My patient with a medicated adhesive patch is having an MRI. Should the patch be removed before the procedure?

The nonadhesive backing of some medicated or transdermal patches (TPs) contain aluminum or other metals that can become heated during an MRI1.  FDA is aware of skin burns at the patch site in several patients wearing an aluminized TP during an MRI2.

The following TPs have been reported by the FDA to have aluminized backing: Androderm (testosterone transdermal system); 2. Catapres-TTS (clonidine transdermal system); 3. Nicoderm (nicotine transdermal system); 4. Nicotrol (nicotine transdermal system); 5. Prostep (nicotine transdermal system);6. Habitrol (nicotine transdermal system); 7. Nicotine transdermal system (generic nicotine transdermal system); 8. Transderm Nitro (nitroglycerin transdermal system); 9. Trasnsderm Scop (scopolamine transdermal system).

Other TPs that have metal backing but not necessarily carrying FDA warning include Flector (diclofenac), estradiol, Duragesic (fentanyl), Synera (lidocaine and tetracaine), methyl salicylate and menthol (over the counter), Oxytrol (oxybutynin), Exelon (rivastigmine), Neupro (rotigotine), and Emsam (selegiline)3.  

In short, it is advisable that TPs with metal backing (either listed above or others)  be removed prior to MRI.

 

References

  1. Kuehn B. FDA warning: remove drug patches before MRI to prevent burns to skin. JAMA. 2009;301:1328
  2. https://www.accessdata.fda.gov/scienceforums/forum06/k-26.htm , accessed April 19, 2017.
  3. http://www.pharmacytimes.com/contributor/alexander-kantorovich-pharmd-bcps/2016/08/transdermal-patches-that-must-be-removed-before-mri , accessed April 19,2017.
My patient with a medicated adhesive patch is having an MRI. Should the patch be removed before the procedure?

When should I consider bicarbonate (BC) replacement in my patient with renal insufficiency?

Metabolic acidosis is one of the earliest complications of chronic kidney disease (CKD), with a direct correlation between the decline in glomerular filtration rate (GFR) and reduction in serum BC1.

Epidemiologic studies in patients with CKD have reported an independent association between serum BC (<22 meq/L considered low) and adverse renal outcomes and mortality1. Limited data from small interventional trials of alkali therapy supplementation and dietary interventions (eg, increased fruit and vegetable intake) have shown the benefits of raising serum BC. Specifically, 1 study involving patients with CKD stages 4 and 5 and another involving CKD stage 2 hypertensive nephropathy reported slower decline in creatinine clearance/eGFR in patients receiving BC replacement2,3.  

Less is known on the potential benefit of BC replacement in patients with acute kidney injury with a recent Cochrane review finding no randomized controlled trials4 and national guidelines not recommending either for or against its use in this setting5. Of note, BC therapy has also been associated with sodium and fluid overload, an increase in lactate and PCO2, and a decrease in serum ionized calcium6.

References

  1. Dobre M, Rahman M, Hostetter TH. Current status of bicarbonate in CKD. J Am Soc Nephrol 2015;26:515-523.
  2. de Brito-Ashurst I, Varagunam M, Raftery MJ, et al. Bicarbonate supplementation slows progression of CKD and improves nutritional status. J Am Soc Nephrol 2009; 20: 2075–2084.
  3. Mahajan A, Simoni J, Sheather SJ, et al. Daily oral sodium bicarbonate preserves glomerular filtration rate by slowing its decline in early hypertensive nephropathy. Kidney Int 2010;78: 303–309.
  4. Hewitt J, Uniacke M, Hansi NK, et al. Sodium bicarbonate supplements for treating acute kidney injury. Cochrane Database of Systematic Reviews 2012; Jun 13; (6):CD009204. doi: 10.1002/14651858.
  5. Palevsky PM, Liu KD, Brophy PD, et al. KDOQI US commentary on the 2012 KDIGO clinical practice guideline for acute kidney injury. Am J Kidney Dis 2013;61:649-72.
  6. Sabatini S, Kurtzman NA. Bicarbonate therapy in severe metabolic acidosis. J Am Soc Nephrol 2009;20:692-695.

 

Contributed in part by Cynthia Cooper, MD, Mass General Hospital, Boston, MA.

When should I consider bicarbonate (BC) replacement in my patient with renal insufficiency?

My patient with recent Clostridium difficile infection (CDI) needs a gastric acid-suppressant. Are histamine2-receptor antagonists (H2RAs) associated with CDI?

Although proton pump inhibitors (PPIs) have received much attention for their link with CDI, H2RAs have also been associated with CDI.  In a study of CDI among hospitalized patients, H2RA was associated with CDI (O.R. 1.53, 95% CI, 1.12-2.10); for daily PPI use the O.R. was 1.74 (95% CI, 1.39-2.18)1.  

A meta-analysis in 2013 reported an overall O.R. of 1.44 (95% CI 1.22-1.7) for CDI in patients treated with H2RAs2.  The estimated number needed to harm with H2RAs at 14 days after hospital admission was 58 for patients on antibiotics vs 425 for those not receiving antibiotics2.

Potential mechanism for H2RA-associated CDI is unclear, but survival of acid-sensitive vegetative forms of C. difficile in the stomach and their enhanced growth in the presence of bile salts related to gastro-esophageal reflux disease have been postulated2.

