The Intersection of Wound Care, Bacteria, and Shakespeare – Healing, Treatment, and Insight
by Michael Miller DO, FACOS, FAPWCA
RAMBLINGS OF AN ITINERANT WOUND CARE GUY PT. 2
I recently recognized a puzzling aspect of my wound care practice; I am just not seeing that many infected wounds. Moreover, I seem to use much fewer antibiotics and antimicrobial agents than almost everybody else I know practicing in wound care.
I have come to the conclusion that there must be a dearth of bacteria in my clinics, nursing homes, and at the house calls I make. At the risk of sounding delusional and daft, allow me to rephrase: I know that there are bacteria everywhere, and on everything, and in fact, I overheard a statement that may truly capture the spirit, “the Earth is covered with poo, it’s just thicker in some places than others.”
I am an avid reader of journals, and am privileged to review for several, both in the US and overseas. I believe we can safely assume that I am (at least in part) seeing the fruits of the most creative minds and their experiences referable to the topics of infection and bacteria (of course, I would be remiss not to include the new kids on the block of bioburden and biofilm…can you say “planktonic” real fast, three times?) I should have, at the very least, a prehistoric understanding of what makes a wound infected, when is a wound infected, how to identify wound infection, and of course, how to treat wound infections.
Due to space constraints and the potential for sheer boredom, I will not reiterate the missives regarding misuse and overuse of antibiotics, such as that from groups like the National ENT organizations - who found that over 90 percent of sinus infections were viral, and thus unresponsive to knee-jerk antibiotics - or that the People’s Republic of China outlawed the overprescribing of antibiotics with very stiff penalties for doing so, or that the FDA has commenced careful oversight of antibiotic use in US livestock.
Our patients play a key role in our folly. I have heard, “Make sure you give me a STRONG ANTIBIOTIC for this”, as if given the choice, we might consider prescribing a “weak” one. Another is the infamous, “Can you give me an antibiotic so I don’t get an infection?” My response is that with literally thousands of bacteria, which one would they like to prevent infection from? Of course, patients are not health care professionals, so the advice they got from their cousin who almost completed paramedic school until he got into the Tool and Die Union should be forgiven.
The overwhelming majority of my patients come to me after seeing at least three, and occasionally more, health care practitioners. Many of these patients have been on at least three antibiotic regimens before seeing me. To avoid confusion, I am talking about oral or intravenous regimens. In addition, the vast majority of those who I see have all too often had their wounds buttered, slathered, or otherwise covered in topical antimicrobial creams and ointments. Equally interesting to me is the varied and confounding dressing combinations using topical antimicrobials. I have seen scads of the infamous Santyl and Polysporin (does anybody really know where this combination came from and why?) Topical Gentamycin is a local favorite -- slimy and green, always got to be Pseudomonas, or the more mystifying, “I can always smell when it’s Pseudomonas” -- in combination with hydrogels, Panafil (may it Rest in Peace), calcium alginates, collagens, or alternating daily with the wound care product du jour. It is easy to assume that our colleagues (both wound care and not) do this because either they truly believe all chronic wounds are infected, or are prone to getting infected, or so nipping the bug in the bud would prevent an infection. If not, at least the lawyers can’t say they did not try to treat it. Of course, the patients get bragging rights by being able to say that their doctor had to use lots of ”strong” antibiotics and still could not cure the infection or heal the wound.
My point is that with numerous experts on bioburden, biofilm (such as Dr. Chris Morrison and his truly remarkable work, in addition to others in the field), critical colonization (I can never remember which one is the NERD and which is the STONE), contamination, and the pervasive increase in antibiotic prescribing for chronic wounds, then why are the wounds I see never infected, otherwise, why are they healing without antibiotics of any kind? Did those previous courses of oral and intravenous antibiotics truly sterilize the wound so that timing-wise, I am seeing a pristine (sterile) wound ready to heal, thanks to the hard work others? Did the use of topical antibiotics invade the biofilm and convert the sessile bacteria to the planktonic (there’s that word again) state, resulting in greater susceptibility? Does my own body have some inherent antimicrobial effect?
I will readily agree that diabetic foot wounds have a propensity to get infected, and with the assistance of my trusty podiatric friend Dr. Kevin Powers, the combination of an extraordinarily performed debriding and limb salvaging surgery, with placement of those wonderful antibiotic beads, and humbly effective wound care performed by myself, we heal a lot of wounds and save a lot of legs. Without doubt, a bedsore with newly exposed bone has osteomyelitis and needs aggressive treatment and antibiotics, no argument there. But where the rubber meets the road is what seems to be a gallimaufry (thank you, Readers Digest) of opinions as to the difference between beneficial inflammation and detrimental infection.
