Month: July 2019

Should I routinely select antibiotics with activity against anaerobes in my patients with presumed aspiration pneumonia?

FA Manian MD, MPH, , , , , , , , , , , , , , , , , , , , , , , , , , Leave a comment

Anaerobes have been considered a major cause of aspiration pneumonia (AP) based on studies published in 1970’s (1-3). More recent data, however, suggest that anaerobes no longer play an important role in most cases of AP (4-7) and routine inclusion of specific anti-anaerobic drugs in their treatment is no longer necessary.

 
An important reason for anaerobes not playing an important role in AP in the current era is the change in the demographics of patients who may be affected. Patients reported in older studies often suffered from alcohol use disorder, drug ingestion, seizure disorders and acute cerebrovascular accident. In contrast, more recent data show that AP often occurs in nursing home residents, the elderly with cognitive impairment, and those with dysphagia, gastrointestinal dysmotility or tube feeding (8,9).

 
In addition, many cases of AP reported in older studies involved delay of 4 or more days before seeking medical attention and, not surprisingly, often presented with lung abscess, necrotizing pneumonia, empyema, or putrid sputum, features that are relatively rare in the current era.

 
Further supporting the diminishing role of anaerobes in AP, are recent microbiological studies of the respiratory tract in AP revealing the infrequent isolation of anaerobes and, even when isolated, often coexisting with aerobic bacteria. The latter observation is important because, due to the alteration in the redox potential (9,10), treatment of aerobic bacteria alone may lead to less oxygenation consumption and less favorable environment for survival of anaerobes in the respiratory tract.

 
We should also always consider the potential adverse effects of unnecessary antibiotics with anaerobic activity in our frequently debilitated patients, including gastrointestinal dysbiosis (associated with Clostridiodes difficile infections and overgrowth of antibiotic-resistant pathogens such as vancomycin-resistant enterococci (VRE), hypersensitivity reactions, drug interactions, and central nervous system toxicity (11,12).
Thus, the weight of the evidence does not justify routine anaerobic coverage of AP in today’s patients.

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References
1. Bartlett JG, Gorbach SL, Finegold SM. The bacteriology of aspiration pneumonia. Am J Med. 1974;56(2):202-7. https://www.ncbi.nlm.nih.gov/pubmed/4812076
2. Bartlett JG, Finegold SM. Anaerobic pleuropulmonary infections. Medicine (Baltimore). 1972;51(6):413-50. https://www.ncbi.nlm.nih.gov/pubmed/4564416
3. Bartlett JG, Gorbach SL. The triple threat of aspiration pneumonia. Chest. 1975;68(4):560-6. https://www.ncbi.nlm.nih.gov/pubmed/1175415
4. Finegold SM. Aspiration pneumonia. Rev Infect Dis. 1991;13 Suppl 9:S737-42. https://www.ncbi.nlm.nih.gov/pubmed/1925318
5. Bartlett JG. How important are anaerobic bacteria in aspiration pneumonia: when should they be treated and what is optimal therapy. Infect Dis Clin North Am. 2013;27(1):149-55. https://www.ncbi.nlm.nih.gov/pubmed/23398871
6. El-Solh AA, Pietrantoni C, Bhat A, Aquilina AT, Okada M, Grover V, et al. Microbiology of severe aspiration pneumonia in institutionalized elderly. Am J Respir Crit Care Med. 2003;167(12):1650-4. https://www.ncbi.nlm.nih.gov/pubmed/12689848
7. Marik PE, Careau P. The role of anaerobes in patients with ventilator-associated pneumonia and aspiration pneumonia: a prospective study. Chest. 1999;115(1):178-83. https://www.ncbi.nlm.nih.gov/pubmed/9925081
8. Bowerman TJ, Zhang J, Waite LM. Antibacterial treatment of aspiration pneumonia in older people: a systematic review. Clin Interv Aging. 2018;13:2201-13. https://www.ncbi.nlm.nih.gov/pubmed/30464429
9. Mandell LA, Niederman MS. Aspiration Pneumonia. N Engl J Med. 2019 Feb 14;380(7):651-663. doi: 10.1056/NEJMra1714562. https://www.ncbi.nlm.nih.gov/pubmed/30763196
10. Walden, W. C., & Hentges, D. J. (1975). Differential effects of oxygen and oxidation-reduction potential on the multiplication of three species of anaerobic intestinal bacteria. Applied microbiology, 30(5), 781–785. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC187272/
11. Sullivan A, Edlund C, Nord CE. Effect of antimicrobial agents on the ecological balance of human microflora. Lancet Infect Dis. 2001;1(2):101-14. https://www.ncbi.nlm.nih.gov/pubmed/11871461
12. Bhalla A, Pultz NJ, Ray AJ, Hoyen CK, Eckstein EC, Donskey CJ. Antianaerobic antibiotic therapy promotes overgrowth of antibiotic-resistant, gram-negative bacilli and vancomycin-resistant enterococci in the stool of colonized patients. Infect Control Hosp Epidemiol. 2003;24(9):644-9. https://www.ncbi.nlm.nih.gov/pubmed/14510245

