This text base course is a transcript of the live event titled "Wound Care Basic Concepts and Treatment" by Dr. Jennifer Gardner, PT, DPT, MHA, CWS. It is strongly recommended to follow along with course handout to ensure understanding of the course material.
>> Jennifer Gardner: Welcome to this presentation entitled “Wound Care Basic Concepts and Treatment.” A typical question I often hear when I tell people that I do wound care is, “Since when do PTs do wound care?” Typically it is considered a nursing function and not a physical therapy function. However it you look at our practice patterns you will see that wound care or integumentary is actually one of our four practice patterns and it is an emerging area of PT practice. In addition, the wound care special interest group of the section on clinical electrophysiology and wound management is currently working with the APTA to develop a wound care certification like those currently available for Neurology, Orthopedics, Pediatrics, etc. Right now there is no certification through the APTA so if a PT wants to become certified, they have to explore another company to get that certification. My certification is through the American Academy of Wound Management, but hopefully we will be getting the one through APTA in the near future. For those of you on the line, many of you might not choose to pursue wound care as your primary focus in physical therapy, but it is important to have a basic understanding. In an outpatient setting, you may have an orthopedic patient who comes in with a non-healing knee replacement incision; or in a rehab or acute setting, you may be treating patients with pressure ulcers. So it is good to have an understanding of what is going on, and what you can do to help that wound heal. This webinar will serve as an introduction to basic concepts in wound healing as well as some treatment options.
Our objectives for today are to: List phases of normal wound healing, identify arterial, venous, diabetic and pressure ulcers based on clinical presentation, differentiate between various dressing types and understand when to use them, list treatment options and the goals of each, identify when a wound is atypical and how to address those atypical wounds, and then identify when a patient may need to be referred to an outside specialist.
I will apologize in advance that I did not include a slide on assessment of wounds, but if you have any questions afterwards, I will be happy to address them or you can have my email address and we can correspond via email. But assessing a wound is a lot like assessing a patient for any physical therapy problem. You want to assess the whole patient, not just the wound. But when looking specifically at the wound, you want to measure it, just like you measure a shoulder for range, you would measure a wound to determine the length, the width, and the depth. If you look at a wound as the face of a clock, length would be from 12 to 6, width 3 to 9, and then the depth would be how deep a Q-Tip or cotton applicator would go into the wound. Based on these measurements, you can get the volume of the wound, or if you just take the length times the width, you will get the square centimeters. Other things you need to assess in a wound include the drainage, if there is any odor, the presence of the different tissue types which we will discuss in a little bit, does the patient have pain, what have they used in the past that has worked or not worked, and then perhaps any tests that they might have had that can help you narrow down what type of wound you are dealing with.
Now we will go back to the slides. The type of wound healing that we are going to be discussing is considered full thickness or secondary intention healing. Primary intention healing is if a patient goes to the operating room and has surgery, and then the surgeon proceeds to close the patient back up with sutures and staples. That is a primary wound closure. A surgeon might also opt to do tertiary or delayed primary closure where they wait to close the wound. So say a gunshot wound or maybe a pretty significant dog bite, they might go in to debride that wound and clean it up, but then they are going to wait a couple of days to make sure further debridement is not necessary or to make sure that there is no infection before they close it. What we are talking about today though is full thickness or secondary intention healing. This is the most effective form of healing when a wound goes through all layers of skin and/or into underlying tissue. Full thickness wounds heal by formation of granulation tissue and a contraction of the wound edges, and it does heal by scar tissue formation. Because of this, a healed wound is not anatomically the same as normal skin, and will only be 80% as strong. So you need to educate your patient that even though they are now healed, they still will have a tendency to re-ulcerate.
So the wound healing physiology follows a cascade of overlapping events that typically occur in a reasonable predictive fashion, and the cascade is the same whether it is an acute wound or a chronic wound; the difference being the amount of time spent in each phase. Acute wounds tend to go through each phase at a normal pace, while the chronic wound might actually get stuck in one of the phases. There are three phases of wound healing. However some literature says that there are four phases. It is not so much important whether there are three or four, but to know what happens in each phase.
The first phase we will talk about is inflammation and hemostasis. This is the central activity of wound healing. The next phase is proliferation. This is where granulation, re-epithelialization, and wound contraction occur. Then the final phase is maturation. This is where the collagen accumulates, matures, and the tissue remodels. Here is a diagram of the different phases in Figure 1 and you can see the wound healing can occur from anywhere from at the time of the injury all the way through 30 days even up to 100 days, and you can also see by the different curves that the inflammatory phase is still going on while the proliferative phase begins, and proliferation is still occurring while wound contraction and epithelialization occurs. It is important to remember that those phases do have some overlap.
Figure 1. Phases of Tissue Repair
Here is a schematic of the inflammatory phase in Figure 2. The inflammatory phase is the first one to four days after injury. This is the first step in the repair process. The first goal of the inflammatory phase is to stop the bleeding. Then once hemostasis is achieved, then it can move on to the next series of events. There are both vascular and cellular responses to the injury and the inflammatory phase is basically a protective role and is usually beneficial to the person.
Figure 2. Inflammatory Phase
First as I mentioned, vasoconstriction occurs. This is to stop the blood loss. When an insult occurs to the blood vessels, there is an immediate constriction to reduce that blood loss and achieve hemostasis. Then platelets come in and begin to coagulate with thrombin and collagen to form a platelet plug. Then once the hemostasis is achieved, we actually begin to get vasodilatation which is triggered by histamine and it allows wound healing to occur. We will also see increased cell membrane permeability and this increases after the trauma or insult to the tissue, and you will see an influx of fibroblasts, neutrophils early in the phase, macrophages a little bit later on, as well as monocytes and mast cells.
Figure 3 shows a little reminder of what the different indicators of inflammation look like. Local indicators of inflammation include redness, swelling, heat, and pain. Then all four of these contribute to an overall decreased functional ability for the patient. In addition to these local indicators, you might also see systemic indicators such as a fever or leukocytosis or just a general feeling of malaise or not feeling well. So in the inflammatory phase there are two parts. It can be acute, which typically lasts 24 to 48 hours, but it may go up to two weeks; or chronic or subacute phase that lasts an additional two weeks. So here is a picture of what acute inflammation looks like in Figure 4. In acute inflammation as we have already discussed, there is vasodilation and that makes the tissue become warm and red, the capillary permeability increases, so you are going to see exudate flowing into the tissue, you will see more swelling occur, and a blood clot might form to help prevent too much blood loss. Then leukocytosis which is an accumulation of the leukocytes at the injury site, and also here is where the macrophages begin to come into play, and you get phagocytosis of any abnormal cells or any infection that might be present within the wound. Then cellular repair begins.
Figure 3 Indicators of Inflammation
Figure 4 Acute Inflammation
However sometimes the wound will not progress as it should from the inflammatory phase to the proliferative phase, and you come to notice that the patient is in a chronic inflammation stage. This may occur for several different reasons. It may occur from an unresolved acute inflammation. An example of this might be if there is a foreign object still in the wound such as a suture. This can continue to cause an inflammation in the wound and not allow the wound to progress. Chronic inflammation may develop from a microtrauma such as in a pressure ulcer where the pressure is not being relieved, then it will continue to cause trauma to that wound and not allow it to move to the next phase. If there is necrotic tissue that is contaminated with infection or as I mentioned if there is a foreign material present can cause chronic inflammation. Frequently we see patients that have an allergic reaction to the suture material used and the suture material might ordinarily be biodegradable and dissolve in other patients, but in a particular patient that is having chronic inflammation, it might be due to a suture that is not dissolving. Once you remove that suture or foreign material, then the patients wound will heal.
Another thing to remember with chronic inflammation is there are no cardinal signs of infection. So you will not see that heat, you will not see that pain, you will not see the redness so much, but you will notice by other reasons why they are not healing. In the chronic inflammation stage, there will be a higher number of monocytes, lymphocytes, histiocytes and macrophages. Here is an example of a chronically inflamed wound in figure 5. Yes we do see granulation tissue, but it is not a real healthy granulation tissue. I will show you an example of what healthy granulation tissue looks like in a moment, but this is more a chronically inflamed example. The granulation tissue is kind of dusky red. There is some yellow tissue, some yellow necrotic tissue in there. So it is just stuck in that inflammatory phase. Here is another example of when there is necrotic tissue in the wound (see figure 6), the body will continue to mount an inflammatory response to that necrotic tissue and it will never allow it to go into the next phase of healing.
Figure 5 Chronic Inflammation
Figure 6 Necrotic tissue
Here is a schematic of the proliferative phase in figure 7. Proliferation begins around day 5 through 20, and the goal as I mentioned earlier is for granulation tissue formation, formation of new blood vessels and then re-epithelialization. The proliferative phase can begin when the wound is essentially clear of foreign substances. It has to be free from infection (or not enough of an infection to prohibit the proliferation to occur), and when the wound has an infiltrate of the macrophages and fibroblasts forming in the matrix. Macrophages release platelet-derived growth factors. That is what PDGF stands for. Macropages also release fibroblast growth factors. These growth factors then attract fibroblasts. The fibroblasts begin to start making collagen which the collagen is the scaffold for the granulation tissue to grow on, as well as elastin which gives the new tissue elasticity. This leads to the growth of that new connective tissue as well as capillary growth. Sometimes our patients will say how come my wound is still bleeding so much. It is important to remind them that bleeding is normal. Bleeding is good and it is expected because of that new capillary growth and the new blood vessels that are coming into that area.
