Mr Alistair McInnes

As far as in the foot is concerned, peripheral neuropathy is the most common complication of all the complications that can affect in diabetes generally speaking. So it's a major comorbidity and to screen for neuropathy is really important because one of the major risk factors for other disease in terms of ulceration and subsequent complications. So in a very simple primary screening if somebody has diabetes and you want to find out if they have sensory motor sensory neuropathy or not, sensory neuropathy is really loss or partial loss of all sensory nerves that pick up from sensations of heat, cold, pressure, light touch, and proprioception, that's to say where the joint is in space. So simple testing we use in clinical practice, the most evidence-based practice, would be looking at loss of sensation to a certain degree, and the degree of which can be measured is using a simple monofilament, which are available commercially. And basically the 5.07 monofilament, and 5.07 is the size of the monofilament, and as it's applied to key points in the foot, which I'll mention in a second, if the patient has to close their eyes and you apply the monofilament for one to two seconds to a site that's a common site for ulceration, i.e. the first metatarsal head, if the monofilament buckles and it seems to buckle after one or two seconds of pressure, it means they can no longer perceive that degree of neuropathy. So the sensory loss being measured is those at risk who have got such a loss of sensation due to a number of complex underlying mechanisms of hyperglycemia over time that destroys the myelin sheath and destroys the sensory nerves. That's one very simple test. In addition to that, if you want to distinguish sensory neuropathy, you may want to use tests for vibration perception using a 1-2-7 tuning fork, and over the bony prominences of the lateral medial malleoli, or over the medial eminence of the first metatarsophalangeal joint, to hit the tuning fork very gently in between your fingers and apply the area. Patients close their eyes and ask them to determine whether they can feel the humming or buzzing of that vibration. It's quite a rough tool. Don't be fooled into making the diagnosis of neuropathy on that alone, because many people as they age lose vibration sensation anyway. But the other thing to do is obviously was for sensory neuropathy testing to look for clinically is to ask the patient about any sensations they have where they have paresthesias often heralds the onset of sensory neuropathy where they feel burning tingling or shooting sensation or they may just feel their feet are like a lump of wood they feel this numbness and or they may indeed be suffering from pain some forms of neuropathy can actually result in a painful foot. So you can have, in diabetes, you can have a situation of the so-called painful painless foot syndrome, first coined by John Ward from Royal Hallamshire Hospital in Sheffield. So for sensory testing, basically, a loss of sensation, if you want to buy a commercial variable monofilament and or it comes with a pen, like a NeuroPen, the other end, you can apply a sharp and dull pinprick. And if they've lost the ability to sense, to feel sharp touch. Again, it's another example of sensorineuropathy. So if you use at least two modalities, sharp and blunt pinprick to see if the patient with their eyes closed can determine it or not, and the monofilament over the sites where ulceration most commonly occurs, the hallux of the big toe, the plantar aspect of the big toe, the apex of the third toe, and the first, third, and fifth metatarsal heads. Five sites on both feet. Test them, and if patients can feel only eight out of ten, only they're said to have sensorineuropathy. neuropathy, a very simple screening test for that. As far as motor neuropathy is concerned, more difficult to discern in a simple clinical setting, but primarily in the foot, the way that motor neuropathy, if present, affects the foot, tends to be an imbalance of loss or paralysis of the small muscles in the foot. These small muscles are the interossei and lumbrical, the small muscles in the toes, and this can lead to an unopposed pool of long extensor muscles, resulting in claw toes. Now, these clawed toes or retracted toes can lead to more pressure on the underlying metatarsal heads, therefore rendering the patient more at risk. So motor neuropathy, depending on which muscle groups have been affected, it can lead to motor imbalance and deformity, which makes the patient even more at risk. Sometimes motor neuropathy can be of greater magnitude. But for a simple clinical test in the foot, look for clawing of the toes, look for some muscle atrophy, and even examine the patient's hands, that first interthenar space, often the very first area of atrophy of the muscle is in the hands, and they often see the terrible wasting in that space, easy to detect. Again, it's real importance of motor neuropathy, as far as the patient's concerned, is it may lead to foot changes that makes them more vulnerable to pressure, and pressure alongside sensory loss can set the scene for developing foot ulceration. Finally, the enigma, or bit of enigma, of autonomic neuropathy. In autonomic neuropathy, the autonomic nervous system can be affected in diabetes. One of the most common clinical presentations of neuropathy is sensory motor neuropathy and also some autonomic loss. And autonomic neuropathy in the foot can be detected primarily from bounding pulses. As a result of the loss of vasomotor tone that controls the pulsatility of blood vessels, If you palpate the pulses between the base of the first and second metatarsals and palpate the dorsalis pedis artery, if it's absolutely thumping, it might be evidence of autonomic neuropathy. So, in contrast to what we understand the diabetic foot often having very poor circulation, which in many cases it does, beware the warm, dry neuropathic foot. The neuropathic foot may be over-perfused with blood supply and you can get a phenomenon of arteriovenous shunting, where the sheer volume of blood is so excess that venules, small venules cannot cope, and you get shunting of vessels where some of the capillaries leading to the surface of the skin may be depriving the area of oxygen. And with AV shunting can be detected not just with pedal pulses being strong and bounding, but look out for predominant veins, as you can see in the back of my hand, predominant veins that are bulging with blood