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Orthopaedics and Trauma Elsevier, ISSN: 1877-1327, http://www.sciencedirect.com/science/journal/18771327 Volume 25, Issue 4, Pages 235-316 (August 2011) 1

Editorial Board, Page i

Editorial 2

Editorial – Goodbye to Bob Dickson, Page 235 David Limb

Mini-Symposium: The Foot and Ankle 3

(i) Understanding the gait cycle, as it relates to the foot, Pages 236-240 Nitin Shetty, Stephen Bendall

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(ii) The foot in systemic disease: management of the rheumatoid or diabetic patient, Pages 241-252 Roland Walker, David Redfern

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(iii) The osteoporotic ankle fracture, Pages 253-257 Iain McFadyen, Adeel Aqil

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(iv) Hindfoot arthritis, Pages 258-268 Paul Hodgson, Kartik Hariharan

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(v) Chronic ankle instability, Pages 269-278 Hiro Tanaka, Lyndon Mason

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(vi) Anatomy and biomechanics of the foot and ankle, Pages 279-286 Edward J.C. Dawe, James Davis

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(vii) Clinical examination of the foot and ankle, Pages 287-292 Howard Davies, Chris Blundell

Quiz 10

Paediatric radiology quiz, Pages 293-299 Ajay Sahu, Sharmila Chhatani, Judith Foster

Spine 11

Bone tumours affecting the spine in children and adolescents, Pages 300-311 George I. Mataliotakis, Athanasios I. Tsirikos

CME Section 12

CME questions based on the Mini-Symposium on “Foot and Ankle”, Pages 312-313

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Answers to CME questions based on the Mini-Symposium on “Radiology”, Page 314

Book Reviews 14

Operative techniques in Orthopaedic Surgery 4th V, Page 315 David Limb

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The Masters experience – arthroscopic surgical techniques, rotator cuff repair, Page 315 Neil Patel

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Operative techniques in Sports Medicine Surgery, Pages 315-316 Neil Patel

Orthopaedics and Trauma Orthopaedics and Trauma presents a unique collection of International review articles summarizing the current state of ­knowledge in orthopaedics. Each issue begins with a focus on a specific area of the orthopaedic knowledge syllabus, covering ­several related topics in a mini-symposium; other articles complement this to ensure that the breadth of orthopaedic learning is supplemented in a 4 year cycle. To facilitate those requiring evidence of participation in Continuing Professional Development there is a questionnaire linked to the mini-symposium that can be marked and certified in the Editorial office.

Editor-in-Chief D Limb BSc FRCS Ed (Orth) Leeds General Infirmary, Leeds, UK

Editorial Committee M A Farquharson-Roberts (Gosport, UK), I Leslie (Bristol, UK) M Macnicol (Edinburgh, UK), I McDermott (London, UK), J Rankine (Leeds, UK)

Editorial Advisory Board D C Davidson (Australia) J Harris (Australia) G R Velloso (Brazil) P N Soucacos (Greece) A K Mukherjee (India) A Kusakabe (Japan) M-S Moon (Korea) R Castelein (The Netherlands) R K Marti (The Netherlands) G Hooper (New Zealand)

A Thurston (New Zealand) E G Pasion (Philippines) L de Almeida (Portugal) G P Songcharoen (Thailand) R W Bucholz (USA) R W Gaines (USA) S L Weinstein (USA) M Bumbasirevic (former Yugoslavia)

EDITORIAL

Editorial e Goodbye to Bob Dickson David Limb

As we move through 2011 we have done so with progressively less input from Professor Robert Dickson, Editor Emeritus of this journal, who attended his last Editorial Board meeting at the Camden Lock offices of Elsevier in May 2011. By the time this issue is in print he will have retired gracefully to his golf and will no longer be called upon for his expert proof-reading and editorial skills. It is a good time to reflect on his contribution to this publication, from his original concept to the professional product that lies behind this editorial. Those who have followed this journal for more than a couple of years will be aware that the original title launched, with Bob Dickson at the helm, was called Current Orthopaedics. The Editorial written by the man himself in Volume 1, Issue 1 in September 1996 was entitled ‘Why this new journal’ and describes the underpinning educational values that still hold today. Indeed, crystal balls may have been involved, as the educational review articles that were stripped down of personal views in favour of balanced opinion, were chosen to cover an orthopaedic and trauma syllabus over a four year cycle. This was before the Curriculum for Trauma and Orthopaedic Surgery in the UK had been written and before the four year higher surgical training cycle leading to professional examination eligibility had been established. However, fast-forward to the first Intercollegiate Specialty Board examination in November 1990 and you will find a familiar name chairing the Board e Bob Dickson himself. They say that assessment drives learning. The chair of the board responsible for assessing trainees in the UK and Ireland was headed up by the man who therefore knew exactly what the candidates needed, and he was able to cater for that need in Current Orthopaedics. He did not go it alone, however. The band of five who conceived and established the journal included Professor John Kenwright, Nuffield Professor of Orthopaedics from Oxford (where Bob had been Senior Lecturer before his own appointment to the Chair in Leeds in 1981), Professor ‘Fred’ Heatley (who subsequently chaired the Specialty Advisory Committee in Orthopaedic Surgery) and Ian Leslie, who became President of the British Orthopaedic Association and is the only remaining original member still on the board. Bob also saw the importance of the cross-fertilization of ideas with

ORTHOPAEDICS AND TRAUMA 25:4

The original board of Current Orthopaedics after Bob Dickson’s retirement lunch e from L to R Prof John Kenwright, Mr Ian Leslie, Bob Dickson, Dr Paul Butt and Prof ‘Fred’ Heatley.

imaging colleagues and therefore the fifth board (see photo) member was Dr Paul Butt, his radiology colleague from Leeds who was able to ensure that the best quality advice on imaging appeared in relevant articles. The original board were reunited when Bob stepped down as Editor of, by then, the renamed ‘Orthopaedics and Trauma’ (See photo), which had changed title for purposes of family brand identity, bringing advantages in the quality of the printed product sent out to subscribers. Bob will now spend more time with his family and on the greens but has no plans to withdraw from orthopaedic education. He has already published eight textbooks and is currently working on a new edition of one, whilst another is in the pipeline. He has made it clear that he is still available in a consultative capacity for this journal and his influence will continue, long past the times of his hard-to-miss contributions to debate at scientific meetings! A

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(i) Understanding the gait cycle, as it relates to the foot

When one stands on tiptoe, the hindfoot inverts, the midfoot is plantar-flexed and the forefoot pronates slightly so there is an arch visible medially. Similarly, if one stands with ones foot flat on the ground and the leg externally rotated, one will see the medial arch rise and rotating the leg internally reverses this effect. This simple process of going up and down on tiptoes involves a number of concepts that need to be understood, which are key to understanding the gait cycle and its clinical applications. There are passive and active mechanisms at work in standing up and down on tiptoe. The active ones are easy to understand; arising from the action of muscles. The passive ones are perhaps more obscure and are a largely a function of four structures: 1 the subtalar joint, 2 the transverse tarsal joint, 3 the midtarsal joints, and 4 the plantar fascia.

Nitin Shetty Stephen Bendall

Abstract The gait cycle is outwardly something complex, which seems difficult to grasp. This really isn’t the case and with a few relatively simple facts to understand it can be easily understood. The purpose of this article is to try and break this complex process into a series of comprehensible steps. The gait cycle is defined and its major components are then described. The key is understanding how the foot can be both a flexible and then a rigid structure in different parts of the gait cycle. This is a function of the subtalar and especially the midtarsal joints. We also look at how the plantar fascia plays a part too. Finally we look at how the cycle may be altered in various clinical scenarios. Which we hope will be of general use but especially to trainees taking final professional examinations.

Subtalar joint motion The talus is a bone without any muscle attachments e rather like the scaphoid in the wrist. It lies on top of the calcaneus and is stabilized by ligaments and surrounded by tendons. Inversion and eversion occur at this joint and one way to consider how this may occur is by viewing the facets of this joint as being like an Archimedes screw or spiral (Figure 1a and b). This is a right-handed screw on the right side, and vice versa on the left.1 On the right hand side with clockwise rotation of the screw one sees hindfoot inversion distally and

Keywords gait cycle; midtarsal joints; plantar fascia

Introduction Gait and topics related to it are clearly important in understanding orthopaedic conditions in the lower limb and their treatment. It is therefore no surprise that this remains an important topic in final professional examinations, such as the UK FRCS(Tr&Orth) examination. The authors are a candidate currently sitting the FRCS(Tr&Orth) examination and a senior FRCS(Tr&Orth) examiner. They have teamed up to explain what they feel are the important aspects of this subject. We both hope that it will be of interest to candidates taking the FRCS(Tr&Orth) examination as well as consultants and other practitioners with an interest in the lower limb, especially foot and ankle conditions.

Anatomy and kinematics We are all familiar with the anatomy of the foot and lower limb, which in the most basic concept is a bony arch. It is quite clearly not a static arch as it can be either flexible or rigid and it can readily adapt to the surface of the ground underneath.

Nitin Shetty MRCS Orthopaedic SpR Brighton and Sussex University Hospitals, Department of Orthopaedics, The Princess Royal Hospital, Haywards Heath, West Sussex, UK. Conflict of interest: none. Stephen Bendall FRCSOrth Consultant Orthopaedic Surgeon Brighton and Sussex University Hospitals, Department of Orthopaedics, The Princess Royal Hospital, Haywards Heath, West Sussex, UK. Conflict of interest: none.

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Figure 1

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MINI-SYMPOSIUM: THE FOOT AND ANKLE

tibial external rotation proximally. This mechanism begins to explain how the arch changes shape but not how the foot changes from being compliant to rigid and load bearing. In understanding this we have to look to the midtarsal joints. Midtarsal joints The calcaneocuboid and talonavicular joints make up the transverse tarsal joint, which is also known sometimes as Chopart’s joint. Mann and Inman in 19642 looked at these joints and described parallel axes through the talus and calcaneus (Figure 2). These axes, called the talonavicular and calcaneocuboid axes, are in the frontal plane. When the foot is in eversion the axes are parallel, motion within the midtarsal joint can occur, and the midfoot is mobile. When the heel is inverted these axes are no longer parallel and motion at these joints is blocked. Inversion and eversion of the hindfoot occurs at the immediately proximal subtalar joint via muscle action and the shape of the subtalar joint facets. These mechanisms within the subtalar and midtarsal joints help us understand at a basic level how the foot manages to be both rigid and flexible during gait. It also begins to explain some clinical aspects, for instance why patients tolerate a pronated or flat foot better than one that is supinated or varus, as in the cavus foot.

Figure 3

cunieform joints move less.3 Thus, when standing on tiptoe the intrinsic structure of the tarso-metatarsal joint and the plantarflexion of the first ray give further stability to the foot. This is reversed when the foot is not loaded and is in neutral alignment. Plantar fascia The plantar fascia attaches to the calcaneum and extends forward as a band-like structure to attach to the plantar aspect of the proximal phalanges of the toes. This results in a structure resembling a bow (as in bow and arrow), where the bones are represented by the bow itself and the fascial band is the bowstring. This in some texts is called a truss, with the fascial band being a tether. One can immediately see that this bow-like structure forms an ideal shock absorber. However, the plantar fascia can function in another way and for this we can consider the model of the socalled Spanish windlass (Figure 4). As the metatarsophalangeal joints extend, the plantar fascia is tightened and the distance between the calcaneus and metatarsal heads shortens. This, via the mechanism described by Hicks,4 locks the midtarsal joints and also brings the heel into slight varus, which, via the subtalar joints, locks the transverse tarsal joint. The metatarsophalangeal joints are arranged in a cascade, with the second metatarsal usually being the longest and the fifth the shortest. The so-called ‘metatarsal break’ is the line joining

Tarso-metatarsal joints The tarso-metatarsal joints are also known as the Lisfranc joint. In cross-section these joints are shaped somewhat like a Roman arch (Figure 3), with the second metatarsal deeply recessed into the midfoot. This renders the second metatarsal rigid compared to the others. In 1953, Hicks demonstrated that when the first ray is either plantar-flexed or dorsiflexed, the other lesser metatarso-

Figure 2

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Figure 4

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MINI-SYMPOSIUM: THE FOOT AND ANKLE

the individual articulations. One can see as one moves higher on tiptoe that the plantar fascia will steadily tighten as one rolls from the medial to the lateral part of the foot. This is due to the orientation of the metatarsal break. Therefore, one can see clearly that surgery on the metatarsals or plantar fascia can potentially have a negative effect on foot function. In summary, these largely passive mechanisms control the shape and thereby the function of the foot and we have some explanation as to how the foot can be both rigid and flexible.

bears the weight, the intrinsic foot muscles remain active so as to stabilize the longitudinal arch. The main stabilizer at this point is in fact the plantar fascia. The Spanish windlass effect comes into play, with the toes dorsiflexing at the metatarsophalangeal joints and so tightening the plantar fascia. The subtalar joint will continue to invert during this interval too, reaching maximal inversion at toe-off. The inversion at this joint is again largely driven by the limb above continuing to externally rotate, but this is enhanced by the plantar fascia’s role as well as other factors such as the obliquity of the axis of the ankle joint and the orientation of the lesser metatarsophalangeal joints. The inversion holds the transverse tarsal joints in a stable position, keeping the foot rigid until toe-off. When a series of cycles is observed, as for example when observing a patient walk, there are various other displacements of the body as a whole. For instance, as one goes through a single gait cycle the trunk will rise at toe-off at the end of the third interval and lower at the point of heel strike at the beginning of the first interval. The pelvis, hip and knee as well as the foot modulate vertical displacement. Similarly, with gait there are not only vertical displacements but also rotatory movements too. The shoulders and pelvis rotate as well as the femur and tibiae. The tibiae rotate about their long axes: in the swing phase and early part of stance phase they rotate internally, and in the later part of stance they rotate externally (during the third interval of stance phase). Finally, when walking the body oscillates from side to side; this is thought to be to try and keep the centre of gravity over the weight bearing foot. This can be noticed by walking with a broad based stance and conversely reduced by walking with the feet close together. When running, there is no period in the gait cycle when both feet are on the ground at the same time. As the pace quickens the time the foot spends on the ground gets less both in time and as a percentage of the overall gait cycle.

The gait cycle By convention we think of a ‘single cycle’ as the motion between heel strike of one foot to the heel strike of the same foot on the subsequent step. Thus, during this one cycle the foot can either be off the ground (otherwise known as swing phase) or on the ground (the so-called stance phase). The stance phase makes up approximately 60% of the gait cycle, with swing phase occupying 40%. In the normal individual this cycle is a fluid motion, but again by convention we divide the stance part of the cycle into three phases; otherwise referred to as ‘intervals’ or ‘rockers’: 1 First interval From heel strike to foot flat 2 Second interval With foot flat e the body is passing over the foot 3 Third interval From the heel lifting off the ground to toe-off First interval As the heel makes contact with the ground the ankle rapidly flexes so the foot is flat. This ankle motion is controlled by the anterior muscles, which contract eccentrically. The posterior muscles are electrically quiet at this time. The foot is loaded and the heel goes into eversion, which is a passive process, and this in turn (via the subtalar joint and transverse tarsal joints) allows the foot to go flat. This phase is mostly centred around the absorption of the forces generated by the heel strike.

Clinical application of the gait cycle As we have mentioned, the gait cycle is from heel strike of one foot to heel strike of the same foot and happens in a little over one second. Clinical evaluation of gait requires a systematic approach and the following aspects need to be considered. 1 Presence of pain e localization of pain and identification of the phase of painful gait. 2 Look for the base i.e. how wide or narrow the stance is. 3 Look for changes in the stride e is it even or uneven and cadence i.e. asymmetry. 4 Observe the shoulder levels for either dipping or elevation. 5 Observe the trunk for lurch, or a fixed tilt. 6 Observe the pelvis for any obliquity or raise or drop. 7 Look at the attitude of the hip, knee and foot in the various phases of gait. Are any of these exhibiting a fixed position? 8 Observe the foot for altered heel strike and toe-off. This is quite difficult to do in the context of examinations but the first two points one can gather before the patient starts moving by asking where the pain is and observing how far the feet are spaced apart. Thereafter is a matter of observing the whole patient, from the shoulder to the foot.

Second interval During this time the body’s centre of gravity is passing over the foot. The ankle joint dorsiflexes and the heel rises. It is in this phase that the changes within the foot from a flexible to a rigid structure occur. The subtalar joint is at the centre of this change and there are several factors that come into play. Which of these might be the most important is not known but they include the external rotation of the tibia proximally, which is brought about by the contralateral swinging limb. This external rotation, as we have previously discussed, brings the subtalar joint into inversion, which in turn locks the transverse tarsal joints. As the forefoot is planted on the ground, the subtalar inversion is passed distally in the foot and serves to make the midtarsal joints more stable via the mechanism that Hicks described. Various muscles have shown to be active during this phase including the triceps surae, tibialis posterior, flexor hallucis longus, flexor digitorum longus and the intrinsic muscles within the foot. Third interval The ankle begins rapid plantarflexion, which is brought about by the posterior muscles, primarily the triceps surae. As the foot

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The painful hip The commonest abnormal gait pattern seen is from a painful hip, referred to as an antalgic gait. The main changes seen include a decreased time in stance phase, to offload the painful hip. One observes the following:  lurching of trunk to affected side in stance phase,  dipping of shoulder on the affected side,  elevation of the shoulder on the opposite side and  shifting of the pelvis onto affected side. The effect of these actions is to move the body’s centre of gravity closer to the affected hip, which reduces the stresses across the joint. In swing phase the hip is often held in flexion, abduction and external rotation. The heel strike is ‘soft’, again to prevent excess loading of the joint.

Gluteus maximus weakness: this leads to a backward lurch of the trunk, with the shoulders held backwards just after heel strike on the affected side. This keeps the centre of gravity posterior to the hip joint, locking the hip in extension and compensating for the hip extensor weakness. Quadriceps weakness: this leads to loss of extension of the knee at heel strike. This is compensated for by trunk flexion, creating an extension moment at the knee. Some patients use their hand to support the upper thigh and to extend it e.g. post-polio weakness (hand to knee gait). Ankle dorsiflexor weakness: this leads to a drop foot or high steppage gait. In mild or moderate weakness the heel strike to foot flat phase is quite rapid. In severe weakness the foot will fall into plantarflexion and heel strike is lost and instead the foot lands onto the toes. This causes relative lengthening and is compensated for by a high steppage gait on the affected side.

The painful knee Painful conditions of the knee usually lead to it being held in a flexed attitude during swing and stance phase and leads to compensatory avoidance of heel strike and toe walking. Flexion contractures of more than 30 are usually apparent with normal walking whereas contractures of less than 30 become pronounced with faster walking. In posterolateral instabilities one can see a varus thrust gait occurring in the stance phase. Similarly, in varus osteoarthritis of the knee one can see a valgus thrust, this is thought to arise form a concomitant weakness of the lateral structures including the iliotibial band. The so-called ‘quadriceps avoidance gait’ is seen in ACL injuries because the quadriceps provides an anterior force to the tibia that could lead to anterior subluxation of the tibia. This gait is characterized by avoidance of loading the limb by decreasing the stride length and avoiding knee flexion during the second interval of stance. Knee contractures can cause a short leg gait, with toe walking on the affected side and a ‘steppage gait’ or ‘hip hiking gait’ on the opposite side.

Ankle plantar flexor weakness (ruptured tendo-Achilles): heel lift-off is delayed and toe push-off is decreased, leading to shortening of the stride on the contralateral side to accommodate the delay of the forward movement of the ipsilateral hip. A flexion moment is created posterior to the knee that might lead to buckling of the knee due to altered ground reaction forces. Spastic gait: this can be seen in cerebral palsy, leading to a crossed limb or scissoring of the lower limbs due to overactivity of the hip adductors. The base is narrow or even crossed. The actual gait depends on the specific muscle group involvement in this condition. Foot and ankle pathology In general, in painful foot conditions the stride length is shortened and normal heel-to-toe motion is lost. With painful pathology affecting the ankle joint and hindfoot, heel strike is avoided, leading to a tiptoeing gait on the affected side. In conditions affecting the forefoot, plantarflexion and toe-off will be avoided.

Leg length discrepancy With shortening less than 1.25 cm, the stance phase of the gait is characterized by dipping of the shoulder and pelvic drop onto the affected side, with elevation of the shoulder on the opposite side. With shortening of more than 3.5 cm, tiptoeing on the affected side with full knee extension during stance phase is observed. To clear the contralateral leg that is comparatively longer, the patient usually compensates by circumduction, hip hitching or a hip stepping gait.

A very tight tendo-Achilles will result in loss of heel contact and heel-to-toe motion. There will be compensatory exaggerated hip and knee flexion in swing phase, to clear the foot off the ground. A tight tendo-Achilles might lead to hyperextension of the ipsilateral knee in stance phase due to an extension moment caused at the knee by the plantarflexion of the ankle. Generally, a flat foot is better tolerated than a cavus foot because with a cavus foot there is heel varus, leading to locking of the transverse tarsal joints, resulting in decreased flexibility of the foot.

Neurological problems and gait There is a wide array of neurological conditions that may affect gait, and the commonest are discussed below.

The cavus foot: this deformity has several aetiologies, the commonest being Hereditary Motor Sensory Neuropathy (HMSN) or Charcot Marie Tooth Disease. The latter is not to be confused with Charcot Disease, seen in neuropathic (including diabetic) feet. The deformity is usually very obvious and a key question to ask is whether or not the subtalar complex is mobile; the relevance being that if a deformity is fixed then most likely a corrective osteotomy or fusion will have to be considered, whereas if a deformity is mobile then conservative treatment or lesser soft tissue surgery along with joint preserving surgery may

Gluteus medius weakness (Trendelenburg) gait: in this gait there is a pelvic drop on the affected side, along with a lateral bend of the trunk over the affected hip and a dropping of the shoulder on the affected side. This effectively moves the centre of gravity nearer to the affected the hip and hence decreases the muscle force required to stabilize the pelvis. The affected leg can also be functionally longer and to compensate for this there might be an increase in hip flexion, knee flexion and ankle dorsiflexion (so-called high steppage gait) to aid toe clearance.

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Even if an ankle is fused in an ideal position, the fusion will still affect the gait cycle. Looking at the three stance intervals, heel strike to foot flat is clearly going to be affected. This can be helped in some patients by cutting a wedge from the heel to allow a smoother contact of the foot with the ground. The second interval is also affected as the body cannot easily pass over the flat foot. However, many patients exhibit an increase in sagittal plane mobility from the un-fused joints. Thus, the first two phases of stance may be slightly shortened and the third phase should largely be unaffected if there some valgus within the hindfoot and there is increased mobility from the other joints.

be possible. The key to this question is answered using the Coleman block test. This is performed by observing the heel from behind and noting its position. One then places a (wooden) block of about 2.5 cm thickness under the lateral part of the foot, leaving the first ray free. If the subtalar complex remains mobile then the hindfoot will adopt a neutral or even valgus position. The flat foot: the commonest condition to consider here, both in clinical practice and in professional examinations, is tibialis posterior tendonitis. In general, and as mentioned previously, the flat foot is more forgiving because the subtalar complex (and in particular the midtarsal joints) is maintained in an unlocked position. The heel strike will involve the lateral aspect of the calcaneum, the second interval will involve a significant collapse of the medial arch and the third interval will be near normal. This this related to the windlass mechanism of the plantar fascia. As the body moves forward the plantar fascia rolls around the extending metatarsophalangeal joints and swings the heel into a more varus or neutral position. One can sometimes see this clinically where a patient with tibialis posterior insufficiency cannot initiate a single leg heel raise but can maintain a single leg heel raise position from a double leg stance on tiptoe.

Other hindfoot fusions Triple fusion refers to fusion of the subtalar, calcaneocuboid and talonavicular joints. As we have seen, these joints function as a unit and fusion of one will inevitably affect the function of the others. In performing a solitary subtalar fusion, one must take care to fuse in around 5 of valgus. The reason is as before, to allow the midtarsal joints to be mobile; they will unlock doing the first and second intervals and lock out later in the third interval from the action of the plantar fascia. The same is largely true of coalitions, notably talo-calcaneal coalitions. In the case of triple fusion, again a position of slight valgus is preferred, although if excessive this will lead to degenerative change within the ankle joint above.

What position should the hindfoot be fused in? Discussion of the different elements of the gait cycle, as they apply to the foot, leads on logically to consideration of the ideal positions in which fusions in the foot/ankle should be performed if one is to maintain as good function as possible.

Conclusions

Ankle fusion A number of different planes need to be considered: first, the most important point to consider is the varus/valgus position. If the ankle is fused in too much varus, the subtalar joint will remain in inversion and so lock the transverse tarsal joint. The second interval of the stance phase of the gait cycle will be adversely affected, as the body will pass over the flat foot with difficulty. Rotation should also be considered. If, for instance, the ankle is fused in excessive internal rotation, then when the centre of gravity passes over the foot within the second interval of stance phase there will be increased stress on the subtalar joint and in the midtarsal area. If on the other hand the ankle is fused in too much external rotation, the patient will push-off during the third interval of stance phase with the medial border of the foot. This places extra stresses around the 1st MTPJ and over time this may lead to a hallux valgus type deformity. The third plane to consider is the degree of dorsiflexion or plantarflexion that the ankle is fused in. If the ankle is fused in too much plantarflexion, this makes the fused limb functionally longer and can lead to a backward knee thrust, an uneven gait and increased stresses within the midfoot joints. Conversely if the ankle is fused in too much dorsiflexion, this makes heel strike at the beginning of the first stance interval uncomfortable and will affect the other two phases too. Therefore, the best position in which to fuse the ankle is in neutral dorsi/plantarflexion, neutral rotation and approximately 5 of valgus, to ensure that there is mobility in the subtalar joint.

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The key messages are:  Gait involves a swing and stance phase.  Stance phase is made up of three intervals.  The key to understanding how the foot goes from being a complaint to a rigid structure lies within the structure of the subtalar and midtarsal joints.  The plantar fascia plays an important role. From here, most clinical situations encountered at the level of the FRCSOrth examination can be understood. One should remember that a varus or cavus foot is stiff whereas a flat or planus foot is pliable. A

REFERENCES 1 Manter JT. Movements of the subtalar and transverse tarsal joints. Anat Rec 1941; 80: 397e410. 2 Mann R, Inman VT. Phasic activity of intrinsic muscles of the foot. J Bone Joint Surg Am 1964; 46: 469e81. 3 Hicks J. The mechanics of the foot, the joints. J Anat 1953; 87(Pt 4): 345e57. 4 Hicks J. The mechanics of the foot II. The plantar aponeurosis and the arch. J Anat 1954; 88(Pt 1): 25e30. FURTHER READING Coughlin M. Surgery of the foot and ankle, 8th edn. Mosby, 2011. Nordin, Frankel. Basic biomechanics of the musculoskeletal system, 2nd edn. Lea and Febiger, 2011.

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(ii) The foot in systemic disease: management of the rheumatoid or diabetic patient

accurate and informative so that others understand the thought processes and decision-making involved. As with all clinical assessment, making good quality decisions begins with a thorough history and examination. An important consideration is the patient’s capacity for activity and reasonable physical aspirations; in other words, the extent to which they are limited by their foot/ankle problem or by other musculoskeletal or systemic pathology. One should ask about exercise tolerance, such as stair climbing, to get an indication of the patient’s cardiovascular fitness. It is important to document other manifestations of the disease, such as peripheral vascular disease in diabetes, and take a detailed history of a patient’s previous operations and interventions. A drug history is also vital, as patients may well be on medications such as antiplatelet therapy, steroids or immune modifying drugs, which may have to be stopped or modified peri-operatively. Finally, the physical examination must be thorough and take account of the patient’s vascular and neurological status and the condition of skin and soft tissues. Inevitably, such consultations will take longer than average but time invested at the start of the relationship results in better decision-making subsequently. Managed well, these patients can have highly satisfying outcomes and are likely to be very grateful. Conversely, poor decision-making can literally be disastrous for the patient, and difficult to salvage.

Roland Walker David Redfern

Abstract The foot is commonly affected in systemic diseases such as rheumatoid arthritis and diabetes mellitus. Treating patients who have foot pathology secondary to systemic diseases requires a multidisciplinary approach, following the principles that we outline in this article. There is very little high quality research in this field in the form of properly controlled clinical trials, and much of what we know owes a debt to the hard work and experience of key individuals and specialist centres.

Keywords acquired; arthritis; diabetes mellitus; foot; foot deformities; foot ulcer; rheumatoid

Rheumatoid arthritis Rheumatoid arthritis (RA) is a systemic polyarthropathy that affects small or larger joints in 1e2% of the population. It affects women more commonly than men and can occur at any age, but most commonly in the third to fifth decades. In our region in the South East of England, a ten-year prospective cohort study of 1154 patients newly diagnosed with RA showed that 27% went on to have orthopaedic surgery.1 In the same study, 12% had major joint replacement within an average of 4 years from diagnosis, which illustrates the aggressive nature of the disease. Diagnostic criteria developed by the American Rheumatism Association include morning stiffness, swelling, nodules, positive laboratory tests and radiographic findings. The aetiology is unclear but seems to be a T-cell mediated inflammatory response. Numerous intracellular messenger proteins are implicated in the inflammatory cascade, but in particular the cytokines interleukin-1 (IL-1) and tumour necrosis factor-a (TNF-a) are highly important in the disease process. TNF-a increases chondrocyte secretion of matrix metalloproteinases, which break down extracellular matrix. Mononuclear cells are the primary cell mediators of tissue destruction in RA.

Introduction The foot is commonly affected in systemic diseases such as rheumatoid arthritis (RA) and diabetes mellitus and is a common region for presentation of such conditions. This article aims to provide the reader with a systematic approach to the assessment of the rheumatoid or diabetic foot and an understanding of the principles of appropriate surgical treatment.

General principles Patients with severe systemic disease are a unique subgroup of the patient population and require a multidisciplinary approach to their management. A good rapport with the patient is always important, but never more so than in cases where the patient suffers from significant co-morbidities. Good communication is also vital with other clinicians involved in the patient’s care. This includes involving allied professionals such as physiotherapists, podiatrists, occupational therapists and orthotists early on in the patient’s treatment. It is vital that documentation and communication between the various teams looking after the patient is

History Poorly localized forefoot pain is a common early symptom of RA. In these early stages there may be synovitis and swelling that limit walking and footwear choices. The diagnosis at this point can be difficult to make and the surgeon should have a low threshold for further investigation. As the disease progresses, other larger joints may become involved and the patient may report deformities of the forefoot such as hallux valgus, hammer or claw toes and dislocation of the metatarsophalangeal joints (MTPJs). Midfoot and hindfoot deformity often occur later in the

Roland Walker MB ChB BSc MRCS (Eng) SPR South East Thames Orthopaedic Rotation, Department of Trauma and Orthopaedics, Royal Sussex County Hospital, Brighton and Sussex University Hospitals Trust, Brighton, UK. David Redfern MBBS FRCS FRCS (Tr & Orth) Consultant Orthopaedic Surgeon, Department of Trauma and Orthopaedics, Royal Sussex County Hospital, Brighton and Sussex University Hospitals Trust, Brighton, UK.

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disease and can become very severe. Overall, the foot is involved at some stage in 90% of patients with RA. Most patients prioritize pain first followed by deformity and difficulty fitting footwear. It is very important to establish the patient’s main concern. It is also vital to ask about and examine the rest of the limb, as it is generally advisable to address proximal pain and deformity in the hip or knee prior to any foot and ankle deformity.

axial instability. This diagnosis must not be missed, and when present it requires urgent investigation and onward referral. Investigations If the diagnosis of RA has not already been made then plain radiographs of the hands and feet may show characteristic periarticular osteoporosis and erosions. Plain X-rays are also useful for monitoring disease progression over time. In the very early stages we have found MRI to be very useful for detecting synovitis and effusions. Laboratory tests should include full blood count, erythrocyte sedimentation rate and C-reactive protein. Rheumatoid factor is positive in about 80% of patients with RA. Anti-nuclear antibody may be positive in juvenile RA. The differential diagnosis is often with other sero-negative arthropathies, such as systemic lupus erythematosus, Reiter’s syndrome and psoriatic arthritis. The patient should be referred to a rheumatologist if newly diagnosed with an inflammatory arthropathy, where more detailed immune and genetic profiling can be performed as necessary.

Examination As with most orthopaedic examinations, simple detailed observation can reveal a wealth of information. Overall limb alignment must be assessed with the patient standing and the knee exposed. The patient’s gait should be studied. Typically, the gait velocity is slower with reduced stride length. There may be longer double limb periods and prolonged heel contact to avoid loading a painful forefoot. Other compensatory actions may also become apparent. Assessing a patient’s shoes for wear will also often give clues about abnormal gait patterns and contact areas as well as the suitability of the footwear. Hindfoot position and its relationship with the forefoot should be assessed. Double and single stance heel raise (weight bearing closed chain tests) as well as open chain testing should be performed in assessing tendon function. Planovalgus deformity is common in RA but one should remember that inability to perform a single stance heel rise is not necessarily due to tibialis posterior tendon pathology in such patients (eg painful midfoot arthritis). One should assess the gastrocnemiusesoleus complex for tightness and if present use the Silfverskiold test to differentiate which part of the complex is tight. The tibialis posterior tendon should be carefully palpated along its course for tenderness and swelling suggestive of tenosynovitis and an increased risk of tendon rupture. The ankle and subtalar joints should be examined for range of movement and evidence of synovitis or instability. Gentle passive pronation and supination of the midfoot in conjunction with palpation of the midfoot joints is sensitive for identifying synovitis here. In the severely rheumatoid forefoot there may be severe hallux valgus deformity and dorsal subluxation/dislocation of the lesser toes at the MTPJ level, with consequent severe metatarsalgia. In earlier disease there may be synovitis without established deformity, evidenced by swelling and pain on palpation, translation and/or a grind test. Examination in all such patients must always be gentle with half an eye on the patient’s face to look for apprehension or discomfort. The clinician must always (gently) assess whether any deformities observed throughout the foot and ankle are passively correctable as this often influences the treatment options available. Attention must also be focussed on any pressure areas and threat of ulceration. The neurological and vascular status of the lower limb should always be documented. If ulcers are established, it is useful to photograph them to document size, location and subsequent response to treatment. A useful adjunct for neurological examination is a 5.07 Semmes-Weinstein monofilament, which applies a standardized 10 g of pressure to the skin. When sensation to this is lost, there is risk of neuropathic ulceration. Neuropathy in RA can be peripheral due to vasculitis, compressive from radiculopathy due to lumbar spine disease or, most worryingly, due to cervical myelopathy as a result of altlanto-

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Medical therapy Medical treatment of RA has advanced dramatically over the past two decades, to such an extent that from 1997 to 2001 there was a 12% reduction in orthopaedic admission of rheumatoid patients in the Swedish National Inpatient Registry. The same trend is seen across the Atlantic, with a 19% reduction in knee surgery in Californian rheumatoid patients from the mid 1980s to 2007. This dramatic reduction in destructive arthropathy requiring surgery has been brought about by disease modifying anti-rheumatic drugs (DMARDS). First-line treatment now involves non-biological therapy with methotrexate, a cytotoxic drug. This is given weekly by mouth and is generally fairly well tolerated. Intra-articular and systemic steroids may also be given initially, with tight control of the disease the main aim. Steroid therapy can then be reduced over time with the aim that no patient remains on steroids longer than 2 years. Bone protection in the form of calcium supplementation and bisphosphonates are used in combination with systemic steroid therapy to prevent osteoporosis. Disease activity is measured with validated scoring systems such as the DAS 28. If patients score more than 5 on the DAS 28, despite methotrexate and steroids, biological treatment is started with anti-TNF drugs such as Infliximab and Etanercept. These drugs are highly effective in 60e70% of patients and can induce remission within a few weeks, sparing patients further joint damage. Currently in the UK, around 6% of RA patients are on anti-TNF therapy, at a cost of £8,000e10,000 per patient per annum. If anti-TNF therapy is not successful, other biological agents that block inflammatory cytokines may be tried, such as Rituximab and Abatacept. Current advice is that methotrexate may be continued in patients undergoing surgery, whilst anti-TNF therapy should be discontinued 2e4 weeks prior to surgery due to an increased risk of both minor and major infection. Despite such advances in medical therapies, the need for orthopaedic intervention is still substantial. Many patients have a long disease history and already have established destructive arthritis. In addition, many newly diagnosed patients will not respond to DMARDs, or may find the side effects intolerable. Steroids lose potency with time and generally patients relapse if DMARDs are discontinued. It is therefore vital that orthopaedic

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surgeons keep abreast of medical developments and understand the point at which surgical treatment should be considered in such patients.

