Michael Trepal, DPM discusses common age related pathologies and treatment modalities in the podiatric geriatric patient population as well as the psychological and physiological pedal concerns often faced in this population.
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TAPE STARTS – [00:00]
Male Speaker: Perfect set-up because I’m going to talk about many of the same things, but we will reach diabetes and emphasize it, so you’ve – we can shorten my talk a little bit, get everyone out. But the broader topic of diabetes is all the people. And as I get closer to it myself, I’m careful of the term. So again, nothing to disclose for this, and our objective is to describe the demographics of it, some of the unique characteristics of aging, and some of the things that we can do.
You get lots of these different timelines, of what we are, you can see, you know, everything comes full circle, we started off non-ambulatory, and we end up in many cases non-ambulatory, and from much of the same reasons that Bob just mentioned about the need to keep going, the need to keep – to get away from that sedentary lifestyle is very much a fact of life, and as it goes – and as all the people lose their mobility, as they lose their ability to engage, they withdraw, they become depressed, the psychological – and there’s so much of a downfall on there that we – in our neck of the woods, down over here, can do many things, not just in terms of direct podiatric interventions, but in dealing with these patients, and some of the things that – interventions that maybe transcend what would normally be considered podiatric.
The ability to have bipedal locomotion is what the sociologists say really cause or develop us to really evolve, right? As we transition through to bipedal locomotion, frees up hands to hunt, to do work, to gather, to communicate, to show emotion, to build, and this need to be bipedal locomotion gets destroyed as many cases as people age.
And we’re kind of unique as a species, as not too many – not too many species that can get around bipedal. And to nobody’s surprise, we are an aging, we are an aging population. And if you see where the biggest growth is, it’s up in here, 80 plus. You see that, yes, there’s more of us, we’re living longer, but the biggest growth in the age relation is in patients at 85 plus. So this is squaring of the pyramid, where in the past, we saw many more young people, that this pyramid is getting square, and in fact, there is the scare in some of the European countries that have extremely low birth rates, that this pyramid is actually going to invert, and there is some fear that you may have more older people than younger people. And think about what that does to the economic needs of a society, the health care needs, the burden, the expense, the living, the services, things.
So this is – this is a very real phenomena that’s occurring. They say the three stages of life, I mean there are many, children and teenagers have energy, have time but no money. Adults have energy, have money but no time. And older people, try to get away from the word elderly, but mature people, they got time, they have money, but no energy. So where you do you feel that you fit in on that spectrum?
So important things in age-related changes, decrease reserve capacity, and this affects everything that we do in our patients. Patients have decreased muscle mass, decreased strength, they have decreased bone mass, osteopenia, osteoporosis. They have decreased reserve of the skin, the epidermis thins, they have decreased Langerhans cells, which serve as an immunologic function.
Obviously, our ability to fight disease and to fight infection, that the immune system becomes senescent. The heart, the left ventricular thickens, it gets stiffness, the cardiac output, the ejection fraction decreases, lungs have decrease tidal volume, the capacity to exchange gases, and the kidneys, they have decreased renal function. And again, this affects everything that we do with a patient, in trying to keep them mobile and it affects us surgically in the operating room. It affects us in prescribing medications to these patients as to what it can be.
And the various – as we age, we lose this functional capacity here, and we’re not the same people. If you look at the changes in the body compartments between age at 25, and at age at 70, certainly, we have more fat, I don’t think that’s a surprise to any. But again, physiologically, structurally, and atomically, we’re very different. So what we do, and again, I’m going to echo, I think I’m on the same rhymes as what Bob says is get, you know, focused on function. Now, some people, you know, they can keep going and they get up and go and for others, it’s much more of an ordeal, and so. This is what we want to keep our patients, doing that, and try to the big extent as possible as to avoid that.
Foot and ankle pain has a higher impact on what happens above. When your foot hurts, and as the saying goes, it hurts all over, and the foot bones connected to the leg bone and et cetera right up there, when ankle arthritis or bunions or hammertoes, or metatarsalgia, it affects the kinetic chain right up the body.
