Myth-Busting in Wound Care: A Panel Discussion

“First, a history lesson: In 1537, France was at war with Charles V and the city of Turin, which sat within disputed territory, had been under siege for some time. Ambroise Paré (1510-90), a 27-year-old French “barber surgeon,” was sent with the infantry to northern Italy. Although we have no way of knowing for sure, it’s a safe bet the French infantry commander had low expectations of his company surgeon. Paré had not even officially been registered as a surgeon, had come from a family of modest means, and was unable to read or speak Latin. Nevertheless, he would become the most famous surgeon of his day, publish numerous scientific works, and be considered the father of prosthetics. We also credit him with performing the first controlled trial in wound care. While an army surgeon, he heard from an old woman how to treat burns with an onion poultice, and he later recorded in some detail the way in which he applied this to part of a burn (and not the other part). He noted the typical burn blisters did not form over the area where the onion poultice was applied. The onion myth apparently proved quite valid and valuable because he successfully treated many burn victims this way. However, one of his greatest accomplishments involved busting a myth that caused great suffering for 16th century soldiers. Gunshot wounds were still relatively new and believed to be toxic. The prevailing wisdom was they should be cauterized with boiling oil to prevent the patient from being poisoned. During the Siege of Turin (May 14–Sept. 7, 1706) Paré ran out of oil and improvised a substitute made of egg yolk, oil of roses, and turpentine. He recorded the following in his diary: ‘That night I could not sleep easily thinking that by the default in cautery I would find the wounded to whom I had failed to apply the oil dead of poisoning; and this made me get up at first light to visit them. Beyond my hopes I found those on whom I had put the digestive dressing feeling little pain from their wounds which were not swollen or inflamed, and having spent quite a restful night. But the others, to whom the said oil had been applied, I found fevered, with great pain and swelling around their wounds. From then I resolved never again so cruelly to burn poor men wounded with arquebus shot.’¹ Many wound care practitioners are familiar with this story. What we do not understand is the courage it took for him to report it. He published this in 1545. Remember that he was relatively uneducated. Because medical texts were published in Latin, he had to publish his findings in French, which meant they had to later be translated for other physicians outside of France and exposed him to even further possible criticism. What is even harder for us to appreciate is the courage it took for him to publish his findings at all. Contradicting academic authority at the time was simply unheard of. As Donaldson points out in a fantastic article I’ve referenced here,¹ Paré must have had incredible self-confidence. I know there have been times I have had second thoughts about publishing something that contradicted current thinking. It guarantees at least some professional discomfort and perhaps a few enemies (assuming you can get the paper past the reviewers of a journal, which is not always possible). Paré had common sense, keen powers of observation, compassion for his patients, and confidence to trust his observations — even if they ran counter to established thinking. He rose from humble beginnings to become surgeon-in-chief to three kings of France. In an era before the germ theory, Paré did a lot of myth-busting with nothing more than the naked eye. One of the things I love about wound care is how visual it is. It’s the perfect field for a keen observer to flourish. Have you done any myth-busting lately?

Here are two of my favorite examples of busted myths (not my discoveries):

Myth: Patients living with venous ulcers need to be checked for deep vein thrombosis (DVT) before being placed in compression; patients experiencing edema and venous ulcers who have no symptoms of DVT do not need to be checked for a DVT prior to the start of compression. No. In fact, compression is one of the treatments for DVT in many countries. These patients do require arterial screening. Myth: Patients experiencing venous insufficiency and/or venous ulcers should be treated primarily with leg elevation. No. The majority of these patients are overweight. Overweight patients living with venous ulcers and edema should be in adequate compression and ambulating, not sitting at home in the recliner.”

— Caroline E. Fife, MD, FAAFP, CWS, FUHM, chief medical officer, Intellicure Inc., The Woodlands, TX; executive director, U.S. Wound Registry; medical director, St. Luke’s Wound Clinic, The Woodlands, TX; co-chair, Alliance of Wound Care Stakeholders; clinical editor of TWC.

“Wound care providers are often cautioned not to be too aggressive with the chronic wound bed because it’s ‘like a garden that should be nurtured.’ This has led to sayings such as, ‘Never put anything in the wound that you wouldn’t put in your eye.’ These admonitions are based on the underlying concept that, on the chronic wound bed, host-healing mechanisms, such as angiogenesis, contraction, and extracellular matrix deposition, are taking place and should not be disturbed. 

