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Differentiating Infected From Non Infected Wounds - How & Why - Part 1 - Diagnosis

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Warren S Joseph
Warren S Joseph, DPM, FIDSA
Roxborough Memorial Hospital
Philadelphia, PA
Editor - Journal of the APMA
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Lecture Transcription

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Hello, my name is Warren Joseph, I’m a podiatrist and infectious disease specialist from Philadelphia, currently working at Roxborough Memorial Hospital in Philadelphia and at Veterans Affairs Medical Center in Coatesville, Pennsylvania. The lecture I’m going to give is titled Differentiating Infected from Non-Infected Wounds - How and Why? This lecture will actually be broken into two parts, in the first part, I will discuss the diagnosis of infection, the so-called wound infection continuum, quite a bit about critical colonization which is to my thinking the pivotal phase in the wound infection continuum. And then discuss biofilms and culturing of wounds. What I’m hoping to do is give you some evidence basis on which to make some decisions in whether or not a wound is infected or not.


Production of this present lecture was made possible by a generous grant from PuriCore, developers of the exciting and new wound care technology; vashe wound therapy, the powerful nature of wound therapy.


In 2004 the Infectious Diseases Society of America Diabetic Foot infection and Guideline Committee, published this classification system for diabetic foot wounds. Basically what we did is we look at the wound and said it is infected or not infected? If it is infected, how badly is it infected? And once we know how badly it is infected, what organism is causing the infection and what antibiotic do you need to treat it. In this classification system, we broke wounds down into four different categories. The first were non-infected wounds, in other words these were wounds lacking purulence or any manifestation of inflammation. We take a pretty strong viewpoint on this. These are evidence-based guidelines and the point is made that we diagnose wound infection by clinical signs and symptoms of wound infection, if those signs and symptoms are lacking, then we assume there is no infection. A mildly infected diabetic foot ulceration or basically a locally infected ulcer must present with signs of either purulence or two manifestations of inflammation. So you’ve been looking for redness, heat, swelling, the classic sign of [___]. In moderate diabetic foot infection can be considered one of this either foot or limb fragment. In this moderate infection we have a patient who is systemically well and metabolically stable but has greater than equal to one of the following. They have that cellulites extending more than 2 centimeters, streaking, deep soft tissue abscess, bone infection, gangrene, any number of those signs of a spreading infection. And finally are severe or life-threatening infections, actually presents with the same clinical signs in the foot as the moderate infection. In other words, the patient has cellulitis extending more than two centimeters, lymphangitic streaking, everything you see above. The differences in a severe infection, the patient is systemically unwell and metabolically unstable, so these are the sicker patients, which make these life-threatening infections. In 2007 this classification system was actually validating independently by Larry Lavery publishing in clinical infectious diseases, were he applied the ideas classification to over 1600 patients with diabetic foot ulcerations and as you would expect, as the severity from when non-infected to mild to moderate, there were is a significant in increase in rate of hospitalization and amputation. And it’s very gratifying having been one of the authors of this classification to see that it’s widely been accepted now and almost any paper that has been published in the last three four years that looks at diabetic foot infection actually is using the ideas say classification. Now early on this slide, I mentioned that it was first published in 2004 so this is getting a little bit old. The new guidelines hopefully will be out in early 2010 and we’ve already work on completing them. I will tell you however that this classification system is not going to change, we have other updates on antibiotic usage, osteomyelitis, and infected wounds versus non-infected wounds but the classification system itself is going to stay the same. The bottom line on this slide is we make the diagnosis of infection based on clinical signs and symptoms of infection.