Figure 7 Proliferative Phase
Fibroplasia is the laying down of the collagen matrix known as granulation tissue. It starts out as type III collagen and then will go to type I. It is undifferentiated tissue. It is not growing back in as muscle. It is not growing back in as tendon. It is growing in as granulation tissue. There is enhanced cell activity that fills in the wound bed and as I mentioned, there is angiogenesis. So it is a building of a vascular network. These new blood vessels will bring in increase oxygen and nutrients, and also help to remove any metabolic waste or any infection that might be in the area. Ideally in the proliferative phase, you will begin to see a decrease in wound size via wound contraction. In the proliferative phase; fibroblasts, myofibroblasts, endothelial cells, and epidermal cells are high. There is a crosslinking of collagen which is formed and I like to explain to patients that collagen is the scaffold that forms the granulation tissue that helps the wound to heal. So when you think of scaffolding used to they are build a building, or when they are cleaning windows, the scaffolding has not only horizontal support, but also vertical support and diagonal support to make that scaffolding very strong. This is the same thing with the cross-linkage of the collagen. It makes it very strong because it has a lot of that cross-linkage.
The new matrix will look like red granules piled on top of each other; hence the name granulation tissue. Granulation tissue as you might expect is highly vascular. It does have that beefy red appearance. It is moist and is very fragile as it is forming and healing, so it does require protection from trauma. Here is an example of what healthy granulation tissue looks like in figure 8. You can see it is a nice beefy red. It has an appearance of granules or little bubbles at the top. That is what you want good healthy granulation tissue to look like.
Figure 8 Granulation Tissue
I mentioned myofibroblasts and these help with wound contraction. Myofibroblasts have the contractile properties of smooth muscle. When the myofibroblasts come in, they connect themselves to the wound’s skin margins and help pull the epidermal layer inward. We will talk about that next. So the clinical presentation as we just looked at is a moist environment, that nice velvety or beefy red granular appearance. You might begin to notice a purplish hue at the edge of the wound bed, which is the migration of the immature epithelial tissue starting to come across the wound bed. You will see a gradual reduction in wound size and you want controlled wound contraction optimally. So if you look in figure 8 we have a little bit of a purplish haze right at edge of the wound bed and and that is epithelialization that is starting to occur.
Clinical considerations: Eschar and slough can occur during this phase and slow the healing process. Eschar and slough are made of dried plasma proteins and dead skin cells. Debridement is necessary to get rid of that dead tissue and promote healing. I will show you some examples of those in future slides. In addition, you want to make sure to control the bacterial load. If for whatever reason the patient gets an infection in that wound, it will definitely slow wound healing. So indicators of an infection include increased drainage, increased pain, foul odor, or just a general feeling of not feeling as well as they usually do. When this occurs, you want to do a wound culture or a wound biopsy to identify the organism, so that the organism can be properly treated so that the infection will go away and allow the wound to heal more quickly.
As I mentioned before, controlled wound contraction is optimal. Sometimes we will see where epithelialization is occurring faster than granulation tissue formation. When this occurs, you might actually get a closed wound, but you are still left with a hole underneath that skin. This is a problem because it sets the patient up for an abscess. If you see in a wound that the epithelialization is occurring faster than the wound is filling in, you want to somehow stop that epithelialization from occurring. This can be done with a silver nitrate to cauterize the edges. You might have a surgeon debride those edges back to a normal wound edge so that the wound can continue to granulate prior to being covered with epithelialization.
As we go into re-epithelialization, this is where the wound is resurfacing and there are changes in the wound edges. As we remember back to the bell shaped curves that I showed you, all these processes are occurring throughout the wound healing, so re-epithelialization actually begins immediately after injury and continues alongside the other phases. The prominent cell that is being active during epithelialization is the keratinocytes. These are the cells that make up the layers of dermis and epidermis as well as line organs and dermal appendages. Dermal appendages are hair follicles and fingernails. The keratinocytes initiate from the epidermal stem cells found in hair follicles and then they migrate from the bulge area of the hair follicle to the basal layer of the epidermis, and then proliferate and differentiate to produce epidermis. This is why if you have heard of more superficial burn wounds, if they are more superficial, they can granulate and epithelialize on their own without a skin graft, but if it goes deeper and there are no longer dermal appendages such as hair follicles in place, then the wound will need a skin graft. That is because without those hair follicles the keratinocytes cannot initiate and proliferate to cover the wound. The epithelial cells migrate from the wound edge and the dermal appendages, and in the next slide I will show you. It is almost like a leap-frog or train fashion, where one cell will migrate and then pull another cell along with it, and so forth until they cover the whole wound. If you have a moist wound environment, this will speed up that process. It is also oxygen dependent. If there is not enough oxygen to the cells, then the epithelialization will not occur as quickly.
As I mentioned in the beginning, partial thickness wounds, scrapes, skin tears, they do not heal by granulation process, but they will heal through this epithelial cell migration. The full thickness and deep wounds will require a base of collagen and granulation tissue first, before the epithelial cells can bridge the gap. The analogy I like to give to patients and to my students is that if you go out and dig a big hole in your front yard, you cannot expect to just throw grass seed out or put a piece of sod down and expect that area to come back to what it was before. First you have to put in dirt and soil to build up the hole, and then you can plant the grass or put down the sod. This is the same thing with wound healing. The wound needs to fill up first with granulation tissue and then it can cover over with epithelialization.
An example of that leap-frogging is shown in figure 9. So one epithelial cell will leap-frog two to three cell lengths and then pull another cell over. There will be cell division by mitosis which we all learned about way back in PT school. There will be that cell division and then those cells will be pulled over in that leap-frogging fashion.
Figure 9. Re-epithelialization
The keratinocytes also help guide the formation of the new blood vessels with growth factors. Macrophages, neutrophils, and a current of injury will stimulate the response of those cells. In chronic wounds, again as mentioned earlier, everything is a little bit delayed so there will be a decrease in the keratinocyte migration, thus causing a delay in the whole process.
I mentioned earlier when dermal appendages are lost, epithelialization can only occur from the wound edges and those dermal appendages again are hair follicles, sebaceous glands, sweat glands, and nails. As the epithelial cells only can advance a few millimeters at a time, sometimes the epithelialization will stop. If a wound is not fully granulated, the cells will go down to the wound base and start to curl under. This causes a ridge around the wound and almost signals to those cells we have met up with some other tissue and we are done. We do not have to keep moving. This is called epiboly. The problem with this is now the body thinks the wound is healed and it will not continue to try to heal that wound. So you will be left with a wound still open, and this is again where you will need to use the chemical cauterization with a sliver nitrate stick or you might have to have a surgeon surgically debride out the wound edges to start back at a healthy wound edge to allow that wound to heel.
Maturation is the final phase. This is once the area has been resurfaced by epithelialization. The collagen matrix continues to mature. It will become thicker. The bundles will become more organized and this will increase tensile strength to the wound. There is a balance in the wound between collagen breakdown and collagen synthesis which helps promote the mature scar. Other things that help in the maturation are something called matrix metalloproteinases or MMPs. These are enzymes that destroy the protein and play a key role in the remodeling phase. However sometimes wounds and tissue will have an overabundance of these MMPs and it will not allow the wound to heal. This is where we might bring in different dressing options to help push back the MMPs so that the wound can go on to heal.
With the scar formation as the wound continues to progress and heal, you will see the scar change from bright red or pink to a gray or white, and the scar will eventually become flatter and more flexible. It is important to realize that this process can go from three weeks to up to two years. So when your patient is healed, the wound is healed, but the skin is not mature and it is not healed. It is important to remind your patients that they still need to protect that area, and they are still prone to breakdown in that area until that wound is fully matured. As I mentioned earlier, new skin is only 70-80% as strong as original skin, and when the wound is first healed, it is only about 15% as strong. You need to protect that area from further trauma until it has a time to more fully mature.
We are going to move into types of wounds now. The four that I am going to spend the most time on are pressure ulcers, neuropathic or diabetic wounds, arterial wounds, and venous wounds. And the ones with the asterisks are the ones that you will most typically see as physical therapists. These are pressure ulcers, diabetic wounds, and venous insufficiency wounds.
When you are talking about how to classify a wound, you go by the depth of tissue injury. Pressure ulcers have a different way of being classified, but all other wounds are classified by the depth of tissue injury. So a superficial wound affects only the epidermis. It is like a stage I in pressure ulcer classification. This will heal by a subcutaneous inflammatory process. Partial thickness wounds extend through the epidermis and into but through the dermis. This is like a stage II in pressure ulcer classifications. They will heal by epithelialization. Then full thickness wounds extend through the epidermis and dermis and may involve subcutaneous tissue, muscle, and possibly bone. This is like a stage III or IV in pressure ulcer classification. They heal as we just mentioned by granulation tissue and wound contraction.
Pressure ulcers are commonly referred to as bed sores or decubitus ulcers, but the better term is pressure ulcer. Bed sores implies that they got them from lying in bed and we know that wheelchair bound patients can get them on their ischial tuberosities from sitting. Decubitus is Latin for again lying down. If a person got them while sitting, decubitus is not really a great term to describe how they got it. A better term is pressure ulcer. Instead of just pressure, a better term for the cause is tissue load, because it is more than just pressure that contributes. It is also exacerbated by friction, shear, moisture, and temperature. Treating pressure ulcers is a huge cost and it can be up to $40,000 for a stage IV. In 2007, CMS decided that any condition that a hospital “caused” would not be reimbursed. This includes pressure ulcers, UTIs, surgical site infections, and there are about 10 more other classifications that if it occurs while a patient is in the hospital, you will not be paid for that additional diagnosis. Consequently there is a huge need for hospitals and nursing staff as well as other healthcare professionals like ourselves, to prevent pressure ulcers from occurring or else the hospital risks losing thousands or even millions of dollars.
Location of pressure ulcers is anywhere there are bony prominences. You can see their ears, occiput, shoulder, etc. The most common place are sacrum and heels, with the sacrum being the most common. More than 95% of pressure ulcers occur over five locations: the sacrococcygeal area, the greater trochanter, the ischial tuberosity, the heel, and the lateral malleolus. Here are a just a couple of diagrams showing how a patient can develop a pressure ulcer no matter what position they are in (figure 10). If they are in supine, they get them on their sacrum, heels, their elbows, scapula or occiput. If they are in prone, as sometimes some facilities will do prone positioning for respiratory patients, then their toes, knees, genitalia, breasts, acromion process, their cheek and ear, are all prone to pressure ulcer development. And in the side-lying position, anything that is against the bed will be an area of possibly breakdown. On the right hand side, you can see that even in sitting, there are areas of pressure that will cause pressure ulcers to occur and here you can see where pressure, shearing, and friction all come into play if the head of bed is elevated higher than 30 degrees.
