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?

Should I be concerned about the umbilical hernia in my patient with cirrhosis and ascites?

Although umbilical hernia in patients with cirrhosis and ascites is common and often “expected” (a rate of 20% during the course of their disease), it can be associated with significant risk of complications such as incarceration, ascites drainage, peritonitis, and spontaneous rupture or evisceration from necrosis of overlying skin.1,2

A 2007 retrospective study involving patients with cirrhosis and umbilical hernia reported a complication rate of 77% and related mortality of 15% among those managed conservatively (mean period of observation ~ 5 years); MELD score could not predict failure of conservative management (median 22 in complicated vs 24 in uncomplicated).3

Because the risk of death with hernia repair in urgent settings is 7x higher than for elective hernia repair in cirrhotic patients, there has been increasing interest in elective repair in patients with well-compensated cirrhosis.3 Interestingly, the reported surgical complication rates among patients with well-compensated cirrhosis appear similar to those in noncirrhotic patients.3 If the patient is expected to undergo liver transplantation in the near future, elective hernia repair can be postponed and managed concomitantly.

Bonus pearl: Did you know that spontaneous umbilical hernia rupture is also known as “Flood syndrome” (should be easy to remember!), first described by Frank B Flood, a surgical resident back in 1961? 4

References

  1. Marsman HA, Heisterkamp J, Halm JA, et al. Management in patients with liver cirrhosis and an umbilical hernia. Surgery 2007;142:372-5. https://www.ncbi.nlm.nih.gov/pubmed/17723889
  2. Coelho, JCU, Claus CMP, Campos ACL, et al. Umbilical hernia in patients with liver cirrhosis: a surgical challenge. World J Gastrointest Surg 2016;8:476-82. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942747/
  3. Martens P, Laleman W. Umbilical hernia in a patient with cirrhosis. Cleveland Clin J Med 2015;82: 404-5. https://www.mdedge.com/ccjm/article/100682/hepatology/umbilical-hernia-patient-cirrhosis
  4. Nguyen ET, Tudtud-Hans LA. Flood syndrome: spontaneous umbilical hernia rupture leaking ascitic fluid-a case report. Perm J 2017;21:16-152. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5499604/ 

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Should I be concerned about the umbilical hernia in my patient with cirrhosis and ascites?

What is the evidence that atrial fibrillation (AF) of less than 48 hour duration may not require anticoagulation?

Although it is often postulated that it takes 48 h for a clot to form in a fibrillating atrium, there are no conclusive studies to back this claim (1). In fact, several studies challenge this presumption by suggesting that atrial thrombus may form within 48-72 h of AF.

A study of patients with acute AF (86% for 48 h or less) reported that 14% of patients developed atrial thrombus within 72 h (2). Another study found that ~1% of patients with AF for 48 h or less had an embolic event (3). A 2016 study of patients undergoing electrical cardioversion within 48 h of AF onset also found a risk of neurological events of ~1% among those who underwent cardioversion without therapeutic AC; none had a CHA2DS2-VASc score <2 or had postoperative AF, however (4).

The 2014 ACC guidelines state that for patients with AF or atrial flutter of less than 48 h duration at “high risk of stroke” (often defined as CHA2DS2-VASc score 2 or greater, or history of stroke or transient ischemic attack), AC is recommended as soon as possible before or immediately after cardioversion, followed by long-term AC therapy (Class I, level of evidence C) (5). For those who are at lower thromboembolic risk, AC before cardioversion is optional without the need for its continuation post-cardioversion (Class IIa, level of evidence C).

 

Bonus Pearl: Did you know that up until 1980s, it was generally held that only freshly formed thrombi broke off and embolized and that “organized” clot developing subsequently within a few days was unlikely to embolize! Another 180!

