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Hi, good evening everyone. And uh uh it's me again. Uh Hammed Hashim. I'm a foot and an consultant um at we and he in uh Northwest London in the UK. Uh Today is our third lecture in the um review course, Foot and Anchor course under the umbrella of Ortho Bema. Um I will speak today about bis virus, rheumatoid foot and diabetic foot. So this is where I come from uh Heatherwood Hospital in an Ascot area in the Northwest London. And again, this is uh the youtube channels where all the education and activities we're running will be there. It's my education and channel and there also be my channel. So quick basic start, which is very important for all of you to understand all the term is will be running through. Uh In this lia, you need to understand what is teleus and telis is two words TLI and P and then you need to understand the different positions with this um uh different names. So when we say Teleus, tele is the ankle and this is the foot. So any deformity related to this, it is deformity of the foot. Anything related to the tele is a deformity of the ankle. And when you have the foot and ankle deforming this, when you say you, you, you, you, you name the deformity as telis. So the commonest one is Telis um con to Telis equi virus or CTV. And basically because it, it is a deformity of the ankle and the foot, we call the TS all other deformities which is related to the foot like the cavovarus. We're speaking about today like the bis Planus or Bino Valgus, we spoke about uh blast lecture. The mainly deformities of the foot, ankle is not involved with. That's why we call it. Uh bis soy means congenital deformity or acquired deformity is mostly congenital, which is affecting both ankle and foot. If ankle only we call tally in, if, if foot only we call this. So you have, you may have a tabu cavus which means high ast foot because there is an element of dorsiflexion of the ankle. I will show you in a minute how uh the ankle is involved. It could be an equinus means blunt deflexion. It could be a calcia means dorsiflexion at the ankle could be vuls which is a po which equal e at the ankle and I'm sorry, in the high foot and um vuls or abduction in the forefoot. And again, we understand that because of the uh configuration of the subtalar joint, you cannot have these two movement alone without and blunt and, and, and, and uh blunt flexion in the ankle. So to have an abduction and e version your ankle, I'm sorry, do your ankle has to be dorsiflexed and to have an abduction and inversion, you, your ankle has to be plan to flexed. So tele valgus which equal pronation, which is equal dorsiflexion in the ankle e version in the hi foot and abduction in the forefoot. And the other way around ation which is equal plantar flection in the ankle inversion in the high foot and abduction in the forefoot. So um we speak about bis cavers and and can you can easily spot. This patient have an high acid foot, blunt the flex with forest tray and the virus of the of the heel. And this is by definition, a bis cavers. What if you have blunt a affection of the first ray only without virus in the heel? This is uh a uncommon condition which is called plantaris. So the difference between cvs and plantaris, both of them are ba ba, both of them are deformity of the foot. But CVAs is deformity of the 4 ft and hind foot which equal blunt affection of the forest ray and virus of the heat. While blanus is only 4 ft blunt without it virus heat. So if you have a CVA without with virus heel, this is not a cavs, this is blunt. And once you see a PC, you have to think about neurology. This is very, very, very important. There is no option even if you are sure this uh CS is idiopathic. Again, you have to exclude the neurological causes and a lot of neurological causes can cause PSS. And we will go to this uh in a minute how this patient will present to you. This patient will present to you mainly with metatarsalgia and sometimes with stress fracture of the lateral border of the foot or base of the 50 m Toral or the 50 me to cell shaft. Because as you can see, basically this patient is loading the lateral border foot more than normal. So the one in black here is a normal foot loading. And as you can see, as we agreed before heal and going from the lateral border up to the first uh mid uh head and the and the toes. And as you can see, there is no overloading or point loading in this normal pattern of weight bearing. One, if the patient has a cava which is equal virus heal and for the situation will be a very high point loading on the foot, which will be under the first meters head, which will be under uh the 50 m head and under the border of the foot. That's why this patient very commonly to come with you with a pain in the lateral border of the foot because he's overloading the lateral border of the foot because of the deformity of ankle and hind foot. And sometimes they come with stress fracture. And very common clinical mistake is to deal with a stress fracture without correcting the main deformity. So the stress fracture happened before you o be because you're overloading this bone, not because of problem in the bone itself. So, bone quality itself is ok. But because you are overloading this foot because of the deformity of your, of uh your foot, uh you have a stress fracture. So the treatment of a stress fracture of a lateral border of the foot in a Kvas foot is correction of CS. This patient may come to um with a history of instability. The problem with this patient, as you can see, the patient is I'm sorry, we'll go back. The patient here is uh uh normally stretching the lateral lateral uh structure of his foot. Normally he has an incompetence in the lateral ligaments. And on the other side, we we understand now the problem of the musculature. So his terus which is per previous uh uh is weak. So bent breva is weak. They have he has a stretched lateral structure because of the virus position of the hand foot and the bladder flection of the first day. So he is commonly to have a giving way because there is the lateral structure of the ankle are weaker at the same time. This patient, the commonest cause of it is neurology as we agreed. And with the neurology, especially the sensory neurology and the motor neurology you have was uh Sharma to this patient would be having a lateral instability because the muscles in the lateral aspect are weaker than the media aspect. Definitely, you will be having a difficulty wearing shoes and constantly you have this patient uh living life with um uh insoles or an arch support or so or insoles because they cannot fit their shoes inside the foot in a normal shoes. Uh When you see this patient, the first question you need to ask about, is it unilateral or bilateral deformity? And uh when did this deformity happen? And is it progressive or not? And does he have any associated problems or uh symptoms or not? Commonly this patient? I'm sorry. Uh If this patient has a unilateral deformity, mostly you will be having a spinal cord injury or some sort of injury or neurology from the spine. If this patient have a bilateral deformity, mostly have, have a generalized neurological problem. Commonly the hereditary since the uh uh neuropathy since motor neuropathy or um uh charcoal marit too, you need to ask you clearly about the neurological spinal trauma and neurological symptoms. And you need to ask about the family history. How will you examine this patient? Same, same protocol as we agreed. First thing to have a look around the patient, have a look. If he has using any aids or any walking aids or sticks, have a look in the shoes. You need to have a look in the shoes, ensure where is the point of wearing the sole of the of the shoes? You basically will see a lot of wearing on the lateral aspect of the, of the shoes on the of or, or, or, or um the sole of the shoes because the patient is overloading his lateral um border of the foot. If patients start to walk, you can ease the spot that the patient has an