Foot and Ankle Surgery

 General Principles

1     Biomechanics

 Take-Home Message

•      The complex bony and ligamentous anatomy of the foot and ankle allows multiple foot positions and motion in three axes of rotation.

•      Transverse tarsal joints provide both fl exibility and stability to the hindfoot and midfoot.

•      The midfoot is an important bridge between hindfoot and forefoot and is stabilized by longitudinal and transverse arches.

•      The gait cycle is composed of a stance and swing phase, the mechanics of which are infl uenced by important soft-tissue contributions.

 Ankle Biomechanics   

 Ankle joint:  articulation between tibial plafond, medial malleolus, lateral malleolus, and talus.

•      Mortise widens and ankle is more stable in dorsifl exion due to shape of talar dome.

•      R esponsible for most sagittal plane motion of foot and ankle: dorsifl exion (10–23°) and plantarfl exion (23–48°). Secondary motion rotation and inversion and eversion.

•      M edial deltoid ligament complex is the main stabilizer of the ankle during stance.

Functions to resist lateral translation and valgus forces, i.e., talar tilt.

•      Lateral ankle ligaments function as a restraint to varus forces.

 A. R.  Kadakia ,  MD (*) •  P. J.  Switaj •  B. S.  Ho •  M.  Alshouli •  D.  Fuchs •  G.  Ochengele

 Department of Orthopedic Surgery ,  Northwestern University – Feinberg School of Medicine, Northwestern Memorial Hospital,   Chicago ,  IL ,  USA

 e-mail: Kadak259@gmail.com; paul.switaj@gmail.com; bryant.s.ho@gmail.com; mtshouli@gmail.com; dfuchs0011@gmail.com; gochenjele@gmail.com

© Springer-Verlag France 2015                                                                                              837

C. Mauffrey, D.J. Hak (eds.), Passport for the Orthopedic Boards and FRCS Examination, DOI 10.1007/978-2-8178-0475-0_38

Distal tibiofi bular joint:  consists of distal fi bula (medial convex surface) and incisura fi bularis of distal tibia (lateral concave surface).

•      Fibula rotates within the incisura (~2°) during normal gait.

•      Along with syndesmotic ligaments, provides stability against lateral talar translation.

 Hindfoot Biomechanics  

 Subtalar joint : articulation between talus and calcaneus.

•      Functions in eversion and inversion.

•      Limited eversion accommodation contributes to disability derived from even a mild cavovarus foot deformity.

 Transverse tarsal joint (Chopart) : articulation between talus and navicular (TN) and between calcaneus and cuboid (CC).

•      Important for providing stability to the hindfoot and midfoot to produce rigid lever at toe-off.

•      D uring heel strike, these joints are supple and parallel to adapt to uneven ground, then during toe-off become divergent and lock, providing stiffness to the foot.

•      Failure of the posterior tibial tendon to lock the transverse tarsal joints is the biomechanical etiology for lack of a heel rise in patients with posterior tibial tendon dysfunction.

 Midfoot and Forefoot Biomechanics  

 Midfoot : consists of intercuneiform joints, naviculocuneiform joint, and tarsalmetatarsal joints (TMT).

•      Midfoot functions in adduction and abduction.

•      Provides important bridge between hindfoot and forefoot and both fl exibility and stability for normal gait.

•      T MT joint complex (Lisfranc joint) divided into medial, middle, and lateral columns.

–     L  ateral column has most sagittal mobility and allows for fl exibility during necessary for walking on uneven ground.

–     Middle column is least mobile and allows for rigidity during push-off. –  Medial column experiences the most force while in stance.

•      The foot has longitudinal and transverse arches → stabilized by bony architecture, ligaments, and muscle forces.

–     The plantar ligaments are thicker and stronger than the dorsal ligaments.

–     T  he interosseous ligaments are the primary stabilizer of the longitudinal arch. The plantar fascia is a secondary stabilizer.

–     The specialized architecture of the Lisfranc joint complex imparts a bony “keystone” effect which stabilizes the transverse arch. The Lisfranc ligament (from medial cuneiform to base of the 2nd MT) is the largest and strongest of the ligaments which stabilize the Lisfranc joint.

Forefoot: consists of all structures distal to TMT joints.

•      F irst metatarsal is the widest and the shortest and bears 50 % of weight during gait.

•      Second metatarsal experiences more stress than the other lesser metatarsals (commonly involved in stress fractures).

•      Lesser toes are balanced by the extrinsic muscles (EDL, FDL), intrinsic muscles (interossei, lumbricals), and passive restraints (plantar plate, extensor hood, joint capsule, collateral ligaments).

•      Loss of intrinsic function predictably leads to claw toes.

 Foot Positions Versus Foot Motions  

 Foot positions are defi ned in a manner different from foot motions → they are varus/valgus (hindfoot), abduction/adduction (midfoot), and equinus/calcaneus (ankle).

 Foot motions are in three axes of rotation (Table  1 ).

 Gait Cycle   

•                One gait cycle, or “stride,” is measured from heel strike to heel strike.

•                Ground reaction forces are approximately 1.5 times body weight during walking and 3–4 times body weight during running.  Stance phase : 62 % of gait cycle. Heel strike to toe-off

•                Heel strike:

–     Hindfoot valgus, forefoot abduction, dorsifl exion of ankle.

–     Anterior tibialis contracts eccentrically to control rate at which foot strikes the ground.

–     Quadriceps contract to stabilize knee.

–     Hindfoot unlocked/everted for energy absorption.

•                Foot fl at: Single-limb support

–     Gastrocnemius-soleus complex contracts eccentrically.

–     Knee extends, hip extensors under concentric contraction.

–     Hindfoot unlocked/everted for ground accommodation.

 Table 1  Description of foot motion in three axes of rotation

Plane of motion	Motion
Sagittal (X-axis)	Dorsifl exion/plantar fl exion
Frontal (coronal) (Z-axis)	Inversion/eversion
Transverse (Y-axis)	Forefoot/midfoot: adduction/abduction
	Ankle/hindfoot: internal rotation/external rotation
Tri-planar motion	Supination: adduction, inversion, plantar fl exion
	Pronation: abduction, eversion, dorsifl exion

Swing phase : 38 % of gait cycle. Toe-off to heel strike

•                Toe-off:

–     Hindfoot varus, forefoot adduction, plantarfl exion of ankle.

–     Hip fl exors contract. Gastrocnemius-soleus complex contracts concentrically.

–     P  lantar fascia tightens, longitudinal arch is accentuated (windlass mechanism), and transverse tarsal joint locks → allows foot to convert from fl exible shock absorber to rigid propellant.

•                Mid-swing: Foot clearance

–     Ankle dorsifl exors contract concentrically. –  Loss of function results in steppage gait.

•                Terminal swing: Hamstring muscles decelerate forward motion of thigh.

 Bibliography

1 . C hambers HG, Sutherland DH. A practical guide to gait analysis. J Am Acad Orthop Surg. 2002;10:222–31.

2.    Dicharry J. Kinematics and kinetics of gait: from lab to clinic. Clin Sports Med. 2010;29:347–64.

3.    Irwin TA, Kadakia AR. Miller review of orthopedics. 6th ed. Philadelphia: Elsevier Publications; 2012.

4.    Rodgers MM. Dynamic biomechanics of the normal foot and ankle during walk-ing and running. Phys Ther. 1988;68:1822–30.

    2     Ankle Arthroscopy

 Take-Home Message

•      Indications for arthroscopy include treatment of OCLT, debridement of osteophytes and synovitis, removal of loose bodies, and cartilage debridement for ankle fusions.

•      Joint distraction, correct instrumentation, and systematic arthroscopic approach are vital to successful surgical procedure.

•      Arthroscopic portal options include anterolateral, anteromedial, postero-lateral, and posteromedial and require a systematic approach for a thorough procedure.

•      Superfi cial peroneal nerve is most at risk from iatrogenic injury.

 Relevant Anatomy   

•      T ibiotalar joint: comprised of the ankle mortise superiorly and talar dome inferi-orly (Fig.  1).

     Fig. 1  Anatomic dissection of the anterior aspect of the ankle. The anterior aspect of the distal tibia, medial malleolus, and the talus are visualized

•      Distal tibiofi bular joint: convex surface of medial fi bular articulates with incisura fi bularis. Syndesmotic ligaments include anterior inferior tibiofi bular ligament, posterior inferior tibiofi bular ligament, interosseous tibiofi bular ligaments, and interosseous membrane.

•      Deltoid ligament complex: deep and superfi cial deltoid → to resist lateral talar translation and valgus.

•      Lateral ankle ligaments: anterior talofi bular (ATFL), calcaneofi bular (CFL), pos-terior talofi bular (PTFL) →to resist varus forces.

•      A nterior neurovascular structures: superfi cial peroneal nerve (SPN), saphenous nerve, anterior tibial artery, vein, and deep peroneal nerve (DPN) (Fig.  2 ).  

•      P osterior neurovascular structures: sural nerve, tibial nerve, posterior tibial artery and vein.

 Surgical Indications   

•      O steochondral lesions – chronic (debridement with microfracture) or acute (fi xation of bony component)

•      Debridement of synovitis

•      Ankle impingement – excision of soft tissue and tibial/talar osteophytes

•      Removal of loose bodies

•      Cartilage debridement in conjunction with ankle fusion

 Perioperative Considerations   

•      T horough history and physical examination provide a differential diagnosis and guide acquisition of appropriate imaging studies.

•      Positioning: supine, bump under ipsilateral pelvis to achieve neutral foot rota-tion. Flex hip and knee to allow distraction and relax gastrocnemius tension.

•      Use noninvasive distraction methods in a sterile fashion to access tibiotalar artic-ular surface (Fig.  3) . Anterior ankle arthroscopy for impingement and synovitis without distraction minimizes risk to the deep neurovascular structures and articular cartilage as the ankle can be dorsifl exed during the procedure.  

•      2 .7 mm 30-degree angle arthroscope is suitable in most cases. Small joint instruments are useful, in addition to 3.5 mm shaver, 4.0 mm round burr, and microfracture awl.

 Fig. 2  Anterior tibial artery, vein, and deep peroneal nerve ( arrowhead ). The bundle lies deep the EHL at the level of the ankle and visualizing of the structures requires retraction of the tendon. The superfi cial peroneal nerve is also seen distally; it has been transected proximally ( arrow )

     Fig. 3  Patient positioning and noninvasive ankle distractor. Ipsilateral fl exion of the thigh elevates the ankle to allow for posterior portal placement and stabilizes the proximal leg to allow for ankle distraction. The anteromedial and anterolateral portals have been marked in this case

( black lines )

 Portal Placement  

M any arthroscopic portals have been described to access the ankle, but anteromedial and anterolateral remain the staple.

•      Anteromedial: primary viewing portal. Established fi rst. Make portal 2.5 mm medial to tibialis anterior tendon directly at level of joint. Incise skin; bluntly dissect to joint capsule. Enter joint with trochar and cannula; introduce arthroscope and distend joint.

•      Anterolateral: primary working portal. Create once arthroscope is introduced and joint is distracted. Make portal at level of joint line, just lateral to peroneus tertius tendon. Incise skin sharply; bluntly dissect carefully to protect the superfi cial peroneal nerve.

•      P osterolateral: Make portal just lateral to Achilles tendon, 2 cm superior to the distal tip of the lateral malleolus. Incise skin; bluntly dissect to capsule. Direct trochar slightly medially, toward 1st and 2nd interdigital webspace. Portal is at the level of the posterior process of the talus.

•      Posteromedial: rarely indicated given proximity to the posterior neurovascular bundle (posterior tibial artery, vein, tibial nerve). Incision just medial to the Achilles tendon above 2 cm superior to distal tip of lateral malleolus. Enter joint capsule under direct visualization from the posterolateral portal. All instruments must remain lateral to the FHL tendon.

 Diagnostic Arthroscopy   

•      Begins in anterior aspect of joint. Inspect for synovitis, loose bodies, and osteophytes.

•      V isualize articular surfaces of tibiotalar joint. Probe gently for softening to assess for an OCLT (Fig.  4).  

 

 Fig. 4  Osteochondral lesion of the talus with fi ssuring of the articular surface

 Fig. 5  Loose body noted in the anterior aspect of the ankle joint. These commonly reside in the posterior ankle capsule. Use of the shaver to provide suction can “pull” the loose bodies into the shaver and allow for removal

•      View the lateral gutter, between the lateral talar dome and fi bula, both from the anterior ankle and within the tibiotalar articulation. Inspect inferior aspect of syndesmosis.

•      V iew the medial gutter, between the medial talar dome and medial malleolus in a similar fashion.

•      May view the posterior aspect of joint by rotating the arthroscope appropriately, but some pathology may necessitate a posterior portal due to curvature of talar dome.

•      Loose bodies commonly reside posteriorly, so a thorough inspection of the pos-terior aspect is essential (Fig.  5).  

 Complications   

•      Reported complication rates range from 3 to 17 %.

•      Neurovascular injury from portal placement is the most commonly reported complication (SPN is the most commonly injured).

•      O thers include instrument failure, damage to articular cartilage, infection, and complex regional pain syndrome.

 Bibliography

 1.  Bonasia DE, Rossi R, Saltzman CL, Amendola A. The role of arthroscopy in the management of fractures about the ankle. J Am Acad Orthop Surg. 2011;19:226–35.

2 . d e Leeuw PA, van Sterkenburg MN, van Dijk CN. Arthroscopy and endoscopy of the ankle and hindfoot. Sports Med Arthrosc. 2009;17:175–84.

 3.  Glazebrook MA, Ganapathy V, Bridge MA, Stone JW, Allard JP. Evidence- based indications for ankle arthroscopy. Arthroscopy. 2009;25:1478–90.

4 . v an Dijk CN, van Bergen CJ. Advancements in ankle arthroscopy. J Am Acad Orthop Surg. 2008;16:635–46.

    3     Ankle Arthrodesis

 Take-Home Message

•      A nkle arthrodesis is indicated for the patient with recalcitrant arthritic ankle pain.

•      The most common etiology of ankle arthritis is posttraumatic.

•      Surgical techniques can involve arthroscopic or open procedures and rely on adequate joint preparation for bony union.

•      T he results from ankle arthrodesis are excellent overall but with time will result in adjacent joint arthritis; the most common is the subtalar joint.

•      Position of the arthrodesis in neutral dorsifl exion, 5° of valgus, and slight external rotation is critical to maximize function and minimize adjacent joint stress.

 Introduction   

•      N onoperative treatment of symptomatic ankle arthritis includes the use of shoe inserts or shoe modifi cations (SACH heel with rocker bottom), anti- infl ammatory medications, and intra-articular injections (corticosteroid or hyaluronate ) and use of either an ankle-foot orthosis or a rigid lace-up leather brace (Arizona type).

•      The use of a walking cast has been suggested as a trial device to evaluate patient acceptance and degree of pain relief prior to arthrodesis.

 Surgical Indications   

•      P ersistent ankle arthritic pain that is functionally debilitating to the patient and is not relieved by nonoperative treatment methods.

•      Etiology: most commonly posttraumatic arthritis (cause of more than 70 % of ankle arthritis).

•      Other causes of painful arthritis include postinfectious, chronic instability, infl ammatory arthropathy, neuropathic arthropathy, primary osteoarthritis, failed total ankle arthroplasty, and avascular necrosis.

 Perioperative Considerations   

•      Need weight-bearing standing anteroposterior, lateral, and mortise views to assess radiographic changes in the joint, arthritis in the subtalar joints, and bony alignment (Fig.  6).

•      Patient needs to be compliant with postoperative weight-bearing status and should be counseled on smoking cessation.

 Surgical Techniques  

 rthroscopic arthrodesis: typically for patients with little or no deformity of the A ankle and good bone stock and density. Fixation can only be performed with screws.

 Fig. 6  AP and lateral WB views of a patient with end-stage ankle arthritis. Note the signifi cant anterior subluxation of the talus on the lateral radiograph which must be addressed intraoperatively

O pen arthrodesis: particularly useful for patients with severe ankle joint deformity. Better visualization of joint, correction of deformity, and allows use of plate fi xation.

•      Approaches: Options include lateral exposure where the fi bula is either resected or osteotomized and replaced or an anterior approach (between the tibialis anterior and the extensor hallucis longus tendons), and least commonly performed is the posterior approach (in setting of compromised tissues).

•      After achieving operative exposure of the joint to be fused → remove remaining cartilage and subchondral bone from the arthritis joint surfaces (Fig.  7 ).  

•      O btain good bony apposition and reduction with compression of the joint surfaces.

•      Then use rigid internal fi xation (multiple 6.5 mm screws or a plate and screw con-struct) or external fi xation for preexisting septic joint and those with severe osteopenia. Both isolated screw and plate and screw constructs have demonstrated a similarly high union rate that approaches 95–100 % with modern techniques (Fig.  8).  

 Optimal position of ankle joint: neutral dorsifl exion, 5–10° of external rotation, 5° hindfoot valgus (in order to keep hindfoot unlocked for accommodative hindfoot motion) (Fig.  9).  

T ibiotalocalcaneal arthrodesis: can be performed with retrograde nail or a plate for concomitant subtalar and tibiotalar arthrodesis. Use of screws in isolation for a TTC fusion has demonstrated a higher nonunion rate compared to the other constructs.

 Fig. 7  The use of a lamina spreader allows visualization of the tibial articular surface ( arrow ) and facilitates cartilage removal and bony preparation. Alternating the lamina spreader medially and laterally will provide access to the entire joint

 

 Fig. 8  AP and lateral WB views of a patient who is 1 year s/p an open ankle arthrodesis. Note the neutral position of the ankle with bony union at the tibiotalar joint

 Fig. 9  Intraoperative view of the ankle demonstrating a neutral (90°) position of the arthrodesis

 Results   

•      P atient satisfaction has been reported as 90 % following successful arthrodesis, with decreased pain and improved function.

•      G ait studies demonstrate alterations in normal gait, but these changes are often clinically subtle with shoewear. A clear contrast has been demonstrated with barefoot walking with a longer stride length and decreased velocity compared to the normal population and total ankle arthroplasty.

 Complications   

•      A djacent joint arthritis (most common): usually considered an expected sequel of the subtalar joint

•      N onunion: rates range from 0 to 5 % in a recent meta-analysis to 40 %, elevated in tobacco users

•      Malunion, wound healing, infection, and nerve injury

 Bibliography

 1.  Ahmad J, Raikin SM. Ankle arthrodesis: the simple and the complex. Foot Ankle Clin. 2008;13:381–400, viii.

2 . N ihal A, Gellman RE, Embil JM, Trepman E. Ankle arthrodesis. Foot Ankle Surg. 2008;14:1–10.

3.    Stone JW. Arthroscopic ankle arthrodesis. Foot Ankle Clin. 2006;11:361–8, vi–vii.

4.    Thevendran G, Younger A, Pinney S. Current concepts review: risk factors for nonunions in foot and ankle arthrodeses. Foot Ankle Int. 2012;33:1031–40.

5 . T hordarson DB. Fusion in posttraumatic foot and ankle reconstruction. J Am Acad Orthop Surg. 2004;12:322–33.

 Hindfoot

 Anish  R.  Kadakia ,  Paul  J.  Switaj ,  Bryant  S.  Ho ,  Mohammed  Alshouli ,  Daniel  Fuchs , and  George  Ochengele

    1     Arthritis

 Take-Home Message

•      Post-traumatic arthritis is the most common etiology.

•      Classifi ed based on etiology.

•      Nonoperative management (Arizona brace or AFO) is the fi rst-line treat-ment strategy.

•      Arthrodesis is indicated when nonoperative management is not effective to control pain and disability. No role for arthroplasty in the hindfoot.

 Defi nition

•  Infl ammation and degenerative disease of the hindfoot articulations that includes the talonavicular, subtalar, and calcaneocuboid joints.

 Etiology

•      P ost-traumatic arthritis is the most common cause. Mechanical degeneration of the articular surface as a result of post-traumatic articular injury, incongruity, or collapse (Fig.  1).

•      Osteoarthritis is the second most common and is commonly associated with a deformity (pes planus secondary PTTD or cavus).

•      Others include infl ammatory arthropathy, osteonecrosis, gout, or rarely septic arthritis.