Conventional hallux valgus re-alignment procedures can be used in rheumatoid patients with mild to moderate hallux valgus in the presence of well-preserved articular cartilage and relatively inactive disease. However, in the absence of well controlled disease, with clinical evidence of synovitis, or if there is radiologically advanced joint damage, then arthrodesis of the first MTPJ is generally favoured. Attention must also be focussed on any concurrent metatarsalgia and this should be addressed at the same time with either joint preserving or joint excision surgery. Post-operatively the patients may weight bear in a rigid postoperative shoe. Barouk recently reported good clinical results in a series of 55 feet using a scarf osteotomy for hallux valgus in the rheumatoid foot combined with Weil’s osteotomies for the lesser metatarsals.3 Good correction was maintained at 2 years in 95% of feet and only one patient required revision to arthrodesis. Severe hallux valgus or hallux valgus associated with secondary osteoarthritis or significant bone loss is best treated by arthrodesis. The joint surfaces are prepared with either flat bone cuts, domed reamers or osteotomes, with removal of osteophytes. The bone quality is often very poor. The aim is to fuse the 1st MTPJ in 10e15⁰ of valgus and 10⁰ of dorsiflexion from plantargrade (20e30⁰ dorsiflexion relative to the 1st metatarsal). Rather than focussing on exact measurements, it is most helpful to simulate loading of the foot with a flat surface intraoperatively, and the hallux pulp should just make contact with the surface and the toe must not be too straight and likely rub on the medial toe box of their shoes (and equally not so much valgus as to impinge upon or overcrowd the lesser toes). Either a single oblique lag screw and dorsal low profile plate4 or crossed lag screws are used for compressive, stable fixation. If there is significant bone loss, cancellous bone graft from the proximal tibia can be used to augment the fusion, or if a more structural graft is required we use tri-cortical bone from the iliac crest.

Non-operative treatment Most rheumatoid patients in an orthopaedic clinic will have established diagnoses and may already have exhausted more conservative treatments organized by their rheumatologist. It is, however, vital to enquire about and consider orthotics and podiatric input if this might help. We have a close relationship with the podiatrists in our hospital and run a joint clinic with them each month. Steroid injections can be effective in a joint with active synovitis. In our practice we often refer patients to a specialist musculoskeletal radiologist for joint or tendon sheath steroid injections under X-ray or ultrasound control. Local anaesthetic  steroid injections can be useful both diagnostically and therapeutically, and in some cases it is necessary to perform such injections in theatre with sedation by an anaesthetist. Surgery Surgery is often required to alleviate pain and correct deformity. The aim is to create a painless, stable, plantargrade foot. We will consider the forefoot, midfoot and hindfoot/ankle in turn. Forefoot reconstruction: careful pre-operative planning must take account of the severity of the deformities and their correctability, as well as the condition of the articular surfaces. One should remember that assessment of the hindfoot and midfoot is important and concurrent excessive hidfoot valgus/varus must be assessed and addressed with orthoses or surgery if planned forefoot intervention is to be successful. Gastrocesoleus tightness also contributes to increased forefoot loading and can be addressed with physiotherapy or if necessary, a gastrocnemius slide/Achilles tendon lengthening. Whilst we discuss procedures separately, it is very common to combine first ray operations with lesser metatarsal osteotomies and lesser toe correction as a whole forefoot correction to achieve the optimum result. Coughlin showed highly satisfactory results in 47 feet with severe hallux valgus deformity secondary to RA treated with 1st MTPJ arthrodesis.2 Additional forefoot reconstruction was carried out with excision of the lesser metatarsal heads for metatarsalgia and proximal interphalangeal joint (PIPJ) fusion for hammer toes. Excellent or good results were reported for 45 out of the 47 feet. In all feet, the hallux took part in weight bearing on Harris-mat pressure studies after surgery. This type of forefoot reconstruction is generally considered the gold standard in RA.

Other 1st MTPJ procedures The Keller excision arthroplasty has been used extensively in the past in rheumatoid patients. However, it may be associated with higher rates of transfer metatarsalgia.5 We have used the Keller procedure as a salvage operation in the rare cases of failed 1st MTPJ arthrodesis due to infection with a good outcome, but this in our opinion remains its main application. Arthroplasty of the 1st MTPJ remains an attractive proposition, particularly as it is so successful in other joints affected by rheumatoid arthritis. Silastic joints have the advantage of being constrained, however, the results have generally been poor due to silicone synovitis in up to 72% of cases, cystic osteolysis and recurrence of pain.6 Currently, there is insufficient evidence to recommend arthroplasty of the 1st MTPJ in these patients. Arthrodesis of the 1st MTPJ remains the gold standard in this patient population.

Hallux valgus and 1st MTPJ arthritis Whilst hallux valgus is common in the general population, a number of factors make it much more common in RA. Synovitis of the first MTPJ causes ligamentous laxity and subsequent instability. Inactivity and pain with or without peripheral neuropathy causes wasting of the intrinsic muscles of the foot, which may contribute to widening of the forefoot. Subtalar disease often results in excessive pronation which in turn loads the medial column and drives the hallux into valgus. The subsequent malalignment of the flexor and extensor tendons, which subluxate laterally, tends to exacerbate the deformity and cause it to progress.

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Metatarsalgia and MTPJ dislocation: a combination of synovitis and subsequent ligamentous laxity with or without rupture of the volar plate pre-disposes the MTPJs to dorsal subluxation and then dislocation. This is combined with relative weakness of the intrinsics over the long flexors and extensors. As the MTPJ subluxes dorsally, the interossei and lumbricals, which act together to flex the MTPJ and extend the PIPJ, lose mechanical advantage. This perpetuates the problem and can rapidly turn

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a correctable deformity into a fixed one. The lesser toes play little part in load bearing and propulsive gate once the MTPJs are subluxed. In addition, dorsiflexion of the toes causes distal migration of the fat pad. Both factors pre-dispose patients to increased pressure under the exposed metatarsal heads, resulting in metatarsalgia with callosities on the plantar surface. In the normal foot, the proximal metatarsals form an arch, but distally should come to lie in a horizontal plain. On an AP radiograph the metatarsals should form a parabolic cascade, with the second metatarsal longer than the first and subsequent metatarsals being progressively shorter than the second. The aim of surgery is two-fold. The first is to correct any abnormality of the normal metatarsal cascade and offload the symptomatic metatarsal heads. The second aim is to reduce the dislocated MTPJs and in so doing bring the lesser toes back into weight bearing, therefore sharing load and reducing pressure under the metatarsal heads. When the lesser MTPJ anatomy is reasonably well-preserved, we favour a shortening distal metatarsal osteotomy such as the Weil osteotomy. This osteotomy is intra-capsular, with the cut parallel to the ground, allowing the metatarsal head to slide proximally. The osteotomy is fixed with a small twist-off screw and any overhanging dorsal bone spur is excised. This shortens the metatarsal and also decompresses the MTPJ by reducing tension on the collateral ligaments. In combination with extensor tendon lengthening and PIPJ arthoplasty/fusion, the dislocated MTPJs can often be reduced. These may require stabilization with a temporary K-wire. Bolland reported the results of this type of reconstruction in 26 feet, combining 1st MTPJ fusion with Weil’s metatarsal osteotomies.7 Excellent or good results were achieved in 88% of cases with a mean modified AOFAS score of 72/100 (34e90). First MTPJ arthrodesis union rate was 92% at 26.2 months. There was a 12% rate of recurrent metatarsalgia or callosities. The Weil’s osteotomy is not without complications. Scar contracture, stiffness and elevation of the toe are fairly common. Long-term stiffness occurs in as many as 20%.8 There can also be avascular necrosis and recurrence of the deformity. Despite these potential problems, however, the Weil osteotomy remains a useful technique. In severe, destructive arthritis, when the metatarsal head is too damaged to be preserved, excision arthroplasty such as described by Coughlin2 is used. There are numerous varieties of excision arthroplasty described, involving excision of the metatarsal head/base of toe proximal phalanx (or both) and via either dorsal or plantar incisions. Wherever possible we try to preserve the MTPJs of both the first and the lesser rays (Figure 1).

Figure 1 Typical advanced rheumatoid foot with severe hallux valgus deformity, dorsal subluxation of lesser toes and consequent metatarsalgia, with keratotic skin noted under the metatarsal heads.

associated metatarsalgia and hence shortening of the lesser metatarsal is undertaken (see above) and this will often correct a flexible (correctable) claw/hammer toe deformity adequately. If there is residual fixed deformity then osteoclasis may adequately complete the correction or alternatively PIPJ arthroplasty/fusion may be considered. We are also now using minimally invasive osteotomies of the phalanges to treat such deformities, with encouraging results. When undertaking PIPJ fusion, we use an S-shaped incision centred over the dorsal aspect of the PIPJ. The extensor tendon is divided and the joint is opened. The collateral ligaments are released and a fine saw blade is used the remove the subchondral bone. The remaining joint surface is debrided and prepared (with shortening as required) and the PIPJ is then reduced and stabilized with two parallel, fine (approx 1 mm) K-wires, to give rotational stability. The K-wires are removed in clinic at 5 weeks. Hindfoot and midfoot deformity: changes in the hindfoot and midfoot tend to occur with longer duration of disease and therefore present later. They are involved in around two-thirds of patients with chronic RA.9 The main driver of deformity appears to be a combination of subtalar synovitis with subsequent ligamentous disruption, especially the spring ligament, in conjunction with dysfunction of the tibialis posterior tendon. There is pronation at the subtalar joint with hindfoot valgus and loss of the medial arch. Synovitis of the navicularcuneiform or tarsometatarsal joints exacerbates the problem and can lead to prominence of the medial midfoot bones. In severe cases there can be complete lateral dislocation through the transverse tarsal joint with callosity over the exposed head of the talus. Severe deformities can be challenging to treat, with potentially high risks of serious complications. Operations sometimes need to be a la carte, and may combine hindfoot and midfoot/ forefoot correction at the same sitting. Important considerations when correcting severe hindfoot deformities include proximal limb alignment or deformity, the relative presence or absence of ankle arthritis or deformity and soft tissue condition and tension (one needs to predict and avoid undue tension after deformity

Lesser toe deformity: hammer toe refers to hyperextension at the MTPJ, flexion at the PIPJ and extension at the DIPJ. In clawed toes there is hyperextension at the MTPJ and flexion at both the IPJs. These two deformities are common in RA and cause painful callosities over the dorsum of the PIPJs due to rubbing from shoes. If associated with moderate or severe hallux valgus, the toes may cross over or under the hallux, resulting in a painful deformity and significant problems with shoe fitting. Occasionally, lesser toe deformities are addressed individually but it is far more common that they are addressed as part of a more extensive forefoot correction. In most cases there is

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correction). The aim of surgery is to bring the heel back under the tibiotalar joint and to restore the medial arch. It is also important to restore the shape of the foot to facilitate shoe fitting. Finally, it is important to explain to patients that there is a significant investment of time and energy with these procedures, as the total time spent in a cast or protective boot can be up to 12e16 weeks, and full recovery can take up to 12 months or so.

If there is symptomatic ankle arthritis but no significant deformity at this joint, in conjunction with subtalar arthritis, then we have sometimes performed staged (or on some occasions simultaneous) subtalar or triple arthrodesis followed by total ankle replacement, with some success. However, it is vital that a neutral foot position is achieved and that there is adequate soft tissue stability to achieve stable ankle replacement, and generally this is unlikely to be the case with arthritis secondary to end stage tibialis posterior dysfunction (Figure 2a, b and c).

Tibialis posterior dysfunction: in stage I tibialis posterior dysfunction there is pain along the course of the tendon and there may be some weakness but a single stance heel raise is usually possible. In RA this is caused by active tenosynovitis, which can be treated with open decompression of the tendon and synovectomy. Surgery usually improves the patient’s symptoms and can prevent tendon rupture. Stage II and III disease represent a spectrum through weakness of the tendon and a correctable valgus hindfoot to fixed hindfoot valgus with abduction of the transverse tarsal joint and Achilles tendon contracture. In general, these stages require surgical intervention. If the hindfoot and forefoot deformity is still passively correctable then generally the deformity can be treated with a soft tissue reconstruction. We use a curved posteromedial approach and tendon reconstruction with flexor digitorum longus transfer. The pathological posterior tibial tendon is excised and if the proximal musculotendinous unit is mobile (and therefore not fibrosed) then this is tenodesed to the FDL graft just proximal to the medial malleolus. This is combined with a medializing calcaneal osteotomy via an additional lateral calcaneal incision. If the hindfoot valgus is fixed but the forefoot varus is less than 10 and there is no abduction of the transverse tarsal joints, then an isolated subtalar arthrodesis with correction of the heel position may be sufficient. If, however, there is also abduction at the transverse tarsal joints then a triple arthrodesis (i.e. subtalar, talonavicular and calcaneocuboid joint arthrodesis) is required. Knupp et al. published long-term follow up of 24 triple arthrodesis procedures for RA.10 There was satisfactory fusion in all cases and 100% patient satisfaction, however in 15 out of 24 feet there was advancement of midfoot arthritis and in 10 cases there was progressive ankle arthritis. If there is ankle arthritis and deformity at this joint in conjunction with subtalar arthritis, a pantalar fusion is required. A curved lateral incision between the superficial peroneal and sural nerves is used to access the ankle, subtalar and calcaneocuboid joints. The distal fibula is resected, which significantly reduces the tension in the contracted lateral soft tissue following correction of the deformity and allows easy access to the subtalar joint. An additional anteromedial incision is required to adequately prepare the medial tibiotalar joint and talonavicular joint. We favour a locked tibiotalocalcaneal nail augmented by additional cannulated screw fixation of the triple joint complex. It is reasonable to allow such patients some limited weight bearing during the post-operative period with good stability of fixation. Whilst arthroscopic preparation of the ankle joint for isolated tibiotalar fusion has become relatively commonplace, there are also case reports and small series of arthroscopic joint preparation for pantalar fusion that deserve further attention.11,12

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The diabetic foot Diabetes mellitus is a syndrome of chronic hyperglycaemia caused by insulin deficiency or resistance. It affects well over 100 million people world-wide and the incidence of type 2 diabetes is rising in parallel with the increase in obesity. The disease causes damage to numerous organs and body systems. A number of mechanisms contribute to organ damage in diabetes, including glycosylation of proteins in peripheral nerves, activation of the pyolol pathway and disruption of the microvascular circulation. In the foot the majority of problems are caused by neuropathy, ischaemia and infection. Foot complications, particularly infection, are the most common cause of admission to hospital in diabetic patients. History Unlike many orthopaedic consultations, which focus on relieving pain, in diabetic patients the main aim is to reduce risk to the limb and the patient whilst also addressing pain, deformity and loss of function. A general medical history is required, and direct questions should be asked to establish the degree of end organ damage, such as retinopathy, nephropathy and ischaemic heart disease. It is important to ask how long ulcers have been present and whether patients have already previously been hospitalized with diabetic foot complications. The aim is to develop an idea of the degree of risk posed by a patient’s foot problems and available treatment options. Examination: careful attention must be paid to footwear, which can often be a cause of problems in the diabetic patient with neuropathy. Neurological assessment should include recording sensation to either a 10 or 4.5 g Semmes-Weinstein monofilament. Although testing ten defined areas with the 10 g monofilament remains the gold standard, Saltzman showed that loss of sensation to a 4.5 g Semmes-Weinstein monofilament in a single point under the first metatarsal is equally sensitive in predicting risk of ulceration.13 Neuropathic ulcers may be very deep and if painless can be gently probed in clinic. Absent ankle reflexes are an early sign of neuropathy and correspond to increased risk of ulceration.14 Peripheral pulses should be palpated and if absent or reduced, ankle brachial pressure indices (ABPI) should be recorded. An ABPI from 0.8 to 1.0 implies no significant ischaemia. An ABPI between 0.5 and 0.8 warrants further investigation with duplex ultrasonography and possible onward referral to a vascular surgeon. An ABPI of less than 0.5 implies critical ischaemia and should trigger an urgent vascular opinion. Calcification of the vessels is common in diabetes and may give a falsely normal or high reading. An ABPI of above 1.3 implies incompressible

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Figure 2 a Rheumatoid patient with severe planovalgus foot, with dislocation through the talonavicular joint. The surgeon is pointing to the talar head, which is completely dislocated, and the patient had been walking on this. The foot had effectively dislocated laterally through this level. b The talus and distal fibula had to be removed to bring the foot back underneath the leg. This excised bone was then used as autograft as part of a tibiocalcaneal fusion, including a tibionavicular fusion (pantalar fusion without the talus). c There was a good fusion mass by 4 months post-surgery and the patient was able to discard his calliper.

calcified vessels. The clinician must be aware of other signs of ischaemia in this situation and look for reduced skin temperature, sluggish capillary refill and absent leg hair.

Duplex ultrasound arteriography is a safe, non-invasive and effective way of imaging the arterial tree in the lower limb and determining blockages that may be amenable to vascular surgery. All infected wounds should be swabbed and swab results discussed with a microbiologist to target antibiotic therapy where appropriate. Good diabetic control is vital when treating wounds and infections and should be monitored by measuring glycosylated haemoglobin (HbA1C). Dyslipidaemia must be treated and it is often prudent to involve a dietician in the patient’s care early in order to optimize healing potential.

Investigations The main challenge in the diabetic foot is to distinguish neuroarthropathy from infection. This is particularly important if there is an ulcer overlying the affected bone or joint. Plain X-rays are useful to monitor progress. Typically, osteopaenia is more generalized in Charcot joints and more localized in osteomyelitis. MRI can be useful for detecting abscesses but will not generally prove reliable in distinguishing aseptic neuroarthropathy from osteomyelitis. Scintigraphy with Technecium 99 has a 91% sensitivity for osteomyelitis but only 54% specificity.15 Schauwecker et al. compared scans with Indium 111 labelled white cells, technetium 99 and gallium 67 in 57 patients with Charcot joints and osteomyelitis.16 Indium labelled white cells were 100% sensitive in detecting acute osteomyelitis and 60% sensitive in chronic osteomyelitis, with a specificity of 96%. Whilst labelled white cells are more specific for infection, during the acute stages of a Charcot joint there is inflammation in response to micro-fractures, which can result in false positive scans. The gold standard investigation to diagnose osteomyelitis is bone biopsy and culture but this is not often practical.

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The diabetic ulcer Approximately 3e4% of the diabetic population have foot ulcers or deep infection and 15% of diabetics will develop foot ulcers in their lifetime. Diabetic foot ulcers precede 85% of non-traumatic lower limb amputations. Neuropathy, ischaemia and immune deficiency are the main risk factors for the development of diabetic foot ulcers. Aetiology of the diabetic ulcer: sensory neuropathy is the most common cause of ulceration in the diabetic foot due to loss of normal protective mechanisms. Neuropathy affects 50% of patients who have had diabetes for 10 years. The ulcer may start

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rarely causes ulcers, however, in combination with other factors such as neuropathy and pressure it can increase the risk of diabetic ulceration by a factor of nine.17 Ischaemia also significantly impairs healing of established ulcers and creates a relatively anaerobic environment in which infection can thrive. Deformity of any type in the diabetic foot may lead to increased pressure areas whilst weight bearing or wearing shoes. While many orthopaedic surgeons may understandably be cautious about operating on foot deformities in diabetic patients, such procedures may in fact be necessary to prevent future complications due to ulceration. Immune deficiency is also a feature of diabetes. Glycosylation of immune proteins inhibits their function and neutrophil performance is impaired. The result can be infection with microorganisms that would not usually be pathogenic in a healthy person. Diabetic patients are pre-disposed to contracture in the gastrocneumiusesoleus complex. This limits dorsiflexion at the ankle and increases plantar pressure in the forefoot during standing and walking, pre-disposing to plantar ulcers. Contracture of the gastrocnemiusesoleus complex should be assessed clinically using the Silfverskiold test.

The Wagner classification of diabetic ulcers Grade Grade Grade Grade Grade Grade

0 1 2 3 4 5

Skin intact, erythema, at risk Superficial ulcer of skin or subcutaneous tissue Ulcers extend into tendon, bone, or capsule Deep ulcer with osteomyelitis, or abscess Gangrene of toes or forefoot Midfoot or hindfoot gangrene

Table 1

due to acute trauma or be the result of repetitive micro-trauma, for example from ill-fitting footwear. Plantar ulceration is most often found over bony prominences and reflects intermittent excessive pressure with neuropathy. Dorsal ulceration is almost always caused by constant pressure from poorly fitting shoes. Autonomic neuropathy is common in diabetics and results in a dry, scaly and often swollen foot. If the skin cracks, bacteria may enter the soft tissues. Nail growth is abnormal in autonomic neuropathy and can pre-dispose to ingrowing toe-nails and paronychia. Motor neuropathy in diabetic patients can cause intrinsic muscle weakness and subsequent imbalance between these and the extrinsic muscles of the foot, which pre-disposes to hallux valgus and lesser toe deformities. Hammer and claw toe deformities increase plantar pressure under the metatarsal heads, predisposing to ulceration. A combination of motor and sensory neuropathy may also result in subtle abnormalities of gait, which increases pressure on bony prominences such as the medial sesamoid of the 1st MTPJ. Atherosclerosis is more common in patients with diabetes and tends to be more localized to the infra-popliteal vessels in diabetics compared to the general population. Ischaemia on its own

Classification of diabetic ulcers: the Wagner classification was developed in the 1970s by Meggitt and Wagner, and is widely used to describe diabetic ulcers (Table 1).18 The Wagner classification has been adapted to separate out the depth of the ulcer from the degree of ischaemia. This avoids confusion in certain areas, for example where there is limb threatening ischaemia but only a shallow ulcer. The depth-ischaemia classification proposed by Brodsky is a little more complex but perhaps more useful clinically.19 Brodsky also suggested treatments that correspond to the various grades of both ulcer depth and ischaemia (Table 2).

Brodsky’s depth-ischaemia classification of diabetic ulcers Grade

Definition

Treatment

Depth classification 0 At-risk foot, no ulceration 1

Superficial ulceration, not infected

2

Deep ulceration exposing tendons or joints with or without superficial infection 3 Extensive ulceration with exposed bone and/or deep infection or abscess Ischaemia classification A Not ischaemic B Ischaemia without gangrene C

Partial (forefoot) gangrene

D

Complete foot gangrene

Patient education, accommodative footwear, regular clinical examination Offloading with total contact cast (TCC), walking brace, or special footwear Surgical debridement, wound care, offloading, culturespecific antibiotics Debridement or partial amputation, offloading, culturespecific antibiotics

Non-invasive vascular testing, vascular consultation if symptomatic Vascular consultation for bypass or angioplasty, partial amputation if unable to re-vascularize Vascular consultation, major extremity amputation

Table 2

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A further refinement of Brodsky’s depth-ischaemia classification has been developed by the Diabetic Foot Center at the University of Texas San Antonio.20 This includes the presence or absence of infection, and shows greater association with risk of amputation and likelihood of ulcer healing than the original Wagner classification.

therapy, at which point total contact casting may then be used to promote healing. If the ulcer is particularly resistant to treatment, the vascular supply should be investigated even in the presence of foot pulses and normal ABPIs. Partial amputations may be necessary in established osteomyelitis that fails to respond. The involvement of a microbiologist and an adequate number of microbiological specimens is vital for successful treatment of grade 3 ulcers. Correction of deformity is vital in the non-healing diabetic ulcer where deformity is felt to be the major cause of increased pressure. Some general principles apply. Incisions are preferably made through a separate, healthy part of the skin near the ulcer rather than through the ulcer itself. Dorsal incisions are favoured. The opportunity should be taken to debride the ulcer, which is best left open to drain. The surgical incision can be closed. After surgery, careful pressure relief and dressing care are required to promote ulcer healing by secondary intention. Careful attention should be paid to glycaemic control. Chronic toe ulceration is often secondary to hammer or claw toe deformities and is most often treated with amputation. Most ulcers of the hallux are plantar-medial and may be associated with pronation of the digit and hallux valgus. If hallux ulcers are resistant to offloading then resection of the medial condyles of the phalanges, either side of the interphalangeal joint, is often successful. If the joint is infected, excision arthroplasty is a better option. Ulceration beneath the first metatarsal head is common and is often caused by pressure under the medial sesamoid. Ulcers in this area can rapidly progress to grade 3 with osteomyelitis and therefore relatively aggressive surgery to excise the medial sesamoid is indicated. This may be performed through a standard medial approach to the 1st MTPJ. Attention should also be paid to any contribution to overloading of the forefoot by tightness in the gastrocesoleus complex and an Achilles or gastrocnemius lengthening undertaken when necessary. Ulceration under the lesser metatarsal heads may be treated with dorsiflexion osteotomies at the base of the metatarsal, such as the BRT procedure, which offload the metatarsal head and avoid osteotomy or metalwork close to the ulcer. Excision of the metatarsal head is indicated for established osteomyelitis. Ulceration under the fifth metatarsal head may be treated with condylectomy. If this fails, excision of the distal third of the bone can be performed through extension of the same incision. Once again, attention should also be paid to any contribution to overloading of the forefoot by tightness in the gastrocesoleus complex and an Achilles or gastrocnemius lengthening undertaken when necessary. More severe deformities causing ulceration are likely to be associated with Charcot’s arthropathy and are addressed in the next section. A number of studies have shown that Achilles tendon lengthening can be effective in treating plantar forefoot ulcers associated with contracture of the gastrocnemiusesoleus complex, and the technique is growing in popularity. Mueller et al. were able to show reduced rates of ulcer recurrence after tendo-Achilles lengthening and total contact casting versus total contact casting alone (15% vs 49% at 7 months).25 There may also be a role for gastrocnemius slide if the contracture is largely in grastrocnemius rather than the soleus or the Achilles tendon.

Treatment of diabetic ulcers: patients with grade 0 ulcers, or more accurately the patient at risk of ulceration, must be carefully advised and followed up. A podiatrist or chiropodist should look after the patient’s feet on a regular basis to take care of nail cutting, pad pressure areas and advise on footwear. Patients should be advised to keep feet warm and not to smoke. Grade 1 and 2 plantar ulcers can largely be treated with local debridement (either in clinic or theatre) and total contact casting with antibiotic therapy in the case of superficial infection. Casting relieves pressure areas and shares up to 30% of the patient’s weight. Total contact casts should avoid excessive padding and should incorporate the toes, preventing excessive dorsiflexion of the MTPJs. Bony prominences should be padded with felt or foam. The first cast should be changed at a week as swelling subsides. Subsequent cast changes may occur every 2 weeks. Overall, healing rates are reported between 70% and 100%. Frigg et al. showed primary healing rates of 85% in an average of 4.2 months with total contact casting for grade 1 and 2 ulcers.21 However, 56% of patients suffered recurrent ulcers after healing despite custom-made orthopaedic shoes and foot care advice. In approximately a third of recurrent ulcers, significant deformity was a contributor and these patients underwent corrective surgery. Nearly two-thirds of recurrences could be treated again with total contact casting. In addition to recurrence, 14% of patients acquired new ulcers from poorly fitting casts. This is the main complication of total contact casting but can largely be treated by changing the cast frequently and by meticulous wound care. An alternative to a total contact cast is a pneumatic walking boot. Faglia et al. recently reported similar efficacy to total contact casting, however, as such devices are removable compliance can be an issue.22 Katz et al. wrapped fibreglass casting tape around a pneumatic walking boot to improve compliance and showed similar rates of ulcer healing to total contact casting.23 However, a number of other studies show greater success and more rapid healing in total contact casts versus off the shelf devices. For this reason, total contact casting was still recommended over and above removable pneumatic boots in a recent review concerning offloading the diabetic foot.24 We discuss both options with patients and make decisions on a case-by-case basis. However, significant deformity is a relative contra-indication to offloading with a pneumatic walking boot. Dorsal ulcers are rarer and are more commonly caused by deformity and ill-fitting shoes. They do not respond as well to total contact casting as plantar ulcers, which are pressurerelated. In these situations a soft surgical shoe with a wide, high toe box and good outpatient ulcer care is often sufficient. Gentle probing of the wound can detect grade 3 ulcers if bone is felt. If there is significant deep infection the patient should be admitted for intravenous antibiotics. The aim is to down-grade the ulcer with surgical debridement and adequate antibiotic

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union, late displacement and collapse and subsequent Charcot joint. This theory is simple and makes sense in the foot, however, it does not adequately explain neuroarthropathy in non-weight bearing joints such as the elbow or shoulder. The neurovascular theory suggests that autonomic dysfunction leads to increased blood flow to the joint via arteriovenous shunting. This hyperdynamic circulation leads to bone resorption, via increased osteoclastic activity. Finally, there is evidence of an inflammatory component in neuroarthropathy, with raised levels of the cytokines TNF-a and interleukin-1 found in association with the condition, although causality has not been established. Neuroarthropathy in diabetes is a strange condition as it does not correspond well with severity or duration of neuropathy or type of diabetes as one might reasonably expect. This feature serves to highlight the multifactorial aetiology of a Charcot joint.

Dressings and wound therapies for diabetic ulcers Dressing/therapy

Recommended for

Foams, hydrofibres and crystalline sodium chloride gauze Calcium alginates Hydrogels Hydrocolloids

Sloughy wounds with exudate

Negative pressure therapy

Infected or exudative wounds Dry wounds Mild to moderately exudative wounds Deep wounds after adequate debridement

Table 3

History and examination: clinical presentation of a Charcot joint is varied. Presentation types can be thought of as acute or chronic. Acute cases may present with a fracture, dislocation or rapidly developing deformity. Marked erythema, warmth and swelling can give the appearance of septic arthritis or cellulitis. Elevation of the limb reduces the erythema, as this is largely dependent and distinguishes a Charcot joint from cellulitis. A careful history may reveal a traumatic event. Despite the limb by definition being neuropathic there is pain in up to half the cases, although it is not always in proportion to the degree of joint destruction. Chronic Charcot joints present more often with deformity, classically widening of the foot, collapse of the longitudinal arch and even a rocker-bottom appearance. There may be ulceration over bony prominences, particularly the plantar aspect of the midfoot. Vascularity should be assessed although it is often adequate. Footwear and risk of ulceration are prime concerns.

Various dressing and wound care therapies can enhance wound healing when compared with simple moist saline dressings or hydrogel.26 Most work by removing fluid and exudate from the wound that contain factors such as proteolytic enzymes that impair wound healing. Local policies and cost will dictate the availability of these options, which are summarized in Table 3. Importantly, none of these dressings alone appear as efficacious as total contact casting with simple dressings, so they are best used as an adjunct to established treatment protocols. During subsequent follow up, ulcer healing should be documented by taking measurements and photographs as well as radiographs, to determine progression or resolution of osteomyelitis. Once healed, patients must be educated to prevent recurrence and provided with good footwear. They should be followed up by a podiatrist/chiropodist and their primary physician. A multidisciplinary approach to these problems is important to achieve optimal results. Charcot’s neuroarthropathy Jean Martin Charcot described neuroarthropathy due to syphilis in 1868. Currently, however, diabetic neuropathy is by far the most common cause of this destructive arthropathy, with the foot and ankle the most commonly affected sites. The prevalence of Charcot’s neuroarthropathy is estimated to be between 0.12% and 1.4% of the diabetic population. In the UK, that amounts to as many as 25 000 individuals. The incidence appears to be rising although it is difficult to determine if this is a true reflection of more disease or simply better awareness of neuroarthropathy as a complication of diabetes. Either way, it is clear that neuroarthropathy presents a significant burden on health resources and in particular the foot and ankle surgeon.

Classification of the Charcot foot: Eichenholtz described three distinct stages in the pathophysiological process of developing a Charcot joint.27 The first stage is characterized by acute inflammation. Radiographs show fracture and fragmentation of the bone associated with osteopaenia and eventual collapse of the joint. In the second stage there is coalescence with new bone formation. Clinically, the foot returns to a normal colour and temperature. In the third stage there is consolidation and healing, with persistent deformity. A modification of Eichenholtz’s classification adds an initial stage zero, in which there is warmth and erythema without radiological changes. It is supposed that early intervention here may prevent progression to destructive arthropathy. Brodsky has described an anatomical classification to describe the common patterns of neuroarthropathy in the foot and ankle.19 Type 1 Charcot joints are the tarsometatarsal joints and naviculocuneiform joints of the midfoot. This type of midfoot collapse is the most common pattern in diabetics with neuroarthropathy and often causes a fixed planus or even rockerbottom deformity. Type 2 disease involves the triple joints of the hindfoot, i.e. the subtalar, talonavicular and calcaneocuboid joints. Charcot changes here result in valgus collapse of the hindfoot. Type 3A is rarer and involves the ankle joint. This may

Aetiology of the Charcot joint: the pathophysiology of neuroarthropathy is not entirely understood and it is highly probable that a number of processes contribute to joint destruction. The neurotraumatic theory suggests that arthropathy is the effect of continuous micro-trauma and overuse or misuse of the joint due to impaired pain transmission and proprioception. As the protective feedback of pain is absent, the damage continues, resulting in arthritis and deformity. Occasionally, the process may be initiated by a single traumatic episode such as an ankle fracture, which despite standard treatment may go on to delayed

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often relate to trauma such as a fracture or severe ligamentous injury. Varus or valgus collapse may occur and there is risk of ulceration of the malleoli. Type 3B feet are those which develop a pathological fracture of the tubercle of the calcaneus. Trepman added two more categories to this classification.28 Type 4 disease involves a combination of patterns and type 5 deformity is in the forefoot alone.

years. The acute stage is characterized by erythema, swelling and inflammation. In this situation immobilization in a full contact cast, rest, non-weight bearing and elevation are key. As the swelling can rapidly subside, frequent cast changes are initially required to prevent rubbing and ulceration as the less swollen foot becomes mobile inside the plaster. Once the acute stage has settled and the patient has clinical and radiological features of type 2 disease, the cast is converted into any number of offloading devices. We have used pneumatic walking boots with some success in more minor deformity. In severe deformity custom-made thermoplastic anklefoot orthoses or removable bivalve casts are preferred. After consolidation the patient may return to an accommodative shoe

Non-operative treatment of the Charcot foot: the aim of treatment is to prevent deformity, minimize risk of ulceration and to keep patients mobile until the third stage of the disease, in which there is bony healing and consolidation. It is vital to explain to patients at the outset that this process may take months or even

Figure 3 a AP X-ray of a diabetic patient with a painful swollen foot after a minor injury, initially referred as an acute Lisfranc injury, although assessment revealed a neuropathic foot and a more insidious onset. b and c Charcot midfoot obvious on CT images, with fragmentation and disorganization of the tarsometatarsal joints. d, e and f The patient was protected in a diabetic boot and waited 3 months for the Charcot process to move into a cooler phase before undertaking reconstruction of the foot, which had become severely rocker-bottom. A good result was obtained but he required boot protection for 6 months after surgery before moving into custom-made shoes. A cautious approach is required in such cases.

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with a wide toe box and soft upper, with a custom-made orthotic insole.

time required for an arthrodesis procedure and an elective amputation below the knee with post-operative limb fitting and physiotherapy may give highly satisfactory results (Figure 3).

