My elderly patient on chronic warfarin with recent hospitalization for soft tissue infection is now readmitted with gastrointestinal bleed and a newly-discovered supra-therapeutic INR? Why did her INR jump?

Assuming no recent changes in the dose of warfarin, one potential culprit may be her recent antibiotic exposure. Of the long list of antibiotics associated with elevated INR, quinolones (e.g. ciprofloxacin, levofloxacin), trimethoprim-sulfamethoxazole, macrolides (e.g. azithromycin), and azole antifungals (e.g. fluconazole) are generally thought to carry the highest risk of warfarin toxicity, while amoxacillin and cephalexin may be associated with a more modest risk. 1-3

Other drugs such as amiodarone (Did she have atrial fibrillation during her recent hospitalization?), acetaminophen (Has she been receiving at least 2 g/day for several consecutive days?), and increasing dose of levothyroxine (Was she thought to be hypothyroid recently?) should also be considered.3,4

Also remember to ask about herbal supplements (eg, boldo-fenugreek, dong quai, danshen) that may potentiate the effect of warfarin. 3 Of course, poor nutrition in the setting of recent illness might have also played a role.5

As far as the mechanisms for drug interaction with warfarin, some drugs act as cytochrome p450 inhibitors (thus reducing the metabolism of warfarin), while others influence the pharmacodynamics of warfarin by inhibiting the synthesis or increasing the clearance of vitamin K-2 dependent coagulation factors.3

Antibiotics may increase the risk of major bleeding through disruption of intestinal flora that synthesize vitamin K-2 with or without interference with the metabolism of warfarin through cytochrome p450 isozymes inhibition.

Check out a related pearl on P4P: https://pearls4peers.com/2015/06/25/is-there-anyway-to-predict-a-significant-rise-in-inr-from-antibiotic-use-in-patients-who-are-also-on-warfarin  

 

References

  1. Baillargeon J, Holmes HM, Lin Y, et al. Concurrent use of warfarin and antibiotics and the risk of bleeding in older adults. Am J Med. 2012 February ; 125(2): 183–189. https://www.ncbi.nlm.nih.gov/pubmed/22269622
  2. Juurlink DN. Drug interactions with warfarin: what every physician should know. CMAJ, 2007;177: 369-371. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1942100/pdf/20070814s00018p369.pdf
  3. Ageno W, Gallus AS, Wittkowsky A, et al. Oral anticoagulant therapy: Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 Suppl):e44S-e88S. doi:10.1378/chest.11-2292.  https://www.ncbi.nlm.nih.gov/pubmed/22315269
  4. Hughes GJ, Patel PN, Saxena N. Effect of acetaminophen on international normalized ratio in patients receiving warfarin therapy. Pharmacotherapy 2011;31:591-7. https://www.ncbi.nlm.nih.gov/pubmed/21923443
  5. Kumar S, Gupta D, Rau SS. Supratherapeutic international normalized ratio: an indicator of chronic malnutrition due to severely debilitating gastrointestinal disease. Clin Pract. 2011;1:e21. doi:10.4081/cp.2011.e21. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3981245

 

Contributed by Rachel Weitzman, Medical Student, Harvard Medical School, Boston, MA.

My elderly patient on chronic warfarin with recent hospitalization for soft tissue infection is now readmitted with gastrointestinal bleed and a newly-discovered supra-therapeutic INR? Why did her INR jump?

My patient with ulcerative colitis has had colectomy. Can she still get C. difficile infection?

Yes! Although a common cause of colitis, an increasing number of reports in the literature suggest C. difficile can cause enteritis as well.Antibiotic use is a major risk factor in most reports, with nearly one-half of the cases reported in patients with inflammatory bowel disease, many post-colectomy. 1-3

Mortality of C. difficile enteritis based on the first 83 cases in the literature appears to be 23%,1 but as high as 60%-83% depending on the report!2 Its diagnosis post-colectomy requires a high index of suspicion, as patients may not complain of “diarrhea” with chronically loose stools in the ileostomy bag.  Be particularly on the lookout for C. difficile enteritis in these patients when there is increased stool output, fever, hypotension, and/or leukocytosis2, and when in doubt, send a stool specimen from the ileostomy bag for C. difficile testing.