 A. R.  Kadakia (*) •  P. J.  Switaj •  B. S.  Ho •  M.  Alshouli •  D.  Fuchs •  G.  Ochengele

 Department of Orthopedic Surgery ,  Northwestern University – Feinberg School of Medicine, Northwestern Memorial Hospital,   Chicago ,  IL ,  USA

 e-mail: Kadak259@gmail.com; paul.switaj@gmail.com; bryant.s.ho@gmail.com; mtshouli@ gmail.com; dfuchs0011@gmail.com; gochenjele@gmail.com

    © Springer-Verlag France 2015                                                                                              849

C. Mauffrey, D.J. Hak (eds.), Passport for the Orthopedic Boards and FRCS Examination, DOI 10.1007/978-2-8178-0475-0_39  Fig. 1  Nonoperatively treated calcaneus fracture with resultant post-traumatic arthritis. Note the loss of height and obvious articular incongruity and joint space narrowing. The patient had no anterior ankle impingement or pain and was treated with an in situ subtalar arthrodesis

 Pathophysiology

•      Post-traumatic articular incongruity leads to abnormal joint contact forces and loading, resulting in mechanical wear.

•      Deformity/instability can also lead to joint subluxation, decreased contact area, and increased contact pressure.

–  Post-traumatic deformity, end-stage posterior tibialis tendon disorder (PTTD), tarsal coalitions, and cavovarus are commonly associated.

•      Infl ammatory processes such RA lead to articular cartilage destruction and wear.

•      A bnormal purine metabolism results in precipitation and deposition of monosodium urate crystals in joint spaces, resulting to severe infl ammatory response.

 Radiography

•  Weight-bearing x-ray (AP, lateral, and oblique views) of the hindfoot

–     Joint space narrowing or loss (Fig.  2)  

–     Subchondral sclerosis/cysts

–     Osteophytes and bony erosions

–     Hindfoot malalignment and deformity (Fig.  3)  

 Computed tomography (CT) scan

–     In the setting of deformity, the obliquity if plain radiographs prevent appropri-ate visualization of the joints. CT is critical in these cases to accurately determine the presence of articular erosion.

 Classifi cation

 Based on Etiology

•      Mechanical (post-traumatic)

•      Degenerative (osteoarthritis)

     Fig. 2  Joint space narrowing in a patient who has isolated talonavicular ( arrow ) arthritis

              

 Fig. 3 T he severe malalignment of the hindfoot precludes visualization of the hindfoot joints in particular the subtalar joint in patients with a pes planus deformity. In these cases, this may be misinterpreted as subtalar DJD. A CT is appropriate in these cases to determine viability of the joints to determine if the patient is a candidate for joint salvage or requires an arthrodesis

•      Infl ammatory (rheumatoid, seronegative spondyloarthropathy)

•      Metabolic (gout, pseudogout (chondrocalcinosis))

•      Neuropathic  Treatment

 Nonoperative

•      Nonsteroidal anti-infl ammatory drugs (NSAIDs)

•      Activity modifi cation (avoidance of impact and uneven ground)

•      B racing such as an ankle-foot orthosis (AFO) or rigid lace up brace such as Arizona brace with an associated rocker bottom shoe modifi cation

•      Corticosteroid/anesthetic injections: both diagnostic and therapeutic

•      Treatment of underlying causes such as gout, RA

 Operative

 Failure of nonoperative treatment with persistent pain and disability is an indication for arthrodesis. Goal of surgery is to obtain a solid fusion and position the hindfoot in 0–5° of valgus, neutral abduction/adduction, congruent talus-fi rst metatarsal axis (Meary line) and create a plantigrade foot (Fig.  4 ). In many patients a concomitant contracture of the Achilles tendon is present, and an Achilles lengthening should be considered at the time of arthrodesis if a fi xed equinus contracture is present.

•      Single joint fusion is indicated for isolated joint arthritis. However, isolated joint fusions, especially TN (TN > ST > CC), are associated to severe hindfoot motion limitation and higher nonunion rate. As such, fusion procedures usually involve ST and TN fusion or triple (ST, TN, and CC) fusion (Fig.  5 ).  

    

 Fig. 4 P ostoperative clinical appearance of a patient s/p subtalar and talonavicular arthrodesis for a severe pes planus deformity. Note the neutral adduction/abduction and restoration of the longitudinal arch

•      I n the setting of stage 3 PTTD, a TN and ST fusion without violation of the CC joint may be employed. In many cases additional midfoot correction is required to obtain a plantigrade foot (Fig.  6).  

•      A triple arthrodesis is an effective strategy to treat pan hindfoot arthritis and deformity and is typically required for any congenital deformity.

•      Subtalar bone block arthrodesis is an effective option to treat post-traumatic arthritis secondary to a calcaneus fracture with loss of height. This operation is only indicated if the patient has ankle impingement (pain or limited dorsifl exion). The higher risk of nonunion and technical diffi culty is why this should not be performed if the patient is asymptomatic in the ankle.

•      T ibiotalocalcaneal (TTC) fusion is an option for subtalar arthritis with associated tibiotalar arthritis or if there is a concern for bone stock and fi xation as may seen in neuroarthropathy or sever osteonecrosis.

              

 Fig. 5  Attempted isolated TN fusion that resulted in a nonunion ( a ) that was successfully revised with a combined TN and ST fusion ( b )

 Fig. 6  The radiographic appearance of the patient in Fig.  4with collapse of the medial arch and subtalar DJD noted on CT ( a) . Postoperative radiograph demonstrating restoration of the arch and additional 1 TMT fusion that was required to create a plantigrade foot ( b )

 Complications

•      Wound complications: Higher in a lateral approach for subtalar joint in severe pes planus deformity and bone block arthrodesis s/p calcaneus fractures.

•      Nonunion risk factors: prior ankle arthrodesis, isolated TN fusion, and smoking

•      M alunion: Resultant malposition of foot and abnormal joint loading. Post- traumatic talar neck fractures with varus require a triple arthrodesis to prevent persistent cavovarus deformity.

•      Adjacent joint arthritis: The ankle is most common.

 Bibliography

1.    Anand P, Nunley JA, DeOrio JK. Single-incision medial approach for double arthrodesis of hindfoot in posterior tibialis tendon dysfunction. Foot Ankle Int. 2013;34(3):338–44.

2.    Herscovici D, Sammarco GJ, Sammarco VJ, Scaduto JM. Pantalar arthrodesis for post-traumatic arthritis and diabetic neuroarthropathy of the ankle and hindfoot. Foot Ankle Int. 2011;32(6):581–8.

3 . R adnay CS, Clare MP, Sanders RW. Subtalar fusion after displaced intra-a rticular calcaneal fractures: does initial operative treatment matter? J Bone Joint Surg Am. 2009;91(3):541–6.

4.    Rammelt S, Zwipp H. Corrective arthrodeses and osteotomies for post-traumatic hindfoot      malalignment:      indications,       techniques,            results.   Int           Orthop. 2013;37(9):1707–17.

5.    Rammelt S, Pyrc J, Agren PH, Hartsock LA, Cronier P, Friscia DA, et al. Tibiotalocalcaneal fusion using the hindfoot arthrodesis nail: a multicenter study. Foot Ankle Int. 2013;34(9):1245–55.

    2     Ankle Instability

 Take-Home Message

•      The lateral ligamentous complex is most commonly involved (ATFL > CFL > PTFL).

•      Nonoperative management is the fi rst-line treatment for all acute inju-ries → therapy (peroneal strengthening and proprioception) and functional bracing.

•      Surgical reconstruction indicated for persistent instability → Anatomic repair is most appropriate fi rst-line treatment (Brostrom-Gould).

•      Concomitant hindfoot varus may require lateral slide/closing wedge calca-neal osteotomy.

 Introduction

•      Acute injuries →Traumatic injury to the lateral ligamentous complex presenting with pain, swelling, and ecchymosis.

•      Chronic instability →Repeated episodes of “giving way” or recurrent ankle sprains without signifi cant trauma.

•      These symptoms can be debilitating to athletes, and recurrent ankle sprains are felt to be an etiologic factor for ankle arthritis.

 Etiology

•      Injury and incompetence of the ligamentous structures (most commonly laterally)

•      Certain factors put patient at risk for ankle instability:

–     Mechanical: varus hindfoot alignment, generalized ligamentous laxity

–     Functional: muscle weakness (peroneal tendons), impaired proprioception, and impaired neuromuscular control

•      S uggested mechanism of injury →inverted, plantar fl exed foot with an internally rotated hindfoot, and an externally rotated leg

 Fig. 7  Intraoperative photograph of the ATFL ( white arrow )

 

 Fig. 8  To perform the anterior drawer test, ne hand stabilizes the anterior distal tibia, while the other is cupped around the posterior calcaneus ( a ). The heel is translated anteriorly with respect to the tibia, and any subluxation should be noted ( b) . Note the sulcus that is created over the anterolateral ankle with an unstable ankle ( arrow )

 

 Fig. 9  Intraoperative photograph of the CFL ( white arrow ). Note how the fi bers become taught with dorsifl exion of the ankle

 Fig. 10 Inversion stress test in a patient with severe laxity of the CFL

•  Can lead to chronic instability

 Pathophysiology

 Ankle Joint Stability

•      L ateral ligamentous structures: most commonly involved (medial side rarely injured). Always compare to contralateral lower extremity.

–     Anterior talofi bular ligament (ATFL) (Fig. 7  ) →most commonly injured →once injured, causes stress on the remaining ligaments; tested by anterior drawer test (Fig.  8). Also assessed with inversion in plantarfl exion.  

–     Calcaneofi bular ligament (CFL) (Fig.  9) →second most commonly injured; tested by talar tilt stress (inversion test) in dorsifl exion (Fig.  10)  

–     Posterior talofi bular ligament (PTFL)

•      C an check joint hyperlaxity by calculating the Beighton score. Signs of ligamentous laxity should be evaluated using the Beighton scoring system. Out of a possible nine points, four points indicates a generalized ligamentous laxity.

–     5th fi nger metacarpophalangeal joint extension past 90° (bilateral, 2 points)

–     Thumb to volar forearm (bilateral, 2 points)

–     Hyperextension of the elbow (bilateral, 2 points)

–     Hyperextension of the knee (bilateral, 2 points)

–     Hands fl at on fl oor with forward trunk fl exion (1 point)

 Fig. 11  Anterior osteophytes are identifi ed by their prominence relative to the remaining tibia and by the lack of cartilage inferior to the bone ( a ). After excision of the osteophyte, the normal articular surface is easily seen ( b )

  Fig. 12  Varus stress radiograph of a patient with signifi cant talar tilt >15°

 Radiography

•      Standard weight-bearing anteroposterior, lateral, and mortise views to assess avulsion fractures, arthritis, or osteochondral lesions. A common fi nding is anterior tibial osteophytes in patient with chronic instability; this must be addressed at the time of surgical intervention (Fig.  11).

•      Anterior drawer stress x-ray and talar tilt views are helpful in cases of suspected ankle instability. Absolute values for normal talar tilt vary widely; however, the talar tilt is less the 15° in 95 % of patients (Fig.  12 ).  

•      MRI →Not required to make the diagnosis of an acute injury. May consider to evaluate for OCLT or syndesmotic injury if appropriate clinical suspicion is

 Fig. 13 Large adhesion in a patient that obliterates the anterolateral aspect of the ankle

     Fig. 14  Loose bodies can be the source of instability in patients who have functional instability without any mechanical laxity. Arthroscopic excision of the loose body is critical in order to relieve the symptoms

given. Recommended in the setting of chronic instability with ankle pain to evaluate for intra-articular pathology (OCLT, loose body, anterior tibial osteophyte, synovitis) given the high incidence of concomitant intra-articular pathology

(Figs.  13and  14 ).  

 Classifi cation

•      Malliaropoulos classifi cation of acute ankle sprains (Table  1)

•      There is no relevant classifi cation for chronic instability.

 Table 1Malliaropoulos classifi cation of acute ankle sprains

Grade	I	II	III
Injured structures	Partial	ATFL	ATFL and CFL
Decrease in range of movement	<5	5–10	>10
Edema	up to 0.5 cm	0.5–2 cm	> 2 cm
Stress radiographs	Normal	Normal	>3 mm laxity

 Treatment  Nonoperative : initial treatment for most cases

•      Acute injury (nonoperative in all cases as fi rst-line treatment)

–     R  est, immobilization, and protected weight bearing immediately, then early mobilization with functional bracing and early rehabilitation (peroneal strengthening and proprioception). Demonstrated superior to cast immobilization

•      Chronic instability

–     P  hysical therapy (including peroneal strengthening and proprioceptive training), functional bracing

–     O  rthotic treatment for cavovarus deformity (lateral heel wedge, decreased arch, well-out for fi rst metatarsal)

 Operative: following failure of nonoperative management with persistent instability

•      Two methods:

–     Gould modifi cation of Brostrom (anatomic repair) → Imbrication of elongated ATFL and CFL into distal fi bula. Additional reinforcement with a fl ap of the inferior extensor retinaculum that improves stability of the subtalar joint (Fig.  15 ).  

–     Non-anatomical reconstructions: reserved for revision cases, long-standing instability, or patients with generalized ligamentous laxity.

•      Watson-Jones, Evans, and Chrisman-Snook: all involve peroneus brevis transfer. These all create signifi cant subtalar stiffness and less restriction of anterior translation compared to an anatomic reconstruction.

•      A utograft or allograft reconstructions have been utilized for revision cases or for patients with ligamentous laxity as these can be placed into a more anatomic position (Fig. 16).  

•      Arthroscopic exam: controversial, high percentage of intra-articular pathology found, but unknown clinical benefi t proven. Consider if MRI demonstrates intra- articular pathology.

 Complications

•      Recurrence (especially with hindfoot malalignment that is uncorrected)

•      Persistent pain

•      Post-traumatic osteoarthritis (associated with signifi cant long term instability)

     Fig. 15Brostrom anatomic reconstruction for lateral ankle instability. The ATFL and CFL are incised from the fi bular origin ( a ). Utilizing suture anchors in this case the ligaments are imbricated ( b ). Final appearance of the ligaments shows them taut ( c )

     Fig. 16Anatomic allograft reconstruction of the lateral collateral ligaments. The graft is fi xated within the talus and routed from anterior to posterior through a fi bular drill hole ( a ). Subcutaneous passage to the calcaneal insertion is then performed superfi cial to the peroneal tendons to prevent subluxation ( b ). Some authors prevent passing the tendon deep to the peroneal tendons to recreate the CFL’s anatomic origin. There is no data to demonstrate superiority of one technique over the other. Final appearance of the reconstructed ankle ( c )

 Bibliography

1 . d e Vries JS, Krips R, Sierevelt IN, Blankevoort L. Interventions for treating chronic ankle instability. Cochrane Database Syst Rev. 2006;(4):CD004124.

2.    DiGiovanni CW, Brodsky A. Current concepts: lateral ankle instability. Foot Ankle Int. 2006;27:854–66.

3.    Ferkel RD, Chams RN. Chronic lateral instability: arthroscopic fi ndings and long-term results. Foot Ankle. 2007;28:24–31.

4.    Maffulli N, Ferran NA. Management of acute and chronic ankle instability. J Am Acad Orthop Surg. 2008;16:608–15.

    3     Talar Osteochondral Defects

 Take-Home Message

•      Lateral OCLT are usually of traumatic etiology, smaller, more shallow and more symptomatic than medial lesions. However, lateral lesions have superior surgical outcome.

•      Persistent ankle pain after acute sprain →obtain MRI to rule OCLT.

•      Lateral lesions have less potential for spontaneous resolution.

•      Choice of operative treatment is dependent on lesion size.

•      Arthroscopic verse open procedure has comparative results.

 Defi nition

• O steochondral lesions of the talar dome is a cause of ankle pain and disability. Presenting symptoms includes pain, swelling, and mechanical symptoms such as catching and locking. Up to 10 % are bilateral.

 Etiology

•      Acute trauma

•      Repetitive microtrauma

 Pathophysiology

•      Osteochondral lesions of the talar dome may result from acute trauma or repeti-tive microtrauma. Pathophysiology differs based on lesion location. Recent data has demonstrated that both medial and lateral OCLT are found most common in the central talar dome in the sagittal plane.

•      Lateral talar dome

–     Tends to be traumatic etiology, typically inversion or inversion-dorsifl exion mechanism

–     Lesions usually smaller, more shallow and more symptomatic than medial lesions (Fig.  17 )  

–     Superior surgical results

 

 Fig. 17  Arthroscopic view of a lateral talar osteochondral defect. ( a ,  b ) Note the shallow nature of the defect with the clear detached articular surface ( a ,  b )

 Fig. 18  Ankle radiograph demonstrating an obvious lucency of the medial talar dome ( arrow ) consistent with an OCLT

•      Medial talar dome

–     Tends to be atraumatic etiology

–     Lesions usually larger and deeper than lateral lesions

 Radiography

•      Ankle x-ray

–     M  aybe normal or subtle radiolucency, articular surface irregularity, or subchondral bone fragmentation (Fig.  18 )  

•      CT/MRI

–     Further evaluate lesions apparent on x-ray or for persistent ankle pain after trauma such ankle sprain/fracture despite appropriate management (Fig.  19 )  –  Helpful for classifi cation of lesions

 Classifi cation

•      The Berndt and Harty radiographic staging classifi cation (Table  2 )

•      The Ferkel and Sgaglione CT staging classifi cation (Table  3 )

•      The Hepple and associates MRI staging classifi cation (Table  4 )

•      Arthroscopic evaluation is the reliable means of determining lesion size and the intactness of articular surface of lesions.

     Fig. 19  MRI demonstrating a medial

OCLT with fl uid inferior to articular surface

( arrow ) that denotes instability of the lesion

 Table 2  The Berndt and harty radiographic staging classifi cation of OCLT

Stage 1	Small area of subchondral compression/depression
Stage 2	Partial fragment detachment
Stage 3	Complete fragment detachment, non-displaced
Stage 4	Complete fragment detachment, displaced

 Table 3  The Ferkel and Sgaglione CT staging classifi cation of OCLT

Stage 1	Cystic lesion within talar dome with an intact roof in all views
Stage 2a	Cystic lesion with communication to talar dome surface
Stage 2b	Open articular surface lesion with overlying non-displaced fragment
Stage 3	Non-displaced lesion with lucency
Stage 4	Displaced fragment

 Table 4  The Hepple and Associates MRI staging classifi cation of OCLT

Stage 1	Articular cartilage
Stage 2a	Cartilage injury with underlying fracture with surrounding bone edema
Stage 2b	Cartilage injury with underlying fracture without surrounding bone edema
Stage 3	Detached but non-displaced fragment
Stage 4	Displaced fragment
Stage 5	Subchondral cyst formation

 Treatment

 Nonoperative

•      Indication: Non-displaced fragment. No proven risk of DJD with nonoperative management.

•      Short leg cast immobilization

•      Restricted weight bearing

 Operative

•      I ndication: displaced fragment in the acute setting. Persistent pain or mechanical symptoms in the chronic setting.

•      Treatment choice is based on size of lesion.

•      Results of arthroscopic verse open procedures are comparable.

•      Lesion with intact cartilage cap: retrograde drilling ± bone grafting.

•      Lesion < 1.5 cm ² : debridement and microfracture/drilling (Figs.  20and  21 )  

•      Lesion > 1.5 cm ² cm with displaced cartilage cap: joint restorative procedures – osteochondral autograft, chondrocyte implantation, or osteochondral allograft

•      Lesions >3 cm ² : osteochondral allograft (Fig.  22).  

 Complications

•      Nonunion of autograft/allograft

•      Persistent pain

•      Tibiotalar arthritis

 

 Fig. 20  Microfracture technique of a tibial ( a ) and talar ( b ) osteochondral lesion

     Fig. 21  Final appearance of a talar osteochondral defect following microfracture. Note the blood that is emanating from the microfracture holes made in the talus

 Bibliography

1 . C hoi WJ, Park KK, Kim BS, Lee JW. Osteochondral lesion of the talus: is there a critical defect size for poor outcome? Am J Sports Med. 2009;37:1974–80.

2.    Choi WJ, Kim BS, Lee JW. Osteochondral lesion of the talus: could age be an indication for arthroscopic treatment? Am J Sports Med. 2012;40:419–24.

3.    Cuttica DJ, Smith WB, Hyer CF, et al. Osteochondral lesions of the talus: predic-tors of clinical outcome. Foot Ankle Int. 2011;32(11):1045–51.

4.    Orr JD, Dawson LK, Garcia EJ, Kirk KL. Incidence of osteochondral lesions of the talus in the United States military. Foot Ankle Int. 2011;32:948–54.

5 . V entura A, Terzaghi C, Legnani C, Borgo C. Treatment of post-traumatic osteochondral lesions of the talus: a four-step approach. Knee Surg Sports Traumatol Arthrosc. 2012;21:1245–50.