Operative treatment of the Charcot foot: the indications for surgery in a Charcot foot are severe uncontrolled deformity, ulceration, infection and persistent pain. Two main surgical strategies exist. The first is excision of bony prominences with or without debridement of ulcers and infected bone. The second strategy is re-alignment and arthrodesis to reconstruct the shape of the foot in order to relieve pressure and facilitate shoe fitting. The evidence for this type of surgery is largely experiential in the form of case series and is therefore open to bias. Decision-making is therefore not easy and will be based on multiple factors, with a large emphasis on patient involvement in the decision-making process. Exostectomy is similar to procedures used for chronic ulcers. Various principles should be applied. Incisions should be longitudinal, not transverse, and away from the pressure areas if possible. Plantar incisions should be avoided. Careful soft tissue dissection should be carried out, raising full thickness flaps as a single layer to expose the bone. Attempts should be made to diagnose infection pre-operatively as bony resection needs to be more extensive to treat osteomyelitis. The patient may also require prolonged intravenous antibiotic therapy post-operatively. Bony resection should leave smooth, rounded surfaces and try to minimize the risk of creating a new pressure area. Post-operatively, wounds should be offloaded with padded casts and non-weight bearing. Deformity correction and arthrodesis of a Charcot foot is a major undertaking. In our experience patients can expect to be immobilized in a cast or boot for a minimum of 12 weeks, and full recovery can take up to a year. The risk of infection can be overstated and in correctly chosen patients results are highly satisfactory. Whilst some authors have reported success with arthrodesis in the acute stages, we prefer to wait until stage 2 or 3 before operating i.e. in a cold, elective setting. We favour internal fixation with plates and screws over external fixators which are poorly tolerated in this patient population and not suited to porotic bone. There is also a high risk of pin site complications with external fixators. Intramedullary devices are useful load sharing devices and allow early mobilization. Arthroscopy is also a useful adjunct. For example, the ankle joint may be arthroscopically prepared for fusion before being fixed with percutaneous screws or a nail, thereby reducing significantly soft tissue dissection. Despite rigid internal fixation, cast immobilization and non-weight bearing is mandatory for at least the first 6 weeks following major reconstruction. Partial weight bearing in a boot or cast can often begin from 6 weeks onwards. Assal and Stern performed extended midfoot fusions with a medial column screw in 15 patients with advanced midfoot Charcot collapse (type 1).29 13 of the patients had non-healing ulcers pre-operatively. Post-operatively, all 13 plantar ulcers healed with no recurrence. Only one patient suffered deep infection and required an amputation. One patient required revision surgery for a symptomatic non-union. This small study shows that very satisfactory results can be achieved in these patients when one bears in mind that without correction of deformity more than one of these patients was likely to have subsequently required amputation for infection. Finally, it is worth stating that amputation remains an elective option in severe Charcot deformity that is complicated by pain, ulceration or infection. Some patients are not willing to invest the

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Summary Treating the orthopaedic problems of patients who have systemic diseases requires a multidisciplinary approach, following the principles that we have outlined in this article. There is very little high quality research in this field in the form of properly controlled clinical trials, and much of what we know owes a debt to the experience and dedication of key individuals and centres who specialize in treating these demanding foot pathologies. A

REFERENCES 1 Musa R, James D, Koduri G, et al. Which patients require multiple joint surgery by 10 years of rheumatoid arthritis? Results from the ERAS group St Albans. Poster 391. British Society for Rheumatology Annual General Meeting, 2008. 2 Coughlin MJ. Rheumatoid forefoot reconstruction. A long-term followup study. J Bone Joint Surg 2000; 82-A: 322e41. 3 Barouk LS, Barouk P. Joint-preserving surgery in rheumatoid forefoot: preliminary study with more than two year follow-up. Foot Ankle Clin 2007; 12: 435e54. 4 Politi J, Hayes J, Njus G, Bennett GL, Kay DB. First metatarsophalangeal joint arthrodesis: a biomechanical assessment of stability. Foot Ankle Int 2003; 24: 332e7. 5 Henry APJ, Waugh W. The use of footprints in assessing the results of operations for hallux valgus. A comparison of Keller’s operation and arthrodesis. J Bone Joint Surg 1975; 57-B: 478e81. 6 Rahmann H, Fagg PS. Silicone granulomatous reactions after first metatarsophalangeal joint hemiarthroplasty. J Bone Joint Surg 1993; 75-B: 637e9. 7 Bolland BJRF, Sauve PS, Taylor GR. Rheumatoid forefoot reconstruction: first metatarsophalangeal joint fusion combined with Weil’s metatarsal osteotomies of the lesser rays. J Foot Ankle Surg 2008; 47: 80e8. 8 Hofstaetter SG, Hofstaetter JG, Petroutsas JA, Gruber F, Ritschl P, Trnka HJ. The Weil osteotomy: a seven-year follow-up. J Bone Joint Surg Br 2005; 87: 1507e11. 9 Vidigal E, Jacoby RK, Dixon AS, Ratliff AH, Kirkup J. The foot in chronic rheumatoid arthritis. Ann Rheum Dis 1975; 34: 292e7. €rnkvist H, Ponzer S. Triple arthrodesis in 10 Knupp K, Skoog A, To rheumatoid arthritis. Foot Ankle Int 2008; 29: 293e7. 11 Gougoulias NE, Agathangelidis FG, Parsons SW. Arthroscopic ankle arthrodesis. Foot Ankle Int 2007; 28: 695e706. 12 Sekiya H, Horii T, Kariya Y, Hoshino Y. Arthroscopic-assisted tibiotalocalcaneal arthrodesis using an intramedullary nail with fins: a case report. J Foot Ankle Surg 2006; 45: 266e70. 13 Saltzman CL, Rashid R, Hayes A, et al. 4.5-gram monofilament sensation beneath both first metatarsal heads indicates protective foot sensation in diabetic patients. J Bone Joint Surg Am 2004; 86-A: 717e23. 14 Abbott CA, Carrington AL, Ashe H, et al. The North-West Diabetes Foot Care study: incidence of, and risk factors for, new diabetic foot ulceration in a community-based patient cohort. Diabet Med 2002; 19: 377e84.

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15 Sella EJ. Current concepts review: diagnostic imaging of the diabetic foot. Foot Ankle Int 2009; 30: 568e76. 16 Schauwecker DS, Park HM, Mock BH, et al. Evaluation of complicating osteomyelitis with Tc-99m MDP, In-111 granulocytes, and Ga-67 citrate. J Nucl Med 1984; 25: 849e53. 17 Lavery LA, Peters EJ, Williams JR, Murdoch DP, Hudson A, Lavery DC. Re-evaluating the way we classify the diabetic foot: restructuring the diabetic foot risk classification system of the International Working Group on the Diabetic Foot. Diabetes Care 2008; 31: 154e6. 18 Wagner FW. A classification and treatment program for diabetic, neuropathic and dysvascular foot problems. AAOS Instructional Course Lectures 1979; 28: 143e65. 19 Brodsky JW. The diabetic foot. In: Coughlin MJ, Mann RA, eds. Surgery of the foot and ankle. Vol. 2. 8th edn. Mosby, 2006: 1281e1368. 20 Oyibo SO, Jude EB, Tarawneh I, Nguyen HC, Harkless LB, Boulton AJ. A comparison of two diabetic foot ulcer classification systems: the Wagner and the University of Texas wound classification systems. Diabetes Care 2001; 24: 84e8. 21 Frigg A, Pagenstert G, Sch€afer D, Valderrabano V, Hintermann B. Recurrence and prevention of diabetic foot ulcers after total contact casting. Foot Ankle Int 2007; 28: 64e9.

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22 Faglia E, Caravaggi C, Clerici G, et al. Effectiveness of removable walker cast versus non-removable fiberglass off-bearing cast in the healing of diabetic plantar foot ulcer: a randomized controlled trial. Diabetes Care 2010; 33: 1419e23. 23 Katz IA, Harlan A, Miranda-Palma B, et al. A randomized trial of two irremovable off-loading devices in the management of plantar neuropathic diabetic foot ulcers. Diabetes Care 2005; 28: 555e9. 24 Cavanagh PR, Bus SA. Off-loading the diabetic foot for ulcer prevention and healing. J Vasc Surg 2010; 52(suppl 3): 37e43. 25 Mueller MJ, Sinacore DR, Hastings MK, Strube MJ, Johnson JE. Effect of Achilles tendon lengthening on neuropathic plantar ulcers. A randomized clinical trial. J Bone Joint Surg Am 2003; 85-A: 1436e45. 26 Wukich DK. Current concepts review: diabetic foot ulcers. Foot Ankle Int 2010; 31: 460e7. 27 Eichenholtz SN, Springfield III , Charles Thomas. Charcot joints; 1966. 28 Trepman E, Nihal A, Pinzur MS. Current concepts review: Charcot neuroarthropathy of the foot and ankle. Foot Ankle Int 2005; 26: 46e63. 29 Assal M, Stern R. Realignment and extended fusion with use of a medial column screw for midfoot deformities secondary to diabetic neuropathy. J Bone Joint Surg Am 2009; 91: 812e20.

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(iii) The osteoporotic ankle fracture

Risk factors While it is commonly assumed that ankle fractures in the elderly are osteoporotic fragility fractures, studies suggest that the risk factors differ from typical fragility fractures seen in the hip and spine. The bone density in patients who sustain ankle fractures is similar to age-matched counterparts who have not sustained a fracture.3,4 Increased body mass index, prior falls and diabetic neuropathy may be stronger risk factors than decreased bone mineral density for ankle fractures in the elderly. Smoking, polypharmacy, the need to use arms to rise from a chair and engagement in strenuous activity or rarely leaving the home have also been identified as risk factors.5

Iain McFadyen Adeel Aqil

Abstract Conservative management of osteoporotic ankle fractures is associated with high displacement rates and elderly patients are often unable to restrict their weight bearing, leading to longer hospital stays. Operative surgery is challenging and may lead to loss of reduction or implant failure from screw ‘cut out’. This paper describes some of the operative techniques in this difficult group of patients.

Treatment The aim of treatment for elderly hip fractures is clearly established, that is to avoid the complications associated with immobility and bed rest, while attempting to restore function and enable resumption of activities of daily living. It is accepted that the benefits of early surgery outweigh operative risks in most instances. While the aim of treatment of osteoporotic ankle fractures is similar, the benefits of surgery are not as widely accepted and non-operative treatment is still considered to represent a viable option. A review of the literature published in 2007 of the management of ankle fractures in the elderly suggested evidence appeared to support surgery.6 However the review could only find four comparative studies between 1983 and 2007 with participant numbers ranging from 47 to 126 and only one prospective randomized study using a validated functional scoring system to assess outcomes. This Israeli study was of 84 patients with 65 available for follow up. It compared conventional internal fixation with plaster cast treatment and used the American Orthopaedic Foot and Ankle Society (AOFAS) score to measure outcomes. The non-operative group had better AOFAS scores at 3 years, the cost of operative treatment was significantly higher and 33% of patients required removal of internal fixation.7 Other randomized controlled studies have shown better functional results such as range of motion with operative treatment, but importantly they have also reported higher complication rates, particularly infection rates up to 12%. The non-operative groups had difficulties with maintaining fracture reduction (especially with traditional casting techniques) in up to 27% of patients.8,9 However other studies have reported much lower complication rates. A large study of 33704 patients using the American Medicare database identified low rates of complications (under 2%) in elderly patients 2 years after surgery.10 The North American Evidence Based Trauma Working Group considered the current available evidence to be of poor quality, noting that non-consecutive case series, non-randomized and retrospective reviews dominated the literature and felt that larger, well constructed randomized controlled studies were needed.11

Keywords ankle; fracture; osteoporosis

Introduction There has been a significant increase in the incidence of ankle fractures in the elderly population, but uncertainty persists regarding their management, particularly whether operative fixation offers enough advantages over non-operative treatment to justify the risks. US Medicare figures show that increasing age is strongly associated with decreasing likelihood of operative treatment of ankle fractures.1 However there is a lack of clear evidence to support such caution, which may explain the great variations seen in management. For example, in some areas of the United States, operative treatment is five times more likely than in others. Additionally, there is a wide variation of reported techniques used. In the absence of definitive evidence, treatment is likely to continue to depend on individual surgeon preferences. This article reviews the current evidence.

Incidence Studies in Finland have found that the incidence of ankle fractures in patients over 65 rose steadily from 1970 to 1997 at a rate higher than could be explained by changing population demography alone.2 Since 1997 the increase has levelled off. This differs from other fractures associated with increasing age. The authors postulated that a healthier, older population with improved functional ability and reduced risk of injurious slips, trips and falls could partly explain this phenomenon. Currently in developed countries the incidence is about 2 per 1000 population per year and is far higher in women than in men.

Operative treatment

Iain McFadyen MBChB MRCS Ed FRCS (T&O) Consultant Trauma Surgeon and Chief of Trauma Brighton and Sussex University Hospitals, Brighton, East Sussex, UK. Conflicts of interest: none.

Osteoporotic ankle fractures are associated with more complex fracture configurations and fragmentation and are thus less stable after reduction. Additionally the holding strength of screws in osteoporotic bone can be diminished up to 10 fold.12 Thus a variety of techniques have been developed to improve the strength of fixation in weaker bone.

Adeel Aqil MBChB MRCS Ed Training Registrar, Trauma and Orthopaedic Surgery, Brighton and Sussex University Hospitals, Brighton, East Sussex, UK. Conflicts of interest: none.

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Some simple ways of improving implant stability have been developed from biomechanical studies, such as extending fibula screws into the tibia to improve stability e ‘tibia-pro-fibula’ screws.13 Koval et al. evaluated supplementing a lateral fibula plate with two intramedullary k-wires in the fibula.14 Biomechanical cadaveric testing demonstrated that this construct had 81% greater resistance to bending and double the resistance to torsional loading compared with a lateral plate alone (Figure 1). Twenty patients over the age of 50 were treated with this construct. Of the 19 available for follow up, all had united without displacement. Intramedullary fixation of the fibula without plates has also been studied and has been shown to have biomechanical advantages as well as lower post-operative wound complications. A study of intramedullary Rush nails compared to standard plating favoured the former with respect to incision size and post-operative wound complications.15 Possibly more promising is the use of fibula locked intramedullary nailing. A small series in elderly osteoporotic Weber B fractures reported good to excellent results in 9 out of 11 cases with no wound problems at the insertion site.16 Biomechanical studies have consistently shown the advantage of locking-plate technology over non-locked fixation in osteoporosis.17,18 There has been an increase in the use of locked plates despite their use in osteoporotic ankle fractures not yet having been fully evaluated and it is uncertain how this technique will translate into clinical benefit. A recent retrospective review from the Netherlands showed a significant increase in wound complication rates with locking plates compared with third tubular plates in distal fibular fractures; 5.5% with the conventional plates and 17.5% in the locking plate group.19 While the two groups were comparable with respect to patient and fracture characteristics, the two plates used were different in thickness and were applied to different surfaces of the fibula. The third tubular plates were more frequently applied to the posterolateral surface in an anti-glide position whereas the locking compression plates were more frequently applied to the lateral sub-cutaneous surface. As a locking compression plate is bulkier, this may have contributed to wound problems. In many other fractures, wound healing problems have been improved by implanting locked plates using

a minimally invasive technique. However, thus far this has not been reported in ankle fractures. A recent study compared a minimally invasive technique for fixation of the distal fibula with a standard open plating technique. It did not demonstrate any clear advantage of one technique over the other.20 Thus in Weber B fractures in the elderly, anti-glide plating is the preferred mode of fixation for many surgeons, because of the biomechanical and soft tissue advantages of placing the plate on the posterolateral surface rather than using conventional plates on the lateral surface (Figures 2 and 3).21 Biomechanical studies have shown that using a third tubular plate in an anti-glide position is at least as stable as using a lag screw with a locking compression plate as neutralization on the lateral surface.22 With neutralization plating, the screws inserted in the distal fibular metaphysis are important for plate stability, whereas with anti-glide plating the most important screw conferring stability to the construct is the screw immediately proximal to the fracture, which will usually be in cortical bone. While a comparative clinical study of anti-glide versus neutralization plating has not been performed in osteoporotic ankle fractures, screw purchase in the osteoporotic cancellous bone of the distal fibula can be so poor that it would seem sensible to opt for a plate construct that depends more on purchase in cortical bone than cancellous bone. Augmenting screw fixation in osteoporotic bone with bone cement has been validated in biomechanical studies but has not yet been properly evaluated in clinical studies in osteoporotic ankle fractures.23 While this may be an option to improve fixation in bone, additional foreign material within bone can make the treatment of infection more difficult. Intramedullary trans-calcaneal fixation has been advocated to achieve enough stability to allow early weight bearing (see Figures 4 and 5). This has been described in elderly patients in two case series from the United Kingdom. The first paper described the use of an unlocked expandable retrograde calcaneo-tibial nail in 12 patients with a mean age of 84.24 The second paper used a locked nail in 13 patients with a mean age of 79.25 In neither study were the ankle or subtalar joints opened and there was no attempt

Figure 2 Mortise view of antiglide plate placed on the posteriolateral surface of the fibula.

Figure 1 Lateral fibula plate augmented with two intramedullary k-wires.

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Figure 3 Lateral view of antiglide plate placed on the posteriolateral surface of the fibula.

at formal arthrodesis or resection of joint surfaces. Patients were allowed to mobilize fully weight bearing immediately after surgery. At follow up (mean 67 weeks in one study and 11 months in the other) there were no reported wound complications and all fractures united without loss of fracture position. Furthermore all achieved favourable Olerud-Molander (OMAS)26 symptomatic and functional outcome scores, and good patient satisfaction was also reported. The option of nail removal after fracture union was

Figure 5 Lateral view of ankle showing hindfoot nail used in fixation of bimalleolar ankle fracture in a patient with osteopenia.

offered in the expandable nail study but was only accepted by five patients. Six elected to retain the implant despite the surgeon’s recommendations. After removal of the nail, collapse of the hindfoot was not observed. This suggests that trans-calcaneal fixation might not be as destructive as might be imagined and is supported by an earlier study using Steinmann pin fixation in a similar fashion to augment cast immobilization of ankle fractures. Good results were observed in the patients over 65 in this earlier study but patients were not allowed to weight bear for 6 weeks after surgery and all of the Steinmann pins were removed.27 This suggests that in frail patients this technique protocol permits early mobilization, is tolerated well and is associated with a low complication rate. Thus the potential benefits outweigh the disability due to fixation of the subtalar and ankle joints. That 10 patients in these two studies died during the follow up period from unrelated causes emphasises the poor general state of this group of patients and importance of early mobilization to reduce hospital stay and lessen the likelihood of further complications.

Post-operative complications The overall complication rate following operative fixation of ankle fractures increases with age. While osteoporosis is an important factor, is not the only cause. Increasing fracture severity is not only associated with a general increase in complication rates, but is also strongly predictive of reoperation including ankle fusion or replacement. Medical co-morbidities, diabetes in particular, have been shown to be stronger risk factors for complications than osteoporosis or age alone,28 but the data is confused by the fact that certain co-morbidities are associated with osteoporosis; for example, there is an increased

Figure 4 Mortise view of ankle showing hindfoot nail used in fixation of bimalleolar ankle fracture in a patient with osteopenia.

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2 Kannus P, Palvanen M, Niemi S, Parkkari J, Jarvinen M. Stabilizing incidence of low-trauma ankle fractures in elderly people Finnish statistics in 1970e2006 and prediction for the future. Bone 2008; 43: 340e2. 3 Hasselman CT, Vogt MT, Stone KL, Cauley JA, Conti SF. Foot and ankle fractures in elderly white women. Incidence and risk factors. J Bone Joint Surg Am 2003; 85-A: 820e4. 4 Greenfield DM, Eastell R. Risk factors for ankle fracture. Osteoporos Int 2001; 12: 97e103. 5 Seeley DG, Kelsey J, Jergas M, Nevitt MC. Predictors of ankle and foot fractures in older women. The Study of Osteoporotic Fractures Research Group. J Bone Miner Res 1996; 11: 1347e55. 6 Strauss EJ, Egol KA. The management of ankle fractures in the elderly. Injury 2007; 38(suppl 3): S2e9. 7 Salai M, Dudkiewicz I, Novikov I, Amit Y, Chechick A. The epidemic of ankle fractures in the elderly e is surgical treatment warranted? Arch Orthop Trauma Surg 2000; 120: 511e3. 8 Vioreanu M, Brophy S, Dudeney S, et al. Displaced ankle fractures in the geriatric population: operative or non-operative treatment. Foot Ankle Surg 2007; 13: 10e4. 9 Makwana NK, Bhowal B, Harper WM, Hui AW. Conservative versus operative treatment for displaced ankle fractures in patients over 55 years of age. A prospective, randomised study. J Bone Joint Surg Br 2001; 83: 525e9. 10 Koval KJ, Zhou W, Sparks MJ, Cantu RV, Hecht P, Lurie J. Complications after ankle fracture in elderly patients. Foot Ankle Int 2007; 28: 1249e55. 11 Petrisor BA, Poolman R, Koval K, Tornetta 3rd P, Bhandari M. Management of displaced ankle fractures. J Orthop Trauma 2006; 20: 515e8. 12 Willett K, Hearn TC, Cuncins AV. Biomechanical testing of a new design for Schanz pedicle screws. J Orthop Trauma 1993; 7: 375e80. 13 Panchbhavi VK, Vallurupalli S, Morris R. Comparison of augmentation methods for internal fixation of osteoporotic ankle fractures. Foot Ankle Int 2009; 30: 696e703. 14 Koval KJ, Petraco DM, Kummer FJ, Bharam S. A new technique for complex fibula fracture fixation in the elderly: a clinical and biomechanical evaluation. J Orthop Trauma 1997; 11: 28e33. 15 Pritchett JW. Rush rods versus plate osteosyntheses for unstable ankle fractures in the elderly. Orthop Rev 1993; 22: 691e6. 16 Ramasamy PR, Sherry P. The role of a fibular nail in the management of Weber type B ankle fractures in elderly patients with osteoporotic bone e a preliminary report. Injury 2001; 32: 477e85. 17 Freeman AL, Tornetta 3rd P, Schmidt A, Bechtold J, Ricci W, Fleming M. How much do locked screws add to the fixation of “hybrid” plate constructs in osteoporotic bone? J Orthop Trauma 2010; 24: 163e9. 18 Kim T, Ayturk UM, Haskell A, Miclau T, Puttlitz CM. Fixation of osteoporotic distal fibula fractures: a biomechanical comparison of locking versus conventional plates. J Foot Ankle Surg 2007; 46: 2e6. 19 Schepers T, Lieshout EM, Vries MR, Van der Elst M. Increased rates of wound complications with locking plates in distal fibular fractures. Injury 2011. 20 Hess F, Sommer C. Minimally invasive plate osteosynthesis of the distal fibula with the locking compression plate: first experience of 20 cases. J Orthop Trauma 2011; 25: 110e5. 21 Cornell CN. Internal fracture fixation in patients with osteoporosis. J Am Acad Orthop Surg 2003; 11: 109e19.

prevalence of peripheral arterial disease in osteoporotic postmenopausal women compared with age-matched women with normal bone density.29 However as bi-malleolar and tri-malleolar fractures occur more commonly in osteoporotic bone, osteoporosis is itself associated with increased risk of reoperation. The strongest risk factor for post-operative complications in elderly ankle fractures is complicated diabetes, defined as diabetes with end organ damage, such as peripheral neuropathy or arterial disease. Compared to patients with uncomplicated diabetes these patients have 3.8 times increased risk of overall complications, 3.4 times increased risk of non-infectious complications (e.g. malunion or nonunion) and five times higher likelihood of needing revision surgery.30 The cumulative effect of co-morbidities has not been evaluated, but it is obvious that the risks associated with operative treatment of, for example, a tri-malleolar ankle fracture in a frail osteoporotic patient with obesity or complicated diabetes will be high. In such patients particular care must be taken to reduce the risks. Nonoperative treatment may be attractive at first sight but, unfortunately, it is this group of patients who are least likely to be able to manage non-weight bearing protocols required by treatment in a cast. These patients are also at risk from the complications of poor mobility and prolonged inpatient care. Thus many surgeons favour an aggressive treatment strategy in such patients to provide sufficient ankle stability for early ambulation.

The future Currently a large British multi-centre randomized study to compare non-operative versus operative treatment in elderly ankle fractures is half complete.31 The researchers are comparing close contact casting e a technique adapted from total contact casting used in diabetics with frail skin e against standard open reduction and internal fixation techniques. It is interesting that this group recognizes that conventional casting may not be adequate in elderly ankle fractures and that a very specific casting technique is needed for these patients. The same argument could be true for operative treatment, where standard fixation techniques may not be adequate and modifications may be needed.

Conclusion Osteoporotic ankle fractures in the elderly present particular challenges, especially as they have a high level of co-morbidities, particularly complicated diabetes. Non-operative cast immobilization is associated with high risk of fracture displacement and does not facilitate early weight bearing and mobilization in a group of patients for whom immobility is contra-indicated. Attempts to decrease the risks associated with surgery in this group have included augmenting conventional stabilization techniques, avoiding placing direct lateral fibula plates and hindfoot nail fixation. To date there is no conclusive evidence as to the preferred method of treatment and further studies are needed. A

REFERENCES 1 Koval KJ, Lurie J, Zhou W, et al. Ankle fractures in the elderly: what you get depends on where you live and who you see. J Orthop Trauma 2005; 19: 635e9.

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22 Minihane KP, Lee C, Ahn C, Zhang LQ, Merk BR. Comparison of lateral locking plate and antiglide plate for fixation of distal fibular fractures in osteoporotic bone: a biomechanical study. J Orthop Trauma 2006; 20: 562e6. 23 Collinge C, Merk B, Lautenschlager EP. Mechanical evaluation of fracture fixation augmented with tricalcium phosphate bone cement in a porous osteoporotic cancellous bone model. J Orthop Trauma 2007; 21: 124e8. 24 Lemon M, Somayaji HS, Khaleel A, Elliott DS. Fragility fractures of the ankle: stabilisation with an expandable calcaneotalotibial nail. J Bone Joint Surg Br 2005; 87: 809e13. 25 Amirfeyz R, Bacon A, Ling J, et al. Fixation of ankle fragility fractures by tibiotalocalcaneal nail. Arch Orthop Trauma Surg 2008; 128: 423e8. 26 Olerud C, Molander H. A scoring scale for symptom evaluation after ankle fracture. Arch Orthop Trauma Surg 1984; 103: 190e4.

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27 Childress HM. Vertical transarticular pin fixation for unstable ankle fractures: impressions after 16 years of experience. Clin Orthop Relat Res 1976; 120: 164e71. 28 SooHoo NF, Krenek L, Eagan MJ, Gurbani B, Ko CY, Zingmond DS. Complication rates following open reduction and internal fixation of ankle fractures. J Bone Joint Surg Am 2009; 91: 1042e9. 29 Mangiafico RA, Russo E, Riccobene S, et al. Increased prevalence of peripheral arterial disease in osteoporotic postmenopausal women. J Bone Miner Metab 2006; 24: 125e31. 30 Wukich DK, Joseph A, Ryan M, Ramirez C, Irrgang JJ. Outcomes of ankle fractures in patients with uncomplicated versus complicated diabetes. Foot Ankle Int 2011; 32: 120e30. 31 Ankle Injury Management Trial. http://wwwndorms.ox.ac.uk/ clinicaltrials.php?trial¼aim

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(iv) Hindfoot arthritis

Other causes of ankle arthritis include inflammatory arthritis, avascular necrosis of the talus, congenital deformity, sepsis, haemophilia, pigmented villonodular synovitis and as a result of previous ankle surgery. Rheumatoid arthritis (RA) is the most common inflammatory arthropathy causing ankle arthritis. Fifty per cent of RA patients can be found to have ankle hindfoot involvement.6 However, most patients will also have involvement of the hindfoot, midfoot and forefoot in addition, and coupled with bone destruction and deformity, immunosuppression and polyarticular arthropathy poses significant challenges to the treatment of these patients. Other inflammatory arthritides that commonly affect the ankle are sarcoidosis and psoriatic arthritis. Sepsis can lead to ankle arthritis, with common infective organisms being Staphylococcus, Streptococcus, gonococcus and meningococcus.7 Patients with a bleeding disorder such as haemophilia may suffer repeated episodes of intra-articular bleeding, which can in turn lead to arthritis. Surgical management of these patients often requires a multidisciplinary approach and is best undertaken in centres where the relevant skill base is available.

Paul Hodgson Kartik Hariharan

Abstract Ankle and subtalar arthritis are commonly encountered by foot and ankle surgeons, but their prevalence is not as common as arthritis of the hip or knee. Trauma is the most common aetiology for both, but primary osteoarthritis and inflammatory arthropathies are also encountered. Clinical and radiological assessments are vital for correct diagnosis and for formulating an appropriate management plan. The recognition of abnormal alignment is particularly important as failure to do so will result in poor clinical outcomes of treatment. Both conditions can be managed using non-operative and operative treatment. Ankle arthritis in particular has generated much controversy with regards to the definitive treatments of arthrodesis and arthroplasty.

Keywords ankle joint; arthritis; arthrodesis; arthroplasty; subtalar joint

Anatomy and pathomechanics The low incidence of primary OA of the ankle is surprising, given that the ankle joint experiences a greater force per unit area than either the hip or the knee. This can be explained by several factors in which the ankle differs from these joints. First, the thickness of the articular cartilage of the ankle is less, and more uniform than that of the knee.8 Thinner articular cartilage has a higher compressive modulus i.e. stiffer cartilage (there is an inversely proportional relationship between cartilage thickness and compressive modulus), and thinner cartilage tends to allow for increased joint congruency. The ankle moves mainly as a rolling joint as oppose to the rolling, sliding and rotational movement seen in the knee. Therefore the ankle maintains congruency throughout movement and at high loads, again protecting against degeneration.9 The histological appearance of ankle articular cartilage differs from that of the hip and knee; the superficial layer makes up a higher proportion of the overall cartilage thickness in the ankle, and as the superficial regions are more responsible for compressive deformity this may play an important role in resistance to development of OA.9 Several studies have demonstrated that there are significant differences between the biochemical and biomechanical properties of ankle versus knee cartilage, ankle cartilage having a lower water content and a higher sulphated-glycosaminoglycan (sGAG) and collagen content, with a higher equilibrium modulus and dynamic stiffness.9 Interestingly, chondrocytes derived from ankle cartilage are less susceptible to the effects of soluble proinflammatory mediators and cytokines, including interleukin 1 (IL-1) and fibronectin fragments.10 In addition to this they do not express mRNA from key degradatory enzymes, including matrix metalloproteinase-8 (MMP-8), which play important roles in the development and progression of OA.11 These findings suggest that the ankle cartilage may possess intrinsic properties that protect it from developing primary OA. Disruption of normal joint loading mechanics predisposes cartilage to degenerative changes. This is clinically evident in the

Ankle arthritis Prevalence The prevalence of osteoarthritis (OA) of the ankle is thought to be 1% worldwide.1 Primary OA of the ankle is relatively rare, with approximately nine times more patients presenting with primary osteoarthritis of the hip or knee. In one study, the clinical incidence of OA was reported as 41% in the knee but only 4.4% in the ankle.2 An inspection of 50 cadavers for the presence of degenerative morphological changes classified 66% of knees compared to only 21% of ankles with severe degeneration.3 In terms of patient numbers, total knee replacement is performed more than 20 times more frequently than ankle arthrodesis and replacement combined.4 Aetiology Epidemiological studies indicate that trauma is the most common cause of ankle OA, but ankle OA may be associated with several associated risk factors including ageing, obesity, joint malalignment and genetic predisposition.5 In a study of 406 ankles with end-stage OA, post-traumatic OA accounted for 78%, 13% was secondary arthritis and primary OA accounted for only 9% of the cases. Of the 78% of post-traumatic OA cases, 62% was attributed to fracture events and 16% to ligamentous posttraumatic OA1 (Figure 1).

Paul Hodgson MB BCh MRCS(Eng) FRCS(Orth) Specialist Registrar Orthopaedics, Royal Gwent Hospital, Newport, UK. Conflicts of interest: none. Kartik Hariharan MBBS FRCSI FRCS(Orth) Consultant Orthopaedic Surgeon, Royal Gwent Hospital, Newport, UK. Conflicts of interest: none.

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Figure 1 Radiographs demonstrating ankle OA secondary to chronic lateral ligament instability (a) and following an ankle fracture (b).

post-traumatic ankle, either due to mal-union of fractures or chronic ligamentous instability. Congruency of the ankle joint plays an important role in preventing primary OA, therefore any mal-union seen after a fracture can alter the contact area and stresses. This has been demonstrated in cadaveric studies, showing that 1 mm lateral talar shift reduces the contact area between 15% and 42%.12,13 This may also depend on the integrity of the medial ligaments.13 In addition to this, fractures that lead to angular deformity at the ankle (such as tibial shaft fractures) also significantly increase the risk of subsequent ankle OA. It is unlikely that a single soft tissue injury will lead to ongoing problems, but recurrent instability might do.14 Patients presenting with ankle OA frequently give a history of recurrent giving way and instability, and arthroscopic studies of ankles with chronic instability have confirmed evidence of chondral damage.15

treatment. An indication of this should have been gained from a thorough patient history, which may reveal co-morbidities such as diabetes and vascular disease. This will also reveal previous trauma and surgery to the foot or ankle. Radiographic evaluation Plain radiographs (AP and lateral) should be obtained of the ankle and foot with the patient weightbearing. This will reveal the extent of ankle OA and alignment, but will also show evidence of degenerative disease in the subtalar and midfoot joints. A grade (0e3) of ankle OA can be given on the basis of the X-ray findings using the classification system described by Pell, Myerson and Schon.16 If there is concern about the presence of degeneration in the subtalar and/or midfoot joints then further imaging can be useful (e.g. Broden subtalar view, CT, MRI). At times it can be difficult to establish the joint responsible for the patient’s pain, and in these circumstances selective joint injections under image guidance can be very helpful for aiding formulation of a management plan.

Clinical evaluation Patients usually present with pain, which is felt both anteriorly and in the medial and lateral gutters. Rest or night pain is uncommon, and the pain is usually exacerbated by standing and walking. Stiffness is a common complaint, limiting patient mobility. Alternatively, some patients report instability, which may indicate this being the cause of OA, but more often the ankle giving way is precipitated by pain and is indicative of a functional instability. Examination findings are important and guide decisions on the most appropriate treatment. It is important to establish the hindfoot alignment in the coronal plane, and whether such deformity is correctable. The range of ankle movement is an important finding, including the presence of any equinus deformity. This should be examined eliminating movements in the subtalar and midfoot joints. Dorsi-flexion is usually more reduced than plantar flexion because of large anterior osteophytes. The use of walking aids should be documented, and footwear examined to assess patterns of wear. It is also important to palpate and move the subtalar and midfoot joints to assess if there are any signs of degenerative disease in these joints, as this may have a significant bearing on treatment options. A full neurovascular examination of the extremity is mandatory, again because any abnormality may influence

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Treatment The treatment options for ankle arthritis can be either nonoperative or operative. The clinician’s decision is based on the level of symptoms, clinical and radiological findings, and the general condition of the patient. It is important to equate the level of symptoms with the need for surgical intervention, which is not without risk. Non-operative treatment: simple measures, including lifestyle modification and weight loss, can sometimes be sufficient. Lifestyle changes may range from stopping certain sporting activities to an alteration in working patterns. Weight loss decreases the joint reactive forces in an exponential manner and can therefore be very effective. Medical therapy can include simple analgesia, opioid analgesia or non-steroidal anti-inflammatory drugs. Care must be taken to minimize side effects such as gastroenterological sequelae. Treatments such as chondroitin sulphate and glucosamine have no strong evidence to support their use, but some patients may benefit from taking them.

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Other than oral medications, intra-articular injections of corticosteroids can improve pain by reducing inflammation.17 In the majority of patients the effects tend to be only temporary, and most clinicians are concerned about the potential for joint sepsis with repeated use. Hyaluronic acid injection preparations (e.g. Synvisc) have no clinical evidence to support their use. Orthoses can be useful in improving pain, gait and stability. This can be in the form of modified footwear or an ankle support/brace. Gait pattern can be improved by using a rocker bottom sole or a solid ankle cushioned heel (SACH) shoe. A period of time of ankle immobilization in a walking plaster or boot can reduce pain felt with acute inflammation, or give the patient and surgeon an indication of what an ankle arthrodesis might provide.