The ankle and the foot are indeed the foundation for the musculoskeletal system. And as we age, gait changes, again same things that Bob mentioned. We walk slower, stride length decreases, arm swing decreases, there’s forward flexion at the head and the torso. All right, that’s due to a lot of different muscle wasting, can be osteoporosis, you get an increased lordosis, lordosis and kyphosis, increased flexion of the shoulders and knees, and increase lateral sway. You see someone older – then, again, there’s lots of reasons for that, some of that are just antalgic gait because of painful hips, of painful knees, some of it is reduction in muscle mass, some of it is maybe is due to foot pain, maybe due to heel pain that we see this way.
Foot problems impair balance, we know that, and are a major risk for falls. Some of the more common things that we see as someone, you know, ages, we’re not worried in a 12-year old that a juvenile bunion is going to cause that individual to fall. But in someone who’s older, okay, that bunion – that bunion pain, coupled with, perhaps, reduced plantar sensation, toe flexor weakness, toe shoe gear problems, limited capacity to dorsiflex the ankle, stiffness, again predominant factors in causing a fall. And again, the data shows, again, no surprise here, that as we age, foot problems get more, more common, and in fact it’s rare to do a population of patients greater than 60 years old without finding a significant number of foot deformities.
Fall aging prevalence, 30% of those over 65 – wow, that’s one out of three fall annually, half are repeat fallers. Each decade of life, falls increased, over those – half of those in nursing homes and hospitals fall each year. Fall prevention, my wife works in an extended care facility and fall prevention is a major, major issue in any extended care facilities.
What can we do in here? Again, a lot of these is preventable. Acute injury, whether that be a paronychia, whether that be an inflamed corn, whether it be a painful inflamed plantar fasciitis, where we can be part of the team, we interview these patients, we talk to them, we see their families, we see that many times, patients are in polypharmacy, their dermatologist gave them a steroid for something, their internist gave them a sleeping pill, their cardiologist gave them a platelet inhibitor, so they’re taking all these drugs and they may not understand. So part of what we do is not to take necessarily these patients off of drugs, but how we can contribute to their overwhelming, over health condition.
Rehab, exercises keep them going. Prescribed exercises, sensory impairments of the foot, now we may not be able, in a neuropathic foot, to correct it, but we certainly can adapt or deal, and as Bob kept saying, modify it, evaluate for osteoporosis, and perhaps even encourage proper diet. Dietary, put patients on vitamin D. All right, we see osteoporosis in patients all the time.
I routinely sent patients for DEXA scans. There’s nothing wrong of ordering a DEXA scan on the patient. If it comes back, you know, recommend some dietary changes or send them to their internist or younger – even younger females, osteoporosis is a disease that starts in your 20s. And we’ve reached massive maximum bone density at age 25. After you hit 25, it’s all downhill over that.
So we can do a lot in identifying that and helping patients deal with it. Internists, postural – ask patients, observe. When they sit in your chair and they stand up, do they look a little dizzy, a little woozy? Is it – is that that they’re having a problem of hypotensive medications. Again, refer them back to their internist.
Footwear, I mean, who – this is – this is our domain. Foot – are they wearing proper shoes? Are we informing them what to do? Do we talk to them about their environment? Hip protectors? Again, four risk factors, there’s so many different things over here and to a large extent in the center of it, it sits and resides at the foot.
Looking at shoes, I always, every time I have a patient in there, I’d look at the shoes. Shoes are a roadmap as to what’s going on. You know, all too often the patient sits in the chair, we come into the room, we’re busy and the shoes are often in the corner there and we don’t look at them.
I make a habit of checking shoe wear and checking the shoes in every single patient by seeing all the patient come in, you know, I’m converting that just not into they’re coming in to get their nails cut. I mean I view my – if they want to get their nails cut, go down the hall to the beauty parlor or something and get that done. I’m trying to convert that into much more meaningful visits for the patient and part of that is looking indeed at the shoe and the shoe gear. Not only is this an accident waiting to happen, it – what is this telling me about how they’re – about how they are functioning.
We can tell a lot about how the patient is functioning by just watching them, the so called, ‘get up and go’ test. All right? And in other words, how long does it take when they stand up. Again, just don’t walk out of the room and say, ‘okay, fine. See you in sixty-one days’ to cut your nails again. Watch them get up and then get – this has been a documented test, less than 10 seconds is normal. If it takes 10 to 20 seconds after a patient gets up to try to get their balance and to regain their posture, they are frail and if it’s greater than 20 seconds then they probably need to be referred to a geriatrician or a generalogist to try to see what’s the underlying.