Figure 10. Pressure Ulcer Locations
The National Pressure Ulcer Advisory Panel has come up with a staging system, but this is only for pressure ulcers. We will go through those different stages and classifications. First is a deep tissue injury. I am not going to read the whole definition because I want to make sure that we get through the whole presentation. Basically it presents as a purple or maroon area of discolored intact skin or it may be a blood filled blister. So here is an example of a deep tissue injury and full definition (figures 11 and 12) The skin is intact, but there is definitely tissue damage going on beneath the surface of the skin. With proper positioning and topical treatment, this could resolve, but chances are if you see deep tissue injury, that wound is going to progress to a stage III or IV pressure ulcer. It is very important when a patient is admitted to a facility and deep tissue injury is identified that the clinician documents deep tissue injury noted and expect progression of this wound to a stage III or IV in the next several days. This will help protect yourself and will help insure reimbursement for that pressure ulcer, because the damage had already occurred before that patient came to that facility.
Figure 11 Definition of Deep Tissue Injury and Figure 12 Deep Tissue Injury
A stage I, the most important to remember is that it is intact skin, but it is nonblanchable redness. Basically you would see redness and when you press lightly on that redness, it does not turn white. It stays red. Here is an example of a stage I pressure ulcer in figure 13. If you were to press on that pressure ulcer, it would stay red. It would not blanch, and then you would know that stage I has occurred. If it blanches, it is not yet a stage I and you can prevent the stage I from occurring by repositioning that person off of that bony prominence.
Figure 13. Stage 1 Pressure Ulcer
Stage II is partial thickness, loss of dermis, and will present as a shallow open ulcer with a red or pink wound bed. There will be no necrotic tissue. It may also appear as an intact or ruptured, serum filled blister. It is important to know that stage II pressure ulcers are not used to describe other types of wounds. So if a patient has a skin tear, a tape burn, perineal dermatitis from incontinence, if they have any kind of maceration or excoriation, that is not a stage II, you would call it a partial thickness wound. Here is a stage II i Figure 14. You can see just the epidermis is involved. The dermis is still intact.
Figure 14. Stage II Pressure Ulcer
Stage III is full thickness tissue loss. Subcutaneous fat may be visible, but the bone, tendon, or muscle is not exposed. In a stage III, you might see some necrotic tissue, but if you cannot see any of the wound base, then you have to call it unstageable. We will talk about that in a minute. It may also include undermining or tunneling. Undermining is where there is a flap of skin covered the wound, so the wound does not look as big when you first look at it, but when you stick a Q-Tip in, you can go under the rim of the skin. That is called undermining. It is almost like a roof of skin that is covered up some of the wound. Tunneling is where you can stick a Q-Tip in and it just kind of continues tunneling to another area. It is Important to remember with stage III wounds is the depth with vary by anatomical location. So on areas where is not a lot of subcutaneous tissue such as the bridge of the nose, the ear, and the malleolus, a stage III might be relatively shallow. In places where there is more adipose tissue such as the sacrum, a stage III might be extremely deep. Stage III wounds do not have bone or tendon visible or palpable. Here are examples of stage III in figure 15. You see a little bit of yellow slough, but you can also see at least 50% of the wound bed so you know that is a stage III.
Figure 15. Stage II Pressure Ulcer
Stage IV involves full thickness tissue loss with exposed bone, tendon, or muscle, and you again may have slough or eschar. Here is a stage IV in figure 16. You could debate whether this is a stage IV or whether this is an unstageable because it does have a lot of the wound bed covered with necrotic tissue, but the sacrum was palpable and was observable with this wound, so it was called a stage IV.
Figure 16 Stage IV Pressure Ulcer
Then unstageable is where the wound tissue base is covered by slough or eschar. Typically you would want to debride eschar and slough, except in one case where if you see stable eschar on the heels, you will not want to debride it. Stable eschar is considered dry, adherent, and intact eschar without any redness or bogginess around the eschar. This will work as the body’s natural cover and eventually the eschar will come off and you will be left with a healed heel. Figure 17 shows an unstageable pressure ulcer. Predebridement you cannot stage it; however the right sided picture shows post-debridement and you could probably call this a stage IV because it is down into muscle. As I mentioned, unstageable wounds cannot be accurately staged because the wound base is not visible. Eschar is black necrotic tissue characterized by gray, leathery or black tissue. Slough is usually yellow, green, and more moist than eschar. Here are examples of eschar in figures 18, and here are examples of slough in figure 19. So you can see that the eschar has a drier appearance to it. It is usually an older wound while the slough is usually wetter and usually indicates a more acute wound. You cannot backstage. Once a wound is a certain stage, it is always that stage and you would characterize it as a healing stage II or healing stage III.
Figure 17 Unstageable Pressure Ulcer
Figure 18. Examples of Eschar
Figure 19. Examples of Slough
Next we will talk about neuropathic or diabetic foot ulcers. These are caused by a lack of sensation in the foot. The typical locations include metatarsal heads, the lateral foot, toes, or any area of pressure and friction. Here are some examples of some neuropathic wounds in figure 20. The ones on the plantar aspect may occur because the patient has something in their show that they could not feel. I have had patients with acorns in their shoes. One patient had a pacifier in a shoe that he did not know about and it caused a toe wound. It is because they do not feel an insult causing that injury until they notice blood or something on their sock.
Figure 20. Neuropathic Wounds
Sussman is one of the authors of one of my reference texts, and she wrote that the “patient with neuropathy often has a dysvascular component as well and this must be addressed by a medical team, rather than just one specialty.” So a team approach in treating neuropathy is best and can help maintain the patient’s ambulatory ability. The overall goal is to prevent or delay amputation and salvage the limbs as much as possible. The pathogenesis of neuropathy or diabetic wounds is poorly understood. They do know that there is a tri-neuropathy where all three, sensory, motor, and autonomic neuropathy play a role, and diabetic neuropathy can be gradual onset. That is usually painless, but sometimes it can have a sudden onset and be very painful until that complete loss of sensation occurs. Diabetes is not the only disease that can cause neuropathy. There are many others that can cause a neuropathy, see Figure 21. It is important if a patient says they do not have diabetes, to dig a little deeper and see what other systemic disorder they might have that could cause that neuropathy.
Figure 21. Disease that can cause neuropathies
There are over 54,000 lower extremity amputations every year, and 50% to 84% of these were preceded by a foot ulcer. The mortality rate after amputation is 50% within three to five years. There is also a rate of a contralateral amputation of 50% within four years. Of these amputations, 86% could have been prevented by proper footwear and patient education. Sometimes the patients may have adequate blood flow to heal the wound, but they just have such severe neuropathy, that that is why they get the wound. So when you are looking a patient with a diabetic wound, you want to make sure to look at all of these systems, neuromuscular, vascular, musculoskeletal, as well as integumentary. So any areas of callouses can indicate areas of high pressure and stress, and these are areas that will most likely break down in the future.
I just want to tell you about a couple of scales that are used to classify diabetic foot ulcers. The Wagner scale was developed by a podiatrist and it grades the wounds based on the depth of the ulcer and whether there is any infection or necrosis. See Figure 22. So a grade 0 is a preulcerative lesion, a healed lesion or presence of a bony deformity, but the skin is intact. Then it goes all the way to gangrene of the foot requiring amputation.
Figure 22 Wager Scale
Just as a review, there are two types of gangrene, one is dry. This is due to a loss of nourishment to a part, loss of blood flow to the area followed by mummification. The area is dry, black and shriveled, and has a well-defined line of demarcation. These can auto-amputate if left long enough. Wet gangrene is more of a concern because it is necrosis of the tissue followed by destruction caused by excessive moisture. This is where bacterial gases begin to build up in the tissue. The line of demarcation is ill-defined and the limb can be painful, purple, and swollen. These are not something that we want to touch as physical therapists. We want to immediately refer to a vascular surgeon. Here are examples of dry gangrene and wet gangrene in figure 23.
Figure 23 Wet and Dry Gangrene
Another classification is the University of Texas Diabetic Foot classification system, see figure 24 This looks at a few more things where neuropathy is present and it looks at infection, circulation, and a combination of infection and ischemia to assign risk and predict the outcome of wound healing. Grade 0 to 3 go from pre- or post-ulcerative lesion, but it is a healed area, all the way to wound penetrating bone or deep abscess. Then you would add on A to D whether the patient has an infection, ischemia, or both.
Figure 24 Univ of Texas Diabetic Foot Classification System
A common thing noted with diabetic foot ulcers is a Charcot joint. Charcot arthropathy is relatively painless. It is a progressive and degenerative process, and may include single or multiple joints and it is caused by underlying neuropathy. Again it is usually painless and the foot may present as swollen and red. You might see in the acute phase that the involved foot is 5 to 10 degrees hotter than the uninvolved. Unfortunately Charcot foot is frequently misdiagnosed and mistreated, and often you will just see a Charcot foot without any skin opening or ulceration. Numerous theories behind the Charcot foot are multiple microtraumas to the joints cause a microfracture which then leads to relaxation of the ligaments and joint destruction. Another theory is that there is increased blood flow and bone reabsorption to the area. This might be noted by bounding pulses. Another theory is changes in the spinal cord lead to tropic changes in the bones and joints, or it could be caused by osteoporosis due to abnormal brittleness of the bones leading to spontaneous fractures in the foot.
Here are two examples of the Charcot foot. You can see that there is more swelling. You can see on the picture on the right side in figure 25 that it looks like the arch might have fallen. Here is another example of an acute Charcot foot in figure 26, where you can see redness. It looks like it is probably warm. It is swollen. Here is a more chronic Charcot foot in figure 27. No open areas noted, but you can see the foot now has a rocker bottom inside of a nice arched that most people’s feet have. It is not a rocker bottom or a flat foot caused by those fractures. Here is an example of a Charcot foot with an open wound in figure 28. This is an x-ray of a Charcot foot (in figure 29) so you can see where the arch is dropped and causing that rocker bottom effect again.