high arch, uh high media arch. And if this have a have a neurological background, this patient will be walking with a shuffling or high steady gait because of the foot drop, you have to have a look on the hand and very commonly with marit to find gathering of the hand because of the atrophy of the muscle. And definitely you have to look on the spine to ensure there is no signs of spinal uh operation. There is no sign of spinal trauma, there is no clear aggressive deformity, there is no clear signs of dysraphism where patient is while patient is standing, have a look from the back. You you expecting to find this patient uh he in vs have a look from the side. You're expecting to find a high altitude with a blunt orlex it very straight. And you're expecting this patient if he has a neurological origin of the problem to have a clouding of the tubes, definitely while patient is standing at the same stage, do a common block test. So both uh be food or whatever you use or whatever a book or something underneath the first tray, according to the idea we explained about the tri. But so this patient, the tri but this is has been, this is the first tray has been blunt reflex. It so the whole thing to for the whole thing to to change it has to go this way. So if you raise the first tray from the ground, you normally should see a corrected hind foot virus. This is means this is uh the the the standard bisques which is 4 ft driven. If this doesn't happen, means the hind foot, either the hind foot is the origin of the deformity or the hind foot become rigid and arthritic and it's not moving anymore. So common block test will give you two results. Number one correction of the head virus on uh raising of the fest ray, which equal is this deformity is driven from the forefoot and the high foot is supper or the other way around. Even if you raise the first ray, the deformity of the hind foot will not correct. And this is gives me one of two meanings. Either the the deformity is hind foot driven, not 4 ft driven, or the deformity is 4 ft driven, but the hind foot become arthritic and it is not suffer anymore. Once you sit your patient on the couch, have a look on the sole and definitely you will be looking at the pressure areas and you will see the pressure areas very clearly under the first ray and over the lateral border of the foot, you may find ulceration, especially if the patient is neuropathic by any means, either spinal cord problem or trauma or uh charcoal too. And this is because of the hyperkeratosis and overloading and over attrition. There, you find some ulceration and once you correct the heel virus into normal on into neutral position, you will see clearly a pronation of the forefoot. So it's very important to comment on the full foot position after correction of the hill. When you start to ask this patient to move again, same system, sorry, we'll do an active range of motion, then basic range of motion and basic range, basic range of motion. And you need to comment on the deformity if this deformity is correctable or not. So if the hand foot is corrected into neutral and if it's neutral is the 4 ft is correctable or not, you definitely, as we understand uh that the muscle imbalance is one of the main causes how the bisques happens. We need to come to an itchy tendon and how we examine and we agreed on this before we need to examine Brune long tip and tip post. And Bruneus ps, you definitely need to do a thorough uh neurovascular examination and CVS called test is very positive to check if the patient has a in the achilles or a gastro contraction. So, what's the best anatomy behind the bis cavers? So as we agreed again, the idea of the tri boot. So bis gave us start by blunt it for t which is in the bipolar foot. And this poin forefoot equal that to be corrected, that the foot is blunt reflexed and the hind foot is in virus causes of KVAS is a lot. Um ve is not, not an uncommon cause. It's a common cause. Then you have may have it congenital. Like in, in patient with cla foot or abos, you may have it traumatic as we agreed. If unilateral, it may have it from a crush injury in the back, from a compartment syndrome in the leg. It may be neuromuscular and this is the commonest charcoal ptosis by in a baby that B UCB ataxia or stroke. Uh If you have a look in the x-ray, I need you to understand that you cannot comment on an X ray for base gave unless the patient is standing weight bearing and your x-ray should be an eb later and oblique use, you spot three angles and you need to measure them correctly is the mars angle, hips angle and the calcaneal pitch. So if you look in the mirrors angle, this is the angle. So basically, it's between the axis of the talus and the axis of the uh first meter person. And normally it is 0 to 5 if it is more than five bis bis gave us if it's less than zero by minus, it is a bis planus. Then heps angle is between the axis of the calcaneum and the first meat cell axis. And this is normally an obtuse angle as you can see. And if this angle is going beyond 150 this means the patient is in bisc can cal pit basically you doing at line here. This number 3 g line here under the ground and normal. This is 16 to 32 degrees. If this Kinia which is increasing means sorry if this CIN bit is increasing, this mostly in CVAs and if it's as low as is in uh plants. So in this X ray, you can spot these angles on an X ray. So this is a tibiotalar angle. Ignore this one. This normal should be 90 but ignore about it. Ignore it. Uh This is the me angle, it the ax of the the and the first mid cell. This is the hep angle between the, the material axis of the calcaneum and the first meals axis and uh the Calcaneal bridge. This one is not here. You kinda spot here very easily, sorry you can hear what we call the kite angle. So the angle between the, the the angle between the axis that he has and the calcaneum and definitely with uh uh cava this angle will be reduced in this x-ray. You can easily spot the uncoverage of the tenor navicular joint. And as you can see, this is the axis of the head of the TS and this is the articular surface of the navicular. And you need to spot this clearly to see if the patient how, how much uncoverage of the T is there. This is not a perfect solve man's view, but it gives you an idea where is the position of the hindfoot? And you can easily spot that the hind foot is in. Vs. And if you look on this x-ray, you can easily spot that this is the the axis of the talus. And normally it should be running with the same axis of the foot which is going through the second metatarsal. But as you can see because of the cap, the, the forefoot is out ducting and because the forefoot is out ducting, the heel isn't going into virus. Uh You need an MRI scan if your deformity is unilateral because the risk of having a spine problem, either injury or dystrophy or compression or whatever is there. You have to have an MRI scan of the spine. When you asking the exam about the management of this, gave us, we all again agreed that it is neurological until proven otherwise. So you need to have an MDT approach. You have to involve the podiatrist. You have to involve the neurologist. Very, very important. Don't touch this patient even if you are sure that it is an idiopathic PVI unless you get an a neurologist opinion, which says that it is idiopathic definitely as any treatment we have to start with non operative. So non operative for Best gave us will be uh show, show where modification will be some orthotics and insoles. Either this is still a Subbu uh hi foot to use and uh um corrective orthotic or it is become rigid and we need to use an accommodative orthotics neurological treatment under the neurologist. We need to have a very good goal with the neurologist until we get uh proper management. What if I operate on the base givers and the non operative treatment is not enough for the patient. So we have few principles. You need, you need to understand this by heart. Number one is the colo of how to correct the foot deformity and this