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Classifications
1. Lauge-Hansen
Cadaveric study which relates the fracture pattern to an injury mechanism
The first word in the designation refers to the foot's position at the time of injury; the second word refers to the direction of the deforming force.
"eversion" is a misnomer; it more correctly should be "external" or "lateral" rotation
Type of injury (foot position/direction Pathology of force)
Supination/adduction Transverse # of fibula/tear of collateral ligaments - vertical # medial malleolus
Supination/eversion (external 1.Disruption of the anterior tibiofibular ligament rotation) 2.Spiral oblique fracture of the distal fibula 3.Disruption of the posterior tibiofibular ligament or fracture of the posterior malleolus 4.Fracture of the medial malleolus or rupture of the deltoid ligament
Pronation/abduction 1.Transverse fracture of the medial malleolus or rupture of the deltoid ligament 2.Rupture of the syndesmotic ligaments or avulsion fracture of their insertion(s) 3.Short, horizontal, oblique fracture of the fibula above the level of the joint
Pronation/eversion 1.Transverse fracture of the medial malleolus or disruption of the deltoid ligament 2.Disruption of the anterior tibiofibular ligament 3.Short oblique fracture of the fibula above the level of the joint 4.Rupture of posterior tibiofibular ligament or avulsion fracture of the posterolateral tibia
Pronation/Dorsiflexion (Pilon) 1.Fracture of the medial malleolus 2.Fracture of the anterior margin of the tibia 3.Supramalleolar fracture of the fibula 4.Transverse fracture of the posterior tibial surface
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2. AO/ Danis-Weber [Click for Image ]
Type Pathology
A Avulsion # fibula - shear # of med malleolus
B Fibula # at level of syndesmosis - # med malleolus/ tear of deltoid ligament
C Fibula # above level of syndesmosis - medial injury + tear of ITFL and interosseous membrane
Maissoneuve's fracture
Spiral fracture of proximal fibula associated with very unstable ankle injury
Bosworth Fracture
A lesion described by Bosworth may be the cause of failure to reduce a posterior fracture-dislocation of the ankle. The distal end of the proximal fragment of the fibula may be displaced posterior to the tibia and locked by the tibia's posterolateral ridge; the bone cannot be released by manipulation because of the pull of the intact interosseous membrane. In these cases the fibula is exposed, and a periosteal elevator is used to release the bone; considerable force may be necessary. The fibular fracture then is fixed.
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Bosworth fracture with entrapment of fibular behind tibia. A, Anteroposterior view. B and C, Lateral views.
Rationale behind ORIF of ankle fractures
Tibiotalar congruency
Ramsey and Hamilton (JBJS (B) 1976) showed that a 1mm lateral shift of the talus in the ankle mortice reduces the contact area by 42% Posterior malleolus fracture >33% leads to a significant loss of tibiotalar contact DeSouza (JBJS (A) 1985) showed 90% satisfactory results could be obtained even if up to 2mm of lateral displacement was present Generally Young ORIF if >1mm displacement or >2 o talar tilt Old can accept up to 2mm of displacement Always take into account the ambulatory needs of the patient and judge treatment accordingly
Surgical technique
Standard AO fixation Interfragmentary screw and 1/3 tubular neutralisation plate for fibula and lag screw fixation for medial malleolus Syndesmosis screw is required if fibula is unstable at end of fixation (engage 3 cortices and ensure the ankle is at 90 o when inserting screw, and that the screw is not lagged) Screw needs to be removed before weight bearing can be commenced Alternative fixation for Type B fractures of the fibula is the anti-glide plate which has been shown to be biomechanically superior to a lateral plate Posterior malleolus fractures need to be fixed if there is > 25% of the articular surface involved. This is often underestimated on lateral radiographs.
Post-operative management
In studies comparing the effect of early movement vs immobilisation and weight bearing vs non-weight bearing, the conclusion is that there is no difference in the final result whichever regime is used.
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Arthritis
Incidence increases with severity of injury Degenerative changes in 10% of anatomically fixed 85% if not adequately reduced - changes apparent within 18 months Klossner "Late results of operative and non-operative treatment of severe ankle fractures" Acta Chir Scand Suppl. 293: 1-93, 1962
Prognosis
There is a reduction in the incidence of arthrosis in patients where an anatomical reduction has been achieved (Phillips et al JBJS 67A: 67-78, 1985)
Prospective trial shows higher total ankle scores in those that are operatively treated- especially so in those pts more than 50 yrs old
PILON / PLAFOND FRACTURES
(Pilon = Hammer / Plafond = Ceiling)
Reudi & Allgower Classification
(Ruedi TP, Allgower M: Clin Orthop 1979;138:105-110)
Type Pathology
I Undisplaced
II Displaced with joint incongruity
III Marked comminution with crushing of the subchondral cancellous bone
Reudi
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& Allgower classification. (Clin Orthop 1979;138:105-110)
Initial treatment
Reduction of any dislocation and covering of exposed wounds if present Assess neurovascular status Check for evidence of compartment syndrome Splint fracture which may require temporary skeletal traction
Investigations
X-ray plus CT
Timing of surgery
Type II and III - goal is to keep talus centred under the tibia while soft tissue heal over 7 to 21 days Study by M.Sirkin et al 1999, a series of pilon fractures underwent immediate external fixation and ORIF of the fibula, and formal ORIF of the tibial articular surface was performed on a delayed basis (avg. delay 12-13 days); - using this protocol, no patient that presented with a closed injury developed a full thickness skin necrosis and none required secondary soft tissue coverage The historically high rate of infection and skin necrosis following ORIF of these injuries is most related to operative timing - in the study by MJ Patterson and JD Cole (JTO 1999), all patients underwent a two staged technique for the treatment of complex pilon fracture - initially all patients underwent immediate fibular fixation and placement of a medial fixator
Surgical options
1. ORIF
Medial and anterior incisions with full thickness flaps developed at level of the periosteum. These incisions must be at least 7 cm apart to protect the viability of the intervening skin bridge Steps 1. Fibula # brought out to length and fixed with plate (DCP) 2. Tibial # exposed and reduced, held with temporary K-wires - usually 4 main fragments 3. K-wires replaced with interfragmentary screws and fixed with buttress plate 4. Closure of wounds - tension must be avoided and if present close deep layers and return later for delayed 1 o closure of skin
2. Fine wire fixation with circular frames
Using either the Ilizarov or hybrid external fixators This can be combined with limited internal fixation of the tibia using interfragmentary screws and fixation of the fibula
3. Trans-articular external fixation
Will align the tibia but will not address the central depression of the joint surface. Useful as first part of 2 -stage procedure (to allow soft tissue management & CT & planning)
Outcomes
Operative treatment of high-energy pilon fractures will take an average of 4 months to heal 75% of patients that do not develop wound complications may expect a good result Subsequent arthrodesis rate ~ 10% Bourne et al " Pilon fractures of the distal tibia" CORR 240:42-46, 1989 36% satisfactory results in intra artic fracture treated with closed means 76% satisfactory for operative treatment 32% at 4.5 yrs had undergone ankle arthrodesis for failed result
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INVESTIGATIONS NON-OPERATIVE TREATMENT OPERATIVE TREATMENT
Non-Augmented Augmented Preferred Method
Ankle Instability - Q&A - Click to view
INVESTIGATIONS [Back To Top]
1. Plain radiography: AP standing, lateral
2. EUA - Stress x-rays under anaesthesia (GA or peroneal block)
3. Arthroscopy - Cook et al found that 25% of patients arthroscoped for instability symptoms had another intra-articular pathology, usually treatable arthroscopically
NON-OPERATIVE TREATMENT [Back To Top]
Most patients with ankle instability will improve with non-operative rehabilitation.
Programme [ Orth Clin N Am.- Jan '94 ]
Phase 1: RICE (immobilze in POP for 2-3wks)
Phase 2: Strengthening of peroneal & dorsiflexor muscles, stretching of TA. Isometric exercises using furniture or rubber bands.
Phase 3: Proprioceptive training. W hen pain & swelling gone. = wobble board exercises. Progress thro functional activities- walking, running, figure-of-eight running, hopping, jumping & cutting.
In severe strains protect ankle with pneumatic brace or taping for sports for 3-6mnths.
OPERATIVE TREATMENT [Back To Top]
Prior to considerations for surgery, ensure that subtalar instability is not present
Indications:
Failed non-operative management +ve anterior drawer & talar tilt tests clinically stress x-rays tibiotalar tilt > 20 deg. anterior translation > 5mm.
Aims:
Restore functional stability.
Results:
A wide variety of reconstructive techniques have had a high degree of success.
Most authors report a good or excellent result in 80% to 85% of patients.
Techniques:
The methods of reconstruction fall into two general types: non-augmented and augmented .
Non-Augmented Methods: [Back To Top]
Brostrom originally described this technique in 1966 [ Brostrom, L. Acta Chir. Scand. Vol 132. 1966. p 551-565. ]
Brostrom recommended a mid-substance repair of the free ends of the ligaments with fine continuous sutures.
Karlsson and associates modified this by shortening of the ligaments with reinsertion onto the fibula through drill-holes.
Gould and associates modified the Brostrom technique to include repair of the lateral talocalcaneal ligament and reinforcement of the repair with suturing of the lateral extensor retinaculum to the distal aspect of the fibula. This modification is important in patients who have excessive inversion and laxity of the subtalar joint. [ See Picture .]
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Advantages:
1. The normal joint anatomy & mechanics is restored. 2. Motion of the subtalar joint is preserved. 3. There is no associated donor-site morbidity 4. No weakening of eversion strength due to sacrifice of a peroneal tendon. 5. A single, smaller, more cosmetically acceptable incision may be used.
Disadvantages:
1. Inability to achieve stability with only the weak & attenuated local tissues 2. Failure to reconstruct the calcaneofibular ligament adequately 3. Failure to address the relatively frequent problem of subtalar instability.
Augmented Methods [Back To Top]
Employ the peroneus brevis tendon to limit instability of the ankle.
Evans Watson-Jones Chrisman- Snook (preferred) Peroneus brevis tendon is anchored to the fibula, limiting inversion of the Peroneus brevis graft is brought through the fibula from ant. to post. to ankle and Evans tenodesis plus the graft is routed anteriorly through the talar neck to reconstruct ATFL. It is then brought post. and inferiorly to the calcaneus anterior reconstruct ATFL. to reconstruct CFL. talar translation indirectly, while also limiting motion of the subtalar joint.
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Preferred Operative Technique: [Back To Top]
Longitudinal incision, running just posterior to the prominence of the lateral malleolus. This incision can be extended to allow harvest of the peroneus brevis tendon if augmentation of the reconstruction is found to be necessary.
The anterior talofibular ligament and the calcaneofibular ligament are reconstructed.
The ligaments are divided just distal to their fibular attachments.
The joint is inspected and debrided as necessary.
Occasionally, one or both ligaments are avulsed from the fibula with a piece of bone. This so-called os subfibulare should be excised.
The bone at the anatomic attachment sites of the anterior talofibular and calcaneofibular ligaments is roughened, and the ligaments are reefed and reattached to the fibula with the use of drill-holes. The repair is oversewn with the proximal stump of the ligament to reinforce the repair.
During the repair, the ankle is held in neutral and the foot is held in eversion.
Augmented reconstruction with Peroneus Brevis is added if:
The anterior talofibular ligament and the calcaneofibular ligament are so disrupted and frayed that they cannot be repaired Hypermobility of the subtalar joint Previous failed reconstruction of the ankle.
Expose the peroneus brevis, while maintaining the integrity of the superior peroneal retinaculum
Anterior third of the tendon is isolated distally and split from the distal position to the musculoskeletal junction. This tendon portion is transected at its proximal aspect. A drill hole is made through the distal fibula, and the split portion of the peroneus brevis is passed through this hole. The tendon is tensioned with the foot in mild plantar flexion and eversion.
This augmentation procedure results in significant loss of eversion and inversion.
Post-operatively:
2 weeks NWBing BK cast with the ankle in neutral and the foot in eversion. At 2 weeks the patient is allowed to bear weight as tolerated. 6 weeks postop, range-of-motion exercises, progressive resistance exercises, and proprioceptive exercises are begun. At 3 months, full sports activities can be resumed with the ankle taped or braced. Most athletes should continue to use tape or a brace indefinitely during sports activities, but bracing is not routine after 3 months for most work-related activities or activities of daily living.
Bibliography:
R.A. Marder; Instructional Course Lectures 1995, Volume 44:349
Jim Barries Foot & Ankle Hyperbook
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Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Ankle Sprains
Functional Anatomy Pathomechanics Clinical
Investigations Management Chronic Ankle Instability
FUNCTIONAL ANATOMY
Lateral Ankle Ligaments
The lateral aspect of the ankle capsule is augmented by the anterior and posterior talofibular ligaments and the calcaneofibular ligament . Of these three structures, the anterior talofibular and calcaneofibular ligaments are the most important clinically.
The anterior talofibular ligament
is a thickening of the ankle capsule
extends a relatively short distance from the anterior edge of the distal part of the fibula to the talar neck, anterior to its lateral articular facet.
The orientation of the anterior talofibular ligament depends on the position of the ankle joint:
In plantarflexion, it is parallel to the long axis of the foot in dorsiflexion, it is aligned with the tibial and fibular shafts.
Strain in the anterior talofibular ligament is minimum in dorsiflexion and neutral, and it increases as the ankle is moved progressively through plantarflexion. Inversion and internal rotation moments applied to the ankle increase the strain in this ligament.
The calcaneofibular ligament
A discrete, extra-articular, round ligament that spans the ankle and subtalar joints as it courses obliquely from the inferior tip of the distal part of the fibula to insert posteriorly on the mid-lateral part of the calcaneus.
This ligament is extra-articular but it has an intimate connection to the overlying peroneal-tendon sheath.
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Strain increases as the ankle is moved from plantarflexion to dorsiflexion, with the greatest strain occurring when an inversion moment is applied with the ankle in dorsiflexion.
Because of its unique anatomic orientation, the calcaneofibular ligament also has a major role in the stabilization of the subtalar joint.
Deltoid Ligament
Consists of deep and superficial components.
The deep fibers connect the medial malleolus to the medial border of the talus, while the superficial portion has a broad, fan-shaped attachment to the navicular, the sustentaculum tali, and the posterior part of the talus.
The deep portion resists external rotation of the talus
The superficial component resists abduction of the talus.
Distal Tibiofibular Syndesmosis
The ankle mortise is stabilized by:
the anterior and posterior tibiofibular ligaments
the inferior transverse ligament
the interosseous ligament
Strain increases in the anterior and posterior tibiofibular ligaments with dorsiflexion
Strain increases in the anterior tibiofibular ligament with external rotation of the talus
PATHOMECHANICS [Back To Top]
Analysis of ankle stability under physiologic loading of the joint demonstrated that articular contact provides 100% of inversion stability and 30% of rotational stability.{12} In reality, however, inversion ankle injuries usually occur during loading or unloading of the ankle.
Lateral Ankle Ligaments
Inversion injuries.
Injury of the anterior talofibular ligament occurs first, followed by a varying degree of injury of the calcaneofibular ligament.
Black and associates chose to describe injuries to it as single if one ligament was ruptured and as double if more than one ligament were ruptured.
Singer and Jones classified injuries of the lateral ankle ligaments as stable or unstable and subdivided unstable injuries according to the degree of the talar tilt and anterior drawer that is present under stress.
CLINICAL [Back To Top]
Stress Tests
See Foot & Ankle Examination
It is difficult to be certain which ligament is being evaluated with each of the clinical tests.
The anterior drawer test [ Picture1 ][ Picture2 ]
can be performed with the patient either sitting or supine. W hen the patient is sitting, the knee should be flexed over the edge of a bench or table and the ankle should be allowed to fall into equinus . The examiner then stabilizes the distal part of the leg with one hand and applies an anterior force to the heel with the other hand, in an attempt to subluxate the talus anteriorly from beneath the tibia. This maneuver usually is not painful if the patient has an acute injury.
The modified anterior drawer test can be used when the patient is supine . W ith the knee hyperflexed , the ankle in equinus , and the foot fixed by one of the examiner's hands to the ground or table, a force is applied with the other hand on the anterior aspect of the distal part of the leg, in an attempt to translate the tibia posteriorly .
The talar tilt test
is performed with the patient seated and with the ankle and foot unsupported in 10 degrees to 20 degrees of plantarflexion . The examiner stabilizes the medial aspect of the distal part of the leg, just proximal to the medial malleolus, with one hand and applies an inversion force slowly to the hindfoot with the other hand. The lateral aspect of the talus should be palpated during inversion of the hindfoot to determine if tilting is occurring at the tibiotalar joint. Comparison with the normal ankle is helpful to detect any side-to-side difference. It has been noted that the talar tilt test may be positive only if gross instability is present.
If the anterior drawer or talar tilt test suggests abnormal laxity or if pain, swelling, and muscle spasm are present to a degree that prevents satisfactory clinical assessment, then stress radiographs are performed to measure laxity.
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INVESTIGATIONS [Back To Top]
Stress Radiographs
anterior drawer test - > 3mm of anterior excursion = rupture of the anterior talofibular ligament. (measured as the shortest distance from the posterior lip of the tibia to a constant point on the talar dome.)
talar tilt test - > 10deg. = complete rupture of both the anterior talofibular and the calcaneofibular ligaments.
Ankle Arthrography and Peroneal Tenography
Arthrography is useful for detection of tears of the lateral, medial, and syndesmotic ligaments of the ankle.
Peroneal tenography has proved to be more accurate in the diagnosis of disruption of the calcaneofibular ligament.
Magnetic Resonance Imaging
Can demonstrate accurately the normal and torn anterior talofibular and calcaneofibular ligaments
Major role in the evaluation of osteochondral lesions of the talus.
Arthroscopy
Useful in the treatment of certain conditions that may persist after an ankle injury, such as osteochondral defects of the talar dome, loose bodies, painful ossicles within the ankle ligaments, and the hypertrophied inferior border of the anteroinferior tibiofibular ligament. However, arthroscopy does not play a role in the diagnostic workup of an acute ankle injury.
MANAGEMENT [Back To Top]
The results of early mobilisation are superior to early surgical repair of acute ankle ligament injuries. The literature shows clearly that excellent results can be achieved in most patients with grade III lateral ankle ligamentous injuries by conservative treatment with a combination of immobilization and early protected mobilisation
Possible exceptions:
high level athletes with an initial talar tilt on stress radiograph of >15 degrees patients with significant disruption of both medial and lateral ligamentous structures patients with bony avulsion.
Patients with residual functional instability after conservative treatment are best treated with an anatomical repair such as a modified Brostrom technique.
See Ankle Instability
Bibliography:
Kaikkonen A, Kannus P, Jarvinen M. Surgery versus functional treatment in ankle ligament tears. A prospective study. Clin Orthop 1996;326:194-202.
