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Wound Care: Basic Concepts and Treatments

Wound Care: Basic Concepts and Treatments
Jennifer A. Gardner, PT, DPT, MHA, CWS
September 6, 2017
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Wound Care

So, the question I get asked frequently is, since when do therapists do wound care? I always get asked that question. Why are you, as a therapist, doing wound care? Or, you're no longer a therapist because you do wound care now. I have to explain to people that wound care or integumentary, is one of our four practice patterns. The integumentary system is not an area that people typically associate with physical therapy. Usually, they think of neuromuscular or musculoskeletal disorders as what therapist s treat, not wound care. The Wound Care Special Interest Group of the Academy on Clinical Electrophysiology and Wound Management is very active in wound care and encouraging physical therapists to be active in wound care. Currently, we do not have a certification just for wound care in the American Physical Therapy Association so we have to go through other organizations, such as the American Board of Wound Management if we want to become certified. We are working on the development of a certification so that it will be something similar to a certification in neuro, orthopedics, pediatrics, et cetera.  We will be going through basic wound care and some basic dressings and treatment otherapist ions today. Even if you don't choose to specialize in wound care, it's important to have a basic understanding. For example, you may see someone in an outpatient setting who has a non-healing incision after a total knee or a total hip replacement and you may be the first person to identify that there is a problem with the wound healing. If you're in a rehab, or acute care, or long-term care setting, you may have patients with pressure injuries or other types of wounds that, again, you might not be the individual taking care of those wounds, but you need to be able to identify them and give other members of the healthcare team the heads up that those wounds are present. This course will serve as a basic introduction.

Types of Wound Healing

Primary Intention Healing

Primary intention is when a person has a suture, or perhaps a laceration, and the wound is closed by sutures, staples, et cetera. The wound doesn't have to granulate or fill in by granulation tissue and it doesn't have to re-epithelialize. The wound edges are pulled together and closed by the sutures or staples. Rarely do wound care specialists have to deal with this type of wound unless for whatever reason it opens up.

Tertiary Intention Healing

Tertiary, or delayed primary healing is when a surgeon will leave the wound open to granulate prior to closing it with sutures or staples.  A lot of times we see this tertiary intention when there's an infection expected or suspected, or if there's a traumatic injury such as a person riding a motorcycle who slid and has some road rash and deeper lacerations. There may be some fear that gravel or debris is in the wound, so the doctor will leave the wound open to granulate and heal a little bit before they close it primarily.

Secondary Intention Healing

Secondary intention, also called full thickness healing, is where we will concentrate the most today. These are the wounds that have to heal by granulation and re-epithelialization.

Full thickness, or secondary intention healing, is the most effective form of healing when a wound goes through all layers of skin and/or into the underlying tissues. If a doctor tries to prematurely close a wound (prior to full granulation process occurring) that has some significant detherapist h to it, then the patient may become suscetherapist ible to an abscess. I like to use the analogy of gardening or planting trees.  You can't just dig a hole, and then cover it over with grass, or cover it over with mulch, without allowing that hole to be filled in with dirt first. The same thing is applicable regarding a wound. The wound needs to be filled in with granulation tissue first before you can close it with epithelialization.

Full thickness wounds heal by formation of granulation tissue, and contraction of the wound edges. They will have scar tissue formation and the tissue will not be the same tissue that it was prior to the injury. It is important that patients' understand that their wounds, even though they appear healed once they're fully closed, that they're still only 80% as strong as the tissue that was present there before. The patients need to understand that they will always be prone to a future breakdown in that same area. So, when patients have pressure injuries and/or diabetic foot ulcers, it's important that they understand, that even though they go on to heal, they're going to be at risk for future re-ulceration because the tissue strength is not as durable as it was before.

Wound Healing Physiology

When we look at wound healing, we like to think of it as a series of overlapping events. Typically they should occur in a reasonably predictive fashion. They should go through the first phase, which is inflammation and hemostasis, and then advance to proliferation, and finally, maturation. The problem occurs when a wound stays in one phase longer than we expected or that it just can't advance to the next stage for a number of different reasons. Whether a patient's wound is an acute wound or a chronic wound, that healing cascade should be the same. The difference is an acute wound will move through the phases much quicker and we will get healing in a quicker time than we will with chronic wounds. Hopefully, with good wound care, we are able to move these chronic wounds through these phases in a reasonable fashion as well. So, as I mentioned, there are three phases of wound healing, though some books might say there are four. This is because sometimes they will combine inflammation with hemostasis, or they'll make hemostasis the first phase of wound healing and then inflammation the second phase. It's not really important to know whether there's three or four, but understand that there are different phases and that wounds need to go in a reasonable, orderly fashion through these phases.

