Chapter 5 Foot and ankle
Structured oral examination question 1#
Lateral ligament instability of the ankle
Tell me what this diagram (Figure 5.1) represents and name the structures labelled 2, 3 and 5.

This diagram is a representation of the lateral aspect of the ankle showing the bony and ligamentous structures. Structure 2 is the anterior talofibular ligament, structure 3 is the calcaneofibular ligament and structure 5 is the posterior distal tibiofibular ligament.
What structures are injured in a lateral ligament injury?
The mechanism is usually a rotational injury with sequential failure of the ligaments from front to back, hence the anterior talofibular ligament or ATFL is most commonly injured followed by the calcaneofibular ligament or CF Land the posterior talofibular ligament is the least frequently injured.
How would you go about diagnosing a lateral ligament injury to the ankle?
In the acute se tingI would expect the patient to give a history of an episode of a twisting incident resulting insignificant pain and swelling. There may be a history of recurrent sprains and instability. Acutely the lateral side of the ankle anterior and inferior to the distal end of the fibula would be swollen and tender but discomfort may make it difficult to elicit definite signs of instability. In apa tien t with a chronic history the clinical signs of instability would be a positive anterior drawer testor talar tilt t est.
Tell me more about those two tests.
The patient is examined siting with their legs over the edge of the couch or siting in a chair to relax the gastrocnemius soleus complex. For the anterior drawer test the distal tibia is stabilized in one hand. The other hand is used to grasp the heel then draw the foot anteriorly in relation to the talus. Pain or excess anterior translation or a sulcus sign developing at the anterolateral corner of the ankle are signs of an ATFL injury. The other ankle must be examined for comparison. The talar tilt t est involves inversion of the ankle while placing a finger on the anterolateral corner of the joint. The lack of a firm endpoint or tilt in excess of the normal side suggests instability and the CF Lis considered to be injured if this testis positive.
What other clinical findings may be positive in apa tien t with recurrent ankle sprains?
Ankle sprains are more common inpatients with a cavus foot or hypermobility.
If you suspect a lateral ligament injury how will you proceed in managing this patient?
The first step in management would be rehabilitation with physiotherapy, concentrating on peroneal strengthening and proprioceptive training. If the dynamic stabilizers of the ankle are well- conditioned the majority of patients recover well from a ligament injury. Bracing may be of benefit.
What percentage of patients recover?
The vast majority.
[That’s a bit vague] Do you know a figure?
Sorry. Around 20% of patients develop symptoms of chronic ankle instability such as recurrent sprains, weakness and instability. Candidates should know this and may lose a mark.
How do you determine severe injuries?
Severe extensive bruising, severe pain on moving the foot, inability to bear weight are features of a severe injury. The options for acute grade III injuries include cast immobilization or functional management. Cast immobilization involves 3 weeks in a below-knee walking cast followed by 12 weeks proprioceptive rehabilitation. Functional management involves early mobilization with external support and a protocol of rest, ice, compression and elevation. This is followed by a rehabilitation programme that comprises ROM exercises, muscle strengthening, proprioception (wobble boards) and activity -specific training.
What if the patient continues to have significant symptoms despite adequate rehabilitation?
Apa tien t that fails to recover would require investigation. I would begin with simple weight- bearing radiographs of the ankle. Other investigations includes tress X-rays of the ankle and/or ultrasonography to assess the degree of ligamentous injury and if the patient is still having significant pain and swelling an MRI scan to look for additional pathology.
What other conditions would you be looking for?
My differential diagnosis for an ankle sprain that does not improve would be peroneal tendon pathology such as a split tear or subluxing tendons, intra-articular pathology such as an osteochondral defect of the talus or loose body, or non-union of an anterior calcaneal process fracture.
Do you know any scoring systems for chronic lateral instability?
No, sorry. Karlsson score, American orthopaedic foot and ankle score (AOFAS) and the foot and ankle outcome score (FAOS).
What are the surgical options for management of an isolated lateral ankle ligament complex injury in a young patient who has failed to respond to non-operativ e treatments?
The options f all into three broad categories. (1) Anatomic repair, (2) non-anatomic reconstruction, (3) anatomic tenodesis reconstruction.
What is an anatomic repair?
Anatomic repair involves the use of endogenous ligamentous tissue to restore the ligament. This is considered in cases when adequate tissue is present.
The Broström and the ‘modified Broström’ are the most widely used procedures for anatomic repair of the lateral ligament complex.
The complication rate is lower (fewer wounds, less risk of injury to the superficial peroneal nerve and decreased incidence of degenerative joint disease) compared to non-anatomical reconstructions with minimal effect on subtalar movement and a quicker rehab.
Failures have been atiribut ed to a variety of factors, including generalized ligamentous laxity, poor tissue quality , previous surgical repair, long-standing instability, and cavo-varus deformity.
What do you mean by a non-anatomic reconstruction (checkrein procedure)?
Non-anatomic reconstruction does not replicate the normal course and anatomy of the ATFL and CFL. Examples of non-anatomic reconstructive procedures include the Chrisman–Snook procedure, the Watson-Jones procedure and the Evans reconstruction, all utilizing the neighbouring peroneus brevis tendon to restrict motion without repair of the injured ligaments.
What do we mean by anatomical reconstruction?
These procedures utilize autogenous tendon gratis such as semitendinosus, gracilis or plantaris that are rerouted in such a way as to replicate the anatomic positions of the A TFL and CFL origin and insertion sites.
Are intra-articular lesions common in this group?
Various studies have found chondral injuries in a significant proportion of patients with chronic ankle instability. In one study associated intra-articular pathology amenable to arthroscopic treatment was identified in 83% of patients undergoing Brostrom repair [1]. Arthroscopic abrasion, curettage, drilling or microfracture can be used for the OCLs.
Apa tien t asks how successful a ligament repair will be, what will you tell them?
I would expect a successful result in approximately 80% of patients.
What are the reported results of using a free hamstring graft?
The reports are good but there are some reports of weakness of knee flexion beyond 70°, particularly when both gracilis and semitendinosus tendons are harvested. This ligament reconstruction can be performed through short incisions effectively making it a minimally invasive technique. The harvested graft semitendinosus or gracilis) is secured in a tunnel in the calcaneum using interference or biotendinosis screws then passed through a tunnel in the fibula and finally secured under tension into a further tunnel in the talus. This leaves the stabilizing evertor muscles intact together while reconstructing the A TFL and CF Land so may also be considered to be an anatomic repair.
The selected fixation device should be secure enough to maintain appropriate graft tension intra operatively to support healing and potentially allow for early joint motion
Thankyou.