 

Contributed by Amar Vedamurthy, MD, MPH, Mass General Hospital, Boston, MA

Should I routinely select antibiotics with activity against anaerobes in my patients with presumed aspiration pneumonia?

My patient with anemia has an abnormally high mean red blood cell corpuscular volume (MCV). What conditions should I routinely consider as a cause of his macrocytic anemia?

FA Manian MD, MPH, , , , , , , , , , , , , , , , , , , , 2 Comments

Anemia with mean corpuscular volume (MCV) above the upper limit of normal (usually ≥ 100 fL) is considered macrocytic anemia. The numerous causes of macrocytic anemia can be divided into major categories (1,2) (Figure 1).

First, a reticulocyte production index should be calculated and if elevated the MCV can be above the normal range due to the large size of reticulocytes. Once high MCV is not thought to be related to reticulocytosis, the majority of macrocytic anemias can be categorized according to one of two major mechanisms: 1. Liver disease; and  2. Impairment of DNA synthesis, which includes nutritional deficiencies (folate, B12), drug effect (e.g co-trimoxazole, anti-neoplastic agents and certain anti-retroviral drugs) and “idiopathic” causes (myelodysplastic syndromes).

Mild macrocytosis can also be seen in hypothyroidism and hypoproliferative anemias such as aplastic anemia.  Macrocytosis without anemia or liver disease can also be a manifestation of heavy alcohol intake.

Macrocytic anemia in liver disease is due to excess lipid deposition in the red blood cell (RBC) membrane, not impairment of DNA synthesis. Enlarged RBCs are usually round and  often have a targeted appearance in liver disease; acanthocytes (spur cells) may also be present (Fig 2). In contrast, in disorders of impaired DNA synthesis, enlarged RBCs are often oval-shaped (macro-ovalocytes) (Fig 3).

Other common abnormalities seen with macrocytic anemia include hypersegmented neutrophils (eg, induced by B12 or folate deficiency), and in the case of myelodysplastic syndromes, hypogranulated neutrophils and Pelger-Huet neutrophil abnormalities.

Bonus pearl: Did you know that the MCV unit, fL, stands for femtoliters or 1/1,000,000,000,000,000 L? 

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Figure 1. Major causes of macrocytic anemia. MDS: myelodysplastic syndrome.

 

Macrocytic_Anemia_Figure 1

Fig 2. Round macrocytes with targeting and abundant acanthocytes (spur cells) in a patient with hepatic cirrhosis.

 

Macrocytic_Anemia_Figure 2

Fig 3. Oval macrocytes in a patient with large granular cell leukemia and an MCV of 125 fL who received cyclophosphamide.