R.A. Marder; Instructional Course Lectures 1995, Volume 44:349
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Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Arthritis in Children
Matt Smith, 2006
JUVENILE CHRONIC ARTHRITIS (JCA)
Approximately 1:1000 children will develop swelling of one or more joints persisting for more than 3 months with no specific cause found. 50% of these will progress to JCA.
Aetiology - unknown
Diagnostic Criteria
Age under 16 at onset Persistent arthritis in one or more joints for 6 weeks (minimum) to 3 months after other aetiologies have been ruled out. E.g. infection, malignancy, blood dyscrasias, Reiter's, hypogammaglobulinaemia
Classification by onset (Schaller)
1. Systemic onset (Still's disease)
Age: usually under 5years but can be any age Sex: <5yr female = male; >5yr female > male Fever (high with spikes up to 40 °C daily) plus one of the following
1. Maculopapular rash 2. Iridocyclitis 3. RhF +ve 4. Cervical spine involvement 5. Pericarditis
Generalised lymphadenopathy Hepatomegaly Splenomegaly Sites: knees, wrists, ankle, feet
2. Polyarticular onset
Age: any, even before age 1year! Sex: female > male 5 or more joints involved in the first 3 months Seronegative (RhFactor -ve) Sites: knees (60%), wrists, hands RhFactor +ve
Older children (9-10 years) with persistent activity and rapid joint destruction affecting mainly the hands and feet.
3. Pauciarticular (most common)
4 or less joints involved in the first 3 months Type I Younger onset <6yr, with females mainly affected. ANA +ve. Danger because of development of iridocyclitis. Presence of ANA related to eye involvement. Type II Older onset 9yr+, with males mainly affected. Association with HLA-B27.
Lab tests
HB WCC ESR RhF ANA Systemic - ++ ++ +ve +ve Polyarticular + + + -/+ve 30%+ve (in those with RhF+ve) Pauciarticular - - + or - -ve -ve (M) +ve (F)
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Radiological changes
Early features limited to periarticular osteopenia Late features occur after 6 months and include growth disturbance, chondrolysis, joint destruction and erosions. These features are more common in the RhF +ve patients.
Prognosis
80% will eventually be able to lead normal functional lives. Death can occasionally occur in the systemic onset group because of infection or the development of amyloidosis. 60% if seen within 1 year of onset will have normal function at 5 years compared with 25% of those seen after 1 year. Functional outcome is related to joint contractures and destruction.
Poor prognostic factors
Onset < 1year IgM (RhF) +ve Eye involvement Hip involvement leads to a greater functional deficit
Medical Management
Aim: to suppress activity and therefore prevent joint deformity Multidisciplinary approach with rheumatologist, PT, OT, child psychologist etc PT to help prevent joint contractures and keep healthy muscles working. Hydrotherapy affective. OT for splints and orthoses
Drug treatment
NSAID's - Ibuprofen, voltarol, naproxen etc. - Aspirin used to be the drug of choice but dangerous with children under the age of 5 years because of the risk of Reye's syndrome. Disease modifying drugs - Methotrexate: shown to be effective in polyarticular disease - Gold, penicillamine, azathioprine etc. Corticosteroids - Systemic: the use of steroids does not affect the ultimate prognosis and there are many complications related to their use, in particular growth disturbance, adrenal suppression etc. - Intra-articular/tendon sheath: can be effective in controlling flare ups
Surgical treatment
Hip - Soft tissue releases for contractures - Total joint replacement Knee - Soft tissue releases for contractures - Synovectomy - Epiphyseal stapling - Supra-condylar osteotomy - Total joint replacement (rarely needed) Foot and ankle - Orthoses - Triple fusion
Summary
Type % Joints Features Progression (%) Systemic (Still's) 25 many Fever, rash, organomegaly 25 Polyarticular: RhF -ve 15 many Mild fever 30 Polyarticular: RhF+ve 15 many Severe joint destruction 25 Pauciarticular I (F) 30 large Iridocyclitis 15 Pauciarticular II (M) 15 large Spondylitis, HLA-B27 15
Other arthritides
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Juvenile psoriatic arthropathy Ankylosing spondylitis Reiter's disease Acute rheumatic fever
FIGURE 12“1 Algorithm for evaluation of a child with joint pain and/or swelling. Chronic is considered <6 weeks. ANA, antinuclear antibody; ASO, antistreptolysin-O; PPD, tuberculin skin test; PVNS, pigmented villonodular synovitis; ESR, erythrocyte sedimentation rate; CRP, C-reactive protein.
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Lovell & Winters Paediatric Orthopaedics
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Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Arthrodeses of the Foot & Ankle
TALO-NAVICULAR ANKLE ARTHRODESIS SUBTALAR ARTHRODESIS DOUBLE ARTHRODESIS TRIPLE ARTHRODESIS ARTHROSESIS
ANKLE ARTHRODESIS [Back To Top]
Indications:
posttraumatic arthritis
infection
paralytic conditions
salvage of failed total ankle arthroplasty.
Position:
neutral dorsiflexion to 10deg. equinus
5deg. valgus
7deg. external rotation (equal to opposite side)
Techniques:
Approaches:
Approach Eponyms Description anterior longitudinal incision beginning 8 cm proximal to the ankle and ending at the medial cuneiform. Blair, Morris, Anterior longitudinal Dissect the interval between the extensor hallucis longus and extensor digitorum longus, and retract the Hand, Dunn neurovascular bundle medially. Incise the capsule and periosteum in line with the skin incision. Anterior Transverse Charnley see below Oblique Ollier, transverse incision extending from the talonavicular joint anteriorly to 1 cm below the lateral malleolus Transmalleolar - 10 cm longitudinal incision over the subcutaneous surface of the distal fibula, ending 1.3 cm distal to the Horwitz; Adams Lateral lateral malleolus. After subperiosteally exposing the fibula, osteotomize it 7.5 to 10 cm from its distal end Anteromedial incision; Use an osteotome to remove a longitudinal wedge of bone about 10 cm long and 1 to Transmalleolar - Stewart & Harley 1.5 cm wide from the medial tibia including the inner third of the medial malleolus; also include the medial Medial side of the body of the talus. Posterior Campbell allows for TA lengthening also. Arthroscopic
Fixation Methods:
Charnley External compression clamp Blair posterior tibial cancellous screw into the talar head Baciu and Filibiu Dowel technique
Technique (Charnley):
Transverse incision across the anterior aspect of the ankle, extending from 1 cm proximal to the tip of the medial malleolus to 1 cm proximal to the tip of the lateral malleolus. Curve the incision distally at its middle so that subsequent sectioning of the extensor tendons is not directly beneath the skin incision. Raise the skin and subcutaneous fat as a proximally based flap to expose the extensor tendons.
Between sutures, divide the tendons of the tibialis anterior, extensor hallucis longus, peroneus tertius, and extensor digitorum communis muscles. Treat the extensor digitorum communis tendon as a unit, but do not include the peroneus tertius.
Divide and ligate the anterior tibial vessels, section the deep branch of the peroneal nerve, and incise the joint capsule transversely.
Subperiosteally expose the distal tibia and the medial and lateral malleoli.
Divide the deltoid and lateral ligaments of the ankle, then plantarflex the foot.
Partially divide the distal ends of the tibia and fibula with a power saw. Complete the bony division posteriorly with an osteotome.
Place the foot in the desired position and remove a section of bone about 6 mm thick from the superior surface of the talus.
Pass a heavy Steinmann pin through the open wound and through the anterior portion of the body of the talus so that its pull will counterbalance the pull of the tendo calcaneus.
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Do not violate the subtalar joint.
Apply the Charnley clamps to the distal pin and, using them as guides, insert a proximal pin through the distal tibia. Tighten the clamps and correct any rotatory deformity.
Repair the divided extensor tendons and close the wound. Apply a short leg cast
.
Compression arthrodesis of ankle. A, Distal pin should be inserted anterior to transverse axis of body of talus to counteract pull of tendo calcaneus. B, If pin is inserted through or posterior to axis, force of tendo calcaneus will separate osseous surfaces anteriorly. C, Osseous surfaces should not be flush anteriorly as shown; rather, talus should be displaced as far posteriorly as possible to preserve prominence of heel. (Modified from Charnley J: J Bone Joint Surg 33-B:180, 1951.)
SUBTALAR ARTHRODESIS [Back To Top]
For isolated subtalar arthrosis
Position = 5deg. valgus; too much valgus causes lateral impingement. Varus alignment locks the midtarsal joint.
Mann et al 1998, 48 subtalar fusions were performed w/ 93% satisfactory results.
Technique:
Ollier incision
joint capsule of talocalcaneal joint is incised & laminar spreader is inserted into sinus tarsi to expose entire subtalar articulation; - excise articular cartilage & subchondral bone. Resect according to correction required.
Insert Bone graft.
Compression screws can be passed proximal to distal (talar neck to calcaneus) or distal to proximal.
TALO-NAVICULAR ARTHRODESIS [Back To Top]
Results in reduced motion of the calcaneo-cuboid joint & subtalar joint.
Best for sedentary patients.
DOUBLE ARTHRODESIS [Back To Top]
= Both midtarsal joints.
Similar to Triple, since it restricts subtalar motion.
TRIPLE ARTHRODESIS [Back To Top]
stiffness following islolated arthrodesis:
subtalar arthrodesis limits talonavicular motion to about 26%, and limits calcaneocuboid motion to about 56%;
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talonavicular fusion will limit subtalar motion to about 9% so that there will only be about 2 deg of motion;
calcaneocuboid fusion decreases talonavicular motion down to 67% and subtalar motion down to 92%;
outcomes:
CL. Saltzman MD et al JBJS 1999, 67 feet in 57 patients who underwent triple arthrodesis were evaluated at an average of 25 and 44 years following surgery; - indications for surgery: polio (55%), CMT (9%), spinal cord abnormalities (6%), CP (4%), Guillain-BarrÃÆ'© syndrome (1%); - pseudarthrosis occurred in thirteen feet - 55 % of feet were painful at 44 years and all showed some degenerative changes; - despite the foot pain and radiographic signs of degenerative changes, 95% of patients were satisfied with results of the procedure; - the authors note that the indications for triple arthrodesis have change during the past few decades (less often for neuromuscular disorders and more often for severe degenerative arthritis or severe flat foot), and note that the prevalence of pseudoarthrosis is less frequent;
RF Pell MD et al. Jan. 2000. Vol 82-A. p 47., the authors followed 183 triple arthrodeses procedure over an average of 5.7 years; - authors noted high correlation between patient satisfaction and post-operative foot alignment; - 91% of patients indicated that they would have the procedure again, under similar circumstances; - postoperative ankle arthritis (clinical and radiographic) was common but did not seem to affect patient satisfaction; - authors noted that feet w/ post-traumatic changes (25) required the least correction where as the 22 feet w/ RA and the 70 feet w/ tibialis posterior rupture needed the most correction; - average time to fusion was 10.7 weeks;
contra-indications:
contra-indicated in young children (less than 10-12 yrs) because the procedure limits foot growth
Ollier Incision:
begins over dorsolateral aspect of the talonavicular joint, - continue incision obliquely & inferoposteriorly to end about 1 inch inferior to lateral malleolus; - superiorly expose long extensor tendons to toes and retract them medially, w/o opening their sheaths; - inferiorly expose the peroneal tendons and retract them inferiorly; - divide origin of EDB muscle & retract it distally; - this exposes sinus tarsi;
NV bundle enters approx 1.5 cm medial & distal to anterior process of the calcaneus;
Continue dissection to cuboid and distal calcaneus thru deep portion of peroneus sheath;
Identify, posterior facet of the subtalar joint;
Identify the calcaneocuboid joint which is found just distal to the anterior beak of the calcaneous;
The talo-navicular joint lies superior and medial to calcaneocuboid joint;
Identify neck of the talus, and elevate the extensor tendons off the neck;
Procedure:
Incise the capsules of the talonavicular, calcaneocuboid, and subtalar joints circumferentially to obtain as much mobility as possible. If this release allows the foot to be placed in a normal position, removal of large bony wedges is not required. If correction is impossible after soft tissue release, appropriate bony wedges are removed
Identify the anterior articular process of the calcaneus, and excise it at the level of the floor of the sinus tarsi for better exposure of all joints. To make this osteotomy, use an osteotome placed parallel to the plantar surface of the foot; preserve the bone for grafting.
Next, with an osteotome, remove the articular surfaces of the calcaneocuboid joint to expose cancellous bone. Remove an equal amount from both bones unless wedge correction of a bony deformity is required.
Next remove the distal portion of the head of the talus with Ú ¼-inch and Ú ½-inch straight and curved osteotomes. Remove only enough bone to expose the cancellous bone of the talar head unless a medial wedge is required to correct a fixed deformity. A small lamina spreader can be inserted for better exposure.
A second medial incision may be necessary to expose the most medial portion of the talonavicular joint. Beginning at tip of medial malleolus and in line w/ medial border of foot, extending 6 to 7 cm toward great toe longitudinally & ending between anterior & posterior tibial tendons
Remove the proximal articular surface and subchondral bone of the navicular, and shape and roughen the surfaces for a snug fit with the talus. Excise the articular surfaces of the sustentaculum tali and the anterior facet of the subtalar joint.
Now approach the subtalar joint and completely remove its articular surfaces. For better exposure of the posterior portion, use the small lamina spreader to expose the subtalar joint. Remove appropriate wedges from this joint if necessary; otherwise, make the joint resections parallel to the articular surfaces.
Cut the removed bone into small pieces to be used for bone grafting. Place most of the bone graft around the talonavicular joint and in the depth of the sinus tarsi.
Smooth Steinmann pins, screws, staples or Kirschner wires may be used for internal fixation.
Obtain intraoperative roentgenograms to ensure correct positioning of the foot and the pins.
Close the muscle pedicle of the extensor digitorum brevis over the sinus tarsi to decrease the dead space. Close the wound over a suction drain, and apply a well-padded, long leg cast with the knee in 45 degrees of flexion. If wires or pins are used for internal fixation, apply a short leg cast.
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Bibliography:
Jim Barrie's Foot & Ankle Hyperbook
Campbell's Operative Orthopaedics
Orthopaedic Knowledge Update - Speciality Series - Foot & Ankle
Sponsored Links www.ebimedical.com
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Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Arthroscopy of the Foot & Ankle
Indications Positioning & Distraction Portals Technique Complications
Indications [Back To Top]
Indications for Diagnostic Ankle Arthroscopy Indications for Operative Ankle Arthroscopy 1. Chondral lesions 2. Osteoarthritis 1. Persistent post-traumatic disorders 3. Impingement exostosis 2. Arthritis 4. Meniscoid lesions of the ankle 3. Non-specific synovitis 5. Chronic lateral instability of the lateral collateral ligaments 4. Osteochondritis dessicans and osteonecrosis of the talus 6. Septic arthritis 5. Joint evaluation prior to some ligamentous reconstruction procedures 7. Rheumatoid synovitis 8. Post-traumatic synovial impingement
Positioning & Distraction [Back To Top]
A good joint distraction allows up to 5 to 10mm of joint opening. With increased joint opening there is less chance for operative complications and lessens the need for accessory portals.
Several positioning alternatives exist:
supine position supine with the leg hanging dependent over the edge of the table supine with a bolster under the hip to internally rotate the ankle into a neutral position.
Distraction methods may either be non-invasive or invasive:
Non-invasive methods applies force by traction onto the skin. A sterile commercially produced strap is applied with one loop at the heel and one loop over the dorsum of the midfoot. This strap is then attached using a velcro strap to a sterile bar attached to the operative table. The velcro strap allows easy variation of distraction force during the case.
Invasive distraction involves pins placed proximal and distal to the joint. This can cause direct neurovascular injury & traction nerve injury.
Arthroscopic portals [Back To Top]
There are 5 portals developed for arthroscopy of the ankle joint.
1. Antero-medial portal
First portal as least dangerous
Site: Just medial to the tibialis anterior tendon, and just lateral to the course of the saphenous vein and nerve as they pass across the joint line.
Danger: tibialis anterior tendon, saphenous vein, & saphenous nerve.
View:
tip of the medial malleolus deltoid ligament antero-medial synovial wal the medial tibio-talar articulation most of the articular facet on the medial aspect of the talus the medial shoulder of the talus and tibia anterior half of the talar dome and the anterior synovial wall
2. Anterolateral portal
Site:lateral to the peroneus tertius tendon & EDL.
Danger: terminal branches of the superficial peroneal nerve. By flexing and inverting the foot it is possible to put the superficial peroneal nerve under tension and visualise it subcutaneously so as to avoid its injury.
View:
tip of the lateral malleolus anterior talo-fibular ligament occasionally the posterior talo-fibular ligament the talo-fibular joint the antero-lateral synovial wall portions of the facet on the lateral aspects of the talus the distal tibio-fibular articulation the tibio-fibular synovial fringe and recess.
3. Antero-central portal
Rarely used.
Site: just lateral to EHL tendon
Danger: anterior tibial artery & the deep peroneal nerve. EHL & EDL. Terminal branches of the superficial peroneal nerve.
View: anterior aspect of the ankle joint can be viewed.
4. Posterolateral portal
Site: 2cm above the tip of the lateral malleolus, lateral to the Achilles tendon, and posterior to the short saphenous vein and sural nerve.
Danger: the above structures.
View: the posterior joint cavity
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the tip of the lateral malleolus the posterior talo-fibular ligament the talo-fibular articulation the postero-inferior tibio-fibular ligament posterior aspect of the tibio-fibular articulation posterior aspect of the distal tibia the trochlear surface of the talus the posterior synovial wall medial malleolus, and the posterior aspect of the deltoid ligament
5. Postero-medial portal
less commonly used due to the close proximity of the posterior tibial artery and nerve
Transmalleolar portals have also been described.
Technique of diagnostic arthroscopy [Back To Top]
Mark landmarks with marking pen: tibialis anterior tendon, dorsalis pedis artery, EHL, EDL, peroneal tendons.
Inject 50ml saline into the joint.
Use a 2.7mm arthroscope.
Systematic Examination:
Visualization from the anteromedial portal: - deltoid ligament; - medial malleolus; - medial gutter (medial talomalleolar joint); - talar dome (osteochondral lesions) - anterior gutter; - tibiofibular joint: - synovitis, fibrocartilagenous protrusion; - posterior tib-fib ligament; - anterior tib-fib ligament; - anterior talofibular ligament (arising from the tip of the fibula);
Examination is made first of the central aspect of the tibio-talar joint, visualising the talus and the distal aspect of the tibia.
Plantarflexion of the foot allows the surgeon to pass the obturator over the talar dome into the posterior compartment allowing visualisation of the postero-medial and postero-lateral aspects of the joint.