Figure 5.1 Diagram of the lateral ankle ligaments.
Structured oral examination question 2#
Ankle arthritis
Describe the findings on this X-ray (Figure 5.2).

This is an AP weight-bearing radiograph of a left ankle showing narrowing of the joint space and some subchondral sclerosis. There is also evidence of a previous fibula fracture superior to the syndesmosis and varus angulation of the ankle. These findings are consistent with post-traumatic arthritis.
What are the most common causes of arthritis of the ankle?
The most common cause of ankle arthritis is pos t-traumatic arthritis. Other causes include inflammatory, neuropathic and septic arthritis. Primary osteoarthritis is thought to be relatively uncommon. In a recent epidemiological survey, the onset of ankle osteoarthritis was atiribut able to a previous rotational fracture (37.0% of cases), recurrent sprains (14.6%), a single sprain (13.7%), pilon fracture (9.0%), tibial shaft fracture (8.5%) and osteochondral lesion of the talus (OLT) (4.7%) [2].
How is this patient likely to present?
The patient is likely to complain of pain, restriction of movement, deformity and difficulty in undertaking activities of daily living (ADLs).
Are you aware of any classification systems for arthritis of the ankle?
No, I am not aware of any classification systems specific to the ankle. The Kellgren and Lawrence Radiographic Criteria can be used [3].
The X-ray you have been shown belongs to a 42-year-old manual worker who had an ankle fracture 7 years ago that was managed non-operativ ely. Describe your management strategy for this patient.
I would first want to take a full history and examine him, then obtain a lateral standing radiograph.
Tell me about the management options a vailable for ankle arthritis.
I would start with conservative measures and the options include NS AIDs, activity modification footwear modification with a cushioned sole and rocker boft om shoe, an ankle brace or AFO, intra-articular steroid injection or visc o-supplementation and physiotherapy. PRP injections have been used inpatients with osteoarthritis. One study reported a strong positive effect on pain and function after four PRP injections a t weekly intervals [4].
What surgical options are available?
There are two types of surgical option a vailable, those aimed to ‘buy time ’ or provide temporary relief and definitive treatments. The temporizing measures are debridement of the joint which can be performed arthroscopically or open depending on the extent of disease and should be aimed at treating identifiable causes of symptoms such as removing loose bodies, trimming anterior osteophytes which may give impingement symptoms, or debriding loose areas of articular cartilage and areas of synovitis. The other option is distraction arthroplasty [5]. The definitive surgical options are ankle fusion or ankle replacement.
What about arthroscopic debridement and osteophyte resection?
This may be helpful inpatients with mild arthritis with a large osteophyte restricting motion or causing painful impingement at the extremes of motion. R est pain is unlikely to be relieved. This operation is unlikely to be successful with this particular patient.
What about distraction arthroplasty?
Distraction arthroplasty can be used on several joints including the hip, knee and ankle to preserve the joint space and decrease the weight-bearing load by using an external fixator to distract the respective joint. This is usually combined with an attempt at articular cartilage repair such as subchondral drilling or microfracture. Results of motion distraction are better than fixed distraction. Continuous joint movement is essential for cartilage regeneration and reduces overloading protecting fibrocartilage regeneration. Distraction arthroplasty is best suited for post-traumatic ankle osteoarthritis.
Would you offer him distraction arthroplasty?
My concerns about offering him distraction arthroplasty are that he is a young patient with a physical occupation. The distraction device needs to be kept in place for at least 3 months, which is a significant treatment commitment. Ankle function declines following joint distraction such that at 5 years around 50% of patients will either have gone on to ankle arthrodesis or replacement. Due to the relatively small number of studies with only level 4 evidence and no long-term follow-up I would rather offer him ankle arthrodesis [6].
Isn’t fusion an outdated treatment now that ankle replacements are available?
No, total ankle replacements are not suitable for every patient and ankle fusion is still considered the ‘gold standard’, especially so for younger patients with severe post-traumatic ankle arthritis.
So which patients should be considered for ankle replacement surgery?
Ankle replacement surgery could be considered in low-demand patients over the age of 60 years who have inflammatory arthritis or osteoarthritis. Bilateral disease or arthritis affecting adjacent joints is a relative indication. Contraindications include younger, more-activ epa tien ts, significant ankle instability, particularly deltoid ligament insufficiency, significant deformity, especially varus or valgus of more than 10°, peripheral vascular disease, a poor soft -tissue envelope, marked osteoporosis or avascular necrosis of the tibial plafond or talar dome.
Do you know anything about the types of ankle replacement available?
The earlier designs involved a two-component design such as the Agility total ankle replacement, which required fusion of the distal tibiofibular joint. Most modern designs are three- component uncemented mobile bearing prostheses.
Apa tien twants to know how longan ankle replacement will last. What will you tell them?
The 10-year survival is about 85%, but there are fewer data available compared to knee and hip replacements [7–10].
The 42-year-old patient we began by discussing wants an ankle replacement. What would you tell him?
He is a young patient in a manual job. He wouldn’t be a candidate for total ankle replacement and I would explain to him that if his symptoms have not been controlled by non- operative measures then he requires definitive surgical treatment and an ankle fusion would be a better option for him.
He still w ants a replacement, as he is keen to get back to hill walking and sports and doesn’t want a stiff ankle. What will you tell him now?
He would be at risk of early failure with an ankle replacement due to his age and level of activity . Postoperative complications of total ankle replacement include infection, loosening , progressive intracomponent instability or deformity, subsidence and polyethylene failure. A fusion would provide a stable, pain-free ankle that would allow him to return to the majority of activities that he wishes to do. I would explain that many patients return to sports after ankle fusion. I would also explain that an ankle fusion would only sacrifice the residual movement that he has at his ankle joint and that his subtalar, midfoot and forefoot movements would still be present.
What position should his ankle be fused in?
The ankle should be fused in 5° of hind-foot valgus, 10° of external rotation and the foot should be plantigrade.
What complications will you warn him about?
Infection wound healing problems, neurovascular injury, DVT/PE, delayed union, malunion, non-union, hardware failure and the risk of exacerbating or developing arthritis in other joints (subtalar joint).
Anything new on the horizon?
Ankle osteochondral allograft reconstruction involves replacing all or a large part of the arthritic ankle joint with a cadaveric bulk osteochondral allograft. Although in theory this procedure is a potentially desirable option for a young patient with advanced ankle arthritis reported results suggesta high failure rate.
Thankyou.