Figure 25 Charcot Foot
Figure 26 Acute Charcot Foot
Figure 27 Chronic Charcot Foot
Figure 28 Open Wound with Charcot Foot
Figure 29 X-ray of Charcot Foot
Now we are going to move into chronic venous insufficiency wounds or venous ulcers. They are typically seen on what is called the “gaiter“ region of the leg, which is usually the medial malleolus, but it can be on the lateral. Chronic venous insufficiency accounts for 70% to 90% of all leg ulcers. It is relatively common. It affects 1% of the general population, and 3.5% of those over 65 are affected and have a recurrence rate of 70%. Women are typically affected three times more than men. Over ¼ of patients with venous ulcers also have arterial disease, which we will talk about in a little bit, how that can compromise how you are going to treat that venous ulcer.
The mechanism behind venous insufficiency ulcers is poorly understood. They do suspect that there is a sustained hypertension in the veins which is somehow causing the veins to not work properly. The first complaint patients might say or a first time when a patient is going to see their doctor, they might say that their legs are swelling so much and just feel really heavy. But if I put my legs up at the end of the day, they feel a lot better.
We are going to talk briefly about the venous pump. When we ambulate, the calf muscle contracts and helps pump blood from the lower extremities through the veins and the veins have one-way valves. However when the valves are incompetent, it allows blood to leak back down into the interstitial space, because there is nowhere else for it to go. This causes edema and hemosiderin staining. Hemosiderin staining is a brown staining of the skin from the hemoglobin that is breaking down in the interstitial space. Here is a diagram of normal veins in figure 30. While you are walking you can see the blood flow is being pushed back up. When you are sitting or standing, you are not getting that calf muscle pump, so the valves are shut. Then in a varicose vein or an incompetent vein, the valve is no longer shut and it allows for backward flow of the blood. This is also where people with venostasis can be more prone to blood clots, and vice versa; people who have had blood clots are more prone to venous insufficiency because the valves have been compromised by the blood clot.
Figure 30 Veins
Here are some examples of venous insufficiency or venous stasis ulcers. If you look at the top picture in figure 31, if you see around the wound, some of that brownish staining, that is the hemosiderin staining I was referring to. We will talk about treatment for these in a few minutes.
Figure 31 Venous Ulcers
Finally the last classification I want to touch on is wounds associated with arterial disease. These are not wounds that we can have a big effect on as therapists, but it is important for us to recognize when this occurs and get them referred to vascular surgery. Peripheral arterial disease and arterial wounds are caused by an inadequate blood flow to the leg. This is due to narrowing or complete blockage of the arteries. Sometimes the first clue you might have that a patient has this is that they do not have any hair on dorsum or their feet. Their toenails might be thickened. They might have delayed capillary refill. Some of the symptoms they might complain of are intermittent claudication where if they walk a block or two, they start to get cramping pain in their calf. As soon as they sit down, the pain goes away, but when they walk again, it comes back. Then they might complain of nocturnal pain saying "when I put my foot up at night it really hurts, but if dangle my foot over the edge of the bed, it feels better". This is because the arteries do not have to fight gravity to get the blood flow to the toes. When they put the leg down, the blood can flow more freely in the arteries. Then it begins to not just be night pain, but rest pain altogether, and then they present with ulceration and gangrene. Ischemia is also common in some other diseases such as sickle cell, Berger’s disease, and Raynaud’s disease.
As I mentioned, intermittent claudication is characterized by cramping or an aching sensation while ambulating. It is relieved by resting, and then if an occlusion occurs higher up, typically the pain is in the calf, but if the patient has an occlusion in their upper thigh, they might actually complain of pain in the buttocks with walking. This is where it is tricky for us as physical therapists to differentially diagnose. Is the patient having back pain causing the pain in the buttocks, the upper thigh, and the leg? Maybe they have degenerative disk disease or maybe they have a herniated disk that is causing this pain, or is there something else going on? So if you are doing everything right PT-wise to treat a low back problem and they are not getting better, you might want to consider this as a problem and refer them to a vascular surgeon. So here is a gentleman clutching his calf while walking because of the pain and the diagram on the right shows a normal artery and then what a narrowed artery looks like. You can see that there is going to be decreased blood flow getting through that artery.
Nocturnal pain usually precedes rest pain. It occurs at night as the blood flow goes through more of the core of the body and not the extremities. The pain is usually in the toes, across the base of the metatarsals and in the plantar arch. They can relieve the pain with standing, dangling their feet over the edge of the bed, and sometimes with walking, but not far distances. Rest pain is a continued progression of the arterial disease. Pain is worse at night. They need a narcotic to treat it. Pain is decreased by dependency, increased by heat, elevation and exercise. Usually you will see it with two or more significant arterial occlusions. Patients with rest pain will have an ankle brachial index of less than 0.5 mm Hg. An ankle brachial index is where you take the systolic in the arm and then the systolic pressure of the leg and you divide the ankle pressure by the brachial pressure to get your ratio. 1 is normal, anything less than 1 you want to be concerned about. At 0.8, you can still use compression for a venous wound, but 0.5 of less you want to make sure that they see a vascular surgeon for potential revascularization. Finally at its most severe, you will see ulceration and gangrene. This is the distal portions of the foot, the toe, the heel, and usually are very painful. The ulcers generally do not bleed. They do not drain a lot. As I mentioned, pain is relieved by dependence of the limb. Here are just a few more examples of arterial ulcers in Figure 32. This is not something that we can treat as physical therapists. We need to refer to a vascular surgeon and get them revascularized. Once they have adequate blood flow, then we can start treating the wound. But it is important to get that blood flow before beginning any treatment.
Figure 32. Arterial Ulcers
Here is the question: How do I know what dressing to use? There are so many dressings out there, so many options. There is not any right or wrong per se, but how do I know when to use what? We are going to go through some of the treatment options, some of the dressing options first. Again there is no right or wrong, and that is why we practice medicine because it is a trial and error. Something might work for one person and not work for someone else. We will go through them and please feel free to ask questions as we go along.
So dressing options are picked based on several different factors: the pathophysiology of wound; what type of wound; if the patient has to dress their own wound, is it going to be easy for the patient to do; how much drainage do they have and what is the quality of it; is there infection?; what is the wound depth?; what is the patient’s social and economic issues?; and the different properties of the dressing. You also want to consider if the dressing is going to be easy to apply for the patient or the caregiver. Is the dressing cost effective? It might be a more expensive dressing, but if you only have to change it every three to five days, you are actually going to save money because you are not changing daily. Can that particular dressing be used on an infected ulcer? Will it stay where I put it?
The purpose of a wound dressing is basically to provide an environment conducive to wound healing. So depending on what phase of healing the wound is in, what the wound looks like, you are going to pick different dressings. So if the wound has necrotic tissue, you want to debride it. If the wound has a foul odor, you want to deodorize it. If the wound needs to granulate, you want to promote granulation via your dressings, or if the wound looks great and is fully granulated, there are options you can use to help epithelialization. So an ideal dressing criteria is kind of Goldilocks. She did not like her porridge too hot. She did not like her porridge too cold. She liked it just right. She did not like the bed too hard or too soft, but just right. Wound healing is the same thing. You do not want it too wet. You do not want it too dry. You want it just right. You want it to be just moist to keep those cells alive, to prevent a scab from forming, and to get that wound to heal. Dressings need to allow for gaseous exchange so that oxygen, water vapor, and carbon dioxide can pass into and out of the dressing. It is important that it is thermally insulating so that it maintains the core body temperature of the wound. If a wound gets cold, it will stall the wound healing. So that is why two to three times a day dressing changes are not optimal, because you are opening that wound, exposing that wound, and cooling it off and exposing it to microorganisms. You want to make sure that the dressing will keep the wound free of contamination and microorganisms, and it has to be nontraumatic and nonadherent to the wound base.
As I mentioned, moist wound healing is the way to go (See Figure 33). The traditional theory or as I like to say the “old school” thought was that wounds should be cleaned and kept dry so the scab can form. Wounds should be exposed to air and sunlight as much as possible. When tissue loss is present, the wound should be packed to prevent surface closure before the cavity is filled. This is correct, but you have to be careful when you are packing the cavity with what you are packing it with and how hard you are packing it. That wound should be covered with dry dressings. Is this theory right? No. That is because a scab is a barrier to wound healing. It slows down migration of the epidermal cells that we mentioned earlier. Allowing a wound to be open to air reduces the temperature of the wound, thus slowing down the flow of blood, oxygen, and nutrients to the wound, and it promotes infection in the wound because all the organisms in the environment could get in that wound. Then packing a wound with dry gauze can dry out the wound, cause trauma to the wound bed, and prevent wound healing. No more wet to dry!
Figure 33 Theory
I would like to say that my facility practices this, but I do still have some doctors that still think wet to dry is where it is at. Seriously wet to dry dressings are not standard anymore because they rip off good tissue with the bad. There are so many better options out there. Wet to dry should be put out to dry and not used anymore.
Moist wound healing does not allow a scab to form, so it allows for migration of those epidermal cells. In the process of not allowing the wound to dry out, it helps with autolytic debridement which is basically where the body’s own mechanisms help to debride the wound, and it protects granulating tissue and encourages epithelialization.
The first category we are going to look at is nonadherent dressings. The intentions of these dressings are to not stick to the wound bed and to maintain a moist wound environment. Unfortunately they do not always work as well as intended and can stick to wounds, either because the drainage dries and adheres it to the wound bed or sometimes the granulation tissue can actually grow through the dressing. One example is Telfa. It is an absorbent pad with a plastic film that prevents adherence. These can be used for minor wounds and wounds with minimal drainage. Petrolatum or oil-based/oil emulsion dressings also known as Vasoline gauze or Adaptics can be nonadherent as well, but they may cause problems such as maceration and an increased susceptibility to infection. There are other things called contact layers. They can be made with silicone, and they actually allow water and electrolytes to cross the dressings but not cells and proteins that can cause sticking to the wound bed. Here is an example in figure 34 on the left of Telfa, and on the right an example of Adaptic.
