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The four local risk factors for skin ulcers are friction, which denudes the epithelium, shearing, which pulls the dermis and the subdermal tissues and disrupts blood flow with the arterioles, moisture, which denudes the epithelium and maceration, particularly moisture with urine and stool decubitus ulcer, decubitis ulcer. They both are very damaging to the skin. Then of course, pressure, which impairs blood flow. Other less important local risk factors are localized edema, infection and hypoxia related to poor blood flow, such as with peripheral occlusive disease.
Systemic risk factors for decubitus ulcers are malnutrition, both over and under. Immobility, of course. That’s probably the biggest. Immobility for one reason or another. Anemia is a risk factor for decubitus ulcer formation. Hypotension, hypoxemia of course. Neurologic injury such as hemiplegia, paraplegia, quadriplegia. Diabetes with the impaired wound healing that occurs with diabetes. Same thing with steroid treatments, and then vascular insufficiency; venous stasis, arterial insufficiency.
Four common types of skin ulcers: first the skin tears, then venous stasis ulcers, arterial insufficiency ulcers and pressure ulcers and I’ll talk about all these within the next 20 minutes.
Skin tears are caused by trauma to thin, fragile skin. They occur typically on transfers of frail elderly people. You treat these by cleaning them with water and preserving the skin that remains and replace it, and then cover it with a non-stick dressing such as - a clear dressing - like a Tegaderm or Op-site. Because the skin surrounding that is so fragile, if you put some form of Duo-Derm or something you’ll pull off healthy skin. Most nursing facility nurses know what their favorite thing is to use and they’ll always ask you if they can put an Op-Site. In fact, they even call and leave a message and say, "We’re going to put a … I’m putting on
Next is venous stasis ulcers. These are caused, initially it is thought, these are caused by deep venous thrombosis. That initiates the whole chain of events that causes increased venous pressure. Most often, not ever diagnosed and asymptomatic. But eventually what happens is people develop incompetent perforator valves, the valves in the big veins of the legs, and out in the periphery there is increased venous pressure which locally results in fibrin deposition and then tissue necrosis within the center of the deposits of fibrin, and ulcer formation. The clinical characteristics are that these typically have a medial leg location. The two things in the differential are pressure and arterial insufficiency ulcers. There are some nice clues though. Medial location is one, surrounding hemosiderin discoloration is a
This is a good picture that points out a few of these things. This is a venous stasis ulcer. The only thing I don’t like about it is it’s lateral. But you know that this is a venous stasis ulcer because it’s got this intense hemosiderin deposition, there’s also a fair amount of this tight edema. You can see where he had his socks on, which tells you that he was probably not wearing a compressive stockings, and a pretty significant deep big ulcer. Here’s a little bit more common one. Again you
The treatment for these is compression in one way or another. Oftentimes when people have such severe edema, one way to compress them initially is the use of Ace wraps, working from the distal to the toe, working your way all the way up. These aren’t very popular with the patients, of course, but they can squeeze out enough edema that more definitive things can be done, like fitting for compressive stockings, Teds, Jopst, Juzios. Juzios are the best I think. They are stronger than Teds, not as tough to use as Jopst, they are more comfortable for patients and they do a nice job. Una boots can be used for compression in people who actually have the ulcer. These things are used eventually prophylactically. And then mechanical pumps can be used prophylactically too. Also to treat a current ulcer, these
Arterial insufficiency ulcers. Several clues that someone might have an arterial insufficiency ulcer: one is that the toes are commonly involved. The toes and the heels. How many times have you seen a person with a hip fracture, after they have their hip fracture they have a big ulcer on the heel that was fractured. It’s from immobility and prolonged pressure, plus or minus arterial insufficiency. The toes are commonly involved. Pedal pulses are diminished or absent. Now in terms of managing them - it’s not that tough to diagnose these things, in terms of you might want to get some studies like a tissue oxygenation and maybe study their ankle brachial indices, can provide you some indication of how likely they are to heal. Although that’s not foolproof and I don't really even know what the numbers are
Now, pressure sores, with their various stages. Stage I pressure ulcer is a non-blanchable erythema, a tissue injury that causes non-blanchable erythema. Stage II is a partial skin thickness ulcer that goes through the epidermis but not fully through the dermis. Stage III is a full skin thickness ulcer that is down to fascia, but not through the fascia. A stage IV is a full skin thickness ulcer that goes through the fascia down to underlying bone, muscle or viscera. Diagrammatically this is a stage I ulcer with this non-blanchable erythema. The treatment for this is mostly prevention. Preventing this from getting worse, and really the money savings in the decubitus ulcer business is prevention. These things are tremendously expensive to heal, in terms of supplies and the manpower hours that go into treating these wounds. So if you are at a facility where you have a decubitus ulcer problem, spend a great deal of effort if you can in employing successful prevention strategies.
The treatment for this sort of condition is just to reduce whatever the offender is, and it’s usually pressure. So therefore, reduce pressure, get these people turned, get them some kind of a foam mattress, get them a foam pad over a pressure point, whatever it takes. Minimize the friction and shearing forces, keep them clean
The principles of local wound care. The first is to debride. You want to have a nice healthy granulating base, and there’s different ways that you can debride. One is to debride surgically, sharp debridement. Very viable thing, especially when you are talking about these bigger ulcers with loads and loads of necrotic tissue. It’s the fastest way to get it done. Another way to do it is chemical debridement for less extensive debridement, using such things as collagenase - goes by the trade name of Santyl. It’s an enzyme that breaks down necrotic tissue and the tissue can be washed right out of the wound. You don’t even need to know the details on
This is called a Geo-Mat cushion. There’s all sorts of different cushions on the market. I guess the only thing I would say is that there are many better cushions on the market than the old egg-crates. Egg-crates are inadequate. This is an air-fluidized bed. Talking about great expense when you get to these, though. This is a sharp debridement. Now if you have a big wound like this on somebody’s backside, it’s going to take forever to get this thing cleaned up unless you do sharp
This is an example of a wet to dry dressing doing its job. It’s nice and dried out. It’s pulling off debris, but then when you see what’s left there, it’s beautiful healthy granulating tissue, and it’s time to switch from wet-to-dry to some other form of dressing, because continuing using wet-to-dry will only pull off healthy tissue as you go on from here. I would switch this person to some sort of a Duo-Derm dressing. This is the healthy fibrinous exudate that exists under Duo-Derm, and then some old fashioned pitfalls. "If it’s wet, dry it. If it’s dry, wet it", that’s not the way it should be. Heat lamps should not be used. Heat lamps have been
Maybe the most important thing I can say of all is, don’t culture these things. These things tend to be polymicrobially infected and there’s no way of knowing that what you culture in that soup that you culture is really what’s infecting the wound. The most typical organisms are: staph, proteus, bacteroides and Pseudomonas. You might well culture these things and have staph that’s resistant to methicillin that’s just colonizing the wound and then you are going to have big trouble and