There is insufficient literature to draw conclusions on the success of this technique, but it can be used for patients with mal-alignment (such as after fracture mal-union) and partial articular involvement. Joint sacrificing surgery Ankle arthrodesis e ankle arthrodesis has been considered the gold standard treatment for end-stage ankle OA, and in particular post-traumatic OA.21 It still remains the treatment of choice in the young and active patient, in whom an ankle replacement may wear or loosen prematurely because of high demands and physical load. Other indications include OA secondary to previous sepsis, inflammatory arthritis, large osteochondral defects and talar avascular necrosis. It can also be used as a salvage procedure for failed ankle arthroplasty.22 There is a wide variety of methods/techniques that can be used, but it is generally accepted that the optimum position for fusion is neutral dorsi-flexion, 5 of hindfoot valgus and external rotation equal to that of the contra-lateral leg (or 5e10 if the other side is abnormal). The talus should be positioned in the axis of the tibia, as an anterior position causes an increased extension force on the knee during gait. Fusion in equinus leads to a vaulting gait as there is a premature heel rise during the stance phase.23 Ankle arthrodesis does carry a risk of non-union in the presence of risk factors e.g. smoking or the use of non-steroidal antiinflammatory drugs (NSAIDs). The overall surface area of fusion is relatively small and the foot creates a large lever arm across the ankle, causing large stresses across the fusion site. Occasionally there may be a paucity of blood supply on the talar side of the fusion, with avascular necrosis. Smoking is a significant risk factor with a relative risk of nonunion four times greater than in non-smokers.24 Other risk factors for non-union are infection, patient noncompliance, neuropathy and vascular compromise (including avascular necrosis of the talus). Surgical factors include malalignment and excessive stripping of the soft tissues. NSAIDs have been shown to contribute to fracture non-union,25 but there is no evidence to show reduced union in surgical arthrodesis. However, due to NSAIDs’ inhibitory effects on angiogenesis seen in fracture healing, some surgeons would avoid their use in the postoperative period after arthrodesis. Operative technique e the operative technique utilized is largely dependant on whether or not any deformity exists. Whatever the method used, adequate joint preparation, meticulous care of the soft tissues and adequate and optimal positioning of the arthrodesis are all of paramount importance in achieving optimal results. In those with deformity, an open technique is favoured. This can be performed using an anterior, anterior-lateral, lateral or a posterior approach. The lateral malleolus and sometimes the medial malleolus may require resection if there is significant angular deformity. The lateral approach requires excision of the distal fibula for joint access and it is common practice to then use this for cancellous bone graft, if healthy. When there is little or no deformity present the surgery can be performed using a mini-arthrotomy (one or two incision techniques) or arthroscopically.26 The latter has become more popular in recent years. It does require a surgeon with adequate experience in ankle arthroscopy, and the ability to convert to an open technique if required. Although the overall rate of fusion between the

Operative treatment: operative treatment can broadly be divided into joint sparing and joint sacrificing procedures. Joint preservation Ankle debridement e debridement can be performed using an open or arthroscopic technique, with the latter nowadays being favoured by most surgeons. It can address impinging osteophytes, inflamed synovium, impingement lesions, loose bodies and chondral defects.18 In rheumatoid patient synovectomy may be a suitable option if there are minimal erosions. Debridement is not suitable in end-stage OA or when there is marked deformity. Articular distraction e the use of a spanning external fixator, such as an Ilizarov frame, has been shown to provide improvement in symptoms in patients with post-traumatic OA.19 The procedure involves open or arthroscopic joint debridement followed by application of the fixator. The joint is then gradually distracted by 5 mm, in 1 mm increments per day. The patient is allowed to weight bear, and hinges can be incorporated after approximately 6 weeks to allow some ankle movement. The frame is usually removed between 12 and 15 weeks. It is postulated that with distraction, the joint surfaces are not in contact (even with loading) and this increases the hydrostatic pressure within the joint, which increases proteoglycan synthesis.19 Results using this technique have been varied in the few studies that have been carried out, with the good results of Marijnissen et al.19 not being repeated by others. There is no Level 1 evidence currently available to suggest the validity of this operation in the setting of ankle arthritis but anecdotal evidence suggests that it may have a role in the treatment of the early stages of the disease. Lateral ligament reconstruction  calcaneal osteotomy e patients with chronic lateral ligament deficiency may present with an isolated medial wear pattern and varus mal-alignment.14 Such patients should be assessed arthroscopically for the pattern of wear, and to check joint congruency when the joint is reduced. The lateral ligament complex can be reconstructed to provide joint stability and congruence.14 This may be augmented with the use of a lateralizing calcaneal osteotomy which serves to lateralize the ground reaction force and thereby spare the medial side. Supramalleolar osteotomy e corrective osteotomies to improve joint alignment and change loading patterns are more commonly performed for the hip and knee, but are occasionally used in the treatment of ankle arthritis in its earlier stages.20

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open and arthroscopic techniques is comparable, the latter is thought to have a faster time to union, less blood loss, less morbidity associated with wounds and soft tissues, shorter hospital stay and quicker mobilization.26 Surgeons with greater experience of arthroscopic arthrodesis have reported using this technique for patients with up to 15e25 of deformity, providing some of the hindfoot deformity can be corrected with a calcaneal osteotomy.26 The methods of fixation also vary. No evidence exists to suggest one method is superior, but options available can be broadly classified into external and internal fixation. Simple cast immobilization has also been described. External fixation was popularized by Charnley in the 1950s using a compression clamp device. Pins are placed transversely through the tibia and talus and are connected medially and laterally by compression clamps. The main disadvantage of this technique is that it provides very little rotational stability, and in view of this the technique was modified by Calandruccio to give a triangular configuration. Modern external fixators tend to incorporate fine wires (e.g. Ilizarov, TSF), and this technique can allow good compression in osteoporotic bone. This is also a useful technique in patients with a past history of infection and in those who have multiple scars or skin issues in the surgical field. Repositioning of the arthrodesis site and additional compression can be made relatively easily in an outpatient setting in addition to being able to keep the patient mobile. It is also useful in the presence of limb length discrepancy, when lengthening procedures can be incorporated into the process.27 The preferred option in most ankle fusions is internal fixation, which includes screws, plate fixation and on-lay grafts and intramedullary nails. Internal fixation is favoured because of the lower rate of non-union compared to external fixation, and it is much better tolerated by patients. The higher rate of union may be due to the fact that internal fixation provides greater rotational and sagittal stability than external fixation devices.28 Screw fixation has been shown to be superior to plates,21 with a higher rate of union. This is because greater compression can be achieved with screws. Plate fixation requires greater exposure and soft tissue stripping, which can adversely affect local bone vascularity. The orientation of screw placement varies significantly between surgeons, but it is widely accepted that at least two screws are required. Biomechanical studies have shown that crossed screws (Figure 2) provide a more rigid construct than two parallel screws,29 and the addition of a third screw adds to rotational stability.21 Most surgeons using an internal fixation technique adopt a postoperative regime of 6e8 weeks of non-weightbearing, protected by a plaster cast, followed by a further 6e8 weeks of partial or protected weightbearing. There is anecdotal evidence to suggest that the use of arthroscopic fusion techniques may allow earlier mobilization.26 Outcomes e the rate of union in recent studies using internal fixation methods has generally been greater than 90%. The investigation of choice to identify a non-union is CT (Figure 3). Treatment of a non-union depends on whether the patient is symptomatic. Some fibrous non-unions may be asymptomatic and may necessitate no further treatment. In symptomatic cases, the cause should be identified if possible, and measures taken to correct it. Revision fusion with bone graft

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Figure 2 Open ankle arthrodesis with excision of distal fibula and crossed compression screws.

harvested from the iliac crest is the standard technique although other forms of treatment including the use of synthetic bone substitutes and bone morphogenic proteins have also been used.30 Non-invasive low intensity pulsed ultrasound treatments have been used to promote union but there is no evidence to support this for arthrodesis. Other complications include infection, mal-alignment, neurovascular injury and thromboembolism. Late complications include prominent metalwork (necessitating removal) and tibial stress fractures. Long-term outcome studies have found that the majority of patients with a successful isolated ankle arthrodesis will develop substantial and accelerated arthritis in the ipsilateral foot (subtalar, talonavicular, naviculocuneiform, calcaneocuboid and tarsometatarsal joints) but not the knee, and that these changes correlate with reduced function and pain.31 However, others have reported that degenerative changes in these joint are radiologically evident prior to surgery, hence such changes may not be an actual consequence of ankle arthrodesis.32

Figure 3 Sagittal CT image demonstrating non-union of an ankle arthrodesis.

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Gait pattern is altered due to loss of ankle motion.33 Patients often report difficulty walking on uneven surfaces, and gait velocity as well as stride length are reduced resulting in poorer gait efficiency. This can be improved by the use of an orthosis with a rocker bottom sole. Arthrodesis may lead to limb length loss and require a shoe augment. Ankle arthroplasty e the use of total ankle replacement (TAR) is becoming an increasingly popular alternative to arthrodesis in patients with end-stage ankle arthritis (Figure 4). TAR was first introduced in the 1970s and over 20 different types of prosthesis have been developed. Early designs tended to yield poor results, with an unacceptably high complication rate, and most failed in the short and intermediate term.34 The increasing success and evolution of hip and knee arthroplasty provided the motivation for development of TAR with increased longevity and improved function. Indications e TAR is the main alternative to arthrodesis. It has been used in patients with rheumatoid arthritis. In primary and post-traumatic OA some surgeons would reserve the use of TAR to older or less physically active patients, with its use in higher demand patients being avoided because of the perceived risk of earlier failure. In these patients arthrodesis may be favoured. In patients with radiological evidence of ipsilateral midfoot and hindfoot OA, TAR may be a more favourable option than arthrodesis even in the younger patient, because of the risk of increasing symptoms in these joints with a fused ankle.31 Contra-indications to TAR are mal-alignment (valgus/varus), active or recent infection, vascular insufficiency, poor bone stock,

neurological impairment (including neuropathy e.g. Charcot), avascular necrosis of the talus and severe ankle joint laxity.35 A previous ankle arthrodesis can be converted to TAR but this is a challenging procedure and requires preservation of both malleoli.22 Subtalar deformity must also be assessed pre-operatively. Severe deformity may preclude the use of TAR, but in mild or moderate cases the arthroplasty may be coupled with a corrective calcaneal osteotomy or subtalar arthrodesis36 (Figure 5). Similarly, midfoot disease such as talonavicular arthritis can also be treated concomitantly. Prior to surgery, close attention should also be paid to identifying any longitudinal mal-alignment, for example from previous tibial fractures. Surgical approach e most surgeons and modern prosthetic designs favour implantation via an anterior approach, developing a plane between tibialis anterior and extensor hallucis longus so that the neurovascular bundle is protected by EHL during retraction, to gain adequate exposure.35 A sandbag can be placed under the ipsilateral buttock so that the ankle lies in neutral rotation, and a tourniquet is used. Following implantation of the prosthesis (according to the manufacturer’s guidelines), the capsule and extensor retinaculum should be closed, and most surgeons will use a single drain.35 At the time of surgery it is important to ensure that there is sufficient ankle dorsi-flexion. Failure to achieve dorsi-flexion beyond neutral will result in early failure. If this is the case then an Achilles tendon lengthening is advisable.

Figure 4 Radiographs showing a modern design total ankle replacement.

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Figure 5 AP and lateral radiographs showing a total ankle replacement combined with a calcaneal osteotomy to correct varus mal-alignment.

insufficient talar bone stock remaining (most commonly seen in rheumatoid patients), then tibio-talo-calcaneal fusion using an intramedullary device may be required. Arthrodesis or arthroplasty? e a recent systematic review evaluating the intermediate and long-term outcomes of both these options has found similar results in terms of scoring (using AOFOS scores), and revision rate; 9% and 7% for arthroplasty and arthrodesis respectively. The incidence of below knee amputation was 1% in the arthroplasty group and 5% in the arthrodesis group. The study concluded a lack of data to make a confident assessment of superiority and suggested that further comparative studies are required.38

Post-operative regimens may vary depending on the prosthetic design. For example, the Mobility (Depuy) design requires an anterior tibial bone block to be resected for implantation of the tibial component, which is then replaced. The recommendation is for a period of 4e6 weeks, plaster immobilization to allow consolidation. Other designs may not require this length of immobilization. Evolution of TAR e the first generation of TARs was introduced in the 1970s, with most designs comprising of two components. There were constrained and unconstrained designs, with almost all using cement fixation. The results for these prostheses were generally poor, with an unacceptably high complication rate, and most failed in the short and intermediate term.34 The increasing success in both design and outcomes of hip and knee arthroplasty, coupled with poor results from the first generation of TAR, led to the evolution of the second generation TAR. The medium-term outcomes of the newer generation of TAR appear to be encouraging, with 5-year survival greater than 90% and 20-year survival of almost 75%.37 Complications of TAR e some complications will be similar to those encountered with arthrodesis, and will often depend on patient factors. These include infection, wound problems and thromboembolism. If such surgery is performed in patients with co-morbidities, such as inflammatory arthritis, then they should be followed up regularly in the post-operative period to ensure that problems are identified early and treated. Other early complications are related to surgical technique and include neurovascular injury and fractures of malleoli (intra-operatively and post-operatively, when they may be stress fractures).35 Loosening is the most common late complication, with no identifiable cause in the majority, although this will be accelerated in cases with mal-alignment or component mal-position.35 Failure of a TAR represents a significant challenge irrespective of the cause. If the cause is infection then this will necessitate removal of the prosthesis and eradication of the infection. The treatment options then are arthrodesis22 (usually requiring bone graft) or in the worst cases below knee amputation. Even without infection, failure is usually associated with loss of bone stock, which will mean that revision arthroplasty is not feasible.22 Therefore, bone graft interposition arthodesis is required to best maintain leg length equality. In cases where there is

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Subtalar disease Disease of the subtalar joint usually presents with pain and instability when walking on uneven ground. Similarly to the ankle, primary OA of the subtalar joint is rare, and again the most common aetiology is trauma i.e. talus or calcaneal fractures, with the latter being more common.39 An acquired flatfoot deformity as a result of rupture or disruption of the tibialis posterior tendon results in subtalar joint deformity and disease, but this topic deserves a mini-symposium of its own and will therefore not be discussed here. Other subtalar joint pathologies include instability (which can be linked with ankle instability) and sinus tarsi syndrome. Subtalar OA Aetiology and prevalence: primary subtalar OA is rare and degeneration usually occurs as a consequence of trauma or instability. Other causes are inflammatory arthritides (in which case other surrounding joints are also usually affected) and tarsal coalition.39 The most common cause is a mal-united calcaneal fracture. Calcaneal fractures are the most common tarsal fractures (65%) and account for up to 2% of all fractures, usually as a result of a fall from height with men being affected more than twice as often as women. The long-term outcome of calcaneal fractures will depend on the severity of the injury and the treatment received. Studies have shown improved results with operative intervention of

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calcaneal fractures40 but even if a good reduction is achieved patients can still go on to develop symptomatic OA. However, it has been demonstrated that in patients requiring a subtalar fusion following a calcaneal fracture, those who were initially treated with operative fixation have better functional outcomes and fewer wound complications.41

Radiological assessment should include anteroposterior and lateral weightbearing views, axial calcaneal views and Broden’s view (foot in neutral flexion, leg internally rotated 30e40 ) (Figure 6). The X-ray is centred over lateral malleolus and four radiographs are taken, with the tube angled 40, 30, 20, and 10 towards the head of the patient to assess the subtalar posterior facet, although a more comprehensive assessment can be made using computerized tomography.43 Stephen and Sanders (1996) have described a CT classification graded into three types, depending on the presence of a large lateral exostosis, calcaneal body alignment and degree of subtalar joint OA.43 MRI may also be of benefit, showing more subtle changes of oedema isolated to the subtalar joint. Often, a diagnostic intraarticular injection is helpful to clarify that the symptoms are arising from the subtalar joint, and this may be useful in assessing the possible success of any potential subsequent subtalar fusion.

Anatomy and pathomechanics: the subtalar joint comprises of the inferior surface of the talus and the three articulating surfaces on the superior surface of the calcaneum; the anterior, middle and posterior facets. Its unique shape makes its movement complex, but in general terms it allows mobilization on uneven ground. It is closely coupled with the talonavicular and calcaneocuboid joints in allowing hindfoot motion and function. Mal-united intra-articular fractures often lead to deformity with patients having difficulty with proper fitting footwear. This is due to the heel profile being shortened and widened as a result of the fracture, with the heel widening also causing problems with lateral subtalar impingement, which may encroach on the peroneal tendons or the sural nerve. The intra-articular mal-union, as with any other joint, invariably will lead to degeneration and subsequently pain.40 With a joint depression type injury, the talus subsides somewhat and adopts a more dorsi-flexed position, which can in turn result in anterior ankle impingement and pain.42 The ankle joint may also be affected by varus (or less commonly valgus) mal-union of the heel, which will inevitably alter the loading pattern of the ankle joint (leading to eccentric wear).

Treatment: Non-operative treatment e appropriate management will depend on the level of symptoms, previous treatment and on patient factors dictating suitability for surgery. Non-operative treatment includes simple analgesia, steroid/ local anaesthetic injections and footwear modification or orthoses. Orthoses are designed to limit joint motion and loading and may range from an insole (UCBL type) to a custom made ankle-foot orthosis. Operative treatment e operative management needs to take into account the cause of the arthritis and hindfoot alignment. In some patients following a calcaneal fracture, the joint itself may be spared and pain can be due to impingement from a lateral exostosis. In this case joint preservation is possible and an exostectomy may be all that is required.43 Similarly, when the joint is relatively spared but heel malalignment is the main concern then a corrective osteotomy may be possible, which might avoid the need for fusion. With joint degeneration the operative treatment of choice is a subtalar arthrodesis.

Clinical and radiographic evaluation: careful clinical evaluation is essential to address the site of pain, alignment, tendon dysfunction (peronei) and sensory loss (sural and posterior tibial nerves). Pain is usually felt laterally, inferior to the fibula. Movement of the subtalar joint should be isolated and assessed for pain and reproduction of symptoms. As with assessment of the ankle, a careful neurovascular examination is mandatory, and indications of abnormalities will be alluded to in the patient’s history.

Figure 6 Broden’s view radiographs showing the posterior subtalar joint; normal (a) and with degenerative change following a calcaneal fracture (b).

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Figure 7 Lateral radiographs showing a seemingly united subtalar joint as part of a triple fusion (a), and sagittal CT image of the same patient showing non-union of the subtalar joint (b).

Sinus tarsi syndrome There is debate as to whether this is a real clinical entity or simply a reflection of other pathology. It was first described by O’Connor in 1958.46 The sinus tarsi is the cavity between the inferior aspect of the talar neck and the superior surface of the calcaneum, containing ligaments, nerves and vessels. It is postulated that injury to the nerves may cause hindfoot instability due to a loss of proprioception.47 Aetiologies include trauma (70%), inflammatory/crystal arthritides, pes cavus and planus, and chronic hindfoot instability. Histological assessment of the soft tissue has demonstrated synovial hypertrophy, haemosiderin deposition and scar tissue.47

Although joint preparation can be performed arthroscopically, the majority favour an open approach via a lateral utility incision i.e. from just below the tip of the fibula towards the base of the fourth metatarsal. Preparation of the posterior subtalar joint alone is usually sufficient.39 The need for bone graft will be determined by the degree of residual deformity, and the graft can usually be harvested from the ipsilateral iliac crest. Multiple methods of stabilization are available including staples, dowels and compression screws. Screws are the most popular method and most surgeons will introduce these via the calcaneus, although entry from the talus is also described. The number of screws used depends on surgeon preference, but using a single large calibre (6.5 mm or greater) compression screw does not yield inferior results to multiple screws.44 In cases with a calcaneal fracture mal-union and talar dorsiflexion causing anterior ankle impingement, it is important to restore the effective height of the calcaneum to relieve the anterior impingement. This can be achieved by performing a distraction fusion using an iliac crest tri-cortical bone graft.42 Post-operative regimens can vary between surgeons, but a commonly used regime is 6 weeks in a below knee plaster, nonweightbearing, followed by 6 weeks protected weightbearing in an orthotic boot. Outcomes e most studies report high success rates with primary subtalar fusion, regardless of the technique used, with union rates ranging between 86% and 100%.39 However, these figures may be falsely high given that clinical and radiological assessment methods may not identify all cases of non-union. The best method to assess union is using CT (Figure 7), and although this would be ideal in all cases it represents a large radiation dose and has resource and cost implications.39,45 It is recommended that any patient with persistent hindfoot pain should be assessed with CT to determine union. Using this method, it is estimated that union rates are approximately 95%.39 Other complications include infection, complex regional pain syndrome, nerve injury (superficial peroneal), tendon injury and prominent metalwork necessitating removal.39

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Figure 8 Sagittal T2 MRI image showing oedema localized to the sinus tarsi, in keeping with sinus tarsi syndrome.

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Figure 9 AP and lateral radiographs demonstrating a tibio-talar-calcaneal (TTC) fusion using an intramedullary retrograde nail.

ankle replacement and a subtalar fusion can give good results.36 This option is especially useful if pre-operative radiographs demonstrate evidence of midfoot degenerative change, as this is likely to become increasingly symptomatic if both joints are fused.27,31 If mal-alignment is present then TAR is contra-indicated because of the risk of early failure.36 In this situation fusion of both subtalar and ankle joints is the best option. This can be performed by individually fusing each joint, but a better option to provide more stability and rotational stiffness is the use of a tibio-talar-calcaneal intramedullary retrograde nail49,50 (Figure 9). With modern designs, compression can be applied to each joint, increasing the chance of union.

The syndrome presents with chronic lateral ankle pain and symptoms of instability, especially when walking on uneven surfaces. Pain is usually related to activity and resolves at rest. Symptoms may be reproduced on clinical examination by inverting and everting the hindfoot. Symptoms are usually eliminated for several hours with an injection of local anaesthetic into the cavity.47 Plain radiographs including stress views are usually normal. Arthrogram examination may reveal a complete absence of the micro recesses along the interosseous ligament that are seen in a normal example.47 MRI may demonstrate oedema localized to the sinus tarsi (Figure 8). Electromyography (EMG) shows abnormal reduction or complete loss of electrical activity in the peroneus brevis and longus during gait, with a reversal of these abnormalities after local anaesthetic injection into the sinus.47 Non-operative treatment entails repeated hydrocortisone injections, immobilization and orthoses to correct any hindfoot mal-alignment that may be present. The success of these measures is approximately 60%.47,48 In cases that do not respond, surgical intervention may be required. This can range from sinus tarsi debridement (ensuring that the interosseous ligament is preserved) to subtalar fusion in recalcitrant cases.47,48

Conclusion Hindfoot arthritis involving the ankle, subtalar joint or both is less common than that of the hip and knee. The most common cause for degenerative change in both joints is trauma. It is important to make a full clinical and radiological assessment of each patient in order to make appropriate management plans. Important factors to assess are: - Medical co-morbidities that may increase the risk of postoperative complications - Neurovascular status of the limb - Joint movement (and associated pain) and alignment - Site of pain/symptoms; diagnostic local anaesthetic injections are often helpful - Patient expectations - Radiological examination; weightbearing X-rays, CT, MRI. There is a wide range of treatment options, and each case must be assessed individually to provide the patient with appropriate treatment. Options include: - Non-operative treatments; lifestyle changes, analgesia, orthoses, therapeutic injections - Joint sparing surgery - Joint sacrificing surgery; TAR, arthrodesis.

Combined disease In some patients, degenerative change in both the ankle and subtalar joints may co-exist. This is more commonly seen in inflammatory conditions such as rheumatoid arthritis. The management of such patients can be challenging, and conservative measures such as orthoses should be considered. Key concerns that must be taken into account are alignment, site/source of pain, mobility of joints involved, condition of midfoot/forefoot joints and patient factors such as vascularity and body habitus. If no significant mal-alignment is present and the ankle joint retains a reasonable range of movement, then combining a total

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18 Cheng JC, Ferkel RD. The role of arthroscopy in ankle and subtalar degenerative joint disease. Clin Orthop Relat Res 1998; 349: 65e7. 19 Marijnissen AC, Van Roermund PM, Van Melkebeek J, et al. Clinical benefit of joint distraction in the treatment of severe osteoarthritis of the ankle: proof of concept in an open prospective study and in a randomized controlled study. Arthritis Rheum 2002; 46: 2893e902. 20 Takakura Y, Tanaka Y, Kumai T, Tamai S. Low tibial osteotomy for osteoarthritis of the ankle. Results of a new operation in 18 patients. J Bone Joint Surg Br 1995; 77: 50e4. 21 Mann RA, Rongstad KM. Arthrodesis of the ankle: a critical analysis. Foot Ankle Int 1998; 19: 3e9. 22 Hopgood P, Kumar R, Wood PL. Ankle arthrodesis for failed total ankle replacement. J Bone Joint Surg Br 2006; 88: 1032e8. 23 Coughlin MJ, Mann RA, Saltzman CL. Surgery of the foot and ankle. 8th edn. Mosby Inc, 2007; 93. 24 Cobb TK, Gabrielsen TA, Campbell DC, Wallrichs SL, Ilstrup DM. Cigarette smoking and nonunion after ankle arthrodesis. Foot Ankle Int 1994; 15: 64e7. 25 Murnaghan M, Li G, Marsh DR. Nonsteroidal anti-inflammatory druginduced fracture nonunion: an inhibition of angiogenesis? J Bone Joint Surg Am 2006; 88: 140e7. 26 Winson IG, Robinson DE, Allen PE. Arthroscopic ankle arthrodesis. J Bone Joint Surg Br 2005; 87: 343e7. 27 Harris N. Ankle arthritis. Curr Orthop 2001; 15: 352e5. 28 Thordarson DB, Markolf KL, Cracchiolo A. Arthrodesis of the ankle with cancellous-bone screws and fibular strut graft. Biomechanical analysis. J Bone Joint Surg Am 1990; 72: 1359e63. 29 Friedman RL, Glisson RR, Nunley JA. A biomechanical comparative analysis of two techniques for tibiotalar arthrodesis. Foot Ankle Int 1994; 15: 301e5. 30 Bibbo C. Practical use of adjuvant rhBMP-2 to augment bone healing in foot and ankle surgery. Techniques in Orthopaedics 2011; 26: 28e31. 31 Coester LM, Saltzman CL, Leupold J, Pontarelli W. Long term results following ankle arthrodesis for post-traumatic arthritis. J Bone Joint Surg Am 2001; 83: 219e28. 32 Sheridan BD, Robinson DE, Hubble MJW, Winson IG. Ankle arthrodesis and its relationship to ipsilateral arthritis of the hind- and midfoot. J Bone Joint Surg Br 2006; 88: 206e7. 33 King HA, Watkins TB, Samuelson KM. Analysis of foot position in ankle arthrodesis and its influence on gait. Foot Ankle 1980; 1: 44e9. 34 Bolton-Maggs BG, Sudlow RA, Freeman MA. Total ankle arthroplasty. A long-term review of the London Hospital experience. J Bone Joint Surg Br 1985; 67: 785e90. 35 Jackson MP, Singh D. Total ankle replacement. Curr Orthop 2003; 17: 292e8. 36 Kim BS, Knupp M, Zwicky L, Lee JW, Hintermann B. Total ankle replacement in association with hindfoot fusion: outcome and complications. J Bone Joint Surg Br 2010; 92: 1540e7. 37 Buechel Sr FF, Buechel Jr FF, Pappas MJ. Twenty-year evaluation of cementless mobile-bearing total ankle replacements. Clin Orthop Relat Res 2004; 424: 19e26. 38 Haddad SL, Coetzee JC, Estok R, Fahrbach K, Banel D, Nalysnyk L. Intermediate and long-term outcomes of total ankle arthroplasty and ankle arthrodesis: a systematic review of the literature. J Bone Joint Surg Am 2007; 89: 1899e905. 39 Davies MB, Rosenfeld PF, Stavrou P, Saxby TS. A comprehensive review of subtalar arthrodesis. Foot Ankle Int 2007; 28: 295e7. 40 Buckley R, Tough S, McCormack R, et al. Operative compared with nonoperative treatment of displaced intra-articular calcaneal

Complications are not infrequent and patients must be counselled and consented appropriately prior to embarking on surgery. Patients should be encouraged to titrate their level of symptoms against the need for surgery and potential risks. Potential complications include: - Infection, which may lead to limb loss in severe cases - Non-union in arthrodesis - Loosening and component subsidence in TAR - Thromboembolism - Potential accelerated degenerative changes in surrounding joints with arthrodesis. A

REFERENCES 1 Valderrabano V, Horisberger M, Russell I, Dougall H, Hintermann B. Etiology of ankle osteoarthritis. Clin Orthop Relat Res 2008; 467: 1800e6. 2 Cushnaghan J, Dieppe P. Study of 500 patients with limb joint osteoarthritis. Analysis by age, sex, and distribution of symptomatic joint sites. Ann Rheum Dis 1991; 50: 8e13. 3 Muehleman C, Bareither D, Huch K, Cole AA, Kuettner KE. Prevalence of degenerative morphological changes in the joints of the lower extremity. Osteoarthr Cartil 1997; 5: 23e37. 4 Praemer A, Furner S, Rice DP. Musculoskeletal conditions in the United States. 1st edn. Park Ridge, III: American Academy of Orthopedic Surgeons, 1992. 5 Saltzman CL, Salamon ML, Blanchard GM, et al. Epidemiology of ankle arthritis: report of a consecutive series of 639 patients from a tertiary orthopaedic center. Iowa Orthop J 2005; 25: 44e6. 6 Rush J. Management of the rheumatoid ankle and hindfoot. Curr Orthop 1996; 10: 174e8. 7 Hirsch E, Sherman M, Lenet MD. Gonococcal arthritis. J Am Podiatr Med Assoc 1989; 79: 190e4. 8 Shepherd DE, Seedhom BB. Thickness of human articular cartilage in joints of the lower limb. Ann Rheum Dis 1999; 58: 27e34. 9 Treppo S, Koepp H, Quan EC, Cole AA, Kuettner KE, Grodzinsky AJ. Comparison of biomechanical and biochemical properties of cartilage from human knee and ankle pairs. J Orthop Res 2000; 18: 739e48. 10 Cole AA, Kuettner KE. Molecular basis for differences between human joints. Cell Mol Life Sci 2002; 59: 19e26. 11 Chubinskaya S, Kuettner KE, Cole AA. Expression of matrix metalloproteinases in normal and damaged articular cartilage from human knee and ankle joints. Lab Invest 1999; 79: 1669e77. 12 Ramsey PL, Hamilton W. Changes in tibiotalar area of contact caused by lateral talar shift. J Bone Joint Surg Am 1976; 58: 356e7. 13 Clarke HJ, Michelson JD, Cox QG, Jinnah RH. Tibio-talar stability in bimalleolar ankle fractures: a dynamic in vitro contact area study. Foot Ankle 1991; 11: 222e7. 14 Harrington KD. Degenerative arthritis of the ankle secondary to longstanding lateral ligament instability. J Bone Joint Surg Am 1979; 61: 354e61. 15 Taga I, Shino K, Inoue M, Nakata K, Maeda A. Articular cartilage lesions in ankles with lateral ligament injury. An arthroscopic study. Am J Sports Med 1993; 21: 120e6. 16 Pell RF, Myerson MS, Schon LC. Clinical outcome after primary triple arthrodesis. J Bone Joint Surg Am 2000; 82: 47e57. 17 Friedman DM, Moore ME. The efficacy of intra-articular steroids in osteoarthritis: a double-blind study. J Rheumatol 1980; 7: 850e6.

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41

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44 45

fractures: a prospective, randomized, controlled multicenter trial. J Bone Joint Surg Am 2002; 84-A: 1733e44. Radnay CS, Clare MP, Sanders RW. Subtalar fusion after displaced intra-articular calcaneal fractures: does initial operative treatment matter? J Bone Joint Surg Am 2009; 91: 541e6. Carr JB, Hansen ST, Benirschke SK. Subtalar distraction bone block fusion for late complications of os calcis fractures. Foot Ankle 1988; 9: 81e6. Stephens HM, Sanders R. Calcaneal malunions: results of a prognostic computed tomography classification system. Foot Ankle Int 1996; 17: 395e401. Mann RA, Beaman DN, Horton GA. Isolated subtalar arthrodesis. Foot Ankle Int 1998; 19: 511e9. Coughlin MJ, Grimes JS, Traughber PD, Jones CP. Comparison of radiographs and CT scans in the prospective evaluation of the

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49

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fusion of hindfoot arthrodesis. Foot Ankle Int 2006; 27: 780e7. O’Connor D. Sinus tarsi syndrome: a clinical entity. J Bone Joint Surg Am 1958; 40A: 720. Taillard W, Meyer JM, Garcia J, Blanc Y. The sinus tarsi syndrome. Int Orthop 1981; 5: 117e30. Bernstein RH, Bartolomei FJ, McCarthy DJ. Sinus tarsi syndrome. Anatomical, clinical, and surgical considerations. J Am Podiatr Med Assoc 1985; 75: 475e80. Niinim€aki TT, Klemola TM, Leppilahti JI. Tibiotalocalcaneal arthrodesis with a compressive retrograde intramedullary nail: a report of 34 consecutive patients. Foot Ankle Int 2007; 28: 431e4. Pelton K, Hofer JK, Thordarson DB. Tibiotalocalcaneal arthrodesis using a dynamically locked retrograde intramedullary nail. Foot Ankle Int 2006; 27: 759e63.

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(v) Chronic ankle instability

history, physical examination and radiological investigations but consideration of the pathomechanics of the condition.

Hiro Tanaka Ankle joint anatomy and biomechanics

Lyndon Mason

The ankle joint complex consists of three articulations: the talocrural, subtalar and distal tibiofibular joints. The three joints work together to allow coordinated movement of the hindfoot in three cardinal planes: the sagittal plane (plantarflexionedorsiflexion), the frontal plane (inversioneeversion) and the transverse plane (internal and external rotation). Hindfoot motion does not occur in isolation but rather in a coordinated, coupled motion best described as pronation (dorsiflexion, eversion and external rotation) and supination (plantarflexion, inversion and internal rotation).4 The talocrural joint or ‘mortice’ is formed by the articulation of the dome of the talus, the medial malleolus, the tibial plafond and the lateral malleolus. In isolation, the ankle joint is a modified hinge joint allowing dorsiflexion and plantarflexion. The sagittal plane motion of the ankle joint passes through the tips of the malleoli. Since the lateral malleolus is longer and is posterior to the medial malleolus, the plane is oblique to the plane of the floor and also to the transverse plane. As the ankle dorsiflexes, it also rotates externally and vice versa.5 The biomechanics of the ankle is complex, with three factors contributing to stability. In a loaded ankle the osseous anatomy is the most critical as the talus compresses into the bony mortice resulting in primary stability. In an unloaded ankle a combination of static ligamentous restraints and musculotendinous units play more vital roles, with each ankle ligament contributing a different function depending of the position of the foot and ankle in space.

Abstract Injuries to the ligaments of the ankle are common, especially in athletes. Symptomatic ankle instability develops in as many as 10e40% following an acute injury. The causes of symptoms are multifactorial, encompassing pre-existing patient factors predisposing to instability, functional instability and mechanical instability. Chronic ankle instability occurs when patients suffer recurrent episodes of ankle sprains and the majority can be successfully treated with a functional rehabilitation programme. Those that fail require consideration of surgical intervention. A full history, clinical examination, radiological investigation and an understanding of the pathomechanics involved are vital to ensure that the most appropriate surgical strategy is adopted. Pain and swelling are commonly associated symptoms and may be more disabling than the episodes of instability. Concurrent intra and extra-articular pathologies must be addressed to achieve a successful functional outcome. Surgical options include arthroscopy, ligament reconstruction techniques, hindfoot alignment procedures and gastrocnemius release. This article focuses on the anatomy, pathomechanics and treatment of chronic lateral ankle instability. Medial, syndesmotic and subtalar instability are also discussed.

Keywords ankle injuries; ankle joint; joint instability; lateral ligament ankle; subtalar joint

Lateral ligaments The lateral ankle ligament complex is composed of three main ligaments: the anterior talofibular, calcaneofibular and posterior talofibular ligaments (Figure 1). The anterior talofibular ligament (ATFL) is the weakest of the lateral ligaments. It has a load to failure 2e3.5 times lower than the calcaneofibular ligament (CFL) and two times lower than the posterior talofibular ligament

Introduction Injuries to the lateral ankle ligament complex or “ankle sprains” are the commonest sports related injury, accounting for 16e21% of all musculoskeletal injuries. The incidence in the UK of 52.7/ 10 000/year equates to 300 000 injuries/year.1 Following ankle injury the majority of patients undergo a functional rehabilitation programme, which is usually successful in returning patients to functional normality. There is little role for surgery in the acute phase.2 However, some patients develop residual symptoms of pain and/or instability as a consequence, which may be underestimated in clinical practice. Symptomatic ankle instability can develop in as many as 10e40% of patients following an acute event, even after adequate conservative treatment.3 Chronic ankle instability does not exist as a single pathologic entity and the symptoms of “sprained ankle syndrome” are frequently multifactorial. Treatment is not only based upon a proper

Lateral ligament complex of the ankle

Posterior talofibular ligament

Hiro Tanaka MB BCh MSc FRCS(Ed) FRCS(T&O) Consultant Orthopaedic Surgeon, Royal Gwent Hospital, Newport, UK. Conflicts of interest: none.

Calcaneofibular ligament

Lyndon Mason MB BCh MRCS Specialist Registrar Orthopaedics, Royal Gwent Hospital, Newport, UK. Conflicts of interest: none.

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Anterior talofibular ligament

Figure 1 The lateral ligament complex of the ankle (to be redrawn).

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to dorsiflexion the lateral malleolus externally rotates by 11 and the distance between the tibia and fibula increases by 1.5 mm.