References

  1. Ward PC. Investigation of Macrocytic Anemia. Postgrad Med 1979; 65: 203-207. https://www.ncbi.nlm.nih.gov/pubmed/368738
  2. Green R, Dwyre DM. Evaluation of macrocytic anemias. Semin Hematol 2015; 52: 279-286. https://www.sciencedirect.com/science/article/abs/pii/S0037196315000554

 

Contributed by Tom Spitzer, MD, Director of Cellular Therapy and Transplantation Laboratory, Massachusetts General Hospital, Boston, MA.

My patient with anemia has an abnormally high mean red blood cell corpuscular volume (MCV). What conditions should I routinely consider as a cause of his macrocytic anemia?

Should my patient with cirrhosis and esophageal varices be considered for partial splenic embolization?

FA Manian MD, MPH, , , , , , , , , , , , , Leave a comment

 

Although limited, the weight of the evidence suggests that patients with cirrhosis and esophageal varices may benefit from partial splenic embolization (PSE).

A 2006 small randomized-controlled trial comparing PSE and endoscopic ligation vs. endoscopic ligation alone in patients with cirrhosis, thrombocytopenia and esophageal varices reported reduced risk of recurrence of varices, progression to variceal bleeding and death over a mean follow-up of 4.8 years. 1

A 2016 meta-analysis of PSE in the management of gastroesophageal variceal hemorrhage arrived at a similar conclusion with respect to reducing the risk of recurrence of varices, variceal hemorrhage and mortality. 2 The studies included in this meta-analysis, however, were small with only 1 randomized-controlled trial (RCT) in the series.

A 2019 small retrospective of patients undergoing transjugular intrahepatic portosystemic shunt (TIPS) placement with or without PSE found a significant benefit in primary shunt patency (period between placement and first shunt dysfunction), but not secondary shunt patency (period between placement and permanent shunt dysfunction) or mortality over a 5-year follow-up.3

Adverse effects of PSE include post-embolization syndrome—a constellation of symptoms such as fever, pain, and nausea/vomiting— reported in 78%-100% of patients. More severe complications up to 15%-30% may also occur with PSE, particularly when around 70% or more of splenic volume is embolized. These complications include pleural effusion/ascites, spontaneous bacterial peritonitis, pulmonary embolism, liver failure, portal vein thrombosis and splenic abscesses which may develop between 10 days to 3 months following the procedure.  Up to 6% of patients undergoing PSE may die of the procedure-related complications. 4-6  

For these reasons, careful selection of patient for PSE and limiting the extent of splenic necrosis to 50% with close monitoring of clinical and ultrasound follow-up, particularly in patients with a volume of splenic necrosis >50%,  have been suggested.6

 

Fun fact: Did you know that splenic embolization was first performed by Frank E. Maddison of Madison, Wisconsin, in 1973 using autologous clot to treat recurrent gastrointestinal hemorrhage arising from esophageal varies?

 

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References

 

  1. Ohmoto K, Yoshioka N, Tomiyama Y, et al. Improved prognosis of cirrhosis patients with esophageal varices and thrombocytopenia treated by endoscopic variceal ligation plus partial splenic embolization. Digestive Diseases and Sciences 2006;51:352-58. https://link.springer.com/article/10.1007/s10620-006-3137-8
  2. Wang P, Liu R, Tong L, et al. Partial splenic embolization has beneficial effects for the management of gastroesophageal variceal hemorrhage. Saudi J Gastroenterol 2016;22:399-406. http://europepmc.org/articles/PMC5184739/
  3. Wan Y-M, Li Y-H, Xu Z-Y, et al. Comparison of TIPS alone and combined with partial splenic embolization (PSE) for the management of variceal bleeding. European Radiology 2019; https://doi.org/10.100/s00330-019-06046-6
  4. N’Kontchou G, Seror O, Bourcier V, et al. Partial splenic embolization in patients with cirrhosis: efficacy, tolerance, and long-term outcome in 32 patients. Eur J Gastroenterol Hepatol 2005;17:179-84. https://www.ncbi.nlm.nih.gov/pubmed/15674095
  5. Hadduck TA, McWilliams JP. Partial splenic artery embolization in cirrhotic patients. World J Radiol 2014;28:6:160-168. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4037542/
  6. Smith M, Ray CE. Splenic artery embolization as an adjunctive procedure for portal hypertension. Semin Intervent Radiol 2012;29:135-39. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3444868/
  7. Maddison FE. Embolic therapy of hypersplenism. Invest Radiol 1973;8:280-281. https://journals.lww.com/investigativeradiology/Citation/1973/07000/Embolic_Therapy_of_Hypersplenism.54.aspx

 

Contributed in part by Theodore R. Pak, MD, PhD, Mass General Hospital, Boston, Massachusetts.