The scope can then be rotated 180deg. allowing the surgeon to change the field of view and visualise the inferior aspect of the distal tibio-fibular joint proximally and intra-capsularly, as well as the talar neck and anterior insertion of the capsule distally
Anterior 8 point system - from Stoller, MRI Arthroscopy & Anatomy of the Joints Posterior 7 point system - from Stoller, MRI Arthroscopy & Anatomy of the Joints
Arthroscopic Views [click on Image]
Complications of ankle arthroscopy [Back To Top]
1. Damage to tendons or neurovascular structures (see portals above)
2. Instrument breakage
3. Neurological secondary to the use of distraction pins
4. Infection is rare
Guhl (1988) reported 13 cases of complications in 131 surgery cases. Complications arising from Guhl's report included one broken pin, two cases of infection, two misdiagnoses, one scarring of the peroneal tendon from the distraction device, four nerve injuries, and three painful scars (complication rate of 7.6%). Other studies have show a 15% complication rate (Martin et al, 1989), and a 17% complication rate (Barber, Click, and Britt, 1990).
Soft tissue infection over a joint is a contraindication to arthroscopy.
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Bibliography:
Ankle Arthroscopy by David Chia
Schneider et al. Arthroscopy of the ankle joint
Stoller - MRI, Arthroscopy & Surgical Anatomy of the Joints. Lipincott Williams.
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Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Bibliography
The following Websites & Books were used in compiling the Orthoteer Summaries: ( Bold= Essential)
Books:
Review of Orthopaedics - Mark Miller
Campbells Operative Orthopedics - Terry Canale
Principles of Orthopaedic Practice - Dee & Hurst
Apley
Orthopaedic Knowledge Updates
Websites:
South Australian Orthopaedic Registrars' Notebook
Entrez-PubMed
University of Washington Radiology Webserver
Journals:
Current Orthopaedics
The Journal of Bone and Joint Surgery
BASIC SCIENCE
Sciences Basic to Orthopaedics - Sean Hughes & Ian McCarthy; WB Saunders, 1998.
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The Developing Human - Moore & Persuad
duPont PedOrtho Education Modules Resident Education Home Page, ALFRED I. DUPONT INSTITUTE British Society for Children's Orthopaedic Surgery
McGloughlin & Mann.Surgery of the Foot and Ankle. 1999. Mosby.
Barton. The Upper Limb & Hand. 1999. Electronic Textbook of Hand Surgery eRadius - International Distal Radius Fracture Study Group Copeland. Operative Shoulder Surgery. 1995. Churchill Livingstone.
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Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Biomechanics of the Foot & Ankle
Ankle Joint Range of Motion Stability Kinetics Foot
Gait Muscle Activity Load Transmission Subtalar Joint Midtarsal Joints
TMTJ's Fat Pads Summary
ANKLE JOINT - Biomechanics
Hinged synovial jt btn tib, fib & talus Tibiotalar, fibulotalar & dist. Tibiofibular artics Intrinsically stable with additional ligamentous stability most imp are: - ant inf talofib lig - med (deltoid) lig - lat lig
Composite joint of:
1. Syndesmosis between the distal tibia and fibula 2. A diarthrodial mortise between the distal tibia, fibula, and talus.
The Ankle Mortise is a uniplanar hinge joint .
The axes of movement are along a line just distal to the palpated tips of the medial and lateral malleoli
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In the horizontal plane, the ankle axis projects from anteromedial to posterolateral
In the coronal plane, from medial-cephalad to lateral-caudad.
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Ankle jt motion:
Mostly in sagittal plane ROM varies widely, usu around 45o 10-20o dorsiflexion 25-35o plantarflexion walking req's approx 10-15o dorsi & 15-20o plantar
Dorsiflexion of the ankle results in eversion of the foot, plantarflexion in inversion.
The axes of rotation change depending on whether the ankle is in dorsiflexion or plantarflexion. No true single joint axis exists. These instant centers vary depending on the joint position, different individuals, direction of motion & weightbearing status.
The distal fibula:
static buttress for the talus the fibula bears one sixth of the weight transmitted downward from the knee during static weightbearing. The distal fibula moves distally (average, 2.4 mm) when moving from nonweightbearing to weightbearing. (pulled distally by the active contraction of the flexors of the foot). This distal movement may increase ankle stability by deepening the mortise and by tightening the interosseous membrane, thereby pulling the fibula medially.
Trochlea of the talus:
Wedge-shaped, with the mediolateral width greater anteriorly than posteriorly.
Ankle Range of Motion: [Back To Top]
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Ankle Joint Stability [Back To Top]
Ankle stabilisers:
1. Shape of talus 2. interosseous membrane 3. Ant. & post. talofibular ligaments 4. calcaneofibular ligament 5. Deltoid ligament 6. Ankle joint capsule
Because the talus narrows posteriorly, in plantarflexion the tautness of the ligaments provide most of the stability.
Ankle Kinetics [Back To Top]
Ankle has a larger weight-bearing surface area than the hip & knee joints. Therefore, lower loads per unit area (stresses) can be transmitted. Also, a small amount of articular incongruity causes relatively larger stresses. Thus the need for perfect anatomical articular reconstruction following fractures & the higher failure of ankle arthroplasties.
Ankle free body diagram for calculating Joint Reaction Force (J in diagram):
The Ground reaction force (W) is known [BW x g]; The direction of the Achilles Tendon force (A) & W are known. Therefore the magnitude of J & A can be calculated.
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One sixth of the load of the leg is borne by the fibula.
The compressive force across the ankle joint is produced by the contraction of gastrocnemius & soleus through the Achilles tendon. Only 20% is contributed by the Anterior tibial muscle group during early stance phase.
FOOT [Back To Top]
26 bones, 57 synovial jts & numerous ligs/tendons Adapts to surfaces, distribute loads, avoids injury Hindfoot - talus & calcaneus Midfoot - Cuboid, cuneiforms & navicular Forefoot - Metatarsals & phalanges
Subtalar jt:
Artic btn talus & calcaneus Oblique axis @ 42 o to plantar surface & 16 o medial to midline of the foot
20 o inversion & 5 o eversion
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Walking req's 6 o motion
GAIT & FOOT MOTION [Back To Top]
The subtalar and transverse tarsal joints can be modelled as in Figure 6 .
The subtalar joint functions as a mitered hinge, and the transverse tarsal joint as a pivot.
External rotation of the leg causes inversion of the heel and supination of the forefoot. - from heel strike to foot-flat during the stance phase of gait
Internal rotation of the leg causes eversion of the heel and pronation of the forefoot. - occurs from foot-flat to toe-off.
Muscle Activity during Standing [Back To Top]
Active supports for the longitudinal arch:
Tibialis posterior - flexes the midfoot through it's broad insertion into several tarsal bones. Supports the talar head & neck through a sling-like action. Peroneus Longus Tibialis Anterior - also decelerates the foot as it strikes the ground preventing slapping of the foot on the ground.
Muscle Activity during Gait [Back To Top]
From heel strike to foot flat, the anterior compartment of the leg (tibialis anterior) contracts eccentrically, thus lengthening, while the gastroc soleus is quiescent.
During foot flat the gastroc soleus complex is contracting eccentrically, and the anterior tibialis is quiet.
During heel rise the gastroc soleus complex contracts concentrically, and the tibialis anterior (anterior compartment) is quiescent.
From heel strike to foot flat there is progressive eversion of the subtalar joint, which unlocks the transverse tarsal joint and
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causes internal rotation of the tibia.
Heel rise is the opposite.
The Achilles tendon provides the motor for the heel rise phase of gait.
Mechanisms of Running-The difference between running and the normal walking gait cycle is that at one point during the running cycle the person is airborne and not bearing weight on either leg. The forces on heel strike are thus larger.
SUBTALAR JOINT [Back To Top]
Motion between talus and calcaneus consists of rotation about a single oblique axis. Subtalar motion has been modeled as screw-like with calcaneal inversion (varus) & forward translation.
The axis of subtalar rotation passes in the plantar & lateral direction from the neck of the talus through the sinus tarsi to the lateral wall of the calcaneus.
Subtalar rotation = ~45 degrees.
MIDTARSAL JOINTS (Chopart's joint) [Back To Top]
The midtarsal articulation consists of the calcaneocuboid joint and the talonavicular joint. With varus / inversion of the hindfoot (subtalar joint), the midtarsal joints are not parallel, and this joint (Chopart's joint) is locked. See Figure 8. As the subtalar joint everts, these joints (Chopart's joint) become parallel and allow motion [see Figure 8] . This flexibility is important during the heel strike and the subsequent stance phase of gait, when the hindfoot is in valgus; it allows pronation of the foot, absorbing some of the energy from heel strike.
TARSO-METATARSAL JOINTS (Lisfranc's joints) [Back To Top]
A Gliding motion occurs at the TMTJs during gait.
The 2nd TMTJ is recessed into the midfoot, forming a key-like lock with the middle cuneiform. It is more stable than all the other TMTJs. This is important during the toe-off stage of the stance phase, since the 2nd TMTJ bears the majority of the transmitted load through the forefoot.
FAT PADS
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Metatarsal Fat Pad [Back To Top]
When the toes extend beyond 50deg. the MT fat pad is locked under the MT heads - occurs during toe-off.
Heel pad
To absorb the energy of the ground reaction force at heel strike, the skin and soft tissues are compartmentalized into a unique shock-absorbing mechanism. Under the thick skin are slanted spiral chambers that contain adipose tissue beneath the calcaneus. These chambers are so placed as to take their deep origin from the calcaneus and, passing posteriorly and curving laterally, to attach to the skin. A second spiral system, located more superficial to the calcaneus, converges on itself as it spirals laterally. The two systems represent a right-handed spiral that opens laterally beneath the calcaneus and a second spiral that closes as it passes laterally, superficial to the first (Figure 9). The cushioning provided by this system accounts for the ability of the resist repeated loads for long periods, as hiking.
The arched structure of the foot:
5 longitudinal arches from calcaneus along the rays supported by plantar fascia from calc to plantar aspect of prox phalanges - heavy ligamentous structure - The plantar fascia originates on the plantar calcaneus and passes distally, inserting into the base of the flexor mechanism of the toes at the proximal phalanges. - It is primarily a medial structure. - only elongates slightly on loading - fcts as cable btn heel & toes & shock absorber
- during standing , bones of long arch & PF act as truss - PF prevents force acting down from collapsing long arch - When toes dorsiflex, PF is put under tension & long arch is raised = windlass action & basis of jack's wind up test - This is a passive function during heel rise and serves to bring about some inversion of the calcaneus, which results in some external rotation of the tibia and locking of the midtarsal joint, thereby providing a rigid lever arm. - Bones of foot are thus held together & fct as single unit - Above = truss model “ see beam below 1 transverse arch
Note Beam model:
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The biomechanics of Reciprocal Gait:
Manner or style of locomotion Reciprocal “ LL used alternatively to provide support & propulsion Others are swing-thru (swing-to & drag-to) & swivel
Gait analysis:
Clinical examination of gait pattern Many parameters, techniques & purposes Photography & video may be used - subjective Gait laboratories give quantitative data using - Motion analysis systems - Force plates - Electromyography equipment
Gait Cycle:
One stride, 2 steps (one by each LL) Stance phase (foot in contact with ground) & swing phase Double support when both feet in contact with ground ↑ speed & ↓ double supp. Until no double supp = running events during gait cycle: - heel contact - flat foot - heel off - toe off - mid swing abnormal gait = disturbance in above i.e. foot drop toe contact B4 heel
Range of motion:
varies with person, speed, ground surface & footwear hip = 5-10 ext to 30-40 flex knee = <5 ext to 70 flex
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ankle = 15 plant (peak @ flat foot & toe off) to 10 dorsi (peak heel off)
Ground Reaction forces:
Newton's 3rd = + & opp force by ground to ody wt Measured with force plate/platform GRF mag & direction varies during stance phase Ploting vectors of GRF during gait cycle gives the typical butterfly diagram (fig 42) Plotting the vertical GRF against time for both feet gives double hump (fig 43) First peak is due to deceleration of body mass at heel strike Second peak is due to pushing off at toe off
Joint forces & Moments:
Can be calculated using biomechanics & data collected in gait lab Position measured using motion analysis system External forces & moments on foot measured using force plate Weight of each body seg using anthropometric data Muscle & lig forces estimated using electromyography & mathematical models
Foot Pressure Measurement
Foot provides support, balance & propulsion Constantly changing loading pattern as COM moves relative to COP Foot pressure divides into 2 vectors vertical & horiz (shear) Shear divides into 2 components AP (y-axis) & ML (x-axis) Normal foot has normal pressure distribution “ abnormal & it changes Info about foot relates to rest of body
Load Transmission in the Foot [Back To Top]
All the metatarsal heads are in contact with the ground during stance.
50% of the load is borne by the MT heads & 50% by the heel. The load on the 1st MT head is twice that on each of the other MT heads.
During the stance phase the center of load progresses forward along the foot rapidly to the great toe. As the foot progresses to toe-off the load is transmitted mainly through the 2nd metatarsal head (since it is longer than the others).
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Foot Pressure systems:
Barefoot pressure measuring devices - Measure pressure btn plantar surface of foot & ground - Dynamic Pedobarograph (DPBG) In-shoe pressure measurement - Measure press btn plantar surface of foot & inner sole of shoe - GaitScan (GS) Sole-shoe pressure transducers - Measure pressure btn sole of shoe & ground Shear or vert & horiz pressure measurers
Barefoot Measurement systems:
Foot pressure / impression
1882 “ Beely “ plaster of paris - postulated highest pressure → deepest imprint - didn't work but set out principles - now similar systems with indentable foam “ FootPrint - other systems have been developed
Semi-quantitative systems to measure plantar loading
Kinetograph (1935) - Properties of rubber “ ability to deform under load - Ridged (2) rubber sheet & inkpad → imprint on paper - Series of parallel lines with width α pressure - Deformable mat technique Harris & Beath mat (1947) - Improved on kinetograph to incorporate 3 sets of ridges - Increased density of ink in high pressure areas - Subjective as determined by amount of ink applied methods of calibration have been described Podotrack (PDT) - Uses chemical reaction of special carbon paper instead of ink - No ink mat req'd - Standard & uniform ink layer within the carbon paper - Can be calibrated using plastic card provided - Easily portable sheets fixed to floor with adhesive strips - Sheets = antistatic, anti-allergic, inexpensive & easy to use - Reproducible results Grieve (1980) - Aluminium foil sandwiched btn foam & rubber mat - Upper surface of rubber mat embossed with pyramidal lattice - Pressure on the foam causes aluminium foil to deform - Depth of penetration is α load applied
Development of Quantitative systems:
Barograph (Elftman 1934) - Rubber mat with pyramidal projections resting of glass plate - Light & cine-camera underneath to film contact area
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- Opaque white fluid enhanced image which appears as dots or squares - Few results prob due to calibration & data collection problems Plastic Pedobarograph (Barnett 1954) - Recorded force distribution via 640 Perspex rods in a Perspex jacket - Filmed changes at 30 frames/sec - Produced 2d graph DPBG (started in 1957) - Started as PVC sheet in near contact with optically clear glass plate illuminated by lights around the edge - As deformable film comes into contact with the glass, light is scattered - Changes in the normal internal reflection are recorded with a monochrome camera & processed electronically to give pressure contours - More recently interfaced with microcomputer → quality colour images Many other systems developed along the way incorporating Optical filters, FP's, liquid crystal sheets of cholesteric crystals (colour changes), & high resolution pressure mats Musgrave footprint (Musgrave Park Hosp, Belfast 1985) - Initially foam rubber transducers - Later Force Sensitive Resistors (FSR) - 2048 sensors connected to PC via ADC with powerful usable software - calibrated statically & dynamically using hydraulic/pneumatic probe EMED (Novel, Germany 1980) - Barefoot & in-shoe - Various products with various sensors - Based on Nicol capacitance pressure mat platform Podinamic Sensor (Italy 1990) - Capable of capturing multiple steps
In-Shoe Measurement systems:
Instrumented insoles to register foot loading in normal & sporting activities Measure foot-shoe interface Can record successive steps Results useful for clinical assessment, shoe design, orthosis design, pre & post-op assessment Many available in-shoe transducers: Capacitive - 1960's onwards - piezoelectric discs - capacitive pressure pads - sponge rubber & copper foils - Computer DynoGraphy (CDG) & EMED are have commercially available systems “ can be expensive Strain Gauge - Silicon beam in PVC - Beryllium Copper cantilever system - Not been particularly effective Force Sensing Resistors - Thin & flexible - Electrodynogram (EDG), data logger around waist → transferred to PC - Podinamic in-sole system (similar to barefoot system) - Tekscan (Scholl) - FSR's require a power source as they are active transducers - Also difficult to calibrate due to wear & environment sensitivity Piezoelectric - Polyvinylidene fluoride (PVDF) = piezoelectric film - No external source of voltage req'd - Inherent charge from loading collected via electrodes - Converted to voltage α pressure applied - Gaitscan uses this system - PVDF is long chain semi-crystalline polymer with high level piezo activity - Easy to cut - Similar impedance to human tissue - Stable & resistant to moisture & most chemicals Microcapsule - Miniature transducers incorporating a colour indication device Projection devices
Shear Pressure:
Important variable remains a mystery No reliable system to measure it in-shoe Magneto-resistive principle has been tried
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Difficulties arise in locating the required points such as metatarsal heads However Dundee have demonstrated 95% reliability
Sole-Shoe Measurement systems:
Device for measuring sole to shoe pressures Measuring device is actually placed on the sole of the shoe (?outside) Information used in shoe design
The Ideal Foot Pressure System:
Must be supported by reliable software, hardware & sensors (transducers) Should take into account - Hygiene - Comfort - Repeatability - Linearity of transducers - Reproducibility of data in different formats - Reliable technical support - Ease of use and cost
Dundee University Foot Pressure Analysis Laboratory (DUFPAL):
Uses 3 systems “ DPBG, GS & PDT GS is synchronised in real time with bilateral 4-channel dynamic EMG The following activities are being carried out both clinically & research: - Barefoot pressure measurement - In-shoe pressure measurement - Dynamic EMG - Dynamic 3d goniometry - Anatomical & physiological foot assessment - CAD/CAM - Orthotic design & manufacturing - Other investigations with other departments - Foot & ankle biomechanics - Lower limb alignment - Foot & ankle proprioception
Dynamic Pedobarograph (DPBG):
Pressure platform & active measurement area large enough for any foot Measurement & pressure resolutions 4x more precise than any other system Adjustable sampling rate NOT portable “ walkway 5.5m long & 1.25m wide 1 footprint captured per run provides graphical information on - maximum pressure - average pressure & vertical force against time - overall loading of foot (contour maps) - specific load and time graphs for 16 areas per foot Basic system - Glass plate surrounded by strip lights - Top surface covered by opaque reflective deformable film - Light totally internally reflected btn top & bottom of glass due to light travelling from high to low refractive index medium (glass to air) - When deformable sheet touches glass, due to higher refractive index of plastic (comp to air) some light escapes - The amount of light scattered back from the deformable sheet is α to the pressure. - The scattered light is reflected via a mirror positioned @ 45o under the glass to a video camera connected to a computer - Data is stored analysed & displayed
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Early PVC systems had 10-15% error Now eliminated & accuracy & calibration improved with modrn computers Measures in kgcm-2 (pressure) & Kg (force) rather than SI units of Nm-2 & N
GaitScan system (GS):
8 discrete piezoelectric transducers per insole PVDF copolymer film sandwiched btn copper sheet & circuit board Embedded in customised insole of rubberised cork & leather
Transducers calibrated individually with dynamic jig Small lightweight pre-amplifier on ankle connected to console by trailing lead Connected to PC via ADC Captures 20 sec of data at a time
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1 of 1 10/6/2007 10:54 AM BOFSS Syllabus for FRCS (Tr & Orth) http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. BOFSS Syllabus for FRCS (Tr & Orth)
from the BRITISH ORTHOPAEDIC FOOT SURGERY SOCIETY
The British Orthopaedic Foot Surgery Society recommends the following syllabus of study in foot and ankle surgery for the FRCSOrth examination. This syllabus has been recommended to the Intercollegiate Board in Orthopaedic Surgery. We do not recommend at what stage of training any particular part of the syllabus should be studied: this will depend on your clinical attachments and your local training programme. Thorough knowledge of history taking and clinical examination.