applies to all four deformities especially Cavs. Firstly, number one, you need to get the heat underneath the cuff. So you need the heat under the tibia. You need to have the foot plan to grade and to do the heat under the tibia, you'd have to do one of two, either number one lensing of to ales or a shifting Calcaneal uh displacing cal osteotomy um uh media um later cal osteotomy displacement to have the foot square on the ground. You have either to dorsiflex, the first ray, first ray osteotomy release of the blunt fascia. Then you have to have a balance in muscle to overcome the reason that or the cause of the muscle anatomy behind uh the base CVAs and this balance equal that you need to move one of the invertors to become an inverter. So you can transfer the tibia posterior to the dos and move the foot and you can get the brunneus longus to be transferred to the bruneus to give it some eer uh power. If your foot is still flexible, definitely, you will do uh a 4 ft surgery to treat the, the driving cause. And if the, if the virus is fixed it, so you don't have any option to correct anymore. And the option here will be a combined forefoot and hand foot surgery and mostly it will be a fusion right through this. You have after the colo, you have the role of stones. So you have two soft tissue to release tender achilles which is tied and plantar fascia, a lot of debates about the plantar fascia release many centers at the moment, doesn't do a plantar fascia release. But the classic teaching is still, you have to release the tender achilles and plantar fascia to get the give sorted. Uh, you have two tendon transfers to do. And again, as I told you, you move from Berne longest to Brevis to give the more e force and allow the Berne Brevis to be, to balance uh, uh, uh, uh uh the tip, the tip post. Otherwise it is to get the inverter, weaker or to weaken the inverter by moving the TPO from an position of inversion to a some of the foot to be weaker inversion and uh uh um to, to balance the weak, be previous osteotomies. If you will, do you have two osteotomies to do either lateral displacing osteotomy of the calcemia to correct the he virus or first MTB or cuneiform, uh first MT or cuneiform dorsiflexion osteotomy to correct the blunt reflection of the first tray and definitely in the severe or rigid cases. The option you have is to have a high foot, corrective fusion or fusion. So you have, as I told you, you will have a clawing of the tooth and the clawing of the tooth has two reasons. Number one, the same pathology which cause uh the PCA which is a neurological cause. And the other one is is trying of the foot to overcome the weak uh um uh es inverters. I'm sorry, the weak uh es and Bronta flexors, uh dorsiflexors. So what's happened? The first ray is blunt, reflexive and the blunt reflex of uh and the I'm sorry, the dorsiflexors of the foot are so uh weak, which is the tip. And so the the patient is start to recruit the, the A HL or the extensor ha as long as to do the job of the tibia. And T I will go in a minute in the muscle imbalance in the charcoal. But to understand I we in the, in the first lecture, we agree that we have counteracting muscles on both sides of the ankle. So tip and is overcome by the Benni Longus tip ant is elevating the first ray and blood Benne Longus is dropping the first ray tip ant is dorsiflex in the first ray. While Benne Longus is blunter fixing the first ray. On the other side, you have Bernes Brevis versus TPO. Bernes Brevis is an eter and TPO is an inverter in the this ca especially if the shark to the coast, the tip post is a stronger o or overpowering the brevis and the brunneus strong is overpowering the tip. And so you have a weak tip, ant and a weak tip, a weak uh re weak tip. And so no dorsiflexion of the first ray. That's why the first ray drop or blunt reflex and weak BN Brevis. So no eer so the inverter are more stronger. That's why the he goes into virus. Again, you have encounter acting muscles, maintaining your ankle and foot balances, tip post and be Brevis TPO is an invertor. Benes Brevis is an eter in charar and base gave us tip post is stronger than the previous tip post is causing the hea to go into virus and the forefoot to go into a while the be vus is weak. That's why the aversion is weak. The other group of muscle counteracting muscles is the tip and which is normally dorsiflex in the first tray. And the Bennis Longus which normally blunter flexing the first ray in Charco marit or your bene longus is stronger or overpowering the tip. And so the the blunt reflexing force on the first ray is stronger than dorsiflex. That's why the blunter flex. The first tray goes into blunter flexion for the patient to compensate for the weak tip ant or the dorsiflexors of the ankle because your tip aunt is the main dorsiflexor of your ankle because tip aunt is weak, the patient to overcome this weakness of the tip and or the ankle dorsiflexion. He recruit the E HL the extensor Haasis longus to do the job of the anterior. And with time the extensor Harri longus is over recruited. It starts to cause a clawing of the first um of the hallux of the great toe. That is one of the causes why the hallux go in clothing with um um ABIs SCS to treat this surgically. The option you have is to do what's called Jones procedure. And it's basically as you can see here, we use the IB joint. So get the IBJ it, insert a uh a wire through and get the A HL detach the hal from here and move it around the, the the the first metatarsal neck. So it doing the job of blunter of dorsiflexion rather than blunter flexing. And there is no more movement in the IV joint. So joints, procedure basically is fusion of the ib joint of the great toe and moving the HL to hook around the neck of the first minute dos. So doing the dorsiflex action of the first metatarsal without any clothing because of the fused IB joint. If you have clawing of the toes, the option you have is to release the flexors. So do flexor tono toy or to fuse the IB joint or even to excite them. So if we come to the commonest cause of PCA, which is char marit, uh it's basically in, in simple terms, it's a demyelination of nerves of the different nervous system. That's why it gives an hereditary. So HSM N means hereditary sens motor neuropathy, hereditary sensory motor neuropathy means because if there is demyelination or problem of the myelin of your breath nerve, so your sensory and motor nerves are dysfunction. It is a very common cause in bilateral uh cava feet. It's a type of an autosomal dominant problems and it's most commonly aggressive inherited neurological disease. If you have it, it's always presented in the second decade of life and it's a bit progressive. Uh It's not uncommon to be honest. Uh There are two types. The mo the most aggressive is type one when the demyelination and patient have a, give us a second uh decade and the type two is a bit less aggressive with some uh valerian degeneration and it's always the late onset and the patient will be on the a side rather than the spastic side. I now we'll go in the same pathology I explained from a minute ago is about the affected muscle. So basically what chaco marit does, it, it makes some muscles weak and other muscles stronger. So it imbalance the muscles around the foot and ankle. And as we agreed, the bene believe it is antib until will be weaker and the tip post and brunneus fungus will be stronger. And when you see that the same happened with the the intrinsic muscles of the hand and feet. And that's why you have to examine the hand because you will see the guttering in the web spaces. Cas happens because as we agreed be Longus, which is a blunter flexor of the first ray overpower the tibialis anterior, which is a dorsiflexor of the first ray and virus happen because the tibialis posterior which is uh normally an inverter overpowering the bruneus, which is normally an everter. The hammer too happened because weak recruit the two extensors that as we agreed and clo the other clots under char of meito