Should my patient with cirrhosis and esophageal varices be considered for partial splenic embolization?

My previously healthy patient developed a viral illness with fever and headache few days after swimming in a community pool. Can swimming pools be a source of viral infection?

FA Manian MD, MPH, , , , , , , , , , , , , , , Leave a comment

Yes! Swimming pools have been implicated in the transmission of a variety of pathogens,  including enteric viruses (eg, echovirus, coxackie virus, hepatitis A virus, norovirus) which account for nearly one-half of all swimming pool-related outbreaks.  Adenoviruses also account for a significant number of swimming pool outbreaks.1,2

The most commonly reported symptoms in swimming pool outbreaks have been gastroenteritis, respiratory symptoms and conjunctivitis. However, aseptic meningitis and hepatitis may also occur. 1

Because viruses cannot replicate in the environment outside of host tissues, their presence in swimming pool is the result of direct contamination by those in the water who may shed viruses through unintentional fecal release or through body fluids, such as saliva, mucus, or vomitus.  The finding of E. coli in 58% of pool water samples in 1 CDC study suggests the presence of stool as a primary source of infection.3

On average, each person has 0.14 grams (range 0.1 gram to 10 grams) of fecal material on their perianal surface that could rinse into the water if pre-swim shower with soap is omitted.4-5 Coupled with the potential for inadequate disinfection or chlorination of pool water, it is not surprising that swimming pools may serve as a source of infection.  

CDC recommends keeping feces and urine out of the water, checking the chlorine level and pH before getting into the water and not swallowing the water you swim in.3 

Bonus pearl: Did you know that pool water has also been associated with Cryptosporidium and Giardia and waterslides with E.coli-0157 outbreaks?

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References

  1. Bonadonna L, La Rosa G. A review and update on waterborne viral diseases associated with swimming pools. Int j Environ Res Public Health 2019;16, 166. Doi:10.3390/ijerph16020166. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6352248/
  2. Keswick BH, Gebra CP, Goyal SM. Occurrence of enteroviruses in community swimming pools. Am J Public Health 1981;71:1026030. https://www.ncbi.nlm.nih.gov/pubmed/6267950
  3. CDC.Microbes in pool filter backwash as evidence of the need for improved swimmer hygiene—Metro-Atlanta, Georgia, 2012. MMWR 2013;62:385-88. https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6219a3.htm
  4. Gerba CP. Assessment of enteric pathogen shedding by bathers during recreational activity and its impact on water quality. Quant Microbiol 2000; 2:55-68 https://arizona.pure.elsevier.com/en/publications/assessment-of-enteric-pathogen-shedding-by-bathers-during-recreat
  5. CDC. Model Aquatic Health Code. 8.0 Annexes: fecal/vomit/blood contamination response Annex (6.0 policies and management), 2008. https://www.cdc.gov/healthywater/pdf/swimming/pools/mahc/structure-content/mahc-fecal-vomit-blood-contamination-response-annex.pdf
  6. CDC. Surveillance of waterborne disease outbreaks and other health events associated with recreational water—United States, 2007-2008 and surveillance of waterborne disease outbreaks associated with drinking water—United States, 2007-2008. MMWR 2011;60. 1-76. https://www.ncbi.nlm.nih.gov/pubmed/21937976

 

 

My previously healthy patient developed a viral illness with fever and headache few days after swimming in a community pool. Can swimming pools be a source of viral infection?