Although the pathophysiology of C. difficile enteritis is not fully understood, few observations are particularly intriguing: 

  • Small bowel mucosa may be colonized by C. difficile in about 3% of the population, potentially serving as a reservoir.2
  • Patients with ileostomy may develop a metaplasia of the terminal end mimicking colonic environment.4  
  • Exposure of rabbit ileum to C. difficile toxin A also causes significant epithelial necrosis with destruction of villi and neutrophil infiltration.5

 

References

  1. Dineen SP, Bailey SH, Pham TH, et al. Clostridium difficile enteritis: a report of two cases and systematic literature review. World J Gastrointest Surg 2013;5:37-42. https://www.wjgnet.com/1948-9366/full/v5/i3/37.htm
  2. Boland E, Thompson JS. Fulminant Clostridium difficile enteritis after proctocolectomy and ileal pouch-anal anastomosis. Gastroenterology Research and Practice 2008; 2008: Article ID 985658. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2633454/pdf/GRP2008-985658.pdf
  3. Freiler JF, Durning SJ, Ender PT. Clostridium difficile small bowel enteritis occurring after total colectomy. Clin Infect Dis 2001;33:1429-31. https://pdfs.semanticscholar.org/333b/d84978cfc4ac8fd21a15bc8fd26ff3160387.pdf
  4. Apel R, Cohen Z, Andrews CW, et al. Prospective evaluation of early morphological changes in pelvic ileal pouches. Gastroenterology 1994;107:435-43. http://www.gastrojournal.org/article/0016-5085(94)90169-4/pdf
  5. Triadafilopoulos G, Pothoulakis C, Obrien MJ, et al. Differential effects of Clostridium difficile toxins A and B on rabbit ileum. Gastroenterology 1987;93:273-279. https://www.ncbi.nlm.nih.gov/pubmed/3596162
My patient with ulcerative colitis has had colectomy. Can she still get C. difficile infection?

Should I be concerned about piperacillin-tazobactam nephrotoxicity in the absence of vancomycin?

Nephrotoxicity associated with piperacillin-tazobactam (PT) combined with vancomycin (V) has been increasingly reported1,2,  with  some recommending that an alternative to V be used when PT is also on board 2. However, there are several reasons why the nephrotoxic potential of PT either alone or with antibiotics other than V also deserves further study before such recommendations can be widely embraced3.

First, most studies of VPT combination do not include comparative V or PT alone arms making it difficult to assess the relative contribution of these 2 antibiotics to kidney injury when used in combination. A small study that did include a PT-only  arm reported a similar rate of acute kidney injury (AKI) in PT and VPT arms ( 15.4% and 18.8% , respectively), both significantly higher that than of  V-only group (4%).4

 Other reasons not to readily dismiss PT as a cause of nephrototoxicity include the  lack of association between higher V trough levels and AKI in patients receiving VPT2, the association of PT with lower rates of renal function recovery in critically ill patients when compared to other selected β-lactams5,  and higher magnesium and potassium renal tubular loss with the use of PT compared to selected cephalosporins and ciprofloxacin6.  As with other penicillins, PT-associated acute interstitial nephritis may also occur7-8.

In short, even in the absence of V, nephrotoxic potential of PT should not be automatically dismissed.

 

Disclosure: Ref 3 was also authored by the creator of this pearl.