specifically will be a weak intrinsics muscles of the foot. Mary has a common association as a neurological problem with hip dysplasia because you understand that for a normal hip to develop, it has to have a normal muscle action around it because the muscles are imbalanced. The hip dyspas is very common association with charcoal and the same cause you have, you will have an aggressive, severe muscular scoliosis, which mostly will be a left curve, which is an uh atypical curve and will be Thora thoracic curve and maybe kyphotic as an investigation. You have X rays and we agreed about the x rays uh on a bi cavus charco marit at the end of the day is a bilateral bi cavus condition. So the X rays will be the same you may have because we understand that the charco marit cause cause cavus because of muscle imbalance. We may do an emg and definitely because it's an autosomal dominant inheritance, we may do a genetic testing for a patient, MRI scan uh or spine. If you have a lateral deformity, this is to exclude the spine causes and definitely the treatment of char com marit. As we agreed for PCA treatment is an MDT. You have to have a neurologist. But the at, at, at the end of the queue is the orthopedic surgeon because the treatment of char comatus is basically non operative until proven otherwise. And non operative again, the same treatment will be fourth, we modification will be insoles and the insoles will be added because this is definitely an accommodative one would be arranged ino with depression of first ray and later which are are underneath the he if you will operate same story, all what we aim for is to achieve a bl grade is stable, show foot. And depending on the deformity, every deformity will be corrected. Same story as we agreed on. The bi gave us nothing in you. Uh There's some in common Bi Cas deformities and you need, I need you to have a look on this X ray, I'm sorry. And this picture and to keep it in mind and keep your, your, your eye memory, remembering every definition of this. So the, the classic one is the best Cavovarus. This is the one we spoken about the whole uh lecture. Then you may have a best equinal cavovarus. And Quino means that uh the, the cal bit is low means that the foot is in blunt reflection with a cavus, so blunt of friction at the ankle and cus at the mid foot. And this cavus as you can see. So the calcium again, this is means the cainia bit is very high. The calcium is dorsiflexion and the foot is uh uh and the forefoot is plantar flexion and this is will have the highest. Then there is this uh vulva cavus and basically this is uh about the position of the hind foot. So the hind foot rather than being in virus will be in valgus while they still the la the the uh midfoot is in blood reflection. So another two uncommon deformities and uh we quickly go through them is Equinovarus and Equinovalgus foot. So, Equinovarus foot, the commonest to have it is a residual from a Talaus uh correction. So, if you don't cor correct your tabs completely. You will end by a residual club for deformity or equinovarus. And basically this patient will be walking on the later board of the foot. As you can see in this uh clinical picture. Other causes which is uh a bit rare causes is cerebral palsy. If the patient has a muscular dystrophy by a baby that or uh Hemed commonly with the tibia heed, the patient has um weak uh I'm sorry, has lost media structures. That's why. Oh normally the food goes into virus uh following a stroke. Definitely because following a stroke, this this the the muscle im balancing and the deformity will uh be an equinovarus. Uh Again, virus is tibia posterior uh overpower and equinus is gastro uh complex overpower uh treatment if it's a residual club foot deformity. So it will do the same against the bones, technique and ankle. Uh foot orthos. Uh you may need uh if, if, if there is a cerebral palsy, especially a spastic cerebral palsy, you need some uh uh um uh Botox injection to relax the muscles which is over contracted like the TPO and the gastrochilus. Definitely you have some, you need some physiotherapy. And if you fail in all this, you need to lengthen the achilles and you need to do a split transfer of the tibia anterior and uh even do a split transfer spread tendon of the tibia posterior. In uh more advanced cases, you may need to do a calcaneal osteotomy. And uh if the patient is rigid deformity, you may need to fuse other way around is Equinovalgus foot. And again, valgus quino, the same is because of the uh speciality of the today's complex and equinus. I'm sorry. Valgus is because of uh overpower of the previous. The high foot will be in equinus and it will be benefit callosities over the tailor head on the media aspect of the foot. Communist cause of this is lost lateral structure of the an in uh feri heel and cerebral palsy in the frill heeria, the ankle is called bone and socket ankle and it lost fibular. There is no fibular fri hemi media. I mean there is no distal fibula. There was like uh uh uh bone and socket, ankle easy for the ankle to go in in uh valgus and equinus treatment. Again, the same, you will be doing some physiotherapy, doing bracing buttocks, uh ait dens and dens if you can, if it non-operating measures are uh uh do fail. And at the end, either calm osteotomy and if it's a deformity will be um a sub arthrodesis. Uh The second topic in this literature will be the rheumatoid foot and rheumatoid foot is a, a, an, an exact picture of a rheumatoid hand rheumatoid is a systematic inflammatory disease with a AAA body arthralgia everywhere. The pathology is done in the sinuum and you all, all of you are much better than me in understanding the bas or the bas cascade behind the rheumatoid, the rheumatoid hand, the rheumatoid rheumatoid foot are the same, same in diagnosis, same in pathology and same in treatment. So with the moto foot, you can see uh the 4 ft as you, you, you definitely um spot there is a hallux vs and always there most of the time uh clinically, it is more symptomatic and this is not the main complaint of the patient. The patient have uh body arthralgia and uh joint pain. His pro his biggest problem is in the bunion or the helix valgus. Definitely in x-ray, you will see an erosive arthroplasty and this erosive arthroplasty would be very articular because the problem is start in the synovium. You will have after after some time of the uh sinusitis and uh destructive process in the joint, the MTB joint would be dorsally subluxing, there is no more fat back there. And definitely you agree with any rheumatoid disease. The soft tissue are very weak and one of the weakest structure uh because of the rheumatoid is the blatter plate. And once the blatter plate goes, the joint is the dorsal subx. You. When the joint, the MTB joint dorsally, this MTB joint dorsally sub lax, you'll definitely see the metatarsal head very prominent and because it's prominent, it will be a avoid loading will be some oc and blunt. The tendon is there because the blunter has gone the main main strut to stop the dirty, the, the hyper extension of the TB joint has gone TB joint will go in hyper extension and the flexor tendon will still be embowering. And that's why you will see hammer toes or even close toes. So again, problem is the synovium body arthralgia, ar body arthritis, inflammatory arthros, which is erosive arthros with the time it starts to cause um, joint arthritis and at the same time, soft tissue uh destruction. And as you understand, definitely that trauma is a very destructive uh inflammatory condition, especially for soft tissue. The ear, soft tissue to get damaged is the blader blades. And once the blan blade is done, the MTB joints in the rest of toes, dorsiflex and dislocate dorsally. And this is the br that's why you feel the, the metatarsal head are prominent and there is some call and blunt and tendons underneath it because the MTB joint lost the main start against or main resistance against hyper flection. Hyper, I'm sorry, extension, the MTB will go in an extension