St. Louis (KSDK) -- Your high heels may be doing more harm than you think.
Doctors say they're seeing more and more women coming in with foot problems because the high heel heights are soaring and there seems to be less support in some of those shoes.
Ten or 15 years ago, the problems were a lot easier to fix, but now doctors say women are set on wearing higher heel, so they're doing a lot more long term damage.
"The higher the heels the worse the problems," said Dr. Rick Lehman, an orthopedic surgeon. "As these new shoes come out the incidents of foot problems have gone through the roof."
Dr. Lehman said the high heels can cause bunions, plantar fasciitis and achilles tendon problems.
Dr. Lehman says if you're going to wear high heels, make sure to stretch your feet, wear a wide enough shoe and give your feet a break if they start to hurt.
Thursday, November 17, 2011
Neuropathy diminishes pain, sensations in feet
The condition is caused by poor blood-glucose control associated with diabetes
Dealing with neuropathy
• Keep blood glucose levels in your target range.
• If you have problems, get treatment immediately.
• Check your feet every day. If you can’t feel pain, you might not notice an injury.
• If your feet are dry, use a lotion on your skin but not between your toes.
• Wear well-fitting shoes and socks.
• Use warm water to wash your feet, and dry them carefully.
• Get special shoes, if needed. If you have foot problems, Medicare may pay for shoes.
• Be careful with exercising. Talk with a diabetes clinical exercise expert.
Source: American Diabetes Association, www.diabetes.org
It’s a very uncomfortable situation: the loss of sensation on your feet.
Not being able to feel whether the ground is hot or cold, or whether your shoes don’t fit right. Or worse, not noticing the damage you could be causing to your feet.
“When you realize you’ve lost pain, you are in trouble,” says Dr. Andrew Boulton, professor of medicine in the division of endocrinology, diabetes and metabolism of the University of Miami Miller School of Medicine.
Boulton has witnessed the consequences of not feeling pain.
The patient who walked around without noticing he had a nail through his shoe. Another one who took a stroll on the beach not realizing the hole slowly carved on his foot by the hot sand. Or the man who felt asleep near a chimney and woke up to the smell of something burning — his feet.
Boulton is an expert on neuropathy, a disease prompted by poor glucose control, among other factors. The condition causes nerve damage, impairing feeling in the foot.
Neuropathy acts similarly to an electrical circuit being disrupted. The nerves send messages to your brain about heat, cold, touch and pain. Nerves communicate how and when to move your muscles, and also have control over systems like sweat glands or digestive functions. So when these nerves are damaged, communication stops.
It’s important to take steps to prevent foot injuries, Boulton says.
“Use your eyes and look where you are walking,” he says. “All this is preventable. This doesn’t need to happen if you look after your feet.”
This is important advice since diabetes is the most common cause of foot ulcers, says Dr. Robert Kirsner, professor of dermatology at the University of Miami Miller School of Medicine.
“Because patients don’t have sensation, they may not have any symptoms,” Kirsner says. “That’s why it’s critical that patients with diabetes examine their feet regularly, and when they go to their physician, their feet get examined.’’
Ulcers or foot wounds can cause serious problems if they don’t heal because, in worst cases, this increases the chances of amputation.
“If we can heal the ulcer faster and better, those complications can be diminished,” he says. Eliot Prince, a patient of Kirsner, is well aware of the importance of looking after your feet.
The 47-year-old Miami native credits Kirsner for saving the toes on his left foot. About seven years ago Prince, who had been diagnosed with diabetes in 1992, had noticed that two toes on his left foot were darkening and had started to swell.
He went to Nassau, hoping that the salty waters of the island would heal his foot. He was putting his socks on when his hand slipped, removing some of the skin. He flew back to Miami the next day. At the hospital he was told it could be gangrene and that his two toes might have to be cut off.
“I didn’t have gangrene but if you would have seen them you’d thought I had gangrene because my toes were black.”
He wanted a second opinion, and a friend told him about Kirsner.
“He cut off the skin, examined it. He knew what he was looking for,” Prince says. Kirsner told him that the wound was treatable and prescribed him a cream that eventually healed his foot.
People with neuropathy can also develop ulcers. They have to wear special shoes to remove pressure from the wound, Kirsner explains.
“That’s the most important thing with neuropathic foot ulcers, to remove pressure off the wound,” he says.
Special shoes or boots improve the way people walk by making them take fewer steps and shortening the length of their stride.
Another foot-related complication is excessive dryness, a sign that the sweat glands aren’t working properly. In those cases, special moisturizers are prescribed to help deal with the discomfort. When you have dry, cracked feet, you are more likely to get a fungus infection, Kirsner explains.
Fungus cause microscopic changes on the skin; it’s an opening that allows bacteria to come in and cause an infection.
“A fungal infection on a diabetic patient is more important than in other patients because infections on diabetic patients have more complications,” Kirsner adds.
By Douglas Rojas-Sosa
Dealing with neuropathy
• Keep blood glucose levels in your target range.
• If you have problems, get treatment immediately.
• Check your feet every day. If you can’t feel pain, you might not notice an injury.
• If your feet are dry, use a lotion on your skin but not between your toes.
• Wear well-fitting shoes and socks.
• Use warm water to wash your feet, and dry them carefully.
• Get special shoes, if needed. If you have foot problems, Medicare may pay for shoes.
• Be careful with exercising. Talk with a diabetes clinical exercise expert.
Source: American Diabetes Association, www.diabetes.org
It’s a very uncomfortable situation: the loss of sensation on your feet.
Not being able to feel whether the ground is hot or cold, or whether your shoes don’t fit right. Or worse, not noticing the damage you could be causing to your feet.
“When you realize you’ve lost pain, you are in trouble,” says Dr. Andrew Boulton, professor of medicine in the division of endocrinology, diabetes and metabolism of the University of Miami Miller School of Medicine.
Boulton has witnessed the consequences of not feeling pain.
The patient who walked around without noticing he had a nail through his shoe. Another one who took a stroll on the beach not realizing the hole slowly carved on his foot by the hot sand. Or the man who felt asleep near a chimney and woke up to the smell of something burning — his feet.
Boulton is an expert on neuropathy, a disease prompted by poor glucose control, among other factors. The condition causes nerve damage, impairing feeling in the foot.
Neuropathy acts similarly to an electrical circuit being disrupted. The nerves send messages to your brain about heat, cold, touch and pain. Nerves communicate how and when to move your muscles, and also have control over systems like sweat glands or digestive functions. So when these nerves are damaged, communication stops.
It’s important to take steps to prevent foot injuries, Boulton says.
“Use your eyes and look where you are walking,” he says. “All this is preventable. This doesn’t need to happen if you look after your feet.”
This is important advice since diabetes is the most common cause of foot ulcers, says Dr. Robert Kirsner, professor of dermatology at the University of Miami Miller School of Medicine.
“Because patients don’t have sensation, they may not have any symptoms,” Kirsner says. “That’s why it’s critical that patients with diabetes examine their feet regularly, and when they go to their physician, their feet get examined.’’
Ulcers or foot wounds can cause serious problems if they don’t heal because, in worst cases, this increases the chances of amputation.
“If we can heal the ulcer faster and better, those complications can be diminished,” he says. Eliot Prince, a patient of Kirsner, is well aware of the importance of looking after your feet.
The 47-year-old Miami native credits Kirsner for saving the toes on his left foot. About seven years ago Prince, who had been diagnosed with diabetes in 1992, had noticed that two toes on his left foot were darkening and had started to swell.
He went to Nassau, hoping that the salty waters of the island would heal his foot. He was putting his socks on when his hand slipped, removing some of the skin. He flew back to Miami the next day. At the hospital he was told it could be gangrene and that his two toes might have to be cut off.
“I didn’t have gangrene but if you would have seen them you’d thought I had gangrene because my toes were black.”
He wanted a second opinion, and a friend told him about Kirsner.
“He cut off the skin, examined it. He knew what he was looking for,” Prince says. Kirsner told him that the wound was treatable and prescribed him a cream that eventually healed his foot.
People with neuropathy can also develop ulcers. They have to wear special shoes to remove pressure from the wound, Kirsner explains.
“That’s the most important thing with neuropathic foot ulcers, to remove pressure off the wound,” he says.
Special shoes or boots improve the way people walk by making them take fewer steps and shortening the length of their stride.
Another foot-related complication is excessive dryness, a sign that the sweat glands aren’t working properly. In those cases, special moisturizers are prescribed to help deal with the discomfort. When you have dry, cracked feet, you are more likely to get a fungus infection, Kirsner explains.
Fungus cause microscopic changes on the skin; it’s an opening that allows bacteria to come in and cause an infection.
“A fungal infection on a diabetic patient is more important than in other patients because infections on diabetic patients have more complications,” Kirsner adds.
By Douglas Rojas-Sosa
Tuesday, November 8, 2011
EXERCISE AND NEUROPATHY: Not mutually exclusive
A classic case of innovative research turning conventional wisdom on its head is changing the way clinicians approach exercise in patients with diabetic neuropathy.
For decades, patients with type 2 diabetes and peripheral neuropathy were cautioned against weight-bearing exercise out of fear that the accompanying stress on the foot would lead to plantar ulcers. Then, in 2003, scientists began to report surprising findings.
“Prior to those studies, the feeling was that weight-bearing exercise was too risky to recommend to patients who lacked sensation,” said Joseph LeMaster, MD, MPH. LeMaster, for many years an associate professor in the Department of Family and Community Medicine at the University of Missouri, will move to the University of Kansas this fall. “There was evidence that people with neuropathy had increased plantar pressures, and those were considered an independent risk factor for foot ulcers.”
In 2003, LeMaster and his colleagues published a study of 400 diabetes patients with a history of foot ulcers and found that increased weight-bearing activity didn’t increase the risk of reulceration. Moreover, the most active subjects saw the most significant risk reduction, and the effects were the same regardless of whether subjects retained foot sensation.1
That same year, researchers from Washington University in St. Louis reported in Clinical Biomechanics that diabetes patients with a history of plantar ulcers were 46% less active and accumulated 41% less daily stress on the forefoot than nondiabetic and diabetic control subjects without a history of such ulcers.2 At first, the finding seemed so counterintuitive that people weren’t sure what to make of it. The authors ultimately concluded, conservatively, that subjects with a history of plantar ulcers were susceptible to injury at relatively low levels of tissue stress.
These studies flung open the door to further investigations, however. In 2004, scientists confirmed in Diabetes Care that neuropathic patients who exercised more had lower rates of ulceration than those who were relatively sedentary.3 Two years after that, in 2006, researchers in Italy reported that, far from being deleterious, exercise could help prevent neuropathy’s onset or modify its natural history.4 Right on cue, then, in 2008, Washington University researchers reporting on the Feet First study noted that promoting weight-bearing activity did not lead to significant increases in foot ulcers.5 Finally, in 2010, the American Diabetes Association, together with the American College of Sports Medicine, acknowledged this accumulating body of evidence and published new guidelines that, for the first time, endorsed weight-bearing exercise for patients with diabetic neuropathy in the absence of foot ulcers.6
“The new guidelines represent a big change,” said Michael Mueller, PT, PhD, a professor of physical therapy at Washington University School of Medicine. “For the first time, people with diabetic neuropathy are explicitly encouraged to do weight-bearing exercise.”
Although this rhythmic chronology outlines what appears to be a straightforward investigation that changed medical practice, the story is more nuanced. A number of questions have bedeviled researchers, and continue to. For example, what’s the chicken and what’s the egg? That is, do people get more ulcers because they get less exercise, or do they exercise less because of their ulcer history? Or, for that matter, are other variables involved that no one yet understands? These and other issues, such as how to distinguish those at highest risk of ulceration from their peers and how to adjust exercise regimens accordingly for individual patients, are only now starting to become clear.
Foundations
Back in 2002, Mueller published a paper in Physical Therapy whose relevance to this issue was not immediately clear, but which turned out to have a big impact. In that article, he proposed a “Physical Stress Theory” (PST) of tissue adaptation, the premise of which was that changes in the relative level of physical stress cause a predictable adaptive response in biological tissues.7 In a nutshell, the theory suggests that tissues respond to stress in predictable ways: stress levels that are too low lead to reduced stress tolerance and atrophy; mid-level stress produces no change; moderately high levels increase tolerance; and too much stress leads to injury and tissue death. The goal for practitioners seeking to increase their patients’ strength and resilience was to identify the levels that increased tolerance and work carefully from there.
Mueller also made several points that affected later researchers:
1. Stress exposure is a composite value comprising magnitude, time, and direction of stress application.
2. Extreme deviations from the maintenance stress range have serious consequences.
3. Individual stresses combine in complex ways to contribute to the overall level of stress exposure, and tissues are affected by the history of recent stresses.
4. Excessive stress can arise due to a brief, high-magnitude stress; a long duration of low-magnitude stress; or a repetitive application of moderate stress.
5. Inflammation occurs immediately after injury, reduces the injured tissue’s stress tolerance, and requires that the tissue be protected from further stress until the inflammation subsides.
Many of these points turned out to be crucial to understanding how to manage diabetic neuropathy in the context of exercise.
Variability
The lead author of the 2004 study in Diabetes Care was David Armstrong, DPM, MD, PhD, professor of surgery and director of the Southern Arizona Limb Salvage Alliance (SALSA) at the University of Arizona College of Medicine in Tucson. An important aspect of his team’s findings was not just that more active subjects were less prone to ulcers, but that variability in activity was an important predictor of ulcer risk. Eight of 100 patients with diabetic neuropathy ulcerated during the average evaluation period of 37 weeks, and although they were significantly less active than those who remained ulcer-free, there was also much more variability in their exercise levels, as measured by high-capacity computerized accelerometer/pedometers.
“People who had wide swings in activity were at greater risk,” Armstrong told LER. “An example would be someone who’s not very active, then suddenly remembers their grandkid’s birthday and leaps off the couch, runs to the car, then spends an hour and a half walking around the mall. They do more in a couple of hours than they usually do in two days.”