Investigation of foot problems including:
Plain radiological investigations. Complex scanning including ultrasound, CT, MRI and radioisotope bone scanning. Invasive investigation such as arthrography. Principles of gait analysis applied to the foot and ankle, including foot pressure studies.
Swellings and Tumours about the foot and ankle. Surgical approaches to the foot and ankle. Reflex sympathetic dystrophy. Principles of ankle arthroscopy. Management of ingrown toenails. Conservative management of the foot and ankle including:
The principles and use of orthoses Shoe wear modifications Appliances Principles and variety of prostheses following amputation Principal techniques of physiotherapy as applied to the foot and ankle The role of manipulation and injection techniques
TRAUMA
The classification, management and outcomes following injuries to the: Ankle Os calcis Talus and peritalar soft tissues Tarsal bones Tarso-metatarsal joint Forefoot and toes Tendo Achilles injuries, recognition and treatment Investigation and management of lateral ligament injuries of the ankle
PAEDIATRIC FOOT PROBLEMS INCLUDING:
Congenital talipes equinovarus Congenital vertical talus Metatarsus varus and adductus Acquired neuromuscular disorders Disorders of deletion or duplication Disorders of growth Osteochondroses Tarsal coalitions Accessory navicular Inflammatory disorders. Acute and chronic infective disorders of the foot in childhood.
ELECTIVE ADULT FOOT DISORDERS
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Indications, techniques and outcomes of the surgical treatment of pain and deformity of the first ray Lesser toe and ray disorders and the investigation and treatment of metatarsalgia The pathogenesis of deformities of the mid and hindfoot including congenital, post traumatic, neurological and degenerative conditions The principles of correction of deformities of the ankle, hindfoot and midfoot by soft tissue and/or bony procedures such as fusion or osteotomy The pathology, prevalence and classification of posterior tibial tendon ruptures and their management The diabetic foot, pathology, conservative treatment and surgical management including neuropathic ulceration, Charcot deformities and amputations The rheumatoid foot, pathology, conservative treatments and surgical management of forefoot, hindfoot and ankle disease
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Classification
Type 1 - Enlargement of the 5th MT head
Type 2 - Lateral bowing of 5th MT
Type 3 - Widened 4-5 IMT angle
Surgical Treatment
If conservative treatment fails.
1. Chevron osteotomy for Type 1
'L' shaped capsule incision.
60deg. angle.
fix with K-wire.
2.
Midshaft oblique osteotomy for Types 2 & 3
Oblique osteotomy directed in a dorsal proximal to distal plantar direction.
Distal fragment then rotated medially.
Fix with mini-fragment screw.
(similar to Scarf procedure)
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1 of 1 10/6/2007 10:56 AM Calcaneal Fractures http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Calcaneal Fractures
Anatomy
Superior surface is divided into 3 articular facets:
Posterior - largest and convex on shape Middle - on the sustentaculum tali, concave in shape Anterior - often confluent with the middle facet, concave
Between the middle and the posterior facets lies the interosseous sulcus (calcaneal groove)
The anterior surface is saddle shaped, articulating with the cuboid bone
Principle functions of the calcaneum
1. To act as a lever arm for the gastrosoleus complex 2. To provide a foundation or vertical support for body weight 3. To provide support for and to maintain the lateral column of the foot
Any fracture that impairs one of these functions will significantly affect the patients gait if not corrected or restored.
Associated injuries
Bilateral calcaneal fractures occur in 5 - 9% of patients
Compression fractures of the lumbar/dorsal spine occur in 10% patients with calcaneal fractures
Other injuries of the lower extremity occur in 26%, e.g. ankle, tibial fractures
Soft tissue injuries
Laterally the peroneal tendons can be subluxated or dislocated from the fibular sulcus
Medially the fracture fragments can injure or entrap the neurovascular bundle.
Flexor hallucis longus can interpose in fractures of the sustentaculum tali, trapping the tendon.
Compartment syndrome develops in 10% of calcaneal fractures, with half of these develop clawing of the lesser toes or other chronic problems such as stiffness and neurovascular dysfunction. Fasciotomy should be carried out when pressure of >40mmHg are encountered.
Classification
Extra-articular fractures
25-30% of all calcaneal fractures
Divided anatomically into:
Anterior process Tuberosity (beak or avulsion)
More common in diabetics
Medial process
Sustentaculum tali
Body
Intra-articular fractures
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70-75% of all calcaneal fractures
These fractures can result in an infinite variety of patterns with varying degrees of displacement.
There are two main fracture lines:
Primary fracture line running from the plantar aspect obliquely upwards into the posterior facet, which divides the calcaneum into anteromedial and posterolateral fragments.
Secondary fracture line which begins at the crucial angle (of Gissane) and extends posteriorly.
Essex-Lopresti identified two distinct fracture sub-types that occur
1. Tongue type - Where the secondary fracture line extends directly posteriorly producing a large superior, posterior and lateral fragment with the rest of the body forming the inferior fragment.
2. Joint depression type (seen more frequently) - The secondary fracture line begins at the crucial angle extends posteriorly, but deviates dorsally to exit the bone just posterior to the posterior articular facet. This fragment contains the majority of the posterior facet.
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Lateral views will show Bohler's tuber angle and the crucial angle of Gissane clearly.
Bohler's angle - Normal = 20-40deg. (should compare to opp. side) - indicates disruption of the posterior facet .
AP (dorsoplantar) view will delineate the calcaneocuboid joint.
Axial best demonstrates the tuberosity, body, middle and posterior facet
Oblique views ( Broden's ) can define the subtalar joint incongruity (done by internally rotating the foot 45deg. with the heel resting on the radiographic plate & directing the beam cephalad in angles varying from 10 degrees to 40 degrees)
CT
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This is the investigation of choice. Coronal and axial views are needed.
Sanders classification
Type 1: undisplaced
Type 2: two parts (split)
Type 3: three parts (or split/depression)
Type 4: comminuted
Type 1 will do well with non-operative treatment, types 2 and 3 can be treated effectively with ORIF, and type 4 defies operative reduction
Treatment
Extra-articular fractures
Admit for elevation, ice packs and compression bandaging.
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Commence vigorous exercises to regain subtalar and ankle movement once the swelling has begun to subside.
If significant widening of the calcaneum exists some authors perform a closed manipulation (manual), to decrease heel width and decrease the chance of late peroneal tendon irritation.
If Bohler's angle has been reduced by more than 10 o then calcaneal height can be restored by using a transverse pin, applying traction and subsequently incorporating the pin in a POP cast for 4 weeks.
Prognosis
Virtually all patients with undisplaced extra-articular fractures have a good result, even if there is displacement patients generally do well. Fracture union always occurs, and with early movement, joint stiffness is a minimal long-term problem.
Intra-articular fractures
4 treatment options
1. Treatment without reduction
Compression dressing, elevation and ice packs
Early movement beginning at 24 hours
NWB mobilisation after the first week
Surgical shoe fitting at 14 days
PWB in the shoe after 6 weeks to FWB after 8 weeks
2. Closed reduction and fixation
This technique can be used in certain types of fracture, utilising a Steinman pin to manoeuvre the fragment and then advance the pin to hold the fracture.
3. Open reduction and internal fixation
Using a lateral approach, the subtalar joint is reduced and held with reconstruction plates.
Problems occurring with this treatment option include skin edge necrosis (8%) and deep infection (2%).
4. Primary arthrodesis
Either isolated subtalar fusion or triple fusion, as there can be unrecognised damage to the calcaneocuboid joint or talonavicular joint.
Prognosis
Lance (1964) reviewed 227 intra-articular fractures, only 55% of patients had good results, although this was better than the group treated operatively.
Lindsay and Dewar reviewed 147 patients after 8 years, 76% of patients treated conservatively had good results, with only 60% of patients treated with primary or late arthrodesis had good results.
Prognostic factors:
1. Degree of displacement of the posterior facet is the most important factor 2. Decreased tuber angle, with a persistent severe decrease (0 o or less) is associated with poor long-term results. 3. Patient age, Essex-Lopresti recommended that patients over 50yr should not be treated as aggressively as the results are worse. 4. Degree of comminution - 5-15% of intra-articular fractures are so comminuted that they are not amenable to surgery and will have a poor outcome.
Premature weight bearing before 6weeks is related to redisplacement of the fracture fragments, and weight bearing after surgery should be delayed to 12 weeks.
Other sources of persistent pain following calcaneal fractures
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1. Subtalar joint
Secondary degenerative changes present as pain on weight bearing, which is aggravated by inversion and eversion.
Subtalar arthrodesis alone may not control the symptoms, as unrecognised degenerative changes in the calcaneocuboid or talonavicular joint will not be treated by a limited hind foot fusion.
2. Peroneal tendonitis
Stenosing tenovaginitis of the peroneal tendon sheath. Surgical decompression and rerouting of the tendons can give relief.
3. Bone spur
Heel spur arising from a malunion can become painful, treated primarily with pressure relieving pads. Surgical excision should only be undertaken as a last resort.
4. Calcaeocuboid OA
Treated with local steroid injections or a triple fusion should symptoms persist.
5. Nerve entrapment
Either from the healing fracture or from iatrogenic injury.
Cochrane Collaberative Review of Interventions in Calcaneal Fractures (from Cocharane Musculoskeletal Reviews )
A substantive amendment to this systematic review was last made on 29 June 1999. Cochrane reviews are regularly checked and updated if necessary.
Background: Fracture of the calcaneus (os calcis or heel bone) comprises one to two per cent of all fractures.
Objectives: To identify and evaluate randomised trials of treatments for calcaneal fractures.
Search strategy: MEDLINE, EMBASE, CINAHL, the Cochrane Controlled Trials Register, and the Cochrane Musculoskeletal Injuries Group Trials Register were searched. We checked reference lists of relevant articles and contacted trialists and experts in the field. Date of the most recent search: October 1998.
Selection criteria: Randomised and quasi-randomised trials comparing interventions for treating patients with calcaneal fractures.
Data collection and analysis: Two reviewers independently assessed trial quality, using a 12 item scale, and extracted data. Wherever appropriate and possible, results were pooled.
Main results:
Of the six relevant randomised trials identified, four were included, one excluded and one is ongoing.
All four included trials had methodological flaws.
Three trials, involving 134 patients, compared open reduction and internal fixation with non-operative management of displaced intra-articular fractures. Pooled results showed no apparent difference in residual pain (24/40 versus 24/42; Peto odds ratio 0.90, 95% confidence interval 0.34 to 2.36), but a lower proportion of the operative group was unable to return to the same work (11/45 versus 23/45; Peto odds ratio 0.30, 95% confidence interval 0.13 to 0.71), and was unable to wear the same shoes as before (12/52 versus 24/54; Peto odds ratio 0.37, 95% confidence interval 0.17 to 0.84).
One trial, involving 23 patients, evaluated impulse compression therapy. At one year there was a mean difference of 1.40 pain units on a visual analogue score (scale 0-10) (95% confidence interval 0.02 to 2.82) in favour of the treated group. The impulse compression group had greater subtalar movement (mean difference 14.0 degrees, 95% confidence interval 3.2 to 24.6) at three months. On average, patients in the impulse compression group returned to work three months earlier than those in the control group.
Reviewers' conclusions:
Randomised trials of management of calcaneal fractures are few, small and generally of poor quality.
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Even where there is some evidence of benefit of operative compared with non-operative treatment, it remains unclear whether the possible advantages of surgery are worth its risks. Given this it seems best to wait for the results of one large ongoing trial on open reduction and internal fixation against conservative treatment.
One very small trial suggests that impulse compression therapy for intra-articular calcaneal fractures may be beneficial.
More large-scale, high quality randomised controlled trials are needed to confirm these results, and to test other interventions in the treatment of calcaneal fractures.
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7 of 7 10/6/2007 10:57 AM Compartment Syndrome http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Compartment Syndrome INCIDENCE & AETIOLOGY Compartment syndrome of the foot occurs in 10% of calcaneal fractures & 41% of crush injuries. PLANTAR COMPARTMENTS
the 9
compartments of the foot can be placed into 4 groups
Interosseous Compartment: 4 intrinsic muscles between the 1st and 5th metatarsals
Medial Compartment: abductor hallucis; FHB
Calcaneal / Central Compartment: FDB; Quadratus plantae; Adductor Hallucis
Lateral Compartment: Flexor digiti minimi brevis; abductor digiti minimi DIAGNOSIS HIGH INDEX OF SUSPICION
Unlike its counterpart in the leg or forearm, there are no classic signs in the foot. Pain on passive stretch, dysesthesias, and diminished pulses are not consistent findings.
Tense swelling may be suggestive.
Pressure measurement of all major compartments is required. Absolute pressures >30mmHg requires decompression, or less than 20mmHg below the diastolic blood pressure. SURGICAL FASCIOTOMY 2 dorsal incisions over the medial aspect of the 2nd MT & lateral aspect of the 4th MT. one 6cm medial incision - releasing the medial, calcaneal & lateral compartments.
- medial approach: can be used to decompress the medial and central compartments as well as the remaining foot compartments; extends from a point below the medial malleolus (3 cm from the sole)to
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proximal aspect of first metatarsal; once the neurovascular bundle has been retracted out of the way, the fascia overlying the abduction hallucis and FDB is released; medial intermuscular septum is opened longitudinally; the lateral plantar neurovascular bundle is found coursing over the quadratus plantae (central compartment) as they course laterally; the remaining compartments (central, lateral, intrinsic) are entered thru blunt dissection; the lateral compartment is found by retracting the FDB out of the way; - dorsal approach: often the dorsal approach is not necessary unless there is concomitant metatarsal or Lisfranc fractures; accomplished through 2 dorsal incisions centered just medial to the 2nd metatarsal and just lateral to the 4th metatarsals (to maximize skin bridge); avoid injury to sensory nerves and extensor tendons; superficial fascia is divided and interosseous are elevated off the metatarsals to further decompress the compartments; bluntly dissect thru the central, medial, and lateral compartments; separate medial incision may be needed to release the abductor; fasciotomy incisions may be used for fracture fixation;
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2 of 2 10/6/2007 10:57 AM Diabetic Foot http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Diabetic Foot
Prevalence Neuropathy PVD Injury
Clinical Investigations Treatment Charcot foot
Prevalence of diabetic foot problems [Back To Top]
1% of the UK population is diabetic 12% of diabetic admissions are with foot problems
Pathology
33% of diabetic foot ulcerations are neuropathic, 33% are ischaemic and 33% are of a mixed nature
Neuropathy [Back To Top]
Symmetrical distal polyneuropathy Involves motor, sensory and autonomic systems;
Autonomic
Autonomic involvement has 2 effects: Reduced sweating, leading to dry plantar skin which can fissure Alteration of normal autoregulation of the microcirculation; thickening of the basement membrane of the capillaries, AV shunting, loss of sympathetic tone , loss of postural vasoconstriction and increased peripheral flow
Sensory
May be painful or painless Those with painful neuropathy don't tend to get ulcers Painless sensory neuropathy causes stocking distribution sensory loss . Reduced ability to sense pinprick, light touch and vibration. Probably the main factor leading to ulceration. The neuropathic foot is therefore a warm, dry, insensitive foot with clawed toes and increased pressure under the metatarsal heads. Veins are often distended
Motor / Myopathy
Motor involvement causes weakness of the intrinsic muscles causing imbalance between the long flexors and extensors, causing a cavus foot and claw toes . The weight bearing contribution of the toes decreases and the fat pad under the metatarsal heads is drawn forwards, decreasing cushioning and increasing vertical and shear forces. The metatarsal and heel pads are atrophied for unclear reasons.
Peripheral Vascular disease [Back To Top]
Atherosclerosis appears earlier, progresses quicker and shows less male bias in diabetics. Vessels in the lower limb most involved are distal superficial femoral, tibial and peroneal vessels. There is controversy over how much small vessel disease there is. It has been assumed that there is microangiopathy like that in the retina, but this is disputed. It is possible that for the toes to become gangrenous even when ankle pressures normal. 2 Features of vascular disease in diabetes: 1. It occurs mainly distally, affecting popliteal arteries more than the iliac and femoral arteries 2. There is arterial wall calcification
Injury [Back To Top]
Mechanical stress is the precipitator of ulceration in both the neuropathic and ischaemic foot. In the ischaemic foot low pressures over a period of time may lead to necrosis. The most common sites are the curve of the 1 st and 5 th metatarsal heads. The sole of the foot has a relatively good blood supply and tends not to ulcerate early. In the neuropathic foot ulceration precipitated by direct high pressure injury (unfelt) or gradually through repetitive stress. Callosities develop under metatarsal heads and the heel. Subcutaneous tissue trapped
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between bone and thick unpliable skin producing high shear forces, leading to sterile deep haematoma. This à ¢Ã‹Å“deep' ulcer then tracks to the skin.
