Biofilm and Infected Wounds

By Liping Tang, PhD

Infection is the single most likely cause of delayed healing in chronic wounds. In most cases, identification of chronic wound infection (e.g., diabetic foot ulcers and venous leg ulcers) is not obvious because chronic wounds do not exhibit the same classic inflammatory signs of infection as those found in acute wounds. More arduously, those common signs of infection—pain, erythema, heat, and purulent exudate— vary as we age and occur differently in those with underlying diseases or weakened immune systems. Diagnosis is generally based on the doctors’ experience and could be confirmed with microbiological culture of tissue biopsy. However, culture could take a few days, and the results may not always be reliable because of sampling error. A fast and accurate diagnosis of wound infection would relieve the patient of significant discomfort and improve the treatment outcome.

The incorporation of silver into wound dressings has been a breakthrough to combat the effects of antibiotic resistance, despite silver safety concerns. Regardless of its recent popularity, silver is not a new tool in health care.

As a cost-effective alternative to topical antibiotics, silver is now widely available in wound dressings. However, what does silver really do within the wound bed? Silver uses a multifaceted approach to combating infection that attacks bacteria internally.

Silver has become one of the most commonly used alternatives to topical antibiotics in recent years because of the growing concern over antibiotic resistance. Silver offers a multifaceted antimicrobial approach that makes it less likely for resistance to develop. With its limited and uncommon cytotoxicity, silver can be used to treat infected wounds over time and prevent further complications.

Before the discovery of penicillin in 1928, silver was the primary antimicrobial agent available. Now, as antibiotic resistance plagues the health care field, silver has new value for wound care. Additionally, silver has demonstrated limited cytotoxicity when used topically, thus making it a suitable alternative to antibiotics.

Emily Greenstein, APRN, CNP, CWON, FACCWS

Wound care has evolved from treatments based on superstition to systematic, evidence-based care. The history of wound healing dates back to 2000 BCE. Various civilizations over the centuries had differing approaches to wound care.

Centuries ago, science took a back seat to superstition. Infectious diseases were seen as a sign of supernatural powers or the wrath of God. We now know that it was smallpox that led to the downfall of the Aztecs. We also know that bubonic plague was not a divine punishment, but it was caused by bacteria transmitted by fleas on rodents traveling on trading ships.

Of all the types of chronic wounds in lower extremities, venous leg ulcers are the most common, and they account for up to 70% of lower leg ulcers. Infection is a common complication in these wounds, however, and may contribute to chronicity. Biofilm is another common complicating factor. Preventing infection, removing unhealthy tissue from the wound, providing dressings that manage exudate, and using advanced modalities can help heal these chronic wound types and prevent a recurrence.

Wounds typically heal in four sequential but overlapping phases — hemostasis, inflammatory, proliferative and remodeling — ultimately leading to tissue regeneration. Healing sometimes stalls for various reasons, a key one being extensive inflammation, which disrupts the normal cascade of healing and leads to chronic and hard-to-heal wounds. A vicious cycle of ongoing inflammation, pain and poor quality of life often follows. Understanding how to break this cycle is essential for wound care clinicians who want to optimize healing outcomes and patient quality of life.

Wound healing can stall for a number of reasons. Wounds that have not healed or significantly reduced in size after four to six weeks are considered chronic. They are characterized by a multitude of impeding factors including biofilm, excess matrix metalloproteinases (MMPs) and extracellular matrix degradation, inflammation, fibrosis, unresponsive keratinocytes and fibroblasts, and atypical growth factor signaling.