 

 Fig. 22  Large (>3 cm ²)  osteochondral defect ( arrow ) that was approached via an anterior ankle arthrotomy ( a) . The entire ½ of the articular surface was abnormal ( b) . Given the large surface area involved an allograft reconstruction ( c ) was performed

    4     Heel Pain

Take-Home Message •      P lantar fasciitis is the most common cause, present classically with “startup” pain in the AM that improves after the fi rst few steps. •      Location of pain provides diagnostic clue. –     Inferior heel pain - > plantar fasciitis –     Medial         heel        pain → Baxter’s   neuritis   (Lateral plantar   nerve compression) –     Posterior heel pain → retrocalcaneal bursitis, Haglund’s deformity, insertional and Achilles tendinitis/tendinosis –     Pain with lateral and medial compression → calcaneal stress fracture •      N onoperative management is the fi rst treatment. Plantar fascia-specifi c stretch is most important for PF.

 Defi nition  Heel pain is a common foot problem that causes signifi cant discomfort and disability. The differential diagnosis for heel pain is broad and includes plantar fasciitis, calcaneal stress fracture, calcaneal apophysitis (Sever disease), central heel pain (fat pad atrophy, fat pad contusion), and nerve entrapment (tarsal tunnel syndrome, entrapment of the fi rst branch of the lateral plantar nerve) and posterior heel pain (retrocalcaneal bursitis, Haglund’s deformity, insertional Achilles tendinitis/ tendinosis).

 Etiology

•      Repetitive microtrauma (stress fracture, Baxter’s neuritis in runners)

•      Infl ammatory

•      Degenerative

•      Drug induced (fl uoroquinolone use with Achilles pathology)

 Pathophysiology  Etiology is multifactorial, as such presentation and pathophysiology unique to each disease process.

 Plantar Fasciitis

•      Most common cause of heel pain. Affects both sedentary and active.

•      Presents classically as “start-up” plantar medial heel pain and preference for toe walking for fi rst few steps and improvement with progressive walking

•      Repetitive microtrauma to plantar fascia →microtears and infl ammatory response → reparative response

•      Other risk factors: obesity, pes planus, pes cavus, gastrocnemius contracture, and excessive femoral anteversion increase the traction load at the origin of the  plantar fascia during weight bearing

•      About 50 % have heel spurs, however not cause of heel pain.

 Calcaneal Stress Fracture

•      Heel absorbs about 110 % of body weight during walking and 200 % during running.

•      R epetitive loading of the calcaneus results in fatigue fractures. Common in active individual and military recruits.

•      Risk factors: female, female athlete triad, hormonal defi ciency, and osteopenia

 Calcaneal Apophysitis (Sever Disease)

•      Common cause of heel pain in pediatric population

•      Overuse injury of calcaneal apophysis

•      Natural history: self-limiting, resolves with closure of the apophysis

 Central Heel Pain (Fat Pad Atrophy, Fat Pad Contusion)

•      The heel pad provides signifi cant shock absorber function to the hindfoot.

•      Fat pad atrophy can result from infl ammatory disease process, corticosteroid injection, trauma, and advanced age.

•      Fat pad contusion from trauma can present as central heel pain.

 Nerve Entrapment

•      Entrapment of the First Branch of the Lateral Plantar Nerve (Baxter’s Neuritis)

 The fi rst branch of the lateral plantar nerve is a mixed (sensory and motor) nerve. Compression of this nerve occurs between the deep fascia of the abductor  hallucis and inferomedial margin of the quadratus plantae.

C ommon in running athletes and presents as plantar medial heel pain that mimic plantar fasciitis

 Tarsal tunnel syndrome can have similar presentation; however, symptoms originate more proximal and tend to involve entire foot and not just heel.

 Posterior Heel Pain

 Retrocalcaneal bursitis and Haglund’s deformity

•      Infl ammation of retrocalcaneal bursa (lies between anterior surface of Achilles tendon and the posterosuperior calcaneus tuberosity).

•      Haglund’s deformity: enlargement of the calcaneal posterosuperior tuberosity

 Insertional Achilles tendinitis/tendinosis

•      Infl ammatory changes at the tendon insertion site from repetitive microtrauma

•      Progressive bony metaplasia and prominence at the calcaneal insertion

 Fig. 23  Inferior plantar spur ( arrow ) commonly seen in patients with plantar fasciitis

     Fig. 24  Lateral radiograph of a calcaneal stress fracture. Note the linear and vertically oriented increased density in the calcaneus ( arrowheads ). The fi nding is subtle but more easily identifi ed as the normal lines of stress are oriented from the tuberosity towards the posterior facet, with the fracture line crossing multiple normal lines of stress

 Radiography

 Plantar Fasciitis

•        Weight-bearing x-ray

–                      Usually normal

–                      Heel spurs (Fig.  23 )   Calcaneal Stress Fracture

•        Heel x-ray: Initially normal, but few weeks after onset of symptoms, radio-dense line becomes apparent (Fig.  24).  

•        MRI: fracture apparent in setting of normal x-ray (Fig.  25 )  

 Calcaneal Apophysitis (Sever Disease)

•        Heel x-ray

–                      Apophyseal sclerosis not specifi c fi nding

–                      Apophyseal fragmentation more specifi c fi nding

 Fig. 25 Sagittal STIR image of a calcaneal stress fracture. Note the hypointense signal ( arrow ) delineating the fracture line with adjacent bony edema (high signal)

•        MRI

–  Apophyseal infl ammation, rule out other diagnosis

•      Bone scan

–     Apophyseal increased uptake

 Central Heel Pain (Fat Pad Atrophy, Fat Pad Contusion)

•      Weight-bearing x-ray

–     Heel spurs

–     Rule out other pathology

 Baxter’s Neuritis

•      EMG/NCV: increased motor latency of the abductor digiti quinti

•      MRI: fatty atrophy of abductor digiti quinti or space-occupying lesion

 Retrocalcaneal Bursitis and Haglund’s Deformity

•      Foot x-ray: Haglund’s deformity on lateral view

 Insertional Achilles Tendinitis/Tendinosis

•      Lateral Heel x-ray: bone spur, intratendinous calcifi cation/ossifi cation (Fig.  26 )  

•      Ultrasound/MRI: evaluate tendon degeneration

 Treatment

 Plantar Fasciitis

•      Nonoperative

–     Plantar fascia-specifi c and heel cord stretching protocol

–     NSAIDs, low impact activity, physical therapy

–     Orthotics: Night splints, heel cushion inserts

–     Corticosteroid injection if failed non-op

 Fig. 26 Lateral radiograph of a patient with insertional calcifi c Achilles tendinosis. A large posterior heel spur is diagnostic ( white arrow )

–     High-energy extracorporal shock wave therapy and PRP have demonstrated effi cacy in some trials compared to standard non-op treatment in the short term. Cannot be recommended over standard non-op management at this time.

•      Operative

–     Plantar fascia release. Release only medial ½. Baxter’s nerve release for con-comitant Baxter’s neuritis symptoms

–     Gastrocnemius recession instead of a PF release if contracture is present

 Calcaneal Stress Fracture

•      Rest/activity modifi cation and protected weight bearing

•      Cushioned heel orthotics

 Calcaneal Apophysitis (Sever Disease)

•      Rest/activity modifi cation and heel cord stretching

•      Brief immobilization with short leg cast for persistent pain

•      Cushioned heel orthotics

 Central Heel Pain (Fat Pad Atrophy, Fat Pad Contusion)

•      Cushioned heel cups

 Baxter’s Neuritis

•      NSAIDs, cessation of aggravating activity, heel cord stretching

•      Orthotics: cushioned heel inserts, correct for any underlying deformity.

•      Operative

–     S  urgical release and decompression of Baxter’s nerve, deep fascia of the abductor hallucis must be released (Fig.  27).  

–     Medial ½ plantar fascia release for concomitant plantar fasciitis symptoms

 Fig. 27 Inferior retraction of the muscle belly of the abductor exposes the deep fascia ( a ). Appearance after incision of the deep fascia ( b ). The lateral plantar nerve lies directly superior to the deep fascia, and careful dissection must be performed

 Retrocalcaneal Bursitis and Haglund’s Deformity

 Nonoperative

•      NSAIDs

•      Shoe modifi cation (open or low back shoes) or padding to minimize mechanical irritation

•      Corticosteroid injection of the bursa, avoid tendon injection → risk of rupture  Operative

•      Retrocalcaneal bursectomy and resection of Haglund’s deformity

•      <50 % release of Achilles tendon mandates repair with anchors to calcaneus.

 Fig. 28 Intraoperative photograph of a patient who had insertional Achilles tendinosis. After debridement of the diseased tissue and Haglund’s deformity, more than 50 % of the Achilles was detached. Repair with suture anchors is important in preventing postoperative rupture

 Insertional and Non-Insertional Achilles Tendinitis/Tendinosis

 Nonoperative

•      NSAIDs, activity modifi cation (limit impact, push-off).

•      Heel cord stretching and therapy with eccentric training (most critical).

•      Shoe modifi cation or padding to minimize mechanical irritation or small heel lift.

•      Avoid corticosteroid injection →risk of rupture.

 Operative

•      Tendon and prominent bone debridement with repair to bone with anchors

(Fig.  28).

•      Tendon augmentation with FHL, FHL transfer if > 50 % tendon debrided (Fig.  29 )  

 Complications

 Plantar Fasciitis

•      Fat pad atrophy from corticosteroid injection

•      Longitudinal arch collapse and chronic foot pain from excessive plantar fascia release

•      Injury to the lateral plantar nerve

 Fig. 29 Intraoperative photograph of a FHL transfer in a patient who had a severe insertional Achilles tendinosis. After resection of the nonviable tissue, the FHL was transferred through a drill hole in the calcaneus and fi xed with an interference screw

 Baxter’s Neuritis

•      Inadequate decompression

•      Injury to the lateral plantar nerve

 Retrocalcaneal Bursitis and Haglund’s Deformity

•      Achilles tendon rupture from corticosteroid injection or excessive debridement

 Insertional Achilles Tendinitis/Tendinosis

•      Achilles tendon rupture from corticosteroid injection or excessive debridement

 Bibliography

1. D iGiovanni BF, Moore AM, Zlotnicki JP, Pinney SJ. Preferred management of recalcitrant plantar fasciitis among orthopaedic foot and ankle surgeons. Foot Ankle Int. 2012;33(6):507–12.

2. G arrett TR, Neibert PJ. The effectiveness of a gastrocnemius-soleus stretching program as a therapeutic treatment of plantar fasciitis. J Sport Rehabil. 2013;22(4):308–12.

3.    Ngo KT, Del Toro DR. Electrodiagnostic fi ndings and surgical outcome in iso-lated fi rst branch lateral plantar neuropathy: a case series with literature review.

Arch Phys Med Rehabil. 2010;91(12):1948–51.

4.    Schon LC, Glennon TP, Baxter DE. Heel pain syndrome: electrodiagnostic sup-port for nerve entrapment. Foot Ankle. 1993;14(3):129–35.

5.    Schon LC, Shores JL, Faro FD, Vora AM, Camire LM, Guyton GP. Flexor hal-lucis longus tendon transfer in treatment of Achilles tendinosis. J Bone Joint Surg Am. 2013;95(1):54–60.

6.    Sinnaeve F, Vandeputte G. Clinical outcome of surgical intervention for recalci-trant infero-medial heel pain. Acta Orthop Belg. 2008;74(4):483–8.

7.    Wiegerinck JI, Kerkhoffs GM, van Sterkenburg MN, Sierevelt IN, van Dijk CN. Treatment for insertional Achilles tendinopathy: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1345–55.

 Midfoot

 Anish  R.  Kadakia ,  Paul  J.  Switaj ,  Bryant  S.  Ho ,  Mohammed  Alshouli ,  Daniel  Fuchs , and  George  Ochengele

1     Arthritis  

 Take-Home Message

•      Primary osteoarthritis most common.

•      N onoperative management with a carbon fi ber plate and midfoot rocker shoe modifi cation is the fi rst-line treatment strategy.

•      Operative management consists of a tarsometatarsal arthrodesis with realignment in the cases of midfoot deformity (RA and chronic Lisfranc).

•      Arthrodesis of medial and middle columns is effective and does not signifi -cantly adversely affect foot function.

•      Arthrodesis of lateral column adversely alters foot function as it alters ground accommodation. Therefore, interpositional arthroplasty (tendon, implant, collagen matrix) has been advocated as an alternative treatment instead of arthrodesis for the 4th and 5th TMT joints.

 Introduction   

• Arthritis of the midfoot is a signifi cant cause of pain and disability. Midfoot articulations include naviculocuneiform (NC) and tarsometatarsal (TMT) joints.

  A. R.  Kadakia , MD () •  P. J.  Switaj  •  B. S.  Ho  •  M.  Alshouli  •  D.  Fuchs  •  G.  Ochengele

 Department of Orthopedic Surgery ,  Northwestern University – Feinberg School of Medicine, Northwestern Memorial Hospital,   Chicago ,  IL ,  USA

 e-mail: Kadak259@gmail.com; paul.switaj@gmail.com; bryant.s.ho@gmail.com; mtshouli@gmail.com; dfuchs0011@gmail.com; gochenjele@gmail.com

© Springer-Verlag France 2015                                                                                              879

C. Mauffrey, D.J. Hak (eds.), Passport for the Orthopedic Boards and FRCS Examination, DOI 10.1007/978-2-8178-0475-0_40

 Etiology   

•      Primary osteoarthritis is the most common cause of hindfoot arthritis.

•      Posttraumatic arthritis is second.

•      Infl ammatory.

 Pathophysiology   

•      The middle column has limited motion but is exposed to large forces.

•      Abnormally high forces through the midfoot lead to the incompetence of sup-porting soft tissue structures →joint subluxation →increased contact pressure →degeneration.

•      Infl ammatory processes and posterior tibialis tendon dysfunction (PTTD) can lead to midfoot collapse and arthritis.

•      Gastrocnemius contracture will increase forces across the midfoot possibly accelerating the disease.

 Radiography   

• AP (1st, 2nd, 3rd, and N-C joints), oblique (3rd, 4th, and 5th TMT joints), and lateral WB radiographs:

–     J  oint-space narrowing or loss (The lateral view may reveal joint-space narrowing not appreciated on the AP or oblique radiographs (Fig.  1 ))  

–     Subchondral sclerosis/cysts

–     Osteophytes and bony erosions – best seen on lateral view

–     Disruption of Meary’s line (loss of colinearity between talus and 1st MT) with apex deformity at midfoot and longitudinal arch collapse on lateral view

–     Forefoot abduction deformity. Critical to differentiate from PTTD fl atfoot deformity where TN in abduction > TMT (Fig.  2)  

 Treatment   

Nonoperative

•      A stiff carbon fi ber plate inserted underneath the insole of the shoe or a rocker- bottom shoe will offl oad stress on the midfoot during gait and may relieve mild degenerative symptoms.

•      Rigid deformity should be managed with accommodative, not corrective orthot-ics that support and offl oad the deformity.

•      Corticosteroid/anesthetic injections: both diagnostic (determine symptomatic joints) and therapeutic

 Operative

 Indication is failure of nonoperative with persistent pain and disability. Arthrodesis is the treatment of choice. Goal of surgery is to obtain solid fusion and restoration of normal foot alignment.

•      Medial and middle column arthrodesis ensuring a normal anatomic alignment. Residual deformity will predictably result in a poor outcome (Fig.  3 ).  

 Fig. 1  Patient with midfoot arthritis primarily at the middle column. Note the subtle asymmetric narrowing on the AP radiograph. The presence of 2nd TMT degeneration is clearly seen on the lateral radiograph ( arrow )

•      Interpositional arthroplasty (motion sparring) of lateral column is preferred for symptomatic 4th and 5th TMT arthritis given the biomechanical advantage. However, no signifi cant data is present to support motion-sparing procedures over arthrodesis.

•      A simultaneous gastrocnemius recession and/or hindfoot osteotomy might be required to restore normal foot alignment (Fig.  4).  

 Fig. 2  AP WB radiograph demonstrating abduction deformity of the foot that is clearly focused at the TMT joints ( arrowhead ). Note the minimal amount of TN joint subluxation despite the severe deformity, indicating this is a midfoot driven fl atfoot and not related to PTTD

 Complications   

•      Nonunion/malunion

•      Wound complications

 Bibliography

1 . N emec SA, Habbu RA, Anderson JG, Bohay DR. Outcomes following midfoot arthrodesis for primary arthritis. Foot Ankle Int. 2011;32(4):355–61.

2.    Patel A, Rao S, Nawoczenski D, Flemister AS, DiGiovanni B, Baumhauer JF. Midfoot arthritis. J Am Acad Orthop Surg. 2010;18(7):417–25.

3.    Russell DF, Ferdinand RD. Review of the evidence: surgical management of 4th and   5th          tarsometatarsal     joint           osteoarthritis.       Foot        Ankle     Surg. 2013;19(4):207–11.

4. V erhoeven N, Vandeputte G. Midfoot arthritis: diagnosis and treatment. Foot Ankle Surg. 2012;18(4):255–62.

5. Z onno AJ, Myerson MS. Surgical correction of midfoot arthritis with and without deformity. Foot Ankle Clin. 2011;16(1):35–47.

 Fig. 3  A Lapidus and 2nd TMT arthrodesis was performed in this patient who presented with complaints of hallux valgus and midfoot pain with radiographic evidence of midfoot DJD. The patient had osteopenic bone and therefore plate fi xation was chosen

2     Kohler’s Disease  

 Take-Home Message

•      Pediatric avascular necrosis of the navicular of unknown etiology.

•      Boys preferentially affected.

•      25 % can be bilateral.

•      Usually self-limiting with favorable prognosis, surgery is not indicated.

•      Immobilization with short leg walking cast is indicated for activity-related symptoms.

•      Immobilization decreases duration of symptoms.

 Defi nition   

•      Avascular necrosis of the navicular bone of unclear etiology. Occurs in pediatric population. Patients usually present with pain (dorsomedial), swelling, and warmth/redness and limp.

•      However, some patients are asymptomatic.

 Fig. 4  Extended midfoot arthrodesis with concomitant medial slide calcaneal osteotomy was required in this patient who presented with midfoot arthritis and secondary hindfoot valgus deformity. Note the restoration of the longitudinal arch in the postoperative radiograph

•      More common in boys (up 80 % of cases).

•      25 % of cases are bilateral.

 Etiology  

•      Unknown

 Pathophysiology  

•      Blood supply: the central 1/3 of the navicular is a watershed area → avascular necrosis

•      Late ossifi cation →predisposition to injury and mechanical compression

 Radiography   

• Foot X-ray

–     Active disease: sclerosis, fragmentation, and fl attening of navicular

–     P  ost resolution: bone remodeling and reconstitution, asymptomatic deformity can persist

 Treatment   

•      Usually self-limiting with good prognosis. Symptoms usually associated with activities.

 Nonoperative

•      NSAIDs, activity modifi cation (eliminate impact)

•      Shoe insert orthotics (accommodative)

•      Immobilization with short leg walking cast

–  Indication: activity-related pain and failure of above modalities

 Operative

•      No indication for surgery

 Complications   

• Very good prognosis without post-resolution sequela. Deformity is usually asymptomatic.

 Bibliography

1 . B orges JL, Guille JT, Bowen JR. Köhler’s bone disease of the tarsal navicular. J Pediatr Orthop. 1995;15(5):596–8.

2.    DiGiovanni CW, Patel A, Calfee R, Nickisch F. Osteonecrosis in the foot. J Am Acad Orthop Surg. 2007;15(4):208–17.

3.    Tsirikos AI, Riddle EC, Kruse R. Bilateral Köhler’s disease in identical twins.

Clin Orthop Relat Res. 2003;409:195–8.

3     Sinus Tarsi Syndrome  

 Take-Home Message

•      Sinus tarsi syndrome presents as lateral heel pain that is relieved by local anesthetic injection into sinus tarsi and associated with feeling of instability.

•      Highly associated with ankle inversion injuries.

•      M RI and arthroscopy reveal infl ammatory changes and partial ligamentous tear.

•      Nonoperative management is the fi rst-line treatment: serial local anes-thetic/corticosteroid injections are effective.

•      Favorable results for both arthroscopic and open excision and debridement.

 Defi nition   

•      Sinus tarsal syndrome (STS) is a clinical entity that represents local pain in the lateral heel over sinus tarsi – located between the talus and the calcaneus.