Clinical Assessment [Back To Top]
An ulcer needs to be assessed as to whether it is ischaemic, neuropathic or a combination A decision about whether it is infected is also necessary Neuropathic ulcer - Under metatarsal head, surrounded by thick hyperkeratosis, pink punched out base, readily bleeds, painless. Foot warm with palpable pulses and distended veins Ischaemic ulcer - not surrounded by hyperkeratosis, dull fibrotic base, doesn't bleed easily, painful to touch Infection - Surrounding cellulitis, discharge, erythema Neurological examination
Investigations [Back To Top]
For nerve function:
1. Biothesiometer;
Measures vibration perception threshold. A hand held vibrator whose amplitude of vibration can be varied. There are normal tables allowing the results to be expressed as a standard deviation score from the normal for the patient's age. Measured at the medial malleolus and the great toe. If SD score is >1.9 for hallux and >2.1 for medial malleolus then there is risk of ulceration
2. Semmes Weinstein hairs - Nylon monofilaments of the same length but different diameters. If the 5.07 hair can be felt, the patient has protective sensation
3. Nerve conduction studies - Take longer, can give spurious results if some fibres conducting and others not
For blood supply:
1. Doppler ultrasound;
Ankle/brachial index produced by measuring pressures in dorsalis pedis, posterior tibial and brachial arteries. Normal = 1. Less than 1 indicates peripheral vascular disease. To be treated with caution in diabetics as calcification of the arteries makes them relatively incompressible
2. Angiography
For infection:
1. C+S;
There is polymicrobial colonisation of foot ulcers. Most commonly staph aureus, Ecoli, streptococci. Anaerobes eg. Bacteroides species and streptococcus can be found if looked for. But only give antibiotics if clinical evidence of cellulitis, abscess or evidence of osteomyelitis.
2.WCC, ESR
3.Plain Xray for bone infection
4.Technetium and indium labeled white cell scans
Treatment
1. Prevention 2. DM control 3. Mx complications renal etc. 4. Eliminate infection 5. Optimise arterial inflow if ischaemic component 6. Local ulcer healing – debridement, relief of pressure
Prevention of complications! Screening, pt education, good BM control, regular podiatrist.
Eliminate infection
Augmentin is a good broadspectrum antibiotic but not to be used on everyone with a positive culture swab Removal of infected bone Drainage of abscesses
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Dry gangrene- allow autoamputation, Wet gangrene- debride /amputate
Key to healing in diabetic foot ulcer is relief of pressure
Mueller et al. 1989 RCT: TCC vs NWB& dressings. TCC is most effective.
Neuropathic ulcers
Healed by moderation of the causative mechanical forces Options: strict bedrest, expensive, risk of complications non wt bearing on crutches Total contact plaster cast: Below knee plaster cast with minimal padding, rocker for walking, hole cut where ulcer is. Ulcer debrided and excess callus removed prior to application. Changed weekly, then three weekly intervals
Ischaemic ulcers
Made worse by a total contact plaster Arteriography will determine whether angioplasty, bypass surgery or amputation is necessary
Ulcers of mixed aetiology
Usually more one than the other, if it doesn't bleed, ischaemic, if it does, neuropathic
Prevention of further ulceration
Good diabetic control Well fitting shoes with adequate cushioning, total contact insoles, 30 degree rocker sole to prevent undue loading of metatarsal heads.
The role of surgery:
1. Debridement of infected ulcers, drainage of abscesses and excision of infected bone 2. Revascularisation of ischaemic foot 3. For fixed deformities - Correction or resection as in any foot , eg. Resection of distal metatarsals (all) for prominent metatarsal heads. 4. Amputation (see notes on amputation ) - Digital, Ray, Symes if heel pad healthy, Below knee.
Charcot [Back To Top]
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A chronic painless degenerative process affecting the weight-bearing joints of the foot.
Rare complication of diabetes, only in 1 % of diabetics
Age - 5 th and 6 th decades in insulin dependent diabetics usually of more than 12 years duration
Aetiology
Repeated minor trauma in the neuropathic foot. Spontaneous fractures, dislocations and subluxations can occur. Autonomic neuropathy can increase blood flow leading to weakening of bone by osteoporosis. Can begin after acute trauma or even during bedrest.
Pathology
Eichenholz scale of progression:
Stage 1. Swollen hot erythematous foot, some pain, may follow some minor trauma. Destruction X-rays show healing fracture(s). Mimics infection!
Foot collapses, arch flattens, rocker-bottom appearance of foot. Progressive Stage 2. bone destruction, new bone formation subluxation/ dislocation. (Midtarsal 60%, Coalescence MTP 30%, Ankle 10%)
Stage 3. Stable but deformed shape to foot, can create pressure points for ulceration. Consolidation May span 2-3 years
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Brodsky classification – describes distribution: Brodsky1 TMT, midtarsal; Brodsky2 peritalar.
Early treatment – goal – obtain durable, plantigrade foot
Exclude infection, by WCC, ESR, MRI (will show infection), aspiration of joints, white cell scans- technetium scan looks similar but indium leukocyte scan hot for infection cold in Charcots. Biopsy not indicated. N.B Charcot although often painless can be painful.
Good metabolic control (BMs)
Treat with NSAIDS,
Prevent progressive destruction of joints and further deformity: Avoid weight bearing & total contact cast to keep patient active and prevent disuse osteoporosis. May require plaster for several months. Can usually stop Total con. casting when skin temp normal.
Late treatment
If rocker bottom deformity already present wait till bone scan negative then reconstruction (eg. midfoot wedge osteotomy)
modified shoewear
Surgical Indications:
Severe instability with deformity, ulceration, infection. Stabalise with IF: retro nail for ankle. Best to wait for Eichenholz 2 (heal ulcer and infection)
Persistent ulceration despite healed fixed deformity. Options: shave prominences, corrective osteotomies with fusions – triple, tibio-talo-calc.
amputation – hindfoot, trans-tibial.
Updated by Naqui 1.05.05 using Orthoteers, Current Orth., Hyperbook & Miller.
Bibliography:
Klenerman - Current Orthopaedics 1996.
Jim Barrie - Foot & Ankle Hyperbook
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5 of 5 10/6/2007 10:58 AM Foot & Heel Pain http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Foot & Heel Pain
from: South Australian Registar's Notebook + Apley & Solomon
Painful Heel Painful Tarsus Painful Forefoot
Painful Heel [Back To Top]
Children: Severs disease (apophysitis) usually male aged about 10 years with increased density and fragmentation of the calcaneal apophysis Raise heel and avoid strenuous activities, severe cases may require POP Adolescents: Calcaneal knobs (often bilateral) usually female 15 - 20 years
Young Adults: Retrocalcaneal Bursitis (w/ Haglund's lump) above the Achilles tendon insertion or plantar fasciitis (enthesopathies) Older Adults:
1. Plantar fasciitis 2. Pagets may affect the calcaneum resulting in a chronic ache 3. Chronic bone infection (Brodies abscess with sclerotic margin) 4. Diabetes 5. Entrapment of medial calcaneal branch of posterior tibial nerve 6. Tarsal Tunnel Syndrome
Plantar Fasciitis:
Pain at the attachment of the plantar fascia to the medial tubercle of the calcaneus. Treat with NSAIDs and orthosis, rarely needing release of plantar fascia.
Painful Tarsus [Back To Top]
Kohlers disease (osteochondritis of the navicular) usually children less than 5 years old present with a painful limp and tender warm swelling over the navicular Rest and strap for a few weeks results in relief and eventually ® normal looking navicular Brailsfords disease similar to Kohlers but older women affected The "overbone" In adults with high arches, ridge of bone on dorsal surfaces of the med cunieform and 1st metatarsal- adjust shoes, bevel lump
Painful Forefoot [Back To Top]
1. Metatarsalgia:
Symptom not a diagnosis and may be primary or secondary to other conditions
Primary metatarsalgia due to chronic imbalance in weight distribution between the toes and metatarsal heads due to absent or ineffective muscle function
Secondary metatarsalgia caused by:
1. Intractable plantar keratoses (most common) 2. rheumatoid arthritis 3. gout 4. neuromuscular disorders 5. stress fracture 6. Freiberg's infraction 7. Mortons neuroma 8. plantar fasciitis 9. tarsal tunnel syndrome 10. intermittent claudication 11. osteoarthritis Any foot condition with faulty weight distribution may cause this condition
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2 of 2 10/6/2007 10:58 AM Freiberg's disease http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Freiberg's disease
Friebergs
Definition Osteochondritis of the 2nd metatarsal head
History Initially reported in 1914 by A.H. Freiberg as a series of 6.
Features:
Most commonly recognized in the 2nd decade Thought to be secondary to a pressure effect as the second metatarsal is both the longest and the least mobile. Causes a painful synovitis with resultant loss of function.
Treatment:
Conservative: Anti inflammatories Activity modification Metatarsal bars
Surgical Dorsal closing wedge osteotomy Alows debridement of the joint and rotation of the healthy plantar area into the articulating position. Joint Debridement and metatarsal head remodelling
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Albert H. Freiberg, 1868-1940 Freiberg spent all his life in his birthplace, Cincinnati, apart from a period of study in Germany and Austria. He established himself as an orthopaedic surgeon in the city and played an important part in the establishment of orthopaedic facilities there. His influence on the development of American orthopaedics was felt for two reasons: first, he was an active medical author, one of the leaders of thought-he has been called the philosopher of orthopaedic surgery. The second reason for his eminence was his committeemanship; an able, kindly speaker, he had the ability to turn discussions.
He is best remembered for describing flattening of the head of the second metatarsal. It is interesting to note that he considered that it was an injury. Since then opinion has swung towards osteochondritis and back again; most people would now agree that Freiberg was right.
In 1910-11 he was President of the American Orthopaedic Association. It is ironic that Freiberg, whose name is attached to the second metatarsal, should have just missed working with Keller, who campaigned against damaging the first metatarsal head, at the Walter Reed Hospital. Freiberg spent the war there and Keller joined the staff after it was over.
Freiberg's original Description: Infraction of the Second Metatarsal Bone A TYPICAL INJURY by Albert H. Freiberg, M.D., F.A.C.5., Cincinnati, Ohio, 1914 As a part of the general symptom-complex of weak or so-called "flat foot" we very commonly encounter pain in the
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forefoot, in the region of the metatarsal heads. When seen as a paroxysmal affection concerning the fourth metatarsal, in particular, we are dealing with the metatarsalgia of Morton. Very frequently, however, we are consulted by patients because of pain in the heads of the other metatarsals which is not of paroxysmal character but rather dependent upon the use of the foot in weight-bearing. This may or may not be in the presence of other signs of yielding and strain in the foot mechanism elsewhere than in the metatarsal region, but the dependence of the pain purely upon the weight-bearing function will cause us to ascribe the symptom to static incompetence of the foot. Under these circumstances we shall find that the most common seat of the pain is the second metatarso-phalangeal joint instead of the fourth, as in Morton's disease. The joint is usually tender to pressure and frequently somewhat thickened. The well-known plantar callus is frequently seen; almost uniformly soin cases of long standing. I have often found thickening of such degree in the second metatarso-phalangeal joint that I have sought for organic change m the radiogram; always without finding it, however, until I encountered Case i of the series which I am now reporting. In this case I felt justified in the diagnosis of infraction of the distal end of the second metatarsal, a condition which I have thus far failed to find described in literature.
During the past few years I have encountered six cases of in-fraction of the distal end of the second metatarsal bone. I feel justified in speaking of it as a typical injury because in each of my six cases not only was the same bone end involved, but the conditions under which the patients presented themselves were very similar, as was also the character of the trauma which produced the lesion.
Ten years ago the first patient in whom I recognised this lesion was referred to me by Dr. E. W. Mitchell, of Cincinnati- The patient was a girl of sixteen. She had been suffering from pain in the ball of the foot for about six months. The pain was precisely like that which we so often encounter in the metatarso-phalangeal region in connection with static incompetence of the foot. At the time I examined the patient she complained of pain in weight-bearing only. In attempting any unusual exertion, as in walking considerable distances, she was compelled to limp and the pain became severe.
The patient was quite sure that the condition dated from and was due to a game of tennis in which she "stubbed" her foot. The pain was severe at the time; it was considered a sprain and she was able to be about the next day. My examination disclosed a well formed and apparently
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strong foot. The metatarsophalangeal articulation of the second toe was thickened, on palpation, and very tender to pressure. Passive movement of this joint was very painful and accomplished by slight grating. The X-ray (Fig. x) showed quite clearly that the distal end of the second metatarsal had been crushed in, causing the articular surface to lose its curved outline. There was apparently a small loose body in the joint about two mm. in diameter.
The treatment consisted in applying a felt pad to the plantar surface of the foot by means of adhesive plaster, so that its anterior end was placed just back of the injured joint. In this case I also had a steel plate inserted between the layers of the sole of the boot in order to deprive the foot of the motion in the metatarsophalangeal joints, in walking. I have not done this in my later cases.
The patient was able to walk painlessly without the pad within six weeks and has had no further trouble with this foot. The other foot has always been entirely normal.
I find it.unnecessary to report each of my cases in detail, as they have great similarity except as noted below.
Three of my six cases have shown loose bodies in the radiogram, and grating upon examination. In two of these three cases I was unable to give definite relief by mechanical support alone and, therefore, removed the loose bodies by means of an arthrotomy from the dorsal surface of the foot. This resulted in entire relief from discomfort and pain.
It is a curious fact that in two of the six cases, no injury whatever could be recalled by the patients in spite of careful questioning on my part. In one of these cases operative removal of small corpora libera was necessary. I have no doubt of the traumatic origin of these three cases.
Two of my cases were women below middle age, but the remaining four wee girls under eighteen years of age. In two of the six cases there was evidence of static incompetence of the feet. I have no reason to believe that this stood in any particular relationship to the condition which is here described.
Having observed six cases of this character in my own practice there would appear little doubt that the condition which I have described is not extremely infrequent. It is very likely that the similarity of symptoms to those of weak feet has caused it to be overlooked. While those cases in which there are no loose bodies will be relieved by the use of the felt pad if sufficiently long continued, the contrary will be true of the other cases. The cases with loose bodies will require arthrotomy as a rule. As in my first case, this may be unnecessary where the bodies are very few in number and very small.
It seems worthy of note that in my six cases only one foot has been the seat of this injury. While it is common enough to see only one foot affected in cases of metatarsal pain from static weakness, the contrary is the rule. This would seem, therefore, to be a point of some diagnostic importance. Not a little interest attaches to the mechanism by which this injury to the foot takes place. Under normal circumstances the second metatarsal bone is slightly longer than the first. In the presence of a diminished power of toe flexion and especially of the great toe, it is apparent that forcible impact of the ball of the foot against the ground not sufficiently guarded by the flexor power of the toes will cause the distal end of the second metatarsal to bear the brunt of the blow. It seems likely to me that we have here the explanation of the mechanism of this injury.
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4 of 4 10/6/2007 10:58 AM Hallux Rigidus http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Hallux Rigidus
Definition
Stiff and painful first MTP joint associated with degenerate changes
Epidemiology
Most common condition affecting 1st MTP joint (Duvries 1959, Moberg 1979) Affects 1 in 40 patients > 50 years old (Gould 1978) May affect adolescents, possibly due to Osteochondritis dissecans of1st Metatarsal head “ if so leads to more severe symptoms later Females > males “ debatable Positive Family history in 50%
Aetiology
Not known osteochondral defect / osteochondritis dissecans definitely lead to hallux rigidus Possible predisposing factors include : trauma / repetitive microtrauma / abnormal shape of metatarsal head / long or short 1st metatarsals / tight intrinsics / pes planus
Clinical assessment
Pain on walking, relieved by rest Stiffness in dorsiflexion Plantar flexion may be present Swelling “ synovitis / bunion / exostosis Hallux valgus deformity can occur with hallux rigidus “ this is uncommon Skin irritation over exostosis Pain on flexion may be caused by stretching tight MTP joint capsule / EHL / inflamed synovium May have positive Tinel sign because of compression of 1st webspace digital nerve from osteophyte Check neurovascular status of foot Check midfoot / hind foot - sitting, standing and walking
Xray assessment
AP/Lateral weight bearing films Sesamoid views may sometimes be useful Look at shape of Metatarsal head Reduced joint space “ may be deceiving if there is a gross flexion deformity Subchondral sclerosis / Metatarsal head cysts / osteophytes “ 'dripping candle wax' on lateral film / sesamoid hypertrophy In young patients “ look for osteochondral defect Lateral film “ evaluate for elevation of 1st metatarsal in relation to 2nd Sesamoidal involvement is unusual
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Treatment
Non surgical treatment
Stiff insoles “ reduces excursion of MTP joint; but reduces room in the shoe, and can lead to pain because dorsum of the toe is pushed against the top of the shoe Insoles to correct hindfoot pronation / pes planus Taping of the toe “ acts like a splint to reduce MTP excursion Injection with steroid and local anaesthetic “ too many injections will accelerate degenerative process
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Surgical treatments
Arthroscopy of 1st MTP joint “ for OCD / Ost Diss “ similar to knee Dorsal cheilectomy - removal of 1/3 of articular surface of metatarsal head, not just the osteophytes “ very good pain relief and restores some movement by removing the dorsal block to extension. GOOD OPERATION Moberg closing wedge osteotomy “ moves less worn part of the articular surface of the metatarsal head to articulate with the proximal phalanx Excision arthroplasty “ Kellers operation “ DO NOT DO THIS OPERATION “ leads to a floppy cocked up toe, shortens the 1st ray and causes transfer metatarsalgia “ Patients are never happy! Replacement arthroplasty “ Silastic implants loosen and then need to be removed, leaving a large area of bone loss ( effectively a 2 stage Kellers); Newer implants have only very short term results. A multicentre study on the Moje Replacement is ongoing. Watch this space.
1st MTP joint fusion
Good pain relief Shoe wear restriction Must fuse in correct position Complications “ malunion / non-union / prominent implants / infection / nerve & vessel damage / failure of pain to resolve
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4 of 4 10/6/2007 10:59 AM Hyperkeratotic Pathology of the Plantar Foot http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Hyperkeratotic Pathology of the Plantar Foot
1. PLANTAR KERATOSES
Anatomy Causes Diagnosis Conservative treatment
Surgical management of Surgical management of Surgical management of Localised intractable plantar Discrete callus beneath tibial Diffuse intractable plantar keratoses sesamoid keratoses
2. KERATOTIC DEFORMITIES OF THE LESSER TOES
Hard corn Soft corn
1. PLANTAR KERATOSES
Anatomic considerations [Back To Top]
Transfer of load laterally from 1 st ray can occur in disorders of the 1 st ray such as hallux valgus or instability of first metatarsocuneiform joint. This can cause callus formation under 2 nd and 3 rd metatarsal heads where the tarso metatarsal joints are quite rigid. The 4 th and 5 th TMT joints are quite flexible so rarely get callus formation due to transfer from the first ray
Postures of the foot that can precipitate callus formation are
Equinus deformity of ankle joint, causing increased forefoot loading Cavus foot, generally reduced weight bearing area therefore more pressur Flatfoot, if it produces a hallux valgus deformity, can cause callus over medial aspect of great toe at the IP joint Varus forefoot, with lateral border more plantar flexed than medial border causes callus of lateral side of foot Valgus deformity, opposite of above Abnormal alignment of MTP joints, eg subluxation or dislocation, causes plantarward force on metatarsal head and callus formation
Causes [Back To Top]
Bony Prominent fibular condyle head
Long metatarsal
Mortons foot
Hypermobile first ray
Postrauma effects
Abnormal foot posture
Systemic disease Rheumatoid arthritis
Psoriatic arthritis
Dermatological lesions Wart
Seed corn
Hyperkeratotic skin disorde
Soft tissue causes Atrophy of plantar fat pad
Crush injury sequelae
Plantar scar secondary to trauma
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Hallux valgus leading to transfer lesions
Subluxed or dislocated metatarsal head
Iatrogenic Secondary to metatarsal surgery
Hallux valgus surgery. Eg shortening or dorsiflexion of 1 st ray
Diagnosis [Back To Top]
History
How long have they been there? History of previous surgery/ trauma PMH What treatment has been attempted?