I mentioned in the previous slide that we diagnosed infection by looking for the clinical signs and symptoms of infection in particular the signs of inflammation. However, a lot of people feel that those signs maybe somewhat altered in the diabetic state, for example, if the patient is ischemic, they may not get inflammatory response and you would expect they would have red hot swollen foot, and neuropathic patients won’t have pain. However, I’m not one of these people who believes that everybody with the diabetic foot infection does not show signs of infection. It just doesn’t pan up. I’ve seen many patients with severely uncontrolled diabetes who present with massive diabetic wound infections with all the classic signs and symptoms of infection. So although I do agree that there might be some alteration in the signs and symptoms, I still feel that most of them are present, most of this sign of inflammation are going to be present regardless of the fact that the patient has diabetes or not. A couple of the other signs that we could look for an infection other than just those classic inflammatory markers includes perhaps delayed wound healing. If you’ve got patients whose wounds not healing who has good circulation and you know is being off loaded maybe infection is delaying that wound healing. I will tell you though in the vast majority of times, I think if you have a wound, let’s say in the plantar aspect of the foot, you think you’re offloading it properly, that patient may still not be offloaded especially if you’re using some sort of removable device and that’s been shown by Armstrong and others that you know as soon as the patient gets home basically, they stop using whatever offloading device you gave them. So always go back to the offloading first, however, if you know that the patients offloaded during an instant total contact cast something along those lines or straight total contact cast maybe considering infection as one of the causes for the delayed wound healing. You also see changes in granulation tissue instead of the usual reddish beefy tissue, the granulation tissue maybe pale, it maybe very friable with a tendency to hemorrhage when just slightly touched or debrided or curetted and you might have the edema present in the granulation tissue that you wouldn’t find in otherwise healthy granulation tissue and then we have also the microbiological diagnosis of infection which we will talk about in a bit more detail.


Especially in the wound literature and in the nursing literature, you hear a lot about the so called wound infection continuum, and you may not know it by that particular name but I think you understand it or recognized it when I start talking about each individual part of that continuum. And we’re gonna go into some of these in quite a bit more detail. But basically what the wound infection continuum says is that the wound goes through varying states of bacterial presence. The most basic and the earliest being so-called bacterial contamination and these are cases where there’s no replication of the bacteria, there are just a couple of bacteria sitting around on the wound. This is normal but relatively short-lived state. The next state is so-called colonization, now with colonization, you not only have the bacteria sitting around on the wound but they’re actually replicating. They’re producing, they’re growing but they’re not causing any damage to the wound itself and this tends to be normal state that you see in clinically non infected wounds. The pivotal stage is what’s known as critical colonization and because it’s so pivotal, I think we’re going to go into this in quite a bit more detail. What the whole concept of the critical colonization is that you have bacteria on the wound, the bacteria are replicating and they are causing damage to the wound but they’re not causing enough damage to actually demonstrate the clinical signs and symptoms of infection so this is considered an abnormal state but we really don’t know when it’s going on. And the final stage of the wound infection continuum is frank clinical infection, and this is a situation were you have replication of the bacteria, the bacteria are causing damage and the damage is getting to the point that the host needs to respond, so it sends in to white blood cells and because it sends to the white blood cells, you get the inflammatory response, you get redness, heat, swelling and you get pus. This of course is also an abnormal state.


This slide graphically demonstrates the wound infection continuum, what you see is all the way to the left contamination where the bacteria are present but not replicating and not causing any damage, and next to that is colonization where the bacteria are present,. They are replicating but they’re still not causing any damage and this of course is the most normal state you see on wounds. Then the so called critical colonization where the bacteria is replicating and possibly causing some local damage but not enough to get the host response. And finally, the infection state where the bacteria is not only replicating and causing damage but the host is actually responding to it and you get the classic clinical sign and symptoms of infection. Some people say that the difference between colonization and critical colonization occurs at a specific number of organisms and the off quoted number is 10 to the 5th colony forming units, I’m going to show you that’s really not based in any science and probably not a good marker.


I wanna spend sometime talking about the critical colonization phase because in the wound infection continuum this is really the pivotal phase where the wound can go in any number of different directions. And once again critical colonization is defined as where the bacteria are replicating and possibly causing damage but without any sort of overt host response. So when you have a critically colonized wound, the common thinking is as well the wound can go one of three ways: 1) that wound can deteriorate into the clinical infection so in words it will shift to the right on that graphic slide; 2) the wound can remain in that critically colonized state and just not go one way or the other just continue bacteria, continued local response but nothing more than that; or 3) with proper intervention, perhaps the wound can revert back to the so-called normal or colonized state.