Figure 5.2 X-ray showing ankle arthritis.
Structured oral examination question 3#
The rheumatoid foot
Please have a look at this radiographic print and tell me what you see. (See Figure 5.3.)

This is an AP radiograph of a forefoot. There is a hallux valgus deformity with subluxation of the second metatarsophalangeal joint and destructive change of all the metatarsophalangeal joints. There may be deformities of the lesser t oes and I would like to see a lateral view to clarify this.
A lateral view would be very helpful. What do you think is the underlying diagnosis?
The changes suggest that this is an inflammatory polyarthropathy such as rheumatoid arthritis.
Could it be anything else?
The appearances could be secondary to a neuropathic process.
What might be the commonest neuropathic process that could cause these appearances?
A peripheral neuropathy such as that associated with diabetes mellitus would be the commonest.
How would you confirm your diagnosis?
A detailed history would be most informative Specifically, I would enquire about pain, swelling and sensory alteration.
OK. This lady gives a clear history of progressive, painful, bilateral small joint swelling and post-immobility stiffness. She has gr eat difficulty finding comfortable shoes and describes the feeling of walking on pebbles. She is not aware of any diabetes or sensory loss. What are your thoughts at this stage?
This appears to be an inflammatory arthropathy. Candidates may be asked about the revised diagnostic criteria of the American College of Rheumatology (ACR)/European League against Rheumatism (EULAR). This requires confirmed synovitis of one or more joints, with absence of alternative explanation for the synovitis, and achieving a score of 6 or greater out of 10 from domains including: Numbers and location of the involved joint(s). Serological abnormality. Elevated acute-phase response. Symptom duration. These criteria replaced the previous set from 1987, which were felt to lack sensitivity in early disease. The advent of increasingly effective treatment paradigms, incorporating the use of conventional and biologic DMARDs, has made it possible to prevent destructive disease in patients who are identified early in the course of disease rather than after progression to irreversible radiographic changes.
Yes. Her feet are making her life pretiy miserable and she would like you, as an orthopaedic surgeon, to do something to make them better. Your examination finds marked active synovitis and plantar tenderness under the metatarsal heads as well as a minimally correctable hallux valgus. There is some hammering of the lesser toes with a cock-up deformity of the second toe. Sensation and perfusion appear good. What are you going to do?
First, I would want to know if she is known to a rheumatology service and has had any attempt at non-operativ e intervention.
She has never seen a rheumatologist and has never sought help for her feet other than from you via her GP.
I would advise her that operations are helpful but that she should be formally assessed by a rheumatologist to confirm the diagnosis and achieve disease control using DMARDs. I would also advise review by the local podiatry and/or orthotics service as simple footwear modification may be all that is necessary to control her symptoms. The key buzz phrase to mention (if appropriate) is that patients with rheumatoid arthritis require a (contemporary) multidisciplinary approach to their management. This may also include involvement of vascular surgeons, occupational therapists and physiotherapists.
I think that is appropriate advice at this stage. However, she returns to you a year later. Her synovitis is controlled by biological agents, but she has not found insoles and modified shoes helpful. How would you manage her at this point?
I would suggest surgery in the form of forefoot reconstruction. This consists of excision of the lesser metatarsal heads, correction of lesser toe deformities and excision or fusion of the first metatarsophalangeal joint.
Why?
This is a proven intervention with good results.
How good?
More than 80% of patients report significant improvement.
Would you fuse or excise the first metatarsophalangeal joint?
I would be guided by her age and functional demand in combination with the quality of the soft -tissue envelope of her foot. I would prefer to fuse the joint as I believe this aids maintenance of gait but, in a low-demand patient excision is associated with reduced complications and more rapid rehabilitation [ 11].
How would you secure the arthrodesis?
I would use an oblique compression screw augmented by a dorsal locking plate as biomechanical and clinical studies have shown this to be the most reliable method.
Would you always excise the lesser metatarsal heads in apa tien t of this age who now appears to have their disease under control?
No. It would be appropriate to perform shortening osteotomies such as Weil osteotomies to preserve the metatarsal heads if they are not badly diseased.
Surely that just prolongs the procedure and increases the risk of complication?
Yes, but it is very difficult to salvage a rheumatoid foot without metatarsal heads if the disease progresses in subsequent years.
Tell me about the principles of surgery in rheumatoid arthritis.
Surgery is indicated when symptoms and/or deformity are uncontrolled or geting worse. The overall objective is to produce a stable, plantigrade foot. Arthrodesis is the favoured procedure, but the risk of complications as ares ult of osteopenia, reduced vascularity and immunosuppression are to be borne in mind.
What steps can a surgeon take to minimize the risk of complications?
A drug history is 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. Biological agents should be stopped in the run up to surgery and not resumed untilt here is good evidence of postoperative healing. It should go without saying that meticulous handling of soft tissues is necessary. Incisions must be planned with care, both to maintain adequate skin bridges and to ensure satisfactory wound closure if significant deformities are being corrected.
How long would you stop biological agents for?
Two weeks pre- and postoperatively [12,13].
What about other disease-modifying anft-rheuma tic drugs? Which other ones would you stop?
Studies have shown that there is generally no need to stop drugs such as methotrexate or leflunomide. Peri operative management of RA medications [ 14]: Steroids: low dose (≤ 7.5 mg/day) or any dose if for < 3 weeks should be given as usual daily dose. Methotrexate: continue, as does not impair wound healing or increase peri operative infection risk. Other DMARDs: hold postoperatively until bowel and renal function are restored. TNF antagonists: stop one dose cycle preoperatively and restart when wound healed.
I would like to backtrack a bit. Would you alter your management if she also had signs and symptoms of hindfoot arthritis?
Generally, I would plan to address the most symptomatic area first. However, a less symptomatic and fixed hindfoot deformity should be corrected before proceeding to the forefoot. Flexible hindfoot deformity could be left un til more symptomatic.
Which hindfoot joints are most commonly affected in rheumatoid arthritis?
The talo-navicular joint is most commonly affected, followed by the subtalar and calcaneocuboid joints.
Can you outline the arguments for and against isolated talo-navicular fusion in RA?
Isolated talo-navicular fusion is a lesser procedure than triple fusion for both patient and surgeon and effectively eliminates hindfoot motion Historically, a non-union rate of up to 37% has been reported, although more recent studies suggest the non-union rate using contemporary fixation is much less. A triple arthrodesis is more reliable and allows greater deformity correction.
Thankyou.

