reported as a potential cause, affecting about 1% of patients. 1

Besides many case reports, couple of large epidemiologic studies support the association between PN and FQs. A case-control pharmacoepidemiologic study of a cohort of men aged 45-80 years without diabetes found that current users of FQs were nearly twice as likely to develop PN (RR 1.83, 95% C.I. 1.49-2.27), with the highest risk found among current new users of FQ.2 The risk appeared similar among the 3 most commonly used FQs (levofloxacin, ciprofloxacin, moxifloxacin).

Another epidemiologic study with “pharmacovigilance analysis” based on the FDA Adverse Event Reporting System found significant disproportionality of PN for FQs compared to many other antibiotics. 3 The median onset of PN after exposure to FQ was 4 days (range 0-91). Contrary to initial reports of the mild and reversible course of FQ-associated PN, 1 study reported that 58% of patients had symptoms lasting greater than 1 year.4`

These findings prompted the FDA to update its boxed warnings for FQs in 2016 to stress the potential rapidity of onset and permanence of FQ-associated PN while strongly discouraging their use in conditions for which alternative therapy exists, such as in acute bacterial sinusitis, acute bacterial exacerbation of chronic bronchitis and uncomplicated UTI.5

So while our patient may have other causes for her neurologic complaints, FQ exposure should also be in the differential!

References

  1. Dudewich M, Danesh A, Onyima C, et al. Intractable acute pain related to fluoroquinolone-induced peripheral neuropathy. J Pain Pall Care Pharmacotherapy 2017;31:144-7. https://www.ncbi.nlm.nih.gov/pubmed/28358229
  2. Etminan M, Brophy JM, Samii A. Oral fluoroquinolone use and risk of peripheral neuropathy: A pharmacoepidemiologic study.Neurology 2014;83:1261-63. https://www.ncbi.nlm.nih.gov/pubmed/25150290
  3. Ali AK. Peripheral neuropathy and Guillain-Barre syndrome risks associated with exposure to systemic fluorquinolones: a pharmacovigilance analysis. Ann Epidemiol 2014; 24:279-85. https://www.ncbi.nlm.nih.gov/pubmed/24472364
  4. Francis JK, Higgins E. Permanent peripheral neuropathy: A case report on a rare but serious debilitating side-effect of fluroquinolone administration. Journal Investigative Medicine High Impact Case Reports 2014; 1-4. DOI:10.1177/2324709614545225. https://www.ncbi.nlm.nih.gov/pubmed/26425618
  5. FDA.https://www.fda.gov/Drugs/DrugSafety/ucm511530.htm.  Accessed December 8, 2017.
My diabetic patient complains of new onset tingling, burning, and numbness in her feet and ankles while taking levofloxacin for sinusitis. Could it be the antibiotic?

Is intermittent urethral catheterization preferred over continuous indwelling catheters for short-term management of urinary retention in my hospitalized patient?

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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References

  1. 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
  2. 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
  3. 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
  4. 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
  5. 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

 

 

 

 

Is intermittent urethral catheterization preferred over continuous indwelling catheters for short-term management of urinary retention in my hospitalized patient?

How exactly do urinary tract infections (UTIs) cause delirium in my elderly patients?

 UTIs are often considered in the differential diagnosis of causes of delirium in the elderly. Though largely speculative, 2 possible pathophysiologic basis for this association are suggested:1-3

  •  Direct brain insult (eg, in the setting of sepsis/hypotension)
  • Indirect aberrant stress response, involving cytokines/inflammatory pathways,  hypothalamic-pituitary-adrenal [HPA] axis and sympathetic nervous system (SNS). One or both pathways can interact with the neurotransmitter and intracellular signal transduction systems underlying delirium in the brain, which may already be impaired in the elderly due to age-related or other pathologic changes.

The indirect aberrant stress pathway suggests that not only pain and discomfort (eg from dysuria) can contribute to delirium but UTI-associated circulating cytokines may also cause delirium.  Indeed, a large study of older adults undergoing elective surgery found a significant association between delirium postoperatively (postop day 2) and serum proinflammatory cytokine levels such as IL-6. 4  

The corollary is that bacteriuria is unlikely to be associated with delirium in the absence of significant systemic inflammatory response, pain or discomfort.

 

References

1.Trzepacz P, van der Mast R. The neuropathophysiology of delirium. In Lindesay J,  Rockwood K, Macdonald A (Eds.). Delirium in old age, pp. 51–90. Oxford University Press, Oxford , 2002.

2.Flacker JM, Lipsitz LA. Neural mechanisms of delirium: current hypotheses and evolving concepts. J Gerontol A Biol Sci Med Sci. 1999; 54: B239–B246 https://www.ncbi.nlm.nih.gov/pubmed/10411009

3. Maclullich AM, Ferguson KJ, Miller T, de Rooij SE, Cunningham C. Unravelling the pathophysiology of delirium: a focus on the role of aberrant stress responses. J Psychosom Res. 2008;65:229–38. https://www.ncbi.nlm.nih.gov/pubmed/18707945

4. Vasunilashom SM, Ngo L, Inouye SK, et al. Cytokines and postoperative delirium in older patients undergoing major elective surgery. J Gerontol A Biol Sci Med Sci 2015;70:1289-95. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4817082/pdf/glv083.pdf

Contributed by Henrietta Afari MD, Mass General Hospital, Boston, MA

How exactly do urinary tract infections (UTIs) cause delirium in my elderly patients?

What is an abnormal post-void residual (PVR) volume?

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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References

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

What is an abnormal post-void residual (PVR) volume?