Although this term critical colonization has been generally accepted in the wound world, I’d like to point out that most of the recommendations when you’re looking at critical colonization are based on low level of evidence. So this is more hypothetical than really factual and really proven science. The critical colonization is not always associated with those overt signs of infection, in fact almost by definition, but what you may see and these are the signs and symptoms that you will look for in critical colonization includes failure of wound healing, poor quality granulation tissue, I spoke earlier about that pale friable tissue, increased wound friability the granulation tissue just plaques apart and possibly bleeds very easily with just the lightest touch, increase wound drainage, and I don’t necessarily mean purulence here, this could be just serous drainage where the patients constantly having to change the dressing or complains when they come to see you that no matter how often they change the dressing, the wound just is soak, the dressing is soaked and sometimes leaking. These are all possible signs of that critical colonization. The diagnosis of chronic wound infection is based on clinical signs of inflammation I talked about before, but also some of these local wound signs and symptoms. But again this is not based on more evidence or more particularly high level of evidence and I’d like this quoted more research into assessment and treatment of skin ulcer infection is necessary. We really need to understand it. Is it just the inflammatory signs and symptoms which the idea say tends to point to or are there some of these other more subjective signs specifically looking at the wound that may point to this critical colonization? Basically what’s happening is that there is a chronic inflammatory phase, in other words the cause of the presence of bacteria, the wound is stuck in the inflammatory phase, it doesn’t move on to repair and that’s why you get this failure of wound healing and the increase drainage in granulation tissue and wound friability. So these is all things that need to be really researched in quite a bit more detail so that we can understand exactly what defines wound infection.


I really like this quote from Martin Robson, MD that “health is not a germ-free state,” we tend a think that we always have to kill the bacteria, we always to have attacking them, but really our lives will be pretty miserable without the presence of bacteria. Instead what health is, is a balance between factors that lead to host resistance and the bacteria that are constantly present, it’s almost like a seesaw or some people called it teeter tooter with a bacteria on one side and the host on the other and we need to keep that nice level balance because they need us and we need them. It really is a truly symbiotic relationship. So infection occurs when there’s some sort of impairment in host defenses which allows the bacteria to become more pathogenic than they otherwise would be or when something allows an increase in bacterial inoculum so that the bacteria then overwhelmed the host defenses. But not all bacteria are created equal, some of them are going more virulent than others and of course we are familiar with some of the virulent ones including staph aureus.


When exploring the microbiology of wounds, the first question we have to ask is – is a wound ever sterile? And in fact the only way to sterilize a wound is to heal it, you will always grow back bacteria from a wound. I love one of this great what I called ___ myths that’s out there that in order to delay primary closure of a wound, you need that two or three negative culture, of course that’s never been based to any good literature any good evidence. But think about that, if a wound always has bacteria on it, how are you ever going to get three negative cultures, so we really have to re-think a lot of these myths that are out there that have been perpetuated over the years. Again, really the only way to sterilize a wound is to actually heal it. On top of that, the organisms that you find in the wound tend to changed over time, you might start off with an acute wound primarily with gram-positive organism such as staph aureus and the streptococcus particularly when we are looking at diabetes wound group B streptococcus, but what happens over time, you then get a shift towards more gram negatives if the patients been on a lot of antibiotics, they may develop resistant organisms, if the patients been soaking their foot they may develop water loving organisms such as pseudomonas colonizing that wound. So bacteriology of the wounds is not stable, it is a changing factor, it is always something new going to be there, but again just because the bacteria are there doesn’t necessarily mean they are actually causing clinical infection. Now the presence of bacteria in and of itself really does not seem to inhibit wound healing, this gets back to that quote about health not being a germ free state. In fact if you look at the initial study that is done on vacuum assisted closure, the study actually showed that the bacteria load played no appreciable role whatsoever in wound closure. In fact, the patients that healed that had the vac device on had higher bio-burden, higher bacterial counts than the patients who did not have the vac device and who did not heal. And in another study there was done by Alper, they found that wounds under occlusion healed despite an increased number of bacteria. Now I’m not going back to the ancient philosophy of so called ____ pus, which suggests that, basically pus is good. However, we just don’t always need to be so focused on this need to de-colonize wounds to decrease bio-burden into so called sterilized them, it’s just not going to happen. What maybe more important in whether wound heals or not is which species are present. A lot of these bacteria are notorious colonizers and really not pathogens whereas others tend to be a little bit more virulent. So that really maybe more the issue, which bacteria are present not how many bacteria are present.