Figure 5.3 AP radiograph of rheumatoid forefoot.
Structured oral examination question 4#
Cavus foot
These are photographs of the left foot of a 20-year old man (Figure 5.4). Describe them.

These clinical photographs show the anterior, medial and posterior views of a left foot with a cavus deformity. The hindfoot is in varus and there is a high medial arch. There doesn’t appear to be any significant clawing or abnormality of the toes. There is some shortening of the medial column of the foot and I can’t see any obvious callosities beneath the metatarsal heads.
What is the likely underlying cause?
The causes of a cavus foot may be broken down into congenital or acquired. The common causes of congenital deformities are idiopathic, a sequelae of clubfoot or due to arthrogryposis. The acquired deformities may be due to trauma (compartment syndrome, crush injury) or neuromuscular conditions. The neuromuscular causes may be grouped into central nervous system disease such as cerebral palsy or Friedrich’s ataxia, spinal cord lesions such as spina bifid aor spinal dysraphism, peripheral nervous system lesions such as an HSMN or muscular causes such as muscular dystrophy. A cavus foot develops a high arch as the result of imbalance in the musculature of the foot. In the cavovarus foot the heel is in varus and the forefoot in equinus with pronation of the first and sometimes second ray. It is important to distinguish between a cavovarus foot and a calcaneocavus foot. In the calcaneocavus foot the calf muscles are weak and the heel is in calcaneus and often valgus.
HSMN?
Hereditary sensorimotor neuropathies. These are a group of inherited neurological conditions. Char cot–Marie–Tooth is the most common of these conditions.
Can you go into more detail? How do these conditions lead to a cavus foot deformity?
The hereditary sensorimotor neuropathies are a group of related conditions that may lead to cavus foot deformity due to muscle imbalance. The conditions are diagnosed by the pattern of deformity and a positive family history. The most commonly recognized is Charcot–Marie–Tooth (CMT) disease, which affects approximately 1 in 2500 people. These patients commonly have weakness of the intrinsic muscles, tibialis anterior and peroneus brevis. Type I with an autosomal- dominant inheritance pattern tends to present in the second decade and patients have peroneal muscle weakness, abnormal (slow) nerve conduction studies, absent reflexes and hand involvement. Type II presents in the third or fourth decade. Reflexes and nerve conduction are normal; however, the foot deformity may be more pronounced. Genetic analysi sis able to diagnose and group these conditions more accurately and at least 17 types of CM Thave been described.
What causes the deformity in CMT?
In CMT the tibialis anterior and peroneus brevis muscles are weak and the strength of the antagonistic muscles tibialis posterior and peroneus longus causes the deformity. In detail, the peroneus longus contracts stronger than the weak tibialis anterior causing plantar flexion of the first ray. The posterior tibialis contracts harder than the weak peroneus brevis causing forefoot adduction. In addition, the long extensors to the toes are recruited to assist ankle dorsiflexion, causing claw toe deformities.
What symptoms is this patient likely to complain about?
Common complaints include pain to the forefoot under the metatarsal heads, lateral aspect of the foot, instability of the ankle with a history of frequent ankle sprains and deformity of the foot with problems fiting footwear or alteration of g ait.
What are the main findings you would look for in the examination of a cavus foot?
On general inspection I would be looking to see if the deformity was bilateral and whether there were stigmata of a generalized condition such as intrinsic muscle wasting involving the hands. With the patient standing I would look to see if the heel was in varus, neutral or valgus alignment, assess the height of the longitudinal arch by inspection and also look for any toe deformities. While the patient was standing I would also look at the spine for any stigmata of an underlying abnormality, such as a hairy patch or scoliosis. With the patient siting I would inspect the soles of the feet for callosities or areas of ulceration and look for any clawing of the toes. I would undertake a neurological examination of the lo wer limbs to assess sensation, deep tendon reflexes and power of the major muscle groups, particularly the tibialis anterior (ankle dorsiflexion), tibialis posterior (inversion), peroneal longus (resisted plantar flexion) and peroneus brevis (eversion). I would also like to see the patient walk to see if they had a broad-based ataxic gait (Friedrich’s ataxia) or drop-foot gait.
What is shown in these diagrams (Figure 5.5)?