(PTFL).6 The ATFL is intra-capsular and originates 1 cm proximal from the tip of the lateral malleolus just anterior to the fibular facet. It extends distally and medially inserting onto the neck of the talus and functions as a check-rein when the foot is in an equinus or inverted position. It is therefore most vulnerable when the ankle is in plantarflexion and is the most frequently injured ligament. It is usually disrupted through its midsubstance. The ATFL is taut in plantarflexion and acts to prevent anterior displacement of the talus from the ankle and excessive inversion and internal rotation. The CFL originates adjacent to the ATFL, approximately 8 mm from the tip of the fibula, and courses distally and posteriorly across both the ankle and subtalar joints to insert onto the lateral aspect of the calcaneus just behind and above the peroneal tubercle. It forms the floor of the peroneal tendon sheath. When the ankle is dorsiflexed, the ATFL is loose and the CFL is taut. The PTFL is short, thick and is the strongest of the three ligaments and hence is rarely injured. It originates from the medial surface of the lateral malleolus and inserts into the posterior aspect of the talus. The talar and fibular insertions of the PTFL are broad. The PTFL is under tension only when the ankle is in extreme dorsiflexion, and provides restraint to both inversion and internal rotation when the ankle is loaded.7

Subtalar joint anatomy and biomechanics The subtalar joint is formed by the articulation between the talus and os calcis. The joint is divided into anterior and posterior articulations separated by the sinus tarsi and canalis tarsi. The anterior joint consists of the talonavicular joint including the anterior and middle facets of the calcaneum. The posterior joint contains the posterior facet and its corresponding inferior talar surface. The anterior joint lies more medial than the posterior joint and has a higher centre of rotation. This results in a subtalar joint axis of rotation that is 42 upwards in the sagittal plane and 23 medial to the midline of the foot in the transverse plane10 (Figure 2). There is debate in the literature regarding the key ligamentous stabilizers of the subtalar joint, in both their terminology and reported functions. It is generally accepted that there are three ligamentous groups; the peripheral, deep and the retinacular ligaments. There are three peripheral ligaments, the calcaneofibular ligament (CFL), lateral talocalcaneal ligament (LCTL) and fibulotalocalcaneal ligament (FTCL). There are two deep ligaments, the cervical ligament (CL) and interosseous ligament (IOL).

Medial ligaments The deltoid ligament has significantly higher load to failure than its lateral ligament counterparts and thus requires much greater force to injure. The anatomy of the deltoid ligament comprises of both superficial and deep components. The superficial deltoid originates from the anterior colliculus of the medial malleolus and inserts into both the navicular and the sustentaculum tali of the os calcis. The deep deltoid ligament is a key component of ankle stability. It originates from the posterior colliculus and inserts into the non-articular medial surface of the talus. Classically the superficial deltoid ruptures first followed by the deep deltoid at its talar insertion due to forced abduction or eversion. The biomechanical function of the deltoid ligament is to resist abduction and lateral translation of the talus. The deep deltoid ligament provides the greatest restraint against talar shift.8

Subtalar joint motion (pronation and supination) occurs around a single oblique axis

Syndesmosis The syndesmosis refers to the distal articulation between the tibia and fibula, and forms the stable roof of the talocrural joint. The joint is stabilized by a thick interosseous membrane that runs throughout the length of the two bones. There are three ligaments at the ankle: the anterioreinferior tibiofibular ligament (AITFL), the posterioreinferior tibiofibular ligament (PITFL) and the interosseous ligament (IOL). The AITFL is the most commonly injured and results in the so-called ‘high ankle sprain’. The IOL is both stronger and stiffer than the AITFL but is commonly injured in combination with the AITFL. The PITFL is smaller than the AITFL and is composed of both a deep portion, the transverse tibiofibular ligament, and a superficial portion. The PITFL contributes most towards the stability of the syndesmosis,9 and acts to deepen the talocrural joint by projecting inferior to the tibia, preventing posterior translation of the talus. Biomechanically, a limited degree of motion is necessary at the syndesmosis for normal ankle function. When the talus is wider anteriorly than posteriorly, as the ankle moves from plantarflexion

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Figure 2 Subtalar joint motion (pronation and supination) occurs around a single oblique axis (to be redrawn).

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In addition to the stability provided by the osseous anatomy and ligamentous structures, the peroneal musculotendinous units provide a compensatory pronation moment during supination at the talocrural joint. Gauffin determined that the ankle everters are unable to withstand a supinating moment lever arm greater than 3e4 cm,14 and if this is surpassed then ligamentous injury will occur. Medial ankle sprains are rare in isolation and are more commonly combined with either a lateral ligament complex injury or fractures. A medial ankle sprain can occur after eversion and internal rotation injuries. The reported incidence of syndesmotic sprains range from 1% to 17% of all ankle injuries.15 The primary causative force is external rotation. This causes failure of the AITFL and tearing of the interosseous ligament but the PITFL is usually preserved. Although isolated subtalar joint injuries have been reported, these injuries typically occur in combination with chronic ankle instability. A significant proportion is due to an acute highenergy injury, and subtalar injuries may be present in 10e25% of individuals who have chronic ankle instability. A proposed mechanism of injury results from a sudden deceleration of the calcaneus with progression of the talus.

The CFL is integral in preventing excessive supination at the subtalar joint, and its rupture may cause combined instability at the ankle and subtalar joints.

Pathomechanics of ankle sprains Lateral ankle sprains most commonly occur as a result of excessive supination of the hindfoot about an externally rotated lower leg during the initial phase of heel strike. There is often sequential failure of the ligaments starting with the ATFL, followed by the CFL.11 Isolated ruptures of the CFL are rare and may play a role in subtalar instability. Chapman classified acute injuries into three grades: Grade 1 e ligament stretch without macroscopic tearing, Grade 2 e macroscopic tearing of the ligament, Grade 3 e ligament rupture.12 Chronic lateral ankle instability most often follows Grade 3 injuries. There is little research describing predispositions to a firsttime ankle sprain. A pathomechanical model proposed by Fuller13 describes the cause of lateral ankle sprain as an increased supination moment around the subtalar joint axis. In the normal ankle, on heel strike the centre of pressure (COP) of the foot lies lateral to the subtalar joint axis and the ground reaction force (GRF) exerts a pronation moment. However, individuals with a rigid supinated hindfoot (calcaneal varus) would have a laterally placed subtalar axis relative to the GRF and this increased supination moment could cause excessive inversion and injury to the lateral ligaments (Figure 3). In addition, increased plantarflexion causes the subtalar joint axis to drift laterally and thus increases the risk of injury14 (Figure 4). Inman described great variation amongst individuals in the alignment of the subtalar joint axis,10 thus those individuals with a laterally placed subtalar axis would be predisposed to injury.

Pathomechanics of chronic instability Chronic ankle instability (CAI) is defined as the occurrence of recurrent bouts of lateral ankle instability. The most common factor predisposing an individual to chronic instability is an initial acute event; however, the mechanisms of chronic instability are thought to be different from the acute injury. Classically, there are two factors thought to cause chronic instability although these are not mutually exclusive from one another. In 1965, Freeman16 introduced the concept of functional instability, which occurs as a result of proprioceptive changes following ligament injury. Tropp et al17 expanded on this model and defined mechanical instability as abnormal motion of the talus within the ankle joint due to pathologic laxity of the ligaments, and functional instability as motion beyond voluntary control but within the normal physiological range. In addition to instability, a significant proportion of patients develop chronic symptoms, which contribute to the overall morbidity and which may accentuate the sense of instability. Pain, swelling, locking and stiffness are commonplace and arise from pathologies that might not fall neatly into the two categories. Mechanical instability The precise definition of mechanical instability varies in the literature. It is traditionally thought of as the result of anatomical insufficiencies such as either ligamentous laxity, synovial changes or a fault in the kinematics of any of the three joints around the ankle. Mechanical instability can be measured via clinical examination, stress radiography or arthrometry. Karlsson et al.3 investigated the relationship between the degree of mechanical instability demonstrable with stress testing and symptoms. They determined that 10 mm or more of anterior draw or 9 of talar tilt was consistent with CAI. Alternatively, a difference of 3 mm of anterior draw or 3 of talar tilt with the functionally normal side was also significant. Since there is great variation in the normal physiologic ranges of motion, a comparison with the functionally stable ankle is the most accurate determinant.

Figure 3 The subtalar joint axis of rotation passes through the talus. In the normal ankle (a), the ground reaction force acts lateral to the axis producing a pronating torque. In (b), where the heel is in varus, the force produces a supinating torque. (Reproduced with kind permission from Tropp H 2002 Journal of Athletic Training).

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Figure 4 Diagram showing the lateral drift of the subtalar joint axis from (a) neutral to (e) plantarflexion and inversion, increasing the risk of injury. (Reproduced with kind permission from Tropp H 2002 Journal of Athletic Training).

Functional instability Injuries to the lateral ligaments results in neuromuscular changes to the stabilizing muscles around the ankle, leading to a proprioceptive deficit. Weakness of the peronei have been reported amongst individuals with CAI as well as impaired reflexive response times. Most patients presenting with CAI will invariably have an element of functional instability and it is often the predominant problem.

over the lateral gutter (ATFL) and Molloy’s impingement test may reveal impingement syndrome due to post-traumatic synovitis.19 Tenderness over the deltoid ligament usually indicates a more complex injury. Peroneal tendon subluxation may manifest itself as a sense of instability and can be unmasked with the foot in maximal dorsiflexion and eversion. Hindfoot examination must also exclude a gastrocnemius contracture (Silfverskiold test) and a varus heel, both of which would accentuate the instability. Neurological status should be assessed and documented, as sural and peroneal nerve palsies are a rare complication of lateral ligament injuries. The two most important tests for evaluation of ankle instability are the anterior draw test and inversion stress test (talar tilt test).

Other factors DiGiovanni et al.18 demonstrated the presence of multiple other pathologies in patients presenting with CAI, which may cause pain, disordered kinematics or mechanical impairments, and this can manifest themselves as a sense of instability. Synovial hypertrophy with anterolateral impingement, osteochondral injuries, intraarticular loose bodies, degenerative changes and peroneal tendon injuries are common. Pre-existing factors will also contribute biomechanically towards CAI such as a varus hindfoot, tight tendoAchilles or gastrocnemius, and generalized joint laxity.

Anterior draw test: with the patient relaxed, anterior subluxation of the talus can easily be demonstrated. With the foot in 20 of plantarflexion, the tibia is pushed backwards against the fixed foot or the foot drawn forwards against the tibia (Figure 5). The characteristic sign is the ‘suction sign’ as the skin is sucked inwards over the lateral gutter.

Clinical evaluation Inversion stress test: excessive hindfoot inversion with the foot in a plantigrade position may indicate tibiotalar laxity, and is usually positive where there is complete CFL disruption. Both ankles should be tested simultaneously to determine asymmetry (Figure 6). It is sometimes difficult to differentiate between ankle and subtalar motion, and palpation of the talar neck may help.

History Patients presenting with chronic ankle instability usually report a preceding history of a significant ankle sprain. Typically, patients complain of repeated episodes of giving way, particularly on walking on uneven ground. Aside from instability, intermittent swelling and pain may accompany these episodes. The presence of pain, especially if consistent on weightbearing, should raise the suspicion of intra-articular pathology such as an osteochondral lesion or soft tissue impingement. The mechanism of injury, in particular the position of the foot at the time of injury, is important but often the patient’s account does not correlate well with the injured structures.

Medial and syndesmotic instability test: the Kleiger test can demonstrate medial and syndesmotic instability. With the knee flexed to 90 , the foot is externally rotated. A positive test reveals pain in the area of injury. The ‘squeeze test’ for syndesmotic injury involves squeezing the fibula at the mid-calf. The pain should be felt distally at the level of the syndesmosis.

Clinical examination A thorough examination is essential to determine intra-articular and extra-articular causes of symptoms. Tenderness is usually maximal

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Molloy impingement test: the Molloy impingement19 test is the cardinal physical sign for ankle synovial impingement. The ankle

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Radiographic investigation Although various imaging modalities have been utilized in the evaluation of ankle instability, the two key investigations are stress radiography and MRI. Stress radiography The purpose of stress radiography is to demonstrate mechanical instability of the tibiotalar joint. The inversion stress view is a comparative antero-posterior radiograph taken with the foot in neutral and the hindfoot in maximal inversion. Both anterior draw and talar tilt are tested (Figure 7). Muscle guarding due to pain may limit its sensitivity and intra-articular local anaesthetic has been shown to improve accuracy. There is no consensus as

Figure 5 The anterior draw test. It can be performed either with the foot fixed or free.

is dorsiflexed with finger pressure in the joint line. The appearance of or increase in pain under the finger is a positive test. The test may have to be repeated at different points on the joint line. This is both highly sensitive and specific for predicting synovitis and hypertrophy.

Figure 7 Stress radiography showing abnormal 18 of talar tilt and 6 mm of anterior draw.

Figure 6 The talar tilt test, which is best performed bilaterally for comparison.

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to what is the normal range of talar tilt (0e23 ). Chrisman and Snook20 determined that a 10 difference between the two sides was 97% sensitive for ATFL and CFL injury. According to Safran,21 a 5 difference may be clinically significant. Syndesmotic instability can be demonstrated radiographically with the Kleiger test (Figure 8). Comparative views are recommended, but instability is likely where: (1) the tibiofibular clear space on the mortice view is >5 mm, (2) the tibiofibular overlap on the antero-posterior view is <6 mm, and (3) there is tibiofibular overlap on a mortice view of <1 mm. Magnetic resonance imaging The primary purpose of MRI is to identify conditions that may give rise to symptoms of instability such as osteochondral lesions, peroneal tendon tears, impingement syndrome and loose bodies. Although MRI can identify the degree of injury to the ligaments, it does not confirm whether or not the ankle is mechanically unstable. MRI is useful for patients presenting primarily with chronic pain, to determine whether arthroscopic treatment should be offered prior to consideration of ligament reconstruction (Figure 9). Figure 9 T2 weighted MRI showing an unstable osteochondral lesion of the medial talar dome.

Other investigations Arthrography or MRI-arthrography is of limited value in the evaluation of chronic lateral instability. A rupture of the CFL allows contrast medium to enter the peroneal tendon sheath but penetration into the subtalar joint is not indicative of injury. Peroneal tendography can be utilized in a converse manner and may be useful when a tendon tear is suspected. Ultrasound is a comparatively new technique and is largely operator-dependent. Ligament ruptures can be identified and stress testing can be performed. It may prove to be a useful technique in the assessment of subtalar instability.

Non-surgical treatment Early rehabilitation of acute injuries is the main aim. A combination of isokinetic strength training with proprioception training shortens rehabilitation and can be prophylactic for recurrent injury. In the case of CAI, rehabilitation follows a similar course; the aim being to improve the functional component of any instability. Ankle supports such as an ankle stirrup brace may be utilized, as needed. Patients with pure mechanical instability are less likely to respond to conservative measures.

Surgical treatment Surgery should be considered following complete workup and failure of conservative management. Surgical planning should initially be based on the presence or suspicion of any intraarticular pathology and whether or not ankle arthroscopy is indicated. Ankle arthroscopy DiGiovanni,18 Kibler22 and Ogilvie-Harris23 all found a high incidence of intra-articular pathology in CAI. Synovitis, impingement lesions, osteochondral lesions, spurs and loose bodies are all amenable to arthroscopic treatment, which can lessen symptoms of mechanical instability (Figure 10). Malviya et al.24 performed an initial ankle arthroscopy with screening and found a similarly high incidence of intra-articular pathology. Treatment of these lesions resulted in 53% of their patients not requiring lateral ligament reconstruction. Kibler believed that fluid extravasation from ankle arthroscopy did not compromise ligament reconstruction and practice varies as to whether the arthroscopy is performed as a combined or staged procedure. With a high reported rate of resolution of symptoms with an arthroscopy alone, it would seem logical to perform an initial arthroscopy and subsequently proceed to ligament reconstruction only if required. Further research is

Figure 8 The Kleiger test of syndesmotic instability. Significant widening is noted with no tibiofibular overlap on the mortice view.

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described a modification in which the inferior extensor retinaculum is advanced to reinforce the repair (Figure 11). The incision is performed anterior to the lateral malleolus, parallel to its border in a curvilinear approach. Dissection is carried out down to the joint capsule. The capsule and ATFL are divided at the lateral malleolus, leaving a cuff of tissue, and imbricated via transosseous sutures or anchors. The peroneal tendon sheath is then opened to determine the quality of the CFL. Avulsions proximally or distally can be reattached in the same manner but a midsubstance tear may prove impossible to

Figure 10 (a) A syndesmotic impingement lesion with synovitis. (b) An unstable osteochondral lesion of the medial talar dome.

required in this area. The authors’ practice is to perform an initial ankle arthroscopy in all suspected cases of intra-articular pathology, and subsequently proceed to ligament reconstruction 10e12 weeks post-operatively if instability has not resolved. A combined procedure is only performed where no intra-articular pathology is identified. Surgical stabilization of chronic lateral ankle instability There are over 20 different described surgical reconstruction procedures available for chronic lateral ankle instability. All have reported success rates of over 80%. There are two main approaches to surgical stabilization: anatomical and non-anatomical. In contemporary practice, the anatomic repair remains the procedure of choice although the techniques have to be individualized according to the patient and their anatomy. Biomechanical studies have shown more stability with anatomic repair versus non-anatomic but the clinical outcomes may largely be the same. There are only a few randomized controlled trials comparing the two techniques.

Figure 11 The Brostrom-Gould lateral ankle ligament reconstruction: (a) The surgical approach between the branches of the superficial peroneal and sural nerves. (b) Tears of the ATFL and CFL. (c) Direct repair and imbrication of ligaments. (d) The Gould modification with mobilization and advancement of the inferior extensor retinaculum. (Reproduced with kind permission from J Baumhauer 2002 Journal of Athletic Training).

Anatomic stabilization: Brostrom25 described a repair whereby the ruptured lateral ligaments are reapproximated to the bone, resulting in restoration of normal anatomy. Gould et al.26

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imbricate. Additional stability to the subtalar joint may be obtained by imbrication of the inferior extensor retinaculum over the repair to the periosteum of the fibula, as described by Gould.26 Post-operatively, a walking plaster or boot is applied for 4e6 weeks. Thereafter, the patient may commence proprioceptive training with a U-stirrup support. Athletes are instructed to use protective taping/bracing for 6 months after the repair. Reported functional outcomes are excellent, with 87e95% success rates.25e27 The advantages of anatomical repair include minimal surgical exposure, repair of host anatomy, preservation of ankle and subtalar joint motion and low morbidity. Unsatisfactory outcomes are reported in patients with generalized hypermobility, long standing ligament insufficiency and previous surgery. Other relative contraindications include obesity, hindfoot malalignment and very high demand athletes. The most severe common complication is iatrogenic injury to the superficial peroneal or sural nerve. Non-anatomic stabilization: non-anatomic reconstruction utilizes a tendon or other graft as a weave tenodesis. The most common graft involves the use of peroneus brevis. The commonly used techniques are the Evans28 (Figure 12) and ChrismaneSnook (Figure 13) procedures.20 The Evans procedure involves harvesting half of the peroneus brevis tendon, leaving the free arm attached distally to the base of the fifth metatarsal. The free arm is then passed though a drill hole in the lateral malleolus, from anterior to posterior, and is then sutured to itself. The degree of tension can be adjusted according to the position of the foot. The Evans tenodesis does not recreate the normal biomechanical functions of the ATFL and CFL. Whilst ankle motion is

Figure 13 The ChrismaneSnook ankle tenodesis. One-half of peroneus brevis is harvested, leaving it attached at the fifth metatarsal base. It is passed anterior to posterior through the distal fibula and through a calcaneal bone tunnel and sutured back on itself. (Reproduced with kind permission from J Baumhauer 2002 Journal of Athletic Training).

not affected, anterior translation is not well controlled and subtalar motion is decreased. The ChrismaneSnook procedure uses a split peroneus brevis tendon detached proximally, similar to the Evans procedure. It aims to reconstruct the function of the ATFL and CFL more accurately and involves weaving the tendon from anterior to posterior through the fibula and subsequently though a drill hole in the calcaneum before the tendon is sutured back upon itself. As a result, stability is better than the Evans procedure but it has the highest incidence of loss of inversion. Post-operatively, patients are placed in a walking plaster or boot for 6 weeks and a U-stirrup for a further 6 weeks. Active proprioceptive training is commenced at 6 weeks. Reported early results are similar to anatomic repair, with 80e90% success rates. The greatest limitation of these procedures is the decrease in subtalar joint motion and the risk of sural nerve injury. Long-term follow-up studies have shown gradual deterioration of stability, restriction of range of motion, increased risk of degenerative changes and less satisfactory overall results as compared to anatomic reconstructions. The advantage of non-anatomic reconstruction is the increased strength of the repair, which is particularly important in athletes where stability is more important than motion. In most cases, reconstruction is reserved for when the tissues are so severely attenuated that an anatomic repair cannot be carried out. Surgical stabilization of syndesmotic instability Surgical treatment of syndesmotic instability should be considered in symptomatic patients where mechanical instability is demonstrated on radiography. Syndesmotic stabilization can be performed in the subacute phase (6 weekse6 months) and

Figure 12 The Evans ankle tenodesis. One-half of peroneus brevis is harvested, leaving it attached at the fifth metatarsal base. It is passed from anterior to posterior through a drill hole in the fibula and sutured to itself. (Reproduced with kind permission from J Baumhauer 2002 Journal of Athletic Training).

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treatment of mechanical instability are excellent and the technique employed should be chosen based upon functional demand, patient factors and the pathological anatomy of the injury. A

REFERENCES 1 Bridgman SA, Clement D, Downing A, Walley G, Phair I, Maffulli I. Population based epidemiology of ankle sprains attending accident and emergency units in the West Midlands of England, and a survey of UK practice for severe ankle sprains. Emerg Med J 2003; 20: 508e10. 2 Kannus P, Renstrom P. Current concepts review. Treatment for acute tears of the lateral ligaments of the ankle. Operation cast or early controlled mobilization. J Bone Joint Surg 1991; 73A: 305e12. 3 Karlsson J, Lasinger O. Lateral instability of the ankle joint. Clin Orthop 1992; 276: 253e61. 4 Rockar Jr PA. The subtalar joint: anatomy and joint motion. J Orthop Sports Phys Ther 1995; 21: 361e72. 5 Lundberg A, Goldie I, Kalin B, Silvik G. Kinematics of the ankle/foot complex: plantarflexion and dorsiflexion. Foot Ankle 1989; 9: 194e200. 6 Attarian DE, McCrackin HJ, Devito DP, McElhaney JH, Garrett WE. Biomechanical characteristics of human ankle ligaments. Foot Ankle 1985; 6: 54e8. 7 Stormont DM, Morrey BF, An KN, Cass JR. Stability of the loaded ankle: relation between articular restraint and primary and secondary static restraints. Am J Sports Med 1985; 13: 295e300. 8 Harper MC. Deltoid ligament: an anatomical evaluation of function. Foot Ankle 1987; 8: 19e22. 9 Ogilvie-Harris DJ, Reed SC, Hedman TP. Disruption of the ankle syndesmosis: biomechanical study of the ligamentous restraints. Arthroscopy 1994; 10: 558e60. 10 Inman VT. The joints of the ankle. Baltimore, MD: Williams & Wilkins, 1976. 11 Brostrom L. Sprained ankles: I, anatomic lesions on recent sprains. Acta Chir Scand 1964; 128: 483e95. 12 Chapman MW. Sprains of the ankle. Inst Course Lect 1975; 24: 294e308. 13 Fuller EA. Center of pressure and its theoretical relationship to foot pathology. J Am Podiatr Med Assoc 1999; 89: 278e91. 14 Gauffin H. Knee and ankle kinesiology and joint instability [master’s thesis]. Linkoping, Sweden: Linkoping University, 1991. 15 Hopkinson WJ, St Pierre P, Ryan JB, Wheeler JH. Syndesmosis sprains of the ankle. Foot Ankle 1990; 10: 325e30. 16 Freeman MAR. Instability of the foot after injuries to the lateral ligament of the ankle. J Bone Joint Surg Br 1965; 47: 669e77. 17 Tropp H. Commentary: functional ankle instability revisited. J Athl Train 2002; 37: 512e5. 18 DiGiovanni BF, Fraga CJ, Cohen BE, Shereff MJ. Associated injuries found in chronic lateral ankle instability. Foot Ankle Int 2000; 21: 809e15. 19 Molloy S, Solan MC, Bendall SP. Synovial impingement of the ankle. A new physical sign. J Bone Joint Surg Br 2003; 85: 330e3. 20 Chrisman OD, Snook GA. Reconstruction of lateral ligament tears of the ankle. An experimental study and clinical evaluation of seven patients treated by a new modification of the Elmslie procedure. J Bone Joint Surg Am 1969; 51A: 904e12. 21 Safran MR, Benedetti RS, Bartolozzi 3rd AR, Mandelbaum BR. Lateral ankle sprains: a comprehensive review: part 1: etiology, pathoanatomy, histopathogenesis, and diagnosis. Med Sci Sports Exerc 1999; 31: 429e37.

Figure 14 Syndesmotic reconstruction with suture button fixation. The syndesmosis has been reduced following arthroscopic debridement.

multiple methods have been described. The commonest techniques are insertion of a syndesmotic screw, bioabsorbable screws and suture button fixation.29 Reduction of the syndesmosis is facilitated by reduction clamps under radiographic control. Arthroscopic debridement should be performed concurrently, to allow accurate reduction of the syndesmosis and to treat any intra-articular pathologies. If the joint surface is already degenerate on both sides then arthrodesis or arthroplasty may be needed. The aim of surgery is to allow a degree of fibrotic healing of the syndesmotic ligaments using an implant strong enough to resist diastasis, to ensure early mobilization and to allow a degree of physiologic micromotion (Figure 14). There are a number of controversies with regards to implant positioning, post-operative management and implant removal but no technique has been shown to be superior.

Conclusion Chronic ankle instability is not a single pathologic entity, and comprises a spectrum between functional and mechanical instability. Treatment should be based upon careful evaluation of the pathomechanics of the injury, clinical assessment and stress radiography. Arthroscopy should be considered where patients present with chronic pain suggestive of intra-articular pathology. Factors predisposing the patient to chronic instability such as a gastrocnemius contracture or hindfoot varus should be noted and treated as part of the surgical plan. A focused course of conservative management will often resolve patient symptoms, particularly if functional instability is the predominant problem. The results of surgical

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22 Kibler WB. Arthroscopic findings in ankle ligament reconstruction. Clin Sports Med 1996; 15: 799e804. 23 Ogilvie-Harris DJ, Gilbart MK, Chorney K. Chronic pain following ankle sprains in athletes: the role of arthroscopic surgery. Arthroscopy 1997; 13: 564e74. 24 Malviya A, Makwana N, Laing P. Is reconstruction always necessary in chronic lateral ankle instability? J Bone Joint Surg Br Proceedings 2005; 87B: 374. 25 Brostrom L. Sprained ankles VI. Surgical treatment of ‘chronic’ ligament ruptures. Acta Chir Scand 1966; 132: 551e65.

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26 Gould N, Seligson D, Gassman J. Early and late repair of lateral ligaments of the ankle. Foot Ankle 1980; 1: 84e9. 27 Ahlgren O, Larsson S. Reconstruction for lateral ligament injuries of the ankle. J Bone Joint Surg Br 1989; 71: 300e3. 28 Evans DL. Recurrent instability of the ankle e a method of surgical treatment. Proc R Soc Med 1953; 46: 343e4. 29 Van den Bekerom MP, de Leeuw PA, van Dijk CN. Delayed operative treatment of syndesmotic instability. Current concepts review. Injury 2009; 40: 1137e42.

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(vi) Anatomy and biomechanics of the foot and ankle

of the tibia. The interosseous ligament is a thickening of the interosseous membrane. This ligament is more flexible and allows a subtle diastasis of the tibia and fibula during ankle dorsiflexion.1 Lateral ankle stability is conferred by the lateral ligament complex. This consists of the anterior talofibular ligament (ATFL), calcaneofibular ligament (CFL) and the posterior talofibular ligament (PTFL). The ATFL is a thickening of the anterior capsule and its primary function is to resist inversion when the ankle is plantarflexed. The ligament runs anteriorly from the lateral malleolus to the talus at 45
to the frontal plane.2 The ATFL also resists external tibial rotation and anterior draw of the talus. There is an angle of 105
between the ATFL and the CFL allowing the two ligaments to act synergistically. The CFL lies in a horizontal position during ankle plantarflexion but comes to lie in a vertical orientation during dorsiflexion. It remains under tension throughout this arc of movement, although the tension is greatest during ankle dorsiflexion where the ligament mosteffectively resists inversion. During ankle plantarflexion the CFL also guides calcaneal inversion, which may be observed when a patient with normal feet stands on tip-toes. The PTFL runs from the lateral malleolus to the posterolateral talus. The lateral ligament complex tends to fail in a predictable sequence during inversion injury. The sequence is ATFL, CFL and PTFL. Once the ATFL has ruptured there is a significant increase in internal hind-foot rotation which predisposes to further ligament injury.3 Major stabilizers on the medial side of the ankle joint are the medial malleolus and the deltoid ligament. The deltoid ligament is by far the strongest ligament stabilizing the ankle, with a tensile strength of 714N. This compares with the strongest lateral ligament, the CFL with a tensile strength of 346N.4 The ligament is formed from superficial and deep parts. The superficial deltoid is divided into three slips which originate from the anteroinferior medial malleolus and insert into the navicular, calcaneonavicular ligament and the sustentaculum tali and tuberosity of the calcaneum respectively. The superficial deltoid acts mainly to prevent hind-foot eversion. The deep deltoid ligament originates from the posterior border of the anterior colliculus, intercollicular groove and posterior colliculus before running transversely to insert into the non-articular surface of the medial talus. The posteromedial aspect of the ligament is covered by the tibialis posterior tendon sheath.5 Sectioning the deep deltoid ligament results in greatly increased lateral talar shift and external talar rotation.6

Edward J C Dawe James Davis

Abstract The foot is a complex anatomical and biomechanical structure. It functions to allow stable stance, ambulation and the effective transfer of force through the lower limb. A thorough understanding of how the foot and ankle achieve this is essential for planning surgery and avoiding the consequences of nerve injury, poor wound healing and disrupted function. This review looks at the current understanding of foot function in the context of gait, biomechanics and relevant surgical anatomy.

Keywords ankle; biomechanics; foot

Introduction The foot is a complex anatomical structure. It acts to transmit force between the lower limb and the ground, allowing stable ambulation and stance. During gait the foot functions as a flexible shock-absorber, deforming to uneven surfaces before undergoing a series of biomechanical changes which allow it to act as a rigid lever to exert force. The dense concentration of structures required for normal foot function makes the foot and ankle a treacherous area for the surgeon. A thorough understanding of the complex anatomy of this area is essential for safe surgical intervention.

Anatomy of the foot and ankle Ankle Ankle joint stability: the ankle joint gains its stability from bony congruence, the joint capsule as well as ligamentous support. The inferior tibiofibular joint is a syndesmosis with three main supporting ligaments. Firstly the anterior inferior tibiofibular ligament (AITFL). This is a flat, strong ligament which runs from the anterior edge of the lateral malleolus to the anterolateral tubercle of the tibia. The posterior inferior tibiofibular ligament (PITFL) consists of both superficial and deep portions. The deep part runs from the posterior margin of the tibia to the osteochondral junction on the posteromedial aspect of the distal fibula, whilst the superficial part functions along with the AITFL to ensure that the fibula remains held tightly within the incisura

Applied anatomy of surgical approaches to the ankle A number of different surgical approaches are used to access the ankle joint. These will be considered in a clockwise direction starting with the direct lateral approach to the distal fibula. Laterally the fibula lies subcutaneously and approach to fractures here can be carried out in relative safety. There are however several important structures that must be considered when performing this simple approach. Running just posterior to the fibula are both the sural nerve and, accompanying it, the short saphenous vein. Identifying and protecting the vein with its less easily identified nerve is essential in order to prevent numbness on the lateral aspect of the foot or a painful neuroma. Another structure at risk with higher fibular fractures is the superficial peroneal nerve which exits the lateral compartment of

Edward J C Dawe MBBS BSc(Hons) MRCS(Eng) Dip(SEM) Specialist Registrar in Trauma and Orthopaedic Surgery, Brighton and Sussex University Hospitals, UK. James Davis FRCS Consultant in Trauma and Orthopaedic Surgery, Torbay Hospital, Devon, UK.

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the leg 15 cm above the ankle. More extensive dissection is this area may uncover the peroneal tendons in their common tendon sheath. These play an important role as dynamic stabilizers of both the medial and lateral longitudinal arches. Damage to these tendons is one of the causes of pain after ankle injury. This occurs by tendon dislocation, instability, tendinitis or rupture. The anterolateral approach to the ankle is a useful approach which is extensile both proximally and distally to expose the fibula as well as the calcaneocuboid, talonavicular and talocalcaneal joints. This may be useful for approaching fractures of the talus as well as for triple fusion or ankle arthrodesis. The incision should be made 2 cm anterior to the fibula and curving downwards such that it passes 2 cm medial to the lateral malleolus and ends 2 cm medial to the base of the fifth metatarsal. The structures most at risk during this dissection are the dorsal cutaneous branches of the superficial peroneal nerve. These are superficial to the deep fascia and should be identified and protected. The deep fascia in this region is thickened by the superior and inferior extensor retinaculae. These should be incised to reveal the extensor muscles. Peroneus tertius is the most lateral of these and is supplied by the deep peroneal nerve. Identify the lateral margin of this muscle and retract the extensors medially to expose the distal fibula and ankle joint. From this position the anterior elements of the syndesmosis are visible. At the distal end of the wound the extensor digitorum brevis muscle is visible below the fat pad of the sinus tarsi. Excising the fat pad and detaching this muscle at its origin allows access to the mid-tarsal joints for arthrodesis (Figure 1). The direct anterior approach to the ankle may be used for arthrodesis, fixation of pilon fractures or total ankle replacement. The malleoli may be used to centre the incision, which should be just through the skin. Care must be taken to avoid first the superficial peroneal nerve and secondly the neurovascular bundle

formed from the anterior tibial artery (palpable as the dorsalis pedis pulse) and the deep peroneal nerve. The anterior tibial neurovascular bundle runs just medial to the extensor hallucis longus (EHL) tendon and crosses over at the level of the ankle joint to lie on the lateral side of the tendon between EHL and extensor digitorum longus (EDL). The deep peroneal nerve, which has supplied all the muscles in the anterior compartment of the leg, goes on to supply the skin of the first webspace in the foot. These structures are best approached from proximal to distal and once identified, should be retracted medially along with the EHL tendon. One other approach is to develop a plane between tibialis anterior (TA) and FHL, although care must be taken to protect the deep peroneal nerve at the proximal extent of the wound. A medial approach can be used for the fixation of medial malleolar fractures. This may be performed through an anterior, posterior or direct medial incision. The anterior incision allows visualization of the ankle joint, whilst the posterior incision allows visualization of the posterior tibia. For arthrodesis the direct medial approach may be used in combination with a medial malleolar osteotomy to improve access. Incisions in this area should curve anteriorly at the level of the tip of the medial malleolus and should avoid the most prominent part of the malleolus in order to avoid wound problems and discomfort from footwear. Anterior to the medial malleolus the great saphenous vein runs with the saphenous nerve. These should be identified carefully and protected. Behind the medial malleolus there is the retinaculum covering the tibialis posterior (TP) tendon. The retinaculum may be incised for access and later repaired but care should be taken to avoid damage to the TP tendon. This should be retracted anteriorly. The remaining structures behind the medial malleolus may be gently retracted posteriorly to allow limited access to the posterior tibia. The structures running behind the medial malleolus may be approached through a posteromedial approach. This is useful in exploring soft tissue entrapment such as tarsal tunnel syndrome. The incision should be made between the Achilles tendon and the medial malleolus. This may be deepened into the fat which lies between the two structures. The deep fascia is incised and the flexor hallucis longus identified. The other long flexors have all become tendinous at this level and so FHL is easily identified. For this reason the muscle is sometimes known as the “beef to the heel”. The FHL muscle along with the neurovascular bundle containing the posterior tibial artery and nerve may then be retracted laterally whilst the FDL tendon is retracted medially. This allows access to the posterior tibia and joint capsule (Figure 2). Finally, the posterolateral approach to the ankle is a useful approach for internal fixation, allowing fixation of both posterior malleolar fractures and distal fibular fractures through the same incision. The patient should be positioned prone and the incision made midway between the posterior border of the lateral malleolus and the Achilles tendon. There is an inter-nervous plane between the peroneus brevis (supplied by the superficial peroneal nerve) and the FHL tendon (supplied by the tibial nerve). At this level the peroneus longus and brevis run in a combined tendon sheath before passing under the peroneal retinaculum posterior to the lateral malleolus. Peroneus brevis continues to insert into the base of the fifth metatarsal whilst peroneus longus runs around the peroneal groove in the cuboid to insert into the medial cuneiform. Peroneus

Figure 1 Neurovascular structures in a coronal section 1 cm proximal to the ankle joint. A: Superficial peroneal nerve. B: Anterior tibial artery and vein with the deep peroneal nerve. C: Long saphenous vein with saphenous nerve. D: Posterior tibial artery and vein with the tibial nerve.

