Vancomycin was first discovered in 1950 and approved by the FDA in 1958. It became a standard treatment for methicillin-resistant Staphylococcus aureus (MRSA) infections in the 1980s. Vancomycin works by inhibiting peptidoglycan biosynthesis in the bacterial cell wall. It has activity against gram-positive bacteria and is used to treat various hospital-acquired infections caused by MRSA such as pneumonia, bloodstream infections, and surgical site infections. Key considerations for vancomycin treatment include monitoring for potential adverse effects like red man syndrome, nephrotoxicity, and ototoxicity. Therapeutic drug monitoring is important to maintain concentrations above the minimum inhibitory concentration for optimal bacterial killing

1. Presented by
Helena H. Quezon
Clinical Approach to Advanced Pharmacology
MSNE 5356

2. Vancomycin “Vanquish”
 Vancomycin was first discovered in 1950 and was approved by
the Federal Drug and Agency (FDA) in 1958.
 It became an option to treat an increasing Penicillin resistant
Staphylococcus infection in the 50’s.
 The emergence of Methicillin resistant Staphylococcus aureus
(MRSA) in the ‘80’s.
 It provides empiric antibiotic coverage for Gram positive bacteria
(aerobic and anaerobic) only.
(Barber et al., 2016)
Reference
Barber, K. E., Bell, A. M., Stover, K. R., & Wagner, J. L. (2016). Intravenous Vancomycin
Dosing in the Elderly: A Focus on Clinical Issues and Practical Application. Drugs & Aging,
33(12), 845–854. http://doi.org/10.1007/s40266-016-0420-z

3. Conditions Treated
 Vancomycin has been the gold standard for
treating MRSA, a leading cause of hospital
acquired infections (HAI) such as:
 ventilator associated pneumonia (VAP)
 Bacteremia (septicemia)
 Catheter associated urinary tract infection (CAUTI)
 Central line associated blood stream infections
(CLABSI)
 Surgical site infections (SSI)
(Levine, 2006)

4. Peptidoglycan (PG), also known as murein,
is the substance that layers the bacterial
cell wall created by a polymer matrix of
peptide chains.

5.  Gives structural integrity critically needed for the
bacteria to survive in varying osmotic pressures within
its environment.
 Is maintained by the activity of transglycosylase and
trans peptidase enzyme activity
 Disaccharide pentapeptides to strengthen glycan
strands and provide a meshwork for nearby peptide
strands of immature PG areas of the cell wall (Prince,
2009).

6.  inhibits peptidoglycan biosynthesis of bacterial cell wall
 blocks transglycosylase and trans peptidase activity
 prevents transpeptidation linking
 stops bacterial cell wall maturation
(Zhanel, Schwezer, & Karlowsky, 2012)
* http://image.slidesharecdn.com/8-drugresistance-150727150817-lva1-app6891/95/8-drug-resistance-30-638.jpg
*

7. The inhibitory effect of Vancomycin interferes
with the specific sequence in cell wall synthesis
that changes cell shape and size, increase
stress responses in hypotonic environment to
promote cell death
(Prince, 2009).

8. Adverse Drug Reaction
 Red man or red neck syndrome is caused by rapid
intravenous infusion of the drug.
 Ototoxicity with tinnitus as a symptom is linked to an
increase in serum concentration and prolonged
duration of Vancomycin treatment.
 It is potentiated by concomitant use of ototoxic
drugs.
(Barber et al., 2016)
Nephrotoxicity is defined by Rybak (2009), as “ a rise
in serum creatinine of more than or equal to 0.5 mg/dL
above baseline”(p. 92).