One of the hot topics nowadays is the role of bio-films on wounds. You’re gonna read a lot about this in literature, hear about it in lectures, in fact they even pick up a copy I think it’s popular mechanics magazine recently and there was a whole article on the role of bio-films in wounds. So what exactly are these? Well some bacterial species produce a glycocalyx, now this is a combination of bacteria and polysaccharides that literally form a film over the wound. And this inhibit antibiotic penetration, the bacteria basically are nice and comfortable sitting in this matrix where the bacteria can penetrate. Staph aureus and pseudomonas aeruginosa are the most organisms that are known the cause these bio-films and within them the bacteria become quiescent, they just kind of lie I weight, there is no stress on them because they know that the antibiotics can’t get to them either systemically or applied topically because they are encased within this film. So the organisms actually almost become more antibiotic resistant because they can’t be touched by the usual drugs that would be used either systemically or topically. But with also come out of the study of bio-films is this whole concept is what’s known as quorum sensing. And what quorum sensing is that bacteria are actually capable of communicating, they can send up chemical signals and talk to each other within these bio-films. They can say, okay it’s time to become more aggressive, we’re getting some antibiotics through here or it’s time to eat, let’s destroy more tissue, so the bacteria are able to send this signals between their colonies that are encased in the bio-films, telling them almost instructing them on when to become more pathogenic or when to become more quiescent. And again this is an area that you’re going to be read about in a whole concept of quorum sensing is relatively recent. And the bio-films finally may prevent wounds from healing and basically what they do is they stick to wound in that state of chronic low-grade infection we talk about a little bit earlier when discussing critical colonization and the wound just has the bacteria present, the bacteria is a listening some minor inflammatory response from the body and the body is just constantly sending out enzymes to try to dissolve and kill the bacteria and dissolve the bio-film but what that does instead is inhibit wound healing. So it’s a fascinating topic that’s really going to get a lot of attention in the next few years. However, right now we still have a lot we don’t know about the role of bio-films in wounds.


So it’s pretty evident that bio-films are not necessarily a good thing to have on a wound. So how do you go about removing them, so I guess question is do we even really need to remove the bio-film and that question hasn’t fully been answered at least to my satisfaction although it’s getting there, I’m guessing it’s probably a good thing to remove bio-film. So how do you do it? Well you can physically do it, you just by using cold steal debridement, taking a blade tool wound, curetting a wound, now this is when the bio-films really evident. You’ve all seen wounds have that kind of ____ finish over them and you can almost take a forceps and pick it up from n edge of wound and literally lift it away. That’s when bio-film really is thick and heavy and it’s pretty easy to determine that you do need to debride it. However, some people feel that bio-films is not always that easy to diagnose, in fact, even wounds look relatively healthy may have some microscopic thickness of bio-film over them. And in those cases that curettage and debridement might not be quite this evident but there are other ways to go about it. Ultrasound, there are number of ultrasound devices now both contact ultrasound with some of this debriding units that are being used and non-contact ultrasound let’s say with them missed unit that are able to at least theoretically break up the bio-film. There are also chemicals that can be used to remove the bio-film and those includes surfactants that dissolve bio-film, enzyme that can dissolve bio-film, and possibly even some of the super oxidized water solutions were we going to talk a lot about. If you are interested in bio-films I direct you to a lot of the work that’s been done by Dr. Randy Wolcott in Lubbock, Texas. In the world of wound healing he seems to be the king of bio-films and he has actually written some very interesting papers on this topic.


So what’s the best way to culture a wound? I think you’ve all heard for many, many years that swab culturing is bad, you just don’t take a culture in and run it lightly over the surface of the wound, that’s just going to get you a lot of junk. That being said, there are techniques that can be done with the swab that actually have been shown to be fairly diagnostic of what’s going on in the wound. Probably the most recommended is the so-called qualitative swab, and what this ism is you first debride and irrigate the wound out and then you take a swab and you run it over the wound, applying pressure as you roll it over he surface. The concept is that you’re not just getting the junk that’s sitting on the surface of the wound rather because the pressure you’re using as you roll the swab over the wound, you’re bringing up fluid, you’re bring up bacteria from deeper in the wound to get an idea what might be going on deeper inside and not just sitting on the surface. There’s also a technique that’s known as the semi-quantitative swab, and this is where the swab is actually rolled over defined area of the prepared bed, so again, the bed is prepared first, you need to debrided, you need to irrigate it before you consider using any of this swabbing techniques. And the final swab technique is what’s known as a quantitative swab, it’s also known as Levine technique. And there’s quite a bit that’s actually been written about this, primarily in the wound literature and the nursing literature. The swab is rolled over a specifically defined area 1 square centimeter area and then that swab is agitated in 1 mL of transport media and then serially diluted in order to get actual colony counts. But I’m not solved that the colony counts are all that important, we’ll get into that a little bit. And that brings up the whole issue of quantitative biopsy, in other words doing this culture biopsy looking for 10 to the 5th or 10 to the 6th organisms and for years you’ve heard that that is the gold standard. Well, I really have to ask the question, is it really?