Figure 34 Telfa (left) Adaptic (right)
We are also going to discuss primary versus secondary dressings. Primary dressings are the dressings that are put right up against the wound bed, and secondary dressings are all those other dressings that are put on top. Usually secondary dressings are used to absorb moderate to severe amounts of drainage.
Semi-permeable film dressings can be used as a primary or secondary dressing. They are thin membranes that have an adhesive. They do help promote moist wound environments. They do allow for autolytic debridement. They protect from chemicals, friction, shear, and microbials. They help transmit oxygen into and carbon dioxide and water vapor out of the dressing, but they are not highly absorptive. They cannot be used for infected wounds because of the occlusive matter of the dressing. Indications are minor burns, simple injuries, over suture lines, and prevention and treatment of stage I, potentially stage II pressure ulcers. You want to discontinue use of them when there is a lot of drainage. That might indicate either an infection or may cause maceration. You do not want to use them on deep ulcers, full thickness burns, or infected ulcers. You want to be very careful removing them, because if the patient’s skin is very fragile, you could risk tearing the skin. You want to stabilize a corner of it, lift almost like you wound a piece of taffy, lift and stretch it a little bit, and then lift a little more, stretch a little more, to help stretch and loosen that dressing. Here is an example of Tegaderm in figure 35. You can see it is a clear. We tell patients it is almost like saran wrap. It helps keep the dressing in place.
Figure 35 Tegaderm
Semi-permeable foam dressings are to be used in moderate to highly draining wounds. They are a polyurethane open cell sheet. They absorb drainage and prevent maceration. They help maintain the core temperature of the wound and that moist environment. They also can provide a little bit of protection for the wound by cushioning it, and they often require no secondary dressing if they have their own adhesive border. These are indicated for minor and major wounds, over skin grafts, donor sites and minor burns, over Hydrogels, around tracheostomy tubes, and drainage tubes and catheters to absorb any leakage and to protect. You do not want to use these over minimally draining wounds because it is a foam and its purpose is to absorb. If there is nothing to absorb, it is not beneficial. One the left in figure 36, is an example of a foam without adhesive, and on the right is an example of a foam with adhesive.
Figure 36 Foam without adhesive (left) and with adhesive (right)
Hydrogels are basically a water-based product that help maintain that moist environment. They do conform to the wound shape. They are nonadherent and they can be very soothing. Sometimes we will tell patients to put the Hydrogel in the refrigerator so that when they go to put it on their wound, it is nice and cool and soothing. It can come in a sheet form or in an amorphous actual gel form. It is indicated for dry and necrotic wounds to increase moisture and encourage autolytic debridement. It will facilitate granulation tissue and epithelialization, and it is indicated for simple and complex wounds. But like the foam, you do not want to use when there is minimal drainage, a Hydrogel you do not want to use when there is a lot of drainage because you want to keep that moisture balance. Here is an example of Hydrogel in figure 37. I do not have an example of the sheet.
Figure 37. Hydrogel
Hydrocolloids are a gel-forming polymer with an adhesive, and when the polymer comes in contact with the drainage, it forms a gel. These are the most occlusive type of dressings, so you definitely do not want to use them on infected ulcers. The nice thing about them is they can be left on for three to five days at a time, but you need to make sure to educate the patient and their caregiver that when the hydrocolloid is removed, it is going to have a yellowish gel, and it may have an odor, but that does not mean that there is an infection. You can use it on superficial ulcers. You can use it on necrotic ulcers, but again they cannot be infected. You can discontinue hydrocolloids when the wound is granulated or if hypergranulation which is basically an over-exuberance of that granulation tissue occurs. However I have used it to full closure. You have to see how the wound is responding to the dressing. Again they provide a moist environment. They aid in autolytic debridement. They conform to the wound’s shape. They protect from contamination. They are waterproof. Most of the time they do not require a secondary dressing. Here is an example of a hydrocolloid in figure 38 on the left, and then on the right, you can see this hydrocolloid has been on for a couple of days, now the hydrocolloid has changed from that yellowish-orange to almost a whitish-yellow or opaque color. This is normal with absorption of drainage. It is very normal to have odor. You want to make sure to remind the patient of that so they do not think that the wound is infected.
Figure 38 Hydrocolloid (left), (right-applied few days prior)
Alginates are made from calcium or calcium-sodium salts, and they are actually obtained from seaweed. They turn to gel once in contact with wound drainage. These are indicated for highly draining wounds. If there is an area of bleeding, it can help stabilize the bleeding, cause hemostasis, and they can be used with infected ulcers. But if the level of drainage is insufficient to cause the fiber to turn to gel, then you no longer want to use an alginate. When they come in contact with the wound drainage, then they help maintain a moist environment. They are highly absorbent. They can absorb up to 22 times their weight in drainage. As I mentioned, they do promote and provide hemostasis. Here is an example in figure 39. They can come in a sheet or they can come in a rope. The rope is good to pack cavities in wounds.
Figure 39 Alginate
Hydrofibers are similar to calcium alginates, but they are made from man-made materials, polymer carboxymethylcellulose. They have the same features as the alginates. They are activated by the moisture in the wound. They can absorb a lot of drainage, even more than the alginate. Again they can come in a sheet or in a ribbon. Both of these, the alginates and hydrofibers, can be impregnated with silver which functions as a antimicrobial to help kill infection.
Antibiotic creams and ointments are not recommended for all wounds because they can increase resistance and sensitivity to antibiotics just like oral antibiotics can. They do have their place and they are frequently used. Mupirocin or Bactroban is used with MRSA abscesses. Silver sulfadiazine or Silvadene is typically used in burns and you want to make sure that you have a thickness of 1/16 of an inch. Neosporin or polysporin are petrolatum based ointments. They can have several different antibiotic characteristics. Triple antibiotic has three different types of antibiotics in it, and Cadexomer Iodine contains a sustained release iodine and is indicated for heavily draining or heavily infected wounds.
Use of antiseptics in wounds is not indicated for every wound because they are cytotoxic. However if a wound is very dirty or has a very foul odor with a lot of drainage, these are useful for the first few days to help with that odor. Antiseptics can reduce bacteria by up to 95%. Wounds treated with antiseptics are not guaranteed to not become infected. As I mentioned, antiseptics are cytotoxic so they will not only kill the bad organisms, but they will also kill the good organisms that we actually need to have in wounds to heal.
Silver dressings are antimicrobial. They assist in wound closure by protecting the wound from bacterial contamination and they also help to maintain moist wound environment. They have a fast-kill rate and they have a fairly long wearing time, anywhere from three, five to even seven days. They are effective against a multitude of organisms, gram positives, gram negatives, fungal infections, MRSA, VRE, etc. They are very good dressings to use appropriately. Once you feel like that bacterial burden is gone and there is no longer an infection, you want to move on to something else. Here is an example of a silver antimicrobial in figure 40. The silver is impregnated in that dressing.
Figure 40 Silver Antimicrobial
Recent trends have moved from just not maintaining a moist wound bed to how to prepare the wound bed for granulation and epithelialization to occur. So not only optimizing the moisture balance, but also looking at the chemical environment. As I mentioned way in the beginning of the presentation when we were talking about epithelialization, MMPs help with getting that mature scar but also if there are too many MMPs, it can impede wound healing. This is where these two dressings come into play: Promogran and Prisma. What they have in them is collagen which helps promote the collagen in the wound. It helps form the wound matrix, helps with building that scaffolding, but it also has what is called oxygen reconstituted cellulose (ORC). That binds the MMPs with growth factors and then allows the growth factors to work more effectively. An analogy is say the body is like a wallpaper hanger. You have a guy going along trying to hang wallpaper. He hangs a strip. He goes in and hangs the next strip, and along comes his partner who pulls down the first strip of wallpaper. They are never going to get anywhere because as soon as one wallpaper hanger puts one piece up, another guy takes the other piece down. It is similar in wound healing when the collagen is trying to do its work. The growth factors are trying to their work, but as they continue to build good things, the MMPs come along and eat up those good things. So the ORC binds those MMPs, and distracts those MMPs, so that the growth factors can do what they need to do. Prisma is similar to Promogran, but it has silver in it which helps fight bacteria as I mentioned. An example of Promogran on the left in figure 41, Prisma on the right. It feels almost like a potato chip. It is a very thin wafer. It goes in the wound and then the body absorbs it. So the next time there is a wound dressing change, the Prisma and Promogran will not be noticeable. You cannot see it because it has been absorbed into the wound bed. I have had nurses call and say I cannot get this Promogran out. I have to explain that they are not going to get it out, that it has been incorporated into the wound bed, just put another piece down on top of it, and it will continue to do its function.
Figure 41 Promogran (left), Prisma (right)
Not every wound needs advanced therapies, but advanced therapies are good for wounds that have not healed with conventional treatments. Some of these advanced therapies include dressing materials that have growth factors in them and help fight the MMPs. One particular ointment that is on the market that has platelet derived growth factor in it is Regranex. It is FDA approved only for diabetic ulcers. But some doctors do use it off-label on other types of wounds. It is very expensive. It is a prescription medication and it needs to be refrigerated. It does work. The only problem is that you have to put the Regranex on in the morning and then the wound needs to be changed at night with just a simple saline dressing. So sometimes patients just are not able to do b.i.d. dressing changes. So Regranex has its place, but it is not used as much as it could be.
Biological skin substitutes are an alternative to skin grafting. Rather than giving a patient another wound, we can use these skin substitutes to heal the current wound they have. They can be available for using right off the shelf. You do not need a donor site. They are easy to apply. They minimize contracture and scarring, and they are usually compatible with patients and they do not usually have an immune response to them.
