Pressure/Shear Injury: Characteristics, Pathologic/Etiologic Factors
Skin and Wound Care. Produced by the Emory Nursing Wound Ostomy Continence Nursing Education Center.
Transcript
Okay, in this class we're going to talk about pressure shear injury.
Speaker A:So we've talked about wounds caused by friction, caused by skin tears, caused by tape damage, caused by moisture.
Speaker A:And in this class we'll focus on pressure shear injuries, which are another very common wound seen in clinical practice.
Speaker A:This class is actually going to be divided into two parts.
Speaker A:So the first part will cover definitions, characteristics and pathologic etiologic factors for pressure shear injuries.
Speaker A:And then in the next part, we'll talk about clinical progression and medical device related pressure injuries.
Speaker A:And we are going to differentiate a little bit between pressure shear injuries that occur over bony prominences and pressure shear injuries that occur underneath medical devices.
Speaker A:Because at this point in time, it looks as if the pathology might be just a little bit different.
Speaker A:So that's why we're going to address them a little bit separately.
Speaker A:So looking at the pathology and the etiologic factors for pressure injury, we know the things that we have to be concerned about and that we have to address are intense or prolonged tissue compression, which then results in vessel compression.
Speaker A:We have to address shear force.
Speaker A:We have to be concerned about impaired tissue tolerance.
Speaker A:That explains why some patients are so much more vulnerable than others.
Speaker A:And we're also going to talk about the possible impact of reperfusion injury and the possible impact of direct cell injury.
Speaker A:Now, the impact of reperfusion injury and the role it plays in pressure injury development, the impact of direct cell injury and the role that that plays.
Speaker A:These are areas of ongoing research and we don't have clear answers, but I wanted to at least introduce what they're currently thinking and saying and discussing.
Speaker A:So what is a pressure injury?
Speaker A:Well, you know this, but I wanted to kind of pull in the official definition from the National Pressure Injury Advisory Panel.
Speaker A:So they call a pressure injury localized damage to the skin and the underlying soft tissue.
Speaker A:It typically occurs over a bony prominence or under a medical device, which helps you to do differential assessment.
Speaker A:Interestingly, pressure injuries can present either as intact skin with color changes and palpatory changes, or it can be an open ulcer.
Speaker A:Most of the time, pressure injuries are painful.
Speaker A:Not always, but most of the time.
Speaker A:Pressure injuries currently are thought to occur as a result of intense and or prolonged pressure or pressure in combination with shear.
Speaker A:The tolerance of the soft tissue for pressure and shear may also play a role and that's affected by multiple factors.
Speaker A:So again, as we said, we know that some patients seem less vulnerable than others and we'll talk about those factors.
Speaker A:But here I want you to just kind of lock in that there are two locations where you typically see a pressure injury.
Speaker A:One is over the bony prominences.
Speaker A:That's what you see in the slide on the top.
Speaker A:And the second is under medical devices, which is what you see in the illustration on the bottom.
Speaker A:So location.
Speaker A:We were just reinforcing this over bony prominences.
Speaker A:Why?
Speaker A:Because that's where the soft tissue and the blood vessels and lymphatic vessels are compressed.
Speaker A:So they're compressed between the bone internally and the bed or chair or cast or splint externally.
Speaker A:They can also occur under medical devices.
Speaker A:And again, you've got tissue compression, but here is between the skin surface and the medical device.
Speaker A:What about depth?
Speaker A:Well, for a long time we said that practically all pressure injuries were full thickness.
Speaker A:But now we realize that some pressure injuries present as partial thickness wounds, meaning they're confined to the epidermal and dermal layers.
Speaker A:More commonly they will be full thickness.
Speaker A:They will extend through the skin layers into the fat, the muscle or the bone.
Speaker A:And we'll talk about the different clinical presentations and why.
Speaker A:What about contours?
Speaker A:Because again, you're going to have to be able to differentiate between a pressure injury and other types of wounds.
Speaker A:We'll go back to the causative factors.
Speaker A:So you've got tissue compression between a bone and an external surface or between a device and the skin.
Speaker A:So that tells you the contours are going to be round or slightly oval.
Speaker A:If it's over a bony prominence, if it is an area that's exposed to both pressure and shear, then you can get elongation of the wound bed.