These diagrams show the Coleman block test.
And what is that?
The Coleman block test assesses flexibility of the hindfoot deformity by eliminating the deforming drive of the forefoot. In a cavus foot the first ray is plantar flexed so to place the foot on the ground the hindfoot has to move into varus. In the Coleman block test the foot is positioned so that the lateral border of the foot and the heel are placed on a block and the medial forefoot is allowed to hang off the edge of the block. If the heel assumes neutral to 5° valgus alignment when viewed from behind the hindfoot deformity is considered flexible and driven by the forefoot [15].
What investigations would you use to evaluate this foot further?
In terms of evaluating the foot itself I would first obtain weight-bearing radiographs of the foot and ankle. An MRI scan of the spine is required if the patient has any signs or symptoms suggesting an underlying spinal cause.
What information does the lateral X-ray provide?
The magnitude of the cavus deformity can be quantified using Mear y’s angle, the angle between the long axis of the talus and the first metatarsal shaft. Normally this lies between ±5°. Hibb’s angle is the angle between the long axis of the first metatarsal shaft and the long a xis of the calcaneum. This angle is normally 150° but decreases as the cavus worsens. The calcaneal pitch angle, the angle between the floor and the undersurface of the calcaneum, should be less than 30° but may be elevated in a cavus foot. The radiographs will also show any evidence of degenerative changes to the joints.
What are the principles of managing this condition?
Firstly, it is important to identify and if necessary address the underlying cause of the cavus. The patient should be assessed for neuromuscular causes and referred for a neurological opinion if appropriate. The patient symptoms need to be understood as well as the likelihood of progression. Management can be non-operativ e with the use of orthotics to try and offload pressure areas, prevent rubbing of the toes and improve stability. Surgical treatment needs to be tailored to the individual patient underlying pathology, risk of progression, level of deformity and muscular imbalance. No single surgical procedure is appropriate for all patients and frequently, multiple procedures are required. Correction of deformity without addressing muscular imbalance will not be successful. Surgical procedures are broadly categorized into soft -tissue and bony procedures. Tendon transfers and osteotomies can provide correction of the deformity without the need for arthrodesis. Arthrodesis is usually required for severe arthritic joint disease or if complete muscle paralysis is present.
Thankyou.

Figure 5.4 Cavus foot deformity.

Figure 5.5 Coleman block test.

Figure 5.6a,b AP and lateral radiographs of a cavus foot.
Surgery#
1. Soft -tissue releases
Plantar fascia release
In young children, surgical release of the plantar fascia and short toe flexors may be helpful. This is on the assumption that the deforming force of a contracted plantar fascia leads to a narrow arch base, plantar flexed first metatarsal and heel varus due to the windlass effect.
Gastrocnemius/Achilles lengthening
Occasionally required for contracture, but it is important to make sure a true equinus is present onstanding lateral radiographs.
2. Tendon transfers
The most common tendon transfer incavo varus foot is peroneus longus to brevis transfer to improve power of eversion. It helps stabilize the ankle.
3. Osteotomies
Patients with hindfoot involvement usually require a calcaneal osteotomy to correct the deformity. The osteotomy can include a closing wedge, aver tical displacement, or a combination (triplanar osteotomy).
4. Fusion
For a rigid painful foot in a young adult a triple arthrodesis can be used as a salvage stabilizing procedure that relieves pain but sacrifices joint motion.
Complications include development of ankle arthritis, pseudo-arthrosis, residue deformity, midfoot arthritis overcorrection and AVN talus.
Structured oral examination question 5#
Acquired adult flafooot
I would like you to look at this clinical photograph and tell me what you see (see Figure 5.7a).

This shows the posterior view of feet in a weight-bearing stance. There is marked heel valgus, loss of the medial longitudinal arch and too many toes are visible [16].
What term is used to describe this situation?
Pes planus or flafooot.
Yes. In adults, what are the causes of this condition?
The commonest cause is tibialis posterior dysfunction. Other causes include inflammatory arthritis, Char cot arthropathy, midfoot osteoarthritis and trauma (malunited calcaneum, missed Lisfranc injury, cuboid fracture).
OK. How common is adult flafooot?
It is commoner in females and the incidence increases with age.
Okay. Let’s stick with tibialis posterior dysfunction. Describe a typical patient.
The classic patient would be a female aged between 45 and 65 years with pain along the course of the tibialis posterior tendon exacerbated by activity . Standing on tiptoe may be painful and difficult. There is likely to be later development of increasing planovalgus deformity which may be associated with lateral impingement pain as the distal fibula contacts the calcaneum.
What are the key examination points you would look for?
The most useful testis the ability to perform a single heel raise. I would also assess for hindfoot flexibility. These would guide classification and treatment.
What are the origins and insertions of the tibialis posterior tendon?
It arises from the posterior tibia interosseous membrane and the fibula in the proximal third of the leg and runs in the deep posterior compartment of the leg. The tendon then passes in a groove directly behind the medial malleolus, where it is tightly bound by the flexor retinaculum. The main insertion is on to the navicular tuberosity but equally importantly it also fans out under the plantar aspect of the foot with extensive insertions to the second through fourth metatarsals, all three cuneiforms, the sustentaculum tali and the cuboid.
How do you assess the strength of the tibialis posterior tendon?
The strength of the tendon is evaluated by asking the patient to attempt to invert the foot from a plantar flexed and everted position. This position isolates the posterior tibial tendon, neutralizing synergistic inversion from the anterior tibialis muscle.
How does tibialis posterior dysfunction cause a flatfoot?
The function of the posterior tibial tendon is threefold: it acts as an invertor of the subtalar joint, plantar-flexor of the ankle and an adductor of the forefoot. The combination of these actions serves to elevate the medial arch. The inversion pull of tibialis posterior on the subtalar joint locks the transverse tarsal joint, providing a rigid lever arm with which to push off following the heel-raise phase of gait. With a diseased or poorly functioning tibialis posterior tendon, the unopposed action of the peroneus brevis pulls the forefoot into abduction and the sub talar joint into valgus. It is inactive during the swing phase. After heel contact the tibialis posterior contracts eccentrically to prevent excess hindfoot eversion. The Achilles tendon is a powerful secondary inverter of the heel. It relies on the initial inversion power of the tibialis posterior to shift its mechanical axis more medially, thereby exerting a further inversion force. As the function of the tibialis posterior fails, the Achilles tendon remains close to the subtalar axis, thereby reducing its function as both an inverter and a stabilizer of the subtalar joint. As the imbalance between lateral and medial soft tissues progresses, the hindfoot valgus and forefoot abduction increase. The static stabilizers on the medial side, in particular the spring ligament and the deltoid ligament, attenuate further.
As you have mentioned classification of tibialis posterior dysfunction could you tell me any more about this?
Yes. Johnson and Strom proposed a three-stage classification in 1989. My erson later added a fourth stage [17]. In stage 1 disease, there is no deformity but pain from the tendon. A single heel raise is usually possible but painful. The tendon is inflamed, tender and swollen. In stage 2 disease, there is a flexible planovalgus deformity and weakness of single heel raise. The tendon degenerates and lengthens with the foot changing shape going into valgus. In stage 3 disease, the valgus hindfoot deformity has become fixed and reconstruction is not possible. With stage 4, there is additional tilting of the talus in the ankle mortise leading to significant ankle arthritis secondary to valgus strain.
OK. How would you investigate this patient?
Weight-bearing AP and lateral radiographs of both the foot and ankle would help to assess structural change and exclude other causes of flafooot. They could also show associated degenerate change. The arch index could also be measured.
Would the arch index influence your management?
No. It is mainly used as a research tool.
Is there a place for MRI?
MRI is not routinely needed for the diagnosis of flatfeet. It is useful in detecting early changes within the tendon if there is any diagnostic doubt. MRI is valuable if surgical management is being planned. It is also useful for assessing the medial structures such as the deltoid and spring ligaments and also the peroneal tendon [18]. Figure 5.7d–f. MRI tibialis posterior tendinopathy with fluid around tendon. Some increased signal within the tendon substance.