Inflammation/Hemostasis

The first thing that happens when there is an injury is hemostasis has to occur. This is the initial reaction after the wound happens. It occurs to stop the bleeding and prevent further injury. Once the bleeding has been stopped, then the inflammatory process begins. Once inflammation ramps up to get rid of the necrotic tissue, and gets rid of any bacteria that might be in the wound, then the proliferation phase can move in. The proliferation stage is where we'll get the granulation, the re-epithelialization, and the wound closure. And then the final phase is that maturation phase, where that collagen starts to remodel, and the scar becomes stronger.

Figure 1 is a diagram of the phases of tissue repair. And as you can see, these phases do not occur by themselves, but they occur overlapping and they occur simultaneously. So sometimes even though inflammation begins in the first few minutes, or hours, or days of the wound or the injury, the second phase will start while the inflammatory phase is still going on. The wound in the remodeling phase will start while the granulation tissue phase is still going on as well. That is normal and what we expect to happen. Hopefully, we can have most wounds heal within that 30 day period. The dotted line is in Figure 1 is showing that that collagen accumulation and remodeling continues to occur even after the wound is healed, which can take up to two years before that scar is fully mature. Again, it is important, to remind your patients that even though their wound looks healed, they still need it to continue to mature and strengthen in that final phase of wound healing.

Figure 1. Phases of Tissue Repair.

Figure 2 is a schematic of the inflammatory phase. It's showing where an injury has occurred (an insult to the skin has occurred). In Figure 2, you can see some cells started to migrate in. Those cells are helping with the hemostasis process to occur and then they play a protective role. The macrophages and the phagocytes, help to clean up that wound. They are generally beneficial to the wound and to the body. The problem occurs if we get these responses in too great a numbers and the wound can't go on to the next phase because these responses are too overwhelming. Again, the inflammatory phase is a series of events that occur simultaneously. One of these events is vasoconstriction. So, initially, to achieve hemostasis, we want the blood vessels to constrict to reduce blood loss. Once that initial blood loss is completed, we start to see platelets come in to cause coagulation by thrombin and collagen. Next, we vasodilation occurs and allows cells to come in to do the work that it needs to do. So, while it may seem confusing that I'm saying we need vasoconstriction and dilation, they happen in an orderly fashion. The vasoconstriction happens first to reduce the blood loss and achieve hemostasis, along with the platelets coming in for coagulation. Then we get vasodilation occurring to allow the cells to come in and clean up the wound, kill any bacteria, et cetera. In addition to the vasodilation, we'll see an increase in the cell membrane permeability. We will see an influx of fibroblasts, neutrophils, macrophages, monocytes, and mast cells. Some of the signs that you'll see are redness, swelling, heat, and pain, as well as decreased functional ability in the inflammatory phase. Hopefully, as the patient enters into the proliferation phase, you'll see some of these signs and symtherapist oms go away. There are some systemic indicators of inflammation, including fever and leukocytosis, or elevated white blood count. Sometimes in patients with chronic wounds, you will not see these signs of inflammation and it can be difficult to identify when an infection is present.

Figure 2. Inflammatory Phase.

Acute inflammation.  Acute inflammation is usually the first 24 to 48 hours, but it could last up to two weeks. The subacute phase comes in at the end of that 24 to 48 hours and may last an additional two weeks. Figure 3 is a picture of what you might see in an acutely inflamed tissue. As I mentioned, those vascular responses occur. Vasodilation occurs in response to the injury and allows the tissue to become warm and red. Capillary permeability increases which is why swelling occurs. Next, leukocytosis occurs which is the accumulation of leukocytes at the injury site followed by phagocytosis. This is the phase where cellular repair is beginning.

Figure 3. Acute Inflammation.