When Armstrong and his colleagues first evaluated their data, they were flummoxed.
“We sat there wondering what was going on,” he said.
Their conclusion, however, echoed Mueller’s observations about the importance of tissue stress levels and the consequences of extreme deviation in them.
“We believe what we’re seeing is that it’s just like a lot of other places in the body,” Armstrong explained. “If you don’t use it, you lose it. If skin is allowed to atrophy, then maybe it’s weaker than skin that’s getting tenderized, as it were, by frequent activity.”
Armstrong noted that patients must be monitored carefully, as they were in his study, and that exercise has to be optimized for the individual.
“People can’t run a marathon with profound neuropathy, but we’d like to try to train them so they could slowly become more active,” he said. “We want to dose activity the way you’d titrate a drug.”
As for the chicken-and-egg problem—which comes first, the ulcer or the lower activity levels?—researchers are continuing to probe the reasons first ulcers appear. Manish Bharara, PhD, a research assistant professor at SALSA and a colleague of Armstrong’s, speculated that overall control of blood glucose levels may affect the resilience of damaged tissues.
“In diabetes patients, metabolic control affects other aspects of physiology, and could affect the quality of the tissue that is regenerated as someone heals,” he said.
A couple of Armstrong’s earlier papers may shed light on the issue, as well. In a 2001 article in the Journal of the American Podiatric Medical Association, Armstrong and his colleagues noted that diabetic patients with a history of neuropathy or ulceration took more steps per day inside the home than outside, and that only 15% of them wore their prescribed footwear inside.8 A paper in Diabetes Care in 2003 reported that subjects with foot ulcers wore their off-loading devices for only a minority of steps taken each day.9 Noncompliance with preventive footwear or curative devices could conceivably be similar in effect to low activity levels, then, in that both are associated with ulceration and poor healing. One possible explanation is that, compared to high-activity patients, low-activity patients are taking significantly fewer steps per day in footwear designed to help their feet avoid injury or heal (activity studies have not consistently reported compliance data).
“It even turns out that sometimes just standing for long periods can be potentially dangerous,” Armstrong noted.10 “This is all about better identifying risk and helping us better coach activity. We’re trying to get people moving, and in a lot of ways, that’s how we measure success.”
Individual cases
The Feet First study made it clear that clinicians must carefully consider the patient’s history when prescribing exercise, according to lead author LeMaster.
“In that study, we felt that the exercise program, combined with the careful monitoring we conducted, showed that the benefits of exercise outweighed the risks,” he said. “But it’s quite another thing to say that people who have lots of recent foot ulcers should go out and do this. A good percentage of the people in the study had had prior ulcers, and we didn’t find that to be a predictor [of ulceration during the trial]. But we restricted people from walking if they had any breakdown during the study.”
People with a history of frequent and recurrent ulcers, he added, should be viewed in a different category than those included in the research. Furthermore, the study’s subjects had their feet examined weekly by a physical therapist for the first three months, and had a hotline to call if they showed signs of ulceration later.
Mike Mueller, a coauthor of the 2008 Feet First paper, likened the evolving view of exercise in those with neuropathy to a similar evolution in thinking about exercise in cardiac patients a few decades ago.
“There was a time when the prevailing opinion was that if you’d had a heart attack, you should not exert yourself,” Mueller said. “We came to learn that if you monitor the heart carefully and keep it within a safe range, exercise is beneficial. It’s similar with the neuropathic foot, although we’re still learning what the guidelines should be.”
Adjusting exercise programs to the individual based on variables such as ulcer history is still an emerging field, he noted, and based both on the evidence provided by research and on clinical experience.
“I believe that once you’ve had a full-thickness ulcer, you’re in a whole different category,” he said. “Even a mild one sends up a red flag that you’d better watch this person. There’s so much heterogeneity in the group of people who have diabetes and neuropathy that the program really needs to be tailored to the individual.”
Joint biomechanics
Part of the problem with such tailoring is that only recently has research begun to describe the relationship between biomechanics and diabetic neuropathy.
For example, a 2007 paper in the Journal of Applied Biomechanics found that diabetic subjects with neuropathy had stiffer ankles than diabetic subjects without neuropathy.11 It’s known that normal mobility allows the foot to flexibly dissipate impact, then become rigid during push-off.12 Restricted mobility in the foot and ankle joints, then, could hinder this transition and contribute to abnormal plantar loads.13
Citing such evidence, Smita Rao, PhD, an assistant professor of physical therapy at New York University, published a paper in 2006 outlining how changes in muscle could account for decreased range of motion (ROM) and increased stiffness in patients with diabetes.14 In a subsequent article in Gait & Posture, she and her colleagues reported that decreased sagittal motion of the first metatarsal and lateral forefoot and frontal motion of the calcaneus were key elements that could contribute to increased, sustained plantar loading in patients with diabetes and neuropathy.15
“There’s a big push to emphasize exercise in patients with diabetes and peripheral neuropathy, but those patients are also at higher risk for tissue breakdown, so I wanted to explore the mechanisms that put them at risk,” Rao told LER. “We showed in the Gait & Posture paper that a lot of these patients try to reduce the effects of their stiffness by walking slower and taking shorter steps. When I examine them, I want to look at ankle range of motion, all the mechanical factors that may affect tissue breakdown; but I also want to assess how they walk, find focal regions of high pressure, then put those two together to see if walking is the best activity for this person. Some might need protective footwear, and some should ride a stationary bike instead.”
In her current research, Rao and her colleagues at NYU are examining ways to bring a number of fields together.
“My grandfather had diabetes, so I have a personal connection to the field,” she said. “All these negative effects begin with high blood sugar, so we’re trying to combine medical, surgical, and rehabilitative interventions in patients with diabetes and neuropathy.”
Exercise and balance
Other research has looked at the importance of augmenting exercise with balance training, which has been shown to improve clinical balance measures in neuropathic patients.16 A study published in Diabetes Care in 2010 demonstrated, moreover, that six weeks of such training reduced the risk of falls in 16 older patients with type 2 diabetes and mild to moderate neuropathy.17 In that research, exercise sessions included a balance/posture component (lower-limb stretches and leg, abdominal, and lower-back exercises) and a resistance and strength-training component using machines. The regimen led to better reaction times and affected sensory, motor, and cognitive processes, leading to a significant decline in risk of falls.
Lead author Steven Morrison, PhD, director of research in the School of Physical Therapy at Old Dominion University in Norfolk, VA, told LER that his group’s work was motivated partly by the fact that older diabetes patients’ risk of falling is 10 to 15 times that of healthy age-matched controls, which affects their confidence and ability to exercise.
“To be balanced, you need a certain amount of strength and a certain amount of coordination,” he said. “We found that after six weeks of training, type 2 diabetic individuals become more like the control group—there’s very little difference in terms of how much they sway and what their balance is like.”
Monitoring
David Sinacore, PT, PhD, a professor of physical therapy and medicine at Washington University, and one of the researchers involved in studies of exercise and neuropathy there, emphasized that monitoring—by clinicians or the patients themselves—is crucial to successful exercise programs in those with diabetic neuropathy, particularly if they also have foot deformities such as those resulting from Charcot arthropathy.
“I’m a firm believer that these folks need to exercise for their diabetes,” he said. “But if they start to develop lesions, they need to be addressed.”
Of course, as most clinicians know, there is often a gap between ideal and real-world monitoring levels.
“It’s hard for these patients to check the bottom of their feet regularly, so they sometimes don’t do it,” Sinacore said.
One way to help is with temperature monitoring. Sinacore recommends foot-temperature gauges that patients can use right after exercising, some of which are hook-shaped to ease plantar access.
“When we monitor them here, we check temperature before and after exercise,” he said. “We’re looking for hot spots and temperature differences that may indicate that they’re developing a lesion.”
In such cases, therapists recommend that patients decrease their exercise levels for a while and have their footwear modified to relieve pressure.
David Armstrong agreed that thermometry provides a way of keeping track of the damage caused by weight-bearing exercise.
“We want our patients to dose their activity by checking their skin temperature just as they dose their insulin by checking their glucose,” he said.
His colleague, Manish Bharara, conducts innovative research in this aspect of care.18
“In the last decade we’ve learned that a four-degree difference between two similar sites on both feet is an ulcer risk,” he said. “If the pattern persists over multiple days, the patient should reduce activity and immediately see a doctor.”
Bharara and his colleagues are developing a thermometry scale to address some of the inconveniences typically associated with measuring foot temperature at several sites. Patients stand on it—it’s similar to a bathroom scale—while it measures foot temperature at 20 sites on each foot and records the data. The scale speaks to the patient—telling him, for example, that his right big toe temperature is 5° warmer than the left. Moreover, if the scale detects an abnormal pattern for more than two days, it can be programmed to send a message to the physician’s office and make an appointment.
“Something like this could really help manage patients’ diabetes better, because the biggest barrier is compliance,” Bharara said.
New research
Other researchers are examining variables that affect neuropathic patients’ exercise capabilities, as well. For example, at the Center for Lower Extremity Ambulatory Research at Rosalind Franklin University in Chicago, Bijan Najafi, PhD, associate professor of applied biomechanics, has studied factors including gait initiation in this context.19 As opposed to the measures of steady-state walking—such as rate or number of steps—typically used in exercise studies, a prolonged gait initiation phase (the period between upright posture and steady-state gait) may be associated with increased fall risk.
“During the initiation of the step, there’s an important acceleration phase, and it creates a lot of resistive force,” Najafi said. “We’ve found that neuropathy patients have longer gait initiation. This makes sense, because to reach steady-state gait, people have to gather somatosensory feedback to find the speed at which they can walk safely and minimize energy costs. Neuropathy patients have impaired somatosensory feedback, though. But we believe that if we can provide a good exercise to compensate, we may be able to improve the gait initiation phase.”
One way to help, Najafi thinks, is to take a cue from the dance world.
“If you’re trying to explain a movement problem to a dancer he may not get it, but if you put a mirror in front of him and show him the correct position of the joints, he can improve his motor skills,” he said. “The brain is plastic, and if it realizes there’s an error, it will try to minimize it next time. So we hope that by letting neuropathy patients observe their errors this way, they may improve their motor skills.”
Cary Groner is a freelance writer based in the San Francisco Bay Area.
For decades, patients with type 2 diabetes and peripheral neuropathy were cautioned against weight-bearing exercise out of fear that the accompanying stress on the foot would lead to plantar ulcers. Then, in 2003, scientists began to report surprising findings.
“Prior to those studies, the feeling was that weight-bearing exercise was too risky to recommend to patients who lacked sensation,” said Joseph LeMaster, MD, MPH. LeMaster, for many years an associate professor in the Department of Family and Community Medicine at the University of Missouri, will move to the University of Kansas this fall. “There was evidence that people with neuropathy had increased plantar pressures, and those were considered an independent risk factor for foot ulcers.”
In 2003, LeMaster and his colleagues published a study of 400 diabetes patients with a history of foot ulcers and found that increased weight-bearing activity didn’t increase the risk of reulceration. Moreover, the most active subjects saw the most significant risk reduction, and the effects were the same regardless of whether subjects retained foot sensation.1
That same year, researchers from Washington University in St. Louis reported in Clinical Biomechanics that diabetes patients with a history of plantar ulcers were 46% less active and accumulated 41% less daily stress on the forefoot than nondiabetic and diabetic control subjects without a history of such ulcers.2 At first, the finding seemed so counterintuitive that people weren’t sure what to make of it. The authors ultimately concluded, conservatively, that subjects with a history of plantar ulcers were susceptible to injury at relatively low levels of tissue stress.
These studies flung open the door to further investigations, however. In 2004, scientists confirmed in Diabetes Care that neuropathic patients who exercised more had lower rates of ulceration than those who were relatively sedentary.3 Two years after that, in 2006, researchers in Italy reported that, far from being deleterious, exercise could help prevent neuropathy’s onset or modify its natural history.4 Right on cue, then, in 2008, Washington University researchers reporting on the Feet First study noted that promoting weight-bearing activity did not lead to significant increases in foot ulcers.5 Finally, in 2010, the American Diabetes Association, together with the American College of Sports Medicine, acknowledged this accumulating body of evidence and published new guidelines that, for the first time, endorsed weight-bearing exercise for patients with diabetic neuropathy in the absence of foot ulcers.6
“The new guidelines represent a big change,” said Michael Mueller, PT, PhD, a professor of physical therapy at Washington University School of Medicine. “For the first time, people with diabetic neuropathy are explicitly encouraged to do weight-bearing exercise.”
Although this rhythmic chronology outlines what appears to be a straightforward investigation that changed medical practice, the story is more nuanced. A number of questions have bedeviled researchers, and continue to. For example, what’s the chicken and what’s the egg? That is, do people get more ulcers because they get less exercise, or do they exercise less because of their ulcer history? Or, for that matter, are other variables involved that no one yet understands? These and other issues, such as how to distinguish those at highest risk of ulceration from their peers and how to adjust exercise regimens accordingly for individual patients, are only now starting to become clear.
Foundations
Back in 2002, Mueller published a paper in Physical Therapy whose relevance to this issue was not immediately clear, but which turned out to have a big impact. In that article, he proposed a “Physical Stress Theory” (PST) of tissue adaptation, the premise of which was that changes in the relative level of physical stress cause a predictable adaptive response in biological tissues.7 In a nutshell, the theory suggests that tissues respond to stress in predictable ways: stress levels that are too low lead to reduced stress tolerance and atrophy; mid-level stress produces no change; moderately high levels increase tolerance; and too much stress leads to injury and tissue death. The goal for practitioners seeking to increase their patients’ strength and resilience was to identify the levels that increased tolerance and work carefully from there.
Mueller also made several points that affected later researchers:
1. Stress exposure is a composite value comprising magnitude, time, and direction of stress application.
2. Extreme deviations from the maintenance stress range have serious consequences.
3. Individual stresses combine in complex ways to contribute to the overall level of stress exposure, and tissues are affected by the history of recent stresses.