Tell me what the treatment options are.
For stage 1, I would offer debridement of the tendon followed by 6–8 weeks of casting or splintage, then provision of a definitive arch support orthosis [19]. For stage 2 disease I would offer either a lateral column lengthening or a medializing calcaneal osteotomy in conjunction with a FDL transfer to augmentor replace the tibialis posterior [20]. The Achilles tendon occasionally needs to be percutaneously released if it is tightened and is preventing full correction. In stage 3 disease, triple arthrodesis is recommended [21]. For stage 4 disease, the treatment depends upon the flexibility of the ankle deformity. If it is flexible, a triple arthrodesis combined with ankle bracing or deltoid ligament reconstruction may be adequate, otherwise a triple arthrodesis combined or followed by ankle arthrodesis would be indicated.
You seem very clear about surgical options Whatabout non-operativ e treatment?
I should have mentioned that. It is appropriate to offer analgesia and orthotic treatment to most patients initially . An orthotic providing medial arch support with a heel cup to control heel valgus would be appropriate. There are two aims of orthotic treatment. First, this may offer adequate symptom relief. Second, it may control progressive heel valgus and flattening of the medial archIt’s not great viva tactics to jump straight in to discussing surgical options for a condition unless it is very clear that’s what the examiners want to discuss.
You spoke about an FDL transfer. Tell me about this procedure.
After obtaining informed consent I would make an incision in the line of the posterior tibial tendon, starting posterior to the medial malleolus. I would debride or resect the tendon according to the clinical appearances. The flexor digitorum longus sheath lies directly posterior to the tibialis posterior tendon and would be opened longitudinally as far distally as possible before the FDL tendon is divided. The free FDL tendon is then passed through a tunnel drilled in the navicular and sutured back to itself under tension.
In what direction would you pass FDL through the navicular?
From plantar to dorsal.
What is the aim of a medializing calcaneal osteotomy?
The calcaneal osteotomy directly reduces the heel valgus and brings the weight-bearing axis closer to the long axis of the leg. In addition, it displaces the Achilles tendon insertion medially to prevent it acting as an ever ter of the hindfoot.
When obtaining consent, what would you advise about flexion of the toes after harvesting the flexor digitorum longus?
I would expect flexion of the lesser toes to be maintained by the flexor hallucis longus via the knot of Henry.
Can you tell me alit ile more about the knot of Henry?
The flexor digitorum longus crosses the flexor hallucis longus at the knot of Henry. There are a number of fibrous interconnections between the two tendons that afford a degree of cooperation in movement. This means that flexion of the digits can continue after harvest of either FDL or FHL.
What would you tell the patient about the success rate of the operation?
Chad wicket al. [22] reported that FDL transfer with medializing calcaneum osteotomy provided long-term pain relief and improved function in 85% of patients after a mean follow-up of 15.2 years. Substantial improvements were noted in the American Orthopaedic Foot & Ankle Society (AOFAS), visual analogue scale (VAS), and SF-36 scores. This is scoring a 7. Appropriate up-to-date knowledge of the literature to justify a management decision.
Is there a place for any additional procedures such as first ray fusions or lateral column lengthening?
One concern with stage 2 adult-acquired flafooot deformity is that there is a large variability in disease severity within the classification group including hindfoot valgus, medial column stability, forefoot abduction and supination. The treatment remains controversial with numerous soft -tissue and bony procedures being described. How extensive a procedure is required remains unknown.
What approach would you use for a triple arthrodesis to correct significant, fixed valgus heel deformity?
This is a potentially difficult situation. The joint preparation is s traighfoorward if a lateral utility approach or similar is combined with a dorsal incision over the talonavicular joint. If a significant deformity is being addressed there can be difficulty inclosing the lateral incision once the deformity is corrected. There are advocates of triple arthrodesis via a single medial approach, but this is difficult and not always possible.
One final question. An y new developments?
PRP injections have recently been used in the early stages of posterior tendon dysfunction. We are awaiting randomized controlled data.
Thankyou.

Figure 5.7a Acquired adult flafooot. Loss of medial arch. Valgus heel, ‘too many toes sign’.

Figure 5.7b Midfoot sagift al radiograph sMeary’s angle negative (> 10°). Reduced calcaneal pitch angle (10° approx., normal 20–30°).

Figure 5.7c Anteroposterior (AP) radiographs of midfoot abduction. T alo to first metatarsal an angle > 10°.