So in conclusion to part 1, I think it’s important to stress that not all wounds are infected. You can always grow bacteria from a wound but it doesn’t necessarily mean that, that bacteria is of any clinical importance. And that bring up the second point that infection is a clinical diagnosis, which needs to be made clinically. You base the diagnosis of infection not on whether you can grow back bacteria from a wound or not but rather you base it on what you see on the wound and your clinical judgment.


Production of this present lecture was made possible by a generous grant from PuriCore, developers of the exciting and new wound care technology, vashe wound therapy. The powerful nature of wound therapy.

This lecture by Dr. Warren Joseph explores the differences between infected and non infected wounds. The lecture focuses on diagnosis which includes how to differentiate infected from non infected wounds, the evidence behind the "wound infection continuum", when to culture a chronic wound and the role of biofilms and quorum sensing by bacteria. By the completion of the lecture the listener should have an improved understanding of how a wound is diagnosed as infected.
Goals and Objectives
After participating in this activity, the viewer should be better able to:
1. Distinguish between the clinical findings of an infected vs. non infected wound.
2. Distinguish the Wound Infection Continuum and the evidence behind it
3. Differentiate between the various topical antimicrobial dressings and solutions both on the market and under current research
4. Analyze when and how to appropriately culture a wound

Estimated time to complete this activity is 37 minutes.
Target Audience
Physicians, diabetes educators, and other health care professionals who treat patients with diabetes.
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Differentiating Infected From Non Infected Wounds - How & Why - Part 1 - Diagnosis
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Differentiating Infected From Non Infected Wounds - How & Why - Part 1 - Diagnosis
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Disclosure Information
Differentiating Infected From Non Infected Wounds - How & Why - Part 1 - Diagnosis
It is the policy of PRESENT e-Learning Systems and it's accreditors to insure balance, independence, objectivity and scientific rigor in all individually sponsored or jointly sponsored educational programs. All faculty participating in any PRESENT e-Learning Systems programs are expected to disclose to the program audience any real or apparent conflict(s) of interest that may have a direct bearing on the subject matter of the continuing education program. This pertains to relationships with pharmaceutical companies, biomedical device manufacturers, or other corporations whose products or services are related to the subject matter of the presentation topic. The intent of this policy is not to prevent a speaker with a potential conflict of interest from making a presentation. It is merely intended that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts.
Warren S Joseph, DPM, FIDSA Warren S. Joseph, DPM, FIDSA has disclosed that he receives Honorarium/Expenses, is a Consultant to and serves on the Speaker's Bureau for Pfizer and Merck.
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Promotional Offers: Sometimes we send offers to selected groups of customers on behalf of other businesses. When we do this, we do not give that business your name and address. We provide a variety of mechanisms for you to tell us you do not want to receive such promotional offers. For example, we may provide an opt-in box for consumers to receive an email from another business, and we make clear that by opting in you are submitting your data to a third party.

Protection of Information

In this section of our Privacy Policy, we discuss the security measures we take to protect information that we have collected about you.

We have implemented technology and security policies, rules and other measures to protect the personal data that we have under our control from unauthorized access, improper use, alteration, unlawful or accidental destruction, and accidental loss. We also protect your information by requiring that all our employees and others who have access to or are associated with the processing of your data respect your confidentiality. We use security methods to determine the identity of its registered users, so that appropriate rights and restrictions can be enforced for that user. Reliable verification of user identity is called authentication. We use both passwords and usernames, as well as double opt-n verification, to authenticate users. Users are responsible for maintaining their own passwords.

Access to Information and Choices

In this section of our Privacy Policy, we tell you how to obtain and correct information we have about you, and how to choose what types of information you may share with us.

Correction of Information We Have About You

If you believe that registration information collected by our Web site(s) is in error, you may edit your personal profile any time that you like. You can directly edit most of your user profile on the Web site on which you initially registered. Information that you can not edit may only be changed by contacting Web Customer Support (see CONTACTS). Requests for deletion of your record may result in your removal from the registry, but we may keep certain demographic information about you for product improvement purposes. You may contact Web Customer Support and ask for the changes that you would like to make.

Our Employees

Our employees are required to keep customer information private, as a condition of their employment with the company. Only selected, authorized employees are permitted to access personal information. Our employees with access to personally identifiable information are required to attend a confidentiality/privacy training class, and to sign a confidentiality agreement. All employees and contractors must abide by our Privacy Policy, and those who violate that policy are subject to disciplinary action, up to and including termination of their employment and legal action.
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