Speaker A:And you can also get tunneling and undermining.
Speaker A:If it's medical device related, you'll have contours that match the device.
Speaker A:In other words, where did the device come in contact with the skin?
Speaker A:And if you look at the slide on the bottom, this patient sustained a medical device related injury and it was a bedpan.
Speaker A:And you can see the very clear outline.
Speaker A:And you've probably seen wounds underneath a trach.
Speaker A:You've probably seen wounds underneath the G tube.
Speaker A:You've probably seen wounds that matched the length of tubing, if tubing got caught between the patient and the skin.
Speaker A:So let's back up and talk a little bit about normal tissue perfusion, what it is that keeps skin healthy.
Speaker A:And then we'll talk about how tissue compression and vessel compression causes ischemic damage.
Speaker A:So you know a lot about normal tissue perfusion, you know about the arterial system, and you know that the end point of the arterial system is the capillary bed.
Speaker A:That the capillary walls are very thin and permeable, and that it's at that point where you get an exchange of oxygen and nutrients between the capillary bed and the tissues.
Speaker A:And also you get perfusion from the tissues into the capillary bed of carbon dioxide and other waste products.
Speaker A:So that's where exchange takes place right at the capillary bed.
Speaker A:So we have to think about what are the characteristics of perfusion at that level.
Speaker A:And we know that the capillary bed is a very low pressure system, so that it's not going to take too much external compressive force to start to shut down the capillary bed, to at least partially close the capillaries, to reduce the amount of blood getting through, and to compromise that exchange between the capillary bed and the tissues.
Speaker A:So the question has been asked, how much external force does it take to partially or totally collapse the capillary bed and shut down or significantly reduce blood flow to the tissues?
Speaker A: And the answer is, in: Speaker A:Now, there have been some studies done.
Speaker A:Some of them were done way back where they tried to determine what the pressures were in the capillary bed.
Speaker A:It's really not an easy study to do because you can't just go up to a capillary bed, isolate it, and take a blood pressure.
Speaker A:The physician who tried to do research on pressures within the capillary bed had a very unique approach.
Speaker A:He took little pipettes and drove them underneath the nail bed and help the individuals to access the capillary beds, hooked them up to little manometers, and then monitored pressures.
Speaker A:Well, I'm thinking the pressures were probably a little bit elevated from pain.
Speaker A:And also, he only did the test in healthy adult males, whereas we're frequently dealing with very sick individuals who are already hypotensive at baseline.
Speaker A:But that is some data that we have to go on.
Speaker A:And what he found was that the pressures within the capillary bed range from about 25 to 32 millimeters of mercury.
Speaker A:And based on that, for a long time, people thought, okay, so capillary closing pressure, the amount of external force required to collapse the capillary bed was probably somewhere around 32 millimeters of mercury.
Speaker A:But studies done since that time in much more humane conditions have found that, on average, capillary bed pressures are probably about 17 millimeters of mercury.
Speaker A:So the amount of external force required to collapse the capillary bed is probably much lower than that 32 millimeters of mercury.
Speaker A:So what does that mean to us, we know that the capillary bed is a low pressure system.
Speaker A:We know that any significant external compressive force can partially or totally collapse the capillary bed and either impair or stop perfusion to the tissues.
Speaker A:But there's good news there, because you think, well, how come we're not seeing many more pressure injuries?
Speaker A:Because we turn a patient to the side for two hours, they're probably getting enough pressure to at least partially reduce blood flow through the capillary bed.
Speaker A:But if we turn them every two hours, they don't develop pressure injuries.
Speaker A:Sometimes they can go three hours and not develop pressure injuries.
Speaker A:So here's the other things we've learned.
Speaker A:We know that short term occlusion is well tolerated, and that's because the metabolic rate in the soft tissues is relatively low.
Speaker A:So if you turn a patient onto their right side and you partially collapse the capillary beds along that surface, you're going to reduce blood flow.
Speaker A:But when you turn that patient, those tissues will be well, oxygenated.
Speaker A:They use that oxygen at a very slow rate, and they're going to tolerate several hours with reduced blood flow without tissue ischemia.
Speaker A:So we're not dealing with heart muscle, we're not dealing with brain.
Speaker A:Heart muscle can't go more than three to five minutes.