Examination
General overall picture of patient Posture of foot and toes whilst standing Range of motion of all joints Neurovascular status Look at characteristics of callus, a seed corn?, discrete plantar keratosis under fibular condyle of a metatarsal head? A diffuse keratosis beneath a single metatarsal head, a diffuse callus under several metatarsal heads? Alocalised callus beneath the tibial sesamoid? Distinguish lesion from a wart- a wart will not necessarily be in a pressure area, on trimming, it will show multiple end arteries of a punctate nature
Investigation
Weight bearing AP and lateral views and sesamoid views if indicated Harris mat to determine pressure areas
Conservative Treatment [Back To Top]
Trimming with a sharp knife, may need several sessions Soft metatarsal support to relieve affected area, just proximal to metatarsals If a postural abnormality is present, a well molded orthotic device may be used if a soft metatarsal support does not work If these measures don't work surgery will be required
Surgical management
Depends on the type of callus
Surgical management of Localise intractable plantar keratosis [Back To Top]
Due to a prominence of the fibular condyle
Treated with Duvries metacondylectomy , removal of portion of articular surface of metatarsal and tha plantar condyle 93% Patient satisfaction (Mann and Dufries)
Or Coughlins modification, just removing the plantar condyle, through a dorsal approach (results not published)
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Or chevron osteotomy of distal metatarsal and dorsal displacement of metatarsal head,held with a k wire (Dreeben reported complete relief of symptoms in 67 % of 45 patients)
Surgical management of callus beneath the tibial sesamoid [Back To Top]
Tibial sesamoid shaving through plantar medial approach
Surgical management of Diffuse intractable plantar keratosis [Back To Top]
May be due to long metatarsal, Plantarflexed metatarsal, transfer lesion as a result of adjacent metatarsal osteotomy,
If offending metatarsal too long, shorten it to a line connecting two adjacent metatarsal, with an oblique metatarsal osteotomy
If due to a metatarsal being relatively plantarflexed and metatarsal is not long, a basal osteotomy with a dorsal closing wedge should be used.
Only do metatarsal osteotomy if MTP joint is not contracted.
Distal Metatarsal Osteotomies Diaphyseal Metatarsal Osteotomies
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4 of 4 10/6/2007 10:59 AM Lesser Toe Deformities http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Lesser Toe Deformities
Toes: Important in force and pressure transfer in the late stance phase of gait (Hughes et al 1990). They take 30-40% of peak force and 70% of peak pressure
Hammer - flexion of the PIPJ & extended DIPJ
Mallet - flexion at the DIPJ
Claw Toes - flexion of the IP joints, hyperextension of the MTPJ (intrinsic minus deformity) often associated with a cavus foot and tight TA
Aetiology
Constrictive footwear, restricts the normal movement of the joints and impedes the intrinsic muscle function Neuromuscular diseases - always exclude for all claw toes CMT, Freidrich's, cerebral palsy, myelodysplasia Other causes RA, DM, post compartment syndrome Long toe short shoe
The joints are mobile initially but become rigid and the MTPJ joints sublux
Callosities develop under the metatarsal heads or over the inter phalangeal joints
Examination
1. Neurovascular status 2. Callosities 3. Rigidity of the deformity: is it flexible or fixed? a flexible hammer toe should correct when pushing up on the metatarsal head 4. MTPJ: subluxed, dislocated or congruent? 5. Drawer test for 2nd MTPJ position - flex MTPJ & perform drawer. 6. Tightness of FDL 7. Concomitant hallux valgus
Treatment
Non-operative
In the young patient with a flexible deformity try well fitting shoes with an adequate toe box
Operative
Hammer Toes
Flexible: flexor-extensor transfer (Girdlestone) Fixed: PIPJ arthroplasty - MTPJ soft tissue release DuVries metatarsal head arthroplasty - is a technique to create some space in the MTPJ to allow reduction of the proximal phalanx by excising 2-3mm of the plantar MT head parallel to the joint surface. Aims for a fibrous union which will allow aprox. 15deg. of movement Partial proximal phalangectomy will relieve symptoms but will have a poor cosmetic result
Mallet Toes
Flexible: FDL tenotomy at DIPJ Fixed: DIP excision arthroplasty + FDL tenotomy Terminal Phalangectomy
Claw toes
Flexible: FDL tenotomy or flexor-extensor transfer Fixed: MTPJ subluxed:
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MTPJ soft tissue release and hammer toe correction (fusion or excision arthroplasty of PIPJ) DuVries metatarsal head arthroplasty MTPJ dislocated: Stainsby Procedure = 'V-Y' Dorsal incision (over MTPJ for single toe, web spce for 2 toes); Divide extensor tendon proximally; Remove prox. 3/4 of PP; Reduce Fat Pad with McDonald under MT head; Suture distal extensor tendon end to flexor tendon; K-wire through DIPJ-PIPJ-MTPJ. [Stainsby. Ann R Coll Surg Engl 1997 Jan;79(1):58-68]
Curly toes
Neutral at MTP, Flexed at PIP and DIP -> flexor tenotomy of both FDL and FDB via an incision over proximal phalanx
Over-lapping 5th Toe
A common deformity, usually congenital. Dorsal and medial contracture of capsule and extensor. can release these structures
If troublesome may be corrected by Butlers operation or the Lapidus procedure More Detail
Summary of Lesser Toe Surgical Management: (Blackburn Foot & Ankle Hyperbook)
MTP joint PIP joint Recommendation
flexible flexible MTPJ release and FDL transfer ("type 1 correction")
flexible fixed MTPJ release and PIPJ arthroplasty ("type 2 correction")
dislocated fixed Stainsby procedure ("type 3 correction")
unstable FDL transfer
mallet toe: DIPJ arthroplasty or terminalisation
Current Orthopaedics (1997)11:1-10. MJ. Coughlin.
Blackburn Foot & Ankle Hyperbook
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2 of 2 10/6/2007 10:59 AM Lisfranc Fractures http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Lisfranc Fractures
The Lisfranc injury is named after the French surgeon Jacques Lisfranc, a field surgeon in Napoleonâ™s army.
The original injury described by Lisfranc usually occurred when a soldier fell from his horse, but his foot did not release from the stirrup
Mechanism
Direct: blow or crush Indirect: e.g. windsurfer RTAâ™s are most common cause accounting for 30-60% of all cases Crush injuries Falls from ground level with or without twisting injuries Falls form height
80% of these injuries occur in multiply injured patients
Classification
(Quenu & Kuss 1909)
Isolated: e.g. 1st ray displaced while lateral 4 rays stay in place
Homo-lateral: displacement: i.e. all rays displace in the one direction
Divergent: e.g. 1st ray goes medial, the rest displace laterally
X-rays
Up to 40% of injuries are
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overlooked on initial radiographs
AP/Lateral and 30o oblique
There is a consistent relationship between the medial border of the 2nd and 4th metatarsals and the medial edge of their corresponding
Look for
Widening of intermetatarsal space, particularly the 2nd metatarsal base Lining up of metatarsals with their cuneiforms Associated fractures
Treatment
"There is no place for conservative management of fracture and fracture dislocations of the tarso- metatarsal joint complex". Myerson 1989 "the diagnosis and treatment of injuries to the Lisfranc joint complex"
Fractures presenting with more than 2 mm of displacement and greater than 15o of talometatarsal angulation require operative treatment. Young competitive athletes may require anatomic reduction
Post op: Fixation must be rigid enough to prevent transverse plane & dorsoplantar motion of tarsometatarsal joint and be maintained for at least 12-16 weeks
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Prognosis
Whatever the severity of the initial injury the prognosis depends on an accurate reduction and its maintenance
Lisfranc injuries without fracture have poor prognosis
Late midfoot collapse a common sequela
May occur from displacement in the saggital plane
Posttraumatic arthritis and planovalgus deformity are common and may occur in up to 50%
X-ray findings may not correlate with clinical findings
Symptomatic posttraumatic arthritis â“ consider arthrodesis
Relationship between accuracy of reduction and outcome: Myerson et al Foot and Ankle 1986.
PFC Score = Painful Foot Score Late presentation or failed treatment Sangeorzan BJ. Veith RG. Hansen ST; Foot & ankle 10(4):193-200, 1990 Feb. 16 patients with fractures or fracture-dislocations of the tarsometatarsal (Lisfranc) joint who failed initial treatment were salvaged by arthrodesis using a technique of rigid internal fixation. Preoperative symptoms included local pain
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in all patients, progressive flatfoot deformity with forefoot abduction in 12 patients, and ankle or lateral impingement pain in five. The technique involved exposing the joint, denuding it of cartilage, reduction and fixation with lag screws. A total of 49 joints were fused. When significant deformity was present, reduction was performed before arthrodesis. Clinically symptomatic and radiographically proven non-union occurred in four sites in three patients. 1 healed after revision. Good to excellent results were obtained in 11 patients (69%). Five patients had a fair or poor result. All but one of the patients were subjectively improved. 4 patients were symptom free and returned to their pre-injury lifestyles. Accurate reduction and early treatment had a significant positive relationship with outcome. Injuries that occurred in the workplace and those that incurred a long delay until treatment showed a significant negative correlation to outcome. Neither the age of the patient nor the number of joints fused had a significant impact on result.
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4 of 4 10/6/2007 11:00 AM Morton's Neuroma http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Morton's Neuroma
Aka: Morton's metatarsalgia / Morton's neuroma, (n.b. Morton described neither he thought this was a problem in the 4th MTP joint. Betts described the "neuroma" 70 years later).
The "neuroma" consists of degenerative and fibrotic changes in - common digital nerve near its bifurcation. However, there may be similar changes in adjacent unaffected nerves and it is not known why one becomes symptomatic.
A number of causative factors have been suggested:
·€•‚ƒ„…†‡tethering of the 3rd space nerve by the anastomotic branch between medial and lateral plantar nerves
·ˆ‰Š‹Œ•Ž•traction on nerve by hindfoot valgus, interdigital bursitis or forced toe dosiflexion in high-heeled shoes
The symptoms may be quite non-specific:
·•‘’“”•–—neuralgic pain in a toe and/or interdigital space
·˜™š›œ•žŸtingling of a toe
· ¡¢£¤¥¦§colour changes
·¨©ª«¬•®¯numb or "dead" toe
·°±²³´µ¶·vague forefoot tingling
·¸¹º»¼½¾¿pain usually worse on walking and sometimes at night
·ÀÁÂÃÄÅÆÇrelief on removing shoes
Symptoms -commonest in the 3rd interdigital space, then 2nd. Symptoms in 4th space are rare and should make one doubt the diagnosis. Symptoms in the first space are virtually unknown.
The condition may remain undiagnosed for many years.
Clinical assessment
Often strongly suspected within first minute of consultation. However - may be arrived as part of the assessment of a more generalised metatarsalgia. In any case, a full assessment of the foot should be carried out.
Ask about:
·ÈÉÊËÌÍÎÏconditions which cause a peripheral neuropathy, especially diabetes and chronic inflammatory disorders
·ÐÑÒÓÔÕÖ×trauma to foot
·ØÙÚÛÜÝÞßdiscomfort around ankle which may suggest tarsal tunnel syndrome
·àáâãäåæçspinal problems, especially about any history of root entrapment symptoms.
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Examination begins with assessment of any suggested nerve entrapment in the spine, proximal limb or tarsal tunnel.
Examine whole foot,
·èéêëìíîïlook for other factors producing metarsalgia.
·ðñòóôõö÷local tenderness ± swelling in the intermetatarsal space
·øùúûüýþ Mulder's click on metatarsal compression
· local anaesthetic injection into the affected space may be useful - if it relieves the symptoms this is supportive of the diagnosis.
Imaging
U/S and MRI have been described - but we have not had any success. If ?other forefoot pathology standing AP and lateral forefoot films should be obtained.
Management
· use of shoes with adequate room in the toe-box & avoid high heels
· steroid injection into intermetatarsal space with some success, esp. if the history is relatively short.
· no proven role for orthoses.
· interdigital neurectomy: If symptoms persist despite non-surgical treatment and the diagnosis is regarded as firm enough
I quote a success rate of 75%. warn patients it may take several months to reach full benefit. also a few patients may develop a new neuroma on the severed nerve end which may be more painful than the original problem.
Op: is done through a dorsal interdigital incision with loupes. Others do plantar approach. The nerve is divided 2-3cm proximal to the bifurcation and excised. Deep transverse metatarsal ligment may be partially released but I avoid dividing this important structure. Wound is closed with subcuticular Vicryl. Post-op mobilize FWB
· Decompression of the interdigital space with excision of bursa, division of deep transverse metatarsal ligament and neurolysis of the common digital nerve is suggested but remains unproven.
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2 of 2 10/6/2007 11:01 AM OCD & Osteochondoses of the Foot & Ankle http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. OCD & Osteochondoses of the Foot & Ankle
OCD OF THE TALUS
Aetiology Examination Radiographs XR Classification
MR Classification Treatment
OSTEOCHONDROSES
Sever's Kohler's Iselin's Freiberg's
Clinical Classification Treatment Freiberg's Original Paper
OSTEOCHONDRITIS DISSECANS OF THE TALUS [Back To Top]
Aetiology:
Post-traumatic or idiopathic osteonecrosis
Anterolateral lesions:
may result from impaction of talus on fibula as the dorsiflexed ankle is forced into inversion these lesions tend to be shallow
Posteromedial lesions:
may result from impaction of posteromedial talus on tibia, as plantarflexed ankle is forced into inversion & ER these lesions are deeper and cup shaped
Examination: [Back To Top]
palpate just posterior to the medial malleolus with the ankle dorsiflexed
Radiographs: [Back To Top]
osteochondral # may be anterior or posterior to dome, requiring plantar or dorsiflexion of ankle to be visible on mortise view if radiographs are negative consider repeat radiographs in 2-4 weeks
Radiographic Classification: (Berndt and Harty) [Back To Top]
Note: XR findings may or may not correlate w/ arthroscopic findings nor prognosis
I : small area of compression
II : partially detached osteochondral lesion
III : completely detached, non-displaced fragment
IV : detached and displaced fragment
Bone Scan: - a negative bone scan will r/o the diagnosis
CT or MR Scan: - offers more accurate staging of the lesion;
MR Staging: ( Hepple et al. Foot & Ankle International. 1999. 12:789-93 ) [Back To Top]
1 - Articular damage only
2a - cartilage injury w/ underlying fracture + oedema
2b - cartilage injury w/ underlying fracture + No oedema
3 - detached & undisplaced
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4 - detached & displaced
5 - subchondral cysts
Treatment: [Back To Top]
Non Operative Treatment: - no evidence that non wt bearing cast offers improved results over wt bearing casts; - no evidence that patients need to be immobilized if they are kept non wt bearing
Operative Treatment: - Arthroscopy of the Ankle :
osteochondral lesions of the talus can be debrided, and loose bodies and small osteochondral fragments can be removed
Kumai et al (JBJS(A) Sep 1999 ) noted:
Good clinical results w/ arthroscopy and K wire drilling of the OCD lesions in patients who were younger than 50 years posteromedial lesions can be difficult to access w/ large fragments ORIF may be required, w/ osteotomy of the medial malleolus being required for exposure; - ORIF allows direct observation of the lesion and accurate repair.
Lahm et al. Arthroscopy . 2000;16:299-304 :
reported on the arthroscopic K-wire drilling of osteochondral lesions detected in the early stages via MRI imaging. A clinical score system in which up to 100 points were given in the following categories: "pain," "stability-insecurity," "efficiency-pain-free walking distance," "gait," "differences in circumference," "range of motion," and "power." 42 patients, 22 had retrograde drilling, 13 with cancellous bone grafts, 4 refixations, and 3 curettages. 19 who had K-wire drilling, had a average score of 87%. In 3 patients, repeat surgery was necessary. Most of the K-wire drilling was performed in patients with stage 1 lesions (cartilage intact, no definable fragment). Half of patients with stage 2 lesions (cartilage breached but fragment intact) had drilling and half had cancellous grafts. Patients with stage 3 lesions (cartilage breached, fragment still in situ) were treated with refixation and bone grafting. Removal of the loose body and drilling of the crater were performed in patients with stage 4 lesions (loose body). Results of K-wire drilling were not worse than those of cancellous bone grafts. Lesions can be detected earlier with MRI of the lesion and treated successfully with retrograde drilling.
MRI is a useful tool for assessing the results of arthroscopic drilling & planning further treatment ( Higashiyama et al. Foot Ankle Int 2000 Feb;21(2):127-33 )
OSTEOCHONDROSES OF THE FOOT & ANKLE [Back To Top]
SEVER'S DISEASE
pain at Achilles tendon insertion usually 8-12 years old density + fragmentation of calcaneal apophysis - normal variant symptomatic treatment
KOHLERS'S DISEASE
avascular necrosis of navicular usually 4-8 years old very rare main differential diagnosis: infection symptomatic treatment: will revascularise may need cast during initial illness long term prognosis good
ISELIN'S DISEASE [Back To Top]
Apophysitis of 5th MT base
FREIBERG'S DISEASE
Albert H. Freiberg (1868-1940), Cincinnati Ohio - Link to Freiberg's Original Paper avascular necrosis of a lesser metatarsal head with infraction usually in teenagers or young adults usually 2nd MT possibly caused by trauma
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Smillie Classification (1967): [Back To Top]
1. # alone 2. surface contour altered 3. central portion depressed 4. loose body seperation 5. Flattening
Clinical features [Back To Top]
pain in MTPJ stiffness swelling sometimes large palpable osteophytes
Treatment [Back To Top]
Non-surgical management
analgesia orthosis shoe adaptation steroid injections into joint
Surgery
simple debridement and cheilectomy metatarsal head osteotomy excision arthroplasty
Freiberg's References:
Katcherian DA: Treatment of Freiberg's disease. Orthop Clin North Am 1994;25:69-81. This is a detailed review of Freiberg's infraction and its treatment stages.