References

1. Kaufman E, Lagu T, Hannon NS, et al. Mythmaking in medical education and medical practice. Euro J Intern Med 2013;24:222-26. https://www.ncbi.nlm.nih.gov/pubmed/23312964   
2. Stoddard MF, Dawkins PR, Prince CR, et al. Left atrial appendage thrombus is not uncommon in patients with acute atrial fibrillation and a recent embolic event: a transesophageal echocardiographic study. J Am Coll Cardiol 1995;25:452-9. https://www.ncbi.nlm.nih.gov/pubmed/7829800  
3. Weigner MJ, Caulfield TA, Danias PG, et al. Left atrial appendage thrombus is not uncommon in patients with acute atrial fibrillation and and a recent embolic event: A transesophageal echocardiographic study. J Am Coll Cardiol 1995;25:452-9. https://www.ncbi.nlm.nih.gov/pubmed/9103128  
4. Garg, A, Khunger M, Seicean S, et al. Incidence of thromboembolic complications within 30 days of electrical cardioversion performed within 48 hours of atrial fibrillation onset. JACC: Clinical Electrophysiology 2016;2:487-494. https://cwru.pure.elsevier.com/en/publications/incidence-of-thromboembolic-complications-within-30-days-of-elect
5. Wann LS, Curtis AB, January CT, et al. 2011 CCF/AHA/HRS focused update on the management of patients with atrial fibrillation/American Heart Association task force on practice guidelines. J Am Coll Cardiol 2011;57;223-42. https://www.ncbi.nlm.nih.gov/pubmed/21324629

 

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What is the evidence that atrial fibrillation (AF) of less than 48 hour duration may not require anticoagulation?

Can I rule out primary adrenal insufficiency by obtaining a single morning serum cortisol level in my hospitalized patient with unexplained hyponatremia?

Primary adrenal insufficiency (PAI) can be confidently ruled out when the morning (eg, 6 AM) serum cortisol level is greater than 17 ug/dl. Lower cut-off values are associated with lower probability of excluding PAI: > 10 ug/dl, 62%-67% and ≥5 ug/dl, 36%. 1,2 Conversely, PAI is highly likely when the morning serum cortisol level is less than 3 ug/dl. 3

Since many patients may have serum cortisol levels between 3 ug/dl and 17 ug/dl (ie, in the “indeterminate” range), confirmatory testing commonly performed through cosyntropin stimulation test (CST) is often necessary.

Although the standard CST involves measuring serum cortisol levels at baseline, 30 min, and 60 min with peak cortisol level <18 ug/dl indicative of PAI, several studies have reported that a single post-CST cortisol level obtained at 60 min may also be diagnostic. 3

 

References

  1. Erturk E, Jaffe CA, Barkan AL. Evaluation of the integrity of the hypothalamic-pituitary-adrenal axis by insulin hypoglycemia test. J Clin Endocrinol Metab 83;2350-54. https://www.ncbi.nlm.nih.gov/pubmed/9661607
  2. Bornstein SR, Allolio B, Arlt W, et al. Diagnosis and treatment of primary adrenal insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2016;101:364-89. https://academic.oup.com/jcem/article/101/2/364/2810222
  3. Odom DC, Gronowski AM, Odom E, et al. A single, post-ACTH cortisol measurement to screen for adrenal insufficiency in the hospitalized patient. J Hosp Med 2018;13: E1-E5. https://www.ncbi.nlm.nih.gov/pubmed/29444197
Can I rule out primary adrenal insufficiency by obtaining a single morning serum cortisol level in my hospitalized patient with unexplained hyponatremia?

Should I order a blood transfusion based on the hemoglobin (Hgb) or the hematocrit (Hct)?

Despite the frequent interchangeability of Hgb (g/dL) and Hct (%) by a ratio of ~1:3, directly-measured blood Hgb levels may be preferred for assessing the need for blood transfusion for at least 3 reasons:

First, in contrast to the widely-used automated measurements of Hct, Hgb is not affected by conditions that affect the size of the RBCs or the mean corpuscular Hgb concentration (MCHC). This is because the Hct is not a direct measure of Hgb; rather it’s the proportion of blood occupied by RBCs which, in automated systems, is derived by multiplying the number of RBCs by the mean corpuscular volume (MCV).1-3

This may not be a significant issue when MCHC is normal, but when MCHC is abnormal, HCT may not accurately reflect the blood Hgb concentration. For example, in patients with hypochromic iron deficiency anemia with RBCs containing less hemoglobin (ie, low MCHC), the Hct may overestimate blood Hgb levels. Conversely in hereditary spherocytosis with its attendant low RBC volume and high MCHC, the Hct may underestimate Hgb levels.