Speaker A:Your brain can't go very long at all because the heart muscle is constantly working.
Speaker A:The brain's constantly working, at least we hope it is.
Speaker A:But soft tissue is very different.
Speaker A:They use oxygen at a much slower rate.
Speaker A:So that provides our patients with a degree of protection.
Speaker A:They can tolerate several hours without active blood flow or without normal levels of blood flow.
Speaker A:Now, here's the other thing that we've learned.
Speaker A:Normally, we're all equipped with a pressure injury prevention system.
Speaker A:So you think, you don't walk around worrying about pressure injuries when you go to bed at night.
Speaker A:You don't set your alarm to wake up and turn every three hours during the night.
Speaker A:And that's because you have intact sensation and intact mobility.
Speaker A:And this is the way that system works.
Speaker A:You think about it, every one of you at some point in time have rolled over on your arm during the night.
Speaker A:And when you rolled over on your arm, you essentially cut off blood flow to the tissues.
Speaker A:And they're going to tolerate it for a while, and then they're going to start to become ischemic.
Speaker A:Ischemia hurts.
Speaker A:And so what happens, you wake up, your arm is screaming at you, wake up and get off of me.
Speaker A:Right?
Speaker A:So ischemic pain wakes you up, you turn, you get off Your arm.
Speaker A:So now you've restored blood flow.
Speaker A:Now, right at first you know that the arm is very ischemic, that the tissues in the arm are very ischemic, because you can't even operate your arm normally.
Speaker A:You can't make your fingers do the things they can usually do.
Speaker A:You try, but it doesn't really work.
Speaker A:But then within a few minutes, typically five to 10 minutes, everything is back to normal.
Speaker A:So you see how sensory awareness and mobility work together to protect you.
Speaker A:Even out of a sound sleep, you woke up and you all floated your arm.
Speaker A:Have you ever met a patient who's only got one arm and who said, I didn't wake up?
Speaker A:Nope.
Speaker A:Because sensory awareness, if your sensory pathways are intact and your brain is intact, you will wake up to ischemic pain and you will respond by offloading the area and restoring blood flow.
Speaker A:When you think of people who are at risk for pressure injury development as people who lack normal sensation, lack the ability to process sensory signals appropriately, or lack mobility.
Speaker A:So it's people who are paralyzed, people who are heavily sedated, people who are demented.
Speaker A:So coming back to our etiologic factors, we know that prolonged or intense pressure is one critical factor.
Speaker A:They also talk about pressure gradients.
Speaker A:So if you have high pressures exerted right over the bony prominence, you can see that blood shunts away from the area of high pressure.
Speaker A:And then you have an area of tissue that's acutely ischemic.
Speaker A:So prolonged or intense pressure or very acute pressure gradients, that's an extrinsic factor, shear force.
Speaker A:Shear force causes disruption of blood flow because it literally causes tissue layers to move against each other.
Speaker A:Vessels get compressed or torn and you lose blood flow.
Speaker A:So prolonged your intense pressure shear force.
Speaker A:Two very important extrinsic factors that we know from multiple studies are the primary causative factors for pressure injury development.
Speaker A:Now, there's also been a lot of work looking at reduced or compromised tissue tolerance.
Speaker A:Why some patients seem so much vulnerable than others.
Speaker A:Why are underweight patients, very thin patients, much higher risk than your overweight, obese patients?
Speaker A:Why are patients with poor perfusion at higher risk?
Speaker A:Well, some of these things are pretty obvious, but these are intrinsic factors that make a difference that we're going to talk about.
Speaker A:Now, before we leave this slide, I want you to notice the thing at the very bottom.
Speaker A:And it says most pressure injuries at this point are thought to be bottom up injuries.
Speaker A:So look at the slide in the middle, on the bottom.
Speaker A:So you think, okay, you've turned this patient back to their back, and a lot of the weight is being supported by the sacrococcygeal area.
Speaker A:What happens when the weight supported by the bony prominences?
Speaker A:Remember that you get high pressure right over that bone.
Speaker A:The bone is in contact with the muscle, the bones essentially compressing the muscle, and the muscle is the layer with the highest metabolic rate and the layer that is most sensitive to reduce blood flow to ischemia.