9. Pharmacokinetics
 Creatinine clearance is a good predictor of drug clearance
from the system.
 Drug distribution is dependent on the amount albumin for
protein binding and total body weight.
 A persons actual total body weight (ABW) should be used
for accurate dosing which directly correlates with volume
distribution to avoid over or under dosing.
 It is highly lipophilic, thus the degree of body fat affects the
distribution rate and serum concentration level of the drug.
(Lim, Chong, Noh, Jung, & Kim, 2014)
 *https://images.search.yahoo.com/search/images
*

10. Pharmacokinetics
 Rybak (2009), “patients with normal renal function, the
α distribution phase ranges from 30 minutes to 1
hours, and the ß elimination half life ranges from 6 to
12 hours. The volume of distribution is 0.4-1 L/kg” (p.
83).
 Lim, Chong, Noh, Jung, & Kim (2014), “the distribution
to some of the tissues could be permeability-rate-
limited, and the kinetics of Vancomycin distribution
could also be affected by blood flow, tissue partition
coefficient and tissue volume” (p. 202).

11. Drug Binding Issues
 The drug is primarily eliminated in the kidneys and does not
undergo metabolism (Rybak, 2006).
 Tissue distribution variability depends on the degree of
inflammation of the affected target organ.
 Protein binding capacity of the drug depends largely on the
albumin level for distribution, transport, metabolism and
efficacy of the drug (Wu et al., 2013).
• The bactericidal activity of Vancomycin is dependent on the
inoculum size (Rybak, 2006).
*http://www.mylan.com/-/media/pds/images/us/vancomhclinj1gviallabelpng.png
*

12. Minimum Inhibitory Concentration
According to Lim et al. (2014), “the
antibiotic shows time-dependent bacterial
killing and is most effective when drug
concentrations are three to five times the
minimum inhibitory concentration (MIC) for
growth inhibitory activity against the
bacteria” (p. 196).

13. Communication
Inter-professional collaboration with daily rounding
at the bedside participated by
 medical doctors, nurse practitioners and
physician assistants
 pharmacists
 nutritionists
 infection preventionist
Communication process utilizing a checklist
Alert system built into the electronic health record
(EHR) system

14. Application
Goal when with Vancomycin treatment
 maintain patient safety
 effective and successful drug therapy
 avoid occurrence of drug toxicity with proper
monitoring of drug concentration level
Be abreast with updates with Vancomycin
treatment based on evidence practice

15. REFERENCES
Holt, S., Thompson-Brazill, K., Sparks, E., & Lipetzky, J., (August, 2016). Treating central catheter –
associated bacteremia due to methicillin-resistant Staphylococcus aureus: Beyond
Vancomycin. Critical Care Nurse 36(4). 46-57.
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Levine, D. (2006). Vancomycin: A history. Clinical Infectious Disease 42(Supplement-1): S1-S12. DOI:
https://doi.org/10.1086/491709
Lim, H., Chong, Y. P., Noh, Y., Jung, J., & Kim, Y. S. (2014). Exploration of optimal dosing regimens of
vancomycin in patients infected with methicillin-resistant Staphylococcus aureus by modeling
and simulation. Journal Of Clinical Pharmacy & Therapeutics, 39(2), 196-203. DOI:10.1111/
jcpt.12123
Neu HC, Gootz TD. Antimicrobial Chemotherapy. In: Baron S, editor. Medical Microbiology. (4th ed.).
Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Chapter 11.
Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK7986/
Rybak, M. (2006). The pharmacokinetic and pharmacodynamics properties of vancomycin. Clinical Infectious
Disease 42(Suppl-1). 35-39
Retrieved from: http:// cid.oxfordjournals.org/
Rybak, M., Lomaestro, B., Rotschafer, J., Moellering Jr., R., Craig, M., Dalovisio, J., & Levine, P.
(2009). Therapeutic monitoring of vancomycin in adult patients: A consensus review of the
American Society of Health-System Pharmacists, the Infectious Diseases Society of America,
and the Society of Infectious Diseases Pharmacists. Am J Health-Syst Pharm (66). 82-98. DOI
10.2146/ajhp080434
Wu, J., Wei, R., Wang, H., Li, T., & Weihuan, R. (2013). Underlying the mechanism of vancomycin and human
serum albumin interaction: A biophysical study. J Biochem Molecular Toxicology 27. 463-470. DOI:
10.1002/jbt
Zhanel, G. G., Schweizer, F., & Karlowsky, J. A. (2012). Oritavancin: Mechanism of Action. Clinical
Infectious Diseases, 54S214-S219. doi:10.1093/cid/cir920.
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