4. Excessive stress can arise due to a brief, high-magnitude stress; a long duration of low-magnitude stress; or a repetitive application of moderate stress.
5. Inflammation occurs immediately after injury, reduces the injured tissue’s stress tolerance, and requires that the tissue be protected from further stress until the inflammation subsides.
Many of these points turned out to be crucial to understanding how to manage diabetic neuropathy in the context of exercise.
Variability
The lead author of the 2004 study in Diabetes Care was David Armstrong, DPM, MD, PhD, professor of surgery and director of the Southern Arizona Limb Salvage Alliance (SALSA) at the University of Arizona College of Medicine in Tucson. An important aspect of his team’s findings was not just that more active subjects were less prone to ulcers, but that variability in activity was an important predictor of ulcer risk. Eight of 100 patients with diabetic neuropathy ulcerated during the average evaluation period of 37 weeks, and although they were significantly less active than those who remained ulcer-free, there was also much more variability in their exercise levels, as measured by high-capacity computerized accelerometer/pedometers.
“People who had wide swings in activity were at greater risk,” Armstrong told LER. “An example would be someone who’s not very active, then suddenly remembers their grandkid’s birthday and leaps off the couch, runs to the car, then spends an hour and a half walking around the mall. They do more in a couple of hours than they usually do in two days.”
When Armstrong and his colleagues first evaluated their data, they were flummoxed.
“We sat there wondering what was going on,” he said.
Their conclusion, however, echoed Mueller’s observations about the importance of tissue stress levels and the consequences of extreme deviation in them.
“We believe what we’re seeing is that it’s just like a lot of other places in the body,” Armstrong explained. “If you don’t use it, you lose it. If skin is allowed to atrophy, then maybe it’s weaker than skin that’s getting tenderized, as it were, by frequent activity.”
Armstrong noted that patients must be monitored carefully, as they were in his study, and that exercise has to be optimized for the individual.
“People can’t run a marathon with profound neuropathy, but we’d like to try to train them so they could slowly become more active,” he said. “We want to dose activity the way you’d titrate a drug.”
As for the chicken-and-egg problem—which comes first, the ulcer or the lower activity levels?—researchers are continuing to probe the reasons first ulcers appear. Manish Bharara, PhD, a research assistant professor at SALSA and a colleague of Armstrong’s, speculated that overall control of blood glucose levels may affect the resilience of damaged tissues.
“In diabetes patients, metabolic control affects other aspects of physiology, and could affect the quality of the tissue that is regenerated as someone heals,” he said.
A couple of Armstrong’s earlier papers may shed light on the issue, as well. In a 2001 article in the Journal of the American Podiatric Medical Association, Armstrong and his colleagues noted that diabetic patients with a history of neuropathy or ulceration took more steps per day inside the home than outside, and that only 15% of them wore their prescribed footwear inside.8 A paper in Diabetes Care in 2003 reported that subjects with foot ulcers wore their off-loading devices for only a minority of steps taken each day.9 Noncompliance with preventive footwear or curative devices could conceivably be similar in effect to low activity levels, then, in that both are associated with ulceration and poor healing. One possible explanation is that, compared to high-activity patients, low-activity patients are taking significantly fewer steps per day in footwear designed to help their feet avoid injury or heal (activity studies have not consistently reported compliance data).
“It even turns out that sometimes just standing for long periods can be potentially dangerous,” Armstrong noted.10 “This is all about better identifying risk and helping us better coach activity. We’re trying to get people moving, and in a lot of ways, that’s how we measure success.”
Individual cases
The Feet First study made it clear that clinicians must carefully consider the patient’s history when prescribing exercise, according to lead author LeMaster.
“In that study, we felt that the exercise program, combined with the careful monitoring we conducted, showed that the benefits of exercise outweighed the risks,” he said. “But it’s quite another thing to say that people who have lots of recent foot ulcers should go out and do this. A good percentage of the people in the study had had prior ulcers, and we didn’t find that to be a predictor [of ulceration during the trial]. But we restricted people from walking if they had any breakdown during the study.”
People with a history of frequent and recurrent ulcers, he added, should be viewed in a different category than those included in the research. Furthermore, the study’s subjects had their feet examined weekly by a physical therapist for the first three months, and had a hotline to call if they showed signs of ulceration later.
Mike Mueller, a coauthor of the 2008 Feet First paper, likened the evolving view of exercise in those with neuropathy to a similar evolution in thinking about exercise in cardiac patients a few decades ago.
“There was a time when the prevailing opinion was that if you’d had a heart attack, you should not exert yourself,” Mueller said. “We came to learn that if you monitor the heart carefully and keep it within a safe range, exercise is beneficial. It’s similar with the neuropathic foot, although we’re still learning what the guidelines should be.”
Adjusting exercise programs to the individual based on variables such as ulcer history is still an emerging field, he noted, and based both on the evidence provided by research and on clinical experience.
“I believe that once you’ve had a full-thickness ulcer, you’re in a whole different category,” he said. “Even a mild one sends up a red flag that you’d better watch this person. There’s so much heterogeneity in the group of people who have diabetes and neuropathy that the program really needs to be tailored to the individual.”
Joint biomechanics
Part of the problem with such tailoring is that only recently has research begun to describe the relationship between biomechanics and diabetic neuropathy.
For example, a 2007 paper in the Journal of Applied Biomechanics found that diabetic subjects with neuropathy had stiffer ankles than diabetic subjects without neuropathy.11 It’s known that normal mobility allows the foot to flexibly dissipate impact, then become rigid during push-off.12 Restricted mobility in the foot and ankle joints, then, could hinder this transition and contribute to abnormal plantar loads.13
Citing such evidence, Smita Rao, PhD, an assistant professor of physical therapy at New York University, published a paper in 2006 outlining how changes in muscle could account for decreased range of motion (ROM) and increased stiffness in patients with diabetes.14 In a subsequent article in Gait & Posture, she and her colleagues reported that decreased sagittal motion of the first metatarsal and lateral forefoot and frontal motion of the calcaneus were key elements that could contribute to increased, sustained plantar loading in patients with diabetes and neuropathy.15
“There’s a big push to emphasize exercise in patients with diabetes and peripheral neuropathy, but those patients are also at higher risk for tissue breakdown, so I wanted to explore the mechanisms that put them at risk,” Rao told LER. “We showed in the Gait & Posture paper that a lot of these patients try to reduce the effects of their stiffness by walking slower and taking shorter steps. When I examine them, I want to look at ankle range of motion, all the mechanical factors that may affect tissue breakdown; but I also want to assess how they walk, find focal regions of high pressure, then put those two together to see if walking is the best activity for this person. Some might need protective footwear, and some should ride a stationary bike instead.”
In her current research, Rao and her colleagues at NYU are examining ways to bring a number of fields together.
“My grandfather had diabetes, so I have a personal connection to the field,” she said. “All these negative effects begin with high blood sugar, so we’re trying to combine medical, surgical, and rehabilitative interventions in patients with diabetes and neuropathy.”
Exercise and balance
Other research has looked at the importance of augmenting exercise with balance training, which has been shown to improve clinical balance measures in neuropathic patients.16 A study published in Diabetes Care in 2010 demonstrated, moreover, that six weeks of such training reduced the risk of falls in 16 older patients with type 2 diabetes and mild to moderate neuropathy.17 In that research, exercise sessions included a balance/posture component (lower-limb stretches and leg, abdominal, and lower-back exercises) and a resistance and strength-training component using machines. The regimen led to better reaction times and affected sensory, motor, and cognitive processes, leading to a significant decline in risk of falls.
Lead author Steven Morrison, PhD, director of research in the School of Physical Therapy at Old Dominion University in Norfolk, VA, told LER that his group’s work was motivated partly by the fact that older diabetes patients’ risk of falling is 10 to 15 times that of healthy age-matched controls, which affects their confidence and ability to exercise.
“To be balanced, you need a certain amount of strength and a certain amount of coordination,” he said. “We found that after six weeks of training, type 2 diabetic individuals become more like the control group—there’s very little difference in terms of how much they sway and what their balance is like.”
Monitoring
David Sinacore, PT, PhD, a professor of physical therapy and medicine at Washington University, and one of the researchers involved in studies of exercise and neuropathy there, emphasized that monitoring—by clinicians or the patients themselves—is crucial to successful exercise programs in those with diabetic neuropathy, particularly if they also have foot deformities such as those resulting from Charcot arthropathy.
“I’m a firm believer that these folks need to exercise for their diabetes,” he said. “But if they start to develop lesions, they need to be addressed.”
Of course, as most clinicians know, there is often a gap between ideal and real-world monitoring levels.
“It’s hard for these patients to check the bottom of their feet regularly, so they sometimes don’t do it,” Sinacore said.
One way to help is with temperature monitoring. Sinacore recommends foot-temperature gauges that patients can use right after exercising, some of which are hook-shaped to ease plantar access.
“When we monitor them here, we check temperature before and after exercise,” he said. “We’re looking for hot spots and temperature differences that may indicate that they’re developing a lesion.”
In such cases, therapists recommend that patients decrease their exercise levels for a while and have their footwear modified to relieve pressure.
David Armstrong agreed that thermometry provides a way of keeping track of the damage caused by weight-bearing exercise.
“We want our patients to dose their activity by checking their skin temperature just as they dose their insulin by checking their glucose,” he said.
His colleague, Manish Bharara, conducts innovative research in this aspect of care.18
“In the last decade we’ve learned that a four-degree difference between two similar sites on both feet is an ulcer risk,” he said. “If the pattern persists over multiple days, the patient should reduce activity and immediately see a doctor.”
Bharara and his colleagues are developing a thermometry scale to address some of the inconveniences typically associated with measuring foot temperature at several sites. Patients stand on it—it’s similar to a bathroom scale—while it measures foot temperature at 20 sites on each foot and records the data. The scale speaks to the patient—telling him, for example, that his right big toe temperature is 5° warmer than the left. Moreover, if the scale detects an abnormal pattern for more than two days, it can be programmed to send a message to the physician’s office and make an appointment.
“Something like this could really help manage patients’ diabetes better, because the biggest barrier is compliance,” Bharara said.
New research
Other researchers are examining variables that affect neuropathic patients’ exercise capabilities, as well. For example, at the Center for Lower Extremity Ambulatory Research at Rosalind Franklin University in Chicago, Bijan Najafi, PhD, associate professor of applied biomechanics, has studied factors including gait initiation in this context.19 As opposed to the measures of steady-state walking—such as rate or number of steps—typically used in exercise studies, a prolonged gait initiation phase (the period between upright posture and steady-state gait) may be associated with increased fall risk.
“During the initiation of the step, there’s an important acceleration phase, and it creates a lot of resistive force,” Najafi said. “We’ve found that neuropathy patients have longer gait initiation. This makes sense, because to reach steady-state gait, people have to gather somatosensory feedback to find the speed at which they can walk safely and minimize energy costs. Neuropathy patients have impaired somatosensory feedback, though. But we believe that if we can provide a good exercise to compensate, we may be able to improve the gait initiation phase.”
One way to help, Najafi thinks, is to take a cue from the dance world.
“If you’re trying to explain a movement problem to a dancer he may not get it, but if you put a mirror in front of him and show him the correct position of the joints, he can improve his motor skills,” he said. “The brain is plastic, and if it realizes there’s an error, it will try to minimize it next time. So we hope that by letting neuropathy patients observe their errors this way, they may improve their motor skills.”
Cary Groner is a freelance writer based in the San Francisco Bay Area.
Sunday, November 6, 2011
Orthotic management of the pes cavus foot
Pes cavus foot occurs in about 8% to 15% of the population, but it does not get nearly as much attention in the medical literature as does its counterpart, pes planus.1 Sixty percent of individuals with cavus feet develop foot pain.2
Although medical knowledge regarding pes cavus exists, the research and treatment options, as well as any theories or hypotheses as to why humans develop this deformity, are quite limited. Traditionally, we have considered pes cavus a neuromuscular problem with a surgical answer.3 By combining what is known with what we can hypothesize, perhaps we can establish a new and more successful approach to pes cavus.
Classification of pes cavus foot
Pes cavus has a variety of classifications. However, many of these overlap, which can lead to confusion. The most common classification system categorizes pes cavus as neuromuscular, congenital, or traumatic. Researchers often differentiate idiopathic from congenital pes cavus.4 A large retrospective survey reviewed 465 patients with pes cavus and found that 81% were classified as having idiopathic pes cavus and 19% had neuromuscular pes cavus.5 Another study reviewed 77 patients in a pes cavus clinic and found that 33.8% of cases were idiopathic and 66.2% were neuromuscular.4 Despite this discrepancy between the two studies, each study found that a significant portion of the pes cavus patients had no known etiologic source of deformity.
The high-arched foot has also been classified according to footprint morphology, radiography, visual inspection, and, most recently, the Foot Posture Index (FPI).2,6-8 The FPI is the most comprehensive of these methods because it distinguishes all foot types, not just the cavus foot, using point-based criteria. This statistically validated and consistent tool defines the cavus foot as any foot that has an FPI score between -5 and -12 on a scale from -12 to +12. A normal foot has a score between 0 and +5.
The structure of pes cavus falls into anterior, posterior, and global categories.3 The anterior cavus is either total (indicating plantar flexion of the entire forefoot) or local (plantar flexion of the first ray only). The posterior type has a high calcaneal inclination angle but no forefoot equinus. The global type, sometimes referred to as combined cavus, is a combination of both deformities.
With regard to function, the pes cavus foot has also been classified as either flexible or rigid. The myofascial band of the plantar aponeurosis maintains the deformity with the windlass effect.9 This effect tends to maintain greater rigidity in some individuals and less in others, depending on the flexibility of the patient’s midtarsal joint. The short and long plantar ligaments may also develop contractures due to decreasing motion across their respective joints, maintaining a more rigid cavus foot.10 Although this type of pes cavus classification is often the least emphasized, function may prove to be the most important consideration relative to orthotic therapy. These two variations of functioning cavus feet, though similar in appearance, act very differently. Anecdotally, one popular assumption holds that pes cavus deformity begins as a flexible entity and will become rigid if it is not treated. However, no evidence currently supports this speculation.