Speaker A:So when you turn me back and a lot of my weight is being borne by my bony prominences, the current evidence suggests that compressive force shuts down blood flow or significantly reduces blood blood flow to the tissues overlying the bony prominences, and that that's where the damage begins.
Speaker A:A lot of you have seen patients who started out and maybe they had an area of deep discoloration that we now know as a deep tissue injury, and within a week they have a stage four pressure injury extending to the muscle or the bone.
Speaker A:And this explains why.
Speaker A:Where did the damage start?
Speaker A:At the muscle layer.
Speaker A:That's where you have the highest pressures, the most interference to blood flow, and the tissue layer that is most sensitive to ischemia.
Speaker A:So this is just going to go over some of the things we've already talked about, the impact of prolonged or intense pressure.
Speaker A:So you think you get tissue compression.
Speaker A:So then you have to think, okay, well, now what's running through the tissue and what's going to be the negative impact of that tissue compression?
Speaker A:We've talked a lot about the fact that the blood vessels run through the soft tissue.
Speaker A:So when you compress the tissue over the bone, you're compressing the vessels and you're reducing the rate of blood flow.
Speaker A:If you have very high intense pressure, you may be eliminating blood flow.
Speaker A:You also get lymphatic occlusion, because remember, the lymphatic vessels run right along the arterial vessels and the venous system.
Speaker A:Now, what do the lymphatics do?
Speaker A:They return fluid from the tissues back into the venous system.
Speaker A:So if you occlude the arterial vessels, you get ischemia.
Speaker A:If you occlude the lymphatics in the venous vessels, you get edema.
Speaker A:So now you've got edematous tissue, you've got ischemic tissue.
Speaker A:The edema further compromises blood flow, of course.
Speaker A:And then we think that there's the issue of reperfusion injury.
Speaker A:So what happens with reperfusion injury?
Speaker A:You think, okay, we have compressed the tissue, compressed the vessels, significantly reduce the rate of blood flow, possibly almost stopped blood flow.
Speaker A:And so what's going to happen.
Speaker A:You're talking about blood flow through narrow vessels.
Speaker A:Now you're going to get micro thrombi forming because the blood's just sitting there pooled.
Speaker A:So you're going to start to get little clots.
Speaker A:Then when you restore blood flow, what's going to happen?
Speaker A:Those blood clots are going to flow downstream and they're going to occlude smaller vessels.
Speaker A:So now you've got recurrent issue with ischemia.
Speaker A:You had ischemia, you restored blood flow, and now you have ischemia from the effect of those little clots blocking smaller vessels.
Speaker A:In addition, when you significantly reduce blood flow and you start to change metabolism from aerobic to anaerobic, you start to produce oxygen free radicals.
Speaker A:And then those oxygen free radicals cause further damage to the vessels that cause a lot of edema, can cause sloughing of the vessel lining and further obstruction to blood flow.
Speaker A:We know a lot about reperfusion injury when it comes to the coronary arteries and what happens with mi.
Speaker A:We know much less about reperfusion injury as it relates to of pressure injuries.
Speaker A:So at this point, the effects of reperfusion injury are theoretical and hypothesized.
Speaker A:I just want you to be aware of that.
Speaker A:We definitely know about the impact of tissue compression and vessel compression in terms of ischemia and in terms of edema.
Speaker A:We think reperfusion injury may play a role.
Speaker A:And the other thing that may play a role, some researchers have done some studies that have demonstrated direct negative impact of high intensity pressure on the cytoskeleton of the muscle cell.
Speaker A:So they've shown that if there's high compressive force, it can damage the muscle cell totally apart from the negative impacts of ischemia, edema, and possibly reperfusion injury.
Speaker A:Now the question is, could you get damage to all of the tissue cells?
Speaker A:Could tissue compression cause literally direct damage to keratinocytes, to vascular cells?
Speaker A:Is it just muscle cells that are adversely affected by direct damage, direct compression?
Speaker A:We don't know.
Speaker A:So what we do know is the negative impact of ischemia, the negative impact of edema.
Speaker A:We think that reperfusion injury may play a role.
Speaker A:We think that direct damage to the tissue cells may play a role, but we have much less definitive data in those areas.
Speaker A:So I just wanted you to be vaguely aware of those.
Speaker A:Here's something we do know more about, and that's the inverse relationship between the intensity of the pressure and the time tolerance of the tissues.