Apligraf is FDA approved for diabetic foot ulcers and venous stasis ulcers. It is a bilayered skin substitute. It comes from cow collagen and also human fibroblasts. It is an outpatient surgical procedure, and it does have some bovine collagen in it, but it also comes from neonatal foreskin. So after a boy is circumcised, they will take that foreskin, harvest it and then make Apligraf. It must be thermally controlled and it has to be put on the right way because there is an upside and a down side. So the doctor has to make sure that it is put on correctly, and then you do not want to disrupt it. The dressing is changed once a week. Here is a picture of Apligraf in figure 42 on the left and normal skin on the right. You can see that it contains the two layers of skin like normal skin. It is shipped in this agar and there is a diagram of what color it should be. If it is not in the right color range, then you need to call the company and get another one shipped. The doctor puts it on. It has to be put on by a doctor, the doctor applies it, and secures it either with staples, sutures, Steri-Strips, wound glue, and then you leave it alone. You put a dressing on that can stay on for one week. When the patient comes back, you do not clean the wound, you just clean around the wound, put another nonadherent dressing on and tell the patient to leave it alone until the next visit. The only problem with an Apligraf is when they come back for those follow-up visits, it can be kind of yellow looking. It almost looks like slough, but that is the way it is supposed to look. That is all the organisms working in that wound to heal it faster. You can see here a wound that healed with Apligraf application in figure 43.
Figure 42 Apligraf on the Left, Normal Skin on the Right
Figure 43 Wound healed with Apligraf
OASIS is an acellular collagen matrix. It comes from pig intestine and it is freeze-dried. It can sit on the shelf. It does not need to be in a certain temperature range. You can use it on any wounds, but the only time you would not want to use it is if someone has a sensitivity or religious objection to pig products. You cut to fit the shape of the wound. You moisten it with saline, and you must secure it. Again this is a surgeon application.
Xenaderm is an ointment that can be used in shallow wounds and in perineal dermatitis patients that are incontinent, and they start to get skin breakdown. It does promote stimulation of capillaries. It aids in autolytic debridement. It maintains moisture in the wound and promotes new vasculature in the area. It comes in a tube. Anytime there is dead space or a cavity, you must be sure to fill that space. It used to be considered packing, but really packing should only be done when there is a lot of bleeding noted and you need hemostasis. Otherwise you just want to fill the wound gently with say an alginate rope or packing strips. This will help prevent that epiboly or that rolling under of the skin margins and allow the dead space to fill in with granulation tissue. It is important though to leave a tail hanging out of whatever you packed it with so that you can easily remove the packing the next time you do a dressing change.
As I mentioned secondary dressings are anything that hold the primary dressing in place. This can be anything from film to a foam to a gauze cling. Anything that will help hold that dressing on. Some patients do not tolerate adhesives very well so you must be very careful. If they do not tolerate adhesives, you can either use a skin protectant such as 3M no sting skin barrier to act as a second skin or use stretch netting or tubular bandages to secure the dressing.
As I said earlier, you need to look at the economics of dressing changes. They are not always reimbursed by insurance. So if you can find something that can stay on three to five days that is more cost effective. Medicare Part B is strict with what they will pay for. If a wound does not qualify for what they think they want to reimburse, then they will not pay for it. So you have to be very specific with your documentation in order to get the dressings covered.
Now we will go into treatment options besides dressings. Many adjunctive therapies out there, we are just going to cover a few that PTs have available. Surgeons obviously can do surgical debridements, skin grafts, and muscle flaps. We talked about those four types of wounds earlier: venous, pressure, arterial, and diabetic. There are Gold Standards for each of those types of wounds. The Gold Standard for venous wounds is compression. The Gold Standard for pressure ulcers is to off load the pressure in a turning schedule. If you want to learn more about pressure ulcers, I will be doing another presentation that will go into much more depth about pressure ulcer prevention and treatment. So look for that. The Gold Standard for arterial wounds is revascularization, and in diabetic wounds, you want to off load and encourage frequent foot inspections.
As I mentioned PTs have many options out there. I have wet-to-dry there but as I have already mentioned my disdain for wet-to-dry, I try to stay away from them. Hydrotherapy, whirlpool or pulse lavage are types of mechanical debridement. Whirlpool is not as popular as it used to be, but it is still out there. Sharp debridement, enzymatic debridement, compression wraps, intermittent compression, ultrasound, electrical stimulation, negative pressure wound therapy, hyperbaric oxygen, MIST therapy, and offloading. We will touch briefly on all of these.
Mechanical debridement is the use of an outside force to remove necrotic tissue. This is the use of the wet-to-dry, pulse lavage, and whirlpool. These are familiar to most healthcare practitioners. They have been around for years so every thinks that they are great, but the people in the wound care world are not as fond of these treatments. They are nonselective. They will take good tissue away with bad tissue. With whirlpool, you might have cross-contamination between patients if the whirlpool is not adequately cleaned. However whirlpool and pulse lavage are good when a wound has a large amount of necrotic tissue that you want to moisten and loosen up to make it easier for sharp debridement to be performed. It is not an absolute do not ever use, but you definitely want to use with caution.
Sharp debridement is something we as physical therapists can do. In different states, nurses can also do them. In some states, only advanced practice nurses can do it. As a rule, physical therapists can do it. The new recommendation is that sharp debridement should be used throughout the whole wound healing process to keep the wound free of microscopic debris. Sharp or surgical debridement can actually convert one of those chronic wounds to an acute wound, and jump-start wound healing. As I mentioned depending upon the state practice, PTs and nurses can do it. However, the American Physical Therapy Association has recommended that PT Assistants should not perform sharp debridement because it entails constant reassessment. However they have not made that an absolute recommendation. They have left it up to individual states to make their own determinations. It is selective. It is quick. It is effective. You can do it at the bedside. You can use it with other types of debridement. It does require a level of skill, and sometimes reimbursement might not occur if it is performed by a non-physician, and it can be painful. You also want to be careful with patients that are on Coumadin or have some kind of coagulopathy. You want to make sure that you are not going to cause too much bleeding that you will not be able to control. That is why it does require a level of skill or expertise. Here is just a little illustration of debridement in figure 44. They are using forceps to pull up some dead tissue and then a curette. You can also use a scalpel or scissors to cut out the necrotic tissue.
Figure 44 Illustration of Debridement
Next is enzymatic debridement. Enzymatic debridement is the use of a topical agent to break down and remove nonviable tissue. Currently the only one on the market that can call itself an enzymatic debrider is Collagenase Santyl. As its name implies, it breaks down collagen. Basically what it does is it works at the interface of the dead tissue and the wound base. What you have to do is if there is really thick eschar or really thick slough, you have to crosshatch the tissue so that the Santyl can get down to the base of the necrotic tissue and break the collagen bonds. This is a great product to use with patients who cannot tolerate sharp debridement. It is a pharmaceutical item so a physician’s order is needed. It is not active in a dry environment, but as we have already talked about, wound healing does not really occur in a dry environment so you want to make sure that you maintain a moist environment with the use of Santyl to get effective enzymatic debridement. It is best used on larger wounds, but it can be used on small wounds as well. You want to make sure that it has 50% or greater necrosis. However the company that makes Santyl will tell you to use it until wound healing because it will continue to take away microscopic debris. It is selective and will only work on nonviable tissue. It is slower and some patients do complain of a burning sensation with the use of Santyl.
Next we will talk about the Gold Standard for venous insufficiency or venous stasis ulcers. This is compression therapy. So compression therapy works with exercise to facilitate movement of the fluid from the lower extremity back to the heart. Depending on several things, there are different levels of compression available. When a person has venous disease, approximately 40 mm Hg is recommended. However this is for those who are ambulatory and able to work the calf muscle. In nonambulatory patients, lower compression is better is tolerated. Sometimes patients have to work up to that 40 mmHg of pressure, sometimes it is too hard to get on for them. You might have to go to less compression to ensure adherence to the plan of care which will improve compliance.
I mentioned earlier the ankle brachial index. That is the ratio between the ankle systolic pressure and the brachial systolic pressure. You need to be cautious when putting compression therapy on these patients with an ABI less than 0.8. The recommendations are if they are 0.8 to 1, you can use high compression, 40 to 50 mmHg. If they are 0.5 to 0.8, you can use light compression, 18 to 24 mmHg. If they are less than 0.5, you should not compress until you get them to a vascular surgeon.
There are many different options out there for compression. Some are easily removed by the patient so they can take them off at night and put it back on in the morning. If you feel a patient is not compliant and that is not the best option, you might want to put something on that stays on for a week at a time.
Different types include tubular bandages such as Metagrip or Tubagrip. It gives a light compression. You can double up to give more compression, and you want it tapered at the ankle so that the patient gets more compression at the ankle than at the calf.
Inelastic systems are basically systems that do not expand so that they work by pushing against the calf muscle and help the calf muscle pump work more effectively. So first is the paste bandage also called or more commonly called Unna boots. It is fine gauze and can be impregnated with zinc oxide, calamine, gelatin, glycerin, almost like a wet cast. You put it on from base of toes to the fibular head in a circular fashion. Then you wrap a regular Coban on top. These themselves do not apply compression, but they do not allow the foot to swell anymore and they work with the calf muscle pump to help the pump more efficiently. These should be changed every 7 days. Some doctors will spread it to 10 or 14, but really 7 days is best and if they have a lot of drainage, you might want to do it every three to seven so that you can control the drainage better.
CircAid is typically used more for patients without wounds. It is a nonelastic adjustable garment and you can get it two ways. It can go from above the ankle to right below the knee, or you can get a foot part of it too. It is interlocking nonelastic bands and then Velcro fasteners. What is nice about the CircAid is the patient can adjust it as the edema increases or decreases. So if they feel like their leg is more swollen on one particular day, then they can make it a little looser. If they get up in the morning and their leg is really thin, they can make it tighter, but as the day goes along and their edema increases, they can loosen it up a little.