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posterior joint capsule and inserts into the talar neck just medial to the insertion of the cervical ligaments. Lateral support comes in part from the inferior extensor retinaculum. These have three roots which are lateral, intermediate and medial although it is likely that only the lateral root confers stability.7 The three peripheral ligaments which stabilize the subtalar joint are the calcaneofibular ligament (CFL), which also spans the ankle joint, the lateral talocalcaneal ligament (LTCL) and the fibulotalocalcaneal ligament (FTCL).8 The talus: the anatomy of the talus requires particular mention for several reasons. Firstly it is the only bone in the foot not to receive significant muscular attachments and secondly it is at high risk of avascular necrosis after injury. The talus consists of a body, neck and head and articulates with the tibia, calcaneum and navicular, meaning that around 60% of its surface is covered with articular cartilage. It receives a blood supply from each of the three arteries supplying the foot (Table 1). There is some variability in this supply and an anastamosis usually exists between the artery of the tarsal sinus and the artery of the tarsal canal.9 The calcaneal tendon: is the combined tendon of the gastrocnemius and soleus muscles. It inserts into the inferior third of the posterior part of the calcaneum and transmits the force of the strongest ankle plantarflexors. The tendoachilles is able to withstand up to 17 times body-weight whilst only stressing the gastroesoleus complex to generate 13% of its maximum force. The tendon consists of a spiral of fibres which undergo a 90
rotation during their course from the musculo-tendinous junction to insertion. Hence the medial fibres insert posteriorly and the lateral fibres insert anteriorly. Eighty percent of the tendon is type I collagen with a small proportion of type III collagen. Higher proportions of type III collagen predispose to injury. The tendon is separated from the calcaneum by the retrocalcaneal bursa and from the skin by the subcutaneous calcaneal bursa. The paratenon surrounds the calcaneal tendon and is continuous proximally with the muscle fascia and distally with the periosteum. On the medial and dorsolateral aspects there are gliding membranes lubricated with polysaccharides which reduce friction and allow smooth tendon movement. The blood supply to the tendon is derived from end to end via the paratenon. This creates a watershed area between the more proximal area supplied by the posterior tibial artery and the more distal

Figure 2 The posterolateral aspect of the ankle showing the sites for the posterolateral A: lateral B: and anterolateral C: Note the anterolateral approach is extensile to the mid-foot in order to expose the calcaneocuboid joint.

brevis may be identified as it lies anterior to peroneus longus and it is muscular much more distally than peroneus longus. The sural nerve with the short saphenous vein accompanying it should be running anterior to the lateral malleolus and hence well-outside the scope of the incision. The peroneal retinaculum should be incised and the tendons retracted anteriorly. The muscular FHL may then be retracted medially. Detaching the lateral fibres of the FHL muscle from the distal tibia aids exposure further. This approach may be extended proximally between the lateral head of gastrocnemius and the peroneal muscles. Hind-foot Subtalar joint stability: the subtalar joint allows pronation and supination and consists of two separate joint cavities. Posteriorly the joint is formed between the inferioreposterior talar facet and the superioreposterior facet of the calcaneus. The anterior articulation is formed between the talar head, anterioresuperior facets, sustentaculum tali and the concave surface of the navicular. This talocalcaneonavicular joint functions as a ball and socket. These two joints are separated by the sinus tarsi and have separate joint capsules although they share a similar axis of rotation. There are three lateral groups of supporting structures. These are the deep ligaments, peripheral ligaments and retinaculae. The cervical and interosseous ligaments are deep ligaments which lie between the two joint capsules. The cervical ligament runs from the cervical tubercle of the calcaneus anteriorly and medially to the talar neck. The interosseous ligament lies posterior to the cervical ligament and runs superiorly and medially. It takes its origin from the calcaneus just anterior to the

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The arterial supply of the talus Artery Artery of the tarsal canal

Originating artery Posterior tibial artery

Artery of the sinus tarsi Dorsalis pedis

Perforating peroneal artery Anterior tibial artery

Area supplied Talar neck þ almost all the body of the talus. Medial 1/3 of body supplied by deltoid branches Inferomedial talar head Superolateral talar head

Table 1

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supply from the perforating peroneal artery.10 Hence, between 2 cm and 6 cm proximal to the tendon insertion is the commonest area for tendon rupture to occur. Due to the low metabolic rate and poor blood supply in this region, healing is slow.

fracture-dislocations of the mid-tarsal joints. There are strong intermetatarsal and intertarsal ligaments, although the plantar ‘LisFranc’s’ ligament which runs from the medial cuneiform to the second metatarsal, is most often damaged. This commonly requires surgical repair to regain stability. The surgical approach to this injury is generally made using a two-incision technique. The medial incision is sited between the first and second metatarsals and extends proximally and slightly towards the midline. This affords excellent exposure of the medial and intermediate cuneiforms as well as the medial two metatarsocuneiform joints. The dorsalis pedis artery with the accompanying deep peroneal nerve is found in the centre of the surgical field using this approach so great care must be taken during dissection to avoid damage to these. The second incision is made laterally at the base of the 4th metatarsal and extending proximally. This allows direct visualization of the three lateral tarsometatarsal joints. Care should be taken to ensure the greatest possible width of the skin bridge between the two incisions to reduce the risk of skin necrosis at this site. The approaches should both involve full-thickness dissection with minimal undermining of the skin and gentle retraction.

Applied anatomy and surgical approaches to the hind-foot: as described above, the anterolateral approach to the ankle may be extended to allow access to the talonavicular, calcaneocuboid and calocalcaneal joints. This approach may be used in conjunction with a medial approach for the fixation of talar fractures. The posterior talocalcaneal joint may be approached from laterally during subtalar arthrodesis. The landmarks for this incision are the lateral malleolus and the peroneal tubercle of the calcaneum. This is found 1.5 cm distal and anterior to the tip of the lateral malleolus and acts to separate the peroneus longus and brevis tendons as their courses diverge. The incision should start posterior to the lateral malleolus and curve anteriorly to pass over the peroneal tubercle. The sural nerve and accompanying short saphenous vein should lie well posterior to the incision. The peroneal tendons may be released from their tendon sheaths, which by the level of the peroneal tubercle should be separate. These are both covered by the peroneal retinaculum, which should be repaired during closure to prevent tendon dislocation. The calcaneofibular ligament may be identified running postero-inferiorly from the lateral malleolus. Beneath this lies the capsule of the posterior talocalcaneal joint. Olliers approach, a transverse approach to the mid-foot, is no longer current practice due to the unacceptably high risk of superficial peroneal nerve injury. The lateral approach to the calcaneum as described by Eastwood and Atkins11 is useful for open reduction and internal fixation of calcaneal fractures. Surgery to the calcaneum has proved challenging to surgeons due to the high risk of wound breakdown and nerve damage. This approach seeks to maintain a vascular full-thickness tissue flap using the blood supply from the perforating peroneal artery, whilst avoiding sural nerve damage. However, a thorough history and vascular assessment of the lower limb should be carried out and diabetes, smoking or previous surgery to the posterior aspect of the distal fibula should be considered relative contraindications. The incision is formed of two limbs, a vertical limb and a horizontal limb. These should be separated by at least 90
. The vertical limb should be made 5 cm proximal to the lateral malleolus commencing almost in the midline. This allows the sural nerve to be elevated anteriorly in the flap. The vertical limb should extend downwards to meet the junction between the skin of the sole and the skin of the foot. The horizontal limb may then be made in the skin of the sole of the foot as far anterior as the base of the fifth metatarsal. The flap may then be elevated by subperiosteal dissection to expose the body of the calcaneum. Dividing the calcaneofibular ligament allows access to the subtalar joint whilst splitting abductor digiti minimi in the line of its fibres allows access to the calcaneocuboid joint.

Decompression of compartment syndrome in the foot: the presence of high-energy injury to the foot, such as that which sometimes accompanies LisFranc injuries, necessitates the early recognition and treatment of compartment syndrome. There are nine compartments in the foot. The contents of each are outlined in Table 2. These may all be decompressed using a three-incision technique: The first incision is placed medial to the second metatarsal shaft whilst the second is placed lateral to the fourth metatarsal shaft. These allow decompression of the intermetatarsal compartments. The third incision is sited on the medial side of the foot along the body of the abductor hallucis muscle. Dissection both dorsal and plantar to this muscle allows decompression of the central and calcaneal compartments. Decompression of all foot compartments is desirable, although some surgeons opt to decompress the foot purely through a medial incision whilst accepting the likelihood of damage to the intrinsic muscles of the foot. Dorsal incisions for decompressing the intermetatarsal compartments have a relatively high morbidity with skin necrosis and poor wound healing.

Contents of each of the fascial compartments within the foot Compartment Medial Lateral Superficial Central Deep central (Calcaneal) First to fourth intermetatarsal compartments Distal plantar

Mid-foot Approach to Lisfranc fracture-dislocations: one of the commonest indications for surgery to the mid-foot is for unstable

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Muscle Contents Abductor hallucis Flexor hallucis brevis Abductor digiti minimi Flexor digiti minimi brevis Flexor digitorum longus Flexor digitorum brevis Quadratus plantae Plantar and dorsal interossei Oblique head of adductor hallucis

Table 2

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The choice of which approach to use may be dictated by the type of injury and clinical findings. Despite surgical intervention this condition carries a poor prognosis with a high incidence of contractures, toe-deformities, sensory neuropathy and paralysis.

different structures contribute to normal gait is important when considering gait dysfunction. Muscular activity during gait affords control of the foot such that the centre of gravity of the body progresses smoothly forward without excessive frontal plane motion. These muscle contractions are either concentric (muscle shortening) or eccentric (muscle lengthening). Walking gait is divided into a swing and a stance phase. The stance phase occupies just over 60% of the gait cycle and culminates at the point of toe-off (TO). After this the swing phase occupies the remaining 40%. The gait cycle has been further divided into eight stages (Figure 3).13 During the normal walking gait cycle there are two discrete periods of double limb support; initial and terminal. Together these form around 20% of the gait cycle. Initial double limb support occurs at heel-strike through to the end of the loading response phase. During mid-stance there is purely single limb support. Terminal double limb support occurs from the start of terminal swing until the end of pre-swing at toe-off. During running the periods of double leg stance disappear and there is solely single leg stance with periods of float where neither leg contacts the ground. Gait may also be specifically considered in relation to foot motion in the sagittal plane using the rocker theory which was described by Perry in 1992.14 During the first rocker the ankle plantarflexes after heel-strike bringing the forefoot into contact with the ground. Ankle plantarflexion is brought under control by eccentric contraction of the extrinsic anterior compartment muscles. This prevents a foot slap during gait. The strongest of these is tibialis anterior which descends from the anterior compartment in the leg to insert into the medial cuneiform and the base of the first metatarsal (Figure 4).15 Next during the second rocker the ankle dorsiflexes as the centre-of-gravity of the body moves over the joint. The foot must be flexible here to adapt to uneven ground. Tibialis posterior is the most powerful invertor of the foot. This is active in mid-stance during the second rocker to invert the subtalar joint which creates rigidity in preparation for force transmission at toe-off. The most powerful foot evertors are the peroneus longus and brevis which antagonize the inverting force of tibialis posterior. The dorsiflexion which occurs during the second rocker is controlled eccentrically by both the extrinsic and intrinsic plantarflexors of the foot. The final third rocker occurs as the metatarsophalangeal joints dorsiflex in preparation for toe-off. Here the windlass mechanism is activated, tensioning the plantar fascia under the

Forefoot Applied surgical anatomy of approaches to the first metatarsophalangeal joint (1st MTPJ): the 1st MTPJ is approached via either a dorsal or medial approach. This allows for fusion, arthroscopy, arthroplasty or soft tissue procedures around the joint. The dorsomedial approach to the 1st MTPJ is no longer commonly used due to the high incidence of injury to the dorsal digital nerve.12 The medial approach starts from just proximal to the interphalangeal joint taking care to align with the long axis of the first metatarsal the proximal extent of the incision. The dorsal digital branch of the medial cutaneous nerve lies dorsally in close proximity to the incision. The capsule may then be incised. The dorsal approach begins just proximal to the interphalangeal joint and should remain medial to the EHL tendon in a straight line. The fascia may then be divided in the line of the incision. Deep surgical dissection in this area must avoid the FHL tendon, which lies within a fibro-osseous tunnel on the plantar surface of the joint, kept in place by the medial and lateral sesamoid bones. Anatomy of surgical approaches to the lesser metatarsophalangeal joints: the lesser metatarsophalangeal joints may be approached by two different approaches. These are the dorsal approach and the transverse approach. Dorsally the second and third MTPJ may be approached using an incision medial to the second metatarsal whilst the fourth and fifth MTPJ may be approached through an incision placed laterally to the fourth metatarsal. Care should be taken to avoid the dorsal cutaneous nerves which supply sensation to the toes. These lie on the dorsolateral and dorsomedial surfaces of each metatarsal. If all the distal metatarsals require surgical intervention then a transverse approach may be used. This involves careful dissection to avoid damage to the dorsal veins of the foot but affords excellent access the metatarsophalangeal joints.

Gait Restoring normal or near-normal gait is one of the primary goals of many lower-limb surgeries. Understanding the role that the

Figure 3 Descriptive phases of gait.13

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Figure 4 The three ‘rocker’ phases of foot motion during gait. a Depicts the first rocker, b depicts the second rocker, c depicts the third rocker.15

The subtalar joint is able to invert by 20
and evert by 5
in the normal foot. This is reduced in patients with flat feet and may be reduced to around 12
.19 In normal feet, 1
of tibial rotation results in 1
of subtalar motion. The presence of a flatfoot deformity increases this relationship so a single degree of tibial rotation results in greater than 1
of subtalar motion (Figure 6).17

metatarsophalangeal joints and transforms into a rigid lever which can transmit a propulsive force to the ground. The extrinsic plantarflexors cease their eccentric activity in the terminal stages of the third rocker whilst the intrinsic plantarflexors contract concentrically to add further force and control to toe-off which occurs at the end of the third rocker. During the swing phase the anterior compartment muscles contract concentrically to allow foot clearance and pre-positioning before the next heel-strike.

Motion of the transverse tarsal (Chopart’s) joints Transverse tarsal motion is key to movement between flexibility and rigidity of the mid-foot during gait. One explanation of this is that the axes of the talonavicular and calcaneocuboid lie in parallel in the frontal plane when the subtalar joint is everted. The talonavicular joint or acetabulae pedis behaves as a ball and socket with its axis running through the talar neck. The calcaneocuboid joint is saddle-shaped with its axis through the calcaneal body. These configurations allow flexion and extension of the mid-foot relative to the hind-foot. When the subtalar joint is inverted the axes diverge, increasing the rigidity of the foot and facilitating force transfer to the forefoot.20 During the swing phase the subtalar joint is held in slight supination but at heel-strike there is rapid pronation as the heel

Biomechanics of the foot and ankle Foot function during the phases of gait as described above is permitted to occur by the specific motion of the joints of the foot and ankle. These are described in the next section. Motion of the ankle (tibiotalar) joint The ankle functions almost purely as a uni-planar hinge joint. The talus is on average 2.4 mm wider anteriorly than posteriorly and this mortise shape provides bony stability during dorsiflexion. There is also a small degree of coronal plane rotation. As a result dorsiflexion causes the forefoot to point laterally whilst plantarflexion causes the forefoot to point medially.16 The primary axis of rotation of the tibiotalar joint lies along a line between the tips of the two malleoli and this is angled at 10
to the frontal plane. Along this axis there is a normal range of movement of 10e20
dorsiflexion and 25e30
plantarflexion. Full ankle dorsiflexion provides only 11
of internal tibial rotation. Propulsion during toeoff requires 19
of internal tibial rotation. Hence some subtalar motion is required for normal gait.17 Congenital fusion of the subtalar joint can result in remodelling of the tibiotalar joint to a ball and socket joint. This joint configuration affords sufficient internal tibial rotation to allow a propulsive gait. Motion of the subtalar joint The effect of tibiotalar motion on the subtalar joint is explained using the principle of the ‘mitred hinge’. This is the principle whereby tibial rotation is transformed into pronation and supination of the forefoot by the combined motion of the subtalar and transverse tarsal joints. External tibial rotation results in subtalar supination whilst internal tibial rotation results in foot pronation (Figure 5).18

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Figure 5 The subtalar joint acts as a mitred hinge; external tibial rotation causes subtalar inversion or supination. Internal tibial rotation causes subtalar eversion or pronation.

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Figure 7 The beam model for stability of the medial longitudinal arch. This model assumes arch stability from bony contact and ligamentous support.

predisposes to the formation of dorsal osteophytes which are common features of first metatarsophalangeal arthritis. The plane from the first to fifth metatarsal heads which forms during toe-off is known as the metatarsal break. This is usually between 50
and 70
and represents the instant centres of rotation of each of the five metatarsophalangeal joints. The metatarsal break is usually visible on the soles of well-worn shoes as a transverse crease. Metatarsophalangeal joint movement is essential during the third rocker of gait. As the proximal phalanx passes over the metatarsal head it depresses it. In hallux valgus deformity the ability of the proximal phalanx to depress the first metatarsal head is diminished. This results in transfer of weight to other metatarsal heads, which may result in callosities or ‘transfer lesions’.

Figure 6 The axis of the subtalar joint lies 42
above the coronal plane (A) and 16
medial to the sagittal plane in the midline of the foot (B).

contacts the ground slightly lateral to the longitudinal axis of the lower limb. During the first 15% of the stance phase the lower limb internally rotates. This has the effect of pronating the foot, which allows it to become flexible. Here the foot is able to adapt to uneven ground. As the body-weight passes over the planted foot in late stance the heel inverts, supinating the forefoot and locking the mid-tarsal joints. This makes the mid-foot more rigid and allows effective transmission of force from the forefoot to the ground.17

Arches of the foot There are two longitudinal arches in the foot. These are the medial and lateral longitudinal arches. The medial longitudinal arch consists of the calcaneum, talus, navicular, medial, intermediate and lateral cuneiforms and the first three metatarsals. The talus sits at the apex of the arch and confers stability by acting as a wedge between the calcaneum and navicular. There

Motion of the tarsometatarsal (Lisfranc’s) joints and intertarsal joints The tarsometatarsal joints (TMTJ) contribute little to mid-foot flexibility. What little movement there is results from a gliding motion. Joint stability results both from a high degree of congruency and also from strong ligamentous support. The second metatarsal base is ‘keyed’ into its metatarsocuneiform joint, as the intermediate cuneiform lies slightly more proximal than the medial and lateral cuneiforms. This confers further bony stability. Lisfranc’s ligament runs from the medial cuneiform to the second metatarsal and is a major stabilizer. Movement at the first and second TMTJ is considerably less than that at the fourth and fifth. One study described first TMTJ motion as 3.5
flexion/extension and 1.5
pronation/supination. This compared to 9
flexion/extension and 9
pronation/supination at the fourth and fifth TMTJ.21 Motion of the metatarsophalangeal joints The first metatarsophalangeal joint is highly specialized in order to adapt to the variety of functions it performs. The normal range of motion is from 30
plantarflexion to 90
dorsiflexion. Achieving full painless dorsiflexion is essential for a normal toeoff during gait. The first metatarsophalangeal joint is stabilized by strong collateral ligaments but its congruency depends greatly on position. In neutral there is 0.38 cm2 joint surface area whilst in full dorsiflexion this reduces to 0.04 cm2.22 Whilst most of the joint motion is achieved through a tangential gliding motion, extreme dorsiflexion is achieved by joint compression. This

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Figure 8 The truss model for medial longitudinal arch support. Half the body-weight passes through the apex of the arch whilst standing. The ends of the ach are unable to move apart due to the tight plantar fascia which connects them (dashed line). Hence arch height is maintained.

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4

5 Figure 9 Schematic demonstration of the windlass mechanism for elevation of the medial longitudinal arch following metatarsophalangeal joint dorsiflexion.

6

are a number of important static stabilizers of the arch. These were studied by sequentially dividing structures in cadaveric feet to assess relative contributions to arch stability. The most important primary stabilizer is the plantar fascia, followed by the long and short plantar ligaments and then the spring ligament. Whilst tibialis posterior and other long flexors are important dynamic stabilizers, releasing these structures without releasing any static stabilizers has only a modest effect on arch height. One study found the result of releasing posterior tibial tension to be a reduction of 0.5 mm in arch height.23 There are two models for considering the stability of the medial longitudinal arch; the beam model and the truss model. In the beam model, a load is applied to the apex of the arch generating compressive forces on the dorsal surface and tensile forces on the plantar surface. Stability in this model results from bony congruency and ligamentous attachments (Figure 7). In the truss model, there is a triangular arrangement of structures. The bones of the arch are able to pivot about their apex whilst the tough plantar fascia forms the third side. This is firmly attached to the medial and lateral calcaneal tuberosities proximally and its slips insert into the plantar plate and the fibrous flexor sheathes distally (Figure 8).24 Hicks described the windlass effect whereby the medial longitudinal arch is raised on dorsiflexing the first metatarsophalangeal joint. The plantar fascia spans this joint and has minimal elasticity. When considering the truss model of arch stability, dorsiflexing the first MTPJ shortens the plantar side of the triangle which has to result in drawing the calcaneum closer to the metatarsal head. When this occurs arch height must increase (Figure 9).25

7 8 9 10

11

12

13 14 15 16

17 18 19

Conclusion

20

Understanding the complex anatomy and of the foot is an essential part of Orthopaedic practice. This article aims to provide a concise review of key concepts to aid in refreshing knowledge or exam preparation. A

21 22

REFERENCES 1 Norkus SA, Floyd RT. The anatomy and mechanisms of syndesmotic ankle sprains. J Athl Train 2001 Jan; 36: 68e73. 2 Burks RT, Morgan J. Anatomy of the lateral ankle ligaments. Am J Sports Med 1994 Jan; 22: 72e7. 3 Kjaersgaard-Andersen P, Wethelund JO, Helmig P, Soballe K. The stabilizing effect of the ligamentous structures in the sinus and

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canalis tarsi on movements in the hindfoot. An experimental study. Am J Sports Med 1988 Sep; 16: 512e6. Attarian DE, McCrackin HJ, Devito DP, McElhaney JH, Garrett Jr WE. Biomechanical characteristics of human ankle ligaments. Foot Ankle 1985 Oct; 6: 54e8. Golano P, Vega J, de Leeuw PA, et al. Anatomy of the ankle ligaments: a pictorial essay. Knee Surg Sports Traumatol Arthrosc 2010 May; 18: 557e69. Burns WC, Prakash K, Adelaar R, Beaudoin A, Krause W. Tibiotalar joint dynamics: indications for the syndesmotic screw e a cadaver study. Foot Ankle 1993 Mar; 14: 153e8. Viladot A, Lorenzo JC, Salazar J, Rodriguez A. The subtalar joint: embryology and morphology. Foot Ankle 1984 Sep; 5: 54e66. Hertel J. Functional anatomy, pathomechanics, and pathophysiology of lateral ankle instability. J Athl Train 2002 Dec; 37: 364e75. Mulfinger GL, Trueta J. The blood supply of the talus. J Bone Joint Surg Br 1970 Feb; 52: 160e7. Chen TM, Rozen WM, Pan WR, Ashton MW, Richardson MD, Taylor GI. The arterial anatomy of the Achilles tendon: anatomical study and clinical implications. Clin Anat 2009 Apr; 22: 377e85. Eastwood DM, Langkamer VG, Atkins RM. Intra-articular fractures of the calcaneum. Part II: open reduction and internal fixation by the extended lateral transcalcaneal approach. J Bone Joint Surg Br 1993 Mar; 75: 189e95. Solan MC, Lemon M, Bendall SP. The surgical anatomy of the dorsomedial cutaneous nerve of the hallux. J Bone Joint Surg Br 2001 Mar; 83: 250e2. Descriptive phases of gait; 2011. 6-1-2010. Perry J. Gait analysis: normal and pathological function. Thorofare, NJ: SLACK Inc, 1992. van DR. Mechanical loading and off-loading of the plantar surface of the diabetic foot. Clin Infect Dis 2004 Aug 1; 39(suppl 2): S87e91. Wright DG, Desai SM, Henderson WH. Action of the subtalar and ankle-joint complex during the stance phase of walking. J Bone Joint Surg Am 1964 Mar; 46: 361e82. Ramachandran M. The Stanmore guide to basic orthopaedic science; 2011. Mann RA. Biomechanics of the foot and ankle. In: Surgery of the foot and ankle. 1st edn. St. Louis: C.V: Mosby Co., 1993: 3e33. Nordin M, Frankel V. Basic biomechanics of the musculoskeletal system, vol. 3. Baltimore, MA: Lippincott Williams & Wilkins, 2001. Elftman H. The transverse tarsal joint and its control. Clin Orthop 1960; 16: 41e6. Ouzounian TJ, Shereff MJ. In vitro determination of midfoot motion. Foot Ankle 1989 Dec; 10: 140e6. Ahn TK, Kitaoka HB, Luo ZP, An KN. Kinematics and contact characteristics of the first metatarsophalangeal joint. Foot Ankle Int 1997 Mar; 18: 170e4. Kitaoka HB, Luo ZP, An KN. Effect of the posterior tibial tendon on the arch of the foot during simulated weightbearing: biomechanical analysis. Foot Ankle Int 1997 Jan; 18: 43e6. Sarrafian SK. Functional characteristics of the foot and plantar aponeurosis under tibiotalar loading. Foot Ankle 1987 Aug; 8: 4e18. Hicks JH. The mechanics of the foot. II. The plantar aponeurosis and the arch. J Anat 1954 Jan; 88: 25e30.

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(vii) Clinical examination of the foot and ankle

higher if hip and spinal pathology are suspected from the history. Before looking at the patient, take a moment to examine their footwear once it is removed as the wear pattern may give you an idea of any gait or rotational deformities the patient has and will give you a chance to look at any orthoses or insoles that may have been used. Also note the style of shoes; in particular, if they have been designed to accommodate a fixed deformity in the foot and ankle. Walking aids may also have been brought into the examination room and should be noted if present.

Howard Davies Chris Blundell

Abstract Examination of the foot and ankle can appear to be highly complicated, but if broken down into the component parts of “look, feel and move” supplemented with some simple special tests then it is often possible to arrive at a sound clinical diagnosis. The foot is a dynamic structure, therefore weight bearing and in particular gait is an essential part of the examination, as is an assessment of lower limb neurology. Remember to pay particular attention to a patient’s footwear and any orthoses they may use.

Look Static inspection Front: in the first instance, ask the patient to stand in front of you with legs together if possible, in order to get a good comparison. From the front note the general alignment, including rotational profile, and approximate leg lengths. In a logical order starting distally observe the shape of the foot, looking in particular for hallux valgus and deformities of the lesser toes (Table 1). Hallux valgus is defined as a deviation of the great toe of more than 10 degrees from the midline. It is commonly associated with a bunion, which is in fact a separate deformity and usually comprises part of the metatarsal head with its overlying bursa. It is often the bunion rather than the first metatarsophalangeal joint which is symptomatic due to pressure caused by ill-fitting footwear; overlying erythema and swelling should help to distinguish the cause. A bunion overlying the fifth metatarsal head is termed a bunionette and can make the foot very broad, resulting in difficulty fitting shoes. Claw toes can be as a result of abnormal neurology and this should be borne in mind for the remainder of the examination. At the toe level also note whether there is any under or overriding of adjacent toes, any ulceration or dorsal callosity over the joints or deformity of the nails and try to visualize how the deformity will affect shoe wear and function. From the front one can also assess the state of the skin for scars, swelling, varicosities and erythema. In patients with a sensory neuropathy and intact skin a swollen, warm and red foot is much more likely to represent Charcot neuropathy than an infection and should be investigated urgently.

Keywords ankle; examination; foot

Introduction The foot and ankle comprise a complex array of mobile and planar joints, ligaments and tendons that act synergistically to propel the body forwards whilst walking and to provide a stable weight bearing surface for standing. Whilst the number of joints within the foot can be challenging for the examiner, by following the basic tennets/principles of look, feel and move and by using a logical approach the diagnosis of pathology within the foot can be simple and rewarding. However, the foot and ankle are dynamic structures relying on both intrinsic and extrinsic muscles to stabilize joints and allow propulsion. For this reason it is vital that all patients walk at some point during the examination to assess their gait and foot function whilst the muscles are acting, to make the pathology apparent. It is also important to examine meticulously areas of the foot that are often overlooked such as the plantar aspect and between the toes, and to complete each examination by assessing the foot pulses and any neurological deficit. It is essential that both the examiner and patient are comfortable during the consultation and as such you require a spacious room with an area to walk in, a height adjustable couch with a foot stool and a goniometer to measure angles accurately.

Side: next inspect the feet from the side. It is much easier if the examiner gets the patient to move rather than the other way around. Look carefully at the medial arch and make an assessment of whether it is flat (planus), high arched (cavus) or normal and whether both sides are symmetrical. In extreme planus deformities it may be possible to see the head of the talus push into the ground. Viewing from the side may help identify clawing or other deformities of the lesser toes.

General overview Before the examination can take place the patient needs to expose both lower limbs to above the knee as a minimum, even

Deformities of the lesser toes

Howard Davies MSc FRCS (Tr&Orth) Foot and Ankle Fellow, Sheffield Foot and Ankle Unit, Department of Trauma and Orthopaedics, Northern General Hospital, Sheffield, UK. Conflict of interest: none declared. Chris Blundell MD FRCS (Tr&Orth) Consultant Trauma and Orthopaedic Surgeon, Sheffield Foot and Ankle Unit, Department of Trauma and Orthopaedics, Northern General Hospital, Sheffield, UK. Conflict of interest: none declared.

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Name

Deformity

Mallet toe Hammer toe Claw toe

Flexion Distal Interphalangeal Joint (DIPJ) Flexion Proximal Interphalangeal Joint (PIPJ) Flexion both DIPJ and PIPJ

Table 1

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Back: last, turn the patient to inspect the feet from behind. Subtle swelling of the ankle joint can manifest posteriorly by blurring the sharp outline of the Achilles tendon. Both sides should be compared. This is now an ideal opportunity to watch the patient walk in order to assess their gait pattern.

heel and the medial arch are intimately related to several structures, but in particular the tibialis posterior (tib post) tendon. If the tendon degenerates or ruptures the arch will collapse and the hindfoot will be pushed into valgus. The integrity of the tib post can be tested by asking the patient to perform a heel raise (stand on tip toes). The tib post is a powerful flexor and inverter of the hindfoot, so as the muscle activates to lift the heel the intact tendon will pull the hindfoot into varus. It is important to ask the patient to perform a single stance heel raise on the affected side only, as it is possible to mask a symptomatic leg by compensating with the opposite one. The test should also ideally be performed with the patient standing as close to a wall as possible. This will give them a chance to place their hands against the wall for stability whilst standing on one leg without being able to lean forward and do a “push up” on the wall to help the heel raise and give a false impression of an intact tib post. In subtle cases the flexor hallucis longus (FHL) and flexor digitorum longus (FDL) tendons may compensate for a weak tib post and the patient may be able to perform a single stance heel raise. However, the muscle bellies of FHL and FDL are relatively small and fatigue very quickly, so in this situation the patient is asked to perform multiple heel raises. As they tire the problem will be unmasked. There are many other reasons why a patient may not be able to perform a heel raise, including Achilles tendonopathy, motor weakness and pain or stiffness from arthritic joints in the foot and ankle, all these causes need to be considered before diagnosing tib post deficiency.

Dynamic inspection Gait: ask the patient to walk directly away from you, turn around and walk directly back so that you can watch from both sides. Ensure the patient keeps their head up and looks forward as otherwise this will affect their walking pattern. Gait analysis can be very demanding and complex so we recommend concentrating on a few important principles and features. First consider the cadence, rhythm and symmetry of the gait. Note whether it is antalgic or high stepping, and if there is evidence of a foot drop. In foot drop caused by weakness in the tibialis anterior muscle (e.g. peroneal nerve palsy) you may see recruitment of the extensor hallucis longus and extensor digitorum longus tendons in order to dorsiflex the ankle, but which leads to a simultaneous dynamic clawing of the toes. It may be possible to see a medial arch form during the swing phase of gait in a patient with a mobile flat foot. Patients with stiff ankle joints often walk with external rotation of the foot as this way they can compensate for the lack of ankle dorsiflexion by rolling over the subtalar joint instead. Ankle stiffness can be further examined by stopping the patient and asking them to squat down whilst keeping their heels pressed into the ground. Any loss of dorsiflexion will lead to the heels rising as the patient descends. Causes include intrinsic ankle pathology and a tight Achilles tendon. This is a useful test as patients with a tight Achilles tendon and lack of dorsiflexion can present with metatarsalgia as the forefoot is overloaded during the walking cycle, yet the problem to be addressed is in the hindfoot. Walk the patient as necessary, without causing undue discomfort, until you are sure you have identified most of the above points. Subtle gait abnormalities can be unmasked by asking the patient to walk faster. Remember to consider the knee, hip, spine and neurological causes for unusual gait patterns.

Too many toes: in long standing tib post insufficiency a flat foot deformity can occur, which causes the forefoot to adopt an abducted position. If you observe the patient from behind you will notice that you can see more toes lateral to the tibia than on the normal side. This is known as the ‘too many toes sign’ and whist it is common in tib post insufficiency, be aware that it can also be a feature of external tibial rotation. It is normally reckoned that more than two toes protruding laterally is abnormal (thus “two toes is too many toes”) although in reality it is safer just to note a difference between the two sides.

Tibialis posterior: in a standing position the heel normally adopts a slight valgus position (Figure 1). Both the position of the

Cavo-varus foot: if the heel is in varus rather than in valgus then not only will it be difficult for the patient to perform a single stance heel raise due to lateral instability, but the test will not elicit any useful information as the tib post has to be intact in order for the heel to attain this position. The varus heel will usually be accompanied by a midfoot cavus deformity because the foot naturally wants to adopt a plantigrade position and in order to do so it must form a tripod. As the heel moves medially the forefoot supinates correspondingly which elevates the first ray off the ground, therefore in order to reform the tripod the first ray must flex creating a high medial arch. In these situations we need to ask two questions which may affect further treatment. First, we need to ascertain whether the cavus deformity is driven by (primarily caused by) the plantar flexed first ray or the varus heel. Second, is the hindfoot deformity fixed or flexible? Both these questions can be answered by the Coleman block test. Coleman block test: the idea behind the Coleman block test1 is simply that by standing with the heel on a high surface and allowing the first ray to drop into space without touching the

Figure 1 Normal valgus alignment of the hindfoot.

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swelling or tenderness that might represent a tendonopathy. Continue distally to the insertion of the tendon, where pain will represent an enthesopathy, a bursitis or a bony prominence that impinges between the posterior calcaneum and the Achilles, known as a Haglund deformity. The posterior part of the ankle joint can also be palpated for tenderness and it is possible to feel the joint line at this level. Moving medially, palpate the tib post tendon from its origin behind the medial malleolus to its insertion at the navicular. From observation you will already have an idea whether the tendon is ruptured by the shape of the foot, or dysfunctional by the inability to heel raise, but pain on palpation will unmask a lesser degree of tendonopathy (grade I) that may be amenable to treatment with physiotherapy rather than surgery. Whilst on the medial aspect of the hindfoot, palpate the deltoid ligament, which runs from the tip of the medial malleolus to the talus. The deltoid ligament is unlikely to be damaged by degenerative processes but a traumatic rupture can lead to instability of the ankle joint. The subtalar joint should be palpated from the lateral side. Orientate yourself by finding the sinus tarsi, which is a soft spot just anterior to the distal fibula. Once you have the correct level then you can easily identify the anterior and posterior processes of the subtalar joint. Pain on palpation may represent arthrosis within the joint, though deep palpation in the sinus is usually tender as this area is well endowed with nociceptors. In traumatic situations, ensure you examine the anterior talofibular and the calcaneofibular ligaments that lie anterior and distal to the fibula respectively and which confer stability to the ankle mortice. Swelling and tenderness over the ligaments may indicate a chronic rupture. The peroneal tendons lie posterior to the fibula, with peroneus brevis being closest to bone. The peroneal tendons can dislocate anteriorly if the retinaculum is disrupted and this may be felt as a click as the ankle joint is passively moved from plantar flexion with hindfoot inversion to dorsiflexion with hindfoot eversion.2 Follow the peroneus brevis tendon to its insertion at the base of the fifth metatarsal to palpate for tenosynovitis, which may represent intra-substance tears.

ground, one can eliminate one of the two potential drivers of the cavus foot, which should provide the answers to the above questions. In order to perform the test, ask the patient to stand with the heel and the lateral border of their foot on a block or a thick book, the British National Formulary is perfect (Figure 2). With the first ray overhanging the block in space, ask the patient to try and touch the floor with the great toe. It is often helpful to get the patient to stand on a block with the other foot to keep them balanced and to demonstrate the test in front of them before they attempt it. Once the test is set up, stand behind the patient and look at the heel from the back. If the heel returns to a normal valgus position this tells us that the hindfoot is flexible and the deformity is being driven by a flexed first ray (which has now been eliminated). If the hindfoot remains in fixed varus it tells us that the deformity is driven by the hindfoot. The distinction between flexible and fixed hindfoot deformities is important for pre-operative planning as a cavus foot with a flexible hindfoot deformity may be corrected with a first ray osteotomy and tendon transfers alone, whereas a fixed hindfoot will require an additional calcaneal osteotomy or a subtalar fusion. Skin: following the standing inspection, sit the patient on a high couch in a comfortable position with their affected foot unsupported by the examiner. Ensure that the patient’s hip is not excessively flexed and the plantar aspect of the foot is easy to see. Examine the plantar aspect of the foot looking particularly for calluses under the metatarsal heads and don’t forget to look for lesions between and on the tips of toes.