The classification of pes cavus according to so many different parameters may signal that its origins have escaped the medical community. Classifying pes cavus as idiopathic gives it a place to fit, but this approach may be shortchanging our knowledge of the imbalance in muscle forces and strength associated with this condition.
Pathomechanics of pes cavus foot
Originally, researchers thought posterior tibial tendon dysfunction (PTTD), which is now referred to as adult-acquired flatfoot (AAF), was idiopathic unless it was associated with a specific traumatic incident.11 Lower extremity practitioners learned to test the tibialis posterior muscle to stage this disorder prior to treatment and found that there was a progressive character to the weakness and imbalance that resulted in the deformity.11
Practitioners began to evaluate adolescent flatfoot based on the strength of the tibialis posterior and the overpowering of the peroneus brevis muscle.12 This evolution of thought became a focus of investigation simply because several people pursued the obvious rationale that there must be a mechanical origin to flatfoot, not just a convenient category called idiopathic. Can muscle imbalance, the progression of deformity, and the resultant symptoms also be the basis of a theory for the mechanical origin of pes cavus?
I have yet to encounter non-neurologic pediatric cavus feet. If the tibialis anterior muscle is weak at birth, then the peroneus longus muscle will not have a strong enough antagonist. This would disrupt Kirby’s rotational equilibrium concept,13 leading to progressive plantar flexion of the first ray during osseous development toward adulthood. The plantar flexion of the first ray from the overpowering peroneus longus would force the talus into a more dorsiflexed position. This in turn would increase arch height and calcaneal inclination. This pattern of muscle imbalances and reactions is similar to the pattern that occurs with AAF, but produces a different morphology. The increased arch height would lead to a smaller contact area on the ground. Accordingly, there would be more pressure on the metatarsal heads and heel, resulting in symptoms related to these areas.
The tilting back of the talus in the ankle joint would deplete most of the available dorsiflexion of the ankle joint and lead to ankle equinus, which would lead to gastrocnemius-soleus contracture. The extensor muscles would compensate in stance and swing for the gastrocnemius contracture, producing extensor substitution, which is present in most cavus feet. The higher arch would decrease the contact area, increasing pressure on the metatarsal heads, and limited ankle dorsiflexion would cause that pressure to be experienced over a longer period of time as the tibia moves forward in gait. This would all eventually result in a patient suffering from metatarsalgia, ankle joint pain, heel pain, and antalgic gait changes, all classic signs and symptoms of cavus foot.9
Would early evaluation and intervention with orthotic therapy improve midlife clinical outcomes in these patients? Could early intervention slow down the progression of the deformities that result from a lifetime of compensation and metatarsalgia? Forward-looking studies may prove this true, as more investigators recognize that cavus foot is a mirror image of posterior dysfunction in the child and adult.
Evidence for orthotic therapy
A 1997 paper analyzed gait patterns in nine patients with painful pes cavus.14 The Italian researchers noted the presence of two different types: compensated pes cavus (greater ankle joint laxity) and noncompensated pes cavus. These are now considered functional variations. The compensated pes cavus foot had enough laxity to allow the metatarsal depression to be compensated by ankle joint and midtarsal joint dorsiflexion, reducing pain at the forefoot. Some individuals, because of heredity and genetics, are born with greater hip or ankle range of motion, while others have less than normal range of motion. The same must be true for the range of motion of the midtarsal joint—this is obvious to anyone who has examined a large number of feet. Individuals born with or developing cavus feet are not excused from this inevitability, and, therefore, some have a large range of motion of the midtarsal joint and will compensate for the unusual contact forces of a cavus foot. Those without much midtarsal motion will not be able to compensate.
In the Italian study, gait analysis revealed that the compensated group had increased knee flexion and increased ankle joint dorsiflexion, coupled with prolonged firing of the anterior tibialis muscle into late stance. This finding partially validates a portion of the proposed hypothesis. The noncompensated group, which was more symptomatic, had hyperextension of the knee during stance and an inability of the anterior tibialis muscle to overcome the plantigrade position of the forefoot.14
The researchers also reported that gait patterns were improved with custom orthoses, which distributed loads over a wider plantar surface area, unloading the metatarsal area. The uncompensated group was more likely to require surgical correction, since mechanical intervention was less successful. This may have been because it is difficult to change mechanics when there is little or no motion. Two factors were identified in reducing pain: first, the wider contact surface area of the orthoses; second, the ability to control the compensatory motion and unloading of the metatarsal heads.14
A 2001 study took a different approach, dealing with differences in foot types and related sports injuries.15 Researchers from the University of Delaware, Newark, studied two groups of runners with flat or high-arched feet to determine the differences in their injury patterns. They screened patients based on an arch ratio system.16 Although the FPI was not utilized, the individuals had either a high arch or a flat foot, but none had a normal arch height.
The low-arched runners had more medial and soft-tissue injuries, while the high-arch runners had more lateral and bony injuries. The most common injuries in high-arched runners were plantar fasciitis, iliotibial band friction syndrome, and lateral ankle sprains. The most common type of bony injury observed in the high-arch group was stress fracture; all stress fractures occurred at the fifth metatarsal. This group had increased lateral loading compared with the low-arched individuals, and the center of pressure of the foot remained more lateral than the normal medial shift in normal gait throughout stance. This study has been one of the few to differentiate a true set of injuries experienced by people with cavus feet. Although runners are a unique population, the speed and increased contact forces compared with walkers help exaggerate the differences in injury distribution between the two types of foot morphologies.
Remarkably, only since 2000 have studies begun to focus on orthotic therapy and symptoms related to pes cavus, specifically metatarsalgia. Considering that metatarsalgia is the most common symptom in patients with pes cavus,2 a review of studies on the effect of orthoses on metatarsalgia is relevant.
Researchers from the Washington University School of Medicine in St. Louis measured peak pressure and pressure-time integrals in a study of patients with diabetic neuropathy and a history of plantar ulcers.17 An ulcer or pre-ulcer lesion are clear clinical signs of excessive metatarsal head pressure. We can, therefore, look at this study’s attempts to reduce metatarsal head pressure in patients with diabetes and extrapolate the results to efforts to reduce metatarsal head pressure in cavus feet.
The researchers looked at the use of shoes alone, shoes with custom-molded total contact inserts, and shoes with total contact inserts and metatarsal pads. Both devices used in this study were designed to have a minimum fill or total contact design. The study followed 20 patients, 12 men and eight women, with a mean age of 57 years. When patients were given orthoses, peak plantar pressure and pressure-time integrals were reduced by 16% to 24%, respectively, compared with a shoe-only condition. When patients wore metatarsal pads with the total contact orthoses, the peak plantar pressure and pressure-time integral were reduced by 29% to 47% relative to the shoe-only condition.
This study has applications in many patient groups, but is especially important for patients with pes cavus feet; almost 60% of this population suffer from metatarsalgia.2 Burns demonstrated in 20052 that patients with symptomatic cavus feet and metatarsalgia not only had greater pressure under the metatarsal head region but also that the pressure in that region was maintained for a longer time compared with individuals with noncavus feet.
Some research has addressed whether padding the metatarsal area with soft materials or controlling motion with more rigid materials would reduce symptoms. Canadian researchers assessed patients with rheumatoid arthritis and metatarsalgia. Twenty-four individuals completed three 12-week interventions in random order: shoes alone, soft custom orthoses, and semirigid custom orthoses. The data demonstrated that semirigid devices had a highly statistically significant effect on pain, whereas neither soft orthoses nor supportive shoes alone had a statistically significant effect.
Most recently, an Australian group published three relevant studies on the symptoms and mechanical treatment of cavus foot. Burns et al,2 as previously described, attempted to determine the relationship among pes cavus, pain, and foot deformity. Sixty percent of pes cavus patients complained of pain compared with 23% of patients without the deformity. Pressure-time integrals in all three areas of the foot (rearfoot, midfoot, and forefoot) were higher in the pes cavus group than in normal patients. There was also a significant correlation between higher pressure-time integrals and pain.
In a later study of 130 individuals with painful idiopathic pes cavus,19 the Australian researchers also found that those patients demonstrated a more cautious gait pattern than individuals with normal feet. Peak plantar pressure and mean plantar pressure values were also lower than normal, particularly in the forefoot and rearfoot. Patients with pain limited to the rearfoot were more likely to demonstrate an antalgic gait pattern, lower plantar pressures, and higher pressure-time integrals than those with pain limited to the forefoot.
The same research group also published the first randomized controlled trial20 to investigate the effectiveness of custom orthoses for the treatment of painful pes cavus deformity. One hundred fifty four patients with chronic idiopathic foot pain and bilateral cavus feet received either custom-molded orthoses made of 3-mm polypropylene with a Poron top cover or sham insoles of 3-mm foam. Researchers evaluated patients after three months for changes in quality of life, using the Foot Health Status Questionnaire21 and changes in plantar pressure measurements.
The foot pain scores after three months of insole use improved by 43% with sham insoles and 74% with custom-molded orthoses. The peak pressure was 9% less than at baseline for the sham insole but 26% less than baseline for the custom-molded orthoses. Overall, the custom orthoses had a greater effect on quality of life, including statistically significant increases in activity and decreases in pain. One cannot overlook the value of improvement in both physical and mental health for patients with chronic pain and disability.
Although the clinical studies concerning pes cavus are limited, the information is applicable to clinical scenarios. Cavus gait is specific and often limited by the amount of compensation available at the midtarsal and ankle joint. The runner study revealed that the injury pattern is somewhat predictable and can help guide orthotic fabrication details. The studies by the Australian group revealed that custom orthoses can relieve pain and decrease pressure-time integrals. The positive information gained from this research confirms the value of biomechanical intervention for patients with pes cavus.
Orthotic goals for pes cavus foot
The typical complaints associated with pes cavus are pain, issues with shoe fit, and lateral ankle sprains. By focusing on the pathomechanics of cavus foot issues and applying the evidence in the literature, we can compile a list of prescription components for the ideal custom orthosis.
The overload on the metatarsal heads is due to the limited contact area on the plantar surface of the foot created by the high arch. According to the proposed theory detailed earlier, there is also a domino effect from a weak anterior tibialis muscle, tight gastroc-soleus complex, overactive extensors for ground clearance, and extensor substitution or claw toe contractures that result in metatarsalgia.
Figure 2. Semirigid orthoses with a very minimum arch fill, rearfoot post, 4-mm heel lift, and a forefoot valgus wedge or forefoot padding are recommended for pes cavus.
Increasing the plantar surface contact area with a total contact orthosis ensures that more of the plantar pressure is being borne in the arch area and that the metatarsal heads are bearing less weight for shorter periods. One can accomplish this by using a minimal fill cast correction technique, which raises the arch of the orthosis (total contact), and prescribing a semirigid or rigid device.
Adding a metatarsal bar or a metatarsal pad will shift plantar pressures more proximally, away from the metatarsal heads. Leaving the anterior edge of the orthosis at full thickness (instead of beveled) produces a rocker-type effect, which shortens the time the metatarsal heads bear weight. A forefoot extension of soft durable material attenuates the pressure peaks under the metatarsal heads.
Lateral ankle instability and a laterally deviated subtalar joint (STJ) axis are frequently associated with high-arched feet.22 The STJ axis lies more laterally and exits the foot at a different angle in the pes cavus foot than in the average STJ axis.
This axis deviation leaves the pes cavus foot with more inversion as well as more plantar surface medial to the STJ axis, which increases the likelihood of supinatory moments across the STJ axis. Because the peroneus brevis has a shorter and less efficient moment arm to oppose these supinatory moments, this situation can increase the risk of lateral ankle sprain. The muscle imbalance inherent in the cavus foot leads to a plantar flexed first ray, subsequent rearfoot inversion, and lateral ankle instability by leaving the foot in an inverted position, as described in the theory of cavus pathomechanics.
Leaving the lateral side of the rearfoot post unbeveled increases the surface area and effectiveness of the post by providing a more stable platform to resist inversion of the device. Adding a reverse Morton’s extension or a slight valgus forefoot extension creates a pronatory moment on the forefoot that counteracts the excessive supinatory moment. This makes the cavus foot less laterally unstable.
Rearfoot instability is an extension of the laterally deviated subtalar axis. However, in flexible pes cavus feet, midtarsal flexibility compensates for this later in stance. The forefoot pathology produces midtarsal joint supination, which leads to excessive pronation of the rearfoot.23 Some pes cavus feet suffer from both lateral ankle instability at midstance and rearfoot pronation at late midstance. Adding a flat rearfoot post and a deep (>16 mm) heel cup helps stabilize the rearfoot by limiting rearfoot motion in relation to the supporting surface.
Multiple problems contribute to the apropulsive antalgic gait of the pes cavus foot. Pain in the metatarsal heads or rearfoot can cause shortened strides, which can lead to excessive use of extensor tendons and eventually result in tendinitis, tendon fatigue, and even shin splints.19 Limited ankle joint motion also leads to shorter strides and limited propulsion and is often associated with pes cavus.
Adding a 4-mm heel lift to the rearfoot post actually increases available ankle joint dorsiflexion by plantar flexing the talus. Also bear in mind that a wide orthosis will increase the surface area that contacts the arch of the foot and distribute more pressure to the midfoot and away from the forefoot and rearfoot.
One must understand that, early in treatment, the morphology and pathomechanics of cavus feet are likely to be progressive, especially in the developmental form. Neurologic disorders, such as Charcot-Marie-Tooth disease and muscular dystrophy, create a progressive muscle imbalance.24 Orthotic and shoe interventions are likely to change on a regular basis. Frequent reevaluation and recasting are essential to follow the continually rising arch and shifting of symptoms.