References

  1. Hammond DA, Smith MN, Chenghui Li, et al. Systematic review and meta-analysis of acute kidney injury associated with concomitant vancomycin and piperacillin/tazobactam. Clin Infect Dis 2017;64:666-74.
  2. Navalkele B, Pogue JM, Karino S, et al. Risk of acute kidney injury in patients on concomitant vancomycin and piperacillin-tazobactam compared to those on vancomycin and cefepime. Clin Infect Dis 2017;64:116-123.
  3. Manian FA. Should we revisit the nephrotoxic potential of piperacillin-tazobactam as well? Clin Infect Dis 2017; https://doi.org/10.1093/cid/cix321
  4. Kim T, Kandiah S, Patel M, et al. Risk factors for kidney injury during vancomycin and piperacillin/tazobactam administration, including increased odds of injury with combination therapy. BMC Res Notes 2015;8:579.
  5. Jensen J-U S, Hein L, Lundgren B, et al. Kidney failure related to broad-spectrum antibiotics in critically ill patients: secondary end point results from a 1200 patient randomized trial. BMJ Open 2012;2:e000635. http://bmjopen.bmj.com/content/2/2/e000635
  6. Polderman KH, Girbes ARJ. Piperacillin-induced magnesium and potassium loss in intensive care unit patients. Intensive Care Med 2002;28:530-522.
  7. Muriithi AK, Leung N, Valeri AM, et al. Clinical characteristics, causes and outcomes of acute interstitial nephritis in the elderly. Kidney International 2015;87:458-464.
  8. Soto J, Bosch JM, Alsar Ortiz MJ, et al. Piperacillin-induced acute interstitial nephritis. Nephron 1993;65:154-155. 
Should I be concerned about piperacillin-tazobactam nephrotoxicity in the absence of vancomycin?

Is treatment of pneumococcal pneumonia with bacteremia any different than pneumococcal pneumonia without bacteremia?

In the absence of disseminated infection such as meningitis or endocarditis, there is no convincing evidence that bacteremic pneumococcal pneumonia (BPP) requires either longer course of IV or oral antibiotics.

In fact, although previously thought to have a worse prognosis, recent data have failed to demonstrate any difference in time to clinical stability, duration of hospital stay or community-associated pneumonia (CAP)-related mortality with BPP when other factors such as patient comorbidities and severity of disease are also considered1,2

Although many patients with CAP receive 7-10 days of antibiotic therapy, shorter durations as little as 5 days may also be effective3,4.  Generally, once patients with BPP have stabilized on parenteral therapy, a switch to an appropriate oral antibiotic (eg, a β-lactam or a respiratory quinolone such as levofloxacin) can be made safely5

Although large randomized-controlled studies of treatment of BPP are not available, a cumulative clinical trial experience with levofloxacin for patients with BPP reported a successful clinical response in >90% of patients (median duration of therapy 14 d)6. Resistance to levofloxacin and failure of treatment in pneumococcal pneumonia (with or without bacteremia), however, has been rarely reported7.

 

References

  1. Bordon J, Peyrani P, Brock GN. The presence of pneumococcal bacteremia does not influence clinical outcomes in patients with community-acquired pneumonia. Chest 2008;133;618-624.
  2. Cilloniz C, Torres A. Understanding mortality in bacteremic pneumococcal pneumonia. J Bras Pneumol 2012;38:419-421.
  3. Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007;44:S27-72.
  4. Shorr F, Khashab MM, Xiang JX, et al. Levofloxacin 750-mg for 5 days for the treatment of hospitalized Fine Risk Class III/IV community-acquired pneumonia patients. Resp Med 2006;100:2129-36.
  5. Ramirez JA, Bordon J. Early switch from intravenous to oral antibiotics in hospitalized patients with bacteremic community-acquired Streptococcus pneumonia pneumonia. Arch Intern Med 2001;161:848-50.
  6. Kahn JB, Bahal N, Wiesinger BA, et al. Cumulative clinical trial experience with levofloxacin for patients with community-acquired pneumonia-associated pneumococcal bacteremia. Clin Infect Dis 2004;38(supp 1):S34-42.
  7. Davidson R, Cavalcanti R, Brunton JL, et al. Resistance to levofloxacin and failure of treatment of pneumococcal pneumonia. N Engl J Med 2002;346:747-50.
Is treatment of pneumococcal pneumonia with bacteremia any different than pneumococcal pneumonia without bacteremia?

How does azithromycin (AZ) benefit patients with severe COPD or cystic fibrosis (CF)?

AZ is a macrolide antibiotic which interferes with bacterial protein synthesis by binding to the 50S ribosomal subunit. It is often used to treat acute respiratory tract infections due to Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, as well as Mycoplasma, Chlamydia, and Legionella sp1. Although it has no in vitro activity against many aerobic gram-negative bacilli such as Pseudomonas aeruginosa, its chronic use has often been associated with a significant reduction in the frequency of disease exacerbations in patients with chronic bronchiectasis and colonization due to this organism, including patients with COPD or CF1-3.