Case in point:
In simplest terms, sunburn is the result of solar radiation injuring the skin, whereby it becomes red, hot, swollen, and tender. No one would question the presence of inflammation and therefore, defer on use of antibiotics. Even with the expectation that it would get worse before it got better, our treatment scenario would still not change. Likely, it would be some form of gently applied burn cream and oral NSAIDs. Even in the event that it subsequently blistered and developed open wounds, it is safe to say that we would give sympathy before antibiotics. And yet, when a chronic, open wound develops the same presentation, the vast majority of clinicians seem to become mesmerized, with their first act to be reaching for the prescription pad or the sample closet door. Of course, for far too many clinicians, the presence of odor and drainage clinches the deal because these signs have become almost universally pathognomonic for infection – or have they?
To digress and review, inflammation causes edema, which is a proteinaceous fluid in the tissues. If there is a defect in the skin, this edema fluid drains out. Recognizing that organic tissues, including this edema fluid, need a blood supply to survive, ergo, the loss of blood supply results in death. When tissues die, the ever-present bacteria (remember, thicker in some places than others) proceed to break this down, which is a medical term called “putrefaction” (in the non-medical world, they call it “rotting”). The obvious question then becomes how many of you give antibiotics to corpses? And so, the odor and drainage answer becomes little more than a punchline to an uneducated and misinformed joke.
The rationale for the use of a surface swab as a tool for diagnoses continues to elude me. Yes, I have read the percentages of identification of bacteria using the “Z” track, the “W” track, and the compression elution techniques, but let’s be realistic: using a swab on liquid poo is going to demonstrate well…liquid poo. For my money, I believe that if I am trying to identify infection in a wound, then I am going to the wound itself to find it. A simple, low-risk aspiration biopsy of a gently cleaned wound, or the more invasive and better compensated incisional biopsy provides me a more logical and more realistic assessment of what foreign invaders may inhabit the wound. With the infectious species comfortably and definitively identified, the rest of my workup for a wound infection can resume. This includes lab testing, history, physical examination, and evaluation of all other potential causes of the patient’s presentation before the words “Wound Infection” join the other diagnoses on the face sheet. Only then am I willing to prescribe an appropriate antibiotic.
I would be remiss to remind you that infection is, by definition, a detrimental process. That is to say that its presence should cause the wound and more, the patient, to exhibit signs and symptoms of something bad! For the simple minded like myself, this is actually an elegantly simple conundrum to resolve. Since infection causes bad things only, then if the wound is getting better (smaller, more granulation tissue, less depth, etc.), regardless of any other findings, observations, beliefs, concerns, etc., then it cannot be infected. If you remember that our goal is to promote healing of the wound, then if the wound is improving, we are doing the right stuff to and for it. The haphazard initiation of antibiotics “just in case” or use of topical antibiotics to “prevent infection and promote healing” is counter intuitive. If the wound was at a given state when it became “infected,” then using antibiotics only resolves the “infection” but in actuality, does not improve the status of that wound from when it first became “infected.” Hence, it is at the same status as it was when it became “infected” and thus, is at the same risk due the actual lack of improvement (save for maybe reducing the number of bacteria there temporarily). If our actions were dedicated to improving the wound instead of simply resolving an “infection,” then as the wound becomes healthier, it also becomes less susceptible to “infection.” The point is, why are we spending time, money, and energy chasing something that is not affecting wound healing, and arguably only rarely exists, when our efforts should realistically be directed at wound healing which is, of course, the ultimate goal?
To conclude this month’s edition of Ramblings of an Itinerant Wound Care Guy, it is not so much the recognition that infections may occur in open wounds, more so in acute than chronic, but that our goal should always be to promote wound healing. As specialists in the art of healing wounds, we must use our expertise to identify and then treat appropriately those things that truly mitigate wound healing. The treatment of the low hanging, all too often pseudo-present fruit of infection provides little benefit, but considerable risks and costs across a plethora of categories. For my money, the dedication of even one iota of time, energy, and effort to try to identify or treat something that is often nebulous at best seems tragic. Identifying a wound infection should not require a process so complex and subjective that it makes CSI look like a brownie troop making S’mores. In almost all cases, the presence of true, detrimental infection in a wound makes itself known with a lions roar, not as the result of a prolonged discussion as to the findings of a swab culture and subjective observation of decreased granulation tissue redness. Are there chronic wound infections? As William Shakespeare wrote, it may simply be much ado about nothing.
About The Author
Michael Miller DO, FACOS, FAPWCA is the Founder and Medical Director of The Wound Healing Centers of Indiana and IndyLymphedema, as well as a clinical consultant, teacher, inventor, and published author.
The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, Kestrel Health Information, Inc., its affiliates, or subsidiary companies.
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