–  Pain that is relieved by local anesthetics/corticosteroid injection. –  Associated with hindfoot instability.

•      Canalis tarsi syndrome is a variant of STS → medial side pain

 Etiology   

•      Anatomy: The sinus tarsi is an anatomic space → bounded by inferior talus, the superior aspect of the calcaneus, posterior subtalar facet, and the calcaneonavicular joint anteriorly.

–     Medially continuous with the tarsal canal

–     Space fi lled with fat and contains vessels and ligaments

•      The true etiology of STS is unknown, although several theories have been postu-lated →posttraumatic fi brosis, synovial hyperplasia, hemosiderin deposition, infl ammatory response, compression of herniated synovial membrane, and proprioceptive disorder.

•      T here is high association with previous ankle inversion/supination injuries and independent of lateral ankle ligament complex rupture or osteochondral lesion.

 Pathophysiology   

•      Similar to the etiology, the pathophysiology of STS is poorly understood.

•      Related to posttraumatic ligamentous injury, infl ammatory changes, and instability.

 Radiography   

 X-Ray

N ormal in most cases. Stress radiography may demonstrate instability of the subtalar joint, although this is diffi cult to demonstrate. Clinical laxity to varus stress with a normal stress X-ray of the ankle is suggestive of subtalar instability.

 Subtalar Arthrogram

•      Demonstrates a saclike anterior bulge of the capsule

 MRI

•      V isualize ligament tears, synovial thickening, and fi brosis. Loss of sinus tarsi fat is a useful objective fi nding.

 Classifi cation   

•      There is no classifi cation for this entity

 Treatment   

Nonoperative

•      NSAIDs, ankle/hindfoot bracing, physical therapy (peroneal strengthening and proprioception to minimize instability)

•      Serial local anesthetics/corticosteroid injections

–  Reports of complete resolution

     Fig. 5  Subtalar arthroscopy demonstrated synovitis and soft tissue impingement in a

patient with sinus tarsi syndrome

     Fig. 6  Post-debridement of the same patient demonstrating removal of the offending tissue that theoretically allows impingement free motion of the subtalar joint and mechanical excision of the offending synovitis

 Operative

•      Arthroscopy

– I  n a level IV study, arthroscopy identifi ed pathologies in the subtalar joints of patients with STS → including partial tear of Interosseous talocalcaneal ligament (ITCL), cervical ligament (CL), synovitis, arthrofi brosis, and soft tissue impingement (Fig.  5 ).

•      Treatment of these pathologies led to improved pain and function.

•      Treatment included synovectomy and debridement (Fig.  6).  

•      Open surgical excision/debridement.

•      C oncomitant instability must be addressed if present. Reconstructive procedures that cross the subtalar joint are indicated to improve subtalar instability as opposed to an anatomic repair (Brostrom).

•      S ubtalar arthrodesis is a salvage operation in patients who have failed prior surgical attempts at joint-sparing procedures.

 Complications   

• Persistent pain is the most common complication with debridement. Nonunion can occur with an arthrodesis.

 Bibliography

 1.  Frey C, Feder KS, DiGiovanni C. Arthroscopic evaluation of the subtalar joint: does sinus tarsi syndrome exist? Foot Ankle Int. 1999;20:185–91.

2 . K uwada GT. Long-term retrospective analysis of the treatment of sinus tarsi syndrome. J Foot Ankle Surg. 1994;33:28–9.

 3.  Lee KB, Bai LB, Park JG, Song EK, Lee JJ. Effi cacy of MRI versus arthroscopy for evaluation of sinus tarsi syndrome. Foot Ankle Int. 2008;29: 1111–6.

4. L ee KB, Bai LB, Song EK, Jung ST, Kong IK. Subtalar arthroscopy for sinus Tarsi syndrome: arthroscopic fi ndings and clinical outcomes of 33 consecutive cases. Arthroscopy. 2008;24:1130–4.

5. Z wipp H, Swoboda B, Holch M, Maschek HJ, Reichelt S. Sinus tarsi and canalis tarsi syndromes. A post-traumatic entity. Unfallchirurg. 1991;94:608–13.

4     Coalition  

 Take-Home Message

•      C ongenital fusion of two tarsal bones which could be fi brous, cartilaginous, or osseous (most commonly calcaneonavicular (CN) > talocalcaneal).

•      Can lead to rigid fl atfoot deformity → spastic peroneal fl atfoot.

•      Onset of symptoms corresponds with timing of ossifi cation of coalition.

•      Can be a cause of recurrent ankle sprains.

•      Nonoperative management for asymptomatic – accommodative orthotics.

•      Operative management – surgical resection with interposition (tendon or bone wax) for CN or talocalcaneal (<50 % involved). Triple arthrodesis for revision (CN) or subtalar fusion (>50 % talocalcaneal or revision)

 Defi nition   

•      Tarsal coalition is a congenital abnormal union of two tarsal bones at variable levels

•      Leads to rigid fl atfoot deformity →peroneal spastic fl atfoot

 Etiology   

•      Presumed lack of differentiation of mesenchymal tissue, resulting in failure of normal joint articulation.

•      Genetic predisposition

 Pathophysiology   

•      Abnormal tissue bridge between two tarsal bones

–     Fibrous coalition

–     Cartilaginous coalition

–     Osseous coalition

•      Two most common areas involved are →calcaneonavicular > talocalcaneal

•      Onset of symptoms corresponds with timing ossifi cation of coalition, calcaneo-navicular (8–12), and talocalcaneal (12–16).

–     Sinus tarsi, medial hindfoot, and peroneal tendons

–     Persistent pain following ankle sprain

•      Rigid fl atfoot deformity: restricted subtalar motion results in

–     The subtalar joint lacks the ability to invert and create a normal longitudinal arch. The chopart joints are forced to develop in an abducted position with a pes planus deformity.

–     The peroneal tendons develop in a shortened fashion which accounts for the “spasm” that is felt with attempted inversion.

–     Subtalar arthrosis (late fi nding)

 Radiography   

•      AP, lateral (standing), 45-degree oblique, and Harris axial X-ray views

–     45-degree oblique view →calcaneonavicular (Fig.  7)  

–     Lateral view

•      Calcaneonavicular →elongated anterior process of calcaneus (“anteater sign”)

•      Talocalcaneal →talar beaking (Fig.  8)  

–  Harris heel view → talocalcaneal → irregular middle facet joint

•       CT scan

–     Better characterize size and extent of coalition

 Fig. 7  Oblique radiograph of a patient with a fi brous calcaneonavicular coalition. The anteater sign is evidenced by the elongated anterior process with the associated fl attening ( arrow )

•       MRI

–     Evaluate fi brous or cartilaginous coalition (Fig.  9)  

 Classifi cation  

 On the basis of anatomic location

•      Talocalcaneal

–     Anterior facet

–     Middle facet (most common)

–     Posterior facet

 On the basis of completeness of ossifi cation

•      Synostosis: completely ossifi ed bar, associated with fi bular hemimelia and proxi-mal focal femur defi ciency and Apert syndrome.

•      Synchondrosis: partially cartilaginous bar.

•      Syndesmosis: fi brous bar.

 Fig. 8L ateral radiograph demonstrating talar beaking ( arrow)  in a patient with a talocalcaneal coalition. The prominence is directed superior and distal

     Fig. 9  Coronal T1 MRI of a nonosseous talocalcaneal coalition ( arrow ). There is a lack of bony continuity that distinguishes this from an osseous coalition. The middle facet is irregular with a very thin fi brous bridge present

 Treatment   Most coalitions are asymptomatic.

 Nonoperative

•      Observation for asymptomatic

•      Short leg walking cast immobilization

•      Accommodative full length orthotic

 Fig. 10  Preoperative appearance ( a)  of a CN coalition ( arrowhead)  and the appropriate postoperative appearance after resection ( b ). Note how the resection removes a block of bone from the coalition which should create a square defect ( arrow )

 Operative

•      Calcaneonavicular

–     Coalition resection of a rectangular 1 cm block (Fig.  10)  

–     Interposition: bone wax or EDB (increases risk of wound complications)

•      Talocalcaneal

–  Coalition resection with interposition (bone wax or split FHL)

•      Gold standard indication is lacking.

–     <50 % involvement of middle facet

–     Coalition surface area <50 % of the surface area of the posterior facet –  <16° of valgus

–     Subtalar arthrodesis

•      >50 % involvement, subtalar arthrosis, and revision (Fig.  11 )  

•      Triple arthrodesis

– A  ny coalition with multiple joint arthrosis, revision, or severe hindfoot valgus or abduction

 Fig. 11  Preoperative lateral radiograph ( a ) of a talocalcaneal coalition with associated talar beaking. Postoperative lateral radiograph ( b ) following coalition resection, subtalar arthrodesis, and excision of the talar beaking

 Complications   

•      Hindfoot joint arthritis

•      Persistent pain and deformity

 Bibliography

 1.  Cass AD, Camasta CA. A review of tarsal coalition and pes planovalgus: clinical examination, diagnostic imaging, and surgical planning. J Foot Ankle Surg. 2010;49(3):274–93. doi: 10.1053/j.jfas.2010.02.003 .

2. L emley F, Berlet G, Hill K, Philbin T, Isaac B, Lee T. Current concepts review:

Tarsal coalition. Foot Ankle Int. 2006;27(12):1163–9.

3. T horpe SW, Wukich DK. Tarsal coalitions in the adult population: does treatment differ from the adolescent? Foot Ankle Clin. 2012;17(2):195–204. doi: 10.1016/j.fcl.2012.03.004 .

 4.  Zaw H, Calder JD. Tarsal coalitions. Foot Ankle Clin. 2010;15(2):349–64.

doi: 10.1016/j.fcl.2010.02.003 .

 Forefoot

 Anish  R.  Kadakia ,  Paul  J.  Switaj ,  Bryant  S.  Ho ,  Mohammed  Alshouli ,  Daniel  Fuchs , and  George  Ochengele

    1     Hallux Rigidus

 Take-Home Message

•      Pain and stiffness of the fi rst metatarsophalangeal (MTP) joint consistent with degenerative disease of the fi rst MTP.

•      Nonsurgical management should be attempted fi rst, with the goal of avoid-ing painful fi rst MTP joint dorsifl exion – Morton’s extension carbon fi ber plate.

•      S urgery is determined based on radiographic and physical exam fi ndings. Cheilectomy – >50 % joint preservation or negative grind test. Arthrodesis – <50 % joint preservation with a positive grind test or total joint obliteration or deformity (associated hallux valgus or varus).

 Defi nition   

•  Functional limitation of motion of the fi rst metatarsophalangeal joint in adults due to degenerative arthritis often associated with dorsal osteophyte

 A. R.  Kadakia (*) •  P. J.  Switaj •  B. S.  Ho •  M.  Alshouli

 D.  Fuchs •  G.  Ochengele

 Department of Orthopedic Surgery ,

 Northwestern University – Feinberg School of Medicine, Northwestern Memorial Hospital,   Chicago ,  IL ,  USA  e-mail: Kadak259@gmail.com; paul.switaj@gmail.com;

bryant.s.ho@gmail.com; mtshouli@gmail.com; dfuchs0011@gmail.com; gochenjele@gmail.com

    © Springer-Verlag France 2015                                                                                              895

C. Mauffrey, D.J. Hak (eds.), Passport for the Orthopedic Boards and FRCS Examination, DOI 10.1007/978-2-8178-0475-0_41

 Etiology   

•      Idiopathic arthritis

•      Extrinsic causes

–     Post-traumatic arthritis: intra-articular fractures, repetitive dorsifl exion- compression injuries, and hyperdorsifl exion injury

–     Improper shoe wear: high-heeled shoes, pointed-toe shoes, and shoes with small or short toe boxes

•      Intrinsic causes

–     Secondary to infl ammatory arthropathies

 Pathophysiology   

•      Change in the fi rst MTP joint biomechanics leads to displacement of the instant centers of motion to an eccentric position on the fi rst metatarsal head and higher plantar pressures.

•      Contracted fl exor hallucis longus (FHL) may increase plantar pressures and MTP joint force.

•      Clinical presentation

–     Pain with shoe wear secondary to pressure over dorsal osteophyte

–     Limited range of motion (limited ability to wear heels) –  Pain with activity

 Radiography   

•      Weight-bearing anteroposterior, lateral, and oblique views → Look for narrowing of the joint space, osteophytes at the lateral and dorsal surface of the joint, fl attened fi rst metatarsal head, and subchondral cysts (Fig.  1).

•      MRI scan: look for osteochondral injury in the setting of normal X-rays.

 Classifi cation   Coughlin clinical-radiographic classifi cation of hallux rigidus (Table  1 )

 Treatment Algorithm   Nonoperative : short period of rest followed by activity modifi cations, NSAIDS, intra-articular steroid injections, shoe modifi cation (rigid

sole). Orthotic = Morton’s extension carbon fi ber plate  Operative (Table  2)

•      Simplifi ed

–     C  heilectomy: some preservation of joint space without pain in the central range of motion (Grades 1–3) (Fig.  2)  

–     Fusion for deformity, pain with grind at central range of motion (grade 4), 100 % joint space loss, no motion (Figs.  3and  4 )  

 Complications   

•      Persistent pain

•      Recurrence of osteophyte formation

 Fig. 1  AP and lateral view of a patient with hallux rigidus. Note the narrowing of the joint space on the AP with the common fi ndings of a dorsal osteophyte on the metatarsal head with a loose body within the fi rst MTP. Hallux rigidus is most

easily identifi ed on the lateral radiograph

•      Progression of joint degeneration requiring additional surgery

•      Iatrogenic hallux valgus or varus deformity

•      Nonunion or malunion (ideal position – neutral rotation, slight hallux valgus, and dorsifl exion parallel to the fl oor. Best done with a fl at plate intraoperatively to simulate the fi nal clinical position. Superior to absolute values secondary to anatomic variability)

 Bibliography 

1 . C oughlin MJ, Shurnas PS. Hallux rigidus. Grading and long-term results of operative treatment. J Bone Joint Surg Am Vol. 2003;85-A:2072–88.

2.    Deland JT, Williams BR. Surgical management of hallux rigidus. J Am Acad Orthop Surg. 2012;20:347–58.

 Table 1  Coughlin clinical-radiographic classifi cation of hallux rigidus

Grade	Dorsifl exion	Radiographic fi ndings	Clinical fi ndings
0	40–60° and/or 10–20 % loss compared with normal side	Normal	No pain; stiffness, loss of motion
1	30–40° and/or 20–50 % loss compared with normal side	Dorsal osteophytes; minimal joint-space narrowing, periarticular sclerosis, fl attening of metatarsal head	Pain at extremes of dorsifl exion and/or plantar fl exion
2	10–30° and/or 50–75 % loss compared with normal side	Dorsal, lateral, and possibly medial osteophytes; fl attened appearance to metatarsal head, ¼ or less of dorsal joint space involved on lateral radiograph, mild-to-moderate joint-space narrowing and sclerosis; sesamoids not usually involved	Moderate-to-severe pain and stiffness; pain occurs just before maximum dorsifl exion/plantar fl exion on examination
3	=10° and/or 75–100 % loss compared with normal side. There is notable loss of metatarsophalangeal plantar fl exion	Substantial joint space narrowing, periarticular cystic changes, more than 1/4 of dorsal joint space involved on lateral radiograph, sesamoids enlarged and/or cystic and/or irregular	Constant pain and stiffness at extremes of range of motion but not at mid-range
4	Same as in Grade 3	Same as in Grade 3	Defi nite pain at mid-range of passive motion

Grade	Operative
0	Arthroscopic or open débridement, drilling, or grafting of metatarsal head OCD (if present)
1	Cheilectomy
2	Cheilectomy
3	Cheilectomy
4	MTP joint arthrodesis

 Table 2  Operative algorithm for hallux rigidus

 Fig. 2  Preoperative appearance of the dorsal osteophyte ( top radiograph)  and the postoperative appearance ( bottom radiograph ) following a cheilectomy. No more than 30 % of the metatarsal head should be resected to prevent iatrogenic instability

3.    Seibert NR, Kadakia AR. Surgical management of hallux rigidus: cheilectomy and osteotomy (phalanx and metatarsal). Foot Ankle Clin. 2009;14:9–22.

4.    Simpson GA, Hembree WC, Miller SD, Hyer CF, Berlet GC. Surgical strategies: hallux rigidus surgical techniques. Foot Ankle Int. 2011;32:1175–86.

    2     Hallux Valgus

 Take-Home Message

•      Hallux valgus is defi ned as a lateral deviation of the great toe with medial deviation of the fi rst metatarsal.

•      DJD of the fi rst MTP requires arthrodesis.

•      Hypermobility of fi rst TMT requires Lapidus (fi rst TMT arthrodesis).

•      I ncreased DMAA required redirectional osteotomy of distal metatarsal, in addition to other required osteotomies to correct the IMA.

•      Increased HVI requires an Akin osteotomy (medial closing wedge of phalanx).

 Fig. 3 P atient presented with hallux valgus and hallux rigidus ( a) . Correction of both deformities is best corrected with an arthrodesis ( b ) as an isolated cheilectomy or osteotomy to correct the hallux valgus will not be successful

 Defi nition  H allux valgus is defi ned as a lateral deviation of the great toe with medial deviation of the fi rst metatarsal (Fig.  5).

 Etiology   Related to multiple factors and more common in females

 Extrinsic Causes

I mproper shoe wear (high-heeled shoes, pointed-toe shoes, and shoes with narrow toe boxes)

 Intrinsic Causes

•      Genetic predisposition, ligamentous laxity, and predisposing anatomy (con-vex metatarsal head, pes planus) are contributory.

•      Infl ammatory arthropathies (rheumatoid arthritis), metabolic bone disorders

(gout), neuromuscular disorders (cerebral palsy, stroke)

 Fig. 4  Patient with grade 4 hallux rigidus ( a ) (>50 % joint space loss with central grind). This is best treated with an arthrodesis ( b )

 Pathoanatomy   

•      Medial capsular attenuation.

•      Proximal phalanx drifts laterally, leading to the following conditions:

–     P  lantar-lateral migration of abductor hallucis; change in position causes the muscle to plantar fl ex and pronate the phalanx.

–     Stretching of the extensor hood of the extensor hallucis longus.

–     Lateral deviation of the extensor hallucis longus and fl exor hallucis longus (FHL), causing a muscular imbalance and deforming force for valgus progression and pronation of the great toe.

•      The fi rst metatarsal head moves medially off the sesamoids, increasing the inter-metatarsal angle (IMA).

 Fig. 5  Two patients ( a ,  b)  with hallux valgus deformity. Note the increased medial deviation of the metatarsal head in the patient with a more severe deformity ( b )

•      Secondary contracture of the lateral capsule, adductor hallucis, lateral  metatarsal- sesamoid ligament, and intermetatarsal ligament.

 Radiography   

•      Multiple measurements can be obtained from standard radiographs that guide treatment options

–  Hallux valgus angle (HVA): angle formed by a line along the fi rst metatarsal shaft and a line along the shaft of proximal phalanx (Fig.  6)

•      Normal <15°

–     F  irst to second intermetatarsal angle (IMA): angle formed by a line along the fi rst metatarsal shaft and a line along the second metatarsal shaft (Fig.  7 )

•      Normal <9°

–     H  allux valgus interphalangeus (HVI) angle: angle formed by a line along the shaft of proximal phalanx and a line along the shaft of distal phalanx (Fig.  8 )

 Fig. 6AP radiograph denoting the hallux valgus angle. The acute angle ( HV ) formed by a line parallel to the fi rst metatarsal shaft and a line parallel to the proximal phalangeal shaft is measured

•      Normal <10°

•      Associated with a congruent deformity

–     D  istal metatarsal articular angle (DMAA): angle formed by a line along the articular surface of the fi rst metatarsal and a line perpendicular to the axis of the fi rst metatarsal

•      Normal <10°

•      Associated with a congruent deformity

 Classifi cation   

•      There is no specifi c classifi cation for hallux valgus that is routinely utilized. Specifi c recommendations are based upon the degree of deformity, which is discussed below.

 Fig. 7AP radiograph denoting the intermetatarsal angle. The acute angle ( IMA ) formed by a line parallel to the fi rst metatarsal shaft and

the second metatarsal shaft is measured

•      The use of the term congruency has been utilized and is a source of confusion

–     C  ongruency is determined by comparing the line connecting the medial and lateral edge of the fi rst metatarsal head articular surface with the similar line for the proximal phalanx, and when these lines are parallel, the joint is  congruent; otherwise, it is incongruent (Fig.  9).  