Because P. aeruginosa is invariably macrolide-resistant, the beneficial effect of AZ in chronically infected or colonized patients must be due to factors other than its direct effect on bacterial replication.  Several mechanisms have been invoked including: 1. Inhibition of quorum-sensing dependent virulence factor and biofilm production 2.Blunting of host inflammatory response (eg, ↑IL-10, and ↓ IL-1ß, IL-6, IL-8, TNF-α, and ↓ chemotaxis); and 3. Enhanced antiviral response1.

The latter finding is quite unexpected but AZ appears to augment interferon response to rhinovirus in bronchial cells of COPD patients3.  With respiratory viruses (including rhinoviruses) causing 20-55% of all COPD exacerbations, perhaps this is another way AZ may help the host! Who would have thought!!

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References

  1. Vos R, Vanaudenaerde BM, Verleden SE, et al. Anti-inflammatory and immunomodulatory properties of azithromycin involved in treatment and prevention of chronic lung allograft rejection. Transplantation 2012;94:101-109.
  2. Cochrane review. Treatment with macrolide antibiotics for people with cystic fibrosis and chronic chest infection. Nov 14, 2012. http://www.cochrane.org/CD002203/CF_treatment-with-macrolide-antibiotics-for-people-with-cystic-fibrosis-and-chronic-chest-infection
  3. Menzel M, Akbarshahi H, Bjermer L, et al. Azithromycin induces anti-viral effects in cultured bronchial epithelial cells from COPD. Scientific Reports 2016; 6:28698. DOI:10.1038/srep 28698.

 

 

How does azithromycin (AZ) benefit patients with severe COPD or cystic fibrosis (CF)?

Is the combination of piperacillin-tazobactam and vancomycin (PT-V) nephrotoxic?

Despite its widespread use for over 20 years, PT-V has only recently been linked to higher risk of AKI when compared to vancomycin+/- other β-lactams, particularly cefepime1,2

A 2016 meta-analysis of 14 observational studies reported an AKI incidence ranging from 11%-48.8% for PT-V (used for ≥48 h in most studies), with an adjusted O.R. of 3.11 (95% C.I. 1.77-5.47) when compared to other vancomycin treatment groups1.  Of note, nephrotoxicity associated with PT-V appears to occur earlier than the comparative groups (median 3 days vs 5 days of therapy, respectively), with the highest daily incidence observed on days 4 and 52.

Although the exact mechanism(s) of nephrotoxicity in patients receiving PT-V is unknown, both piperacillin and vancomycin have been implicated in acute renal tubular dysfunction/necrosis and acute interstitial nephritis3-5.

Collectively, these findings are only a reminder to be more judicious in the selection and duration of treatment of even “safe” antibiotics.

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References

  1. Hammond DA, Smith MN, Chenghui Li, et al. Systematic review and meta-analysis of acute kidney injury associated with concomitant vancomycin and piperacillin/tazobactam. Clin Infect Dis 2016 ciw811.doi:10.1093cid/ciw811.https://academic.oup.com/cid/article/64/5/666/2666529
  2. Navalkele B, Pogue JM, Karino S, et al. Risk of acute kidney injury in patients on concomitant vancomycin an dpiperacillin-tazobactam compared to those on vancomycin and cefepime. Clin Infect Dis 2017;64:116-123. https://academic.oup.com/cid/article/64/2/116/2698878
  3. Hayashi T, Watanabe Y, Kumano K, et al. Pharmacokinetic studies on the concomitant administration of piperacillin and cefazolin, and piperacillin and cefoperazone in rabbits. J Antibiotics 1986; 34:699-712. https://www.ncbi.nlm.nih.gov/pubmed/3733519
  4. Polderman KH, Girbes ARJ. Piperacillin-induced magnesium and potassium loss in intensive care unit patients. Intensive Care Med 2002;28:530-522. https://link.springer.com/article/10.1007/s00134-002-1244-3
  5. Htike NL, Santoro J, Gilbert B, et al. Biopsy-proven vancomycin-associated interstitial nephritis and acute tubular necrosis. Clin Exp Nephrol 2012;16:320-324. https://link.springer.com/article/10.1007/s10157-011-0559-1
Is the combination of piperacillin-tazobactam and vancomycin (PT-V) nephrotoxic?