Speaker A:So I want you to think about a lot of you have kids, and so you've gone to their ball games and you have sat in the bleachers.
Speaker A:So if you're sitting on concrete bleachers or wooden bleachers, that surface is totally unyielding.
Speaker A:And when you sit down, all of your weight is going to be concentrated on your bony prominences.
Speaker A:You're going to get rapid onset of tissue ischemia, and it's not going to take long before you're moving around to restore blood flow.
Speaker A:Now, if you have a kid that's big into sports, you have multiple kids, and you're going to lots of games, and sitting on bleachers for prolonged periods of time, you're probably going to get a stadium seat.
Speaker A:You might get the deluxe version.
Speaker A:So what does that stadium seat do for you?
Speaker A:It adds padding that is conformable.
Speaker A:So when you sit in the stadium seat, you sink into that padding and the pressure is distributed much more evenly.
Speaker A:So it brings the intensity of the pressure down.
Speaker A:And what does it do to your time tolerance?
Speaker A:What does it do to the length of time you can sit there?
Speaker A:Before you're wiggling it, extends it.
Speaker A:So mid level pressures are going to be tolerated for moderate periods of time.
Speaker A:High level pressures will be tolerated only for short periods of time.
Speaker A:Now, let's think what that means for us in healthcare.
Speaker A:So we have all replaced our standard hospital mattresses with redesigned hospital mattresses that provide even pressure distribution and a conformable surface so that our patients sink into the surface and get fairly even pressure distribution.
Speaker A:And that buys them time.
Speaker A:It gives them more time before their tissues begin to become ischemic.
Speaker A:And sure enough, more recent study studies have shown that if we're managing a patient on a very conformable surface where pressures are evenly distributed, you can reduce turning frequency without causing pressure injury development.
Speaker A:Now, you might not want to reduce turning frequency because there's many reasons to turn a patient other than skin integrity, but just helpful to realize that as we improve the conformability of the surface, as we allow patients to sink in, as pressures are distributed across the entire body, surface tissue tolerance improves.
Speaker A:But if we take you off of your surface, off of your mattress that has been redesigned, and we take you to X ray or interventional radiology and they just have hard tables, how long can you lie on that hard table before your tissues begin to become ischemic?
Speaker A:So it matters what type of surface the patient's on.
Speaker A:It impacts on the intensity of the pressure, which in turn impacts on the length of time that the tissues can tolerate that pressure without sustaining Damage.
Speaker A:We know that every day in clinical practice, we do, we use two measures to try to prevent pressure injury development.
Speaker A:We just talked about the impact of pressure redistribution surfaces.
Speaker A:When you put a patient on a therapeutic foam mattress.
Speaker A:When you put a patient on an air mattress, you put them on those surfaces to get even pressure distribution and to drive down pressure intensity and prolonged tissue tolerance.
Speaker A:What about when you turn a patient?
Speaker A:Every time you turn a patient, you offload the previous area, restore blood flow and buy them more time.
Speaker A:Right.
Speaker A:So a combination of pressure redistribution surfaces and routine repositioning are the two key elements in pressure injury prevention protocols.
Speaker A:Now, let's talk about what happens if there are repeated periods of impaired blood flow.
Speaker A:So let's say that I have a patient who's very resistant to turning, and it's a crazy weekend.
Speaker A:And so on Saturday, the patient refuses turning at 8, refuses turning at 10.
Speaker A:I finally get the patient to allow me to turn him at 12.
Speaker A:But now it's been from six to 12.
Speaker A:So it's been six hours.
Speaker A:And so there's some microscopic damage in the tissues because there was some ischemic changes in the tissues, but I don't see anything visible externally.
Speaker A:It looks like maybe we got by.
Speaker A:Well, then what if he again refuses turning at 2:00 and 4:00 and I go through another six hour period?
Speaker A:So now I've had two back to back periods of ischemia to these tissues.
Speaker A:Every time you have a period of ischemia, you get some microscopic tissue damage.
Speaker A:That microscopic tissue damage causes an increase in the metabolic rate of the damaged tissue.
Speaker A:It takes more oxygen to repair tissue than to maintain tissue.
Speaker A:So repeated periods of impaired blood flow cause additive damage in the soft tissues.
Speaker A:We have to be very aware of that.