–     T  he implication is that the patient has an intrinsic deformity of either an increased DMAA or HVI. These can be present with an incongruent deformity as well, and therefore each radiograph must be carefully reviewed.

 Fig. 8AP radiograph of the proximal phalanx denoting the hallux valgus interphalangeus angle. A  line is drawn parallel to the proximal and distal articular surfaces. Perpendicular lines are drawn relative to these lines. The acute angle ( HVI ) formed by the perpendiculars is measured

 Treatment   

 Nonoperative

 NSAIDS for associated bursitis, shoe modifi cations (wide toe box, fl at sole), orthotics (arch support in fl at foot and metatarsal pad for second metatarsalgia), toe spacers if fl exible deformity. These will not correct the deformity.

 Operative

A lgorithmic approach to identifying the appropriate surgical intervention. Rigid deformity, pain within the fi rst MTP joint, infl ammatory arthropathy, or radiographic evidence of arthritis requires the fi rst MTP arthrodesis (Fig.  10).

A ll patients should undergo a soft tissue release with all associated osteotomies and the fi rst TMT arthrodesis (Lapidus).

 Fig. 9This patient has an incongruent deformity noted by the lack of parallelism between the articular surface of the metatarsal and the proximal phalanx

 IMA is ≤13° and HVA is ≤40°

•      Distal metatarsal osteotomy (chevron) (Fig.  11)  

•      Distal soft tissue release

•      Medial eminence resection and capsular repair

 IMA is >13° or HVA is >40°

•      Proximal metatarsal osteotomy

•      Distal soft tissue release

•      Medial eminence resection and capsular repair

 Instability of the First TMT/Joint Laxity

•      Lapidus (fusion of the fi rst TMT joint) (Fig.  12)  

•      Soft tissue release

•      Medial eminence resection and capsular repair

 Fig. 10  This patient has a signifi cant hallux valgus deformity with hallux rigidus and pain within the fi rst MTP joint. ( a ) Correction of both the IMA and HVA is easily achieved with an arthrodesis without the need for additional metatarsal osteotomy ( b )

 Increased DMAA (>10°)

•      D istal medial closed-wedge metatarsal osteotomy in addition to what is required based on the angular measurements.

–  IMA is ≤13°, and HVA is ≤40°

•      Distal biplanar closed-wedge metatarsal osteotomy.

•      Translate and redirect the metatarsal head simultaneously.

–     IMA is >13°  HVA is >40°

• P roximal metatarsal osteotomy and distal medial closed-wedge metatarsal osteotomy (Fig.  13 )  

–     Instability of the fi rst TMT/joint laxity

•      Lapidus and distal medial closed-wedge metatarsal osteotomy

 Fig. 11  In patients with a HVA  ≤40 and an IMA  ≤13 ( a ), a distal osteotomy with soft tissue correction is the most appropriate procedure ( b )

 Hallux valgus interphalangeus

•      Akin osteotomy can be done in isolation if no other deformity present.

•      Commonly performed in addition to other procedures.

 Complications   

•      Avascular necrosis (AVN)

–     D  istal metatarsal osteotomy and lateral soft tissue release may be performed simultaneously without increased risk of AVN.

•      Recurrence

–     Can occur with any procedure – highly associated with:

•      Under correction of the IMA

•      Isolated soft tissue reconstruction (modifi ed McBride)

•      Isolated resection of the medial eminence

•      Dorsal malunion

–     Results in transfer metatarsalgia – highly associated with:

 Fig. 12R egardless of preoperative deformity ( a) , in a patient with hypermobility, a Lapidus procedure is required ( b )

•      Lapidus (fi rst TMT fusion)

•      Proximal crescentic osteotomy

•      Hallux Varus (Fig.  14 )

–     Resection of the fi bular sesamoid (original McBride)

–     Over-resection of the medial eminence

–     Excessive lateral release

–     Overcorrection of the IMA

 Bibliography 

1. C oughlin MJ, Jones CP. Hallux valgus: demographics, etiology, and radiographic assessment. Foot Ankle Int. 2007;28(7):759–77.

2. E llington JK, Myerson MS, Coetzee JC, Stone RM. The use of the Lapidus procedure for recurrent hallux valgus. Foot Ankle Int. 2011;32(7):674–80.

 3.  Perera AM, Mason L, Stephens MM. The pathogenesis of hallux valgus. J Bone Joint Surg Am. 2011;93(17):1650–61.

4 . S mith BW, Coughlin MJ. Treatment of hallux valgus with increased distal  metatarsal articular angle: use of double and triple osteotomies. Foot Ankle Clin.

2009;14(3):369–82.

 Fig. 13  In this patient with an IMA >13 and an increased DMAA >10 ( a ), a double osteotomy is required ( b) . A proximal osteotomy in addition to a distal closing wedge osteotomy fully corrects the deformity

     

 Fig. 14  In this patient with clinical hallux varus ( a ), the etiology is the overcorrection of the IM angle with excessive lateral release ( b )

    3     Interdigital Neuroma

 Take-Home Message

•      C lassically, a patient with a symptomatic interdigital neuroma complains of pain located on the plantar aspect of the foot at or distal to the metatarsal heads. The pain is described as burning, often with radiation to the toes.

•      A djacent or multiple neuroma is an uncommon diagnosis and should alert the surgeon to the possibility of alternate diagnoses.

•      E xcision of neuroma from either a dorsal (higher rate of missed neuroma) or plantar (higher rate of painful scar) approach is the surgical treatment of choice.

 Defi nition   

•  A neuralgia of the interdigital nerve in the forefoot due to entrapment of the nerve near the distal edge of the transverse intermetatarsal ligament

 Etiology   

 Extrinsic Causes

•      Mass effect from soft tissues

•      Extrinsic mechanical stresses →improper shoe wear (high-heeled shoes, pointed- toe shoes, and shoes with small or short toe boxes) – result in compression and tensile stress on the nerve (from dorsifl exion)

 Intrinsic Causes

•      Ischemic changes to the perineural tissue

•      Repetitive microtrauma affecting the nerve

•      T raditionally, it was thought that both the medial and lateral plantar nerves send branches to the third web space, creating a larger nerve that was predisposed to increased microtrauma. However, the incidence of a communicating branch to the third web space was noted at 27 %, decreasing support of the anatomic theory.

 Pathophysiology   

•      Histologic analysis has revealed that the nerve is affected distal to the intermeta-tarsal ligament.

•      Fusiform swelling of the nerve has generated the term  neuroma .

•      Chronic entrapment leads to sclerosis and edema of the endoneurium, thickening of the perineurium, deposition of eosinophilic material, and demyelination of nerve fi bers distal to the ligament.

•      T he culmination of this pathologic process is an increased diameter of the affected nerve through intrasubstance hypertrophy and swelling.

     Fig. 15  Coronal T1 image of a Morton’s neuroma ( arrow ). Note that the neuroma is pear shaped and is plantar to the intermetatarsal ligament

 Radiography   

•      Three views of weight bearing of the foot should be performed to rule out any pathologic process of the metatarsophalangeal joint.

•      U ltrasonography has demonstrated a high sensitivity with a variable specifi city in the diagnosis of a neuroma and, however, is not required to make the diagnosis.

•      C urrently, an MRI scan may detect aberrant pathology such as a cyst or ganglion; however, it may show thickening of the nerve (Fig.  15 ). The routine use of MRI to identify a neuroma is not indicated given the diffi culty of interpreting the clinical value of the fi ndings.  

•      I n general, the diagnosis is usually made without the use of ultrasound or MRI and should only be considered with rare clinical presentations.

 Diagnostic Tests   

•      Lidocaine injection test: lidocaine is injected approximately 2 cm proximal to the metatarsal head, below the intermetatarsal ligament → resolution of symptoms confi rms the diagnosis.

•      M ulder’s test: squeeze the transverse arch of the foot and apply pressure between the interdigital space; a positive test will result in a click, as well as pain in the plantar surface of the involved interspace with paresthesias radiating into the affected toes.

 Treatment   

 Nonoperative: shoe modifi cation (soft shoe with wide toe box and fi rm sole that provides metatarsal support), modifi cation of daily activity, NSAIDS, corticosteroid injection 

 Operative: indicated after failure of nonoperative treatment

•      E xcision of the neuroma can be carried out through the dorsal or plantar approach to the web space. Isolated intermetatarsal ligament release is not appropriate.

–     D  orsal approach requires sectioning of the transverse metatarsal ligament (Fig.  16) . However, this approach may result in failure to excise the neuroma in 5 % of cases (Fig.  17 ).  

–     P  lantar approach spares the intermetatarsal ligament and is noted to universally achieve nerve resection, however, results in a painful plantar scar in 5 % of patients.

•      Successful in 75–90 % of cases

     Fig. 16  The intermetatarsal ligament ( arrow ) must be incised with the use of a dorsal approach in order to visualize the neuroma

     Fig. 17  The digital nerve has been transected proximally and elevated out of the wound. Adequate proximal resection must be performed

in order to prevent recurrence. Surgical pathology confi rmed the diagnosis of neuroma

 Complications   

•      Painful plantar scars or plantar keratosis with surgical plantar approach

•      Regeneration or formation of stump neuroma

•      Residual tenderness and/or numbness

•      Infection, plantar fat atrophy (related to steroid injections)

•      Digital ischemia if adjacent vascular structures injured

 Bibliography

1.    Akermark C, Crone H, Saartok T, Zuber Z. Plantar versus dorsal incision in the treatment of primary intermetatarsal Morton’s neuroma. Foot Ankle Int. 2008;29(2):136–41.

2.    Coughlin MJ, Pinsonneault T. Operative treatment of interdigital neuroma. A long-term follow-up study. J Bone Joint Surg Am Vol. 2001;83-A:1321–8.

3 . C oughlin MJ, Schenck RC Jr, Shurnas PS, Bloome DM. Concurrent interdigital neuroma and MTP joint instability: long-term results of treatment. Foot Ankle Int. 2002;23:1018–25.

 4.  Peters PG, Adams SB Jr, Schon LC. Interdigital neuralgia. Foot Ankle Clin. 2011;16:305–15.

5 . T itle CI, Schon LC. Morton neuroma: primary and secondary neurectomy. J Am Acad Orthop Surg. 2008;16:550–7.

    4     Lesser Toe Deformities

 Take-Home Message

•      Lesser toe deformities can present with pain, contractures, and callosities formation at the plantar MTP (claw toes), dorsal PIP (hammer and claw toes), or tip of the distal phalanx (mallet, hammer, or claw toes).

•      Vertical Lachman’s test (drawer test) for the lesser MTP joints that results in pain is highly sensitive for plantar plate rupture.

•      Clinical assessment of degree of fl exibility (fl exible or fi xed) is the key role in treatment.

 Defi nition   

•      Claw toe : fl exion deformities of the distal interphalangeal (DIP) joint and the proximal interphalangeal (PIP) joint with fi xed hyperextension at the metatarsophalangeal (MTP) joint (Fig.  18 ).

•      Mallet toe  : fl exion deformity at the DIP joint with the PIP and MTP joints in neutral position.

•      Hammer toe  : fl exion of the PIP joint with fl exion or extension of the DIP. With weight bearing, the MTP joint will appear extended; however, this should correct with as the foot is elevated from the ground. The MTP extension is secondary to the fl exion deformity of the PIP joint (Fig.  19).  

•      Crossover toe:  Defi ned by rupture of the plantar plate with associated attenuation of the lateral collateral ligament. This results in multiplanar instability of the toe with the end-stage deformity of the second toe (most common) overlapping the great toe (Fig.  20 ).  

 Etiology and Pathophysiology   

•  Lesser toe deformities occur much more commonly in women (up to 5:1 ratio), thought to be secondary to high fashion shoe wear which constricts the forefoot and maintains the MTP joints in hyperextension.

–  A hammer deformity most commonly involves the second toe due to its relative length compared to the remainder of the lesser toes. A short toe box will cause the second toe to buckle and extend at the MTP joint.

 

 Fig. 18 D orsal and plantar view of a patient with severe claw toes affecting primarily the second and third toes. Note the severe callus ( arrowhead)  on the plantar aspect of the second and third metatarsal heads

 

 Fig. 19  Hammertoe deformity of the toes two through fi ve in a patient. As opposed to claw toes, the MTP extension resolves with

removing the foot off the

fl oor

 Fig. 20  Crossover toe deformity of multiple toes in a patient who has longstanding hallux valgus deformity. Note how the toe has deformity in multiple planes. Not only is it extended in the sagittal plane, the toe is deviated in the coronal plane as well

–     C  hronic positioning of the MTP joint in hyperextension will attenuate the static plantar structures, which underlies both claw toes and crossover toe deformities.

–     Cavus deformity, neuromuscular diseases that affect the balance of the extrin-sic and intrinsic musculature infl ammatory arthropathies that lead to attenuation of soft tissue structures and instability of the MTP joint, and trauma have all been implicated in the etiology of claw toes.

–     Claw toes are a noted complication of compartment syndrome involving the deep compartments of the foot.

 Radiography   Three views of the foot weight bearing should be performed to identify if dislocations of the metatarsophalangeal joints have occurred as this will alter surgical management. Additionally, in chronic cases, the presence of arthrosis should be noted as this will alter surgical management as well.

 Classifi cation   The lesser toe deformities are classifi ed as detailed above, but critically differentiated if they are fl exible (reducible) or fi xed (irreducible).

 Treatment   

 Nonoperative

•      Adequate padding, shoe wear modifi cations with an adequate shoe box to pro-vide suffi cient space for the toes and silicone toe caps to protect the toes are useful.

•      O rthotic management may be accomplished by simple (i.e., metatarsal pads) or custom orthotics to include a metatarsal bar and well-outs for the affected metatarsal heads.

 Operative

 Persistent pain despite shoe wear modifi cation or signifi cant pressure sores, creating an at-risk environment for an ulcer, or history of ulceration secondary to shoe wear

•      General principles: fl exible -> soft tissue reconstruction. Fixed -> bone proce-dures required

•      Mallet Toe

–     Flexible – fl exor tenotomy at DIP

–     Fixed – DIP arthroplasty/fusion

•      Hammer Toe

–     Flexible – fl exor tenotomy at PIP or fl exor to extensor tendon transfer (if mild MTP extension noted)

–     Fixed – PIP arthroplasty or arthrodesis (Fig.  21)  

•      Claw Toe

–     Flexible – fl exor to extensor tendon transfer

–     F  ixed – PIP arthroplasty or arthrodesis with associated MTP capsulotomy and extensor lengthening

•      Dislocated or unstable MTP joint

–  Requires shortening osteotomy of the metatarsal

•      Crossover Toe

–     Flexible

•      Direct repair of the plantar plate has demonstrated clinical success and directly corrects the pathology.

•      A lternate options include fl exor to extensor tendon transfer or transfer of the EHB deep to the intermetatarsal ligament.

–     Fixed

•      Metatarsal shortening osteotomy to reduce the MTP with associated soft tissue correction detailed above

 Complications   

•      Recurrence of the deformity

•      Floating toe (noted with a Weil osteotomy)

•      Interdigital joint Instability

•      L oss of active motion of the affected toe (occurs commonly secondary to the altered tendon function from tenotomies or bony shortening)

 Fig. 21 P IP arthroplasty for a patient with a rigid hammer toe deformity of the fourth ( a ). Exposure of the distal aspect of the proximal phalanx ( b)  is followed by resection of the distal 3–4 mm of the phalanx ( c)  to allow the rigid deformity to correct ( d) . Pinning is performed to stabilize the toe for 4 weeks

 Bibliography

1 . C hadwick C, Saxby TS. Hammertoes/Clawtoes: metatarsophalangeal joint correction. Foot Ankle Clin. 2011;16(4):559–71.

2.    Ellis SJ, Young E, Endo Y, Do H, Deland JT. Correction of multiplanar defor-mity of the second toe with metatarsophalangeal release and extensor brevis reconstruction. Foot Ankle Int. 2013;34(6):792–9.

3.    Kwon JY, De Asla RJ. The use of fl exor to extensor transfers for the correction of the fl exible hammer toe deformity. Foot Ankle Clin. 2011;16(4):573–82.

4.    Shirzad K, Kiesau CD, DeOrio JK, Parekh SG. Lesser toe deformities. J Am Acad Orthop Surg. 2011;19:505–14.

5.    Smith BW, Coughlin MJ. Disorders of the lesser toes. Sports Med Arthrosc Rev.

2009;17:167–74.

    5     Freiberg’s Disease

 Take-Home Message

•      Incompetence of the fi rst ray (elevation or shortening) may be a causal fac-tor and must be addressed when treating the second ray.

•      Aggressive early conservative management may prevent late-stage arthritis by minimizing further extrinsic trauma to the metatarsal head.

•      S urgical management: If no arthritis, then dorsal closing wedge osteotomy of the second metatarsal. If arthritis is present, then an MTP arthroplasty with interposition versus metatarsal head excision.

 Defi nition  O steochondrosis of unknown origin that occurs in the metatarsal head, most commonly affects the second and, however, can also affect the third and fourth. Most commonly occurs in second decade of life and in women

 Etiology   Primarily Unknown

 Extrinsic causes: repetitive microtrauma of the subchondral bone secondary to impact activity (running, sports, high-heeled shoes). Increased load transfer during gait secondary to an iatrogenically elevated, short, or unstable fi rst metatarsal most commonly occurs following correction of hallux valgus.

 Intrinsic causes: avascular necrosis, infl ammatory arthropathies, predisposing anatomy (relatively long second metatarsal compared to the fi rst), corticosteroids

 Pathophysiology   

 A disruption in the blood supply due to mechanical or infl ammatory process leading to eventual infarction and weakening of the bony architecture with concomitant disruption of articular surface. Persistent trauma leads to collapse of the weakened metatarsal head that progresses to arthrosis as the cartilage degenerates.

P ain within the affected MTP with swelling, thickening, and decreased range of motion.

 Radiography   Weight-bearing anteroposterior, lateral, and oblique views are required.

 Common fi ndings in Freiberg’s disease include:

 Resorption of the central metatarsal bone adjacent to the articular surface with fl attening of the metatarsal head (Fig.  22 )  

 Osteochondral loose bodies

 Joint space narrowing in late-stage disease with associated osteophyte formation along with collapse of the articular surface (Fig.  23)  

M RI scan: Low T1 and variable T2 fat sat in the subchondral bone of the metatarsal head with fl attening

 Fig. 22Note the fl attening of the metatarsal head that is commonly seen with Freiberg’s disease ( arrow ). This patient had a prior silicone arthroplasty of the great toe and developed Freiberg’s disease secondary to overload from an incompetent fi rst ray

 

 Fig. 23  Focused AP view of the forefoot demonstrating the natural history and long-term sequela of untreated Freiberg’s. Note the signifi cant subchondral cysts and osteophyte formation indicating OA

 Fig. 24Loose body removal in a patient who requires a dorsal closing wedge osteotomy

 

 Fig. 25  A freer is placed in the osteotomy demonstrating the amount of bone that was resected. Note the dorsal to plantar direction of the osteotomy. The intact plantar cartilage will be rotated dorsally and recreate the dorsal articular surface

 Fig. 26Final appearance of the osteotomy after closure. Note the intact plantar cartilage now clearly present dorsally

 

 Fig. 27 R adiograph of a patient with Freiberg’s disease ( a)  with the characteristic fl attening of the metatarsal head ( arrow)  treated with a dorsal closing wedge osteotomy ( b) . Note how the contour of the metatarsal head has been recreated ( arrowhead )

    Classifi cation    

 Smillie radiographic classifi cation of the metatarsal head appearance

Stage I	Fracture of the epiphysis
Stage II	Subsidence of the central portion (altered head contour)
Stage III	Central reabsorption
Stage IV	Loose body separation
Stage V	Flattening, deformity, arthritis of the metatarsal head

     Treatment    

	Nonoperative	Operative
Clinical indication	Early stage of disease/low demand in late stage	Failed conservative treatment and/or advanced stage of disease
Options	(a)  Activity modifi cations (elimination of impact)  (b)  Protected weight bearing in a short CAM walker or short leg cast with toe extensions with crutches  (c)  NSAIDS               (d)  Shoe modifi cations (wide toe box, extra depth, fl at rigid sole)              (e)  Full-length semirigid orthosis with metatarsal bar or pad	1. Early – synovitis: simple débridement and loose body removal (Fig.  24 )                2. Late – joint collapse without arthritis: metatarsal dorsal closing wedge osteotomy with resection of nonviable bone and cartilage (Figs.  25 ,  26 , and  27 )  3. Late – arthritis: resection arthroplasty or interpositional arthroplasty. If severe and low demand, metatarsal head excision can be considered  4. In all cases: correction of the biomechanics of the foot must be performed (restore WB of the fi rst metatarsal and/or shorten second metatarsal as indicated)

 Complications   

•      Progression of joint degeneration

•      Transfer metatarsalgia

•      Limited ROM with extension contracture

 Bibliography

1.    Carmont MR, Rees RJ, Blundell CM. Current concepts review: Freiberg’s  disease. Foot Ankle Int. 2009;30(2):167–76.

2.    DiGiovanni CW, Patel A, Calfee R, Nickisch F. Osteonecrosis in the foot. J Am Acad Orthop Surg. 2007;15(4):208–17.

3 . O zkan Y, Oztürk A, Ozdemir R, Aykut S, Yalçin N. Interpositional arthroplasty with extensor digitorum brevis tendon in Freiberg’s disease: a new surgical  technique. Foot Ankle Int. 2008;29(5):488–92.