When should I pay attention to the minimum inhibitory concentration (MIC) of an antibiotic despite the lab reporting it to be in the “Susceptible” range?

In most situations, you will most likely choose an antibiotic based on the laboratory reporting of “Susceptible” (vs “Resistant”), not the actual MIC value of the drug and that’s fine.  

However, there may be a few instances when you may need to pay more attention to the actual MICs. Many experts recommend caution when “high” MICs within a susceptible range are observed in the following situations:   

  1. Vancomycin MIC >1 ug/ml in Staphylococcal aureus (methicillin-sensitive or –resistant) infections because of its possible association with clinical failure and, at times, increased mortality1,2.
  2. Ciprofloxacin or levofloxacin MIC>0.25 ug/ml in bacteremia caused by Gram-negative bacilli (including Enterobacteriacae as well as Pseudomonas aeruginosa) because of its association with an adverse outcome (eg, longer average hospital stay post-culture and duration of infection) but not necessarily mortality3-5.
  3. Levofloxacin MIC ≥ 1.0 ug/ml in Streptococcus pneumoniae infections, because of its association with an adverse clinical outcome based on drug pharmacodynamics and anecdotal reports of treatment failure6,7.

 

References

  1. Jacob JT, DiazGranados CA. High vancomycin minimum inhibitory concentration and clinical outomces in adults with methicillin-resistant Staphylococcus aureus infections: a meta-analysis. Int J Infect Dis 2013;17:e93-e100.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3780595/
  2. Kalil AC, Van Schooneveld TC, Fey PD, et al. Association between vancomycin minimum inhibitory concentration and mortality among patients with Staphylococcus aureus bloodstream infections: A systematic review and meta-analysis. JAMA 2014;312:1552-1564. https://www.ncbi.nlm.nih.gov/pubmed/25321910
  3. DeFife R, Scheetz MH, Feinglass J, et al. Effect of differences in MIC values on clinical outcomes in patients with bloodstream infections caused by Gram-negative organisms treated with levofloxacin. Antimicrob Agents Chemother 2009;53:1074-79. http://aac.asm.org/content/53/3/1074.full
  4. Falagas ME, Tansarli GS, Rafailidis PI, et al. Impact of antibiotic MIC on infection outcome in patients with susceptible Gram-negative bacteria a systematic review and meta-analysis. Antimicrob Agents Chemother 2012;56:4214-22. https://www.ncbi.nlm.nih.gov/pubmed/22615292
  5. Zelenitsky SA, Harding GKM, Sun S, et al. Treatment and outcome of Pseudomonas aeruginosa bacteremia: an antibiotic pharmacodynamics analysis. J Antimicrob Chemother 2003;52:668-674. https://www.ncbi.nlm.nih.gov/pubmed/12951354
  6. Davidson R, Cavalcanti R, Brunton JL, et al. Resistance to levofloxacin and failure of treatment of pneumococcal pneumonia. N Engl J Med 2002;346:. 2002;346:747-50. https://www.ncbi.nlm.nih.gov/pubmed/11882730
  7. De Cueto M, Rodriguez JM, Soriano MJ, et al. Fatal levofloxacin failure in treatment of a bacteremic patient infected with Streptococcus pneumoniae with a preexisting parC mutation. J Clin Microbiol 2008;46:1558-1560.  http://jcm.asm.org/content/46/4/1558.full

Contributed in part by Nick Van Hise, Pharm.D., BCPS, Infectious Diseases Clinical Pharmacist, Edward-Elmhurst Hospitals, Naperville, Illinois.

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When should I pay attention to the minimum inhibitory concentration (MIC) of an antibiotic despite the lab reporting it to be in the “Susceptible” range?

My patient is being treated for a urinary tract infection with trimethoprim-sulfamethoxazole (TMP-SMX) and has developed hypoglycemia. Can it be related?

Yes! The sulfamethoxazole component of TMP-SMX contains the identical sulfanilamide structural group as sulfonylureas used as oral hypoglycemics1.  It appears to act through mimicking the action of sulfonyureas on the pancreatic islet cells by acting as an insulin secretagogue leading to increased insulin secretion1.   Increased levels of plasma insulin dropping  following interruption of TMP-SMX has been reported,  and is thought to be dose and time dependent1,2.