Speaker A:Patients think nothing happened, everything's okay.
Speaker A:Sometimes nursing staff thinks nothing happened, everything's okay.
Speaker A:But in fact, every period of impaired blood flow that extends beyond the two hours or three hours makes the patient higher risk for pressure injury formation.
Speaker A:We talked a little bit about the impact of pressure gradients.
Speaker A:So when you have what we call peak pressures, so you have a patient on a relatively rigid surface, all of their weights being supported by their bony prominences, tissues compressed here, but not compressed here.
Speaker A:Then blood moves from the point of compression to the area that is not under compression, and you get rapid development of ischemia.
Speaker A:It can also cause interstitial fluid shifts.
Speaker A:So that's why you see across the board that agencies have moved to routine use of very conformable surfaces.
Speaker A:We've changed the COVID of Our mattresses and we've changed the core.
Speaker A:So core contents or core medium in mattresses today is either therapeutic foam, a gel, or air.
Speaker A:Therapeutic foam, gel and air.
Speaker A:They all are conformable liquids or gases, so they will conform to changes in the patient's position, evenly distribute the pressure.
Speaker A:That conformable surface allows the patient to sink it.
Speaker A:That minimizes those peak pressures that cause blood to shunt away and that cause acute tissue ischemia.
Speaker A:So a lot of advances have been made in pressure injury prevention just by learning about the factors leading to pressure injury formation and looking at what can be done in terms of supports or surfaces as well as repositioning.
Speaker A:So those are your two critical elements.
Speaker A:Again, you keep hearing it over and over.
Speaker A:You're going to hear it again when we talk about pressure injury prevention.
Speaker A:Either put them on a pressure redistribution mattress, put them on an alternating pressure surface, and routinely reposition the patient so that you restore blood flow, lymphatic flow, and interstitial fluid flow.
Speaker A:So we've talked about pressure, we've talked about the negative impact of high intensity pressure, prolonged pressure, or recurrent episodes of prolonged pressure.
Speaker A:Now let's talk about shear damage.
Speaker A:So we didn't recognize the impact of shear damage for a long time.
Speaker A:And then studies were done that showed that if patients were exp.
Speaker A:Exposed to both shear.
Speaker A:I mean, sorry, to both pressure and shear, which is sliding force, they were much more likely to develop tissue damage than if they were exposed to pressure alone.
Speaker A:So now a lot of work has been done looking at what happens with shear injury.
Speaker A:What are the factors that combine to cause shear injury?
Speaker A:So it's interaction between friction and gravity.
Speaker A:So let's say I'm lying flat in a hospital bed.
Speaker A:You do not have my head elevated.
Speaker A:Okay, I'm fine.
Speaker A:I'm not experiencing any shear force at this point, but I am being held in place by frictional forces.
Speaker A:So friction causes the skin to become adherent to the underlying surface.
Speaker A:It kind of holds you in place so you don't go flying out of bed.
Speaker A:So, you know when you go to turn a patient or move a patient up in bed and it's almost like their skin has stuck to the sheets, that's the force of friction.
Speaker A:Friction in itself is not a problem.
Speaker A:But now if you come in and you elevate the head of my bed, now you've introduced gravity.
Speaker A:So now friction is trying to hold me in position and gravity is trying to pull me down.
Speaker A:So here's what ends up happening.
Speaker A:You elevate the head of the bed, gravity Causes the deep tissue layers, the bones, the muscles, and the soft tissue to shift down.
Speaker A:The skin's like, not me, I'm sticking with the sheet.
Speaker A:So the skin remains stationary.
Speaker A:Deep tissue layers move, and what happens, you see how tissue layers move against each other, and that's what they're trying to show you in that bottom slide and in the top slide.
Speaker A:When tissue layers move against each other, slide against each other, it causes distortion, angulation, or disruption of arterioles, venules, and lymphatics, all of the vessels that normally keep tissues healthy.
Speaker A:So you can see that if you add shear force to pressure, you're going to get much more severe damage with much faster onset.
Speaker A:So we need to do everything we can to minimize shear forces.
Speaker A:Now, what happens when you get shear forces?
Speaker A:Because shear damage can occur in any direction.
Speaker A:Because remember, you're tearing blood vessels.