    6     Sesamoids

 Take-Home Message

•      Turf toe is a complex injury to the sesamoid complex and plantar plate of the 1st MTP joint. Return to play requires 60° of painless dorsifl exion.

•      T he most effective treatment for pain secondary to the sesamoid is isolated sesamoid resection.

•      Tibial > fi bular

 Defi nition   The sesamoids are embedded within the tendons of fl exor hallucis brevis. They are connected to each other by the intersesamoid ligament, and each sesamoid has an associated ligament inserting onto its respective side of the metatarsal head. The sesamoids function to increase the mechanical force of the fl exor hallucis brevis (FHB) in addition to absorption forces to the great toe during weight bearing.  Etiology and Pathophysiology   

•      T rauma: stress fracture and acute fracture (hyperextension and axial loading of the metatarsophalangeal joint)

•      S esamoiditis: mechanical (repetitive trauma, cavus foot) or infl ammatory disorders (infection, autoimmune disease)

 Radiography   

•      Non-weight-bearing anteroposterior and lateral foot views

•      Oblique views: a lateral 40° oblique view (for assessment of the fi bular sesa-moid) (Fig.  28 ) and a medial 40° oblique radiograph (for assessment of the tibial sesamoid)  

•      An axial view of the fi rst metatarsophalangeal joint → may identify fractures in the sagittal plane not visible on the AP radiograph (Fig.  29 )  

•      Bone scan: nonspecifi c as noted to be increased in 26–29 % of normal individuals

•      CT scan: able to reveal irregular fracture margins in acute or early stress fractures

•      MRI: marrow edema noted in stress fractures. Avascular necrosis (lack of signal intensity) (Fig.  30) . Very useful in the setting of turf toe to identify the presence of articular injury, complete tear of the plantar plate (Fig.  31 ).  

 Classifi cation   

 Turf Toe

•      Grade 1: strain of the capsule without loss of continuity. Normal range of motion with ability to bear weight

•      Grade 2: partial tear of the capsule. Limited and painful range of motion

•      G rade 3: complete tear with loss of continuity of the plantar plate and capsule or associated sesamoid fracture. Inability to bear weight, limited range of motion, severe swelling, and ecchymosis

 Fig. 28Oblique view of the foot demonstrating a linear lucency within the fi bular sesamoid ( arrow ). This is consistent with an acute fracture and not a bipartite sesamoid. The fi bular sesamoid is rarely bipartite in isolation, and the irregular line is consistent with a fracture

 

 Fig. 29  Sesamoid views allow visualization of the metatarsal-sesamoid articulation. This view clearly demonstrates sclerosis ( arrow ), fl attening, arthritis, and fracture

 Fig. 30Coronal T1 image of a patient with osteochondritis of the fi bular sesamoid. Osteochondritis will appear as dark ( arrow ), in contrast to the normal bone that appears bright on T1 imaging

( arrowhead )

     Fig. 31  Sagittal T1 image of an acute grade 3 turf toe injury. Note the disruption of the distal attachment of the plantar plate ( arrow ) with proximal retraction of the sesamoids ( arrowhead )

 Treatment   

 Turf Toe

•      Grade 1: stiff insole with immediate return to play

•      Grade 2: activity restriction for 2 weeks along with a stiff insole

•      Grade 3: up to 6 weeks of rest and immobilization with return to play after 60° of painless dorsifl exion in patients without radiographic abnormality. Operative management for patients who do not respond to the above protocol or any radiographic abnormality (sesamoid migration, hallux valgus, sesamoid fracture, diastasis of bipartite sesamoid, articular impaction)

 Sesamoiditis: mild to moderate pain can be controlled with anti-infl ammatory medication, a stiff-soled or rocker-bottom shoe, and a dancer’s pad (C-shaped pad with a relief for the sesamoids). Severe cases or fracture are treated with a CAM walker for 6 weeks followed by use of a dancer’s pad and activity restriction until resolution of pain. Shoe wear modifi cation (avoidance of high-heeled shoes) is also required.

 Fig. 32Plantar medial and plantar lateral incisions for repair of a Grade 3 turf toe injury

     Fig. 33  Plantar medial approach to the tibial sesamoid must be undertaken carefully to avoid injury to the plantar medial digital nerve (pictured)

 Operative

 Turf Toe

•      Dual incision technique to repair the plantar plate (Fig.  32 ). Avoid damage to plantar medial digital nerve (tibial sesamoid) and plantar lateral digital nerve (fi bular sesamoid) (Fig.  33 ). Repair plantar plate directly or via bony tunnel through the distal aspect of the sesamoid (Fig.  34 ).  

 Fig. 34Bone tunnel made within the distal aspect of the tibial sesamoid to allow fi xation to the proximal aspect of the remaining plantar plate

              

 Fig. 35  Severe cock-up deformity occurred after excision of both the medial and lateral tibial sesamoids

 Chronic sesamoid pain (sesamoiditis, AVN, fracture).

•      C omplete or partial sesamoidectomy. Partial sesamoidectomy for a proximal or distal pole fracture. Repair of the FHB is critical to prevent complications of a coronal plane deformity. Ninety percent of patients will be able to return to preinjury level of activity.

•      Curettage and grafting of long-standing symptomatic nonunion has been described and, however, has not been proven to be superior to excision and is not the most reliable procedure.

•      E xcision of both the tibial and fi bular sesamoid is not routinely performed secondary to the known complication of cock-up toe.

 Complications   

•      C ock-up deformity: increased incidence after excision of both sesamoids

(Fig.  35)

•      Hallux valgus: related to excision of the tibial sesamoid

•      Hallux varus: related to excision of the fi bular sesamoid

•      C hronic pain and neuroma formation at the surgical incision site with the plantar approach to the sesamoids

 Bibliography

1 . A nderson RB. Turf toe injuries of the hallux metatarsophalangeal joint. Tech Foot Ankle Surg. 2002;1:102–11.

 2.  Cohen BE. Hallux sesamoid disorders. Foot Ankle Clin. 2009;14:91–104.

3 . K adakia AR, Molloy A. Current concepts review: traumatic disorders of the fi rst metatarsophalangeal joint and sesamoid complex. Foot Ankle Int. 2011;32: 834–9.

 4.  McCormick JJ, Anderson RB. The great toe: failed turf toe, chronic turf toe, and complicated sesamoid injuries. Foot Ankle Clin. 2009;14:135–50.

 Generalized Conditions

 Anish  R.  Kadakia ,  Paul  J.  Switaj ,  Bryant  S.  Ho ,  Mohammed  Alshouli ,  Daniel  Fuchs , and  George  Ochengele

    1     Neuropathic Foot

 Take-Home Message

•      The neuropathic foot is most commonly a sequela of diabetes but can also result from upper motor neuron (UMN) lesions and hereditary motor-sensory neuropathies (HSMN).

•      S urgical treatment of UMN disorders often include Achilles lengthening, tibialis anterior transfer, and toe fl exor release.

•      S urgical treatment of HSMN requires a thorough evaluation into what drives the pes cavovarus deformity and its fl exibility.

 Defi nition

• M echanical changes in the foot which develop as a result of a disturbance in the normal sensory and motor innervation of joints.

 Etiology

•      Diabetic neuropathy: most common cause of neuropathic foot (see chapters  Paediatric hip conditionsand  Paediatric feet conditions ).

•      Sequelae of upper motor neuron (UMN) disorders: most commonly secondary to traumatic brain injury, stroke, and spinal cord injury.

 A. R.  Kadakia (*) •  P. J.  Switaj •  B. S.  Ho •  M.  Alshouli •  D.  Fuchs •  G.  Ochengele

 Department of Orthopedic Surgery ,  Northwestern University – Feinberg School of Medicine, Northwestern Memorial Hospital,   Chicago ,  IL ,  USA

 e-mail: Kadak259@gmail.com; paul.switaj@gmail.com; bryant.s.ho@gmail.com; mtshouli@gmail.com; dfuchs0011@gmail.com; gochenjele@gmail.com

    © Springer-Verlag France 2015                                                                                              931

C. Mauffrey, D.J. Hak (eds.), Passport for the Orthopedic Boards and FRCS Examination, DOI 10.1007/978-2-8178-0475-0_42

•      Hereditary motor-sensory neuropathies (HMSN): inherited progressive periph-eral neuropathy (e.g., Charcot-Marie-Tooth disease). Specifi c etiology depends on the particular variant. For CMT it is autosomal dominant with a duplication of chromosome 17.

•      Can also be caused by chemotherapeutic agents and certain infectious diseases such as HIV.

 Pathophysiology

•      Diabetic neuropathy (see chapters  Paediatric hip conditionsand  Paediatric feet conditions):

•      Upper motor neuron disorders:

–     Disruption of UMN pathways can lead to paralysis, muscle imbalance, and acquired spasticity, which ultimately may cause deformity.

–     Secondary problems are contractures, calluses, pressure sores, joint sublux-ation, hygiene issues, shoe-wear diffi culties, and dissatisfaction with personal experience.

–     T  he most common deformity is equinovarus caused by overactivity of gastrocnemius- soleus complex and relative overactive tibialis anterior.

•      HMSN, depends on the specifi c type:

–     For CMT the basis is an abnormal myelin sheath protein.

–     Leads to motor imbalance and bilateral → fi rst ray is plantarfl exed due to relative unopposed pull of peroneus longus → forefoot cavus and compensatory hindfoot varus →symmetric pes cavovarus deformity (Fig.  1).  

–     Intrinsic wasting →overpull of extrinsic musculature → claw toe deformity

(Fig.  2).  

–     Variable sensory defi cits →can lead to recurrent ulceration, infection, and arthropathy.

–     F  orefoot-driven hindfoot varus: deformity corrects with Coleman block test. Concomitant intrinsic hindfoot varus: deformity does not correct.

 Treatment  

 Diabetic Neuropathy (see chapters  Paediatric hip conditions and  Paediatric feet conditions):  UMN disorders:

 Nonoperative Care

•      P hysical therapy, stretching, maintenance of joint range of motion. Other modalities include splinting, serial casting, oral muscle relaxants, phenol and lidocaine nerve blocks, and botulinum type A toxin.

•      Phenol block have proven history with longer-lasting effect and are less expen-sive than botulinum toxin. However, botulinum toxin is easy to deliver since it needs only an injection into the muscle belly rather than precise injection around nerve.

 Fig. 1  Anterior view of a patient with HSMN with bilateral cavus feet. Note the ability to see the heel from this view with the elevated arches. The  posterior view clearly demonstrates the varus of the hindfoot

 Fig. 2  Multiple claw toes and signifi cantly claw hallux are seen in more advanced stages of HSMN. Claw hallux and claw toes in young patients should always increase the suspicion of a neurologic disorder

 Surgical Treatment

•      Address equinus deformity with open Z-lengthening or percutaneous lengthening.

•      Varus deformity addressed with split anterior tibialis tendon transfer (SPLATT) to lateral cuneiform or cuboid or total anterior tibialis tendon transfer to lateral cuneiform. Release of toe fl exors often required.

 Hereditary motor-sensory neuropathies (HMSN)

 Flexible Deformity (hindfoot can be passively manipulated):  Nonsurgical management:

•      Not currently recommended given progressive pattern of disease

•      Surgical management:

•      F orefoot driven: closing wedge dorsifl exion osteotomy of fi rst metatarsal (Fig.  3 ), release of plantar fascia, transfer of peroneus longus into peroneus brevis at level of distal fi bula.  

•      H indfoot driven: in addition to abovementioned procedures, include lateral calcaneal slide and/or closing wedge osteotomy (Fig.  4 ).  

•      Clawed hallux can be surgically treated with Jones procedure (arthrodesis of interphalangeal joint and transfer of EHL to the fi rst metatarsal).

•      Consider posterior tibial tendon transfer to dorsum (lateral cuneiform) or length-ening of the tendon to restore balance.

 Fig. 3  Dorsifl exion osteotomy to correct the plantarfl exed fi rst ray is

performed by marking the osteotomy with two K-wires ( a ). Following resection of the wedge, the osteotomy is closed and fi xated with resultant elevation of the fi rst ray ( b )

 Fixed Deformity (hindfoot cannot be passively manipulated):  Nonsurgical management:

•      Attempted with locked-ankle, short-leg ankle-foot orthosis with a lateral T-strap.

•      Rocker sole can improve gait and decrease energy expenditure.

 Surgical management:

•      Triple arthrodesis usually required for hindfoot correction. Posterior tibialis ten-don transfer through the interosseous membrane can correct equinus contracture and dorsifl exion weakness.

•      Must address imbalance of tendon forces even in the setting of an arthrodesis to prevent recurrence.

•      Dorsifl exion osteotomy of fi rst metatarsal, release of plantar fascia.

•      F orefoot correction is performed according to the guidelines outlined previously.

 Fig. 4  Lateral closing wedge osteotomy of the calcaneus in a patient who had concomitant intrinsic hindfoot varus (failure to correct with Coleman block). This is performed in addition correction of the plantarfl exed fi rst ray and is not a substitute for a dorsifl exion osteotomy of the fi rst metatarsal

 Bibliography

1.    Botte MJ, Bruffey JD, Copp SN, Colwell CW. Surgical reconstruction of acquired spastic foot and ankle deformity. Foot Ankle Clin. 2000;5:381–416.

2.    Piazza S, Ricci G, Caldarazzo Ienco E, et al. Pes cavus and hereditary neuropa-thies: when a relationship should be suspected. J Orthop Traumatol. 2010;11:195–201.

3. R oy DR, Al-Sayyad MJ. Complications of surgery of the foot and ankle in hereditary neurologic disorders. Clin Orthop Relat Res. 2001:181–7 .

4. S chenone A, Nobbio L, Monti Bragadin M, Ursino G, Grandis M. Inherited neuropathies. Curr Treat Opt Neurol. 2011;391(13):160–79.

5. v an der Ven A, Chapman CB, Bowker JH. Charcot neuroarthropathy of the foot and ankle. J Am Acad Orthop Surg. 2009;17:562–71.

    2     Rheumatoid Foot

 Take-Home Message

•      Rheumatoid arthritis is a chronic autoimmune disease that results in poly-arthropathy that commonly involves the forefoot.

•      Typical deformity includes dorsal and valgus toe deviation, claw toe defor-mity, and pes planovalgus.

•      Conservative treatment involves proper shoe and orthotic wear and immune- modulating drugs under the direction of a rheumatologist.

•      Surgical treatment of the forefoot includes fi rst MTP arthrodesis, lesser MT head resections, osteoclasis of interphalangeal joints, and extensor brevis tenotomy, while midfoot or triple arthrodesis is needed for pes planovalgus deformity in the rheumatoid foot.

 Defi nition

• C hronic, symmetrical polyarthropathy that most commonly presents in the third and fourth decades and is more prevalent in women

 Etiology

•      Autoimmune disease with a genetic predisposition

•      Cell-mediated immune response against soft tissues, cartilage, and bone

 Pathophysiology

•      ESR, CRP will be elevated, and RF titers positive (most commonly IgM).

•      Chronic synovitis leads to ligament and capsular laxity and cartilage and bony erosion.

•      Forefoot involvement very common:

–     Complaints of forefoot swelling, poorly defi ned pain, and eventually deformity.

–     I  ncompetence of joint capsules and lateral ligaments causes toes to subluxate or dislocate dorsally and deviate into valgus (Fig.  5 ).  

–     Contracture of the intrinsic musculature exacerbates claw toe deformity.

–     Plantar fat pad migrates distally and atrophies, causing metatarsalgia and forming keratoses.

–     As lesser toes deviate, hallux valgus occurs, and transfer metatarsalgia wors-ens (Fig.  6 ).  

•      Midfoot and hindfoot less commonly and less severely involved:

–     Midfoot/hindfoot arthrosis often results in pes planovalgus deformity that can be midfoot driven (tarsometatarsal joints are subluxated with a congruent hindfoot) or hindfoot driven (transverse tarsal and subtalar joint is subluxated with normal midfoot).

•      Tibiotalar joint is also commonly involved and may be caused by chronic subta-lar joint malalignment.

 Fig. 5  Clinical photograph of a patient with RA with swelling of the digits and characteristic valgus deviation of all digits with claw toes

 Radiography

•      Can have signifi cant midfoot and hindfoot arthrosis (talonavicular joint is characteristic)

•      Typically has diffuse osteopenia, symmetrical joint space narrowing, and lack of osteophyte formation (which easily differentiates RA from osteoarthritis) (Fig.  7 )  

 Treatment

•      Vasculitis and soft tissue fragility is common, requiring diligent care of the soft tissues regardless of treatment.

 Conservative

•      Rest, NSAIDs, immune-modulating drugs under the direction of rheumatolo-gists, toe taping, orthoses, careful use of corticosteroid injections to help symptoms related to synovitis, and patient education

 Fig. 6I n severe cases, the joint laxity that occurs results in signifi cant hallux valgus with overlap of the second toe over the fi rst

 Surgical

•      Should discuss use of immune-mediating pharmacologic therapies with rheuma-tologist prior to surgery →while most medications can be continued (prednisone, methotrexate, plaquenil), the newer biologic agents (such as TNF inhibitors) should be discontinued.

•      “Rheumatoid forefoot reconstruction” for deformity correction:

–  First MTP arthrodesis, lesser metatarsal head resection with pinning of lesser MTP joints, closed osteoclasis of interphalangeal joints versus PIP arthroplasty (silicone arthroplasty not recommended) through the use of three dorsal incisions. Extensor brevis tenotomy and Z-lengthening of extensor longus tendons may be necessary (Fig.  8 ).  

•      Pes planovalgus: Midfoot driven, realignment midfoot arthrodesis. Hindfoot- driven and fi xed deformity, triple arthrodesis

•      T ibiotalar arthrosis: Ankle arthrodesis is treatment of choice, ankle arthroplasty emerging as more reliable technique (though it is associated with increased risk of wound complications).

 Fig. 7  Typical radiographic appearance of a patient with RA. Note the multiple joint involvement with symmetric joint space narrowing, osteopenia without osteophyte formation with associated pes planus deformity. The typical dislocation of the lesser MTP joints can be noted as well

 Complications

•      Wound complications common following surgical treatment.

•      C urrent literature controversial whether patients on immunosuppressive therapies have signifi cantly increased infection rates.

•      Late recurrence of deformity has been reported and some consideration for joint sparing lesser toe surgery has been considered. However, no long-term data to support joint sparing treatment to date.

 Bibliography

1.    Aronow MS, Hakim-Zargar M. Management of hindfoot disease in rheumatoid arthritis. Foot Ankle Clin. 2007;12:455–74, vi.

2.    Goodman SM, Paget S. Perioperative drug safety in patients with rheumatoid arthritis. Rheum Dis Clin North Am. 2012;38:747–59.

 Fig. 8 P reoperative AP radiograph ( a)  of a patient with RA with clinical hallux valgus with subluxation of the lesser MTP joints. Post-op AP radiograph ( b ) demonstrating excellent alignment following fi rst MTP arthrodesis with metatarsal head resection of joints 2–5 and osteoclysis of the PIP joints. Interposition of the extensors into the potential space created may decrease risk of late subluxation

3.    Jeng C, Campbell J. Current concepts review: the rheumatoid forefoot. Foot Ankle Int. 2008;29:959–68.

4.    Loveday DT, Jackson GE, Geary NP. The rheumatoid foot and ankle: current evidence. Foot Ankle Surg. 2012;18:94–102.