because blunt a bit has been damaged. And this is the time when the, the flexor tendon will cause a hammer and flow too in the hind foot. You can see a vuls, you will see a valgus angle because uh I'm sorry, a valgus ankle because basically uh the spring ligament, the blat the fascia has gone because the spring ligament and plantar fascia has gone and again and again and again, rheumatoid foot is a soft tissue problem. Before bony problem, the foot will go into, uh, as you see, a severe vuls heel, a widespread osteoarthritis. I'm sorry, it's not osteo, it's a widespread arthritis. Um, and with severe abduction of the forefoot and valgus of the heel, that definitely will be through avicular uh uncoverage up to the avicular subluxation. And there is no question that this patient will have a subfibular impingement. So, again, in the hind foot, the main problem is a problem of soft tissue, your sprain ligament, your blan fascia is very weak and this is the time the hill will go into vuls and the arch will be flat and definitely this will be going aggressively added with uh the arthritis in the joint in bacterial navicular subluxation, prominence of the talar head and loading on the talar head and definitely subfibrillar impingement. Uh again, the soft tissue. So, tivis of tip post and you will have a collapse of media arch because tip posturing or spring ligament rupture or navicular subluxation. You will definitely have a tarsal tunnel syndrome which is compression of the tibial nerve underneath the flexor retinaculum and Mortons, gnoma is very common as any soft tissue problem and rem bursitis you can spot here how, how big and how aggressive are the bursitis. Examination of the rheumatoid foot as examination of the rheumatoid hand is examination of the whole patient, rheumatoid is a systematic disease. It's not a local disease even if it's express itself on the foot or the hand, you have to examine patient head to toe, you definitely have to assist the hip, assist the knee, assist any proximal deformity because your plan of management will depend on what deformities do you have. Uh starting with proximal deformities before distal deformities, you have to assess the skin. You have to assess the tendons. You have to assess the vascular condition. You have to assess the neurological condition and you have to have your investigation including um x-ray MRI scan and CT management. No question. MDTMDT. MDT and MDT start with a rheumatologist. You cannot touch a rheumatoid patient without very good medical care and very good medical control of his uh rheumatology, uh rheumatoid uh and thankfully to uh the the new uh disease, modifying drugs and the biological treatment which and by a lot of rheumatoid patient medically healed without need for any surgery. So, rheumatoid patient is a medical patient until proven otherwise, you never touch the rheumatoid patient with knife unless you have exhausted all the medical measures of controlling the rheumatoid. So, rheumatologist, your MDT will be a rheumatologist will be a physiotherapist, will be orthotic and non operative as any foot and ankle condition, foot wear modification, non non steroidal steroids, disease, modifying uh agents and uh biological treatment. And definitely some targeting the steroid injection um and some accommodative orthotics if no option and the patient is medically controlled, but still in a lot of pain because of the abnormal foot, shave and abnormal foot position. This is the time you will do the surgery and your surgery here. You need to understand there is no soft tissue to depend on and your surgery aiming to have a pain free Blute grade, show foot, not a normal foot. Yeah, the rheumatological foot will never be normal, but you need to have a pain free plan grade and show over foot. So for the first MTB definitely, because there is no dependence in the soft tissue, there is no space for any uh realignment surgery or scarp osteotomies or whatever. The the the the room here is only for first MTB fusion if you want to straighten the laser to. So you have either either to do a virus to do a shortening osteotomy of the, of the MTB uh of the ME A or do A B procedure which is an excision APLS or of the lesser MTB joints in the hind foot. The gold standard is to fuse it. So anchor Arthrodesis, um it's now it's evolving evidence to support at to total ankle replacement. And to be honest in our hands, total ankle replacement is doing a great job of rheumatoid and it, it can easily overcome the ade and now the total ankle replacement is the treatment of choice in um in uh rheumatoid foot. And definitely we cannot ignore the ta trial, which is a ok. Uh multi synthetic pragmatic trial comparing ankle arthrodesis versus ankle replacement and has involved with the rheumatoid patient. Uh You need to go and read the ta trial and we'll give you an insight that the ankle replacement is a good and a valid option. Um uh to ankle arthrodesis. Uh the third and the most important part of this lecture is the diabetic foot. Uh and you need to understand that our problem uh of the diabetic foot is uh uh is a neuropathic foot. Definitely, this is we, we look in the diabetic foot to what what concerns us. So if the patient have an uncontrolled hyperglycemia, so you he will have a neuropathic foot and this neuropathy in the foot would end by uh two series to explain distraction in the foot. So the first to understand the mushy theology in the diabetic foot, you need to understand that the first neurological abnormality will be loss of vibration and position and with loss of vibration position, there is no more protection and there is no more protection. The result will be um abnormal loading and abnormal patient areas. At the same time, you have an autonomic dysfunction. And because of this autonomic dysfunction, your the skin will be dry, would be cracking and easily ulcerating. There will be another uh a motor dysfunction and with the motor dysfunction, the muscle are imbalanced between extrinsic and intrinsic. And this is in by a claw and hammer deformities which may add to the pressure points. So the first and the main problem for us in a diabetic foot is the neuropathy and the neuropathy is sensory neuropathy, autonomic neuropathy and a motor neuropathy, sensory neuropathy. And by loss of protective sensation, starting with vibration and position, then uh loss of uh protective sensation to tactile um uh sensation and vein. And this end by uh pressure areas in in eight ulcers and uh um and foot foot injury, foot problems, autonomic dysfunction which end by dry skin, easily cracks and ulcerates, motor dysfunction, which end by muscle imbalance. And with the muscle imbalance, you will definitely have some deformities of the foot and toes. On the other hand, after other than the neurology is the vascular site, and we definitely agree that the diabetic patient has a vasculopathy and uh um um uh atherosclerosis. And with the vasculopathy, the the healing will be very poor and the soft tissue will be in a poor condition. And this is a very good media for infection. At the same time, systematically, the diabetic patient has a low immunity, high risk of infection and always his infection is poly microbial or makes it if the patient has diabetic foot ulcer, this ulcer will be uh hyperkeratotic will be bin bunched out base will mostly be bless because the patient is neuro and will be almost will be bleeding because there is no normal uh uh there is no normal contraction or I'm sorry. Uh vaso restriction in his visits. And this, you can uh are both in a separate slide because you need to spot easily that the patient has a foot diabetic foot ulcer. This is very, very important. And as you can see, and we, as we understand, it's a pressure point under the first it to the head. And you can see the hyperkeratotic is being is ped out. As you can see the uh this is this, this, this bit, this alpha bed is nearly ok. But it's commonly to come to you with infection and bleeding. So if you ha if you want to investigate a