Multilayer bandages. These are really the Gold Standard in compression wraps. They provide graduated sustained compression and have a series of layers. Some have only two while some have four layers. What is nice about the multilayer dressing is that they work on people that are not ambulatory. Unna boots are only good in ambulatory patients because it works with the calf muscle pump. But if a person is in a wheelchair or bed-bound, that Unna boot is not really effective. So the multilayer dressing is better because it works both in a resting state as well as in a walking state.
Finally what we recommend to patients once they are healed are graduate compression stockings. Again, this assists venous return. They can be measured and fitted for the compression stockings. So you want them to go first thing in the morning when edema is absent or minimal. As I mentioned though it can be difficult to put them on, and they do require to be replaced frequently because they do lose their elasticity after a while and then the patient will not get the adequate amount of compression.
Profore is a four layer wrap and you wrap it from the base of the toes to the fibular head. The first two layers are wrapped in a spiral or circumferential fashion, then the third layer you put on in a figure of eight. Then the top layer or the Coban layer is again in the circumferential wrap or spiral wrap.
The most common company of graduated compression stockings is Jobes. They come in not only stockings but also socks that are actually cotton, not like a Nylon. I have had some patients get them and say they are much more comfortable and easier to get on.
Another aspect of compression therapy is a compression pump. Basically it consists of a sleeve. It can go from the base of the toes to the knee and it can even go from the base of the toes all the way up to the groin. It works at peak pressures of 45 to 60 mmHg and it is recommended that the patient do it one to two hours twice a day. Then they put on their compression bandage. Patients have found, even though at first they are resistant to compression therapy, they do not want to do the wraps, they do not want to do the stockings or the pump. Once they get into the habit, they actually do state that they feel a lot better. Their legs are not as heavy. They do not have as much achiness and so they are usually compliant. The problem is you have to tell your patients that this is a life-long problem and they will have to wear compression the rest of their life. I have a lot of patients say that they are not wearing it in the summer because it is too hot. You may not want to wear it in the summer, but you will get another wound. It is important for them to understand the consequences that if they do not use their compression the way they are supposed, they are going to re-ulcerate. With all compression therapy, you have to be careful with patients that have congestive heart failure. You need to make sure that they are cleared by their primary or their cardiologist because you are increasing the volume of blood going to the heart and if they are already having volume issues, you do not want to put further burden on the heart. So here is an example of the compression pump in figure 45 and then the compression sleeve.
Figure 45 Compression Pump and Sleeve
Now I am going to talk about some different modalities or physical agents. Ultrasound; we all learned ultrasound in PT school. It can be used for wound healing as well. Same type of theory as for regular ultrasound in that it increased plasma membrane permeability to calcium ions and then it helps stimulate cellular activity such as cell migration, proliferation, as well as synthesis and release of growth factors. As we remember, ultrasound has thermal and nonthermal effects. There are a couple of ways that you can do ultrasound with wounds. You can do it around the perimeter of the wound. You can put down an OpSite and put ultrasound gel on top of the OpSite and go right over top of the wound. You can submerge the wound in water and do ultrasound in the water. They all work and they are all effective.
Electric stimulation for tissue repair. The rationale for Estim for tissue repair is that it liquefies and softens necrotic tissue. It reduces pain and edema. It has antibacterial effects. So if a wound is infected, it will help kill the bacteria. It increases ATP generation, improves membrane transport, it increases collagen synthesis, and helps organize the collagen to increase strength. There are two ways you can use Estim in wound healing. You can do the external electrode placement where you put electrodes along the side of each wound. That is a bipolar technique. As we remember, the closer the electrodes, the more superficial the result. So if you have a deeper wound, you would want to put the electrodes farther away, or you can do an internal placement. This is where you place a moist 4x4 in the wound and then put aluminum foil on top, and then hook it to the Estim machine with an alligator clip. This is called a monopolar technique, and you have to use a dispersive. Here is an example of both techniques used on the same patient in figure 46. On the left is bipolar. They have electrodes on each side, and you can see it is a fairly superficial wound, so the electrodes are pretty close together. On the right, they are doing a monopolar so the dispersive is up on the calf, and then the alligator clip and the active electrode are right over the wound.
Figure 46 Bipolar Setup (left) Monopolar (right)
Negative Pressure Wound Therapy is a system that uses special open cell polyurethane foam that you cut to fit the size of the wound. The foam is then placed in the wound and you cover it with a film. It looks kind of like an OpSite, but it is a special, only made film that the company produces. Then a tube is placed over the sponge, and then you attach it to the pump which generates anywhere from 50 to 200 mm of negative pressure. Then drainage is collected in the canister in the pump. Here is an older model of the VAC in figure 47. This one is more commonly seen in nursing homes. They do have a newer model, and I might have picture of that coming up. But you see it is a pump that can hook on the end of the bed. On the right you can see the canister that goes into the pump. You have a clamp and it goes to tubing which has another clamp. You screw the tubing together and then it connects to a Track Pad. You would first put the black foam on, you cut it to fit into the wound bed. If there is any tunneling, undermining, or sinus tracking, you would want to fill that with the foam as well. Then you would cover it with the drape and then you would put this Track Pad on top.
Figure 47 VAC
There are three types of foams that can be used with VAC or negative pressure wound therapy. Black is the sterile large pore foam. It is more effective for granulation tissue stimulation and wound contraction. The white foam is denser with smaller pores, and this can be used when the patient has either an exposed tendon or muscle that you want to protect, if you want to slow down the growth of granulation tissue or if the patient cannot tolerate the black foam because of pain. The granulation tissue does tend to grow into those pores, and that can be painful when removing the foam. So if they are having a lot of pain, you could use the white foam and that would be less painful. Then there is silver foam which is similar to the black foam but it has silver in it for its antimicrobial effects. Here is an example of the black foam in figure 48. What is neat about this one is if you have a sacral wound, you can pack this part into the wound and then you can bridge this part off onto their hip so that they are not lying on that Track Pad or any of the tubing, causing more pressure over that pressure ulcer. Here is an example of the white foam in figure 49. Then this is the silver foam in figure 50.
Figure 48 Black Foam
Figure 49 White Foam
Figure 50 Silver Foam
A lot of times medical professionals will think the only purpose behind negative pressure wound therapy is to remove that excess fluid. That is important, but that is not the only purpose. The main purpose is the negative pressure distorts or stretches the cells and the granulation tissue to promote it to grow. Same thing occurs with muscles. When we want a muscle to grow we put more stress on it. When we want granulation tissue to grow and we want more cell mitosis, then we have to put some pressure on it. So that negative pressure distorts and stretches the cells. It causes cell mitosis, granulation tissue formation, and then stimulates growth in new blood vessels. In addition, that negative pressure or pulling out that fluid will help lower the bacterial count in the wound bed by removing wound fluid which can provide a medium for bacterial proliferation. I like to tell patients that it is almost like a vacuum that we use to vacuum the floor. It does suck up that drainage, pulls it from the interstitial space, helps reduce edema, and reduces pressure on the blood vessels to help promote the flow of oxygen and nutrients to the wound.
Indications for negative pressure wound therapy include stage IV pressure ulcers, venous wounds, arterial wounds once they are revascularized, basically anything. The bottom one is an enteric fistula. This is an abnormal opening from an organ to the skin surface for example, an abnormal opening from say the stomach or the intestines to the skin. So you can put the VAC foam into that fistula and the patient must be NPO, they cannot be eating, nothing can be going through the gut. It will help close up that fistula. Contraindications are the wound must be less than 25% necrotic. You do not want untreated osteomyelitis or bone infection, and you do not want any cancer in the wound. You have to be careful with patients who are having active bleeding. If they have difficult wound hemostasis or if they are on anticoagulants because you do not want them to bleed too much.
Another therapy that is an adjunct to wound care is hyperbaric oxygen therapy. It is a delivery of 100% oxygen through a sealed chamber at a pressure greater than 1 atmosphere. It is capable of causing revascularization and healing of damaged tissue. Medicare has a list of conditions that it will reimburse HBO for, but it is a very specific list. The problem with HBO is that it works really well, but is time intensive. The patient must commit to 5 days a week for 6 to 8 weeks’ worth of treatment, and it is about a 2 or 3 hour treatment. There are two forms available. One is a single person total body chamber and the other one is a multiperson total body chamber. The more common one is the single person one. Here is what it looks like in figure 51. I say it almost looks like a coffin, but it does have glass so the patient can see outside. They always have TVs available so the patients can watch TV and they can watch whatever they want. The facilities usually have DVRs or VCRs so that if the patient wants to watch a movie, they can. There is also a way to communicate. As you see this lady here, she is on the telephone. She can communicate to the patient and the patient can communicate back to here. They get on a stretcher and then the stretcher is pushed into the HBO chamber. The door is shut. Then the technician will start the dive. Basically they lower the oxygen pressure down to greater than 1 atmosphere. Here is an example of the multiperson chamber in figure 52.
Figure 51 Single Person Chamber
Figure 52 Multiperson Chamber
Contraindications or precautions with hyperbaric oxygen is claustrophobia. If a patient is claustrophobic, they might not tolerate this. Ways to get around that are to get them some kind of sedative beforehand to calm them down and help lessen their anxiety, and sometimes you will just say let’s try it. Let’s put you in there and close the door, and see what you think. A lot of times they will get in there and they will be like okay this is not as bad as I thought. So the patient has a call bell. They usually go in with sugar tablets if they are diabetic. Just in case their sugar drops while they are in there, they can take a sugar tablet. The reason for that is they cannot immediately return you back to regular atmospheric pressure. It is about a 10 minute dive down and a 10 back up. So if a patient is having some kind of anxiety or if they are having any kind of episode, it is going to take about 10 minutes to get them back up. There is a way to expedite that if they are really emergent, but for the most part the patients understand that if they are having a problem, they have to let the tech know immediately, because there is somewhat of a process to bring them back up.