5.    Sammarco VJ. Ankle arthrodesis in rheumatoid arthritis: techniques, results, and complications. Foot Ankle Clin. 2007;12:475–95, vii.

    3     Nerve Entrapment Syndromes

 Take-Home Message

•      Nerve entrapment related to space-occupying mass is more likely to improve with surgical treatment than nerve entrapment without a related mass.

•      The fi rst branch of lateral plantar nerve compression between the fascia of abductor hallucis and quadratus plantae is the most common cause of nerve-related heel pain, common in running athlete.

•      Superfi cial peroneal nerve entrapment related to chronic ankle instability and peroneal muscle herniation through fascial defect.

•      N erve entrapment syndromes most commonly cause neuropraxia type of nerve injury with nerve contusion and focal demyelination of axon sheath.

 Defi nition

 Nerve Entrapment

•      Localized pressure causing nerve dysfunction.

•      Tarsal tunnel syndrome →tibial nerve:

–     Boundaries – fl exor retinaculum (medial); talus, calcaneus, sustentaculum tali (lateral); abductor hallucis (inferior)

–     Additional contents – tendons of tibialis posterior, fl exor hallucis longus, fl exor digitorum longus, posterior tibial artery, venae comitantes, numerous septa

•      First branch of lateral plantar nerve (Baxter’s nerve)

•      Anterior tarsal tunnel syndrome →deep peroneal nerve

–     Boundaries – inferior extensor retinaculum (anterior), tibia and talus (posterior)

–     Additional contents – dorsalis pedis artery

•      Superfi cial peroneal nerve.

•      See Table  1 for symptoms and physical exam fi ndings.

 Etiology

•      E xternal compression from adjacent structures – tenosynovitis, engorged or varicose veins.

•      Space-occupying mass – synovial or ganglion cyst, pigmented villonodular synovitis, nerve sheath tumors, lipomas (Fig.  9).  

•      S ystemic disease can cause compression indirectly due to infl ammatory edema – diabetes mellitus, rheumatoid arthritis.

•      See Table  2 for nerve-specifi c etiologies.

 Table 1  Nerve entrapment symptoms and physical exam fi ndings

	Symptoms	Physical exam fi ndings
Tarsal tunnel syndrome	Burning sensation of plantar foot, medial ankle	Positive Tinel and nerve compression tests
	Plantar foot numbness variable	Pain with dorsifl exion-eversion
	Worse with prolonged standing, walking, running	Diminished two-point discrimination
		Wasting of intrinsic musculature
		Hindfoot valgus, pes planus
First branch of lateral plantar nerve	Chronic heel pain, pain at plantar medial foot, may radiate laterally	Maximal point of tenderness at site of compression by fascia of abductor hallucis and quadratus plantae
	Symptoms similar to plantar fasciitis
	Symptoms without weight bearing	Wasting of abductor digiti quinti
	No numbness – nerve has no sensory innervation
Anterior tarsal tunnel syndrome	Burning pain in dorsal fi rst webspace	Positive Tinel sign
	Vague dorsal foot pain	Diminished two-point discrimination
	Worse at night with foot in plantarfl exion	Forced ankle plantarfl exion reproduces symptoms
	Worse with shallow, laced shoes	Weak great toe extension
Superfi cial peroneal nerve	Pain and paresthesias radiating to dorsum of foot	Positive Tinel sign
	Numbness is variable	Diminished two-point discrimination
	Symptoms increase with activity	Palpable fascial defect and peroneal herniation
	May feel a bulge at lateral leg – area of muscle herniation	Forced plantarfl exion and inversion reproduces symptoms
		Signs of ankle instability

 Pathophysiology

•      Pressure on nerve causes ischemia and neuroma formation.

•      N euroma contains bundled disorganized nerve endings within collagenous mass.

•      Can result in loss of sensory and motor function.

•      Pain and paresthesia replace normal sensation.

 Radiography

•      Weight-bearing radiographs of the foot and ankle

–     Detect bony abnormality causing or contributing to nerve entrapment.

–     Evaluate alignment of foot and ankle. –  Rule out other source of symptoms.

•      MRI – if concern for space-occupying mass

•      EMG and NCV – can help confi rm diagnosis but variable sensitivity

     Fig. 9  Axial T2 fat-saturated image of a patient with tarsal tunnel syndrome that was noted to have a ganglion within the tarsal tunnel that required excision in addition to decompression of the nerve

 Table 2  Nerve entrapment etiology

	Etiology
Tarsal tunnel syndrome	Increased nerve tension from hindfoot valgus and pes planus
	Fracture of sustentaculum tali, medial tubercle of posterior process of talus
	Accessory muscle
First branch of lateral plantar nerve	Compression between fascia of abductor hallucis and quadratus plantae
	Lateral plantar nerve injury can occur from insertion of intramedullary nail for tibiotalocalcaneal fusion
Anterior tarsal tunnel syndrome	Anterior osteophytes of tibiotalar or talonavicular joints
	Tightly laced shoes
Superfi cial peroneal nerve	Chronic ankle instability
	Herniation of peroneal musculature through fascial defect
	Iatrogenic injury

 Classifi cation

 Seddon Classifi cation

•      Neuropraxia – nerve contusion, focal demyelination of axon sheath, no Wallerian degeneration, good prognosis

–  Most common resulting injury following nerve entrapment:

•      A xonotmesis – axon and myelin sheath disruption, Wallerian degeneration, endoneurium intact

•      N eurotmesis – complete disruption of nerve including endoneurium, Wallerian degeneration

 Treatment

 Nonoperative : fi rst line unless a space-occupying mass is present

•      Activity modifi cation

•      Medications

–     Nonnarcotic analgesics

–     Centrally acting anticonvulsants

–     Tricyclic antidepressants, selective serotonin reuptake inhibitors

–     T  opically applied compounds – include local anesthetic, anti-i nfl ammatory medication, capsaicin

•      Physical and occupational therapy

•      Injection of local anesthetic with or without corticosteroid medication

–     Useful for diagnosis

 Operative : indicated after 3–6 months of unsuccessful conservative treatment •  Complete nerve decompression (Fig.  10)  

 

 Fig. 10  Intraoperative photograph demonstrating an appropriate incision with decompression of the tibial nerve and the requisite branches. Note release of the abductor hallucis in the distal aspect of the incision, ensuring that both the medial and lateral plantar branches are adequately released

 Table 3  Nerve entrapment treatment options

	Nonoperative	Operative
Tarsal tunnel syndrome	Medial heel and sole wedge if hindfoot valgus and pes planus	Identify nerve proximally
		Release deep investing fascia proximally, fl exor retinaculum, deep and superfi cial fascia of the abductor hallucis
	Short period of immobilization with cast or boot	Assure that all branches – medial calcaneal, lateral plantar, medial plantar – are decompressed
		Release all septa
First branch of lateral plantar nerve	Heel pad	Release superfi cial and deep abductor hallucis fascia
	Arch support if pes planus	Remove heel spur if present
		Release part of plantar fascia if appears pathologic
Anterior tarsal tunnel syndrome	Night splint	Incise inferior extensor retinaculum
	Shoe tongue padding	Decompress both medial and lateral branch of nerve (divide 1 cm proximal to ankle joint)
		Excise bone spur if present
Superfi cial peroneal nerve	Lateral shoe wedge	Identify nerve distally and trace proximally to level that it pierces crural fascia (10–12 cm proximal to tip of lateral malleolus)
	Ankle brace	Partial fasciotomy
	Physical therapy for peroneal strengthening and proprioception	Test for residual tethering with intraoperative plantarfl exion
		Correct concurrent ankle instability

•      Removal of space-occupying mass if present:

– G  reater rate of surgical success if nerve compression secondary to space- occupying lesion

 See Table  3for nerve-specifi c treatment information.

 Complications

•      Recurrence of nerve entrapment – most commonly due to incomplete decompression

•      Revision surgery – decreased success rate

 Bibliography

1.    Ahmad M, Tsang K, Mackenney PJ, Adedapo AO. Tarsal tunnel syndrome: a literature review. Foot Ankle Surg. 2012;18(3):149–52.

2.    Donovan A, Rosenberg ZS, Cavalcanti CF. MR imaging of entrapment neuropa-thies of the lower extremity. RadioGraphics. 2010;30(4):1001–19. PubMed PMID: 20631365.

3 . F lanigan RM, DiGiovanni BF. Peripheral nerve entrapments of the lower leg, ankle, and foot. Foot Ankle Clin. 2011;16(2):255–74.

4.    Hirose CB, McGarvey WC. Peripheral nerve entrapments. Foot Ankle Clin. 2004;9(2):255–69.

5.    Kennedy JG, Baxter DE. Nerve disorders in dancers. Clin Sports Med. 2008;27(2):329–34.

    4     Pes Planus

 Take-Home Message

•      Adult-acquired fl atfoot secondary to dysfunction of the posterior tibial ten-don is the most common cause of pes planus in adults.

•      Correct fl exible deformity with corrective osteotomy (medial slide calca-neal osteotomy) + soft tissue reconstruction (FDL tendon transfer).

•      Correct fi xed deformity with arthrodesis (triple arthrodesis).

•      C orrect forefoot varus/supination with Cotton osteotomy (dorsal opening wedge osteotomy medial cuneiform).

 Defi nition

 Pes Planus (Flat Foot)

•      Loss of medial longitudinal arch.

•      Hindfoot valgus (Fig.  11 ) with forefoot abduction (Fig.  12).  

•      Fixed supination of the forefoot occurs with long-standing disease (Fig.  13 ).  

 Etiology

    Congenital (Flexible) Pes Planus                 

•      Ligamentous laxity.

•      Normal development of infants/children or normal adult variant.

•      In many cases is asymptomatic and does not require treatment. May additionally suffer degeneration of the posterior tibial tendon during adulthood.

    Acquired Pes Planus        

•      Insuffi ciency of the posterior tibial tendon with subsequent strain on the static medial stabilizers of the hindfoot. Asymmetric deformity in contrast to congenital pes planus.

 Pathophysiology

 Congenital Pes Planus

•      Ligamentous laxity, hindfoot valgus, forefoot abduction

•      Normal strength and integrity of the posterior tibial tendon

 Fig. 11 T he left hindfoot has signifi cant hindfoot valgus compared to the right. This is indicative of failure of the ligamentous support of the hindfoot that occurs in stage II, III, and IV PTTD. Simple debridement of the tendon will fail once the hindfoot is in valgus

 

 Fig. 12  The axis of the forefoot deviates into abduction relative to the axis of the hindfoot in patient with late-stage PTTD

 Fig. 13Patient with fi xed forefoot varus after correction of the hindfoot deformity

 Acquired Pes Planus

1.    Posterior tibial tendon (PTT) insuffi ciency – inability to perform a single-limb heel rise with associated pain and swelling (Fig.  14).  

2.    Loss of dynamic arch support.

3.    Arch attenuation (spring ligament > talocalcaneal interosseous ligament > deltoid ligament).

4.    Results in increased hindfoot valgus and forefoot abduction. More long-standing deformity results in fi xed forefoot supination/varus.

5.    Rigid deformity may occur with long-standing disease or arthritis.

6.    Strain across the deltoid ligament may result in ankle valgus with persistent asymmetric ankle joint pressure, placing the joint at risk for ankle arthritis.

 Radiography

 Weight-Bearing AP/Lateral Foot/Ankle

•      Talo-fi rst metatarsal angle on AP (normal =0) – increased angle associated with fl atfoot deformity.

•      Talo-fi rst metatarsal angle on lateral (normal =0) – negative angle (directed plan-tarward) associated with fl atfoot deformity (Fig.  15 ).  

•      Talar head uncoverage – the amount of uncoverage (lack of apposition of the navicular) may direct surgical intervention (Fig.  16 ):

–  >50 % uncovering indicative to perform lateral column lengthening

 Fig. 14Patient with complaints of posterior tibial tendon (PTT) dysfunction. Note the signifi cant swelling along the posteromedial aspect of the hindfoot ( black arrow ). This corresponds to the course of the PTT and is typically tender to palpation

              

 Fig. 15L ateral weight-bearing radiograph of a patient with posterior tibial tendon dysfunction. Note the plantarfl exed position of the talus relative to the fi rst metatarsal

•      L ook for evidence of degenerative changes of the hindfoot – requires triple arthrodesis. Midfoot arthritis may be present and requires realignment midfoot fusion in addition to hindfoot correction.

 AP/Lateral/Mortise Ankle

•      Evaluate for valgus talar tilt, ankle arthritis

 Ultrasound/MRI – not routinely utilized in the decision making process

 Classifi cation

•      Truro classifi cation: posterior tibial tendon dysfunction (Table  4 )

•      Nonoperative management for all stage II is best treated with an articulated AFO and physical therapy focused on strengthening of PTT. Stage III/IV is treated with a rigid AFO or Arizona brace.

 Fig. 16AP weight-bearing radiograph of the foot in a patient with stage IIB PTTD. The navicular is laterally subluxated, resulting in greater than 30 % uncovering of the talar head

 Table 4  Truro classifi cation: Posterior tibial tendon dysfunction

Stage 1	No deformity
	Tenosynovitis
Stage 2A	Flexible hindfoot valgus
	Normal forefoot
Stage 2B/C	Flexible hindfoot valgus
	Forefoot varus >15° or fi xed forefoot varus
Stage 3	Rigid hindfoot valgus
	Rigid forefoot abduction
Stage 4	Deltoid insuffi ciency (ankle valgus) or ankle arthritis

 Table 5Posterior tibial tendon dysfunction treatment options

	Nonoperative treatment	Operative treatment
Stage 1	Immobilization (CAM Walker)	Tenosynovectomy
	Orthotics (medial wedge and arch support) (Fig.  17 )	Equinus correction (GSR/TAL)
	PT
Stage 2A	Orthotics (articulated AFO with focused PT to strengthening PTT)	FDL transfer (Fig.  18 ) +
		Medial slide calcaneus osteotomy (Fig.  19 )
		Lateral column lengthening (>50 % uncoverage)
		Equinus correction (GSR/TAL)
Stage 2B	Orthotics (articulated AFO with focused PT to strengthening PTT)	As per stage 2A
		Cotton osteotomy (stable fi rst TMT) (Fig.  20 ) vs. fi rst TMT fusion – arthritis or instability (Fig.  21 )
Stage 3	Orthotics (AFO, Arizona brace)	Triple arthrodesis (subtalar, talonavicular, calcaneocuboid) (Fig.  22 )  (Some current consideration to perform isolated talonavicular and subtalar arthrodesis)
Stage 4	Orthotics (AFO, Arizona brace)	Rigid ankle: tibiotalocalcaneal arthrodesis or
		Pantalar fusion (Fig.  23 )
		Flexible non-arthritic ankle: may consider deltoid reconstruction (Fig.  24 ) + triple arthrodesis with medial slide calcaneal osteotomy

 Treatment

 Congenital Pes Planus

 Nonoperative : observation, heel cord stretching, orthotics (arch support)

 Operative treatment : indicated for failure of nonoperative treatment

•      G astrocnemius recession (GSR) or tendo-Achilles lengthening (TAL) if equinus contracture

•      Calcaneus osteotomy:

–     Calcaneal lengthening osteotomy (Evans)

–     M  edial calcaneal slide osteotomy, medial cuneiform plantar closing wedge osteotomy, cuboid opening wedge osteotomy (triple C)

 Acquired Pes Planus

 Treatment (Table  5 )

 Complications

•      Nonunion of arthrodesis

•      Failure to achieve satisfactory correction of deformity

•      Failure to achieve pain relief – 10 %

 Fig. 17Standard 3/4 length orthotic. Note the longitudinal arch support. Custom orthotics are useful if the patient has a severe deformity that would not be amenable to over the counter orthotics – however, custom orthotics are 10–20 times more expensive

     Fig. 18  Use of the FDL is the most common tendon transfer to recreate the function of the posterior tibial tendon. The tendon is placed through a drill hole in the navicular and routed from plantar to dorsal

 

 Fig. 19  Note the medial translation of the calcaneal tuberosity. A 1 cm shift is suffi cient

 Fig. 20Plantarfl exion osteotomy of the medial cuneiform is commonly used to correct the fi xed forefoot varus. Use of allograft to achieve the correction is demonstrated here

              

 Fig. 21 S tabilization of the fi rst tarsometatarsal (TMT) joint is critical in fl atfoot reconstruction if there is instability of that joint. After joint preparation – the fi rst MTP is dorsifl exed – which forces the fi rst TMT joint to plantarfl ex secondary to the windlass mechanism. Fixation is typically performed with cross screws

 Fig. 22L ateral radiograph of a patient who underwent a triple arthrodesis for a fi xed hindfoot valgus deformity – stage III

              

 Fig. 23  Lateral radiograph of a patient with stage IV PTTD with ankle arthritis. A pantalar fusion is the gold standard in this case. Performing an ankle replacement and triple arthrodesis is possible – however, there are no long-term results of ankle replacements in this setting

 Fig. 24Allograft reconstruction of the deltoid ligament can be performed in a patient with stage IV PTTD with ankle valgus without evidence of arthritis. Concomitant correction of the hindfoot deformity is required

 Bibliography

1 . A hmad J, Pedowitz D. Management of the rigid arthritic fl atfoot in adults: triple arthrodesis. Foot Ankle Clin. 2012;17(2):309–22.

 2.  Kulig K, Reischl SF, Pomrantz AB, Burnfi eld JM, Mais-Requejo S, Thordarson DB, Smith RW. Nonsurgical management of posterior tibial tendon dysfunction with orthoses and resistive exercise: a randomized controlled trial. Phys Ther. 2009;89(1):26–37.

3 . S chuh R, Gruber F, Wanivenhaus A, Hartig N, Windhager R, Trnka HJ. Flexor digitorum longus transfer and medial displacement calcaneal osteotomy for the treatment of stage II posterior tibial tendon dysfunction: kinematic and functional results of fi fty one feet. Int Orthop. 2013;37(9):1815–20.

 4.  Smith JT, Bluman EM. Update on stage IV acquired adult fl atfoot disorder: when the deltoid ligament becomes dysfunctional. Foot Ankle Clin.

2012;17(2):351–60.

    5     Pes Cavus

 Take-Home Message

•      Primarily progressive, eventually rigid deformity from prolonged muscle imbalance.

•      Etiology primarily neurologic.

•      Rigid deformities should be treated with corrective osteotomies as well as tendon transfers to remove deforming forces.

 Defi nition   Cavovarus:

•      Hindfoot varus, forefoot pronation

 Etiology

•      Neurologic

–     H  ereditary motor and sensory neuropathies – Charcot-Marie-Tooth (typically bilateral disease)

–     Cerebral palsy

–     Stroke

–     Spinal cord lesions (typically unilateral disease)

•      Traumatic

–     Compartment syndrome

–     Talar neck malunion

–     Peroneal nerve injury

•      Residual clubfoot

•      Idiopathic

 Pathophysiology

•      Muscle imbalance

–     Strong peroneus longus (PL) and posterior tibialis (PT)

–     Weak peroneal brevis (PB) and anterior tibialis (AT)

•      Posttraumatic

–     Deep posterior compartment contractures (PT, FDL)

•      Prolonged deformity leads to plantar fascia contraction; fl exible deformity becomes rigid.

 Radiography   Weight-bearing AP/lateral foot/ankle, calcaneus axial

•      Hindfoot varus

•      First MT plantarfl exion

 Classifi cation   Coleman block test – block under lateral forefoot

•      If hindfoot corrects – fl exible hindfoot deformity, forefoot driven

•      If hindfoot does not correct – rigid hindfoot deformity rigid ± forefoot deformity

 Treatment 

 Nonoperative

•      Orthotics – lateral wedge, depression for fi rst ray

•      Ankle-foot orthosis with varus correction for rigid deformities

 Table 6Cavovarus surgical treatment options

Coleman block test fi nding
Flexible hindfoot	PT/PL tendon transfer + plantar fascia release + tendo- Achilles lengthening (TAL) ±1st metatarsal (MT) dorsifl exion osteotomy
Rigid hindfoot	Above procedures + calcaneal osteotomy (lateral slide vs. closing wedge)
Hindfoot/midfoot arthritis or severe deformities	Triple arthrodesis + PT/PL tendon transfer

 Operative (Table  6 )

 Complications

•      Nonunion of arthrodesis

•      Recurrence of deformity

•      Wound breakdown/infection

 Bibliography

 1.  Krause FG, Wing KJ, Younger AS. Neuromuscular issues in cavovarus foot. Foot Ankle Clin. 2008;13:243–58, vi.

2 . R yssman DB, Myerson MS. Tendon transfers for the adult fl exible cavovarus foot. Foot Ankle Clin. 2011;16:435–50.