diabetic food patient, again, you need to look at the systematic problem. So you need to see to have um uh heb one C and to be sure that this is not beyond seven. If heb one c above seven, this means uncontrolled and there is no option to treat this patient until you get uh your blood sugar controlled. Uh Definitely this patient will be having a hypoalbuminemia and hypoproteinemia and this is affecting the wound healing and you, you don't want to operate on a patient with a poor healing, a poor wound healing power. So you need to be ensuring that your albumin is above 30 g. Um total lymph lymphocytic count with TLC will be definitely high because the patient will have some sort of infection, even if not, if a low grade infection that important. And the gold standard. Uh to assess the wound healing is to have a look in the transcutaneous oxygen pressure, which gives you an idea about the healing potential of this patient. And do you need this trans um uh cutaneous oxygen pressure to be above 30 milli uh millimeters mercury to be sure that your wounds will be having a a good healing potential. Uh And brachial uh uh uh index is the pressure index is very, very important because one of the aims designed to show to you that this patient, it has a vasculopathy and has uh um a poor blood supply to the to the lower limb. If your um ankle, brachial, uh pressure index is below um uh 0.45. This means the, the vascularity to the lower limb is weak or, or, or or insufficient and with vascular insufficiency, you don't wait for an ulcer to heal. So you have to have a vascular surgeon in your team X ray to show Osteomyelitis and uh uh and Charcot dis the um uh arthropathy or distraction. And definitely x-ray isn't the best uh um investigation to show osteomyelitis. Um The leukocytic scan is very, very uh sensitive to infection. It can give, basically give you a boost of a hotspot if the patient have an osteolysis infection and will be negative if just a neuropathic joint or um uh Charcot joint. MRI scan is very important but has its own limitation because you will see a bone edema and you cannot differentiate is this edema because of Charcot destruction or because of infection. Definitely deep tiss, deep, deep tissue biopsy will give you an idea about a specific bacterial infection and a specific sensitivity antibiotic. And this will give you a more better option to treat this infection. Diabetic foot is in a speciality. Uh Certainly speciality problem. It is a diabetic foot. So it is uh an MDT nice guidelines in 2019, is stated that an MDT approach should have a diabetologist to control the blood sugar, a podiatrist to look after the foot, diabetic specialist nurse to to uh action. The podiatrists advice orthotist, vascular surgeon, microbiologist, radiologist, cluster technician and TVN, which is tissue viability nurse and different orthopedics and plastics. In some, in some big centers. Plastics is part of the team and in a smaller center, plastics will be available for uh advice and management. So we have this in my diabetic foot team. So diabe my diabetic foot team has a diabetologist, has a podiatrist, has a diabetic species, nurse, have um cluster technician, have a vascular surgeon, have microbiologist, has a radiologist and we TVN and we definitely have an access to plastics. And thankfully, our team has um been awarded a national award from the King because we get the rate of ation below 70% in the area, which is a major, major achievement. And I can promise you this is one of the best service you can offer, offer your patient. We have a dedicated ward for diabetic foot. We have a dedicated uh ward drawn every week. We have a dedicated MDT clinic every week and the service is marvelous. Um When you see a diabetic foot, you need to examine the patient for risk factors. And we agreed from the previous slide that the risk factor will be neuropathy, vasculopathy or limb ischemia, ulceration, callus infection, deformity, gangrene, and charco arthropathy. From these risk factors, you will do what's called risk stratification and know how well your patient uh is spot on these degrees. Is it the low risk patient is a risk patient or a severe risk or a high risk patient? Low risk patient? Basically, he doesn't have any of these risk factors, maybe minimal or early Charcot and uh minimal color. And this patient, all what's need is annual foot assessment. You ask the patient to keep an eye on his foot. You look on uh after the patient once a once a year just to ensure that everything is going in the right way. Moderate risk. This is the patient who starts to have early neuropathy and mild deformity. Then the patient have intake sensation, just neuropathic but not, not badly neuropathic or in in. And the deformity hasn't changed the shape of the foot and it is not causing a pressure point. And in this case, you have to get this patient under the foot protection service and to see uh within six weeks and to do a 3 to 6 months, uh regular assessment if your patient is high risk. And this is when the patient have a previous ulceration, previous amputation uh have a renal replacement, have a critical limb ischemia, have a neuropathy, have a combination of any of this and this patient need to be under the full protection service within 2 to 4 weeks very urgently. And this patient has to be seen in the clinic 4 to 6 weeks, every 4 to 6 weeks. The principles if you're treating a diabetic foot, definitely again, you're treating the cause. Firstly, you have to strictly control the diabetes and this is the role of the diab, you have to have a very good patient education because it is a a multidisciplinary approach including the patient in the center of it. It's a centered patient centered approach for patient centered treatment. You have to optimize your foot. Offloading is a magic word. So your foot has to be offloaded. You don't accept or allow any pressure points in the foot. Infection has to be treated either medically if it's still under control or surgically. If uh the medical or antibiotics fail to control it. Antibiotic has to be under microbiologist advice and to be as much as specific as possible and sensitive as possible. Limb ischemia is very important. And if you have a limb ischemia, either you get a vascular surgeon or an intervention radiologist on board and they have to do um bypass or to do um angioplasty or whatever to regain, to get the, the, the limb vascularity back to normal wound debridement and dressing is definitely, uh if you have a wound debridement treating the outside would be an aggressive department. And we'll go to this in details in a minute. And definitely if you're doing something bony, so your bony either will be a very rigid internal fixation or an arthrodesis. The goal of treatment of the diabetic foot is number one. I'm speaking about the surgical goal, the surgical goal is to reduce the deformity. So avoid any bony prominence or uh uh pressure point, have your foot chewable and Blute great provide some stability. So you don't have any instability in the high foot of the an kit and definitely prevent ulceration by proper offloading and protective base and insults. If you go to debride the infection, your debridement is very specific. It shouldn't be done by a general orthopedic surgeon, it should be done by a diabetic foot surgeon. And if you don't have a diabetic foot surgeon in your unit, it's more better to be done. It's much better to be done by the plastics because they normally do an aggressive debridement over the orthopedics, general orthopedics. So if I will debride, I will be very aggressive, I will not leave any doubt for tissue. We all understand the zones of the tissue to even zone one which is still don't show clearly changes. I will be debriding this. I must end by a very nice clean pink bloody points. Other than this, I will not trust any tissue and I will remove everything, the more you remove, the more you save the patient, you have to keep your wound open because it has to express itself if there is any