Guest Editorial: Wound Infection: Myths and Microbes

This message is for all who make or influence wound care decisions. Patients are counting on you to do what works. Addressing graduates of the Rutgers Department of Kinesiology that included medical doctors, physical therapists, educators, athletic trainers, nurses, and research scientists, Eric LeGrand, former Rutgers football player, inspired his audience from his wheelchair with the message, “Don’t do your job for the paycheck. Do it for the patient.”¹ Science is all you can trust to inform your own patient care decisions. The rest is opinion.

A strong core of wound infection science is available to serve persons with the courage and integrity to conduct evidence-based practice. Yet much science gets lost in translation when applied to patients.² This journal features a sample of sound science you can use to inform decisions about patients with or at risk of developing a wound infection. Evidence-based guidelines^3-5 also are available from researchers who have donated their time and effort to compile evidence for you. 

Let’s focus for now on the science of chronic wound infection, where differentiating between microbial- and tissue-related inflammation is the first challenge. It is tempting to perceive the classical signs of infection (hot, red, swollen with increasing pain and fluid) as infection. This diagnosis seems easy to address with debridement and appropriate antibiotics,⁶ but focusing on the microorganisms rather than cause(s) of tissue damage could result in loss of limb or life. 

Here’s why. For most chronic wounds, complex, ongoing, or repeated causes of tissue injury generate inflammation and delayed healing (Yes! The same symptoms of chronic wound infection). These causes include a myriad of host (patient) and wound environment variables that set the stage for opportunistic invasion by wound microorganisms.⁷ For example:

• One environmental variable familiar to us all is the wound’s need for moisture. Allowing a wound surface to dry (as wet-to-dry gauze does in 4 hours without remoistening⁸) creates a histologically documented 250 micron-wide zone of porous dead tissue at the wound surface, offering a perfect picnic for microorganisms on their way to invade the healthy tissue below.⁹ The resulting increase in infections of wounds dressed with any form of dry or impregnated gauze compared with moisture-retentive dressings is supported by strong evidence in chronic and acute wounds.^10,11
• Diabetic neuropathy is a well-known host variable. Providing consistent protection and offloading of the neuropathic foot heals most diabetic foot ulcers in 12 weeks,¹² but this evidence often is ignored.¹³ Without prompt, consistent, effective offloading of an insensate foot, unnoticed tissue injury progresses to microbial invasion and potential amputation. 

Those host and environmental factors that cause tissue injury must be addressed before the wound can heal. It’s tricky, because causes of tissue injury differ for each patient and require utmost professional expertise and skill to identify and resolve them. If you don’t spot and address them early, the result can be devastating. Causes of injury most typical for chronic wounds singly or in combination include:

• Compromised arterial perfusion, often related to occluded arteries or peripheral arterial disease (PAD), as seen in ischemic ulcers;
• Loss of protective sensation in patients with diabetes-related neuropathy and/or ischemia related to PAD;
• Impaired return of venous blood to the heart as seen in venous leg ulcers; and
• Prolonged or repeated pressure, friction, or shear forces compromise its circulatory support, as in pressure injury. 

Naturally, the signs of inflammation caused by ongoing or repeated tissue injury are the same signs of inflammation caused by invasive infection. Because bacteria thrive on compromised tissue, it would be easy to mistake bacteria as the primary cause of tissue breakdown and call them the “cause” of delayed healing in chronic wounds, but acting on this myth could place patients at risk. 

Opportunistic microbial invasion of compromised tissue doesn’t make it easy to differentiate tissue harm from infection. No one can reliably recognize a strain of organisms or related biofilm by sight,⁶ and strong evidence shows decreasing the bioburden in a diabetic foot ulcer doesn’t improve healing.⁴ Much more definitive research is needed before clinicians can rely on microorganisms or biofilms for valid wound diagnosis, prediction, prevention, or treatment.⁷

The clinical dilemma is how to decide whether the signs of inflammation and delayed healing are caused by microorganisms or by unresolved host and environmental factors that originally compromised the chronic wound tissue. The wrong decision places patients at risk of receiving debridement and antimicrobial therapy when they may really need more rigorous management of the host and environmental factors causing the chronic wound to break down. 

Strong evidence supports an interpretation of clinical wound infection that does not focus on removing the organisms (or their cozy biofilm homes). Instead, it takes us back to basics¹⁴ and challenges all caregivers to close the gap between evidence and practice,¹³ using the following reasoning:

• If removing biofilms allowed chronic wounds to heal, the appropriate combination of sharp debridement and antibiotic/antimicrobial therapy should heal all arterial, venous, pressure, or diabetic ulcers. This doesn’t happen. Guidelines report scant evidence for either.^3-5
• Often bacterial “culprits” are simply replaced by antibiotic-resistant bacteria.¹⁵ In fact, focusing on bacteria may harm patients, because using prophylactic antibiotics on leg ulcers has resulted in delayed healing.¹⁶ This should not be surprising; 90% of the cells in our body are microbes that help us thrive.
• Evidence from clinical practice¹⁷ and blind evaluated randomized controlled trials (RCTs)^18,19 supports true moist wound healing while rigorously addressing all causes of tissue damage to allow healing without using routine sharp debridement, antibiotics, or antimicrobials. The bacterial wound burdens decline as the wounds heal. 

The bottom line is that persons who look past this natural association between bacteria and tissue injury can save limbs and lives by stopping the tissue injury so the bacteria have no compromised tissue to eat and find their end when attacked by white blood cells brought by restored circulation. 

If wound care is to earn scientific credibility, we all need to use consistent evidence and reliable, valid operational definitions^20,21 in order to replicate each other’s work, clearly identifying effective interventions and patients who may benefit from them. This is why we develop evidence-based guidelines and encourage research to improve the evidence base for recommendations that are opinion-based.

The studies cited here are only a few of many in the chronic wound literature. Please don’t take my word for it. Use evidence-based guidelines or find the strongest trustworthy evidence relevant to your own patients at the United States National Library of Medicine, National Institutes of Health PubMed website at: www.ncbi.nlm.nih.gov/pubmed. Search the wound care literature; it is rich with RCTs supporting these ignored principles. As a patient advocate since my “retirement” in 2006, I would be thrilled to see our field renew its attention to those evidence-based practices that would work so well … if only they were used. 

Dr. Bolton acknowledges the pioneering contributions to the science of microbiology of William B. Baine, MD, retired senior medical advisor, Centers for Outcomes and Evidence, Agency for Healthcare Research and Quality, United States Department of Health and Human Services, Rockville, MD. His work is unrelated to the concepts put forth in this Guest Editorial, but his wisdom and rigor in using scientific methods helped her think past the myths and critically evaluate the scientific facts of  wound infection.

The opinions and statements expressed herein are specific to the respective authors and not necessarily those of OWM or HMP. This article was not subject to the Ostomy Wound Management peer-review process.