supply. This is known as Ward's sign, and Ward's sign, named after, again, a famous diabetologist, John Ward at Sheffield Hallam, and Ward's sign is the distended veins on the dorsal aspect of the foot. Loss of sweating is another feature of autonomic neuropathy, to which the autonomic nervous system controls auto-temperature regulation, and as a result of autonomic neuropathy, you might find complete cessation of sweating in the foot. Ironically, sometimes autonomic neuropathy in the general body can lead to gustatory sweating or excessive sweating after certain foodstuffs, so be very careful in the clinical assessment. But as far as the foot's concerned, sensory neuropathy, the monofilament, the chewing fork, and asking the patient of altered sensation. Motor neuropathy, look for clawing of the toes, altered shape of the foot, and look at the hands if there's any other evidence of motor loss. neuropathy, look for bound, feel for bounding pulses, look for absence of cessation of sweating, which may be cracked heels, dry skin, which can act as a portal for infection. And so beware the warm, dry, numb foot is advice to give as far as the neuropathic foot is concerned. The most predominant classification of neuropathy, the most common neuropathy type, is sensory motor loss. And you will get to a certain degree autonomic, but it's very difficult to quantify in the foot. We look for, it's very difficult to quantify, generally speaking, it's usually the more severe autonomic neuropathy is actually a very serious complication of diabetes. But in most peripheral, because it's a small nerves effect, and the way that there are several etiologies that cause the damage to the nerves, usually speaking, all sensory motor and autonomic nerve factors are affected at the same time, and it's really the smaller fibers that we see being affected, but both unmyelinated and myelinated fibers get affected as far as the, so coexisting what the natural, if you're hinting at, Trudy, the natural progression of the disease as many patients present with diabetes, they develop sometimes, many of them develop neuropathy, particularly as they get older, then the onset comes into the background of peripheral arterial disease. So we tend to go from the normal foot to the neuropathic foot to the neuroischemic foot and sometimes that makes assessment very difficult because sometimes the neuropathy can mask severe ischemia And when the warning signs are lost, like pain and so on, and color and so on, and things can change, it's really important you get one of the members of the foot protection team or multidisciplinary team to assess, never be lulled into a false sense of security. Many of the ischemic signs are masked because of the neuropathy. The enigma of the Charcot foot, named after Jean-Martin Charcot, the famous prison neurologist, it's a very strange phenomenon in that many patients go on to develop peripheral neuropathy. up to 50-60% and they're older and yet ironically a very small percentage, maybe even 0.1%, develop a charco foot as a result of neuropathy. In terms of recognition of it when it appears in its acute phase, beware of the foot that's red, hot and swollen that sounds like it's sterilised, it sounds like an infection but there's no break in the skin and there's no signs of infection, no ulcer. And then the person that has autonomic neuropathy, where there's a dry skin and they've got a patent blood supply, often it's predisposed to have a history of trauma. And with that history of trauma, they may present to you with this very hot, very swollen, maybe painless, could be painful foot. And it's really important if it is a charco foot to get a seek opinion. It could be cellulitis infection, it could be the Charcot foot. With Charcot feet, we're picking up more and more of them as patients are living longer. Although it's still relatively rare, it is a patient's room for a long haul because of the work from Professor Jeffcott in a key paper in The Lancet looked at the role of inflammatory cytokines. It looks like one of the reasons why you get this massively increased turnover of bone cells, the osteoblast, osteoclast turnover is rapidly enhanced through the action of these excessive pro-inflammatory cytokines that trigger aspects of the bone metabolism to end up in this very strange increased bony turnover. And what that triggers is these excessive inflammatory cytokines. It means that the bone cells are almost at this bony turnover, it renders the bones much more fragile, prone to fracture, and you end up with if the patient continues to ambulate when they have an acute shock or joint, their walking and bones are like crystal glass. It leads to more fracture, more deformity, more hyperemia, they get this very vicious cycle to which point the foot can become so deformed it can often result in bologna amputation. Conversely, so the real thing to check for clinical observation is, have they got neuropathy? Have they had trauma or not? Examine the foot, send off for x-ray, send off for blood tests. Blood tests include all the inflammatory markers. Look for C-reactive protein, ESR, white blood cell count. The important thing is that whilst these are just markers of inflammation, it could be from infection, or it could be charcoal. But if you're highly suspicious of charcoal, send in to somebody very quickly. Get the patient off their feet. They mustn't continue to wait where all the damage can take place. And the traditional treatment would be to put on a total contact cast, complete loss of ambulation to try to dampen down this massive inflammatory process. I know there's work going on currently where we're looking at all sorts of various pharmaceutical agents that may help to dampen down the pro-inflammatory cytokines, and we're learning a lot, I think, from our colleagues working in the area of rheumatology, with anti-TNS, for example, or maybe the use of steroids, which could be a particular problem, diabetes control, but we've still got a long way to go to get best case treatment. But recognition of it, send off for x-rays, send off for bloods, send off to a multidisciplinary team. If it's red, hot, and swollen, it may be gout, it could be differential diagnosis, could be gout, could be phlebothrombosis, could be cellulitis, be meticulous in your assessment, and the skin's broken, and it's warm, hot, and swollen, then my advice is to get the patient to cease weight bearing and seek opinion from the multidisciplinary food care team.