Also, the reach test, to assess balance in elderly patient – improper balance is a fault. And in this particular test, the subject stands with the physics standing alongside a wall. Subject leans forward as far as possible to the wall without taking a step while losing stability. The length of the fists and movement to – is measured distance of less than six inches indicating increased risk of falling. So you see the patient lean forward and to see what happens. These are all simple little things.
Glasses, all right, it’s important if you’re going to tell people to check their feet if you have diabetics and they’re going to check their feet. You’re going to ask them to look for a cut, a sore or if people are doing things to their feet and they can’t see. Many people can’t afford glasses, they font go to the ophthalmologist. So it’s important, I think, aspect of what we do as comprehensive care. Do it quite well. We’re obviously not going to prescribe glasses, we’re obviously not going to be doing retinal examinations on these patients.
But we can certainly determine if the patient can see.]
Question them about their home situation, a home evaluation – ask if there’s a family there. Is this – are there floor rugs there that patients can trip and fall. What kind of shoes are they wearing at home? Are they wearing defrayed and deformed slippers that can help us – is this a fall waiting to happen?
Assessing osteoporosis, this is the distant – obviously, the result of osteoporosis in the spine. We’re looking old photographs of your parents and grandparents, what it looks like. Well, this obviously is affecting the foot as well. And we’ll see it by taking an X-ray or determining in the foot. Now, this has implications for us and the development of stress fractures. It has surgical implications, if you’re considering a surgical procedure on the patient and its osteoporotic bone, you’re certainly going to modify maybe the procedure you’re doing, the type of fixation that you’re going to use, but also if I notice it here it, very quick to order a DEXA scan on the patient, again, not that I’m going to primarily treat that but make the appropriate referral with the appropriate recommendations for follow-up care.
Osteoarthritis, if you have osteoarthritis in the first MTPJ, as we heard this morning in the very informative radiology talk, if you have it – if you have it in the first MPJ, you almost invariably have it in the hip as well. And again, they’re interrelated. Dealing – you know, there’s a reciprocal relationship. Did the hip cause the first MPJ or did the foot function cause the hip arthritis? And it can work both ways and in both directions.
Skin, normal aging changes in skin that when the skin becomes atrophic, it becomes thinner, there are decreased cellular contractions, so that in an older patient, much more prone to ulcerate. A simple dorsal clavi in the younger individual as compared to a more mature individual.
Much more prone to ulceration and development of osteomyelitis, cellulitis, and complications that that could well be avoided. So we take, you know, much more concern in these patients.
Osteo onychomycosis, certainly a disease as we get older. And again, we can look at this as just a nail cutting routine, a nail cutting visit, or we can, you know, look at this as a true disease. And certainly, it is much more common, and it’s not an insignificant problem. Onychomycosis in the adult – how many times has lead to that?
Okay. Amputations, these get infected. So what we’re doing in a sense is not just not routine foot care, routine nail care. Depending upon the nature of the patient, it can well indeed be limb preservation and all of the other.
Acquired – adult acquired flat foot deformity. Okay. Much more common. It’s a disease of aging. Cause is associated with hypertension, obesity. Diabetics have a higher incidence of this. And again, this is one of those things that you want to catch early.
That 50-, 55-, 60-year-old slightly overweight patient who comes in having posterior medial malleolus pain and some swelling. Okay. Because very frequently, stage I PTTD, and that’s the time to intervene, to do the appropriate, you know, shoe modifications or fosies, the AFOs, would be necessary to stabilize that early on before they come back – and these things can go quick. In a matter of months, you can take, you know, stage I tenosynovitis of the posterior tibial tendon and, you know, two or three months later that PT tendon goes, craps out, and you got a, you know, it won’t be ridged at that point but a completely collapsed hind foot.
And those are difficult. Those surgical procedures are not insignificant in nature. They frequently involve major complex hind foot fusion, sometimes even ankle fusions. So an ounce of prevention here is really worthwhile.