In brief, gastric acid suppression with H2RAs may increase the risk of CDI in hospitalized patients. 

 

References

  1. Howell MD Novack V, Grgurich P, et al. Iatrogenic gastric acid suppression and the risk of nosocomial Clostridium difficile infection. Arch Intern Med 2010; 170:784-790.
  2. Tleyjeh IM, Bin Abdulhak AA, Riaz M, et al. The association between histamine 2 receptor antagonist use and Clostridium difficile infection: a systematic review and meta-analysis. PLoS ONE 2013; 8:e56498.
My patient with recent Clostridium difficile infection (CDI) needs a gastric acid-suppressant. Are histamine2-receptor antagonists (H2RAs) associated with CDI?

What is the clinical relevance of “SPICE” organisms?

 

“SPICE” stands for the following bacterial species: Serratia, Pseudomonas, indole-positive Proteae (e.g. Proteus sp. [not mirabilis], Providencia, Morganella), Citrobacter, and Enterobacter.

These organisms (as well as Acinetobacter sp.) often have inducible chromosomal AmpC ß-lactamase genes that may be derepressed during therapy, conferring in vivo ß-lactam resistance despite apparent sensitivity in vitro (1,2). Because AmpC genes in clinical isolates are not routinely screened for in the laboratory, the following treatment approach to these organisms is often adopted (1).

Third generation cephalosporins (e.g. ceftriaxone and ceftazidime) are usually avoided irrespective of in vitro susceptibility. For less serious infections (e.g. urinary tract infections) or severe infections in carefully monitored clinically stable patients, piperacillin-tazobactam and cefepime in particular may be used due to their lower risk of induced resistance. For severe infections (e.g. pneumonia and bacteremia) in seriously ill patients, carbapenems (e.g. meropenem, imipenem-cilastatin) are often the drugs of choice.  Fluroroquinolones and aminoglycosides may also be considered.

References

  1. MacDougall C. Beyond susceptible and resistant, part I: treatment of infections due to Gram-negative organisms with inducible ß-lactamases. J Pediatr Pharmacol Ther 2011;16:23-30.
  2. Jacoby GA. AmpC ß-lactamases. Clin Microbiol Rev 2009;22:161-182.

Contributed by Avi Geller, 3rd year Medical Student, Harvard Medical School

What is the clinical relevance of “SPICE” organisms?

Is cefpodoxime an appropriate oral antibiotic substitute for ceftriaxone when treating patients with respiratory tract infections caused by penicillin-resistant Streptococcus pneumoniae (PRSP)?

 

Short answer: No! Although cefpodoxime is also a 3rd generation cephalosporin, its invitro activity against PRSP is not comparable to that of ceftriaxone.  In a study of 21,605 strains of S. pneumoniae collected internationally, whereas 89.1% of PRSP isolates were susceptible to ceftriaxone, only 35% were susceptible to cefpodoxime (1).  Among isolates resistant to penicillin and erythromycin, the susceptibility to ceftriaxone was 86.9% compared to that of 22.7% for cefpodoxime.

This information is important since 32%, and 17.6% of all S. pneumoniae isolates tested in this study  were either penicillin-resistant or penicillin- and erythromycin-resistant, respectively.  So, when it comes to the coverage of PRSP, there is no oral cephalosporin “equivalent” to ceftriaxone and that includes cefpodoxime.  In fact, the package insert of cefpodoxime states that cefpodoxime is active against S. pneumoniae “excluding penicillin-resistant strains” (2).

 

References

  1. Pottumarthy S. Fritsche TR, Jones RN. Comparative activity of oral and parenteral cephalosporins tested against multidrug-resistant Streptococcus pneumonia: report from SENTRY Antimicrobial Surveillance Program (1997-2003). Diag Microbiol Infect Dis 2005;51:147-150.
  2. http://www.accessdata.fda.gov/drugsatfda_docs/label/2007/050674s014,050675s017lbl.pdf; accessed June 20, 2016.
Is cefpodoxime an appropriate oral antibiotic substitute for ceftriaxone when treating patients with respiratory tract infections caused by penicillin-resistant Streptococcus pneumoniae (PRSP)?

What is medication overuse headache and how should we approach it?

Medication overuse headache (MOH), also known as rebound headache, is caused by the overuse of medications for acute headaches. It affects 1-2% of the general population, often women, and should be considered in all patients presenting with chronic headaches (1).

According to the International Classification of Headache Disorders (ICHD) (2), MOH has the following characteristics: A. Present on ≥15 days/month in a patient with a pre-existing headache disorder; B. Present for > 3 months with regular use of acute headache medications (eg. ergotamines, triptans, opioids, combination analgesics) on ≥10 days/month, simple analgesics on ≥15 days/month, or any combination of the above drugs on ≥10 days/month; and C. Not readily accounted for by any other ICHD diagnosis. For treatment, experts recommend discontinuation of the offending medication(s) with a taper for medications that may cause severe withdrawal symptoms (e.g. narcotics, benzodiazepines, and barbiturates) (1).

 

References:

 (1) Munksgaard SB and Jensen RH. Medication Overuse Headache. Headache. 2014;54(7):1251-7.

 (2) Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia. 2013;33:629-808.

 

Contributed by Joome Suh, MD, Boston, MA.

What is medication overuse headache and how should we approach it?