A major risk factor for this complication is impaired renal function, but poor hepatic function, and concurrent use of drugs that decrease plasma glucose levels have also been implicated (1,2).  Occasionally there are no obvious risk factors.

sulfapiced

 

References

  1. Forde DG, Aberdein J, Tunbidge A, et al. Hypoglycemia associated with co-trimoxazole use in a 56-year-old caucasian woman with renal impairment. BMJ Case Reports 2012;doi:101136/bcr-2012-007215.
  2. Nunnai G, Celesia BM, Bellissimo F, et al. Trimethoprim-sulfamethoxazole-associated severe hypoglycemia: a sulfonylurea-like effect. Eur Rev Med Pharmacol Sci 2010;14:1015-18.
My patient is being treated for a urinary tract infection with trimethoprim-sulfamethoxazole (TMP-SMX) and has developed hypoglycemia. Can it be related?

How should patients with hospital-associated pneumonia (HAP) be empirically treated under the 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society?

Although empiric selection of antibiotics should be based on the local distribution of pathogens associated with HAP and their antimicrobial susceptibilities, routine coverage of Staphylococcus aureus (not necessarily methicillin-resistant S. aureus [MRSA]) and Pseudomonas aeruginosa or other gram-negative bacilli is recommended1.

In patients not at high risk of mortality (including ventilatory support and septic shock) or risk for MRSA (i.e.prior IV antibiotic use within 90 days, hospitalization in a unit where >20% of S. aureus isolates are MRSA or the prevalence of MRSA is unknown), piperacillin-tazobactam, cefepime, levofloxacin, imipenem or meropenem alone is suggested.

In patients not at high risk of mortality but with factors that increase the likelihood of MRSA, piperacillin-tazobactam, cefepime/ceftazidime, ciprofloxacin/levofloxacin, imipenem/meropenem, or aztreonam, plus vancomycin or linezolid should be considered.

In patients at high risk of mortality or receipt of IV antibiotics during the prior 90 days vancomycin or linezolid plus 2 of the following should be used: piperacillin-tazobactam, cefepime/ceftazidime, ciprofloxacin/levofloxacin, imipenem/meropenem, amikacin/gentamicin/tobramycin, or aztreonam are recommended (avoid double β-lactams).

In patients with structural lung disease increasing the risk of gram-negative infections (ie, bronchiectasis or cystic fibrosis), double anti-pseudomonal coverage is recommended.

 

Reference

  1. Kalil AC, Metersky ML, Klompas M, et al. Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis, Advance Access published July 14, 2016.
How should patients with hospital-associated pneumonia (HAP) be empirically treated under the 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society?

What are some of the major changes in the 2016 Infectious Diseases Society of America and the American Thoracic Society guidelines on pneumonia in hospitalized patients?

The most noticeable change is the elimination of the concept of health-care associated pneumonia (HCAP) altogether1. This action is in part related to the fact that many patients with HCAP were not at high risk for multi-drug resistant organisms (MDROs) , and that individual patient risk factors, not mere exposure to healthcare facilities, were better determinant of  the need for broader spectrum antimicrobials.

Other noteworthy points in the guidelines include:

  • Although hospital-associated pneumonia (HAP) is still defined as a pneumonia not incubating at the time of admission and occurring 48 hrs or more following hospitalization, it now only refers to non-VAP cases; VAP cases are considered a separate category.
  • Emphasis is placed on each hospital generating antibiograms to guide providers with respect to the optimal choice of antibiotics.
  • Despite lack of supportive evidence, the guidelines recommend obtaining respiratory samples for culture in patients with HAP.
  • Prior intravenous antibiotic use within 90 days is cited as the only consistent risk factor for MDROs, including methicillin-resistant Staphylococcus aureus (MRSA) and Pseudomonas sp.

 

Reference

  1. Kalil AC, Metersky ML, Klompas M, et al. Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis 2016 ;63:e61-e111.  Advance Access published July 14, 2016. https://www.ncbi.nlm.nih.gov/pubmed/27418577
What are some of the major changes in the 2016 Infectious Diseases Society of America and the American Thoracic Society guidelines on pneumonia in hospitalized patients?