Skin changes, pigmentation, BM melanoma. We heard another lecture the other day on melanocytic lesions. Skin melanoma of the foot is a different animal than it is on the rest of the body. Okay. It’s not sun-exposed areas. It’s more common in darker skinned individuals than, you know, the classic melanoma where it’s light skin, if it’s Patrick type I or type II. The blue eyes, blond hair, red head, yeah, that’s true for torso melanoma but not of the foot. Okay.
Careful inspection of in-between toes, looking for this pre-malignant lesion that was over here. Another pre-malignant lesion that, in identifying these, whether you adapt skills with dermoscopy or other evaluative tools or have not sent to that out to a dermatologist or another podiatrist who is adept at looking at it. But again, the skin, and particularly pigmentation changes, we can and do save lives. These dysplastic – atypical dysplastic nevi, if left alone almost invariably will degenerate into a malignancy.
Foot melanoma, again, is a disease much more of the older individuals. Again, much more common in the Afro-Caribbean population, and the whites is relatively smaller incidence of it, but nevertheless, someone who is not used to looking at their foot in between the toe, subungual lesion, these are all things that we need to be looking at in the patients.
Again, the foot type is an acral lentiginous. Acral lentiginous, not only meeting the acral areas of the body but it has a specific histopathologic component to it. There is a certain – they also have a different genetic capability to it. They are much common with the BRAF mutation. They have these long fusiform cells that are radial in nature. And these have a fairly high propensity for early metastasis, almost as much as the nodular melanoma. This is fundamentally and histologically different than the nodular melanoma, but deadly just the same.
Pay attention to melanonychial streaks. Again, we heard a good lecture on this yesterday about it. Look for Hutchinson’s sign, a pigment within the nail fold. Look for bands that are greater than 3 millimeters wide variation in pigment. And remember, if you’re going to biopsy it, the place to biopsy is here at the matrix. That’s where you’re going to make the diagnosis.
Diabetes, no doubt, we had a very interesting talk with Bob about the incidence and the progression of diabetes. This is epidemic. As we live longer, more are going to be having diabetes. And there’s the saying, if you ignore your feet, they’ll simply go away. So, this is what we’re looking to avoid. This is what Bob referred to as the salami surgery that starts out as a digital ulceration that ends up with partial metatarsal amputation that goes up to transmet. The transmet breaks down and before you know it, you’re into a BK amputation.
Every 30 seconds, a lower limb is lost somewhere. Not all. Most of these, in my opinion, can be prevented. Again, not every one of them, but certainly a lot more than the case.
And doing all those things, and whether it has props and move the dial back or do other interventions, we have a big role to play at this, if not the biggest role because we do the most comprehensive lower extremity care.
This, again, is a fairly popular slide I have. You know, I don’t know – the implication sometimes is that the amputation is the proximate cause of the mortality, and there may be some truth to that if you take into account the decreased mobility that occurs with it, the psychological depression of it. So there’s probably something to it that had that patient not had the amputation, that they might still be walking around on this planet.
But also remember that the disease process that sets up for the ulceration, that sets up for the atherosclerosis. Whether it be in the atherosclerosis in the tibial artery is the same process of the atherosclerosis that’s occurring in the LAD artery in the heart, it’s the same process. So these are co-morbidities that – there’s probably something to it that if you could prevent amputations, that in reality will be saving lives down the line.
We all ought to be testing significantly for PAD. We ought to be testing it for neuropathy. It’s the easy thing to do. We ought to be looking how that foot lowers, whether you do sophisticated computer-assisted data analysis in the office or you do a pressure mat. But if you’re going to see areas of increased pressure in the face of, say, a foot coupled with peripheral vascular disease, that’s a disaster waiting to happen. And again, Bob did a great setup for me, this is the time to intervene.
Your feet can say a hell of a lot about your heart as well. CAD means PAD and vice versa.
So that’s been referred to as a heart attack of the foot, that terminology. An acute ischemic event in the foot is very akin to an acute ischemic event of the heart. And the comparison, the global estimates, the prevalence and risk factors for peripheral arterial disease, systematic review, it’s increasing across the world.
Again, these slides are all you see in the multiple lectures. When you have PAD in the foot, you have long-term survival. The presence of clinical limb ischemia, okay, the mortality rate, the 10-year is about 10%, 9 out of 10 of those patients will be dead. And remember, claudicators – claudication is treated very different than someone with an ulcer or an acute ischemic event, all right? Claudicators are not – there’s usually not interventions. They don’t die.