MIST therapy is a type of ultrasound but it is designed to deliver therapeutic ultrasound to the wound bed without direct contact with the body or the wound. It emphasizes wound bed preparation to promote wound healing so it helps with cleansing the wound. It debrides the wound, it removes bacteria. It helps promote new blood vessels and attracts the appropriate cells to the wound. It is not a ultrasound like we use regularly in PT. It does not have a warming effect. With regular ultrasound, you have to keep the wand moving and cannot hold it still or you will risk burning the patient. That is not a problem with MIST therapy. You can actually hold it in place for several minutes and it will not harm the person. Saline solution is directed to tip and then atomized through the vibration of the ultrasound. The ultrasound is transmitted through a mist of saline and then it helps wound healing. Here is a picture of the machine in figure 53. It can come with a cart. How long you are going to do it for is based on the size of the wound. You take the length times the width and you multiple that. So if it is a 5 x 2 square cm wound, that is 10 centimeters squared. You would put that in the machine. You would push the buttons and you can go up in minutes based on the size of the wound.
Figure 53 MIST Therapy
Offloading is the use of various techniques. Now we are going into diabetic foot ulcers. It helps alleviate pressure around the diabetic foot ulcer. You need to have adequate offloading or the wound will not be able to heal.
Treatments for neuropathic wounds. The Gold standard is a total contact cast. The cast is changed in one week. They actually recommend to change it the first time after three days to make sure the patient is tolerating it okay, and then you can go to once a week. That is what we usually do. Then once the Charcot phenomena is calming down, you might be able to wean the person back to a splint and then to shoes. This could be used both if the patient does not have a wound, if they are having a flare-up of their Charcot foot it can be used, or if they have a wound it can also be used. It provides decreased plantar pressure by increasing weight bearing over the entire lower leg. It is almost like a CAM walker for someone with a lower extremity fracture. It helps decrease the pressure on the foot by bringing it up to the calf. It does require some education to be able to put it on, but it definitely requires close follow-up and patient compliance. The average use with a total contact cast is 6 weeks. So here is a total contact cast in figure 54. This one is more involved than the one we use in our facility. We actually use one that looks like this. This is called a total contact cast EZ or TCC EZ. This one you actually have to build in the platform for them to walk on. This one comes with a boot. They can take the boot off at night so they do not have wear the boot to bed, but they definitely have to wear the boot to walk in.
Figure 54 Total Contact Cast
Another type is a neuropathic walker. Again this keeps the ankle locked. It is good with Charcot joint, recurrence of Charcot disease, and chronic ulcerations. But reminder that wearing either a TCC or a walking boot is going to change the patients gait pattern, so you might need to give them a cane or a walker depending on their stability while they are wearing it. Here is an example of a walking boot that the patient can remove in figure 55. Here is another one, and here is what is called an OrthoWedge in figure 56. If the person has a wound on the distal aspect of their foot, this helps offload that area. They also have another shoe that is built up in the front, but the heel is open. So if they have a heel wound, it takes the pressure off the heel. You can also make accommodations in patient’s shoes by using this peg insole and you just punch out the peg where the wound is. Here is an example of a boot where you can also punch out the pegs in figure 57.
Figure 55 Walking Boot
Figure 56 Boot and OrthoWedge
Figure 57 Peg Insole
We are winding down here. Atypical wounds sometimes occur. You have treated it with good standard care and it is not getting any better. That is when you need to start thinking that it is an atypical wound. It could be an inflammatory disease such as vasculitis. It could be a malignancy such as malignant melanoma, basal cell carcinoma, or squamous cell carcinoma. It could be associated with other diseases such as pyoderma gangrenosum which is typically associated with irritable bowel syndrome, or calciphylaxis which is associated with end-stage renal disease. It might be an autoimmune disease such as bullous pemphigus which is a blistering disorder or it could be a hereditary disease such as sickle cell anemia or epidermalysis bullosa.
Other wounds include gunshot wounds, other traumatic wounds, skin tears, burns. So they might not fit into the categories that we have talked about, but sometimes they can be treated in the same way as some of those. But in other times, those disorders will not heal no matter what we do. Sometimes they need to be biopsied to determine their etiology. When you get those atypical wounds, it is time to refer to a specialist. What we in the wound industry like to say is it is important to remember that we are not just looking at the hole in the patient, but we are looking at the whole patient. Sometimes we cannot, as PTs, treat the patient effectively just by ourselves. So we need to refer. We might refer to dermatology. We might refer to vascular. We might refer to infectious disease. We might refer to podiatry, general surgery, nutrition, any of those can help with the team effort of healing that wound.
In conclusion, as I mentioned at the beginning of this presentation, it is important to have at least a baseline of knowledge about wound care even if you do not plan on doing wound care specifically. It is important to have a basic knowledge. There are four typical wounds that include diabetic, pressure, arterial and venous. There are a range of treatment options of topical treatments, dressing treatments and modalities to treat those wounds. However wounds frequently do not fall into one of these categories and thus require a referral to an outside specialist, and there are those many different treatment options.
Questions and Answers
Q: How often does Charcot foot occur?
A: It is hard to say how often it occurs. It is quite frequent. It is usually seen in patients that do not have really good diabetes control, and that is why it is so important now to emphasize diabetic control. Get them to endocrinologists. Get them to keep their sugars under control so that those sequelae of diabetes do not occur. Charcot foot is frequent in diabetics, but it is not in every diabetic. You do begin to see Charcot changes in a lot of the diabetics with foot ulcers. I hope that answers your question.
Q: To control heavy exudate, what dressings are optimal?
A: For heavy exudate, the wound foams, algnates re good and the VAC is awesome for heavy exudate because the exudate is going into the canister. If they have a lot of edema, you have to treat the edema first so that may require them actually going on a water pill and doing compression. What is great about all those topical treatments that I told you about, the foams, the silvers, the alginates, they can all be used under compression dressings. So if you have something that is heavily exudating, use a foam and then use one of those compression wraps that will give you some more absorption quality. There are other dressings out there called ExuSorb or Exu-Dry. They actually use diaper technology. Any of you who have young children that wear diapers, you know when they wet, there are beads in the diapers that absorb that urine and then it makes the diaper feel heavier. There are dressings out there that use that same technology, and the beads will incorporate the fluid and wick it away from the wound.
Q: Can you go over Estim again with wounds?
A: I did not go into too much depth because it is not used as frequently. I will back up the presentation to Estim. You can use negative or positive, depending upon what the goals of therapy are. If you want more information on that, I can forward it to Calista and Kami and they can send it out to you. But there is a protocol depending on what your goal of therapy is you would put either the negative or positive electrode on. So if you are looking for antibacterial effects, I believe you would use the negative. I would have to look it up because I have not done it in a while. But depending upon what effects you are looking for, you would use either the negative or the positive and then there are some protocols that alternate where you do negative for 30 minutes, positive for 30 minutes so that you get both effects.
Q: Is pulse lavage still being used? For what?
A: Yes pulse lavage is still being used regularly. Pulse lavage is neat because it combines not only the mechanical debridement factor but it also has some negative pressure with it. Harriet Loehne is one of the premier users of pulse lavage. She is down in Georgia I believe, and she still uses pulse lavage a lot. She uses it for abdominal wounds, say after a morbidly obese person has a panniculectomy and they are left with a very large abdominal wound. It gives a very effective cleaning of the wound and then the negative pressure of the suction of the pulse lavage helps promote wound healing. It is good for undermined or tunneled areas. There is a little attachment that you can use that is a little like a straw but is really flexible. You can put the straw into the undermining and the sinus tracking and get good cleaning of something that you might not be able to. I did use it frequently in my first job, when I first graduated. The problem with pulse lavage is it can aerosolize the bacteria in the wound and they have found that patients that had bacteria in the wound when they cultured both the therapist and the patient’s noses, they found the same bacteria in the nasal passage as was in the wound because the therapist and the patient were inhaling the bacteria that was aerosolized with the pulse lavage. Instead of taking this valuable product off the market, the Centers for Disease Control came up with very specific guidelines for using pulse lavage. It has to be a single patient room, all horizontal surfaces either have to be covered or wiped down after the treatment. Anyone in the room must wear a full protective personal equipment get-up. Head must be covered. Feet must be covered. Face must be covered. You have to wear a mask because of the aerosolization. The reason why pulse lavage kind of fell off the radar a little bit is because of that time intensiveness, that it has to be a single patient room, and you have clean up well afterwards. That is why pulse lavage is not used as regularly, but it is still out there. If you want more information on it, you can Google “pulse lavage”, you can Google “Harriet Loehne,” and you will find more information about pulse lavage.
Q: Can patients wear shoes with stable eschar?
A: Typically when they have stable eschar, you want to protect the eschar. So what we recommend is, and it depends too, one of our surgeons here in the wound center, he does not want you walking at all if you have eschar or any type of heel wound, even if it is on the posterior aspect and not something that you are actually going to ambulate on. But what we frequently recommend is that they get some kind of heel relief shoe. If we go to this picture in the offloading section, this same company called Darco makes a Darco OrthoWedge with heel relief so if they have a heel ulcer, they can wear this and it would keep the pressure off the heel until the heel is healing. Typically we do not want them wearing shoes even though it is stable. Wearing shoes and putting pressure on it can make it go from stable to unstable. You really want to keep the pressure and the weight off of it until it heals.
Q: Is there something you can recommend for pressure?
A: I did not go into detail here because of time restraints, but if a patient is in bed, they need a low air loss surface, and if you Google “low air loss surface” or you go to Hill-Rom’s website or Stryker’s website, you can find information about their pressure redistribution surfaces that they make and sell. In a wheelchair, they definitely have to have cushions. I recommend RoHo. There are a whole bunch of wheelchair cushions, but any time someone is wheelchair bound, they have to have a cushion in that wheelchair. A pillow does not cut it. The cushion must be inspected frequently to make sure that it is still providing adequate pressure relief. They need to be replaced and insurance is difficult. They might only replace every 5 years, but it is important to keep regular maintenance on those wheelchair cushions so that they do not break down. If someone has wounds from sitting, then we usually recommend they go on bed rest because nothing takes the place of absolutely no pressure over a wound. Cushions are good, but no pressure at all is best.