Figure 5.7d–f MRI tibialis posterior tendinopathy with fluid around tendon. Some increased signal within the tendon substance.
Structured oral examination question 6#
Hallux valgus
Please have a look at these clinical photographs and tell me what you see (see Figures 5.8 and 5.9).
These show a frontal view of a pair of feet and an oblique view of the left foot. There are bilateral hallux valgus deformities with the hallux o ver-riding the right second toe. I can only count three lesser toes for the left foot and there is a scar in the web space lateral to the hallux and a medial longitudinal scar over the metatarsophalangeal joint. The toenails appear friable and there is some excoriation around the lesser toes of the right foot.
OK. This 65-year-old lady had her left second toe removed some years ago for a presentation similar to that which she now has on the right. Her left-sided symptoms have also recurred. How would you assess her further?
I would obtain a detailed history, looking to clarify the main source of her symptoms. Can I ask what symptoms she has?
What do you think they are likely to be?
I would expect she has pain from her bunions and toes caused by rubbing on footwear and each other. I would also anticipate she has symptoms due to degenerative change involving the great toe MTP joint or metatarsalgia of the lesser rays.
Let’s say she has all these symptoms to varying degrees. Tell me about your further assessment.
I would complete the history, including questioning about relevant conditions such as diabetes, inflammatory arthritis vascular disease and neuropathy, and proceed to examination. I would assess her gait and the posture of the weighted foot as hallux valgus is often associated with apl anus foot. I would palpate for areas of tenderness, paying particular attention to the hallux MTP joint and lesser metatarsal heads. I would assess the range of movement of the involved joints and look for gastrocnemius tightness. Finally, I would also undertake a grind test to assess pain from loading the MTP joint. Neurovascular status will also be assessed.
You spoke about assessing the range of movement of the involved joints. Can you be more specific?
I would want to assess the range of plantar and dorsiflexion of the hallux MTP joint. It is also important to assess the movement at the first tarso-metatarsal joint as excessive mobility will influence the surgical choice.
Okay, we might come back to that. Outline the value of plain radiographs in the management of hallux valgus.
I would obtain weight-bearing AP and lateral radiographs of the foot. These would allow me to objectively measure various angles, assess uncovering of the sesamoids and look for evidence of arthritic change.
Why weight-bearing?
Non-weight-bearing views tend to underestimate the severity of hallux valgus, and may give misleading information about alignment and relative metatarsal length.
Keep going. What angles?
I would measure the intermetatarsal, hallux valgus and the distal metatarsal articular angles.
What is the normal range of these angles and how would these influence your management? Can you demonstrate these angles on the radiographs (Figures 5.10–5.13)?
The intermetatarsal angle is normally less than 9°, the hallux valgus angle should be less than 15° and the distal metatarsal articular angle is normally a maximum of 15°. The degree of deformity helps determine the surgical options.
What about these radiographs?
These demonstrate severe hallux valgus with an HVA 50°, IMA 22° and DMAA 8° (Figures 5.14–5.16).
If this lady had an intermetatarsal angle of 15° on the right with a hallux valgus angle of 35° and minimal passive correction of the hallux, what surgery would you plan?
If the first tarso-metatarsal joint is not lax, I would plan a scarf osteotomy combined with a lateral release and an Akin osteotomy of the proximal phalanx if necessary.
Why would you choose a scarf osteotomy?
It is a very versatile procedure with stable fixation allowing early postoperative mobilization without a cast. It maintains the length of the metatarsal and facilitates translation angulation and depression of the metatarsal head as necessary. It can also be used to shorten or lengthen the metatarsal [23].
How would you secure the osteotomy?
With two headless compression screws.
Why not use a simpler procedure such as a chevron or Mitchell osteotomy?
For the degree of deformity described, combined with the lack of passive correction of the hallux, I believe the correction that could be achieved with a distal osteotomy would be inadequate. A further disadvantage of a Mitchell osteotomy is that it produces shortening of the first metatarsal, which could lead to transfer metatarsalgia.
Can you draw a scarf osteotomy?
No, sorry.
For your proposed management, what complications would you discuss when seeking consent?
Firstly, I would advise that while early weight-bearing is possible with a scarf osteotomy, it takes up to a year for the foot to fully set ile after such surgery, but that typically 85% of patients are pleased with the outcome. I would advise a 1% risk of deep infection and as lightly higher risk of superficial infection Recurrence is possible with time, although the risk of this is greatest in adolescent cases. A minority of patients will have significant stiffness of the MTP joint afterwards and there can be sensory loss if the dorsomedial sensory nerve is injured. I would mention the possibility of hallux varus as a complication as this is difficult to treat. I would also mention the possibility of intraoperative and postoperative metatarsal fracture.
How would you treat hallux varus?
A subtle varus may improve as the patient returns to normal footwear. While soft -tissue procedures such as abductor hallucis and medial capsular release or transferor a slip of EH Lare described for flexible deformity, arthrodesis of the first MTP joint arthrodesis is a reliable option in the presence of significant stiffness or arthrosis.
So, you have successfully treated this lady’s right foot and she is pleased with the result. Would you go ahead and do the same on the left?
No. The absence of the second toe predisposes to recurrence and I would propose arthrodesis of the hallux MTP joint.
One final question. What do we mean by a congruent versus incongruent hallux valgus (see Figures 5.17 and 5.18)?
If there is no lateral subluxation then the joint is congruent. A congruent first MTP joint is present when alignment of the articular joint surfaces of the metatarsal head and proximal phalanx base occurs in a slight valgus position. An incongruent joint exists when the toe is in a valgus orientation and the articular surfaces do not align properly or concentrically.
Thankyou.

Figure 5.8 AP view of hallux valgus.

Figure 5.9 Oblique view of hallux valgus.

Figure 5.10 Hallux valgus angle (HVA). Angle between long axis of first metatarsal shaft and long a xis of first proximal phalanx. Normal < 15°. Mild 15–20°. Moderate 20–40°. Severe > 40°.

Figure 5.11 Hallux valgus interphalangeus angle (HVI). Angle between long axis of first distal phalanx and long axis of first proximal phalanx. Associated with congruent hallux valgus. Normal < 10°.

Figure 5.12 First to second intermetatarsal angle (IMA). Angle between long axis of first and second metatarsal shaft. Normal < 9°. Mild < 11°. Moderate 12–15°. Severe > 15°.