The true etiology of pes cavus remains one of our unsolved mysteries. The proposed pathomechanical model described above is one that future trials can test. Recent research is both enlightening and encouraging. However, it is apparent that more studies are needed. There are congenital and familial components to these feet, but there is much more to be studied about the progression. We need to recognize patients with cavus feet early in life, and studies need to document the effectiveness of orthoses and other early interventions for affecting midlife outcomes and avoiding symptoms.
Paul R. Scherer, DPM, is a clinical professor in the College of Podiatric Sciences at the Western University of Health Sciences in Pomona, CA. A version of this article appears in his book, Recent Advances in Orthotic Therapy, published by Lower Extremity Review. For more information, call 518/452-6898.
Although medical knowledge regarding pes cavus exists, the research and treatment options, as well as any theories or hypotheses as to why humans develop this deformity, are quite limited. Traditionally, we have considered pes cavus a neuromuscular problem with a surgical answer.3 By combining what is known with what we can hypothesize, perhaps we can establish a new and more successful approach to pes cavus.
Classification of pes cavus foot
Pes cavus has a variety of classifications. However, many of these overlap, which can lead to confusion. The most common classification system categorizes pes cavus as neuromuscular, congenital, or traumatic. Researchers often differentiate idiopathic from congenital pes cavus.4 A large retrospective survey reviewed 465 patients with pes cavus and found that 81% were classified as having idiopathic pes cavus and 19% had neuromuscular pes cavus.5 Another study reviewed 77 patients in a pes cavus clinic and found that 33.8% of cases were idiopathic and 66.2% were neuromuscular.4 Despite this discrepancy between the two studies, each study found that a significant portion of the pes cavus patients had no known etiologic source of deformity.
The high-arched foot has also been classified according to footprint morphology, radiography, visual inspection, and, most recently, the Foot Posture Index (FPI).2,6-8 The FPI is the most comprehensive of these methods because it distinguishes all foot types, not just the cavus foot, using point-based criteria. This statistically validated and consistent tool defines the cavus foot as any foot that has an FPI score between -5 and -12 on a scale from -12 to +12. A normal foot has a score between 0 and +5.
The structure of pes cavus falls into anterior, posterior, and global categories.3 The anterior cavus is either total (indicating plantar flexion of the entire forefoot) or local (plantar flexion of the first ray only). The posterior type has a high calcaneal inclination angle but no forefoot equinus. The global type, sometimes referred to as combined cavus, is a combination of both deformities.
With regard to function, the pes cavus foot has also been classified as either flexible or rigid. The myofascial band of the plantar aponeurosis maintains the deformity with the windlass effect.9 This effect tends to maintain greater rigidity in some individuals and less in others, depending on the flexibility of the patient’s midtarsal joint. The short and long plantar ligaments may also develop contractures due to decreasing motion across their respective joints, maintaining a more rigid cavus foot.10 Although this type of pes cavus classification is often the least emphasized, function may prove to be the most important consideration relative to orthotic therapy. These two variations of functioning cavus feet, though similar in appearance, act very differently. Anecdotally, one popular assumption holds that pes cavus deformity begins as a flexible entity and will become rigid if it is not treated. However, no evidence currently supports this speculation.
The classification of pes cavus according to so many different parameters may signal that its origins have escaped the medical community. Classifying pes cavus as idiopathic gives it a place to fit, but this approach may be shortchanging our knowledge of the imbalance in muscle forces and strength associated with this condition.
Pathomechanics of pes cavus foot
Originally, researchers thought posterior tibial tendon dysfunction (PTTD), which is now referred to as adult-acquired flatfoot (AAF), was idiopathic unless it was associated with a specific traumatic incident.11 Lower extremity practitioners learned to test the tibialis posterior muscle to stage this disorder prior to treatment and found that there was a progressive character to the weakness and imbalance that resulted in the deformity.11
Practitioners began to evaluate adolescent flatfoot based on the strength of the tibialis posterior and the overpowering of the peroneus brevis muscle.12 This evolution of thought became a focus of investigation simply because several people pursued the obvious rationale that there must be a mechanical origin to flatfoot, not just a convenient category called idiopathic. Can muscle imbalance, the progression of deformity, and the resultant symptoms also be the basis of a theory for the mechanical origin of pes cavus?
I have yet to encounter non-neurologic pediatric cavus feet. If the tibialis anterior muscle is weak at birth, then the peroneus longus muscle will not have a strong enough antagonist. This would disrupt Kirby’s rotational equilibrium concept,13 leading to progressive plantar flexion of the first ray during osseous development toward adulthood. The plantar flexion of the first ray from the overpowering peroneus longus would force the talus into a more dorsiflexed position. This in turn would increase arch height and calcaneal inclination. This pattern of muscle imbalances and reactions is similar to the pattern that occurs with AAF, but produces a different morphology. The increased arch height would lead to a smaller contact area on the ground. Accordingly, there would be more pressure on the metatarsal heads and heel, resulting in symptoms related to these areas.
The tilting back of the talus in the ankle joint would deplete most of the available dorsiflexion of the ankle joint and lead to ankle equinus, which would lead to gastrocnemius-soleus contracture. The extensor muscles would compensate in stance and swing for the gastrocnemius contracture, producing extensor substitution, which is present in most cavus feet. The higher arch would decrease the contact area, increasing pressure on the metatarsal heads, and limited ankle dorsiflexion would cause that pressure to be experienced over a longer period of time as the tibia moves forward in gait. This would all eventually result in a patient suffering from metatarsalgia, ankle joint pain, heel pain, and antalgic gait changes, all classic signs and symptoms of cavus foot.9
Would early evaluation and intervention with orthotic therapy improve midlife clinical outcomes in these patients? Could early intervention slow down the progression of the deformities that result from a lifetime of compensation and metatarsalgia? Forward-looking studies may prove this true, as more investigators recognize that cavus foot is a mirror image of posterior dysfunction in the child and adult.
Evidence for orthotic therapy
A 1997 paper analyzed gait patterns in nine patients with painful pes cavus.14 The Italian researchers noted the presence of two different types: compensated pes cavus (greater ankle joint laxity) and noncompensated pes cavus. These are now considered functional variations. The compensated pes cavus foot had enough laxity to allow the metatarsal depression to be compensated by ankle joint and midtarsal joint dorsiflexion, reducing pain at the forefoot. Some individuals, because of heredity and genetics, are born with greater hip or ankle range of motion, while others have less than normal range of motion. The same must be true for the range of motion of the midtarsal joint—this is obvious to anyone who has examined a large number of feet. Individuals born with or developing cavus feet are not excused from this inevitability, and, therefore, some have a large range of motion of the midtarsal joint and will compensate for the unusual contact forces of a cavus foot. Those without much midtarsal motion will not be able to compensate.
In the Italian study, gait analysis revealed that the compensated group had increased knee flexion and increased ankle joint dorsiflexion, coupled with prolonged firing of the anterior tibialis muscle into late stance. This finding partially validates a portion of the proposed hypothesis. The noncompensated group, which was more symptomatic, had hyperextension of the knee during stance and an inability of the anterior tibialis muscle to overcome the plantigrade position of the forefoot.14
The researchers also reported that gait patterns were improved with custom orthoses, which distributed loads over a wider plantar surface area, unloading the metatarsal area. The uncompensated group was more likely to require surgical correction, since mechanical intervention was less successful. This may have been because it is difficult to change mechanics when there is little or no motion. Two factors were identified in reducing pain: first, the wider contact surface area of the orthoses; second, the ability to control the compensatory motion and unloading of the metatarsal heads.14
A 2001 study took a different approach, dealing with differences in foot types and related sports injuries.15 Researchers from the University of Delaware, Newark, studied two groups of runners with flat or high-arched feet to determine the differences in their injury patterns. They screened patients based on an arch ratio system.16 Although the FPI was not utilized, the individuals had either a high arch or a flat foot, but none had a normal arch height.
The low-arched runners had more medial and soft-tissue injuries, while the high-arch runners had more lateral and bony injuries. The most common injuries in high-arched runners were plantar fasciitis, iliotibial band friction syndrome, and lateral ankle sprains. The most common type of bony injury observed in the high-arch group was stress fracture; all stress fractures occurred at the fifth metatarsal. This group had increased lateral loading compared with the low-arched individuals, and the center of pressure of the foot remained more lateral than the normal medial shift in normal gait throughout stance. This study has been one of the few to differentiate a true set of injuries experienced by people with cavus feet. Although runners are a unique population, the speed and increased contact forces compared with walkers help exaggerate the differences in injury distribution between the two types of foot morphologies.
Remarkably, only since 2000 have studies begun to focus on orthotic therapy and symptoms related to pes cavus, specifically metatarsalgia. Considering that metatarsalgia is the most common symptom in patients with pes cavus,2 a review of studies on the effect of orthoses on metatarsalgia is relevant.
Researchers from the Washington University School of Medicine in St. Louis measured peak pressure and pressure-time integrals in a study of patients with diabetic neuropathy and a history of plantar ulcers.17 An ulcer or pre-ulcer lesion are clear clinical signs of excessive metatarsal head pressure. We can, therefore, look at this study’s attempts to reduce metatarsal head pressure in patients with diabetes and extrapolate the results to efforts to reduce metatarsal head pressure in cavus feet.
The researchers looked at the use of shoes alone, shoes with custom-molded total contact inserts, and shoes with total contact inserts and metatarsal pads. Both devices used in this study were designed to have a minimum fill or total contact design. The study followed 20 patients, 12 men and eight women, with a mean age of 57 years. When patients were given orthoses, peak plantar pressure and pressure-time integrals were reduced by 16% to 24%, respectively, compared with a shoe-only condition. When patients wore metatarsal pads with the total contact orthoses, the peak plantar pressure and pressure-time integral were reduced by 29% to 47% relative to the shoe-only condition.
This study has applications in many patient groups, but is especially important for patients with pes cavus feet; almost 60% of this population suffer from metatarsalgia.2 Burns demonstrated in 20052 that patients with symptomatic cavus feet and metatarsalgia not only had greater pressure under the metatarsal head region but also that the pressure in that region was maintained for a longer time compared with individuals with noncavus feet.
Some research has addressed whether padding the metatarsal area with soft materials or controlling motion with more rigid materials would reduce symptoms. Canadian researchers assessed patients with rheumatoid arthritis and metatarsalgia. Twenty-four individuals completed three 12-week interventions in random order: shoes alone, soft custom orthoses, and semirigid custom orthoses. The data demonstrated that semirigid devices had a highly statistically significant effect on pain, whereas neither soft orthoses nor supportive shoes alone had a statistically significant effect.
Most recently, an Australian group published three relevant studies on the symptoms and mechanical treatment of cavus foot. Burns et al,2 as previously described, attempted to determine the relationship among pes cavus, pain, and foot deformity. Sixty percent of pes cavus patients complained of pain compared with 23% of patients without the deformity. Pressure-time integrals in all three areas of the foot (rearfoot, midfoot, and forefoot) were higher in the pes cavus group than in normal patients. There was also a significant correlation between higher pressure-time integrals and pain.
In a later study of 130 individuals with painful idiopathic pes cavus,19 the Australian researchers also found that those patients demonstrated a more cautious gait pattern than individuals with normal feet. Peak plantar pressure and mean plantar pressure values were also lower than normal, particularly in the forefoot and rearfoot. Patients with pain limited to the rearfoot were more likely to demonstrate an antalgic gait pattern, lower plantar pressures, and higher pressure-time integrals than those with pain limited to the forefoot.
The same research group also published the first randomized controlled trial20 to investigate the effectiveness of custom orthoses for the treatment of painful pes cavus deformity. One hundred fifty four patients with chronic idiopathic foot pain and bilateral cavus feet received either custom-molded orthoses made of 3-mm polypropylene with a Poron top cover or sham insoles of 3-mm foam. Researchers evaluated patients after three months for changes in quality of life, using the Foot Health Status Questionnaire21 and changes in plantar pressure measurements.
The foot pain scores after three months of insole use improved by 43% with sham insoles and 74% with custom-molded orthoses. The peak pressure was 9% less than at baseline for the sham insole but 26% less than baseline for the custom-molded orthoses. Overall, the custom orthoses had a greater effect on quality of life, including statistically significant increases in activity and decreases in pain. One cannot overlook the value of improvement in both physical and mental health for patients with chronic pain and disability.
Although the clinical studies concerning pes cavus are limited, the information is applicable to clinical scenarios. Cavus gait is specific and often limited by the amount of compensation available at the midtarsal and ankle joint. The runner study revealed that the injury pattern is somewhat predictable and can help guide orthotic fabrication details. The studies by the Australian group revealed that custom orthoses can relieve pain and decrease pressure-time integrals. The positive information gained from this research confirms the value of biomechanical intervention for patients with pes cavus.
Orthotic goals for pes cavus foot
The typical complaints associated with pes cavus are pain, issues with shoe fit, and lateral ankle sprains. By focusing on the pathomechanics of cavus foot issues and applying the evidence in the literature, we can compile a list of prescription components for the ideal custom orthosis.
The overload on the metatarsal heads is due to the limited contact area on the plantar surface of the foot created by the high arch. According to the proposed theory detailed earlier, there is also a domino effect from a weak anterior tibialis muscle, tight gastroc-soleus complex, overactive extensors for ground clearance, and extensor substitution or claw toe contractures that result in metatarsalgia.
Figure 2. Semirigid orthoses with a very minimum arch fill, rearfoot post, 4-mm heel lift, and a forefoot valgus wedge or forefoot padding are recommended for pes cavus.
Increasing the plantar surface contact area with a total contact orthosis ensures that more of the plantar pressure is being borne in the arch area and that the metatarsal heads are bearing less weight for shorter periods. One can accomplish this by using a minimal fill cast correction technique, which raises the arch of the orthosis (total contact), and prescribing a semirigid or rigid device.
Adding a metatarsal bar or a metatarsal pad will shift plantar pressures more proximally, away from the metatarsal heads. Leaving the anterior edge of the orthosis at full thickness (instead of beveled) produces a rocker-type effect, which shortens the time the metatarsal heads bear weight. A forefoot extension of soft durable material attenuates the pressure peaks under the metatarsal heads.