Claudicators don’t go on to amputations. Claudicators die of MIs and strokes. The treatment for claudication is cilostazol and a supervised exercise program. They don’t need interventions. What they need is control their exercise, their activity, get them out of their sedentary – a controlled exercise period and cilostazol.
ABI is now considered, as part of the follow up to the Framingham risk score, is an active predictor and a risk factor for an end-stage cardiovascular disease, okay? So sentinel cardiac events can be predicted by a low ABI. And again, it’s an easy test to do in the office.
Also, arterial emboli. How many people are – have the AFib? Every time you pick up the – turn on the TV, you’re seeing a commercial for one of the anticoagulants, Eliquis and all of the other varieties of it, all right? In patients with AFib, because of the turbid flow within the heart, okay, they can throw off an emboli.
Now, that emboli can go north up to the brain and cause a stroke, a fatal stroke, and it can – to make a south turn, go south and end up in an artery at the lower extremity. That’s what killed my father, who was a – he had AFib and he had am emboli, went to his leg. He had acute ischemic event. And you know, everything goes downhill when you get into the hospital. They have to do dye for the angiogram, and that craps out the kidneys, and it’s just a systemic organ failure thing.
Oddly enough, the highest incidence of throwing a clot is when – in patients with paroxysmal AFib. Because when they go in or come out of AFib, when the rhythm starts or when the rhythm goes out, people with sustained or chronic AFib but don’t have the same incidence of embolic phenomena. So if the atrial fib, the microemboli goes north, it ends with up micro influx within the brain. If it goes south, it can end up with little focal hemorrhages in it.
Now, again, this little hemorrhage over there – this is a patient who came in to see me had – was running through the airport to catch a plane suddenly felt a sharp pain in his toe. I looked – I mean, he wasn’t diabetic, he wasn’t neuropathic, he had good pulses. You know, you have to try to explain. It didn’t look like a traumatic hemorrhage. Why did that occur?
The pulse was a little bit irregular. He had paroxysmal AFib, and that’s what was the cause of his ulcer over there.
Again, Janeway lesions, you will see these. These are irregular non-tender hemorrhagic macules on the palms or the soles, and these occur in patients with acute bacterial endocarditis, okay. And they result from septic microemboli.
Now, these patients are usually sick if you’re doing consults in the hospital, and you see these lesions on someone who’s in for a cardiac reason or for – they may very well be from septic emboli coming from a heart valve or a heart wall.
Osler nodes is a variation of the same thing. These are red-purple, raised cutaneous nodules, again, caused by septic microemboli. They are tender, they are very painful, and they’re situated at the tip of the toes, in the acral areas of the foot. And these are usually more common in patients with sub-acute bacterial endocarditis, not acute endocarditis. So these are patients that very easily could walk into your office with it.
Pressure ulcers, if the patient is ambulatory and in your office, this is not something that’s generally going to do it. But if the patient comes into your office by an ambulette – they’re brought in, they’re not ambulatory, they’re in a wheelchair, they’re brought to you or you’re doing rounds in the hospital or extended care facility, pressure ulcers are almost always – and I mean that – almost always preventable, okay?
Unfortunately, the prevalence is still too high. They occur during the first few weeks of a hospitalization. Usually, within the first couple of days, they occur in sacral areas, shoulders, and heel. And generally, of this, it’s exactly what the name says, a pressure where that if you have pressure on the skin that exceeds the capillary pressure, which is usually around 32 millimeters of mercury, these things will start to occur.
And they can go – they start off as what’s called a DTI, as a deep tissue injury, and they can progress relatively quick. The incidents in a nursing home, the mortality from a severe pressure ulceration of sacral decubiti is exceedingly high. They get septic very easily and this could be the precipitating factor for end of life.
So basically, what I wanted to say is, yes, we are the experts on the foot. What we do on the foot is second to none in terms of any other profession or occupation. But I urge you, never just treat a foot. Look at a patient with a foot problem, and even though the pathology may not be directly something that we treat, we certainly can identify it and make a referral to the proper.
So I thank you for your time.
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