Figure 5.13 Distal metatarsal articular angle (DMAA). Angle between long axis of first metatarsal and perpendicular to a line along the articular surface. Increased angle associated with a congruent deformity. Normal < 10°.

Figure 5.14 Hallux valgus angle (HVA) (pronation oft oe). Normal < 15°.

Figure 5.15 Intermetatarsal angle (IMA) 22°. Normal < 9°.

Figure 5.16 Distal metatarsal articular angle (DMAA). Normal < 10°.

Figure 5.17 Congruent hallux valgus. Increased HVA, increased DMAA and congruent joint.

Figure 5.18 Incongruent hallux valgus. Increased HV Anormal DMAA and incongruent joint.
Structured oral examination question 7#
Hallux rigidus
This 45-year-old male patient has presented with pain and stiffness of his right big toe. Describe the X-ray findings (see Figure 5.19).

This is a radiograph of a right foot showing loss of joint space, osteophyte formation and sclerosis of the first metatarso-phalangeal joint in keeping with osteoarthritis. The reis also a mild hallux valgus deformity.
So, what is this commonly called in orthopaedics?
Hallux rigidus.
Tell me the range of movement of a healthy first MTP joint.
The joint should be able to dorsiflex between 70 and 90° and plantarflex between 24 and 40°.
How would you manage this patient?
First of all, I would take a full history and examine the foot. I would also obtain a weight- bearing lateral and an oblique X-ray of the foot in addition to the AP view we have here.
OK. If we concentrate on the clinical examination, what specific findings are you looking for to help with your management decision?
I would need to assess the integrity of the skin and the neurovascular status of the foot. I would then palpate for osteophytes and assess the range of movement of the first MTPJ and look to see whether the patient has pain limited to the extremes of movement or throughout the arc of motion. Often the first MTPJ is enlarged, erythematous and swollen. There may be medial-sided numbness present if the medial dorsal cutaneous nerve is compressed by an osteophyte. A grind test of the joint would be informative [24]. This testis usually done with the MTPJ in relative neutral dorsiflexion and can be a pointer to articular cartilage involvement [25]. I also need to evaluate the range of motion and look for any sign of degenerative change at the interphalangeal joint (IPJ).
What is the importance of the IPJ?
Fusion of the first MTPJ may accelerate degeneration in the surrounding joints so if the IPJ is already symptomatic a motion-pr eserving procedure at the MTPJ may be more appropriate.
Are you aware of any grading systems for this condition?
The most widely used is a radiographic grading by Hatirup and Johnson in which Grade 1 is a well-preserved joint space with mild to moderate osteophytes, Grade 2 has a reduced joint space with moderate osteophytes and Grade 3 is complete loss of joint space, marked osteophytes and there may be subchondral cysts within the metatarsal head [26].
Right, so talk me through the management options for apa tien t with hallux rigidus.
In the first instance I would advise non-operativ e treatment. The options include activity modification, NS AIDS, footwear modification or an in tra-articular steroid injection.
And the operative options?
The operative options include cheilect omy with or without a dorsal closing wedge osteotomy of the phalanx (Moberg), fusion and arthroplasty. The choice depends on the grade of the arthritis, patient symptoms and expectations.
So then, back to the operative options for treatment.
In Grade 1 or 2 disease, a cheilectomy, in which the osteophytes and the dorsal 25–30% of the articular surface are resected. No more than one-third of the dorsal metatarsal head articular surface should be excised otherwise there is the risk of dorsal subluxation or overload on the remaining articular surface. Satisfaction rates of 90% have been reported, with improvement in dorsiflexion from 20 to 40°. For Grade 2 or 3 disease inpatients who are young and still highly active I would combine a cheilectomy with a Moberg dorsal closing wedge osteotomy of the proximal phalanx. This shitis the arc of movement further into the dorsiflexion range, reducing symptoms. For patients with severe disease and no ligamentous instability total joint replacement is an option, but early loosening has been a problem. Good results have been reported with hemiarthroplasty of either the metatarsal head or the base of the proximal phalanx, but few large series exist and neither is commonly used in the United Kingdom [28,29]. Arthrodesis of the first MTPJ is still the mainstay of treatment for severe disease and joint preparation with dome-shaped reamers and a lag screw and dorsal plate construct is the most biomechanically sound fixation [ 30]. Keller’s arthroplasty is an option in elderly , low-demand patients however, cock-up deformities and transfer metatarsalgia may develop.
So, back to arthrodesis. What is the optimal position for fusion?
Dorsiflexion of 25° across the MTPJ, valgus of 10–15° and neutral rotation to ensure an effective plane of motion of the IP J.
How will you consent apa tien t for arthrodesis of the first MTPJ?
I will explain that the aim of surgery is to relieve pain and optimize mobility. The risks and complications include wound healing problems, infection, damage to the medial cutaneous nerve, delayed union, malunion, non-union, metalwork irritation and accelerated degeneration in surrounding joints.
If we return to the patient we started discussing. He is a 45-year-old male who is a keen walker. He has significant stiffness and pain on mobilization and dorsiflexion, but a grind testis negative. He has exhausted non-operativ e measures. What treatment will you offer him?
I would offer him a cheilectomy with a proximal phalanx osteotomy as this has the added benefit of improving range of movement over a cheilectomy on its own, although he will be made aware that the risks of this procedure are greater than a cheilectomy. I would also discuss fusion with him and explain that this may become necessary if a cheilectomy failed to provide sufficient relief or he had later progression of disease.
He is not keen on the joint being stiffened up and has read on the internet about joint replacements and is keen for this.
I would inform him that for his age group there would be a significant risk of loosening of the prosthesis resulting in failure, thus the need for revision surgery. A recent systematic review of the literature by Stevens et al. indicated that arthrodesis is superior for improving clinical outcome and reducing pain with fewer complications and revisions compared to total joint replacement. They reported a 20.9% rate of prosthesis loosening causing instability and pain during gait and an 11% chance of revision surgery being required.
He is still not convinced.
I would refer him to a colleague for a second opinion. [Bell] For the FRCS (Tr & Orth) exam joint replacement is very controversial.

Figure 5.19 X-ray showing hallux rigidus.
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