But what if the chronic wound is caused by microorganisms? That is, what if a chronic wound is just a chronic infection? If this is the case, then the fundamental difference between a chronic wound and an acute wound that heals normally is the wound microbiota. Therefore, eradicating the wound microbiota would turn a chronic wound into an acute wound. The ‘Holy Grail’ of wound care is to transform the stalled chronic wound into an acute healing wound. But nobody really believes it’s possible to change a chronic wound into an acute wound because it’s impossible to cure diabetes, completely offload, or fix the many other host impairments that cause chronic wounds. But if biofilm is the primary universal cause, then this transformation is not only possible, it’s desirable. The wound microbiota employs many different strategies and countermeasures to maintain the niche, which is the chronic wound. The host defenses then mount countermeasures against the microbial invaders. So, at a microscopic and molecular level, it’s clear the processes taking place on the surface of the wound are much more like a warzone than a garden. If in our imaginations we go down to the wound bed and look around, what we will see is pure carnage. On the host side, there are fragments of collagen and other structural proteins; fragments of immune cells such as macrophages, neutrophils, and mast cells; and a large numbers of host inflammatory molecules devastating the wound bed in an unregulated fashion. On the microbiota side, the microorganisms are secreting potentially thousands of different molecules to commandeer and subvert host immunity and host healing mechanisms. Molecules such as ospC3, exoU, and ESP are injected or diffused in the wound bed to directly prevent healing. Looking at the wound bed at this subcellular level, the observer sees a very chaotic war. Host molecules are producing friendly-fire damage to host structural proteins, cytokines, and even cellular damage (devitalized tissue). The inflammatory milieu is 1,000-10,000 times normal physiologic levels for tissue injury. And, most importantly, the host cells in the diffusion area of the chronic wound bed are senescent, totally unable to function normally, and unable to defend themselves. This dysfunctional conglomeration of slough, inflammation microbes, and senescent host cells require removal, not nurturing. Chronic wounds that are referred to wound care providers at a macroscopic level have many common attributes. The most fundamental commonality of chronic wounds is they fail to heal. Wound care providers are taught this is due to host impairment, such as diabetes, poor perfusion, repetitive trauma, and more. However, this is just a partial truth (and a minor truth at that). In animal models, when utilizing animals with severe host impairments, as already mentioned, the control wounds in these animals heal — albeit at a slower rate. But the wounds heal. However, when microbiota is introduced into the experimental wound, then all common features of a chronic wound emerge in the animal model. That is, the experimental animal wound will begin to exudate, accumulate slough, and stall in its healing. It’s the wound microbiota and, fundamentally, microorganisms in biofilm phenotype that produce wound behaviors that providers classify as a ‘chronic wound.’ At a macroscopic level, these wounds show exudate, devitalized tissue, accumulation of slough, edges that are undermined or have cliffs, no significant angiogenesis, no significant wound contraction, odor, friable/sclerotic wound beds, and more. These macroscopic findings observable by any wound care provider are the direct result of the brutal ‘war’ taking place between host and microbe. In the 21st century, it seems reasonable that we should have diagnostic tools that allow us to identify the enemy and assess the ‘weapon systems’ being deployed within the wound bed. Relying on 19th century technology of clinical cultures is inadequate. Therefore, clinical assessment will have to suffice until these tools are fully developed. The management is simple: Tip the balance of power in favor of the host over the wound microbiota. Around the world most wound care is being done on a trial-and-error basis using products and methods that decrease the bioburden or suppress the wound microbiota. A newer methodology is to identify the specific microorganisms present and then provide targeted therapy for the microorganisms specifically identified. Yet, even with weapons such as sharp debridement, energy-transfer methods, biologic debridement, topical antibiotics, and broad-spectrum noncytotoxic biocides, the wound microbiota occasionally prevails. When the chronic wound persists multiple different tools have been utilized to ‘ablate’ the wound bed. Debridement taking wide margins, using silver nitrate, painting with betadine, applying full-strength phenol, and other methods have been used to reset the wound bed. Yet, these methods are crude and indiscriminate, therefore leaving behind significant damage to host tissue that quickly becomes reinfected. The nuclear option has become a viable option by utilizing laser technologies to precisely remove a thin layer of the host and microbe battlefield while leaving a clean functional host surface. This effectively converts the chronic wound into an acute wound. Only when the signs of chronic infection are no more and granulation tissue emerges can the wound care provider nurture the wound.”

— Randall Wolcott, MD, CWS, founder, Southwest Regional Wound Care Center, Lubbock, TX.

“Myth: Offloading a sacral ulcer with a ‘donut.’ Often, a patient will present with a sacral pressure ulcer and is frustrated that it’s not getting better (or that it may be actually worsening). Patients often attest they are being compliant with offloading the pressure and keeping the dressing clean. When asked how they are keeping the pressure off when sitting, they’re likely to say they’re sitting on a donut cushion and that they take it with them wherever they go. A donut cushion, while removing the direct pressure, does not evenly distribute the pressure and can create an ‘edge effect,’ essentially strangulating the wound and starving the skin from oxygen. In the seated position, the surface area is much less than a recumbent patient and all the pressure is concentrated in the ischial areas, which is where most donut-type devices apply the most pressure. A seating cushion should adequately and evenly redistribute pressure over the largest area possible. A referral to a seating clinic may be appropriate in certain instances.

