Clindamycin used as a treatment for mastitis.

1. CLINDAMYCIN: A TREATMENT FOR
MASTITIS
CLYNEISHA BYRD
LAMAR UNIVERSITY
MSNE 5356 ADVANCED PHARMACOLOGY
DR. ELIZABETH LONG

2. DRUG CHOSEN
• Approximately 1/3 or breastfeeding women in the U.S. are
affected by lactational mastitis (Reddy, Qi, Zembower, Noskin,
& Bolan, 2007).
• Symptoms include: inflammation of the breast, fatigue, fever,
and breast soreness. Generally mastitis occurs within the 1st
month postpartum. Clindamycin is frequently prescribed to
treat mastitis (Spencer, 2008).

3. PATHOPHYSIOLOGY OF MASTITIS
1. Lactiferous ducts undergo squamous metaplasia →
blockage/inflammation→ vulnerability to bacterial
infection (Epocrates, 2017).
2. Milk Stasis r/t overproduction or ineffective
emptying→ channel for bacterial growth (Epocrates,
2017).
3. Nipple Trauma r/t ineffective infant latch→ entryway
for bacteria (Spencer, 2008).
Postpartum phase hormones
change→ ↑prolactin &
↓estrogen/progesterone →
oxytocin to be excreted
milk ejection occurs when
breast is stimulated via infant
suckling or breast pumping
Alveoli in the breast
contracts→ milk is ejected
through lactiferous duct →
lactiferous sinus →out the
body via the nipple (Mattson
& Smith, 2016).
Normal
Pathway
Abnormal
Pathways
Staphylococcus
Aureus
(S. aureus)
Reddy et al., 2007
End
Result

4. INTENDED DRUG RESPONSE OF
CLINDAMYCIN
• S. aureus is a gram-positive organism and
Clindamycin is routinely prescribed to treat
this bacteria (Reddy et al., 2007).
• Clindamycin is categorized as a lincosamide
antibiotic that has broad spectrum coverage
over skin and soft-tissue infections such as
mastitis (Murphy & McKay, 2015).
• This drug interferes with protein synthesis
by preventing transpeptidation when the
drug binds to the 50S ribosomal subunit.
This causes cell growth and reproduction to
be stopped making the medication a
bacteriostatic agent (Murphy & McKay,
2015).
• The cell wall of staphylococci is
surrounded by murein sacculus and made
of teichoic acids, surface proteins, and
peptidoglycan (Szweda et al., 2012).
• Peptidogylcan is the essential component
of the cell wall (Szweda et al., 2012).
• Clindamycin stops the synthesis of
peptidoglycan which leaves the cell wall
inadequately protected and the gram
positive bacteria cannot survive (Szweda
et al., 2012).

5. PHARMACOKINETICS OF CLINDAMYCIN
• Absorption
• Rapid absorption
• PO: 90% bioavailability
• IV:100% bioavailability (U.S.
Food and Drug Administration,
2017).
• Distribution
• Widely to body tissues and fluids
except cerebrospinal fluid (U.S.
Food and Drug Administration,
2017).
• High protein binding to albumin
(Burian et al., 2011).
• Metabolism
• Primarily in the liver
• Half-life: 2.4 hours ( K.P.
Joseph, personal interview,
November 14, 2017).
• Not effected by first pass
metabolism (Arcangelo et al.,
2017)
• Excretion
• Urine and feces
• Small percentage in breastmilk
(Hale & Rowe, 2014).

6. POTENTIAL INTERACTIONS OF
CLINDAMYCIN
• No major drug-drug
interactions
• Except when used during
surgery being administered with
a muscle relaxant, it can cause
neuromuscular blockade
• ↓muscle tone→ paralysis or
muscle weakness (Kang, 2013)

7. ADVERSE DRUG REACTIONS OF
CLINDAMYCIN
• Clostridium difficile (IV or PO)
• Hypotension and injection site
irritation (IV)
• Rare: Hypersensitivity reactions
such as maculopapular skin
rash, uticaria, vesiculobullous
rash, and Steven-Johnson
Syndrome (IV or PO) (U.S. Food
and Drug Administration, 2017)

8. SIDE EFFECTS
• Changes to the gastrointestinal flora
caused by Clindamycin can lead to:
• Abdominal pain
• Nausea
• Vomiting (Prescribers’ Digital
Reference Guide, 2017)
• Infants may experience
pseudomembranous colitis due to
expose in breastmilk (Hale & Rowe,
2014).

