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Decubitus Ulcers

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 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. Thatís 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 Iíll 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 youíll pull off healthy skin. Most nursing facility nurses know what their favorite thing is to use and theyíll always ask you if they can put an Op-Site.

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.

This is a good picture that points out a few of these things. This is a venous stasis ulcer. The only thing I donít like about it is itís lateral. But you know that this is a venous stasis ulcer because itís got this intense hemosiderin deposition, thereís 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.

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 arenít 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.

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. Itís 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 - itís 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.

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 itís 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.

The principles of local wound care. The first is to debride. You want to have a nice healthy granulating base, and thereís 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. Itís 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. Itís an enzyme that breaks down necrotic tissue and the tissue can be washed right out of the wound.

This is called a Geo-Mat cushion. Thereís 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.

This is an example of a wet to dry dressing doing its job. Itís nice and dried out. Itís pulling off debris, but then when you see whatís left there, itís beautiful healthy granulating tissue, and itís 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 itís wet, dry it. If itís dry, wet it", thatís not the way it should be. Heat lamps should not be used.

Maybe the most important thing I can say of all is, donít culture these things. These things tend to be polymicrobially infected and thereís no way of knowing that what you culture in that soup that you culture is really whatís infecting the wound. The most typical organisms are: staph, proteus, bacteroides and Pseudomonas.