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Kinnard P, Lirette R: Freiberg's disease and dorsiflexion osteotomy. J Bone Joint Surg 1991;73B:864-865. Intra-articular dorsal wedge osteotomy through the distal metaphysis with sufficient bone removal to bring the healthy plantar part of the metatarsal head into articulation with the phalanx was performed on 15 patients. Advanced disease was present in nine patients. The authors reported that all of the patients were able to return to sports, although three had mild discomfort after prolonged jogging. Although the authors observed about 2.5 mm of shortening, the technique appears to restore congruity of the joint.
Smith TW, Stanley D, Rowley DI: Treatment of Freiberg's disease: A new operative technique. J Bone Joint Surg 1991;73B:129-130. The authors discuss metatarsal shaft shortening (4 mm) in 15 patients (16 feet) and the application of a "T" plate. The plate was removed after 12 months. Pain was relieved within 12 months (mean 5 to 7 months) in all but one patient. Swelling was improved in four patients and stiffness was observed in seven of the 16 feet postoperatively. In four feet the toe did not contact the ground in stance. Results were assessed as excellent in five patients; nine were pleased with the results.
Sproul J, Klaaren H, Mannarino F: Surgical treatment of Freiberg's infraction in athletes. Am J Sport Med 1993;21:381-384. The authors reviewed 11 cases of Freiberg's infraction in athletes. All patients underwent debridement and all were reported to have had improvement in symptoms with 80% normal range of motion. Nine of ten patients returned to presurgical sports activities.
Bibliography:
Blackburn Foot & Ankle Hyperbook
Orthopaedic Knowledge Update Speciality Series - Foot & Ankle
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5 of 5 10/6/2007 11:02 AM Other Foot Fractures http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Other Foot Fractures
TALAR Neck Body Head Lateral Tubercle FRACTURES
MIDTARSAL TARSAL Lateral Process Osteochondral Talar dislocations INJURIES DISLOCATIONS
MIDFOOT METATARSAL 5th Metatarsal Navicular Cuboid FRACTURES FRACTURES Fractures
LISFRANC SESAMOIDS INJURIES
TALAR FRACTURES [Back To Top]
1. Neck fractures (50%)
Classification
Hawkins "Fractures of the neck of the talus" JBJS 52A:991-1002, 1970
Type Pathology
I Undisplaced
II Displaced [disloc. subtalar jt.]
III Displaced + dislocation of the body [disloc. ankle jt.]
IV Displaced + dislocation of both body and neck (added by Terry and Canale later) [disloc. T-N jt.]
Treatment and results
Subtalar Hawkins Treatment AVN Non-union Results Arthrosis 6 weeks non-weight bearing in cast (minimum), weight bearing Type I 10% 2% 25% 90% good results starts when signs of union present Immediate closed reduction in A/E if skin compromise present, ORIF via medial approach with 47% unsatisfactory result with Type II lag screw fixation from anterior - 40% 8% 65% healing usually in 8 - 12 weeks posterior. The screw heads must be countersunk below the articular surface. Malunion 30%; 52% 25% of these are open; ORIF 65% unsatisfactory results and Type III required (via medial malleolus 90% 10% (ankle healing occurs in upward of 16 osteotomy) 70%) weeks Type IV ORIF
Hawkin's sign
Radiographic appearance on AP X-ray
At 6-8 weeks disuse osteopenia is seen as subchondral atrophy in the dome of the talus. This would not occur if there was no blood supply. AVN risk 4%.
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Note - AVN does not equate with a poor outcome.
2. Body fractures (shear fractures) (20%) [Back To Top]
Classification (Boyd and Knight)
Type I vertical fracture line, coronal or saggital (A,B,C,D see below)
Type II horizontal fracture line (A undisplaced; B displaced)
Treatment
Type IA + IB with < 2mm displacement - NWB cast 6-8 weeks
Type IC + ID - ORIF
Type II - very little written but closed reduction + cast immobilisation recommended
3. Headfractures (10%) [Back To Top]
Undisplaced - NWB cast 6-8 weeks
Displaced - ORIF
4. Lateral tubercle fractures [Back To Top]
Conservative treatment with excision of fragment if it remains symptomatic
5. Lateral process fractures
Snowboarder's ankle
Undisplaced fractures treat conservatively
Large displaced fragments ORIF
Small fragments or late presentation excise fragment
6. Osteochondral lesions [Back To Top]
Also see Osteochondritis Dissecans of Talus
Occur in 2-6% of all ankle sprains
Occur either anterolaterally or posteromedially. Rarely central.
Classification (Berndt and Harty):
Stage I Small area of compressed Non-operative subchondral bone
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Stage II Partially attached osteochondral Non-operative fragment
Stage III Completely detached but Small defects removed and area drilled; undisplaced osteochondral Large defects can be fixed (Herbert fragment screw/ bioabsorbable pins); Osteochondral grafting has been tried but results not available
Stage IV Completely detached osteochondral Removal of fragment and drilling of bed; fragment Osteochondral grafting has been tried but results not available
7. Total talar dislocation [Back To Top]
Most series are 3-5 cases! No uniformly accepted or predictable treatment
Options:
1. Re-implantation - variable results with regard to AVN + infection, but all develop OA 2. Talectomy 3. Resection and fusion
Treatment should be customised to the clinical situation
Complete dislocation with severe contamination, re-implantation is not indicated
If re-implantation is performed the surgeon should always counsel the patient about the need for subsequent talectomy if infection sets in, or ultimately, amputation
Salvage procedures:
Talectomy Arthrodesis - ankle, subtalar, pantalar
8. Sub-talar dislocation [Back To Top]
Simultaneous dislocation of both the subtalar and talonavicular joints
Classification = Broca - an anatomical description of the direction of the dislocation:
Medial (80%) Lateral (17%) Posterior (2%) Anterior (1%)
Treatment:
Closed reduction and cast immobilisation for 6 weeks Open reduction if closed reduction fails
MIDTARSAL INJURIES (Chopart's Joint) [Back To Top]
Classification (Main and Jowett):
5 broad patterns based on the direction of the force applied and the subsequent displacement
1. Longitudinal stress (40%)
Axial loading of foot Common to have Lisfranc injury in association because the injury mechanism is the same Worst prognosis of the non-crush injuries
2. Medial stress (30%)
Precursor to subtalar dislocation
3. Lateral stress (17%)
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4. Plantar stress (7%)
5. Crush injury (6%)
Treatment: Standard options
Closed reduction + POP cast if stable when reduced Closed reduction + K-wire if unstable ORIF (with K-wires or screws) if CR fails
Crush injuries:
Have high index of suspicion for compartment syndrome In the most severe injuries 1 o amputation may be the only reasonable option
ISOLATED TARSAL DISLOCATIONS [Back To Top]
All are very rare
Treat with closed reduction and cast or open reduction if CR fails. Internal fixation if unstable
MIDFOOT FRACTURES [Back To Top]
1. Navicular
A. Tuberosity #
Symptomatic treatment, but if displaced > 5mm then ORIF as non-union is likely
B. Body #
Classification (Sangeorzan)
Type 1 Fracture is in the coronal plane with no angulation of the forefoot.
Type 2 Fracture line is dorsolateral to plantarmedial, forefoot is displaced medially
Type 3 Fractures with central or lateral comminution
Treatment:
Undisplaced # NWB cast for 6 weeks All displaced, comminuted or fracture dislocations should be treated surgically ORIF with K-wires or screws Ú ± bone grafting for depressed areas
Stress #
Seen in track athletes Management Cessation of training for 6-8 weeks with restricted weight bearing Delayed union or non-union can occur which may require intervention
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2. Cuboid # [Back To Top]
Avulsion - treat symptomatically
Compression - distraction + corticocancellous bone grafting + internal fixation
METATARSAL FRACTURES (excluding those associated with Lisfranc injuries) [Back To Top]
Undisplaced:
Weight bearing as tolerated Can use wooden shoe or weight bearing cast
Displaced
1 st metatarsal # ORIF as only minor malalignment can lead to transfer lesions 2 nd - 4 th metatarsal # If no sagittal plane angulation deformity present then treat as for undisplaced # If sagittal angulation present ORIF with longitudinal K-wires
th 5 metatarsal # [Back To Top]
Jones fracture:
described by Sir Robert Jones in 1902, after he sustained a 5th MT fracture. typically 1.5cm distal to the base of the 5th MT.
Dameron, Lawrence & Botte have described three separate fracture zones
Majority can be treated conservatively but if symptomatic non-union develops then ORIF may be indicated particularly in athletes
Non-union or delayed union more likely in Zone 3
Hypertrophic - longitudinal compression screw
Atrophic - tricortical bone graft + longitudinal compression screw
SESAMOID FRACTURES [Back To Top]
Always conservative treatment for 6 months
If painful non-union, pain despite adequate conservative treatment or degenerative changes develop then treat with excision of sesamoid
Never excise both as this can lead to a cock-up deformity of the hallux
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6 of 6 10/6/2007 11:02 AM Peroneal Tendon Injuries http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Peroneal Tendon Injuries
Martyn Snow, 2005
Anatomy
The peroneus longus and brevis arise from the posterolateral surface of the fibula and the fascia of their compartment. They run over the posterior surface of the fibular tip, where there is an adaptive fibrocartilage on the fibula, with brevis next to the bone. The tendons are kept in place by the presence of a shallow groove on the posterior fibula, the superior peroneal retinaculum (SPR) which tethers the tendons to the fibula, and a fibrocatilaginous lip, which deepens the groove where it meets the retinaculum.
On the lateral surface of the calcaneum the tendons run superficial to the calcaneofibular(CFL) and lateral talocalcaneal ligaments. Distal to the CFL the tendons run superior (brevis) and inferior (longus) to the peroneal trochlea on the lateral calcaneal wall, retained by the inferior peroneal retinaculum (IPR). Here the sheath is thickened and stenosing tenosynovitis may occur. The peroneus brevis is inserted into the inferolateral part of the tubercle of the 5 th metatarsal. The peroneus longus turns through a sharp angle to enter a fibro-osseous tunnel on the underside of the cuboid, where there is usually an accessory ossicle, the os perineum. The longus tendon inserts into the plantar surface of the first metatarsal.
There are avascular zones in brevis at the level of the SPR, and in longus at the IPR and the sharp turn to enter the cuboid tunnel. These are the commonest levels for tears.
Both tendons are plantar flexors of the ankle and evertors of the subtalar and midtarsal joints. As evertors their main opponent is tibialis posterior. In addition the peroneus longus plantarflexes the first metatarsal in opposition to tibialis anterior.
Peroneal tendon tears
Peroneus brevis tears are
· about three times commoner than those of peroneus longus
· often associated with laxity of the SPR
· also associated with a low musculotendonous junction or an accessory peroneus quartus muscle – these may make the tendon stiffer or stretch the SPR
· commonly associated with lateral ligament injuries of the ankle – about 50% also have ankle instability; peroneal tenosynovitis, tears and instability may be present in up to 70% of patients with ankle instability
· usually longitudinal, partial tears – only about 10% are complete tears
· normally centred on the level of the superior peroneal retinaculum
· probably caused by compression of the brevis tendon between the longus tendon and the fibula, especially if the tendon can be squeezed over the edge of the groove because the retinaculum is lax, or if there is a sharp ridge at the edge of the groove
Peroneus longus tears are:
· Strongly associated with pes cavus; 80% in the study by Brandes and Smith (2000); the plantarflexed first ray may increase the stresses in the tendon
· Usually at the level of the inferior peroneal retinaculum or the point where the tendon turns under the cuboid
· Usually partial longitudinal tears
About 10% of patients have combined tears of both tendons.
POPS
Pain at the point where the peroneus longus tendon turns into the cuboid groove is sometimes known as painful os peroneum syndrome; (POPS) (Sobel et al 1994). This may be due to:
· Acute stress fracture of the os perineum
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· Chronic fracture of the os perineum, with or without peroneus longus tendonopathy or tear
· Peroneal tendonopathy or tear at the level of the inferior peroneal retinaculum, often of a stenosing type Peroneal tendon tears
Peroneal tendon instability
Tearing or detachment of the SPR may allow the tendons to prolapse laterally, with pain, swelling and weakness of eversion. The brevis tendon is often torn – it is thought it may be lacerated by the sharp edge of the fibular groove. A shallow fibular groove is commoner in patients with instability. There is a strong association with ankle instability.
Eckert and Davis (1976) described three types of retinacular deficiency:
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Clinical features
Patients with peroneal tendon problems usually present with pain, swelling and sometimes clicking or popping on the posterolateral aspect of the ankle or the lateral aspect of the hindfoot. Those with longus tears may localise the pain to the entry to the cuboid tunnel (POPS) or occasionally under the midfoot. There may be a history of an ankle sprain especially with brevis tears.
Examination will demonstrate
tenderness over the tendon – typically behind the malleolus with brevis
tears and at the entry to the cuboid tunnel or at the IPR with longus tears.
Getting the patient to actively rotate the foot may produce obvious tendon prolapse onto the lateral aspect of the malleolus. With lesser degrees of instability there may be no obvious prolapse but the brevis tendon may be felt to slide laterally, usually in eversion. A brevis tendon which becomes prominent laterally often has a longitudinal tear.
Resisted contraction of each tendon may reproduce thepatients pain.
Active movement may produce a grating or creaking sensation over the tendons.
There may be varying amounts of synovial swelling. Pes cavus suggests a longus tear.
Imaging
· Plain radiography is not usually very helpful. Oblique views of an acutely injured ankle may show an avulsion fragment lying lateral to the lateral malleolus this represents a flake of bone avulsed with the SPR.
· ultrasound can show the tendons well and demonstrate tears. assess the ankle ligaments.
· MR also enables assessment of the depth of the peroneal groove and will demonstrate
intra-articular problems in the ankle such as osteochondral injuries. Tendonopathy shows as enlargement, high signal or a flame shape to the tendon. Tears show as multipart or chevron-shaped tendons, and part or all of the tendon may be subluxed laterally.
There have been no comparative studies of the accuracy or utility of ultrasound and MR.
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Non-surgical treatment
· Simple analgesics or NSAIDs may be used for pain and synovitis.
· Physical modalities such as ice, ultrasound or interferential therapy may be used to settle acute symptoms.
· An ankle brace may be useful in the acute situation or occasionally pallliatively.
· Patients with flexible cavus deformities and a longus tear may benefit from orthotics.
Try non-surgical treatment for patients without overt instability, but would generally advise the correction of SPR instability as primary treatment.
Surgery
Peroneal tendon tears
· Debridement and suture of longitudinal tears, with tubulisation of the remaining
tendon. Krause et al (1998) recommended repair for tears of peroneus brevis where more than 50% of the tendon was intact, but where there was less than 50% tendon remaining they excised the abnormal segment and attached the ends to the peroneus longus.
· Where there is a complete tear with discontinuity of the tendon ends repair without tension is usually impossible except in the acute setting, and the ends of the tendon should be sutured to the adjacent tendon.
· complete tears of both tendons preclude this, and a tendon transfer is required flexor digitorum longus transfer has been reported in two patients by Borton et al (1998)
· Peroneus longus tears at the os peroneum may be debrided and repaired. A fragmented os peroneum is usually excised. Occasionally a defect in the tendon needs to be bridged with a tendon graft (plantaris).
Peroneus brevis tears often have associated SPR laxity and this should be repaired at the same time as the tendon (see below). Stenosing tenosynovitis of peroneus longus may require release of the IPR and/or reduction of the peroneal tubercle.
Van Dijk (1998) described endoscopic debridement and suture of the peroneal tendons. There have been no comparative studies with open surgery.
Superior peroneal retinaculum laxity
Many different types of operation have been described to correct SPR laxity:
· Sliding bone graft to the lateral edge of the groove
· Deepening of the groove by removing underlying cancellous bone and depressing the cortical floor of the groove
· Bankhart-type repair of the type-2 retinacular lesion
· Rotational osteotomy of the distal fibula
· Various forms of retinacular tightening or re-insertion
Obviously, these are not all mutually exclusive. Our standard stabilisation procedure is a Bankhart-type repair. The retinaculum is opened longitudinally, close to where the attachment to the fibular groove should be. The bare area on the lateral malleolus is freshened and one or two suture anchors inserted close to the edge of the groove. The avulsed tissue sleeve is reattached to these and the retinaculum plicated, usually also onto the suture anchor(s). If the groove is shallow, a posterior trapdoor is elevated and cancellous bone removed from the posterior part of the lateral malleolus to allow the floor of the groove to be lowered and the edges of the trapdoor evened. Debridement and repair or tenodesis of tendon tears is usually required.
All reports of stabilisation are small, usually 10-20 patients. Overall, about 85-90% of patients get satisfactory functional results, and some have returned to top-level sport. The rate of recurrent instability is 5-10%. Other complications include neuromas, infection and lateral ankle pain. Symptomatic ankle instability can be corrected through the same incision, usually with a Brostrom-Gould procedure.
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5 of 5 10/6/2007 11:03 AM Rheumatoid Foot http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Rheumatoid Foot
STAGES CLINICAL TREATMENT ANKLE
HINDFOOT FOREFOOT TENDONS OTHER TISSUES
INTRODUCTION
70-90% of rheumatoids have foot involvement
15% present initially with foot complaints.
STAGES [Back To Top]
Stage 1 - synovitis
Stage 2 - Joint erosion & tendon dysfunction
Stage 3 - Progressive deformities
CLINICAL [Back To Top]
Present with Pain or Deformity.
Swelling of the MTPJs Hallux Valgus Claw toes Bursae Morton's neuroma Valgus hindfoot Valgus ankle Tibialis posterior tendon rupture Tarsal Tunnel Syndrome - 2ndry to synovitis of contents.
Look for:
Vascular status - PVD or rheumatoid vasculitis Neurology - neuropathic process more common in rheumatoids. Tendonitis or ruptures (tibialis posterior, proneal) Primary deformity - Forefoot or Hindfoot Which joint is the cause of pain and/or deformity (not easy - may need diagnostic injections)
TREATMENT [Back To Top]
Conservative
1. Medications
2. Footwear - shoes should not be made to correct the deformity, but rather be adjusted to it.
Surgery
Pre-op precautions:
Check the positions of the knees & hips (should correct these first for ankle & hindfoot problems) Skin condition Medications - methotrexate & corticosteroids may need to be stopped.
ANKLE JOINT [Back To Top]
Arthroscopic Synovectomy
useful for cases of marked synovitis & minimal articular damage
Supramalleolar Osteotomy
for stiff hindfoot in equino-varus.
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Ankle Arthrodesis
Operation of choice in most cases.
Arthroscopic arthrodesis if there is minimal osteoporosis & destruction. Intramedullary nail through heel Dowel arthrodesis. If there is gross deformity will need more correction / resection & external fixator.
Ankle Arthroplasty
Indication = severe destruction with a stiff, non-deformed hindfoot (or triple arthrodesis)
2 main types = 1. semi-constrained (Mayo) and 2. LCS prosthesis.
Failures were awful & complication rates high.
This may be improving with newer designs (eg. STAR prosthesis).