Feel Now you have “looked” you can move onto the “feel” part of the examination. Palpation should be used to elicit areas of tenderness, tenosynovitis, swelling and warmth. It is important to palpate every part of the foot and ankle in a logical order and we recommend starting proximally and moving distally. Hindfoot Seat the patient with their leg supported on a stool and begin by firmly palpating the substance of the Achilles tendon for any

Ankle Move to the anterior part of the ankle joint and palpate along the whole margin of the mortice. It is often possible to provoke painful symptoms in the arthritic ankle and may be possible to identify anterior margin osteophytes. Whilst moving across the ankle from medial to lateral there is an opportunity to palpate the tendons that overlie the ankle including tibialis anterior, extensor hallucis longus (EHL), extensor digitorum longus (EDL) and peroneus tertius. In each case, it may be possible to identify tenosynovitis. Midfoot The midfoot consists of the Chopart joints (talonavicular and calcaneocuboid) and the Lisfranc complex (tarsometatarsal joints). The key to examining these joints is to have an appreciation of their location within the foot, which is often more proximal than expected. The talonavicular joint is usually easy to find as the head of the talus can be found medially and can be exposed by inverting and everting the midfoot. Once you have identified the level of the talonavicular joint, move laterally at the same level to palpate the calcaneocuboid joint and distally to palpate the

Figure 2 The Coleman block test.

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cuneiforms and the tarsometatarsal joints. Tenderness in any region is likely to be due to an underlying arthritic joint. Forefoot Palpation of the forefoot is mostly focused on the metatarsal heads and the adjacent joints. Examine each metatarsal head in turn, paying particular attention to any callus formation or tenderness that might represent overloading of the head, often secondary to a short first ray. The metatarsophalangeal joint (MTPJ) may also be thickened and tender due to synovitis, particularly in rheumatoid patients, and is often more apparent on the dorsal aspect of the joint. Acute swelling and significant pain associated with the MTPJ’s may be secondary to a plantar plate rupture and will cause hammering of the toe as a late sign. Patients with deficient plantar plates often develop subluxation of the MTPJ’s, which may eventually lead to frank dislocation. In the early stages it can be possible to elicit a drawer sign of the lesser toes analogous to Lachman’s test in the knee. The significance of a positive result is that in a patient undergoing first ray surgery, a lesser metatarsal osteotomy may be required to relocate the unstable toe. Instability is diagnosed by firmly holding the base of the proximal phalanx with one hand and the corresponding metatarsal neck with the other and translating the toe backwards and forwards such that the MTPJ subluxates and relocates. Ordinarily, there should be no translational movements at the joint. Be careful because this manoeuvre can be very painful in an acutely inflamed joint and there may be only one chance to try it.

Figure 3 Mulder’s click test.

by active. Given the large number of joints in the foot, the examination can be deceptive, as although it may appear that a particular joint is moving, it may be the adjacent joints that are masking stiffness. Therefore, in order to ensure each joint is examined correctly, it is important that the examiner stabilizes the adjacent joints with his or her other hand. Ankle: the main movement of the ankle is plantar and dorsiflexion, usually with an arc of 65 degrees. It is very easy to mistake motion at the ankle for that in the midfoot, and indeed it can be difficult to tell if a patient has an ankle fusion by glancing at them as they walk due to the amount of compensation that can occur in the distal aspect of the foot. For this reason, as you examine the ankle, it is vital that you stabilize the midfoot. We recommend that you grip the heel with the palm of your hand and rest the sole of the foot on your forearm (Figure 4). This way, as the ankle moves you are blocking any motion at the midfoot and getting a true picture. The examination can be made more accurate by using your other hand to palpate the anterior aspect of the talar dome in the mortice to get an idea of how it is moving in comparison to the foot. Very little movement of the talus suggests movement is occurring through the distal joints.

Morton’s neuroma Morton’s neuromata are a common cause of pain in the forefoot and are often described by the patient as a severe burning with the symptoms being relieved when the shoes are removed. In order to examine for a neuroma, palpate firmly between each of the metatarsal heads in turn, ensuring that you distinguish between the space and the metatarsal head itself. In any webspaces that exhibit pain on palpation you should perform a Mulder’s click test to help clarify the diagnosis.3 The basis of the Mulder’s click is that a sizeable neuroma if pushed out from between the metatarsal heads will produce a palpable and occasionally audible click. Beware, however, that the test may be falsely positive for all masses between the metatarsal heads, including bursae. The test is performed by maximally dorsiflexing the foot and applying firm pressure between the metatarsal heads with the thumb of one hand. This manoeuvre ensures that the neuroma is situated between the metatarsal heads. Using the other hand, squeeze the first and fifth metatarsal heads together and feel for a click, which is a positive sign, as the swelling moves from a dorsal to a plantar position relative to the adjacent metatarsal heads (Figure 3). The test should be repeated for each webspace. As neuromata form on digital nerves they often alter sensation to the affected toes, so it is strongly recommended that one checks the sensation along the border of each toe in order to help confirm or refute the diagnosis.

Move Passive movement The final stage of the examination is movement, and again this should be done in a logical fashion starting proximally and working distally, usually with passive movements first followed

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Figure 4 Examination of the ankle joint.

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A common mistake when examining the range of movement of the ankle is not to take into account the effect of a short Achilles tendon secondary to either a valgus or a varus hindfoot. As the calcaneum moves medially or laterally, the axis of pull of the Achilles moves from the midline and eventually acts as a secondary driver of the deformity. As this process progresses, the Achilles tendon gradually becomes shortened as the distance it needs to traverse is decreased. When you measure ankle movement in a patient with hindfoot deformity it can appear that they have a good range of movement; however, to assess it properly the hindfoot, if flexible, has to be brought into a neutral position. Only then will any shortening of the Achilles tendon become obvious as the foot will tend to plantar flex as the heel is brought into line. This is useful as it allows one to distinguish between stiffness secondary to intrinsic ankle pathology and stiffness secondary to a tight Achilles tendon.

aligns with the hindfoot and whether it is able to maintain a neutral position. The Lisfranc complex is situated between the base of the metatarsals and the cuneiforms/cuboid. These are planar joints and so have little movement but can cause significant pain if they are arthritic. They can be examined en mass by stabilizing the cuneiforms with one hand and moving the metatarsals in the plane of motion, which is both dorso-plantar and mediolateral. It is often useful to examine the first tarsometatarsal joint (1st TMTJ) in isolation from the other joints at the Lisfranc level. This can be done by firmly holding the lateral metatarsals whilst moving the first metatarsal shaft up and down with the other hand. In certain patients there can be a degree of hypermobility at the 1st TMTJ, and in these patients standard osteotomies for hallux valgus correction may have a higher recurrence rate.5 Although it is difficult to quantify hypermobility at the 1st TMTJ, a difference in displacement of 2 cm compared to the lateral rays is usually taken as a positive result.

Silverskiold test: ankle dorsiflexion is commonly restricted by a tight Achilles tendon. The Silverskiold test4 can be used to differentiate between a tight gastrocnemius and a tight soleus muscle. It relies on the fact that the gastrocnemius muscle crosses both the knee and the ankle and therefore can be effectively lengthened by flexing the knee. Sit the patient down with the knee fully extended, then dorsiflex the ankle as much as possible and record the range. Now ask the patient to flex the knee and repeat the ankle dorsiflexion. If the two measurements are different and the ankle dorsiflexes further with the knee bent then the gastrocnemius is tight.

Forefoot: the first MTPJ is very susceptible to arthritic change and dorsal osteophytes are commonly present and often palpable. A careful examination here can be extremely valuable in determining appropriate surgery in suitable patients. Holding the first metatarsal for support, put the great toe through its full range of movement. Note the maximum dorsiflexion and plantar flexion and especially whether there is painful impingement of osteophytes against the proximal phalanx at the extremes of movement. Now apply axial pressure across the joint and grind it with small circular movements: pain and crepitus represent an arthritic joint. If the patient has pain only on the extremes of movement along with palpable osteophytes, they may benefit from a cheilectomy, which would remove the obstruction and retain movement in the joint. If the pain is present in the mid-part of motion and on grinding the joint then a fusion or joint replacement would be more appropriate. In hallux valgus, as well as dorsal and plantar flexion, make an attempt to reduce the deformity by squeezing the first and fifth metatarsals together and pulling the great toe medially. This manoeuvre will give you a feel for how easy it will be to surgically reduce the deformity and potentially how successful the outcome is likely to be. Patients with hallux valgus are often

Ankle stability: as well as dorsiflexion and plantar flexion the ankle can be examined for stability in both the antero-posterior and coronal planes. For anterior stability you can perform the drawer test, which is analogous to the Lachman test. With the patient fully relaxed and the foot in a degree of gravity equinus, place one hand behind the calcaneum and the other hand on the anterior aspect of the tibia to support it. Pull the heel forwards and note the degree of anterior translation of the talus against the tibia; it often requires comparison between the two sides to record a pathological result. Remember to move the talus forward perpendicular to the inter-malleolar axis so that the more anteriorly positioned medial malleolus does not give a false negative anterior drawer test. The ankle can also be unstable in the coronal plane, usually secondary to calcaneal-fibular ligament deficiency. Medial and lateral movements are often mistaken for those at the subtalar joint. The key to differentiating between instability of the ankle and subtalar movement is to place a thumb over the upper lateral corner of the talus in the ankle mortice. Grasp the heel and make side to side movements, if the ankle is unstable then you should feel a definite tilt of the talus as it subluxates out of joint. If the ankle is stable then most coronal movement will occur at the subtalar joint, which has a range of approximately 30 degrees. Midfoot: the talonavicular joint allows supination and pronation of the forefoot on the hindfoot. In order to examine this joint the hindfoot represented by the talus must be stabilized with the thumb from one hand on the talar neck whist the forefoot is put through its range of motion by the other (Figure 5). Movement at this complex gives the opportunity to study how the forefoot

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Figure 5 Examination of the talonavicular joint.

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maximal plantar flexion (tib post) and inversion with dorsiflexion (tib ant). Both these manoeuvres should be accompanied by direct palpation of the appropriate tendon. Neurovascular The examination should be completed by assessing the foot pulses and capillary refill as well as performing a full sensory examination, including both dermatomes and individual nerve distributions. Any global sensory deficit should be investigated further with a 10 g Semmes Weinstein filament to test for protective sensation.

Conclusions

short in the first ray, which subsequently causes overloading of the adjacent rays, particularly the second. There will be a tendency for the overloaded second ray to try and shorten itself and this occurs in the form of a hammer toe deformity and instability at the MTPJ which can be assessed as described above. Whilst examining the great toe ensure the Interphalangeal joint is examined for range of movement, pain and osteophytes. Finally, assess the lesser toe MTP, PIP and DIP joints individually for pain, instability and deformities and note whether they are fixed or correctable.

The descriptions given above are a guide as to how one can approach the task of formally and methodically examining the foot and ankle. However, it can only really be learnt through experience and through practice, from a platform of a sound understanding and appreciation of the anatomy and biomechanics of the foot and ankle. Furthermore, the examination of the foot and ankle can only be put into appropriate context with a good understanding of the potential pathologies that can exist. As one gains experience in the assessment of the foot and ankle, an approach to clinical examination will inevitably evolve. However, particularly for those in training, a step-by-step, didactic, methodical approach can help enormously in ensuring that the examination is thorough and that potential pathologies are not overlooked. A

Active movement Assessing the active movements of the foot and ankle will give an idea of the muscle strength that drives them. One must be aware, however, that both pain and any stiffness will limit power across any joint. The main movements to assess are plantar flexion and dorsiflexion of the ankle, inversion and eversion of the hindfoot and flexion and extension of the toes. Both sides should be compared at each stage. The concept of inversion (tib ant and tib post) and eversion (peroneal tendons) can be difficult for some patients to grasp, so rather than asking a patient to perform them, it is easier to place the foot into the position of maximal deformity and ask them to push against the examining hand (Figure 6). Whilst both tib ant and tib post are inverters of the hindfoot they can be examined in isolation by testing inversion with

REFERENCES 1 Coleman SS, Chestnut WJ. A simple test for hindfoot flexibility in the cavovarus foot. Clin Orthop 1977; 123: 60. 2 Mason RB, Henderson IJP. Traumatic peroneal tendon instability. Am J Sports Med 1996 SepeOct; 24: 652e8. 3 Teasdale RD, Saltzman CL, Johnson KA. A practical approach to Morton’s neuroma. Musculo Skel Med 1993 Feb; 39e55. 4 Fernandes JA, Bell MJ. Orthopaedic examination techniques in children. In: Harris N, Stanley D, eds. Advanced examination techniques in orthopaedics. Greenwich Medical, 2003; 209. 5 Faber FW, Klinrensink GJ, Verhoog MW, et al. Mobility of the first tarsometatarsal joint in relation to hallux valgus deformity: anatomical and biomechanical aspects. Foot Ankle Int 1999 Oct; 20: 651e6.

Figure 6 Resisted eversion of the hindfoot.

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QUIZ

Paediatric radiology quiz Questions

Case 2 A 14-year-old girl with a history of coarctation of the aorta and horseshoe kidney, presented with painful wrist movements. She was also noted to have a webbed neck and shield chest. Wrist X-rays are shown [Figure 2(a) and (b)]. What is this appearance of the distal radius and ulna known as? What are the other possible causes?

Case 1 A 13-year-old male presented to the knee clinic with a few months history of mild joint pain, tenderness, swelling and limited movement of the knee joint. What is seen on the radiographs [Figure 1(a) and (b)] and CT scan images [Figure 1(c) and (d)]? What investigations would you arrange next? What are the differential diagnoses?

Figure 2

Figure 1

Ajay Sahu MBBS MS (Ortho) MRCS Specialist Registrar, Department of Radiology, Derriford Hospital, Plymouth, UK. Sharmila Chhatani MBBS MD Specialist Registrar, Department of Radiology, Derriford Hospital, Plymouth, UK. Judith Foster MBBS FRCR Consultant Paediatric Radiologist, Department of Radiology, Derriford Hospital, Plymouth, UK.

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Case 3 A GP refers to a 6-month-old child with a cutaneous cystic lesion over the lumbosacral spine to the paediatric orthopaedic clinic. There is a known family history of spinal problems. Which radiological imaging modality has been used [Figure 3(a)]? What are the findings seen on the MRI spine, midsagittal T1 and axial T2-weighted image [Figure 3(b) and (c)]? What is the diagnosis?

Case 4 A small 15-year-old girl with normal intelligence and motor function presents with an enlarged bulging forehead, protruding jaw and frontal bossing. She was sent by the GP for monitoring radiographs to look for radiographic features of achondroplasia. What are the features on these X-rays to suggest the diagnosis? [Figure 4(aec)].

Figure 3

Figure 4

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Case 5 A 16-year-old boy presented to the emergency department with a painful middle finger after playing rugby. AP and lateral radiographs of the hand [Figure 5(a) and (b)] are shown. What are the findings and the differential diagnoses?

Case 6 An 18-year-old boy presented with multiple bilateral hard lumps around his left knee, elbow and pelvis. The ring and little fingers of his right hand are shortened and he has six fingers on his left hand. He mentioned that these lumps have stopped growing for the last 2e3 years. What are the X-ray findings? What are the associated complications (Figure 6)?

Figure 6

Answers Case 1 The plain X-rays [Figure 7(a)and (b)] of the knee show that there is a lytic expansile mass arising in the metaphysis of the distal femur but spreading distally to involve the epiphysis laterally. The lysis is so complete laterally that the cortex is not visualized but there is no evidence of a soft tissue mass or periosteal reaction. The CT scan images [Figure 7(c) and (d)] show that there is a large soft tissue mass within an expanded distal femur. The lesion appears well defined but contains soft tissue which extends across the growth plate into the epiphysis of the lateral femoral condyle. The appearances are suggestive of a benign lesion but given its extension across the growth plate an aggressive component does exist. The reconstructed images give a better understanding of the lesion [Figure 7(e) and (f)].

Figure 5

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The next line of investigation is MRI. The MRI femur with contrast [Figure 7(g), (h) and (i); coronal T1, STIR sequence and axial T1 respectively] shows that this mass has a component crossing the growth plate into the epiphysis. The lesion has well-defined margins. There is some oedema within the shaft of the femur proximally. Given the involvement of the growth plate and marrow oedema, the lesion is more likely to be an aggressive lesion, although not overtly malignant. The histology suggests that this lesion is a chondromyxoid fibroma. The differential for this lesion includes (1) Fibrous dysplasia (2) Simple bone cyst (3) Nonossifying fibroma (4) Aneurysmal bone cyst (5) Enchondroma

(6) Chondroblastoma (7) Eosinophilic granuloma (8) Fibrous cortical defect (9) Giant cell tumour. Chondromyxoid fibromas present with slowly progressive local pain, swelling, and restriction of motion. The common location is in the long bones around the knee and the site is usually eccentric, either metaphyseal (47e53%) or metadiaphyseal. The features include an expansile ovoid lesion with a lucent centre, bone destruction, a well-defined sclerotic margin (86%), an expanded shell with bulged and thinned overlying cortex in two-thirds of cases, scalloped margin (58%), septations (57%) which may mimic trabeculations, stippled calcifications within tumour in advanced lesions (7%) and no periosteal reaction (unless fractured).

Figure 7

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Case 2 The plain X-ray of the wrist shows deformity of the medial aspect of the epiphysis and metaphysis of the right distal radius. These appearances, in part, are of a ‘Madelung deformity’ [Figure 8(a) and (b)] which constitutes arrest of epiphyseal growth of the ulnar (medial) and volar (anterior) portions of the distal radius and leads to shortening of the radius and relative overgrowth of the ulna. This may be congenital in nature or may have been acquired from previous trauma or other insult. Madelung deformity of the wrist is characterized by a growth disturbance in the volareulnar distal radial physis that results in a volar and ulnar tilted distal radial articular surface. This also causes volar translation of the hand and wrist, and a dorsally prominent distal ulna. It is usually associated with cubitus valgus deformity. Imaging findings are bilateral in 50e66% of patients. It can also predispose to avascular necrosis of the lunate because of carpal wedging between the radius and ulna. The diagnosis in this case is Turner’s syndrome (complete monosomy 45, XO) because of the other associated features. Its incidence is 1:3000e5000 live births. These patients can have associated coarctation, aortic stenosis, horseshoe kidney, primary amenorrhoea, short stature, webbed neck, shield-shaped chest and widely spaced nipples. The different aetiologic groups for a Madelung deformity are as follows: (1) post-traumatic, (2) dysplastic, (3) chromosomal or genetic and (4) idiopathic or primary. Another differential diagnosis is pseudo-Madelung deformity (from trauma or infection). In this, carpal wedging is found between the radius and ulna (due to the triangular shape of the distal radial epiphysis and underdevelopment of the ulna).

Case 3 The imaging modality used here is ultrasound of the lower spine [Figure 9(a)]. It showed that the conus terminates between L1 and L2. However the filum terminale is prominent and is seen right to the end of the spinal canal where a cystic structure arises posterior to the sacral bodies. The concern was raised that there may be tethering of the filum terminale with a possible associated meningocele. Therefore an MR of the spine was performed for further assessment. The MRI lumbar spine shows a large cystic lesion at the level of S1/S2 within the spinal canal. The filum terminale appears lateralized and ventrally displaced. The axial T2-weighted imaging shows a small bony defect in the sense of an incomplete dorsal fusion of the vertebral bodies of the sacral bone and the spinal canal is only covered by a soft tissue layer. Appearances are suggestive of a covered meningocele in the spinal canal at the level of S1/S2. [arrow head Figure 9(b) and (c)]. This is likely to be as a result of spinal dysraphism. Spinal dysraphism is a generalized term for a group of congenital abnormalities that can cause progressive neurological damage and therefore deterioration of neural and physical function. Neural tube defects and spinal dysraphism can be classified under: 1. Open forms: these include myelocele, meningocele and myelomeningocele and are often associated with hydrocephalus and Arnold Chiari Malformation I and II. These forms are classified as spina bifida cystica if their form includes a sac containing neural elements. 2. Closed forms: spina bifida occulta (simple forms) and spina bifida occulta with tethered cord.

Figure 9

Figure 8

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Case 4 The plain radiograph of the pelvis [Figure 10(a)] shows features of achondroplasia with square iliac bones, flattened acetabulae and short femoral necks. The elbow X-ray AP and lateral views [Figure 10(b) and (c)] show lateral bowing of the distal humerus. Achondroplasia is an autosomal dominant disease with defective bone formation. Features include: Neurologic:  Normal intelligence and motor function  Neurologic defects

Case 5 The plain X-rays of the hand [Figure 11(a) and (b)] do not show any fracture. Incidental note is made of an expansile lucent lesion within the diaphysis of the second metacarpal bone. There is scalloping of the cortices but no pathological fracture. There is faint chondroid type calcification within the abnormality. The lucent abnormality is a benign enchondroma. Enchondroma is a solitary, benign, intramedullary cartilage tumour that is usually found in the short tubular bones of the hands and feet. Patients are usually asymptomatic but painless swelling can be seen. The site is usually central and diaphyseal. The epiphysis is only affected after closure of the growth plate. The radiological features include oval or round lucency near the epiphysis with a fine marginal line, “ground glass” appearance, calcification (pinhead, stippled, flocculent or “rings and arcs” pattern) and bulbous expansion of bone with thinning of the cortex. The differential diagnoses are (1) epidermoid inclusion cyst (phalangeal tuft, history of trauma, more lucent) (2) giant cell tumour of tendon sheath (commonly erodes bone, soft tissue mass outside bone) (3) unicameral bone cyst (rare in hands, more radiolucent) (4) fibrous dysplasia (rare in hands, mostly polyostotic) (5) chondrosarcoma.

Craniofacial features:  Shortened base of skull with small foramen magnum  Prognathism  Large skull with frontal bossing and broad mandible Skeletal features:  Relative short stature  Normal trunk length that appears long and narrow, small thoracic cage  Shortening of the proximal limbs  Brachydactyly and trident hand configuration  Limited elbow extension and rotation  Hyperextensibility of most joints, especially the knees.  Genu varum Pelvic features:  Backward tilt of pelvis and hip joints resulting in rolling gait  Square-shaped flat non-flared pelvic bones with tombstone configuration  Flattened iliac wings (“champagne glass”)  Horizontal acetabulum

Figure 10

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Figure 11

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Case 6 The plain X-rays of the knee [Figure 12(a) and (b)] show that there are multiple bony exostoses arising from the lateral borders of the distal femur and medial aspect of the proximal metaphysis of the right tibia. The head of the fibula is expanded and irregular and appears fused to the tibia by an exostosis. There is a very large exostosis involving the whole of the proximal half of the humerus [Figure 12(c)] with massive modelling deformity. The ankle X-ray [Figure 12(d)] also shows multiple exostoses in the distal tibia and fibula, talus, calcaneum and the metatarsals. The diagnosis is of diaphyseal aclasis. Diaphyseal aclasis is autosomal dominant and usually discovered between the ages of 2 and 10 years with a male predominance. The exostoses stop growing when the nearest epiphyseal centre fuses. They are usually multiple painless masses near joints and located usually bilaterally near the metaphyses. The common sites are knee, elbow, scapula, pelvis and ribs. Complications include peripheral nerve and spinal cord compression secondary to involvement of posterior spinal elements or malignant transformation to chondrosarcoma in less than 5% of cases.

Figure 12

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Bone tumours affecting the spine in children and adolescents

even during bed rest and often aggravated at night. The pain may be due to extensive vertebral bony destruction, occasionally resulting in an insufficiency fracture, or infiltration of the paraspinal soft tissues. The symptoms can often be vague and nonspecific and the time to diagnosis can be markedly protracted, resulting in considerable delay to treatment. Muscle weakness is the main neurological symptom that can develop as a consequence of a growing spinal tumour. Chronic compression of the spinal cord can occur in 20% of patients resulting in neurological compromise and, occasionally, paraplegia. Isolated bowel and/or bladder dysfunction in a previously fully toilet-trained child may also alert one to the presence of a spinal neoplasm in the lumbosacral region. In the presence of neurological deficits it is critical to establish the diagnosis and initiate urgent treatment. A high index of suspicion should be present when children present with a painful scoliosis, localized tenderness on examination or a palpable mass (which can be detected in up to 16% of patients). However, in small children pain is not always expressed and other signs such as changes in personality, lethargy, posture, fever, limp or bruising should be always investigated.

George I Mataliotakis Athanasios I Tsirikos

Abstract Children and adolescents may present with non-specific back pain, commonly associated with developmental or psychosocial factors and with a benign and self-limiting course. The assessment of a child with back pain can be challenging and requires skill and expertise coupled with a high index of suspicion. Tumours affecting the vertebral column or the spinal cord should be always considered in the differential diagnosis of back pain in young patients. Bone tumours involving the spine are usually primary and benign, with a favourable outcome if appropriate treatment is applied at an early stage. Any delay in diagnosis can lead to prolonged morbidity, as well as the development of spinal deformity. This can be either a painful scoliosis, which starts as an antalgic deformity but gradually becomes structural, or a deformity affecting the coronal and sagittal planes due to extensive osteolysis as the result of the destructive course of a neoplasm. Primary malignant bony tumours are less common, but are associated with more severe morbidity and often respond poorly to treatment, despite recent advances in surgical techniques, chemo- and radiotherapy. This review summarizes current knowledge concerning bone tumours of the spine and provides a rational approach to the evaluation and management of this group of patients.

Imaging Anteroposterior and lateral radiographs of the spine will, in many cases, indicate the nature and type of neoplastic lesion. Bone scans are useful to determine the metabolic activity of the tumour and to identify whether there is a single, or multiple, location. CT and MRI scans with or without contrast are the most critical imaging modalities for the early detection and differential diagnosis of a spinal tumour. They show in detail the extent of the lesion, intrusion in the spinal canal and expansion into the paraspinal tissues. CT scan can also guide a biopsy, when necessary, to establish an accurate diagnosis. CT and MRI imaging is essential to define the radiotherapy margins of suitable malignant tumours, in the preoperative planning of surgical resection, and to detect tumour recurrence.

Keywords diagnosis; spinal neoplasm; spine; treatment; tumour

Benign tumours Introduction

Osteoid osteoma This is a benign tumour, less than 2 cm in diameter, characterized by a dense, sclerotic nidus of bone surrounded by fibrous tissue.2 It accounts for 11% of all primary benign tumours; 10% of osteoid osteomas affect the spine.3,4 There is a male to female predominance of 2:1. The prevalence is higher between the ages of 6 and 17 years with 70% of osteoid osteomas occurring in patients younger than 20 years and only 3% affecting children younger than 5 years of age.5,6 Predominant sites of spinal involvement are the posterior bony elements, often at the junction of the facet, pars interarticularis and the transverse process, and rarely the vertebral body.7,8 More than 50% of spinal osteoid osteomas are located in the lumbar region followed by the cervical, thoracic and sacral spine.

Spinal tumours should be always considered in the differential diagnosis of back pain in the paediatric and adolescent population. They can originate from the vertebral column or the neural elements and can be primary or metastatic. Spinal neoplasms can also be benign or malignant (Table 1). In children and adolescents, primary benign tumours of the spine are much more common than malignant variants. Overall, less than 30% of all primary bony tumours in children are malignant, with a smaller proportion affecting the spine.1

Clinical presentation Spinal pain is the predominant presenting symptom. This tends to be progressive and constant, unrelated to activities, persistent

George I Mataliotakis Infirmary, Leeds, UK.

MD

Clinical presentation: the main presenting symptom is severe back pain, especially nocturnal, thought to be due to prostaglandin secretion and/or venous congestion.8,9 The pain is usually relieved by aspirin or non-steroidal anti-inflammatory agents (NSAIDs). Adolescent patients with an osteoid osteoma in the thoracic or lumbar spine may present with a painful scoliosis, or with a torticollis if the lesion is in the cervical region (Figure 1). Neurological deficits, including mono- or paraparesis, develop in 25% of patients.10

Clinical Fellow in Orthopaedics, Leeds Royal

Athanasios I Tsirikos MD FRCS PhD Consultant Orthopaedic and Spine Surgeon, Scottish National Spine Deformity Centre, Royal Hospital for Sick Children, Edinburgh, UK.

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Clinical features, presentation, imaging and treatment of tumours affecting the vertebral column in children and adolescents Benign Osteoid osteoma

Osteoblastoma

Occurrence

11% of benign tumours

5% of benign tumours

Spinal involvement

10% affect the spine

40% affect the spine/5%

Aneurysmal bone cyst

Giant cell tumour

20e40% >1 vertebrae

14% affect the spine

10e15% affect the spine/

e Multiple (hereditary multiple exostosis)

7.4
4.5 years

3e9% patients 2e10 years (hereditary multiple exostosis)

Vertebral body/can involve multiple levels

Vertebral growth plates (broad or stalked based)

sacrum (3% lung

54% thoracic/35% lumbar/

Cervical/thoracic

11% cervical e Pain

e Usually asymptomatic

rigidity e Palpable swelling/

metastases) e Pain e Soft tissue swelling e Spinal deformity

e Spinal rigidity e Palpable mass/

e Palpable mass with or without tenderness

e Pathological fractures (11e37%)

tenderness e Kyphosis due to

e Neurological complications uncommon

pathological fractures e Torticollis

e Mechanical symptoms due to direct pressure

e Neurological deficits e Fever/

e Pain/rapid growth ¼ malignancy

Male:female

2:1 70% younger than 20 years

Similar to osteoid osteoma

70e86% patients 5e20 years

Site of vertebral involvement

Posterior elements

Posterior elements/can expand into the vertebral

60% posterior elements/can expand into the vertebral

Region of spine

50% lumbar

body 30e40% thoracic and lumbar

body 70% thoracolumbar

e Severe pain

respectively e Less pain compared to

Female predominance

osteoid osteoma/NSAIDs less effective

bony tumours e Solitary

25% other non-spinal lesion

Age of presentation

e Night pain relieved by aspirin/NSAIDs

Osteochondroma 35% of benign/8.5% of all

2 or more adjacent levels

Symptoms

Eosinophilic granuloma

e Acute onset pain/spinal

e 2/3 scoliosis e Neurological symptoms

tenderness e Scoliosis

e Mono-/para-paresis 25%

69% e Radiculopathy >50%

e Neurological deficits e Pathological fractures (8e21%)

leucocytosis Imaging

e X-rays: 1.5e2 cm lesion with radiolucent core and peripheral calcification

e X-rays: >2 cm lesion similar to osteoid osteoma (larger nidus)

e X-rays: cortical expansion/ central osteolysis/ eggshell thin cortex

e X-rays: radiolucent lesion/ cortical disruption/softtissue expansion/no

e X-rays: destructive lesion/vertebral body collapse (‘vertebra

e X-rays: cartilage-caped

e CT: defines tumour margins e MRI: shows the

e Tc bone scan: 100% sensitive

e Tc bone scan: 100% sensitive

(soap-bubble appearance) e CT: defines tumour margins

primary calcifications e CT: defines tumour

plana’) e CT: defines tumour

e CT: annular lesion with double-attenuating sign

e CT: defines tumour margins e MRI: in the presence of

e MRI: expansile cystic lesion/ fluidefluid levels/cortical

margins e MRI: heterogeneous

margins e MRI: soft tissue

radiculopathy/myelopathy

destruction affecting neural elements

appearance with necrosis and fluid-fluid levels

bony growths in relation to the growth plate

cartilaginous cap that covers the lesion/

Ó 2011 Elsevier Ltd. All rights reserved.

expansion rare/disc spaces spared

assesses spinal cordforaminal compression

e Bone scan/angiography

e Th bone scan: differentiates malignancy (continued on next page)

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e Painful scoliosis e Torticollis

3:1 <5% skeletally immature patients

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Table 1a (continued)

Differential diagnosis

Osteoid osteoma

Osteoblastoma

Aneurysmal bone cyst

e Isthmic spondylolysis on bone scan

e Osteosarcoma

e Giant cell tumour e Telangiectatic

e Osteoblastoma Malignant transformation

No

Benign Giant cell tumour

osteosarcoma

e Aneurysmal bone cyst (CT-guided biopsy recommended)

e Rarely pre-malignant lesions

Eosinophilic granuloma

e Ewing sarcoma (bone biopsy indicated) e Spur-like processes in the cervical spine and sacroiliac

No

e Differentiation to osteosarcoma Treatment

joint e Chondrosacroma (1e20%)

e Surgical resection e CT-guided radio-ablation

e Surgical resection e Radiotherapy for inoperable

e Selective embolisation e Surgical resection/spinal

e Radiotherapy not indicated

or recurrent lesions e Scoliosis may require

reconstruction e Percutaneous sclerotherapy

e Scoliosis may require correction

correction

Osteochondroma

e Vertebral osteomyelitis

e Radiotherapy (limited use)

e Selective embolisation e Surgical resection (use of high speed burr/phenol/ cryotherapy/PMMA) e Radiotherapy (grade 3 tumours)

e Often unnecessary e Surgical resection (persistent pain/ neurological compromise/deformity) e Intralesional cortisone injection/radiotherapy/ chemotherapy

e Usually unnecessary e Surgical resection (persistent pain/ neurological compromise/ pressure to vascular structures/malignant transformation) e Often need for spinal reconstruction

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Clinical features, presentation, imaging and treatment of tumours affecting the vertebral column in children and adolescents Pre-malignant Echondroma Occurrence Spinal involvement Male:female

<1% affect the spine

Ó 2011 Elsevier Ltd. All rights reserved.

Age of presentation Site of vertebral involvement

solitary lesions consisting of hyaline cartilage arising from the growth plate

Region of spine Symptoms

e Often asymptomatic e Pain e Spinal deformity

Imaging Differential diagnosis

e X-rays: bony necrosis/calcifications

Malignant transformation Treatment

e Rarely to chondrosarcoma e Surgical resection/spinal reconstruction

Table 1b

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Clinical features, presentation, imaging and treatment of tumours affecting the vertebral column in children and adolescents Malignant Ewing sarcoma Occurrence Spinal involvement Male:female Age of presentation

Osteosarcoma

Leukaemia

20e25% of all bony tumours

6% of leukaemia presenting with back pain

3.5e5% affect the spine

1e3% affect the spine

5e15 years

50% 10e20 years

Site of vertebral involvement

Vertebral body

90% vertebral body/10% posterior elements/can involve multiple levels

Region of spine Symptoms

Sacrum (pelvis can also be involved) e Persistent pain

2/3 of patients:

e Pain

e Palpable mass e Neurological

e Constant/severe pain e Neurological deficits

e Fever/lethargy e Anaemia e Increased peripheral leucocyte count e Decreased platelet count

compromise e ESR elevated in <50% of patients e High body temperature (25%) e X-rays: destruction/collapse of vertebral body (‘vertebra plana’)/ preserved disc spaces e MRI: defines extent of lesion and adjacent tissue involvement (intraspinal and extraspinal tumour expansion) Differential diagnosis

e Eosinophilic granuloma e Infection

e X-rays: mixed osteolytic/sclerotic lesion

e X-rays: osteolytic lesions with sclerotic

e bone scan: can demonstrate skip lesions or metastases

areas and periosteal reaction/ flattening of multiple vertebrae at

e MRI: modality of choice to define tumour margins and adjacent tissue expansion

adjacent or separate levels due to pathological fractures (10e15%)

e Angiography: preoperatively if resection is planned e Osteoblastoma e Aneurismal bone cyst

e Septic arthritis e Osteomyelitis

e Giant cell tumour e Metastatic lesions Malignant transformation Ó 2011 Elsevier Ltd. All rights reserved.

Treatment

Table 1c

e Metastases to the lungs/ribs, other parts of the spine, lymph nodes, brain, abdominal organs

(CT guided biopsy/CT chest and abdomen) e Metastases mainly to the chest and abdomen

e en block resection often impossible e Combination of chemotherapy/radiotherapy/

e Chemotherapy e en block resection

e Chemotherapy e Radiotherapy

wide resection e Need for spinal reconstruction

e Need for spinal reconstruction e Postoperative radiotherapy

e Spinal reconstruction in the presence of pathological fractures and deformity

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Imaging

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Figure 1 Preoperative posteroanterior spinal radiograph a of a female patient aged 15.3 years with severe thoracolumbar pain which shows a left thoracolumbar scoliosis measuring 41 . Bone scan b indicates increased metabolic activity adjacent to the pedicle of T11 on the right side (black arrow). Further investigation using CT imaging c, d illustrates a radiolucent lesion with a nidus at the junction of the right pars interarticularis and pedicle (white arrows) with cortical erosion into the spinal canal consistent with an osteoid osteoma. The patient underwent surgical excision of the tumour and had complete resolution of her symptoms. Posteroanterior spinal radiograph e at 20 months following resection of the osteoid osteoma and with the patient skeletally mature shows spontaneous improvement of the thoracolumbar scoliosis to 22 .