3.    Ward CM, Dolan LA, Bennett DL, Morcuende JA, Cooper RR. Long-term results of reconstruction for treatment of a fl exible cavovarus foot in CharcotMarie- Tooth disease. J Bone Joint Surg Am Vol. 2008;90:2631–42.

4.    Younger AS, Hansen ST, Jr. Adult cavovarus foot. J Am Acad Orthop Surg. 2005;13:302–15.

5 . Z ide JR, Myerson MS. Arthrodesis for the cavus foot: when, where, and how?

Foot Ankle Clin. 2013;18:755–67.

    6     Tendinopathies

 Take-Home Message

•      Tendinosis is a chronic noninfl ammatory degeneration and should not be confused with tendonitis, an acute infl ammatory disease.

•      Nonoperative treatment should focus on eccentric strengthening.

•      Operative intervention should focus on removing diseased tendon with appropriate tendon transfers if >50 % of operative tendon is removed.

 Defi nition

•      Tendonitis – infl ammation of the tendon

•      T endinosis – chronic damage to tendons with microscopic analysis showing tissue necrosis and mucoid degeneration

 Etiology

•      Anterior tibial (AT) – tendonitis from overuse, partial/complete rupture from trauma. May present as a mass along the anterior ankle (pseudotumor) (Fig.  25 ).

•      Flexor hallucis longus (FHL) – tendonitis from overuse (ballet dancers) or impingement/stenosis along posterior ankle. Prolonged symptoms can lead to partial rupture.

•      Peroneal tendons

–     Subluxation/dislocation from forced eversion/dorsifl exion -> disruption of superior peroneal retinaculum (Fig.  26)  

–     Tendon tears caused by degeneration from tendon subluxation/dislocation, ankle sprains, ankle instability

 

 Fig. 25  Patient with a chronic anterior tibial tendon rupture. Note the extensor recruitment and the stump of the anterior tibial tendon ( arrow ) at the level of the ankle. This patient presented for evaluation of ankle mass  Fig. 26 Subluxation of the peroneal tendons ( arrow ). Note the tendons are displaced anterior to the

posterior border of the fi bula

( line )

•      Achilles

–     Insertional tendinopathy – tendinosis (cause unknown)

–     Non-insertional tendinopathy – infl ammation of peritenon alone from  overuse, fl uoroquinolone antibiotics, mechanical imbalance

–     R  upture – “weekend warrior,” sudden active plantarfl exion against resistance or forced dorsifl exion in plantarfl exed foot

 Pathophysiology

•  Tendinosis degenerative changes → collagen fi ber disorientation; hypocellularity; patchy necrosis, calcifi cation; minimal infl ammatory cells

 Radiography

 AP/Lateral Radiographs of the Foot/Ankle

•      Fracture of lateral ridge of distal fi bula (peroneal subluxation/dislocation)

•      Fracture of os peroneum (peroneal longus rupture)

•      Superior calcaneal tuberosity bone spur and calcifi cation at Achilles insertion (insertional Achilles tendinopathy) (Fig.  27)  

 MRI

•      Fluid around FHL – high-signal intensity surrounding the tendon (Fig.  28 )  

•      A chilles thickening with intermediate intrasubstance signal (non-insertional tendinopathy) (Fig.  29)  

 Ultrasound

•      Dynamic exam peroneal subluxation/dislocation

 Classifi cation   Ogden classifi cation of superfi cial peroneal retinaculum (SPR) tears

(Table  7)

 Fig. 27Lateral radiograph demonstrating calcifi cation of the Achilles tendon at the insertion ( arrow )

     Fig. 28  Axial T2 image consistent with synovitis of the fl exor hallucis longus. Note the increased signal intensity ( arrow ) surrounding the tendon

 Fig. 29Sagittal T1 imaging of a patient with non- insertional Achilles tendinosis. Note the thickening of the tendon ( arrowheads ) and the intermediate-signal intensity within the tendon consistent with degeneration

 Table 7  Ogden classifi cation of Superfi cial Peroneal Retinaculum (SPR) tears

Grade 1	SPR partially elevated off fi bula
Grade 2	SPR separated from cartilofi brous ridge lateral malleolus, subluxation between SPR and ridge
Grade 3	Cortical avulsion SPR off fi bula, subluxation under fracture
Grade 4	SPR avulsed from calcaneus

 Table 8  Anterior tibialis and FHL treatment options

	Nonoperative	Operative
Anterior tibialis	NSAIDs, CAM boot or walking cast	Acute rupture – primary repair
		Chronic rupture – reconstruction with interpositional graft
Flexor hallucis longus	Activity modifi cation	Tenosynovectomy, fi bro-osseous tunnel release

 Treatment  

 Treatment of anterior tibialis, fl exor hallucis longus disorders (Table  8)

 Treatment of peroneal tendon disorders (Table  9 )

 Treatment of Achilles tendon disorders (Table  10 )

 Complications

•      Wound breakdown/infection

•      Tendon re-rupture

 Bibliography

1. C errato RA, Myerson MS. Peroneal tendon tears, surgical management and its complications. Foot Ankle Clin. 2009;14:299–312.

2. H eckman DS, Gluck GS, Parekh SG. Tendon disorders of the foot and ankle, part 1: peroneal tendon disorders. Am J Sports Med. 2009;37:614–25.

 Table 9Peroneal tendon treatment options

	Nonoperative	Operative
Peroneal tendon subluxation/ dislocation	Cast immobilization, protected weight bearing 6 weeks (acute injuries in reduced position)	Reconstruction SPR, fi bular groove deepening
Peroneal tendon tear	NSAIDs, activity modifi cation, physical therapy, lace-up ankle brace	<50 % diseased tendon – tenosynovectomy, debridement, tendon repair ± groove deepening
		> 50% diseased tendon or complete rupture 1 tendon – excision and tenodesis
		>50% diseased tendon or complete rupture 2 tendons – FHL transfer to fi fth metatarsal (MT)
		Hindfoot varus – lateral closing wedge calcaneus osteotomy (Dwyer)

 Table 10  Achilles tendon treatment options

	Nonoperative	Operative
Achilles insertional tendinopathy	Activity/shoe modifi cation, heel lifts, stretching, physical therapy (eccentric strengthening), silicone sleeves/pads, NO corticosteroid injections	Debridement degenerative tendon, resection prominent superior calcaneal tuberosity, excision retrocalcaneal bursa
		If >50 % tendon detached, reattach insertion with suture anchors
		If >50 % tendon excised, FHL transfer
Achilles non- insertional tendinopathy	Activity modifi cation, heel lifts, physical therapy (eccentric strengthening), shock-wave therapy	Mild disease – percutaneous tenotomies
		Moderate disease – debridement, tendon tubularization
		If >50 % tendon excised, FHL transfer
Achilles rupture	Acute – bracing/cast in equinus with early functional rehabilitation (no difference in re-rupture rate)	Acute – direct repair (improved satisfaction in age <45)
	Chronic – AFO	Chronic – VY advancement ± FHL transfer

3. H eckman DS, Gluck GS, Parekh SG. Tendon disorders of the foot and ankle, part 2: achilles tendon disorders. Am J Sports Med. 2009;37:1223–34.

 4.  Jones DC. Tendon disorders of the foot and ankle. J Am Acad Orthop Surg. 1993;1:87–94.

5 . R eddy SS, Pedowitz DI, Parekh SG, Omar IM, Wapner KL. Surgical treatment for chronic disease and disorders of the achilles tendon. J Am Acad Orthop Surg. 2009;17:3–14.

    7     Diabetic Foot

 Take-Home Message

•      The diabetic foot is at a constant risk for recurrent ulcerations, especially due to neuropathy and peripheral vascular disease.

•      Ulcer classifi cation is essential to set a treatment strategy and determine prognosis.

•      Treatment in the setting of infection should include culture-directed ther-apy and a thorough understanding of the different levels of amputations.

 Introduction

•  Diagnosis of foot ulcerations results in the greatest rate of hospital admissions in diabetics, as well as lower extremity amputations.

 Pathophysiology

•      Diabetic neuropathy:

–     S  ensation: sensory loss begins in stocking distribution and progressive proximally. Ninety percent of patients who cannot feel the 5.07 monofi lament have lost protective sensation to their feet and are at risk for ulceration.

–     Autonomic neuropathy: abnormal sweating mechanism leads to a dry foot → vulnerable to fi ssuring cracks →portals for infection.

–     M  otor neuropathy: most commonly involves the common peroneal nerve → resultant loss of tibialis anterior function and foot drop; small intrinsic musculature also affected →claw toes and subsequent toe-tip ulcerations.

•      Hypomobility syndrome:

–     Decreased range of motion in joints from excessive glycosylation of soft tissues

•      Peripheral vascular disease:

–     Occurs in 60–70 % of patients who have diabetes for over 10 years, involving both large and small vessels.

–     Noninvasive vascular examination should be performed when pulses not pal-pable (normal waveform is triphasic); ankle brachial index of 0.45 is minimum for healing and greater than 1.3 is consistent with calcifi cation of vessels.

–     Minimum toe pressures for healing: 40 mmHg.

–     Transcutaneous oxygen measurements of the toes greater than 40 mmHg have been found to be predictive of healing.

 Table 11  Wagner grading system for diabetic foot infections

Grade	Depth of ulcer
0	Skin intact with bony deformity that leads to “at risk” foot
1	Localized superfi cial ulcer without tendon or bone involvement
2	Deep ulcer with exposed tendon or joint capsule
3	Extensive ulcer with exposed bone/osteomyelitis or abscess
4	Partial gangrene
5	Extensive gangrene

 Table 12  Brodsky grading system: Based on ischemia

Grade
A	Normal vascularity
B	Ischemia without gangrene
C	Partial gangrene
D	Complete gangrene

•      Immune system impairment:

–     P  oor cellular defenses, altered chemotaxis of white blood cells, and poor cytotoxic environment (due to hyperglycemia) to fi ght bacteria lead to diffi culty in fi ghting off infection.

•      Metabolic defi ciency:

–     T  otal protein less than 6.0, WBC count less than 1,500, and albumin levels less than 2.5 result in poor healing potential.

 Radiography

•      R outine radiographic series of the foot and ankle should be obtained to determine the extent of bone loss and deformity. Findings can be diffi cult to interpret in the setting of neuroarthropathy. Bony desctruction directly over an open ulcer is highly suspicious for osteomyleitis.

•      MRI can be obtained is an abscess is suspected.

•      MRI has high false-positive rate in the diagnosis of osteomyelitis, particularly with concurrent Charcot arthropathy.

•      WBC-labeled scan or dual-image Tc/In scan is more sensitive and specifi c for osteomyelitis than isolated technetium scan.

 Classifi cation   Wagner classifi cation: based on depth of ulcer (Table  11)

 Brodsky classifi cation: based on ischemia (Table  12)

 Table 13  Diabetic ulcer management based on the Wagner Grading system

Grade	Treatment
0	Extra-depth shoe and pressure relief insoles
1	In offi ce debridement, shoe modifi cation or total contact cast if no infection
2/3	Operative debridement of all exposed bone/tendon and nonviable tissue. Dressing changes and total contact casting once wound bed is healthy
4/5	Local vs. larger amputation

 Treatment

 Ultimate goal is an ulcer-free, functional, plantigrade foot that can fi t within a brace or shoe (Table  13 ).

•      T he Therapeutic Shoe Bill allocated money for neuropathic patients to purchase extra-depth shoes and total contact inserts (3 per year) for ulcer prevention.

•      Workup should include noninvasive vascular studies and surgical revasculariza-tion if indicated and metabolic assessment with delay in surgery if possible until nutritional status is improved. •  Additional treatment includes:

–     Tendo-Achilles lengthening to offl oad the midfoot/forefoot if recurrent ulcer-ations with equinus deformity.

–     Ostectomy of bony prominences (stable deformity) or fusion if instability present.

–     Toe deformities often require joint resection or amputation.

•      Diabetic foot infections are polymicrobial:

–     Should not perform superfi cial wound culture → deep cultures provide most accurate results.

–     T  reat infections with initial broad-spectrum antibiotic coverage once surgical cultures obtained, and adjust once sensitivity returns.

–     Abscesses require surgical drainage and antibiotics.

–     Osteomyelitis is treated with antibiotics and usually surgical debridement.

•      Amputation as needed at different levels with appropriate tendon transfers:

–     Transmetatarsal →lowest energy expenditure, no tendon transfer needed

–     Lisfranc →requires a transfer of peroneals to cuboid to prevent varus; Achilles lengthening

–     Chopart →requires transfer anterior tibialis to talus to prevent equinus; Achilles lengthening

–     Syme’s →next lowest energy expenditure (superior to Lisfranc and Chopart with regard to amount of energy needed to ambulate)

–     Transtibial →superior results with postoperative casting for 3–5 days with conversion to rigid removal dressing

 Bibliography

1 . A nakwenze OA, Milby AH, Gans I, Stern JJ, Levin LS, Wapner KL. Foot and ankle infections: diagnosis and management. J Am Acad Orthop Surg. 2012;20:684–93.

 2.  Arad Y, Fonseca V, Peters A, Vinik A. Beyond the monofi lament for the insensate diabetic foot: a systematic review of randomized trials to prevent the occurrence of plantar foot ulcers in patients with diabetes. Diabetes Care. 2011;34:1041–6.

3. L ipsky BA. Medical treatment of diabetic foot infections. Clin Infect Dis. 2004;39 Suppl 2:S104–14.

4. R obinson AH, Pasapula C, Brodsky JW. Surgical aspects of the diabetic foot. J Bone Joint Surg Br Vol. 2009;91:1–7.

 5.  Wukich DK, Armstrong DG, Attinger CE, et al. Inpatient management of diabetic foot disorders: a clinical guide. Diabetes Care. 2013;36:2862–71.

    8     Charcot Arthropathy

 Take-Home Message

•      Charcot arthropathy is a limb-threatening destructive process that occurs in patients with sensory, motor, and autonomic neuropathy associated with medical diseases such as diabetes mellitus.

•      The Eichenholtz classifi cation describes the evolution of the condition through time, whereas the Brodsky classifi cation is defi ned by location.

•      Initial treatment consists of prompt immobilization and non-weight bear-ing but may warrant arthrodesis or amputation with long-standing deformity.

 Defi nition

• C hronic, progressive, noninfectious destructive process affecting bone architecture and joint alignment in people lacking protective sensation (Fig.  30)

 Etiology

•      I n developed world, diabetic neuropathy is the most frequent cause of Charcot arthropathy.

•      Other possibilities are alcoholism, leprosy, tabes dorsalis, myelomeningocele, and congenital insensitivity to pain.

•      Often challenge is determining whether there is superimposed osteomyelitis.

              

 Fig. 30  Varus deformity of the ankle and hindfoot is a common deformity seen in Charcot. The deformity can be severe with some patient presenting with callous or ulcer over the fi bula as it now contacts the ground

 Pathophysiology   Two traditional theories:

•      N eurotraumatic: exaggerated overuse injury where insensate joints that cannot adopt normal protective mechanisms are subjected to repetitive microtrauma

•      N eurovascular destruction: autonomic dysfunction leads to increased blood fl ow, resulting in osteoclast stimulation, bone resorption, and weakening

 Likely results from a combination of these processes →the development of  abnormal bone with no ability to protect the joint results in gradual bone fracture and subluxation of the joint (Fig.  31 ).  

 Radiography

•      Radiographic appearance dependent on what stage the disease is in (see below).

•      The hallmark deformity associated with this condition is midfoot collapse, described as a “rocker bottom” foot (Fig.  32).  

•      T echnetium bone scan may be positive in all stages. Indium WBC scan may be negative for neuropathic joints and positive for osteomyelitis.

•      Diffi cult to differentiate infection from Charcot based on MRI, although MRI allows detection of subtle changes in early stages of Charcot arthropathy.

 Fig. 31  AP radiograph of a patient with midfoot Charcot in Eichenholtz stage 1. The patient had 2 weeks of swelling without signifi cant trauma. Note the fractures and dislocations through the tarsometatarsal joints

              

 Fig. 32  Rocker bottom deformity in a patient with hindfoot Charcot. Note the severe plantarfl exed position of the talus relative to the forefoot and the break through the talonavicular and metatarso- cuboid joint. Plantar prominence of the cuboid risks ulceration in this patient

 Table 14  Modifi ed Eichenholtz stages for neuroarthropathy

Stage	Clinical manifestations	Radiographs
0: Pre-fragmentation	Acute infl ammation, swelling, erythema with dependent rubor; confused with infection. Lack of systemic symptoms. Pain may not always be present	Normal or regional bone demineralization
1: Fragmentation (dissolution)	Acute infl ammation, swelling, erythema, warmth (typically >2.0 °C in the affected foot). May have ligamentous laxity	Osseous periarticular fragmentation, joint subluxation/dislocation
2: Coalescence	Decreased local swelling, erythema, and warmth	Absorption of fi ne bone debris, early bone healing and periosteal new bone formation
3: Resolution	Resolved infl ammation, more stable but often deformed	Consolidation and remodeling of fracture fragments, joint arthrosis, osteophytes

 Table 15  Modifi ed Brodsky classifi cation for neuroarthropathy

Type	Location
Type 1 (most common – about 60 %)	Tarsometatarsal and naviculocuneiform joints (leads to fi xed rocker bottom deformity)
Type 2	Subtalar, talonavicular, or calcaneocuboid joints (unstable, requires long periods of immobilization)
Type 3	Tibiotalar joint (late varus or valgus deformity produces ulceration and osteomyelitis of malleoli)
Type 4	Combination of joints
Type 5	Only within the forefoot

 Classifi cation   Modifi ed Eichenholtz stages: related to the degree of warmth, swelling, and erythema. Continuum from resorption and fragmentation to bone formation and consolidation that takes 6–18 months (Table  14).

 Modifi ed Brodsky classifi cation: based on anatomic location (Table  15)

 Treatment

•      The goal is to achieve stage 3 (resolution) while maintaining alignment and ambulatory status and minimizing soft tissue breakdown.

 Initial

•      Frequent follow-up with serial radiographs and patient education on diabetic foot care.

•      Immobilization and non-weight bearing →best with serial total contact casting (the aim is to achieve homogenous pressure distribution in plantar arch through gait); can transition to custom brace (AFO or Charcot restraint orthosis walker (CROW) boot) once swelling and warmth subsides.

•      S ome studies use bisphosphonates to help reduce osteoclastic resorption and increase the osteoblastic redeposition of bone.

 Fig. 33  Patient with a rocker bottom deformity with a large plantar prominence ( a ). The patient is in the consolidated phase and therefore exostectomy can be performed ( b) . The exostectomy removes the offending prominence, but does not correct the malalignment of the joints

 Surgical

•      Stable deformity with recurrent ulcers secondary to prominence → exostectomy

(Fig.  33)  

•      Unstable/un-braceable deformity →arthrodesis with internal or external fi xation

(Fig.  34)  

•      Tendo-Achilles lengthening almost universally required

•      Amputation as salvage procedure (Fig.  35)  

 Complications

•      High complication rate (up to 70 %)

•      Infection, hardware malposition, recurrent ulceration, fracture

 Fig. 34  Patient with hindfoot Charcot and rocker bottom deformity ( a ) treated with an extended hindfoot arthrodesis ( b )

 Fig. 35 A P radiograph of patient with poorly treated diabetic neuropathy with osteomyelitis of the fi fth metatarsal ( a ). Reconstructive surgery was not possible and a Syme’s amputation was performed ( b )

 Bibliography

1. K aynak G, Birsel O, Guven MF, Ogut T. An overview of the Charcot foot pathophysiology. Diabetic Foot & Ankle 2013;4:21117 .

2. L owery NJ, Woods JB, Armstrong DG, Wukich DK. Surgical management of Charcot neuroarthropathy of the foot and ankle: a systematic review. Foot Ankle Int. 2012;33:113–21.

3.    Milne TE, Rogers JR, Kinnear EM, et al. Developing an evidence-based clinical pathway for the assessment, diagnosis and management of acute Charcot Neuro- Arthropathy: a systematic review. J Foot Ankle Res. 2013;6:30.

4.    Pinzur MS, Sammarco VJ, Wukich DK. Charcot foot: a surgical algorithm. Instr Course Lect. 2012;61:423–38.

5 . v an der Ven A, Chapman CB, Bowker JH. Charcot neuroarthropathy of the foot and ankle. J Am Acad Orthop Surg. 2009;17:562–71.