Lateral ankle instability and a laterally deviated subtalar joint (STJ) axis are frequently associated with high-arched feet.22 The STJ axis lies more laterally and exits the foot at a different angle in the pes cavus foot than in the average STJ axis.
This axis deviation leaves the pes cavus foot with more inversion as well as more plantar surface medial to the STJ axis, which increases the likelihood of supinatory moments across the STJ axis. Because the peroneus brevis has a shorter and less efficient moment arm to oppose these supinatory moments, this situation can increase the risk of lateral ankle sprain. The muscle imbalance inherent in the cavus foot leads to a plantar flexed first ray, subsequent rearfoot inversion, and lateral ankle instability by leaving the foot in an inverted position, as described in the theory of cavus pathomechanics.
Leaving the lateral side of the rearfoot post unbeveled increases the surface area and effectiveness of the post by providing a more stable platform to resist inversion of the device. Adding a reverse Morton’s extension or a slight valgus forefoot extension creates a pronatory moment on the forefoot that counteracts the excessive supinatory moment. This makes the cavus foot less laterally unstable.
Rearfoot instability is an extension of the laterally deviated subtalar axis. However, in flexible pes cavus feet, midtarsal flexibility compensates for this later in stance. The forefoot pathology produces midtarsal joint supination, which leads to excessive pronation of the rearfoot.23 Some pes cavus feet suffer from both lateral ankle instability at midstance and rearfoot pronation at late midstance. Adding a flat rearfoot post and a deep (>16 mm) heel cup helps stabilize the rearfoot by limiting rearfoot motion in relation to the supporting surface.
Multiple problems contribute to the apropulsive antalgic gait of the pes cavus foot. Pain in the metatarsal heads or rearfoot can cause shortened strides, which can lead to excessive use of extensor tendons and eventually result in tendinitis, tendon fatigue, and even shin splints.19 Limited ankle joint motion also leads to shorter strides and limited propulsion and is often associated with pes cavus.
Adding a 4-mm heel lift to the rearfoot post actually increases available ankle joint dorsiflexion by plantar flexing the talus. Also bear in mind that a wide orthosis will increase the surface area that contacts the arch of the foot and distribute more pressure to the midfoot and away from the forefoot and rearfoot.
One must understand that, early in treatment, the morphology and pathomechanics of cavus feet are likely to be progressive, especially in the developmental form. Neurologic disorders, such as Charcot-Marie-Tooth disease and muscular dystrophy, create a progressive muscle imbalance.24 Orthotic and shoe interventions are likely to change on a regular basis. Frequent reevaluation and recasting are essential to follow the continually rising arch and shifting of symptoms.
The true etiology of pes cavus remains one of our unsolved mysteries. The proposed pathomechanical model described above is one that future trials can test. Recent research is both enlightening and encouraging. However, it is apparent that more studies are needed. There are congenital and familial components to these feet, but there is much more to be studied about the progression. We need to recognize patients with cavus feet early in life, and studies need to document the effectiveness of orthoses and other early interventions for affecting midlife outcomes and avoiding symptoms.
Paul R. Scherer, DPM, is a clinical professor in the College of Podiatric Sciences at the Western University of Health Sciences in Pomona, CA. A version of this article appears in his book, Recent Advances in Orthotic Therapy, published by Lower Extremity Review. For more information, call 518/452-6898.
Friday, November 4, 2011
Regular trips to a podiatrist will help keep you on your toes
It's all too easy to take healthy feet for granted — they take you where you want to go without complaint and don't ask for much in return. But, over time, those puppies can really start barking due to corns, calluses, bunions and other assorted ailments.
Many people are surprised to learn that the normal aging process affects feet as much as any other body part. Feet become wider and flatter, the protective fat pads on the soles thin out and circulation throughout the feet can decrease, all of which can lead to foot pain and damage. But you don't have to suffer alone. You — and your feet — need an ally. That's where a podiatrist comes in.
Doctors of podiatric medicine focus their practices entirely on the foot, ankle and lower leg. Their medical education and training includes four years of undergraduate education, four years of graduate education at an accredited podiatric medical college and two or three years of hospital residency training. Each state requires podiatrists to be licensed to practice there.
"We're primary physicians and specialists for the foot and ankle," says Dr. Marlene Reid, president of the Illinois Podiatric Medical Association. "That's all we do, which means it's best to go to a podiatrist for any foot or ankle condition, large or small."
Unlike many familiar screening guidelines, like getting your first mammogram at age 40 or your first colonoscopy at age 50, there is no definite rule about when to start seeing a podiatrist. "I always suggest coming in for an initial look once you're past your 30s," says Dr. Kirk Contento of Contento Foot & Ankle Center in Palos Heights and Chicago. "We're all about preventing little problems from developing into something major later."
Here are three common foot conditions that become all the more common as we age, and here's what to do about them.
1. Toenail fungus - Podiatrists suggest seeing a podiatrist whenever a nail thickens or becomes discolored. "The doctor can thin the nail, then medicate topically or orally and get the patient started on a good home treatment regimen," Contento says. "Fungal infections often thicken the nail, which can lead to a secondary problem of an ingrown nail." Lasers are also an emerging new treatment for this common problem.
2.Arch strain and heel pain - One word here: Orthotics. Either custom or over-the-counter are fine, as long as you receive adequate arch support. "The tendon that supports the foot's arches weakens over time due to decreased blood flow, which means your arch drops," says Reid. "It usually starts as a vague feeling of weakness or muscle strain and is often misdiagnosed as plantar fasciitis. People tend to ignore it but it can cause the tendon to rupture, which may require surgical repair."
3. Arthritis - People tend to think about big-toe bunions when they think about arthritis in the foot, as arthritis often follows when bunions develop. But Reid, who practices in Naperville, says arthritis can develop in any joint. "Older people often develop arthritis across the top of the foot or in the instep, and it's quite painful," she says. "This is another instance where proper orthotics early on can make a big difference."
One last caveat: If you have diabetes, put your podiatrist on speed-dial because you'll be seeing a lot of each other. "Diabetes is a multi-organ disease that requires constant vigilance because decreased blood flow and neuropathy magnifies everything that happens in the feet," says Contento. "I want to see all my diabetic patients twice a year if they are not having problems and every 2 to 3 months if they are. Diabetics literally should not even be cutting their own toenails due to the risk of infection."
Fortunately, Medicare should cover nail trims every 60 days for people with diabetes. "That's a good interval," Contento says. "It lets me check the feet's skin, neurological status and circulation on a regular basis."
According to Reid, at a certain point, even people 55+ without diabetes should plan on leaving the regular foot care to a pro: "Once reaching or seeing your toes becomes a problem, plan on coming in every few months. An office visit charge of $40-$60 is well worth the peace of mind."
Copyright © 2011, Chicago Tribune
Many people are surprised to learn that the normal aging process affects feet as much as any other body part. Feet become wider and flatter, the protective fat pads on the soles thin out and circulation throughout the feet can decrease, all of which can lead to foot pain and damage. But you don't have to suffer alone. You — and your feet — need an ally. That's where a podiatrist comes in.
Doctors of podiatric medicine focus their practices entirely on the foot, ankle and lower leg. Their medical education and training includes four years of undergraduate education, four years of graduate education at an accredited podiatric medical college and two or three years of hospital residency training. Each state requires podiatrists to be licensed to practice there.
"We're primary physicians and specialists for the foot and ankle," says Dr. Marlene Reid, president of the Illinois Podiatric Medical Association. "That's all we do, which means it's best to go to a podiatrist for any foot or ankle condition, large or small."
Unlike many familiar screening guidelines, like getting your first mammogram at age 40 or your first colonoscopy at age 50, there is no definite rule about when to start seeing a podiatrist. "I always suggest coming in for an initial look once you're past your 30s," says Dr. Kirk Contento of Contento Foot & Ankle Center in Palos Heights and Chicago. "We're all about preventing little problems from developing into something major later."
Here are three common foot conditions that become all the more common as we age, and here's what to do about them.
1. Toenail fungus - Podiatrists suggest seeing a podiatrist whenever a nail thickens or becomes discolored. "The doctor can thin the nail, then medicate topically or orally and get the patient started on a good home treatment regimen," Contento says. "Fungal infections often thicken the nail, which can lead to a secondary problem of an ingrown nail." Lasers are also an emerging new treatment for this common problem.
2.Arch strain and heel pain - One word here: Orthotics. Either custom or over-the-counter are fine, as long as you receive adequate arch support. "The tendon that supports the foot's arches weakens over time due to decreased blood flow, which means your arch drops," says Reid. "It usually starts as a vague feeling of weakness or muscle strain and is often misdiagnosed as plantar fasciitis. People tend to ignore it but it can cause the tendon to rupture, which may require surgical repair."
3. Arthritis - People tend to think about big-toe bunions when they think about arthritis in the foot, as arthritis often follows when bunions develop. But Reid, who practices in Naperville, says arthritis can develop in any joint. "Older people often develop arthritis across the top of the foot or in the instep, and it's quite painful," she says. "This is another instance where proper orthotics early on can make a big difference."
One last caveat: If you have diabetes, put your podiatrist on speed-dial because you'll be seeing a lot of each other. "Diabetes is a multi-organ disease that requires constant vigilance because decreased blood flow and neuropathy magnifies everything that happens in the feet," says Contento. "I want to see all my diabetic patients twice a year if they are not having problems and every 2 to 3 months if they are. Diabetics literally should not even be cutting their own toenails due to the risk of infection."
Fortunately, Medicare should cover nail trims every 60 days for people with diabetes. "That's a good interval," Contento says. "It lets me check the feet's skin, neurological status and circulation on a regular basis."
According to Reid, at a certain point, even people 55+ without diabetes should plan on leaving the regular foot care to a pro: "Once reaching or seeing your toes becomes a problem, plan on coming in every few months. An office visit charge of $40-$60 is well worth the peace of mind."
Copyright © 2011, Chicago Tribune
Thursday, November 3, 2011
Lymphedema presents therapeutic challenges
Although lymphedema in the past has often been overlooked or misdiagnosed, a growing number of certified practitioners are using the conservative treatment techniques of manual lymph drainage and complete decongestive therapy to effectively treat lymphedema patients.
By Harold Merriman, PT, PhD, CLT
The clinical importance of lymphatic system disorders is becoming better known among members of the medical community, including physicians and therapists. Most prominent of these disorders is lymphedema, which involves a buildup of protein-rich lymph fluid in the interstitium.
Some of the most common known causes of lower extremity lymphedema include pelvic or lower extremity cancer and cancer treatment (e.g, lymph node resection or radiation) that can damage the lymphatic system. Other causes of lymphedema may be much more subtle, such as an insect bite or sunburn that could irreversibly damage an already compromised and susceptible lymphatic system. Though lymphedema can be found in all types of individuals, active and fit individuals are less likely than obese individuals to develop lymphedema.
Once the diagnosis of lymphedema has been made, appropriate conservative treatment should be administered. Currently, a certified lymphedema therapist (CLT) is the provider of choice to administer the recommended conservative treatment. Before the 1980s, most of the research and treatment of lymphedema and related disorders occurred in Europe. Now there are also many opportunities for practitioners to obtain advanced training in lymphedema in North America. For example, in North America a number of lymphedema schools teach certification courses that allow practicing clinicians to become certified lymphedema therapists. The Lymphology Association of North America (LANA) administers a nationally recognized lymphedema certification exam to qualified and experienced lymphedema clinicians.1
Though the topic of lymphedema and related disorders is becoming better understood, patients with these disorders may still be ignored, misdiagnosed, or simply unable to find proper treatment. Unfortunately, in many areas of the United States there is a currently a shortage or absence of qualified clinicians who can successfully treat these conditions. This article will briefly review the anatomy and physiology of the lymphatic system and discuss the conservative treatment options for the lymphedema patient.2-5
Lymphatic anatomy and physiology
Lymph originates from blood plasma that leaves the blood capillaries and enters into the interstitum. A percentage of that interstitial fluid then enters the lymphatic system, where it is then called lymph. Lymph matter consists of proteins, water, fatty acids, and cellular components. The typical lymphatic system vessel has a three-layer wall structure and presence of valves, similar to the vessels of the venous system. The inner layer (intima) consists of endothelial cells, the middle layer (media) is made up of smooth muscle, and the outer layer (adventitia) is formed by collagen fibers that are loosely anchored to the extravascular connective tissue.4
The functional unit of the lymph vessel is the lymphangion, which consists of a lymph vessel bordered by two valves. As the lymphangion contracts due to the presence of smooth muscle in the middle layer, the valves provide directionality so that the lymph flows in only one direction. It should be stressed that the lymphatic vessel, unlike the vein, regularly contracts (under the control of the autonomic nervous system) and that this contraction rate can change depending on a number of factors. For example, the lymphangion contraction rate can be stimulated to increase during the hands-on portion of conservative treatment.