Second, Hct results may also be more subject to technical factors in the lab. For example, blood at room temperature between 6-24 h may be associated with RBC swelling and increased Hct without any change in its Hgb concentration.4

Finally, national and international guidelines on blood transfusion generally target Hgb, not Hct results.5-7

For a related pearl, go to https://pearls4peers.com/2016/11/01/should-i-use-a-hemoglobin-level-of-7-or-8-gdl-as-a-threshold-for-blood-transfusion-in-my-hospitalized-patient.

 

References

  1. Tefferi A, Hanson CA, Inwards DJ. How to interpret and pursue an abnormal complete blood cell count in adults. Mayo Clin Proc 2005;80:923-36. https://www.ncbi.nlm.nih.gov/pubmed/16007898
  2. Macdougall IC, Ritz E. The Normal Haematocrit Trial in dialysis patients with cardiac disease: are we any the less confused about target hemoglobin? Nephrol Dial Transplant 1998;13:3030-33. https://academic.oup.com/ndt/article-pdf/13/12/3030/9907456/3030.pdf
  3. Kelleher BP, Wall C, O’Broin SD. Haemoglobin, not haematocrit, should be the preferred parameter. Nephrol Dial Transplant 2001;16:1085-87. https://www.ncbi.nlm.nih.gov/pubmed/11328933
  4. Hayuanta HH. Can hemoglobin-hematocrit relationship be used to assess hydration status? CDK-237/vol 43 no.2, th. 2016 http://www.kalbemed.com/Portals/6/20_237Opini-Can%20Hemoglobin-Hematocrit%20Relationship%20Be%20Used%20to%20Assess%20Hydration%20Status.pdf
  5. Blood transfusion. NICE guideline, November, 2015. https://www.nice.org.uk/guidance/ng24/chapter/Recommendations#fresh-frozen-plasma-2 uk
  6. National Blood Authority: Australia. Patient blood management, November 2016. https://www.blood.gov.au/system/files/documents/nba-patient-blood-management-resource-guide-nov_2016_v3_sm_web_file.pdf
  7. Carson JL, Guyatt G, Heddle NM, et al. Clinical practice guidelines from the AAABB: red blood cell transfusion thresholds and storage. JAMA 2016; 316:2025-2035. https://www.ncbi.nlm.nih.gov/pubmed/27732721

 

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Should I order a blood transfusion based on the hemoglobin (Hgb) or the hematocrit (Hct)?

How should I interpret the growth of “normal respiratory flora” from sputum of my patient with community-acquired pneumonia (CAP)?

Since the primary reason for obtaining a sputum culture in a patient with pneumonia is to sample the lower respiratory tract, you should first verify that the sputum was “adequate” by reviewing the gram stain. Absence of neutrophils (unless the patient is neutropenic) with or without epithelial cells on gram stain of sputum suggests that it may not be an adequate sample (ie, likely saliva)1, and therefore growth of normal respiratory flora (NRF) should not be surprising in this setting.  

Other potential explanations for NRF on sputum culture in patients with CAP include:2-5

  • Delay in sputum processing with possible overgrowth of oropharyngeal flora.
  • Pneumonia caused by pathogens that do not grow on standard sputum culture media (eg, atypical organisms, viruses, anaerobes).
  • Pneumonia caused by potential pathogens such as as Streptococcus mitis and Streptococcus anginosus group that may be part of the NRF.
  • Initiation of antibiotics prior to cultures (eg, in pneumococcal pneumonia).

Of note, since 2010, several studies have shown that over 50% of patients with CAP do not have an identifiable cause.3 So, growing NRF from sputum of patients with CAP appears to be common.