Osteoblastomas Osteoblastomas are histologically similar to osteoid osteomas but are usually larger than 2 cm in diameter. They account for 5% of primary bone tumours, with more than 40% affecting the spine, located mostly in the posterior elements.19 In a small proportion of patients both the posterior elements and the vertebral body are involved and in about 5% adjacent spinal levels may be affected. The thoracic and lumbar spine each account for 30e40% of spinal involvement, followed by less frequent occurrence in the cervical region and sacrum.

Imaging: plain radiographs reveal a well-demarcated lesion, 1.5e2 cm in diameter, with a variable amount of calcification and a radiolucent osteoid-rich core. Due to the small size of the tumour, as well as a lack of calcification in the early stages, the neoplastic lesion may exist for months or years before it becomes visible on X-rays. CT scans demonstrate a circumscribed annular lesion with a double-attenuating sign and are helpful in defining the osteoid osteoma’s location and extent of osseous involvement.8 Bone scan with Tc-99m has up to 100% sensitivity in the diagnosis of osteoid osteomas, even in the early stages.4,9,11,12 It determines the exact location of the nidus and rules out multi-site involvement. Attention should be paid to differentiate an isthmic spondylolysis from an osteoid osteoma, since they can both produce a similar bone scan appearance. MRI is not the imaging modality of choice to establish diagnosis. When used it shows normal to decreased T1 signal in the nidus and normal to increased T2 signal in the surrounding bone due to local inflammatory response.13

Clinical presentation: osteoblastomas cause less back pain than osteoid osteomas but NSAIDs are also less effective in alleviating the symptoms. Two-thirds of affected patients develop a scoliosis, with the tumour being found in the concavity of the curve.20 Neurological symptoms due to intraspinal expansion and spinal cord compression develop in 69% of patients.9 Radiculopathy occurs in more than 50% of patients, whereas myelopathy is uncommon.21 Involvement of the paraspinal muscles may also occur.

Treatment: osteoid osteomas do not carry a risk of malignant transformation. Initial treatment is conservative with NSAIDs, which can provide lasting pain relief in many patients.4,8 Surgical resection of the tumour is indicated in patients with refractory spinal pain, especially those developing a significant scoliosis, and provides rapid alleviation of pain in 95% of patients. Incomplete resection has been reported to occur in up to 23% of patients and this leads to a reoperation rate of 12% in patients with symptoms that persist.14e16 Intraoperative radioisotope scanning has been developed for accurate localization of tumour margins and almost ensures complete surgical excision, with a success rate 94%. Percutaneous CT-guided radiofrequency ablation has also been used for osteoid osteomas that do not invade the spinal canal. Radiotherapy is not indicated. Spontaneous resolution of associated painful scoliosis can occur if the osteoid osteoma is excised sooner than 15 months from the onset of back pain. The presence of back pain for more than 15 months can result in a structural scoliosis, which persists even after tumour removal.3,9,17 Patients who have smaller curves at the initial presentation, and those younger at the time of surgery, are more likely to have spontaneous correction of their scoliosis.4,18

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Imaging: similarly to osteoid osteoma, in osteoblastoma an osteolytic lesion with a larger nidus and calcifications can be found on plain radiographs. Bone scanning localizes the single or multiple lesions. CT remains the best imaging technique for defining the osseous margins of the lesion and assists surgical planning. In the presence of radiculopathy or myelopathy, an MRI should be obtained to define the area of neural compression; the MRI findings include normal to decreased T1 signal, normal to increased T2 signal and often fluidefluid levels.13 Treatment: marginal excision and intralesional curettage can be curative; however, some authors recommend a wider surgical resection whenever this is possible.1,4,8,22,23 A recurrence rate of 10e15% should be expected after curettage; reoperation to complete the tumour resection is then indicated.9 Pain relief occurs in 90% of patients following surgery. Radiotherapy is not recommended due to the risk of myelitis and malignant transformation. It is reserved for inoperable or recurrent tumours, or if surgical excision involves a very significant risks of neurological injury and permanent disability.

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Figure 2 Posteroanterior radiograph of the lumbar spine a shows an absent right pedicle at L3 (white arrow). Increased metabolic activity is noted on bone scintigraphy b adjacent to the L3 on the right side (black arrow). CT scan with 3D reconstruction c demonstrates a destructive lesion with expansion into the vertebral body, right pedicle, transverse process and lamina (white arrow) with obliteration of the cortical wall, as well as erosion into the spinal canal. This represents an aneurysmal bone cyst. On axial CT imaging d the tumour causes destruction of the right corner of the posterior vertebral body, pedicle, transverse process and hemilamina; it invades the spinal canal and neural foramina coming in contact with the right L3 nerve root (white arrow).

Malignant transformation: osteoblastomas can rarely be premalignant lesions, containing plump osteoblasts with nuclear atypia.3 They have no metastatic potential but local differentiation to osteosarcoma can occur. The differential diagnosis between osteoblastoma and osteosarcoma is essential. Osteoblastoma usually originates from the posterior bony elements and can expand into the vertebral body, whereas osteosarcoma tends to arise from the vertebral body and gradually extends into the posterior elements.

The tumour originates from the posterior elements in 60% of patients and can expand towards the vertebral body.25 In 20e40% of patients the lesion involves more than one vertebral body.1,9,26 Clinical presentation: the expansile and osteolytic nature of the tumour can cause an acute onset of back pain, followed by spinal rigidity and a restricted range of motion, which is often the presenting symptom. A palpable swelling, with localized tenderness, an antalgic scoliosis, neurological deficits and pathological fractures leading to vertebra plana constitute another presentation.9,27,28 Neurological compromise may develop due to direct pressure from the enlarging neoplasm or stretching of nerve structures over the neoplasm. Pathological fracture occurs in about 8% of ABCs, but the occurrence rate may be as high as 21% if the tumour affects the spine. Torticollis may develop if the lesion is located in the cervical region.

Aneurysmal bone cyst Aneurysmal bone cysts (ABC’s) are expansile, osteolytic lesions which have a thin wall and contain cystic cavities filled with blood. They affect patients aged 5e20 years in 70e86% of cases, with a female to male predominance. ABCs may be related to trauma or arise from bone with pre-existing neoplastic lesions, such as osteoblastoma or less commonly a malignancy, such as osteosarcoma. They are located in the thoracolumbar region in 70% of patients.24

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Imaging: plain radiographs may show cortical expansion with central osteolysis. The cortex is eggshell thin and blown out, with

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the formation of septations within the core of the osteolytic lesion producing a soap bubble appearance (Figure 2). A CT scan can define the bony margins of the ABC. MRI shows an expanded cystic lesion with fluidefluid levels due to the breakdown of blood and blood products within intratumoural cysts, as well as tumour extension through cortical destruction affecting neural elements and surrounding soft tissues.13,29

Diagnosis: preoperative biopsy is indicated to confirm the diagnosis but carries the risk of contaminating local tissue planes. It is best performed with CT guidance. Grading: GCTs can be categorized as described by Campanacci et al.36 into three grades:  Grade 1, a latent tumour with well-defined margin and intact cortex;  Grade 2, an active tumour with well-defined margin, nonradiopaque rim and thinned, moderately expanded cortex;  Grade 3, an aggressive tumour with indistinct borders and cortical expansion.36 Grading is necessary for surgical planning. However, there is no correlation between tumour grade and the incidence of local recurrence or metastasis.

Differential diagnosis: ABCs must be differentiated in particular from giant cell tumour and telangiectatic osteosarcoma. Treatment: wide local resection of the tumour and curettage followed by bone grafting is the mainstay of treatment but carries a high risk of severe intraoperative bleeding. Selective preoperative embolization can reduce this risk; it goes without saying that attention should be paid to preserve the arterial supply to the spinal cord.9,30 The internal lining of the cyst must be removed during surgery in order to control bleeding. The recurrence rate after such treatment can reach 10e25%; if it occurs, there is an indication for reoperation. The incidence of post-laminectomy kyphosis following surgical resection of the tumour ranges from 37e95%; this is reduced to 9% with retention of the facet joints bilaterally.31 After tumour resection, spinal reconstruction and fixation with instrumentation and bone graft may be required to restore mechanical stability and to prevent the development of deformity. Promising results have been reported with percutaneous sclerotherapy, with or without arterial embolization, using fluoroscopic and/or CT guidance. This is an alternative to surgery, especially in high-risk patients or when resection is technically impossible.32 Radiotherapy is not generally used and has several adverse effects in children, including post-radiation myelopathy, radiation-induced spinal deformity due to growth-plate disruption, sarcoma and gonadal damage. There is only one report on the superiority of 30e40 Gy radiation over surgery for the treatment of ABCs.33

Treatment: in grade 1 tumours, treatment consists of curettage with excision of the pseudocapsule and all reactive surrounding tissues. In grade 2 tumours, curettage is followed by phenol, cryosurgery or the insertion of polymethylmethacrylate cement (PMMA). This may achieve necrosis of any remaining neoplastic cells in the cavity and provide better control of the margins of the lesion.40 These surgical treatments carry a 27e55% risk of local recurrence; the use of a high speed burr on the walls following curettage, and before the local adjunctive measures are employed, in order to remove remaining tumour has reduced the recurrence rates to 12e25%.41e43 In grade 3 GCTs, intralesional resection is associated with recurrence rate of up to 80%. Radical extralesional excision of the tumour is, therefore, indicated. However, this may be technically impossible and the use of local adjunctive measures or radiotherapy should then be considered. In sacral GCTs which do not cross the midline, preservation of urogenital function during wide resection can be achieved if the contralateral nerve supply is preserved. Preoperative embolization of the neoplasm will not only decrease intraoperative bleeding but can also reduce tumour size, allowing more effective surgical resection, which carries less risk for local recurrence. Embolization is often used for grade 2 and 3 lesions.

Giant cell tumours Giant cell tumours (GCT’s) are highly vascular lesions with an unpredictable prognosis, as they are locally aggressive. GCT clusters appear in the lung as metastases34,35 in 3% of affected patients. Less than 5% of GCTs occur in patients who are skeletally immature; 14% involve the spine, especially the sacral region.36e38

Prognosis: the index procedure provides the best opportunity for complete tumour removal. Prolonged disease-free survivals have been reported following curettage and radiotherapy, even though some patients required more than two procedures due to local tumour recurrence.44 Follow-up after excision should include repeat CT and MRI scans to detect local recurrence at an early stage and apply appropriate treatment.

Clinical presentation: back pain is the predominant symptom. Soft tissue swelling and spinal deformity are associated with larger lesions. The incidence of pathological fractures at presentation is 11e37%.39

Eosinophilic granulomas Eosinophilic granuloma (EG) is a benign, self-limiting neoplasm, one of the clinical manifestations of Langerhans’ cell histiocytosis. The tumour derives from a proliferation of lipid-containing histiocytes from the reticulo-endothelial system within the vertebral body. EG behaves as a condition with mixed characteristics of infection and neoplasm.9 In children the mean age at presentation is 7.4
4.5 years and the tumour affects the spine in 10e15% of patients. The thoracic spine is involved in 54% of spinal EGs, followed by the lumbar (35%) and cervical (11%) regions. In almost 1/4 of patients the tumour affects other bony structures outside the spine. EGs originate most commonly within the

Imaging: on plain radiographs, GCTs appear as radiolucent lesions with bony destruction, cortical disruption and soft tissue expansion without primary calcifications. A transitional zone is noted without bony sclerosis. CT scan shows an absence of bone and intralesional mineralization, as well as intraosseous tumour expansion and infiltration beyond its anatomical borders. MRI shows decreased T1 and increased T2 signal. The appearance of the neoplasm may be heterogeneous, with areas of necrosis and fluidefluid levels due to breakdown of blood products. MRI defines the extent of the lesion and affected surrounding soft tissue planes.13

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between 2e10 years of age at a frequency of 3e9% and progress slowly until adulthood.51,52 The cervical and thoracic regions are most commonly affected.49

vertebral bodies and can involve multiple levels. Young children with the condition develop ‘vertebra plana’ due to osteolysis, leading to complete collapse or flattening of the vertebra e the so-called ‘silver dollar’ sign on radiographs; in older children the tumour produces a wedge-shaped deformity.9,45

Clinical presentation: osteochondromas are usually asymptomatic, other than often producing a palpable mass with or without localized tenderness. Most lesions do not protrude into the spinal canal or neural foraminae, therefore neurological complications are uncommon. Mechanical symptoms may occur depending on the location and size of tumour. Malignant transformation is manifest by the exacerbation of symptoms, including the new onset of pain or rapid growth of the lesion.53,54

Clinical presentation: the primary symptom is back pain with localized tenderness at the affected level due to bony destruction and vertebral collapse. This may lead to a restricted range of spinal motion or torticollis, if the tumour affects the cervical region. A palpable mass may be present at the level of the lesion. A localized kyphotic deformity may develop as the result of wedged vertebrae. Neurological symptoms including muscle weakness, monoparesis, and reflex abnormalities may occur, especially if the tumour involves the cervical spine. Spinal EGs may infrequently produce neurological deficits in children due to segmental instability at the level of vertebral destruction.21 Children may also present with fever and leucocytosis.

Imaging: the tumour is often evident on plain radiographs. CT scans show extent and location of the lesion. MRI demonstrates the cartilage cap that covers the lesion, with some peripheral enhancement surrounding the cap on T2-weighted images. Malignant transformation to chondrosarcoma should be excluded if the thickness of the cartilaginous cap is >1 cm.13 However, in skeletally immature patients the size and rate of growth of the cartilaginous cap cannot be assessed as a malignancy marker, as in adults, because in children osteochondromas tend to grow anyway until normal physeal development ends. MRI is also useful to assess the degree of spinal cord compression for lesions with intraspinal extension. With the addition of contrast medium, widening of the epidural space superior and inferior to the lesion may be seen.55,56 Bone scans can assess whether the lesion is active or silent; with the use of thallium 201 it is also possible to differentiate malignant transformation from benign osteochondromas.

Imaging: plain radiographs show a destructive lesion arising in the vertebral body and causing partial collapse, better assessed by CT and MRI scans. The intervertebral spaces are usually spared and expansion to the adjacent soft tissues is rare. MRI may show increased T2 signal. Radionuclide scans and angiography have also been used as complementary techniques to assist diagnosis.45 Differential diagnosis: this includes vertebral osteomyelitis and other benign or malignant neoplasms, such as Ewing’s sarcoma (more likely if the paraspinal soft tissues are affected). A bone biopsy is indicated to establish diagnosis before treatment is decided.

Differential diagnosis: spur-like processes originating from the posterior neural arch in the cervical spine, as well as the inferior aspect of the sacroiliac joint, are normal variants and should not be confused with osteochondromas.

Treatment: EGs are self-limiting, and there is no consensus on the need for treatment.46,47 In the presence of acute onset back pain a short period of bed rest followed by patient mobilization in a spinal jacket or brace provides adequate pain relief and support. Surgical treatment is not usually required unless the patient develops neurological compromise or significant spinal deformity. In this case, surgical curettage or radical resection of the tumour, followed by bone grafting, spinal reconstruction and arthrodesis may be indicated. Intralesional cortisone injection, low-dose adjuvant radiation and postoperative immobilization with Minerva brace or cervical collar can be used for EGs of the cervical spine.47,48 In the presence of multiple EGs, chemotherapy may have a role.47 Vertebral body reconstitution is greater in younger patients and takes place regardless of treatment. Spontaneous restoration of vertebral body height occurs if the growth plates are not involved.

Treatment: osteochondromas require no treatment other than observation unless they cause mechanical or neurological symptoms. Further investigation is indicated if the patient presents initially with a severely painful lesion or develops acute pain and/or increase in size of a previously diagnosed tumour. These changes may be indicative of mechanical pressure or malignant transformation. Tumour excision is recommended when pain persists due to soft tissue compression, in the presence of neurological compromise due to direct pressure on the spinal cord and nerve roots, if the tumour affects adjacent vascular structures and if malignant transformation is suspected. Surgical resection must include all soft tissue coverings and extend to normal bone. Excision of osteochondromas should take into account the risk of injury to adjacent neural elements, visceral organs or blood vessels, as well as the potential need for spinal reconstruction if tumour removal results in structural instability.49 Most chondrosarcomas developing in the setting of an osteochondroma are low-grade, can be treated with wide resection and have favourable prognosis. The reported rate of local tumour recurrence is <2e5%.57 The risk of recurrence is greater in skeletally immature patients. It may, therefore, be preferable to delay resection of osteochondromas until skeletal maturity. Sarcomatous transformation of solitary osteochondromas occurs in approximately 1% of

Osteochondromas Osteochondromas account for approximately 35% of benign and 8.5% of all bone tumours.49 There is a male predominance with a 3:1 male to female ratio. Osteochondromas are cartilage-capped bony growths, appearing in relation to the growth plate, and are either broad based or stalked. They stop progressing at the end of physeal growth. They can be either solitary or multiple. Solitary lesions develop in an isolated bone and are not hereditary. Multiple osteochondromas can occur either spontaneously or as part of an autosomal dominant disorder known as hereditary multiple exostoses (HME), affecting both genders equally or with slight male predominance.50 Spinal osteochondromas as part of HME develop

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Figure 3 Sagittal MRI views of the spine a, b show an extensive osteolytic lesion affecting consecutively the vertebral bodies from C5 to T4 (top and bottom white arrows) and causing complete destruction of the body of C7. Axial MRI views c, d demonstrate vertebral body destruction (white arrows), as well as expansion of the tumour into the spinal canal d. The lesion represents a Ewing’s sarcoma.

patients.55 Malignant transformation of the cartilaginous cap into secondary chondrosarcoma can occur with frequency 1e20% in patients with HME.52,58

palpated adjacent to the spine. The ESR can be elevated in almost 50% of patients; along with fever this can lead to the misdiagnosis of infection.

Pre-malignant tumours

Imaging: radiographs show destruction and collapse of the vertebral body giving the appearance of ‘vertebra plana’ with preservation of disc spaces. The differential diagnosis includes eosinophilic granuloma, in which extensive osteolysis can produce similar radiographic findings.9 Biopsy of the adjacent soft tissue mass can establish a diagnosis. MRI defines the extent of the lesion and involvement of adjacent tissues (Figure 3). In the presence of neurological compromise, and if MRI is not available, myelography combined with CT scan could provide a valid alternative.

Enchondromas Enchondromas are benign solitary tumours consisting of hyaline cartilage and arising from the growth plate. Less than 1% of enchondromas affect the vertebral column. The lesions rarely transform to chondrosarcomas, except in patients with Maffucci syndrome, where malignant degeneration is not uncommon and is associated with the development of haemangiomas. Imaging: enchondromas may demonstrate, on plain radiographs, bone necrosis and calcification.

Treatment: ESs can penetrate extensively surrounding intraspinal and extraspinal soft tissues, to the point that en bloc resection is often technically impossible. Adequate tumour treatment includes a combination of chemotherapy, radiotherapy and wide surgical excision. Radiation and chemotherapy can give short-term local symptomatic relief and make radical excision oncologically appropriate. The standard chemotherapy four drug protocol, including vincristine, doxorubicin, cyclophosphamide and dactinomycin (VACD), can offer a 30e60% 5-year disease-free survival (DFS).60 The new National Comprehensive Cancer Network (NCCN) Guidelines for ES suggest that chemotherapy should include a combination of at least three of the following agents: ifosfamide and/or cyclophosphamide, etoposide, doxorubicin and vincristine.61 The combination of ifosfamide and etoposide (I þ E) is effective in untreated patients with ES with an overall response rate of 96%.62 The regimen and total number of cycles of I þ E are not fully determined, resulting in differences in the reported outcomes across trials.63,64 The incorporation of I þ E to chemotherapy has not improved outcomes in patients with metastatic disease.64

Treatment: this includes surgical excision of the tumour followed by bony reconstruction and spinal stabilization.

Malignant tumours Malignant tumours in children are very rare. Less than 30% of all primary bone tumours in childhood are malignant and relatively few of these affect the spinal column.1 However, spinal malignancies in children have a poor prognosis and the treatment options have limited effectiveness in controlling the disease. Ewing’s sarcoma Ewing’s sarcoma (ES) is the most common malignant bone tumour in children, with the highest incidence between 5e15 years.26 Approximately 3.5e5% of all ESs affect the spine, with the sacrum being the most frequent location. Pelvic involvement can also occur. Clinical presentation: the prominent symptom is persistent back pain and often neurological compromise due to tumour expansion with subsequent pressure on the spinal cord and nerve roots.59 In 25% of patients (hyper)pyrexia develops or a palpable mass can be

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Prognosis: radical surgical resection and adjuvant therapy make periods of disease-free survival feasible; however, complete

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control of disease is still not possible and the overall prognosis remains poor. Metastases involve the lungs and ribs, other parts of the spine, lymph nodes, brain, as well as abdominal organs.

and postoperative deformity in 28% of patients. Therefore, spinal reconstruction with bone graft and instrumentation is required at the time of the index procedure. The more complete the initial tumour removal the better the postoperative survival rate. Several courses of chemotherapy will follow tumour excision. Postoperative radiotherapy is indicated after the spinal wound is totally healed. Local irradiation may also be considered if the tumour is inoperable. The presence of metastases at the initial diagnosis does not necessarily affect overall prognosis. Pulmonary metastases require aggressive treatment with wide resection and this may need multiple thoracotomies.71

Osteosarcoma Osteosarcoma (OS) is the 2nd most common primary malignant bone tumour after myeloma. It accounts for about 20e25% of all bone neoplasms. The prevalence is higher in adolescence and during the pubertal growth spurt, with approximately 50% of affected patients aged 10e20 years. OSs may involve multiple sites simultaneously or consecutively. The axial skeleton is affected in 10% of patients with 1e3% of OSs located within the spine.65 In 90% of patients, the tumour arises in the vertebral body; however, the posterior elements may also be involved.

Leukaemia Leukaemia is the most common malignancy in children. Approximately 6% of affected children will present with back pain as an initial symptom. Other non-specific findings including fever, lethargy, anaemia and increased peripheral leukocyte count.

Aetiology: OS may be primary or secondary. Primary OS occurs without evidence of pre-existing lesions or any prior to exposure to radiation. Secondary OS is associated with Paget’s disease, benign bone tumours and irradiation.66e68 Children with retinoblastoma have a 2000 times higher risk developing an OS compared to normal population.

Imaging: radiographs may not be diagnostic or may show osteolytic lesions with sclerotic regions and periosteal reaction. Flattening of multiple vertebrae at adjacent or separate levels can occur and 10e15% of affected children will develop pathological spinal fractures.

Clinical presentation: constant, severe back pain, often associated with neurological deficits, is the main presenting symptom. This is evident in 2/3 of patients at initial examination.

Diagnosis: a high index of suspicion is the key to early diagnosis. The radiographic evaluation should be supplemented by blood tests including CRP, ESR, white cell and platelet count. CRP, ESR and white cell count are expected to be increased, whereas the platelet count will be decreased. The misdiagnosis of septic arthritis or osteomyelitis is a common scenario in children.

Imaging: the tumour appears as a mixed osteolytic and sclerotic lesion on plain radiographs. MRI is the imaging modality of choice, showing low signal on T1 and T2-weighted images. CT-myelography may be used as alternative to MRI. Bone scan can demonstrate skip lesions and metastases; it is also useful as part of the screening process during postoperative follow-up examinations. Angiography is used mainly for preoperative planning if vertebral resection is planned.

Treatment: chemotherapy and local radiotherapy are the treatment of choice. Chemotherapy protocols for leukaemia in the paediatric population require a combination of drugs including methotrexate. High-dose methotrexate with leucovorin as a toxicity rescue measure is one of most effective regimes to treat an acute lymphoblastic leukaemia.72,73 Spinal reconstruction and stabilization may be required in the presence of pathological fractures and subsequent deformity.

Differential diagnosis: this includes osteoblastoma, aneurysmal bone cyst, giant cell tumour and, less commonly, metastatic lesions. Treatment: a CT-guided biopsy can establish the diagnosis and has to be followed by CT of the chest and abdomen to rule out metastatic disease. Chemotherapy up to 16 weeks prior to surgical resection can achieve primary tumour regression and reduce the risk of micro-metastases, which occur in 10e20% of patients. The introduction of chemotherapy has improved cure rates in OS patients by up to 70%.63,69 Chemotherapy regimens should include at least two of following agents: doxorubicin, cisplatin, ifosfamide, high-dose methotrexate, as well as growth factors.70 One of the treatment protocols involves high-dose methotrexate followed by leucovorin. Another chemotherapy protocol designed by the American and European Osteosarcoma Study Group, and more suitable for paediatric patients, involves high-dose methotrexate with doxorubicin and cisplatin.2,7 Ifosfamide has also been used as part of initial or second-line chemotherapeutic regimes in conjunction with surgery and/or radiotherapy in children. Doses are individualized for children and are based on therapeutic response as well as drug tolerance. The addition of alpha-interferon to high-dose methotrexate is being currently investigated. En bloc tumour resection is recommended. The wide vertebrectomy needed to remove a lesion can lead to segmental instability

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Conclusion Bone neoplasms affecting the spinal column in children and adolescents are most often benign and have a good prognosis. They can be associated with significant and prolonged morbidity and may be difficult to diagnose. Malignant bone tumours involving the spine are much less common but have an unfavourable prognosis and often respond poorly to treatment. Persistent back pain in childhood and adolescence should be thoroughly investigated to exclude underlying pathologies including tumours. Despite the advent of modern imaging techniques and diagnostic tools, the key to early detection and adequate treatment lies with the clinician who possesses the necessary expertise and should have a high index of suspicion.9 A

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CME SECTION

CME questions based on the Mini-Symposium on “Foot and Ankle” C Screw fixation is superior to plate fixation D Significant hindfoot deformity (greater than 15e25 degrees) is a contra indication to arthroscopic fusion E Using a third screw in a screw-only technique does not further improve the stability of fixation

The following series of questions are based on the MiniSymposium on “Foot and Ankle”. Please read the articles in the Mini-Symposium carefully and then complete the self-assessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. After completing the questionnaire, either post or fax the answer page to the Orthopaedics and Trauma Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Orthopaedics and Trauma. Replies received before the next issue of the journal is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be despatched, via email, for your records.

5 In sinus tarsi syndrome, which of the following muscles show an abnormal reduction or absence of electrical activity on EMG studies, reversed by the injection of local anaesthetic into the sinus A Abductor hallucis B Extensor digitorum brevis C Flexor hallucis longus D Peroneus longus E Tibialis posterior

Questions

6 Which of the following contributes most to the blood supply of the talus A Anterior tibial artery B Artery of the sinus tarsi C Artery of the tarsal canal D Dorsalis pedis E Perforating peroneal artery

1 When performing a Coleman block test, the heel adopts a position of physiological valgus. What does this imply about possible future treatment A Correction of the deformity should include a subtalar fusion B Correction of the deformity should include a valgus osteotomy of the calcaneus C The deformity can be managed by 1st ray osteotomy and tendon transfers D The deformity can be managed easily by orthoses alone E The deformity can be managed using tendon transfers alone

7 In which compartment of the foot is quadratus plantae found A Deep central B Distal plantar C Lateral D Medial E Superficial central

2 In what proportion of patients with Rheumatoid arthritis is the Rheumatoid Factor positive A 100% B 95% C 90% D 80% E 60%

8 At heel strike, which of the following best describes the ongoing pattern of muscle activity about the ankle A At heel strike concentric anterior contraction occurs followed by eccentric posterior activity towards the foot flat phase B All muscle groups are electrically silent until heel strike, when eccentric posterior contraction begins C Both anterior and posterior muscle groups are contracting in anticipation of load bearing D The anterior muscles are contracting eccentrically whilst the posterior muscles are electrically silent E The posterior muscles are contracting to absorb heel impact whilst the anterior muscles are electrically silent

3 Which of the following does not differ significantly between samples of articular cartilage taken from the ankle and the knee of the same individual A Compressive modulus B Chemical structure of sulphated glycosaminoglycans C Expression of mRNA from degradatory enzymes D Histological appearance E Water content

9 Which of thee following muscles is least active in the second interval, or rocker, of the gait cycle A Extensor hallucis longus B Flexor digitorum longus C Intrinsic muscles of the foot

4 Which of the following statements concerning ankle arthrodesis is incorrect A Arthroscopic techniques may allow earlier mobilization B It may be necessary to remove both malleoli

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CME SECTION

Responses

D Tibialis posterior E Triceps surae

Please shade in the square for the correct answer. B C D E 1A 2A B C D E 3A B C D E 4A B C D E 5A B C D E 6A B C D E 7A B C D E 8A B C D E 9A B C D E 10 A B C D E 11 A B C D E 12 A B C D E

10 At which point in the gait cycle is the subtalar joint maximally inverted A Early stance B Heel strike C Late stance D Swing E Toe off 11 What is the preferred position for ankle fusion A Neutral dorsiflexion, neutral rotation, neutral valgus B 10 degrees dorsiflexion, neutral rotation, 5 degrees varus C Neutral dorsiflexion, 10 degrees internal rotation, neutral valgus D Neutral dorsiflexion, neutral rotation, 5 degrees valgus E 5 degrees dorsiflexion, 5 degrees external rotation, 5 degrees valgus

Your details (Print clearly) NAME......................

12 In the Kleiger test for syndesmotic instability, which of the following is one of the radiological criteria used A Talar tilt of more than 5 degrees B Tibiofibular clear space of more than 10 mm on mortice view C Tibiofibular clear space on mortice view of less than than 5 mm D Tibiofibular overlap on anteroposterior view of less than 6 mm E Tibiofibular overlap on mortice view of more than 1 mm

......................... ADDRESS..................... ......................... EMAIL...................... RETURN THE COMPLETED RESPONSE FORM by fax to 113-392-3290, or by post to CME, Orthopaedics and Trauma, Academic Department of Orthopaedic Surgery, “A” Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.

Please fill in your answers to the CME questionnaire above in the response section provided to the right. A return address and fax number is given below the response section.

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CME SECTION

Answers to CME questions based on the Mini-Symposium on “Radiology” Please find below the answers to the Orthopaedics and Trauma CME questions from Vol. 25, issue which were based on the Mini-Symposium on “Radiology”

Answers 1

a

b

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d

e

2

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d

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BOOK REVIEWS

The Masters experience e arthroscopic surgical techniques, rotator cuff repair

Operative techniques in Orthopaedic Surgery 4th V

American Academy of Orthopedic Surgeons 2009

Sam W Wiesel, ed, Publisher: Lippincott Williams and Wilkins 2010; ISBN: 978078176370, Pages: 984; Price: £370

Stephen S Burkhart, Felix H Savoie III, eds., ISBN: 9780892035021, Price: AAOS Member $229; Resident $209

Orthopaedic trainees should seek access to this book. I hesitate to say buy it, as a substantial shelf will be needed to support the four volumes and more than four and a half thousand pages (I counted 826 contributing authors!). However, those that take the plunge will be rewarded with a reference of immense detail concerning all forms of operative orthopaedic and trauma surgery. The extent to which it is illustrated is astounding and the artwork appears to be original and focussed on the needs of the text. Although there is inevitable variation from chapter to chapter, the strength of the book is its very visual approach to the subject matter. Take any operation and most likely it will be illustrated with operative photographs, graphics, cadaveric illustrations and/or dry-bones models. I tried a little game of catch-me-out; think of an obscure operation and see how they deal with it. The first I tried was fixation of a Pipkin fracture of the femoral head. There it was, with the classification in graphics and X-rays of each sub type, exposure in graphics and photographs, fixation illustrated on a real case and the postoperative X-rays. The complications and outcomes are then outlined. And so it goes on e the Editor in Chief has orchestrated a comprehensive work that could take the pride of place in any operating department, if it was safe from theft. A couple of decades ago Campbell’s ruled the roost of this genre e I feel the rules have been rewritten. That is not to say that this is the all encompassing text that residents dream about. It assumes an awful lot e you have to know why you are doing an operation before this textbook takes you through how to do it, and that means that a lot of real life experience is needed to get the best from it. However, as you progress through your training you will derive more and more from the contents. Sometimes the extent of the illustration backfires and many operative photos are barely more than 3 cm by 3 cm. I also get the feeling that the paper quality is not the best and a library copy may soon start to show its age. However a proud individual owner will have access to the full contents online. Overall this is an excellent resource and one of the best textbooks of operative trauma and orthopaedics I have seen. A panel of residents has reviewed it during its production and has ensured it caters fully for residents as much as for practicing surgeons. Paperbacks that condense the whole of our speciality into an inch-thick slab are popular with those working for exams but this isn’t that sort of book. This is a book to accompany you through training and into specialist practice and engenders a far richer understanding than any revision aid. A

David Limb

This is a pair of DVD’s in a series from the AAOS and is an educational package which can be used to claim 6 CME points in appropriate circumstances. The first disc goes through history and examination, although not in the order taught by Apley (look, feel, move etc). There is, however, a thorough demonstration of examination techniques with visual demonstrations of a wide range of shoulder tests. There is a mixture of powerpoint slides, clinical videos and arthroscopic videos used to take the viewer through the basics, and indeed advanced aspects, of rotator cuff repair. There is a progression through normal and pathological anatomy and the classification and evaluation of cuff tears. Every step is demonstrated including positioning, portal placements and ancillary procedures such as subacromial decompression, ACJ excision, suprascapular nerve release, subscapularis repair, SLAP repair, and biceps tenotomy/tenodesis. The first disc ends with a discussion of complications and a useful section on rehabilitation. The second DVD then focuses on rotator cuff repair and takes the viewer through partial and small to large tears, single and double row techniques and knotless rotator cuff repairs. A wide range of methods are demonstrated and the quality of the arthroscopic video, with commentary, is on the whole excellent. This would be an informative watch for anyone who is not familiar with shoulder arthroscopy and arthroscopic techniques, covering most of the procedures that might turn up as questions in professional examinations (stabilization being the only real omission). However it comes into its own for those embarking on a shoulder fellowship. Shoulder surgeons may themselves feel that they are already familiar with the majority of what is discussed. One area for improvement is navigation e the compulsory legal material at the start is lengthy and almost prevents one dipping in for a quick refresher on a topic. A lot of backward and forward navigation through menus is needed to move from one segment to another if one choses to look at videos that are not grouped together. A

Neil Patel

FRCS (Tr & Orth)

Consultant Orthopaedic Surgeon, Orthopaedic Department, Darlington Memorial Hospital, Hollyhurst Road, Darlington DL3 6HX, Durham.

Operative techniques in Sports Medicine Surgery Mark D Miller (editor in Chief is Sam W Wiesel). Lippincott, Williams & Wilkins 2010, ISBN: 13:978-1-45110-261-1 and 10:1-45110-261-5, Price: £113.05, 576 pages

FRCS(Ed) Orth

Consultant Orthopaedic Surgeon, Orthopaedic Department, Chapel Allerton Hospital, Leeds LS7 4SA, UK.

This book covers the common operative techniques for sports injuries and conditions involving the shoulder, elbow, groin, hip,

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BOOK REVIEWS

knee and leg. It does not cover hand, wrist, foot or ankle. It isn’t, therefore, an all encompassing book on sports surgery. The book does lean towards quite advanced arthroscopic techniques although some non arthroscopic procedures are described, particularly around the hip and leg. Each chapter is broken down into a specific pathology with the first part describing the anatomy, pathogenesis, natural history, patient history and physical findings, imaging, differential diagnosis, classification, and non operative management. The surgical management and technique is then described, step by step, in great detail. This includes aspects of patient positioning, setup and instruments required as well as a useful table of pearls and pitfalls. The chapter concludes with post-operative management, clinical outcomes, which is referenced, and complications.

ORTHOPAEDICS AND TRAUMA 25:4

The book is primarily aimed at surgeon whose practice involves arthroscopic procedures, particularly in the shoulder and knee joint, and soft tissue procedures for conditions commonly encountered in a sports clinic. It is clear, easy to read with some fantastic illustrations. There is also an online resource available to the reader. Although skewed towards the technical aspects of the relevant procedures, this would still prove useful as an occasional reference for orthopaedic trainees during their training. It is highly recommended for the content it covers. A

Neil Patel

MBBS MSC FRCS(Tr & Orth) MFSEM(UKþI)

Consultant Surgeon, Orthopaedic Department, Darlington Memorial Hospital, Hollyhurst Road, Darlington, Co Durham, UK.

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