9. DRUG BINDING ISSUES OF CLINDAMYCIN
• Evidence shows that chloramphenicol and erythromycin are
medications that affect the binding of clindamycin
• Medications have similar ribosomal binding site
• Medications have similar mechanism of action which causes antagonist
effects if given concurrently.
• Erythromycin is a moderate inhibitor of CYP3A4 and clindamycin is a
CYP3A4 substrate. When medications are given concurrently the clearance of
clindamycin is greatly reduced, and puts the patient at higher risk for
adverse reactions (Prescribers’ Digital Reference Guide, 2017).

10. IMPROVING COMMUNICATION
• There is currently a large gap in communication between providers
and nurses.
• Patients experiencing diarrhea in the hospital setting while on
clindamycin need to be evaluated for C.diff.
• Currently symptoms are getting overlooked and patients are often
given antidiarrheal medication or discharged home without the
proper knowledge of reportable symptoms associated with
Clindamycin (K.P. Joseph, personal interview, November 14, 2017).

11. APPLICATION TO THE PRACTICE SETTING
• Nurses need to inform the provider right away if their patient is
experiencing loose stools or diarrhea.
• Providers and nurses need to educate their patients properly on
adverse effects of clindamycin
• When loose stool is reported, it is important that stool culture
and associated lab work be preformed.
• Monitor for signs of hypoalbuminemia, elevated white blood cells (WBC),
and elevated serum creatinine.
• Elevated WBC may occur before the onset of diarrhea or abdominal pain
(Oldfield IV, Oldfield III, & Johnson, 2014).

12. REFERENCES
• Arcangelo, V.P., Peterson, A.M., Wilbur, V., & Reinhold, J.A. (2017). Pharmacotherapeutics
for advanced practice: A practical approach. Philadelphia, PA: Wolters Kluwer.
• Burian, A., Wagner, C., Stanek, J., Manafi, M., Bohmdorfer, M., Jager, W., & Zeitlinger, M.
(2011). Plasma protein binding may reduce antimicrobial activity by preventing intra-
bacterial uptake of antibiotics, for example clindamycin. Journal of Antimicrobial
Chemotherapy, 66, 134-137. doi: 10.1093/jac/dkq400
• Epocrates. (2017). Mastitis and breast abscess. Retrieved from
https://online.epocrates.com/diseases/108424/Mastitis-and-breast-abscess/Etiology
• Hale, T.W., & Rowe, H.E. (2014). Medication & mothers’ milk. Plano, TX: Hale Publishing.
• Kang, J.M. (2013). Antibiotics and muscle relaxation. Korean Journal of Anesthesiology,
64(2), 103-104. doi: 10.4097/kjae.2013.64.2.103
• Mattson, S., & Smith, J.E. (2016). Core curriculum for maternal-newborn nursing. St.
Louis, MO: Elsevier.

13. REFERENCES
• Murphy, C.S., & McKay, G. (2015). Clindamycin. Practical Diabetes, 32(6), 222-223a.
• Oldfield IV, E.C., Oldfield III, E.C., & Johnson, D.A. (2014). Clinical update for the diagnosis
and treatment of clostridium difficile. World Journal of Gastrointestinal Pharmacology and
Therapeutics, 5(1), 1-26. doi: 10.4292/wjpt.v5.i1.1
• Prescribers’ Digital Reference Guide. (2017). Clindamycin hydrochloride. Retrieved from
http://m.pdr.net/Mobile/Pages/Search.aspx?druglabelid=1864
• Reddy, P., Qi, C., Zembower, T., Noskin, G.A., & Bolan, M. (2007). Postpartum mastitis and
community-acquired methicillin-resistant staphylococcus aureus. Emerging Infectious
Diseases, 13(2), 298-301.
• Spencer, J.P. (2008). Management of mastitis in breastfeeding women. American Family
Physician, 78(6), 727-731.
• Szweda, P., Schielmann, M., Kotlowski, R., Gorczyca, G., Zalewska, M., & Milewski, S.
(2012). Peptidoglycan hydrolases-potential weapons against staphylococcus aureus.
Applied Microbiology and Biotechnology, 96, 1157-1174.