Speaker A:So if it's a pressure injury alone, it's pretty much going to match the shape of the wound because it's this kind of force.
Speaker A:But with shear injury, it's this kind of force.
Speaker A:Damage can go in any direction.
Speaker A:So you frequently have elongated, irregular wounds.
Speaker A:You frequently have tunneling, you frequently have undermining.
Speaker A:So what are the things we try to do to minimize shear?
Speaker A:Well, we, we try to keep the head of the bed as flat as possible.
Speaker A:But, you know, most of our patients require head of bed elevation.
Speaker A:So we have to work with surfaces that minimize friction so that if the patient slides, at least they don't get shear.
Speaker A:You want all tissue layers to slide together.
Speaker A:The third thing we want to talk about is the impact of tissue tolerance.
Speaker A:So we know that some patients are much higher risk than others.
Speaker A:We know that patients who have soft tissue wasting, like this little lady you saw earlier, she's very high risk because she has no padding over her bony prominences.
Speaker A:That means she's going to get high intensity pressure and she's going to get rapid development of ischemia.
Speaker A:What about patients with vascular disease?
Speaker A:So think about how many patients go to surgery every day for coronary artery bypass grafting.
Speaker A:So if they have coronary artery disease, what do you think is going on in their legs?
Speaker A:What do you think is going on at the level of their heels?
Speaker A:They have disease there, too.
Speaker A:We're not focused on their legs, we're not focused on their heels.
Speaker A:We're focused on their heart.
Speaker A:So a lot of times they go to surgery, they go to pacu, they come back to the floor.
Speaker A:Nobody really is focused on their heels until a couple of days later.
Speaker A:And by that time they have deep tissue injuries that result in very severe pressure injuries.
Speaker A:So we want to be aware if a patient has a history of cardiovascular disease, cerebrovascular disease, or lower extremity arterial disease, all of those patients are very high risk for pressure heel injuries.
Speaker A:So we want to keep those heels off the bed.
Speaker A:What about vasopressors?
Speaker A:We know that ICU patients are the highest risk population.
Speaker A:They're critically ill, they're frequently hypotensive, and many times we have to use vasopressors to maintain their blood pressure in a safe range.
Speaker A:But vasopressors cause constriction of the blood flow or constriction of the vessels to the soft tissue.
Speaker A:So, yes, we're shunting blood flow to the critical organs, the heart, the brain, the kidneys.
Speaker A:What's happening to the skin and soft tissue?
Speaker A:Many of you have probably seen ischemic necrotic digits in patients who have been on long term vasopressors.
Speaker A:You might have seen very severe pressure injuries as well.
Speaker A:So vasopressors, hypotension, fever because it drives up the metabolic rate, edema because it compromises blood flow to the tissues, stress because it increases cortisol levels, and of course, you know, all the negative impacts of smoking.
Speaker A:Now, can I make this lady plump?
Speaker A:No.
Speaker A:Can I undo her vascular disease?
Speaker A:Can I take people off vasopressors?
Speaker A:No.
Speaker A:But we can recognize these things that make somebody much higher risk, and we can ramp up our prevention program and hopefully keep that pressure injury from occurring.
Speaker A:So I'm going to summarize part A of this and then we'll move into part B where we talk about clinical progression of a pressure injury and we talk more about medical device related.
Speaker A:So in Part 1, or I guess we just finished Part 3A and we're moved into Part 3B.
Speaker A:So Part 3A, I want you to realize, pressure injuries, where are they located?
Speaker A:They're going to be over bony prominences under medical devices.
Speaker A:They can be shallow super wounds, partial thickness.
Speaker A:Most of the time they're full thickness.
Speaker A:If it's over a bony prominence, typically it starts at that muscle bone interface and comes up if pressure is the etiologic factor.
Speaker A:Remember that the problem is that you've cut off blood flow to the tissue.
Speaker A:So it's very common to have necrotic tissue slough or eschar.
Speaker A:Also very common to have tissue loss, so you end up with craters.
Speaker A:What are the major factors that cause pressure injuries?
Speaker A:We know too for sure, okay, high intensity or prolonged pressure, shear force, we know that compromised tissue tolerance plays a role.
Speaker A:We suspect that reperfusion injury may contribute.
Speaker A:We suspect that direct damage to the cytoskeleton of the cell may play a role.