infection or anything and you can use a negative suction. Racial definitely the negative suction racial induce granulation, minimize this soft tissue, deep space and get any debris or infection away antibiotic. So you have a nice guidelines for diabetic foot. In 2019, you can start with uh uh empiric antibiotic, but you have to go for a specific antibiotic based on a deep tissue sample. And microbiologist advice, wound care is definitely offloading ulcers and avoid barrier to infection and uh absorb exudate to do an offloading, which is very, very important. So you have uh two options. The option is total contact cast or the rocker bottom offloading shoes. Both options are in front of you in the pictures. So the total contact basically is just accommodative to offload the foot. It we keep it there for good 4 to 6 weeks. Um during well, the mission is during in the acute stage, but we have a look on it weekly. So it have to be changed weekly because this foot is very dynamic. Swelling will be reduced. The foot will be losing the side that, uh, the, the, the cast and the cast is not doing the job, the cast to be doing, the job has to be covering the whole foot doesn't allow any pressure point and, uh distributing the pressure simultaneously. And at the same, uh degree on all portion of the foot, it's definitely to be non, non removable because you have, you will have a big problem if you're dealing with diabetic feet uh about patients. Well, the surgical brain spans, if I'm taking a diabetic foot. So to start with any diabetic foot, you have to raise the, the, the, the A 10, the achilles is definitely tight and you don't want this patient to be overloading the fore foot and causing pressure points. There, any pressure point has to be removed. You have to shave any body prominence. You have to keep this foot absolutely Blute great. No pressure points you have, if you be doing it, uh uh uh a pony procedure, you have to be very aggressive in fixation. So if you normally um treat a Weber b ankle fraction in a cast for a diabetic, you have to fix it. If you're fixing a ab ankle fraction, uh with a blade with a bit and screw media laterally and the screws immediately, you have to add uh synthes screws uh for the diabetic. So, diabetic should have double the amount of metal uh um as a normal patient. So you have to be very, very aggressive. If you're going to reconstruct, you have the options of plates or beans in the midfoot and you have the option of hind foot nail if you're doing hind foot reconstruction, and uh if you fail in all this and uh you're unlucky and the patient is uh is uh is lacking luck. So ation will be the answer. So to finish with the Charcot joint or the neuropathic arthros. So to understand Charcot, Charcot is not diabetic. It's not with diabetes. Only Charcot is with any neuropathic condition. So any neuropathic condition can end by a noninfectious distractive process which we call Charcot which end by deformed joint or even dislocated. Sco can happen with any cause of neuropathy. On top of them is the diabetic because it's the most common cause. Sorry. Ok. The whole neural axis should be examined. The patient may have a stroke, may have a spinal cord injury, may have uh he chronic alcoholic has meningo C has Syringomyelia, whatever Syringomyelia is a commonest cause of charco arthros in the shoulder or upper limb. The basi behind Charcot is uh two theories, neurovascular theory and a neurotrauma theory. So, the neurovascular theory, basically because of the nerve damage, the patient has increased local vascularity, increased local vascularity and by hyperemia, bone hyperemia and bone weaknesses. And this is stimulate the osteoclast activity and this makes the bone weaker so easily to deform the neuro traumatic theory. In simple terms, the micro, the patient because has the patient has lost, the protective mechanism is easy to have a minor trauma to the foot and minor trauma or minor fracture in by activation of BB proinflammatory cytokines. And this cause more destruction to the tissue. And because the patient has abnormal remodeling, the, the, the the rather than the, the bone remodel in a normal situation, it in by a de deformans and degenerated joint uh as you can see. So we have grades of uh of Charcot according to um our stage of Charcot, according to the x-ray. So basically from a mild deformity, just hyperemia and osteopenia is the first stage. Then after that, you start to lose the bone archi architecture, you see the X ray and you can spot there's something wrong going on, you cannot spot clearly. What is the problem stage after that is the start the joint to sublux and dislocate. And this is an end by a completely sclerotic deformed joint. Differential diagnosis to this is definitely infection uh gout and cigarettes. So if, if you have a Charcot joint, the foot is active, the foot is hot, swollen, tender, deform it, how to differentiate it between uh being a septic joint or osteomyelitis and a Charcot. So clinically very simply if you elevate the limb, so you're decreasing the vascularity. So, if we depend on the neurovascular uh theory, so the the increased vascularity will be less by the, by independency of the limb. And this is should normally improve the edema in the Charcot. But if the patient has an infection and because of the infection and inflammatory uh mediators, uh there is a local vaso dilatation, whatever you elevate the limb, the edema will not reduce. So to differentiate clinically between a Charcot and an active infection, elevate the level for 5 to 10 minutes. And normally with a Charcot, you will find some improvement in the edema. But in the uh infection, there will be no no improvement. Uh If you go to the lab, definitely the markers will be high in both of them. But the in the markers in uh infection will be shocking. So um the very high numbers but in and the Charcot will not be that MRI scan as we agreed, this is uh if it show a clear collection of us, this is clearly sepsis, but it has a low sensitivity to differentiate between um Charcot and uh sepsis. Because both of them will be having a blood signal body scan, especially the leukocytic scan or the IBC level. The scan is very, very specific to identify infection and by hot spots or positive. And this is a very good one to, to differentiate between Charcot and septic. Definitely, bone biopsy will show us if the ba if there is a bacteria and infection or not, don't spend a lot of time on the classification of Charcot. You need to understand that. Uh uh Brodowski has classified it according to the, to the, uh, um to where the Charcot is the communist are or Taiwan to have a midfoot. Charcot, then type two to have a tr joint which is 10 navicular cuboid and subtalar. The type three is inside the ankle and either it is getting the ankle only or ankle and the pros and number four is combination of this and number five or, or, or stage five, if you go to the forefoot, uh Brodowski is just as I told you, it's just a descriptive classification and um it's, yeah, without Brodowski, you still understand and you still can spot what is the deformity is and what you need to correct. So how you assist a Charcot joint patient will come to you. Um, diabetic neuropathic uh may have a history of mild minimal trauma and this is not uncommon. It's commonly to come to say to you that I have minimal injury, my ankle sprain something like that. Then since that I start to see because the patient is neuropathic, there is not a lot about the pain, but the history will be more about the deformity and changing shape of the foot. And by changing the foot shape, the patient will not be able to fit the normal shoes in. You can have some difficulty walking. When you examine this patient, you can easily spot the hot foot, the foot is swollen, tender. Uh um uh red and there is a deformity going on. Patient is standing, you can see the foot uh in abnormal or deformed position. One specific clinical test is to test the temperature gradient at different points of the foot. And