Myth: Giving antibiotics for chronic hemosiderosis. Often, I will be called by the emergency department physician telling me a patient is being admitted with bilateral lower extremity cellulitis. Both legs are reported red, painful, and swollen, but there is no fever or leukocytosis. There may be some clear, serous drainage, but no purulence. The patient has a history of venous insufficiency and lower extremity edema, but recently the edema has worsened. This very typical patient does not have bilateral lower extremity cellulitis (which is very rare and anatomically unusual), but rather acute chronic hemosiderosis.² The acute or worsening edema causes the veins to become ‘weepy,’ allowing the red blood cells to leak out into the soft tissue and ‘staining’ the skin. By reducing the swelling, the redness fades (but may not go away completely). Bacteria are getting more resistant to antibiotics and indiscriminant use promotes more resistance. In addition, the side-effect profile and complications of antibiotics (Clostridium difficile, renal impairment, etc.) can actually do more harm to the patient.”

— Andrew J. Applewhite, MD, CWSP, medical director, comprehensive wound care center, Baylor University Medical Center, Dallas, TX.

“Myth: Despite the misconception by patients and some clinicians, leaving a wound open to the air to ‘scab over’ does not promote healing. Clinical studies have shown keeping the wound moist leads to improved healing. The scab is a barrier to healing, preventing the generation of new tissue required for wound closure. The presence of the scab or eschar prevents the regenerative wound healing process. When treated by a wound care specialist, this layer of eschar or ‘dead’ cells is removed to create a clean moist wound bed, allowing the tissue regenerative process. While the uninformed clinician or lay person may say the scab stops the bleeding or the wound area looks smaller each time they ‘pick away,’ it’s likely the wound took longer to heal than it would have with appropriately applied wound care. Also, the chance of scarring is increased. There are internal medicine physicians who treat patients using the ‘let it scab over’ approach. They are reluctant to pass the patient to a wound care specialist short of suspecting necrotizing fasciitis. Myth-busting by clinicians to aid patient management of wounds in support of accurate clinical oversight may be helpful. I recently noticed a patient with a large, open wound on the forearm about four weeks in duration from the original injury (> 30 cm wide). The patient was getting into a public pool with no covering and thought that letting it air-dry in the sun and swimming in the pool would help the wound. After asking a few questions I realized it had grown in diameter from the original injury and it did have a foul odor. Information on this topic to aid patient instruction or to be provided in public forums may be helpful.”

— Leah Amir, MS, MHA, chief executive officer, VantageLinks LLC, St. Louis, MO, executive director, Vantage View Institute for Quality Resource Management, St. Louis, MO.

“Myth: It’s best to pop a blister on the skin. Strictly speaking, for injuries that cause enough disruption to the tissues below the skin surface that allows fluid to collect under the skin without actually breaking the skin open, it’s safe to leave the intact blister alone. These are nature’s perfect bandages. I’ll explain to patients that what will happen, all things being equal and assuming there are no complications with the wound, their body will begin ‘growing’ new skin below the blister after about one week. However, if the blister begins to drain on its own and the wound bed is still clean, the surface of the blister should be kept intact. It’s ok to cover it with a Vaseline-impregnated gauze. If the blister has been disrupted to the extent that it could get ripped off and cause further injury, patients should carefully snip the attached edge off completely and keep the fresh wound bed, which may be immature skin, covered with an emollient such as Vaseline or antibiotic ointment. If, however, the blister contains a cloudy or bloody fluid, evaluation by a medical provider who then can refer them to the wound clinic should be suggested.

Myth: Smoking doesn’t cause delayed healing. There are several reasons that smoking is bad for overall health, but, in respect to wound healing, it’s well known that nicotine and other chemicals in tobacco smoke cause even the smallest of arteries to constrict to the point that no oxygen carrying blood can reach the tissue. This same constriction also slows the rate that the body gets rid of toxins that are carried away from wounds and eliminated. For patients living with diabetes and/or a lower extremity wound, this education is extremely important.

Myth: ‘I can order something in the mail to treat my wound without going to the doctor first.’ Believe me, many patients are ordering ‘remedies’ through the mail without seeking a healthcare professional’s input first. And they’re not getting the outcomes they expect or hope for. I’ve had patients who have ordered plastic braces for their toes that have caused injuries and wounds that almost required amputation. Educate your patients on what should and shouldn’t be ordered online or over the phone as well as from whom they order products.”

— Harriet Jones, MD, hospitalist, Merit Health Rankin, Brandon, MS.

References

1. Donaldson IML. 2004. Ambroise Paré’s accounts of new methods for treating gunshot wounds and burns. JLL Bulletin: Commentaries on the history of treatment evaluation. Accessed online: www.jameslindlibrary.org/articles/ambroise-pares-accounts-of-new-methods-for-treating-gunshot-wounds-and-burns
2. Weng QY, Raff AB, Cohen JM, et al. Costs and consequences associated with misdiagnosed lower extremity cellulitis. JAMA Dermatol. 2016. doi: 10.1001/jamadermatol.2016.3816. [Epub ahead of print]