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by Nat Jones, RPh, FAPC, PCCA Clinical Compounding Pharmacist

Getting involved in wound care can be a very rewarding clinical niche. Many medical practitioners have limited experience and training in treating wounds, so when pharmacists have knowledge and compounded options to share, it is usually greatly appreciated. Understanding the pathophysiology of wounds and the pharmacology of the active pharmaceutical ingredients (APIs) used in wound care are needed to interact with prescribers and to formulate a patient-specific compound.

Although there are many types of wounds, this article only focuses on cutaneous wounds. Common types of cutaneous wounds include surgical, arterial, venous stasis, pressure and diabetic.

After a wound occurs, there are four phases of wound healing: hemostasis, inflammatory, proliferative and remodeling.1

Thiruvoth F.M., Mohapatra D.P., Kumar D., et al. (2015) Current concepts in the physiology of adult wound healing. Plast Aesthet Res 2015;2:250-6. Open Access publication at http://dx.doi.org/10.4103/2347-9264.158851

When a cutaneous injury occurs, hemostasis is initiated by platelets through fibrin clot formation. Platelets also release cytokines, chemokines and growth factors to attract macrophages and fibroblasts to the site of tissue injury. The inflammatory phase begins with the arrival of neutrophils, followed by macrophages and lymphocytes, which are essential for effective decontamination at the wound site. The proliferative phase is characterized by new blood vessel formation (angiogenesis), synthesis of collagen, extracellular matrix (ECM) components and re-epithelialization. In the remodeling phase, the collagen laid down during proliferation is gradually replaced by a more stable interwoven type III collagen, along with vascular maturity and regression; this process typically lasts 6-24 months from the time of injury.1

The complex process of wound healing is influenced by a variety of factors. At each healing stage, a different set of specific cytokines and growth factors must interact with their receptors, other growth factors and ECM components at their target sites (see Figures A and B).

Cutaneous wounds 3 days (A) and 5 days (B) after injury. Growth factors such as fibroblast growth factor (FGF), insulin-like growth factor (IGF), keratinocyte growth factor (KGF), platelet-derived growth factor (PDGF), transforming growth factor (TGF) and vascular endothelial growth factor (VEGF), and proteases such as matrix metalloproteinases (MMPs) and plasminogen activator (PA), are thought to be necessary for cell movement.2

Exudate is produced by a complex osmotic and hydrostatic pressure, resulting in a cyclic process that delivers oxygen, nutrients, white blood cells and chemical messengers to the wound site. Wounds can have varying levels of exudate — from leaking to no exudate. Treatment of highly exudative wounds requires frequent dressing changes, along with a base with good adherence and preferably some capacity for absorption.3

Prior to dressing, debridement is a necessary first step for proper wound care.4 A wound formula containing APIs that help facilitate healing is usually needed for successful closure. Commonly used APIs for wound care formulas include misoprostol, phenytoin, naltrexone, minoxidil, N-acetylcysteine and calcium channel blockers, such as amlodipine and nifedipine.

Combination synergy has been observed with misoprostol and phenytoin, as well as with amlodipine and phenytoin; other ingredients, however, have also shown to be beneficial. Hormones and non-API substances — insulin, aloe, arginine, beta glucan and dexpanthenol — may also help wound closure.5-7

When there is justification to treat an infection, antimicrobials may also be used. A partial list includes:

  • Metronidazole
  • Mupirocin
  • Chloramphenicol

The vehicle base chosen to incorporate APIs can be critical to the success of wound closure; appropriate choices are often contingent on the type of wound. For example, an absorptive powder is a good choice for an exudative wound, whereas a hydrating base is beneficial for a dry to normal wound.

In addition, the frequency of wound cleaning and dressing (including instillation of wound formula) also depend on the type, size and status of the wound.

Members with clinical services access may contact our Clinical Services team for help with compounding for wounds and other compounding-related concerns.

A complete version of this article originally appeared in PCCA’s members-only magazine, the Apothagram.

These statements are provided for educational purposes only. They have not been evaluated by the Food and Drug Administration, and are not to be interpreted as a promise, guarantee or claim of therapeutic efficacy or safety. The information contained herein is not intended to replace or substitute for conventional medical care or encourage its abandonment.

References

  1. Cundell, J. (2016) Chapter Two - Diabetic Foot Ulcers: Assessment, Treatment, and Management. Smart Bandage Technologies Design and Application, Academic Press. 37-61. https://doi.org/10.1016/B978-0-12-803762-1.00002-3
  2. Park, J.W., Hwang, S.R., Yoon, I-S. (2017) Advanced Growth Factor Delivery Systems in Wound Management and Skin Regeneration. Molecules. 22(8):1259. Open Access publication at https://www.mdpi.com/1420-3049/22/8/1259
  3. Bradley P. (2018). Wound Exudate. Brit J Comm Nursing, 23(Sup12), S28–S32. https://doi.org/10.12968/bjcn.2018.23.Sup12.S28
  4. Thomas, D. C., Tsu, C. L., Nain, R. A., et al. (2021). The role of debridement in wound bed preparation in chronic wound: A narrative review. Ann Med Surg (2012), 71, 102876. https://doi.org/10.1016/j.amsu.2021.102876
  5. Riepl M. (2022). A Compendium of Compounding Agents and Formulations, Part 2: Metronidazole, Misoprostol, and Phenytoin. Intl J Pharma Compd. 26(2), 94–98.
  6. Vetvicka, V., & Vetvickova, J. (2011). ß (1-3)-D-glucan affects adipogenesis, wound healing and inflammation. Oriental Pharmacy and Experimental Medicine, 11(3), 169-175
  7. Heise, R., Skazik, C., Marquardt, Y., et al. (2012). Dexpanthenol modulates gene expression in skin wound healing in vivo. Skin Pharmacology and Physiology, 25(5), 241-248. doi:10.1159/000341144



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