Chronic inflammation. As I mentioned before, if acute inflammation is allowed to go on unresolved, and it doesn't progress to the next phase, then you will move into chronic inflammation. There are several theories as to why a wound may be chronically inflamed. It may be due to a pressure injury that we're not fully removing the pressure. There might be continuous microtrauma.  Perhaps if the wound is infected, chronic inflammation may have developed because the necrotic tissue is contaminated with foreign material or with bacteria. The problem with chronic inflammation is there will be no cardinal signs of infection that I just mentioned. The redness, the warmth, the pain are not present so it can be difficult to identify chronic inflammation. There will also be a higher number of monocytes, lymphocytes, histocytes, and macrophages in the chronic inflammation phase. Figure 4 is a picture of a wound that's stuck in the inflammatory phase. It's not going on to fully granulate and it can't go on to fully heal because of that. There is some kind of microtrauma or some kind of bacteria keeping it open. Figure 5 is another picture of a chronically inflamed wound because of the necrotic tissue that's present.

Figure 4. Chronic Inflammation.

Figure 5. Necrotic Wound-Chronic Inflammation.

Proliferation Phase 

Figure 6 depicts proliferation and the cells that move in during that time. Collagen fibers are moving in, epithelial cells are moving in to get that wound filled in and closed.  This phase occurs about days five to 20 after the initial injury. The goals are granulation tissue growth, angiogenesis which is new blood vessel growth, and then re-epithelialization (the wound to be covered with skin). In the beginning of the proliferation phase, we want to make sure that the wound is essentially clear of foreign substances. Foreign substances may mean necrotic tissue, or debris such as that from road rash, as mentioned before. You also want to make sure the wound is free from infection. Macrophages and fibroblasts start really moving into the wound to help form that collagen matrix during this phase as well. Macrophages release a platelet-derived growth factor and a fibroblast growth factor. This attracts fibroblasts, which then produce collagen and elastin. Collagen gives the strength to the granulation tissue, while elastic gives it its flexibility. This leads to the growth of new connective and granulation tissue as well as capillary growth.

Figure 6. Proliferation Phase.

Fibroplasia.  Fibroplasia is defined as the laying down of the collagen matrix known as granulation tissue. The first type of collagen that moves in is Type III collagen. As the wound continues to granulate and mature, Type I collagen will move in. That Type III collagen is really undifferentiated tissue so it needs to mature before it becomes the granulation tissue that we're looking for. As I mentioned already, there'll be enhanced cell activity in the wound bed and angiogenesis will occur. Angiogenesis is the building of a new vascular network for increased oxygen and increased nutrition coming into the wound to help it close and the removal of any metabolic waste that's present. Hopefully, you'll see, in proliferative phase, the beginning of a decrease in wound size, because the edges of the wound will move closer together as wound contraction occurs.

Cellular Activity.  As previously mentioned, the cellular activity occuring in this phase are the fibroblasts, the myofibroblasts (which kind of mimic muscle tissue), endothelial cells and epidermal cells. If you look at a wound that's starting to contract in, you'll see some lines along the edges of the wound, and that's the myofibroblasts, at work, contracting that wound. Crosslinking of collagen is formed. The new collagen matrix looks like red granules piled on top of each other. It's called granulation tissue and it's highly vascularized, so you will see increased bleeding in granulation tissue. That is completely normal and it is beefy red, moist and fragile.  It is fragile because it is new tissue that's still trying to mature and grow. It does require protection from a dressing, such as offloading, et cetera. Figure 7 is a picture of what nice, healthy granulation tissue looks like.

Figure 7. Granulation Tissue.

Myofibroblasts and Wound Contraction.  The myofibroblasts have the contractile property of smooth muscle which helps pull the edges of the wound together and helps pull that epithelialization closer together so that we get a decrease in wound size. We want to make sure that the wound stays moist. We want it to have that beefy red appearance and the gradual reduction in wound size is what we want to happen. Sometimes, though, in this phase eschar or slough can form and that will slow the healing process down. 


jennifer a gardner

Jennifer A. Gardner, PT, DPT, MHA, CWS

Dr. Gardner has been a physical therapist for 16 years with the last 11 concentrated solely on wound care. She became a Certified Wound Specialist in 2001 and successfully passed her re-certification in October 2011. Currently, Dr. Gardner is employed at Inspira Medical Center Woodbury as the Manager of Wound Care Services, supervising both inpatient wound care and the outpatient wound center. In addition, she has been adjunct professor at College of St. Scholastica in Duluth, MN for the last 8 years, teaching Integumentary to doctoral physical therapy students.  Dr. Gardner has presented both nationally and internationally on various wound care topics and continues to participate in research studies on new concepts in wound healing.



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