While the lymphangions have a distinct three-layer wall construction with valves, not all lymphatic vessels are that well organized. The first type of vessel that collects what will later become lymph fluid is called the initial lymph vessel or lymph capillary. These vessels are blind or dead-end sacs (tubes) consisting of a single layer of endothelium with junctions that can open and close to let in interstitial fluid. The initial lymph vessels lack valves and are located near the blood capillaries. As this fluid flows unidirectionally toward the heart, the lymphatic vessels become larger in diameter and more organized. The lymph collectors and the even larger lymph trunks have the distinct three-layer wall construction with valves. The diameter of the lymph collectors can be as large as 0.6 mm, and the lymph collectors’ valves are spaced 0.6 cm to 2.0 cm apart.3,5 Lymph then flows into the larger lymphatic trunks. The most important lymphatic trunks are the right lymphatic duct and the thoracic duct, which drain the lymph into the venous system near the heart at the right and left venous angles, respectively. The right lymphatic duct drains the right arm, right side of the head, and right upper trunk; meanwhile, the body’s largest lymphatic trunk, the thoracic duct, drains the left arm, left side of the head, both legs, and the rest of the trunk. 2-5
As the lymph moves unidirectionally in the lymphatic vessels, lymph nodes filter and concentrate the lymph and also provide immune surveillance using T & B lymphocytes. The 600 to 700 lymph nodes found in the human body are concentrated in the neck, axilla, chest, abdomen and—most importantly for the lower extremity practitioner—in the groin. In addition to immune defense, the lymphatic system plays a critical role in fluid homeostasis as well as transport and drainage of excess fluids, proteins, and cellular debris from the interstitial spaces that are not reabsorbed by the venous system. One can think of the lymphatic system as the body’s “sanitation system,” whose purpose is to dispose the body’s “waste material.”2-5
Lymphedema results from mechanical failure of the lymphatic system, which leads to an accumulation of protein-rich edema in the interstitium. Mechanical failure means that the “lymphatic load” (amount of lymph transported in a given time period) exceeds what an impaired lymphatic system can handle (transport capacity). In most cases, lymphedema will present itself in a single extremity, or in bilateral cases one extremity will often be more involved than the other (asymmetry). Though one might picture lymphedema occurring mostly in the upper extremity, often lymphedema (especially primary lymphedema) occurs in the lower extremity as well. 2-5
Diagnosis of lymphedema
Lymphedema is the most common disease of the lymphatic system. It is estimated that lymphedema affects 140 million to 250 million people worldwide and at least 3 million Americans.5 Lymphedema exists in two different forms, primary and secondary. Primary lymphedema is believed to result from an abnormally developed lymphatic system that can present either at birth or later in life. In many cases there is no known cause of primary lymphedema. However, in some cases heat, puberty, pregnancy or minor trauma such as insect bites, infections, sprains or strains may be identified. 2-5
In contrast, secondary lymphedema results from a known insult to the lymphatic system that causes a reduced transport capacity. Specific insults to the lymphatic system include surgery, radiation, trauma, tumor growth, infection, and chronic venous insufficiency. 2-5 The two worldwide most common causes of secondary lymphedema are breast cancer surgery and lymphatic filariasis. It should be stressed that even with the advent of less invasive modern surgical techniques such as sentinel lymph node biopsy and lumpectomy, lymphedema may still occur after breast cancer surgery and treatment. 2-5
Since lymphedema usually begins distally, it will first be noticed in the lower extremity in the toes, feet, and ankles before progressing proximally up into the thighs. Lower extremity lymphedema would typically be caused by a lymphatic insult in the lower extremity and/or pelvic region, but not by an upper-body lymphatic insult such as breast cancer surgery. The classic sign of lymphedema is a positive Stemmer skin fold sign, which can be defined as a thickened skin fold at the base of the second toe such that the tissue cannot be lifted away from the bone.6 A summary of lymphedema clinical features are listed in Table 1. Since there is no pain associated with lymphedema, the classic symptom that brings a patient to a lower extremity practitioner is edema or infection (cellulitis), which becomes more prevalent as lymphedema severity increases.2,4
It should also be mentioned that combination forms such as lipo-lymphedema are not uncommon. Lipo-lymphedema is a condition in which individuals with lipedema (symmetrical accumulation of fat rather than edema in the subcutaneous tissue) later develop lymphedema in addition to the underlying and ongoing lipedema. Unfortunately, many lipedema patients develop lymphedema since the accumulation of fatty tissue from lipedema causes compression of the superficial lymph vessels.2
Table 1. Lymphedema characteristics
Clinical Feature
Lymphedema
Gender
Women > men
Distribution
Unilateral, or bilateral with one leg usually affected more severely (asymmetric)
Pain on pressure
Absent
Easy bruising of affected area (hematoma)
Absent
Distal edema in the foot
Present
Stemmer sign
Present (positive)
Treatment
It is well documented that lymphedema is best treated using conservative methods administered by the certified lymphedema therapist.7-12 Unfortunately at times, lymphedema is still treated with diuretics, which is contrary to treatment guidelines set forth by the International Society of Lymphology and by other lymphedema physician specialists.2,4,12 Perhaps the best known conservative method is manual lymph drainage (MLD) which is a component of complete decongestive therapy (CDT). MLD is a gentle manual treatment technique originally developed in the 1930s by the Danish couple Emil and Estrid Vodder.2,5
CDT consists of two phases; phase I is the treatment phase, and phase II is the self-management phase. CDT and MLD should only be performed after the CLT has determined that no contraindications (e.g., acute infections or cardiac edema) are present. Phase I treatment consists of MLD, compression bandages, exercise (in bandages), and meticulous skin care (to cure/prevent bacterial and fungal infections). Once the reduction in lymphedema begins to plateau, the CLT will transition the patient to the self-management phase II. Phase II consists of compression (typically achieved by a customized garment during the day and bandages at night), exercise (with the limb in either a compression garment or bandages), meticulous skin care, and MLD as needed. Patient compliance with all treatment components (especially during phase II) is the key to a successful long-term outcome, and it is crucial that the patient, therapist, and other caregivers work together as a team.5
One of the most important skills the CLT performs is to provide MLD in the proper sequence. Since MLD increases lymph flow, the therapist does not want this increased lymph flow to overload and further damage an already impaired lymphatic system. For this reason, the CLT may need to initially limit the area to be treated by MLD. For example, if a patient has lymphedema in both legs, then the CLT may elect to initially focus on only one leg. Typically, the lymphedema therapist should first perform MLD on central and uninvolved areas, followed by performing MLD on the involved areas (e.g., the leg). This MLD strategy prepares the uninvolved areas to receive the additional lymph flow from the affected extremity. Again, it is very important that the lymphedema therapist administers MLD in a proper manner and sequence in order to obtain optimal outcomes.5
Proper compression during both phases of CDT is the key to the successful management of the lymphedema patient. If the affected areas do not receive constant and appropriate compression, the improvements achieved by MLD will be temporary (may last only a few hours).5 Therefore, the lymphedema therapist should have a frank discussion with the patient during the initial evaluation outlining the extreme importance of continuous compression of the affected extremity. This discussion should include the reasons why compression is so important, determining the method by which the patient (or other caregiver/family member) can don/doff the compression bandages or garment at home, and alerting the patient to the financial implications of proper compression since two compression garments per affected extremity will need to be purchased about every six months.
In order to achieve appropriate compression during phase I, the lymphedema therapist should use textile-elastic short-stretch bandages that provide a high working pressure when the muscles contract (in contrast with long-stretch Ace bandages, which have a low working pressure). These compression bandages should be applied in such a way that there is more compression distally than proximally. This compression gradient can be achieved by applying more layers of bandage distally and fewer layers proximally.
The lymphedema patient is ready to be fitted for a garment (used for phase II) when the improvements in limb circumference measurements begin to “plateau”. Although ready-made lymphedema garments are available, custom garments are usually made for patients with advanced stages of lymphedema. Compression for lower extremities is often in the range of 40 mmHg to 50 mmHg, and values less than 20 mmHg are not suitable for successful lymphedema management.5
Any exercise or activity that contracts the muscles in the affected area will likely benefit the patient, as activity can promote lymphatic system function. However, the patient should be reminded that during both phase I and phase II, exercises of any type or any strenuous activity should only be performed when the affected extremity is compressed by either a bandage or garment. One helpful strategy when developing an exercise program for a lymphedema patient is to start gradually, and to first start with core muscle and breathing exercises, then proceed to more distal exercises, and finally return to the core muscles and breathing exercises. Examples of distal exercises include toe clenches, ankle curls, heel slides and bike riding.5 It is also very important to carefully monitor the affected extremity of the lymphedema patient during and after the exercise and/or activity to determine if the lymphedema has increased, stayed the same or decreased. Of course, if the lymphedema increases, the intensity and frequency of the exercise should be reduced. 5,12
Lymphedema treatment implications
Only a properly trained lymphedema therapist should treat and educate patients with lymphedema. Unfortunately in North America, extensive instruction during physical therapy schooling is not yet standard. The American Physical Therapy Association APTA), among other groups, is looking for ways to increase the level of expertise among its members. However, with the proliferation of lymphedema certification courses available in North America, many physical therapists and other healthcare professionals are becoming CLTs. These certification courses are 135 hours or more in length and include both didactic and laboratory portions. A number of accelerated certification programs include an extensive pre-course component, allowing the practitioner to take less time off from work. Other important lymphedema resources include the National Lymphedema Network (NLN) and the International Society of Lymphology (ISL).12,13
While lymphedema in the past has often been overlooked or misdiagnosed, a growing number of CLTs are using the conservative treatment techniques of manual lymph drainage and complete decongestive therapy to effectively treat lymphedema patients. An understanding of the pathophysiology of lymphedema on the part of lower extremity practitioners and an ability to recognize the symptoms will enable more patients to get the treatment they need.
By Harold Merriman, PT, PhD, CLT
The clinical importance of lymphatic system disorders is becoming better known among members of the medical community, including physicians and therapists. Most prominent of these disorders is lymphedema, which involves a buildup of protein-rich lymph fluid in the interstitium.
Some of the most common known causes of lower extremity lymphedema include pelvic or lower extremity cancer and cancer treatment (e.g, lymph node resection or radiation) that can damage the lymphatic system. Other causes of lymphedema may be much more subtle, such as an insect bite or sunburn that could irreversibly damage an already compromised and susceptible lymphatic system. Though lymphedema can be found in all types of individuals, active and fit individuals are less likely than obese individuals to develop lymphedema.
Once the diagnosis of lymphedema has been made, appropriate conservative treatment should be administered. Currently, a certified lymphedema therapist (CLT) is the provider of choice to administer the recommended conservative treatment. Before the 1980s, most of the research and treatment of lymphedema and related disorders occurred in Europe. Now there are also many opportunities for practitioners to obtain advanced training in lymphedema in North America. For example, in North America a number of lymphedema schools teach certification courses that allow practicing clinicians to become certified lymphedema therapists. The Lymphology Association of North America (LANA) administers a nationally recognized lymphedema certification exam to qualified and experienced lymphedema clinicians.1
Though the topic of lymphedema and related disorders is becoming better understood, patients with these disorders may still be ignored, misdiagnosed, or simply unable to find proper treatment. Unfortunately, in many areas of the United States there is a currently a shortage or absence of qualified clinicians who can successfully treat these conditions. This article will briefly review the anatomy and physiology of the lymphatic system and discuss the conservative treatment options for the lymphedema patient.2-5
Lymphatic anatomy and physiology
Lymph originates from blood plasma that leaves the blood capillaries and enters into the interstitum. A percentage of that interstitial fluid then enters the lymphatic system, where it is then called lymph. Lymph matter consists of proteins, water, fatty acids, and cellular components. The typical lymphatic system vessel has a three-layer wall structure and presence of valves, similar to the vessels of the venous system. The inner layer (intima) consists of endothelial cells, the middle layer (media) is made up of smooth muscle, and the outer layer (adventitia) is formed by collagen fibers that are loosely anchored to the extravascular connective tissue.4
The functional unit of the lymph vessel is the lymphangion, which consists of a lymph vessel bordered by two valves. As the lymphangion contracts due to the presence of smooth muscle in the middle layer, the valves provide directionality so that the lymph flows in only one direction. It should be stressed that the lymphatic vessel, unlike the vein, regularly contracts (under the control of the autonomic nervous system) and that this contraction rate can change depending on a number of factors. For example, the lymphangion contraction rate can be stimulated to increase during the hands-on portion of conservative treatment.