if you see more than two degrees difference between the suspected Charcot limb and the normal limb, there is definitely an active Charcot limb stability is a very important point. You need to spot if there is any instability in the midfoot or the hind foot because this is will dictate your treatment later on if you plan to manage the Charcot. So your your management, according to the stage of the Charcot, if the Charcot is very early, all what you need is to stop inflammation and maintain the foot in normal shape, doesn't allow the foot to deform. You can do this basically by Lea Bain nonsteroidal. Um some, there is some, some evidence about bisphonate, but the most important is either Twitter contact cast or a rocker bottom shoes to maintain the shape of the foot. Uh I'm sorry, um Total contact c total contact booth to maintain the shape of the foot and doesn't allow the foot to deform and go from stage uh one or 2 to 3 or four. So main treatment is immobilization in the acute stage uh to avoid ulceration and to avoid allowing the foot to deform. This is the shape of the total contact uh boot and definitely to total contact as we have seen before, if uh as we agreed, as I told you, the evidence is start to support because as I told you that the bos start from the osteoclast abnormal activity. So some advocate um uh viscous related infusion over 12 months and support that this is improved pain and bone uh turnover. But this is not a nice uh advice or a nice guidelines if you uh um done this and you pass from stage two, up to stage three and four. So the foot is already deformed. So the option to have is to surgically correct it to Alan grade ch or foot with no prominence. So, excise, any body prominence or exos if the foot starts to be deformed, you need to correct the deformity. You can shorten the foot, you can remove any deformed joints and you can start to answer this in a functional position. This foot will not be normal again, but we can make it bluntly chewable without any pressure points. And this is the main important point you need to understand and indicate your patient that you're dealing with abnormal soft tissue quality, abnormal bone quality, high risk of infection, generally unwell patient. So uh quality of the bone will dictate um fixation. A very, very common to have fixation failure, very, very common to have reconstruction failure. Uh very, very common to have infection or um infected Embron. Very, very common to need um a second stage or even a third stage or a revision surgery. And if you all these fail amputation is an option on the table. You cannot ignore that if you can reduce the amputation rate as, as I told you by a good degree. So we we reach 70 degree reduction in amputation rate. You will be granted an um a national award and this will be a great achievement. You will be very proud of yourself. Charcot and diabetic food is um I know it's not the, the, the, the most exciting or exciting um uh uh um um specialty. But to be honest, when you see a patient, a safe limb or a safe patient, you'll be very, very happy and proud of yourself. Um So, and it is, it's one of the obscure areas of practice in the, in the UK and all over the world. Uh uh Diabetic foot management is not a surgeon management. It is a MDT management. If you don't have a proper MDT, even if you are the best surgeon results will not be the greatest. But if you have a proper team, even your surgical skill is not the greatest. You will have a very good results and you will achieve what you aim for. Thank you so much. So good. Yeah, on time. Thank you, Mr Hashan. You guys questions. Um Yeah, use it as much as you can try to get all the questions and I'll be more than happy to answer it, any questions guys? So it seems no questions. So basically, yeah, I've, I've applied already for um um er accreditation for the course. Um I should be receiving the, the decision by the early uh January or the early New Year. Um, keep feedbacking. So you will receive um a feedback form from uh mid all fill the bit feed feedback form and you will receive your certificate. Uh Next um uh month certificates will be uh Royal College of Surgeon actually did it. Uh Hopefully, uh I hope uh we going, I'm, I'm trying to concise it to make it an hour, hour, 15 maximum. Just uh yeah, to be just to, to get everything on board and understand everything. Uh and um we'll keep it like that. Uh II make it in 10 lectures. So this is the third one. So we still have seven. We'll be, we'll be doing it every Friday at the same time as we agreed. Um will be an hour, not more than this just to give you a chance to understand and digest every information. Uh again, my uh mobile number and my email. If you got any question to ask the video record or this will be uh kept on the will be kept on the uh mid all and would be on uh the youtube channels. I announced it at the early, early in the literature. Ahmed is asking management Weber B acute fracture and diabetic should be aggressively fixed or simply as high for me. So, ah, Weber B uh so basically is, is, is, um, uh an aggressive fixation. If you agree, uh, on a conservative treatment for, uh, Wilbur, be in a normal patient, you shouldn't be agreeing on that on the diabetic. Uh, your fixation should be very aggressive. You should be getting, uh, as much, much fixation, as much metal as you can to maintain everything stable. Remember, this patient have a poor quality bone, bone quality, soft tissue, high foot nail as a primary treatment. Uh has a debate. But yeah, but I don't think it was Weber B. So the debate was, was more um was uh more aggressive ba fraction like a, a triad or um uh by a tri but uh for a Weber B, you need to fix and fixation will need to be very strong. Um And even if the, even in, in, in the bi and Triad is still, there is a debate about uh primary fusion versus very good fixation and uh later fusion if failed, if a fix failed. Uh But yeah, high foot is an option. Think about any question guys. And uh um I hope um there is no question because you understand the lecture very good. This will be a great success for myself. Um uh foot and ankle. Um Topics are not the easiest uh especially if you are not practicing or you don't have a like a proper foot and ankle uh placement, but I promise you it will be an easy one by the end of this course, diabetic foot. Um II II, understand not everyone likes it, but I do like it because basically uh you really help the patient. So you really see an A AAA patient happy. You really see a patient saved either uh saved life or save them. So all of these guys um any question, my mobile number and my um uh email in the chat. Uh Waiting for any question. If you, if you need any question, have to discuss any clinical case, if you have any clinical case. Uh I do a proper diabetic food service. So if you're around the area, you can refer us um diabetic food to wick bar hospital. But Sam is asking is fixation means more than two in these multi screws and this defibrillator locking blade, uh this defibrillator locking blade. Yes. Since both screws, if you will do, you need to use um uh a quadricortical. So four cores and you need to use at least 2 to 3. Uh There's a big, big discussion about the biomechanical analysis and uh the trans fibrillar tibia screws. And uh there's another big debate, but if I'll be fixing, I'll be good putting three screws, uh quadricortical through four corteses and fully it definitely as a position of the screws um to have a very, very proper position. This patient remember is neuropathic. You need uh him or her to uh weight, bear early and to be safe, to weight bear this patient early. You need to have a very, very rigid fixation and you need to be sure that your fixation is, is rigid enough. Any more questions, guys? Uh You're welcome everyone. And um yeah, we shall uh bring this meeting uh this lecture to an end. Um Any question more than happy to receive it and see you next Friday. Good luck and good evening. Thanks for. Thank you. Thank you. Thank you for the day.