References

  1. Wong LK, Barry AL, Horgan SM. Comparison of six different criteria for judging the acceptability of sputum specimens. J Clin Microbiol 1982;16:627-631. https://www.ncbi.nlm.nih.gov/pubmed/7153311
  2. Donowitz GR. Acute pneumonia. In Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases (2010). Churchill Livingstone, pp 891-916.
  3. Musher DM, Abers MS, Bartlett JG. Evolving understanding of the causes of pneumonia in adults, with special attention to the role of pneumococcus. Clin Infect Dis 2017;65: 1736-44. https://www.ncbi.nlm.nih.gov/pubmed/29028977
  4. Abers MS, Musher DM. The yield of sputum culture in bacteremic pneumococcal pneumonia after initiation of antibiotics. Clin Infect Dis 2014; 58:1782. https://www.ncbi.nlm.nih.gov/pubmed/24604901
  5. Bartlett JG, Gorbach SL, Finegold SM. The bacteriology of aspiration pneumonia. Bartlett JG, Gorbach SL, Finegold SM. Am J Med 1974;56:202-7. https://www.ncbi.nlm.nih.gov/pubmed/4812076
How should I interpret the growth of “normal respiratory flora” from sputum of my patient with community-acquired pneumonia (CAP)?

Can my patient with renal insufficiency safely undergo gadolinium-based contrast MRI?

It may be possible for patients with renal insufficiency, including those with end-stage kidney disease (ESKD), to undergo MRI using potentially safer preparations of gadolinium-based contrast agents (GBCAs) with “very low, if any” risk of the feared nephrogenic systemic sclerosis (NSF). 1

In contrast to the so called “linear” chelates of gadolinium (eg, gadodiamide, gadopentetate), “cyclic” GBCA’s (eg, gadoteridol) have not been clearly associated with NSF. 2 A Veterans Administration study involving gadoteridol identified no cases of NSF among the 141 patients on hemodialysis following 198 exposures. 2 In fact, the 2017 American College of Radiology (ACR) Manual on Contrast Media reports the risk of NSF with cyclic chelates as “very low, if any”. 1 Even when a cyclic GBCA is used in patients with ESKD, however, hemodialysis is recommended as soon as possible after MRI. 3

GBCAs are chelates with 2 major components: gadolinium and either a linear or cyclic ligand. Cyclic ligands bind to gadolinium more avidly, resulting in lower probability of circulating renally-cleared free gadolinium which when deposited in tissue is thought to potentially trigger NSF.2

Although NSF is characterized by progressive fibrosis of skin and soft tissue, it may involve multiple organs with an estimated 30% mortality rate. 4

 Bonus Pearl: Did you know NSF is really a new disease, with no evidence of its existence before 1997?

References

  1. “Nephrogenic Systemic Fibrosis”. In ACR Manual on Contrast Media; Version 10.3; May 31, 2017. https://www.acr.org/-/media/ACR/Files/Clinical-Resources/Contrast_Media.pdf
  2. Reilly RF. Risk for nephrogenic systemic fibrosis with gadoteridol (ProHance) in patients who are on long-term hemodialysis. Clin J Am Soc Nephrol 2008;3:747-51. https://www.ncbi.nlm.nih.gov/pubmed/18287249
  3. Wang Y, Alkasab TK, Nari O, et al. Incidence of nephrogenic systemic fibrosis after adoption of restrictive gadolinium-based contrast agent guidelines. Radiology 2011;260:105-111.  https://www.ncbi.nlm.nih.gov/pubmed/21586680
  4. Schlaudecker JD, Bernheisel CR. Gadolinium-associated nephrogenic systemic fibrosis. Am Fam Physician 2009;80:711-14. https://www.aafp.org/afp/2009/1001/p711.pdf

 

Contributed by Richard Newcomb, MD, Mass General Hospital, Boston, MA.

Can my patient with renal insufficiency safely undergo gadolinium-based contrast MRI?