While the lymphangions have a distinct three-layer wall construction with valves, not all lymphatic vessels are that well organized. The first type of vessel that collects what will later become lymph fluid is called the initial lymph vessel or lymph capillary. These vessels are blind or dead-end sacs (tubes) consisting of a single layer of endothelium with junctions that can open and close to let in interstitial fluid. The initial lymph vessels lack valves and are located near the blood capillaries. As this fluid flows unidirectionally toward the heart, the lymphatic vessels become larger in diameter and more organized. The lymph collectors and the even larger lymph trunks have the distinct three-layer wall construction with valves. The diameter of the lymph collectors can be as large as 0.6 mm, and the lymph collectors’ valves are spaced 0.6 cm to 2.0 cm apart.3,5 Lymph then flows into the larger lymphatic trunks. The most important lymphatic trunks are the right lymphatic duct and the thoracic duct, which drain the lymph into the venous system near the heart at the right and left venous angles, respectively. The right lymphatic duct drains the right arm, right side of the head, and right upper trunk; meanwhile, the body’s largest lymphatic trunk, the thoracic duct, drains the left arm, left side of the head, both legs, and the rest of the trunk. 2-5
As the lymph moves unidirectionally in the lymphatic vessels, lymph nodes filter and concentrate the lymph and also provide immune surveillance using T & B lymphocytes. The 600 to 700 lymph nodes found in the human body are concentrated in the neck, axilla, chest, abdomen and—most importantly for the lower extremity practitioner—in the groin. In addition to immune defense, the lymphatic system plays a critical role in fluid homeostasis as well as transport and drainage of excess fluids, proteins, and cellular debris from the interstitial spaces that are not reabsorbed by the venous system. One can think of the lymphatic system as the body’s “sanitation system,” whose purpose is to dispose the body’s “waste material.”2-5
Lymphedema results from mechanical failure of the lymphatic system, which leads to an accumulation of protein-rich edema in the interstitium. Mechanical failure means that the “lymphatic load” (amount of lymph transported in a given time period) exceeds what an impaired lymphatic system can handle (transport capacity). In most cases, lymphedema will present itself in a single extremity, or in bilateral cases one extremity will often be more involved than the other (asymmetry). Though one might picture lymphedema occurring mostly in the upper extremity, often lymphedema (especially primary lymphedema) occurs in the lower extremity as well. 2-5
Diagnosis of lymphedema
Lymphedema is the most common disease of the lymphatic system. It is estimated that lymphedema affects 140 million to 250 million people worldwide and at least 3 million Americans.5 Lymphedema exists in two different forms, primary and secondary. Primary lymphedema is believed to result from an abnormally developed lymphatic system that can present either at birth or later in life. In many cases there is no known cause of primary lymphedema. However, in some cases heat, puberty, pregnancy or minor trauma such as insect bites, infections, sprains or strains may be identified. 2-5
In contrast, secondary lymphedema results from a known insult to the lymphatic system that causes a reduced transport capacity. Specific insults to the lymphatic system include surgery, radiation, trauma, tumor growth, infection, and chronic venous insufficiency. 2-5 The two worldwide most common causes of secondary lymphedema are breast cancer surgery and lymphatic filariasis. It should be stressed that even with the advent of less invasive modern surgical techniques such as sentinel lymph node biopsy and lumpectomy, lymphedema may still occur after breast cancer surgery and treatment. 2-5
Since lymphedema usually begins distally, it will first be noticed in the lower extremity in the toes, feet, and ankles before progressing proximally up into the thighs. Lower extremity lymphedema would typically be caused by a lymphatic insult in the lower extremity and/or pelvic region, but not by an upper-body lymphatic insult such as breast cancer surgery. The classic sign of lymphedema is a positive Stemmer skin fold sign, which can be defined as a thickened skin fold at the base of the second toe such that the tissue cannot be lifted away from the bone.6 A summary of lymphedema clinical features are listed in Table 1. Since there is no pain associated with lymphedema, the classic symptom that brings a patient to a lower extremity practitioner is edema or infection (cellulitis), which becomes more prevalent as lymphedema severity increases.2,4
It should also be mentioned that combination forms such as lipo-lymphedema are not uncommon. Lipo-lymphedema is a condition in which individuals with lipedema (symmetrical accumulation of fat rather than edema in the subcutaneous tissue) later develop lymphedema in addition to the underlying and ongoing lipedema. Unfortunately, many lipedema patients develop lymphedema since the accumulation of fatty tissue from lipedema causes compression of the superficial lymph vessels.2
Table 1. Lymphedema characteristics
Clinical Feature
Lymphedema
Gender
Women > men
Distribution
Unilateral, or bilateral with one leg usually affected more severely (asymmetric)
Pain on pressure
Absent
Easy bruising of affected area (hematoma)
Absent
Distal edema in the foot
Present
Stemmer sign
Present (positive)
Treatment
It is well documented that lymphedema is best treated using conservative methods administered by the certified lymphedema therapist.7-12 Unfortunately at times, lymphedema is still treated with diuretics, which is contrary to treatment guidelines set forth by the International Society of Lymphology and by other lymphedema physician specialists.2,4,12 Perhaps the best known conservative method is manual lymph drainage (MLD) which is a component of complete decongestive therapy (CDT). MLD is a gentle manual treatment technique originally developed in the 1930s by the Danish couple Emil and Estrid Vodder.2,5
CDT consists of two phases; phase I is the treatment phase, and phase II is the self-management phase. CDT and MLD should only be performed after the CLT has determined that no contraindications (e.g., acute infections or cardiac edema) are present. Phase I treatment consists of MLD, compression bandages, exercise (in bandages), and meticulous skin care (to cure/prevent bacterial and fungal infections). Once the reduction in lymphedema begins to plateau, the CLT will transition the patient to the self-management phase II. Phase II consists of compression (typically achieved by a customized garment during the day and bandages at night), exercise (with the limb in either a compression garment or bandages), meticulous skin care, and MLD as needed. Patient compliance with all treatment components (especially during phase II) is the key to a successful long-term outcome, and it is crucial that the patient, therapist, and other caregivers work together as a team.5
One of the most important skills the CLT performs is to provide MLD in the proper sequence. Since MLD increases lymph flow, the therapist does not want this increased lymph flow to overload and further damage an already impaired lymphatic system. For this reason, the CLT may need to initially limit the area to be treated by MLD. For example, if a patient has lymphedema in both legs, then the CLT may elect to initially focus on only one leg. Typically, the lymphedema therapist should first perform MLD on central and uninvolved areas, followed by performing MLD on the involved areas (e.g., the leg). This MLD strategy prepares the uninvolved areas to receive the additional lymph flow from the affected extremity. Again, it is very important that the lymphedema therapist administers MLD in a proper manner and sequence in order to obtain optimal outcomes.5
Proper compression during both phases of CDT is the key to the successful management of the lymphedema patient. If the affected areas do not receive constant and appropriate compression, the improvements achieved by MLD will be temporary (may last only a few hours).5 Therefore, the lymphedema therapist should have a frank discussion with the patient during the initial evaluation outlining the extreme importance of continuous compression of the affected extremity. This discussion should include the reasons why compression is so important, determining the method by which the patient (or other caregiver/family member) can don/doff the compression bandages or garment at home, and alerting the patient to the financial implications of proper compression since two compression garments per affected extremity will need to be purchased about every six months.
In order to achieve appropriate compression during phase I, the lymphedema therapist should use textile-elastic short-stretch bandages that provide a high working pressure when the muscles contract (in contrast with long-stretch Ace bandages, which have a low working pressure). These compression bandages should be applied in such a way that there is more compression distally than proximally. This compression gradient can be achieved by applying more layers of bandage distally and fewer layers proximally.
The lymphedema patient is ready to be fitted for a garment (used for phase II) when the improvements in limb circumference measurements begin to “plateau”. Although ready-made lymphedema garments are available, custom garments are usually made for patients with advanced stages of lymphedema. Compression for lower extremities is often in the range of 40 mmHg to 50 mmHg, and values less than 20 mmHg are not suitable for successful lymphedema management.5
Any exercise or activity that contracts the muscles in the affected area will likely benefit the patient, as activity can promote lymphatic system function. However, the patient should be reminded that during both phase I and phase II, exercises of any type or any strenuous activity should only be performed when the affected extremity is compressed by either a bandage or garment. One helpful strategy when developing an exercise program for a lymphedema patient is to start gradually, and to first start with core muscle and breathing exercises, then proceed to more distal exercises, and finally return to the core muscles and breathing exercises. Examples of distal exercises include toe clenches, ankle curls, heel slides and bike riding.5 It is also very important to carefully monitor the affected extremity of the lymphedema patient during and after the exercise and/or activity to determine if the lymphedema has increased, stayed the same or decreased. Of course, if the lymphedema increases, the intensity and frequency of the exercise should be reduced. 5,12
Lymphedema treatment implications
Only a properly trained lymphedema therapist should treat and educate patients with lymphedema. Unfortunately in North America, extensive instruction during physical therapy schooling is not yet standard. The American Physical Therapy Association APTA), among other groups, is looking for ways to increase the level of expertise among its members. However, with the proliferation of lymphedema certification courses available in North America, many physical therapists and other healthcare professionals are becoming CLTs. These certification courses are 135 hours or more in length and include both didactic and laboratory portions. A number of accelerated certification programs include an extensive pre-course component, allowing the practitioner to take less time off from work. Other important lymphedema resources include the National Lymphedema Network (NLN) and the International Society of Lymphology (ISL).12,13
While lymphedema in the past has often been overlooked or misdiagnosed, a growing number of CLTs are using the conservative treatment techniques of manual lymph drainage and complete decongestive therapy to effectively treat lymphedema patients. An understanding of the pathophysiology of lymphedema on the part of lower extremity practitioners and an ability to recognize the symptoms will enable more patients to get the treatment they need.
Wednesday, November 2, 2011
New frontiers in PTTD
Focus is on ultrasound, hip strength
Research presented in February at the Combined Sections Meeting of the American Physical Therapy Association highlighted underappreciated clinical characteristics of posterior tibial tendon disorder that could influence patient management.
Tendon thickness as measured using high-frequency ultrasound may help determine which patients with Stage II PTTD are most likely to benefit from conservative interventions and which might be better candidates for surgery, according to research from Upstate Medical University in Syracuse, NY.
Ultrasound imaging identified 12 Stage II patients with abnormal tendon thickening, seven with tendon enlargement and five with tendon atrophy. Mean tendon cross sectional area was 39.7 mm2; those with tendon enlargement averaged 53.4 mm2 while those with atrophy averaged 24.6 mm2.
Tendon thickness was not visibly evident prior to imaging, nor were there apparent functional differences between subjects at presentation. However, the researchers did observe significant kinematic differences between the two groups. Patients with tendon enlargement demonstrated significantly greater range of motion for hindfoot inversion/eversion, forefoot plantar/dorsiflexion, and total excursion; forefoot abduction/adduction did not differ significantly between groups.
Although PTTD is typically thought to be associated with tendon enlargement as the result of degeneration, the Syracuse findings show that tendon atrophy also occurs. The kinematic differences related to relative tendon thickness could help explain inconsistencies in patient response to exercise interventions, and knowing the cross sectional area of an individual patient’s tendon could facilitate more effective patient management.
“Targeted exercises to move the foot may be possible in the tendon enlargement group, and conservative or alternative treatments may be indicated,” said Christopher Neville, PT, PhD, an assistant professor of physical therapy at Upstate Medical University, who presented the results at the Combined Sections Meeting. “The tendon atrophy group may be surgical candidates, or if they don’t have surgery, the goal of treatment may be to protect the secondary structures that maintain foot posture and stability.”
A second study from the University of Southern California suggests that practitioners may also want to consider proximal joint kinetics in their patients with PTTD.
After anecdotally noting increased frontal plane motion at the hip in patients being seen for PTTD, researchers compared hip and calf muscle performance in 17 female patients with Stage I PTTD and 17 healthy matched controls. Patients reported a history of symptoms lasting from six months to one year.
They found that the PTTD patients demonstrated significantly lower levels of strength and endurance across the board, with 33.8% less hip extensor torque, 38.5% less hip extensor endurance, 28.5% less hip abduction torque, 27% less hip abduction endurance, and 62.9% less calf muscle strength. Interestingly, these effects were seen in the uninvolved limb as well as the involved limb. The PTTD patients also covered significantly less distance on the six minute walk test (497 m vs 571 m) and reported as much as a 50% increase in pain following the test.
These two sets of findings may be related, said Lisa M. Noceti-DeWit, DPT, ATC, adjunct instructor of clinical physical therapy at USC, who presented her group’s findings at the Combined Sections Meeting. The researchers theorize that because the PTTD patients walk more slowly, their muscles—all the way up the lower extremity—are being underutilized and over time lose their strength and endurance capacity.
“Walking does not depend solely on the actions of the foot and ankle,” Noceti-DeWit said.
The researchers are unable to tell from this study whether the decreased walking velocity occurred as a result of the pain of PTTD or whether other mechanisms may have been involved. Nevertheless, the findings suggest that practitioners treating patients with PTTD should not limit their focus to the most distal aspects of the lower extremity.
By Jordana Bieze Foster
Research presented in February at the Combined Sections Meeting of the American Physical Therapy Association highlighted underappreciated clinical characteristics of posterior tibial tendon disorder that could influence patient management.
Tendon thickness as measured using high-frequency ultrasound may help determine which patients with Stage II PTTD are most likely to benefit from conservative interventions and which might be better candidates for surgery, according to research from Upstate Medical University in Syracuse, NY.
Ultrasound imaging identified 12 Stage II patients with abnormal tendon thickening, seven with tendon enlargement and five with tendon atrophy. Mean tendon cross sectional area was 39.7 mm2; those with tendon enlargement averaged 53.4 mm2 while those with atrophy averaged 24.6 mm2.
Tendon thickness was not visibly evident prior to imaging, nor were there apparent functional differences between subjects at presentation. However, the researchers did observe significant kinematic differences between the two groups. Patients with tendon enlargement demonstrated significantly greater range of motion for hindfoot inversion/eversion, forefoot plantar/dorsiflexion, and total excursion; forefoot abduction/adduction did not differ significantly between groups.
Although PTTD is typically thought to be associated with tendon enlargement as the result of degeneration, the Syracuse findings show that tendon atrophy also occurs. The kinematic differences related to relative tendon thickness could help explain inconsistencies in patient response to exercise interventions, and knowing the cross sectional area of an individual patient’s tendon could facilitate more effective patient management.
“Targeted exercises to move the foot may be possible in the tendon enlargement group, and conservative or alternative treatments may be indicated,” said Christopher Neville, PT, PhD, an assistant professor of physical therapy at Upstate Medical University, who presented the results at the Combined Sections Meeting. “The tendon atrophy group may be surgical candidates, or if they don’t have surgery, the goal of treatment may be to protect the secondary structures that maintain foot posture and stability.”
A second study from the University of Southern California suggests that practitioners may also want to consider proximal joint kinetics in their patients with PTTD.
After anecdotally noting increased frontal plane motion at the hip in patients being seen for PTTD, researchers compared hip and calf muscle performance in 17 female patients with Stage I PTTD and 17 healthy matched controls. Patients reported a history of symptoms lasting from six months to one year.
They found that the PTTD patients demonstrated significantly lower levels of strength and endurance across the board, with 33.8% less hip extensor torque, 38.5% less hip extensor endurance, 28.5% less hip abduction torque, 27% less hip abduction endurance, and 62.9% less calf muscle strength. Interestingly, these effects were seen in the uninvolved limb as well as the involved limb. The PTTD patients also covered significantly less distance on the six minute walk test (497 m vs 571 m) and reported as much as a 50% increase in pain following the test.
These two sets of findings may be related, said Lisa M. Noceti-DeWit, DPT, ATC, adjunct instructor of clinical physical therapy at USC, who presented her group’s findings at the Combined Sections Meeting. The researchers theorize that because the PTTD patients walk more slowly, their muscles—all the way up the lower extremity—are being underutilized and over time lose their strength and endurance capacity.
“Walking does not depend solely on the actions of the foot and ankle,” Noceti-DeWit said.
The researchers are unable to tell from this study whether the decreased walking velocity occurred as a result of the pain of PTTD or whether other mechanisms may have been involved. Nevertheless, the findings suggest that practitioners treating patients with PTTD should not limit their focus to the most distal aspects of the lower extremity.
By Jordana Bieze Foster
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