Note requirements for a joint replacement prosthesis are:
1. Permit normal motion 2. Eliminate pain 3. Accept a salvage procedure 4. Give stability 5. Have no adverse effects on surrounding joints 6. Good fixation 7. Tolerate repeated loading
More detail on Ankle Replacement see Maitrise Orthopaedics and Mr Peter Wood's Website
anklereplacementSTAR1 anklereplacementSTAR2 anklereplacementSTAR3 anklereplacementSTAR4 star
HINDFOOT [Back To Top]
2 main forms of RA affect the hindfoot:
1. Loose mobile type - gross synovitis & planovalgus collapse. Mobile joints. Arthrodesis is difficult to achieve. 2. Stiff dry type - fixed deformity. Responds well to arthrodesis with appropriate excisions.
Talonavicular fusion - operation of choice for early cases since it will stabilize the hindfoot by reducing subtalar motion by 90%.
Triple arthrodesis if the deformity is severe - screws are better than staples.
FOREFOOT [Back To Top]
(Updated by Z Naqui, 2005)
90% of RA pts have forefoot involved. 15% present with forefoot pain.
MTP's loose competence, then toes sublux dorsally and dislocate " pulling plantar fat distally and anteriorly.
Also get IP hyperextension and HV.
OPTIONS
1. Synovectomy of MTPJs - best synovectomy is excision arthroplasty.
2. Metatarsal oblique osteotomies (Helal)
3. Excision of MT heads plus prox. third of PP's (Hoffman type procedure)
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4. 'Pobble' amputation - amputation of all the lesser toes at the MTPJs - only for severe deformity & pain.
5. HV " Keller's or silastic implant (not good), arthrodesis prob. Best
6. Forefoot reconstruction: provide stable medial post by arthrodesis of 1 st MTP. Also reduce plantar fat pad back down " HOFFMAN procedure removing MT heads.
Also see Lesser Toes Summary
TENDONS [Back To Top]
Tibialis Posterior tendon rupture causes planovalgus collapse. May have Tarsal tunnel syndrome also.
Peroneal Muscle spasm can occur.
OTHER STRUCTURES [Back To Top]
1. Neuropathic joints
2. Tarsal Tunnel Syndrome
3. Rheumatoid nodules (indicative of aggressive disease)
4. Rheumatoid ulcers
5. Stress fractures
Sponsored Links www.ebimedical.com
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3 of 3 10/6/2007 11:04 AM Rheumatoid Forefoot http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Rheumatoid Forefoot
Tim Williams, 2006
90% of RA pts have forefoot involved. ( = Hand incidence!) 15% of RA pts initially present with forefoot pain.
Pathology
MTPJ Synovitis & Pannus destruction IPJ's usually Spared
Deformities
2nd-5th MTPJ Synovitis ? Capsular laxity ? P1 Dorsal subluxation / dislocation ? Prominent MT Heads as fat pad drawn distally ? METATARSALGIA & PLANTAR KERATOSES
Subsequent Intrinsic / extrinsic muscle imbalance ? CLAW TOE & DORSAL CORNS
1st MTPJ Synovitis combined with loss of lateral support from lesser toes ? HALLUX VALGUS & BUNION
Larsen Staging (Acta Orthop 1977)
Stage I: No bony deformity. Discomfort and synovitis without significant joint space narrowing. Stage II: Early involvement without fixed deformity. Minimal erosive changes. Stage III: Soft tissue deformity. No significant joint erosive changes. Stage IV: Articular destruction. Severe hallux valgus, dislocation of the lesser MTP joints with fixed hammer toe or claw toe deformities, pes planovalgus (flatfoot), and hindfoot arthroses.
TREATMENT OPTIONS
Multidisciplinary Approach
Non - Operative
Medical Optimisation (Rheumatologists & G.P.) NSAIDS, Steroids, DMD's, anti-TNF etc.. Orthotics Large Toe Box Shoes Metatarsal Pads / Bars Total Contact Insoles Rocker Bottom Shoes Physiotherapy - Try to maintain movement
Operative
1. Lesser MTPJ Surgery - Decompress the Joint to allow relocation
Synovectomy
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Hoffman Procedure (1911) - Excision of metatarsal Heads (1) Fowler Procedure (1959) - Excision of Prox 1/3rd P1 Stainsby Procedure (1998) - Exc. Of Prox 1/3rd P1 & Flex. - Ext. tendon interposition transfer Weil Osteotomy - Oblique MT neck shortening osteotomy (New)
2. Lesser IPJ Surgery
Osteoclasis - 'Crunch' joint straight Soft Tissue release - Plantar capsule & Flexor Brevis Du Vries Procedure - Excision Arthroplasty - Base P2 & Head P1 PIPJ Fusion
3. Hallux Valgus Surgery
MTPJ Fusion - Screw, Plate or Staples Mayo Procedure - Excise MT Head Kellers Procedure - Excise prox. 1/3rd P1 (Largely Historical) Osteotomies - Chevron, Scarf etc. (New)
Forefoot Reconstruction = Combination of above surgeries
Principle 'Don't de-function 1st Metatarsal'
Maintain MT length arcade ( Maestro's)
1st MTPJ Mayo & Hoffman's Procedure 5th +/- Lesser IPJ surgery 1st MTPJ Fusion & Hoffman's 2nd - 5th " " 1st MTPJ Fusion & Stainsby's 2nd - 4th " " 1st MTPJ Scarf & Weil's 2nd - 4th " " (The future)
1st Fusion + Hoffman's 1st Fusion + Stainsby's
4. Amputation
Through MTPJ - Salvage Surgery
Recent papers
Arthrodesis versus Mayo resection: the management of the first metatarsophalangeal joint in reconstruction of the rheumatoid forefoot. Grondal L, Brostrom E, Wretenberg P, Stark A. - Stockholm
JBJS Br. 2006 Jul;88(7):914-9.
31 patients prospectively randomised to either fusion or Mayo resection as part of forefoot reconstruction. No significant differences between outcome for both groups at mean 6 years.
Metatarsal head resection in the rheumatoid foot: 5-year follow-up with and without resection of the first metatarsal head.
Hulse N, Thomas AM - Birmingham J Foot Ankle Surg. 2006 Mar-Apr;45(2):107-12.
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Retrospective study of 45 feet. 16 had only lesser MT excision and 29 had 1st - 5th Mt head excision. 7 /16 ( 47%) of 1st group had revision excision of 1st MT head
Further Reading
The pathological anatomy of claw and hammer toes . MS Myerson 1989 JBJS(Am).
Long-Term Results of the Modified Hoffman Procedure in the Rheumatoid Forefoot. S. Thomas, Kinninmonth, and C. Senthil Kumar, JBJS(Am). 2005;87:748-752
http://dr.barouk.free.fr/anglais.htm - Scarf & Weil Osteotomies - surgical videos and techniques.
Rheumatoid Forefoot Reconstruction. A Long-Term Follow-up Study . M.J. Coughlin JBJS (Am) , Mar 2000; 82: 322 - 41.
Acknowledgements
The Cooke Book - Mr. P. Cooke, Oxford. Forefoot Reconstruction - L.S. Barouk (Springer Publications) Surgery of the Foot & Ankle - Coughlin & Mann (Mosby)
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3 of 3 10/6/2007 11:04 AM Sesamoids http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Sesamoids
Embryology Anatomy Biomechanics Imaging Fractures
Turf Toe Stress fractures Infection Arthrosis
Embryology [Back To Top]
Named sesamoid bones because of resemblance to sesame seeds Most constant sesamoids are those under 1 st MTP joint, but can be present under other metatarsal heads Develop by endochondral ossification Ossification by age 8-12 yrs of age, females earlier Multiple ossification centres which don't always fuse Fibular sesamoid rarely partite Tibial sesamoid bipartite in 10% of population, a quarter of whom have bilateral tibial bipartite sesamoids
Anatomy [Back To Top]
Central ridge, crista divides the under surface/trochlear surface of the 1 st MTP joint, divides the two sesamoids Medial and lateral metatarsaosesamoid ligaments and medial and lateral phalangosesamoid ligaments and intersesamoid ligaments are stabilisers The sesamoids are embedded in the plantar plate in the plantar plate with attached to prox phalanx inferiorly by insertions of medial and lateral heads of flexor hallucis The fibular sesamoid also attached to adductor hallucis, and intermetatarsal ligament The tibial sesamoid is attached to abductor hallucis
Biomechanics [Back To Top]
The functions of the sesamoids are speculated to be
Mechanical protection for flexor hallucis longus tendon which moves in the gap between the sesamoids A pulley function promoting plantarflexion by flexor hallucis brevis Dispersal of the forces from the 1 st metatarsal head
Imaging [Back To Top]
AP standing xray
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Standing lateral Oblique views axial view shows relationship of sesamoids to crista (sesamoid skyline view with toes dorsiflexed)
Isotope bone scan CT MR scan
Acute fractures [Back To Top]
Mechanisms of injury - forced dorsiflexion and abduction, direct trauma, sudden loading of 1 st MTP joint fragments To differentiate from partite sesamoids, look for a sharp line, dorsiflexion views may show increase in separation of fragments. CT scan may help. Treatment-
below knee cast for 3 weeks, followed by a metatarsal bar. Pain may persist for 4-6 months.
If symptomatic nonunion, or chronic pain, consider excision of sesamoid or fragments, through medial , dorsal or plantar incision.
If both sesamoids- avoid resection as a cock up deformity can occur due to loss of function of flexor hallucis brevis
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Turf toe injury [Back To Top]
Exaggerated dorsiflexion with valgus/ varus strain of MTP joint, described by Bowers and Martin 1976 More common since artificial sports surfaces Can range from sprains of the sesamoid complex to ruptures of the complex causing proximal or distal migration of the sesamoid bones to sesamoid complex to a fracture of the sesamoid and dislocation Usually treated with below knee cast, but may need operative reduction and repair through medial approach
Stress fractures [Back To Top]
With MR scanning, sesamoiditis has been shown to be a precursor to stress fracture or AVN of sesamoid Presents with pain on walking Lateral Xrays may show progressive separation of fracture fragments with time Bone scan will be hot Treatment-
Sesamoiditis- NSAIDS, shoewear changes, orthoses with metatarsal relief
Stress fracture- below knee non weight bearing cast for 6 weeks
If persistent pain or nonunion 1. Bone grafting 2. Partial excision 3. Complete excision
Infection [Back To Top]
Treat with excision, if both sesamoids need to be removed a delayed fusion of the 1 st MTP joint can be performed to avoid a cock up deformity
Arthrosis of metatarsosesamoid joint [Back To Top]
Occurs secondary to malalignment, such as hallux valgus. Can also occur in hallux rigidus and inflammatory arthropathies such as R.A. and gout. As splaying of the first metatarsal occurs, the intermetatarsal ligament holds the sesamoid complex laterally. Symptoms more subtle than in sesamoiditis, with aching pain in plantar aspect of the foot rather than focal pain Usually no point tenderness on examination, but motion and compression elicits pain, crepitus may be present If squeezing the 1 st and 5 th metatarsals together allows correction of splaying between the 1 st and second MTs, then it is likely that only a minimal soft tissue release (of the adductor hallucis and superficial and deep parts of intermetatarsal ligaments) will be necessary. If the squeeze test does not reduce the sesamoids, release of the lateral sesamoid ligament will be necessary. Try and avoid excision of the sesamoids.
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Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Sinus Tarsi Syndrome
Adapted from the Blackburn Foot & Ankle Hyperbook
Anatomy Aetiology Pathology
Clinical Investigations Treatment
Anatomy [Back To Top]
The sinus tarsi is an anatomical space bounded by the talus and calcaneum, the talocalcaneonavicular joint anteriorly and posterior facet of the subtalar joint posteriorly. It is medially continuous with the much narrower tarsal canal.
The sinus tarsi contains the cervical ligament and the three roots of the inferior extensor retinaculum.
The tarsal canal contains the interosseous talocalcaneal ligament and the deep and intermediate roots of the inferior extensor retinaculum.
Both the sinus and the canal contain blood vessels - which are important for the nutrition of the talus - and nerves. The extensor digitorum brevis and bifurcate ligament lie anterior to the sinus tarsi.
Aetiology [Back To Top]
The term "sinus tarsi syndrome" was first applied in O'Connor in 1958 to a syndrome of post-traumatic lateral hindfoot pain and instability which was relieved by the injection of local anaesthetic into the sinus tarsi.
The cause of pain has been postulated to be vascular engorgement or nerve irritation, both due to fibrosis.
Frey et al suggests (on the basis of arthroscopic examination) that sinus tarsi syndrome is an inaccurate diagnosis & there is usually an underlying abnormality:
interosseous talocalcaneal ligament tears subtalar instability osteochondral injuries of the subtalar joint arthrofibrosis of the subtalar joint degenerative disease of the subtalar joint fibrous tarsal coalition chronic inflammatory changes in the sinus tarsi connective tissues
Pathology [Back To Top]
Pathological examination of tissue removed from patients with sinus tarsi syndrome include chronic inflammatory changes, fat necrosis, fibrosis and synovial cysts.
Clinical [Back To Top]
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Tenderness over the sinus tarsi, which is relieved by local anaesthetic injection
Pain may be exacerbated by varus tilting of the heel (unlike the pain of lateral impingement which is worse on valgus tilting of the heel) or walking on uneven ground.
A feeling of subtalar opening may be felt on the varus tilt test .
Abnormalities in the ankle are common: up to 50% have ankle instability and/or anterolateral synovitis.
Investigations [Back To Top]
Plain radiographs are generally normal, although degenerative arthritis of the subtalar joint may be seen.
Stress views of the subtalar joint (lateral or Broden views) may show instability
Subtalar arthrography may show obliteration of the anterior micro-recess but sensitivity is not very high.
MR shows inflammatory and fibrotic changes well. The interosseous talocalcaneal ligament may be shown to be torn but some observers find that non-specific changes make this difficult to visualise. MR also shows damage to the subtalar joint and surrounding structures.
Treatment [Back To Top]
Non-surgical symptomatic management & aircast splints
Two surgical techniques are described in the literature:
Excision of the entire contents of the sinus tarsi - Results of this are reported very favourably, with most or all patients relieved of pain. Arthroscopic debridement of the posterior subtalar joint and sinus tarsi - allows diagnosis and treatment with low morbidity. 94% of 49 patients treated by Frey et al were improved at 1-7.75 years' follow-up although half had some residual symptoms.
In addition, surgical treatment may be indicated for concomitant ankle synovitis or instability, subtalar instability or foot deformity.
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2 of 2 10/6/2007 11:05 AM Soft Tissue Impingement http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Soft Tissue Impingement
Edited by Martyn Snow
Anterior.
Chronic ankle pain after an ankle ''sprain'' is a well-documented problem and is seen in 20% to 40% of these patients. Pain is usually located anterolaterally, rarely anteromedially. Wolin described a ''meniscoid'' band between the fibula and the talus in 1950. This mass was thought to be hyalinized connective tissue from the talofibular joint capsule. impingement of this meniscoid tissue led to pain and swelling in the ankle.
The differential diagnosis for chronic pain secondary to ankle sprain includes osteochondral lesions of the talus, calcific ossicles, peroneal subluxation or dislocation, tarsal coalition, subtalar joint dysfunction, degenerative joint disease, and soft tissue impingement.
Anterolateral soft tissue impingement of the ankle occurs at three primary sites:
(1) the superior portion of the AITF ligament;
(2) the distal portion of the AITF ligament, which may involve a separate fascicle;
(3) along the anterior talofibular ligament (ATFL) and lateral gutter near the area of the lateral talar dome
conservative management,
nonsteroidal physical therapy bracing casting steroid injection
Radiographic
MRI can be helpful to rule out other conditions, but can be normal in impingement.
Surgery
Arthroscopic Debridement of the anterolateral gutter with complete removal of the inflamed synovium. However, care must be taken to not excise any of the functional remnants of the ATFL.
Posterior.
In addition to anterolateral impingement, posterolateral impingement of the ankle may also be seen clinically and may occur in combination with anterolateral impingement problems.
Posterior impingement may be associated with;
posterior ankle and/or subtalar synovitis, a prominent posterior talar tubercle os trigonum, flexor hallucis longus tendonopathy. hypertrophy or a tear in the posteroinferior tibiofibular (PITF) ligament, transverse tibiofibular ligament, tibial slip, or pathologic labrum on the posterior ankle
Diagnosis " Clinical +/- MRI
Treatment
Arthroscopic debridement
Open debridement " medial approach
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2 of 2 10/6/2007 11:05 AM Soft Tissue Impingement http://orthoteers.com/(S(o30paf45azn4qf452py0pc45))/printPage.aspx?a...
Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Soft Tissue Impingement
Edited by Martyn Snow
Anterior.
Chronic ankle pain after an ankle ''sprain'' is a well-documented problem and is seen in 20% to 40% of these patients. Pain is usually located anterolaterally, rarely anteromedially. Wolin described a ''meniscoid'' band between the fibula and the talus in 1950. This mass was thought to be hyalinized connective tissue from the talofibular joint capsule. impingement of this meniscoid tissue led to pain and swelling in the ankle.
The differential diagnosis for chronic pain secondary to ankle sprain includes osteochondral lesions of the talus, calcific ossicles, peroneal subluxation or dislocation, tarsal coalition, subtalar joint dysfunction, degenerative joint disease, and soft tissue impingement.
Anterolateral soft tissue impingement of the ankle occurs at three primary sites:
(1) the superior portion of the AITF ligament;
(2) the distal portion of the AITF ligament, which may involve a separate fascicle;
(3) along the anterior talofibular ligament (ATFL) and lateral gutter near the area of the lateral talar dome
conservative management,
nonsteroidal physical therapy bracing casting steroid injection
Radiographic
MRI can be helpful to rule out other conditions, but can be normal in impingement.
Surgery
Arthroscopic Debridement of the anterolateral gutter with complete removal of the inflamed synovium. However, care must be taken to not excise any of the functional remnants of the ATFL.
Posterior.
In addition to anterolateral impingement, posterolateral impingement of the ankle may also be seen clinically and may occur in combination with anterolateral impingement problems.
Posterior impingement may be associated with;
posterior ankle and/or subtalar synovitis, a prominent posterior talar tubercle os trigonum, flexor hallucis longus tendonopathy. hypertrophy or a tear in the posteroinferior tibiofibular (PITF) ligament, transverse tibiofibular ligament, tibial slip, or pathologic labrum on the posterior ankle
Diagnosis " Clinical +/- MRI
Treatment
Arthroscopic debridement
Open debridement " medial approach
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Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Tarsal Tunnel Syndrome & Nerve Entrapments
TARSAL TUNNEL SYNDROME
= Compression of the tibial nerve in the tarsal tunnel
Anatomy:
The tarsal tunnel is formed by the flexor retinaculum behind and distal to the medial malleolus
Contents from ant. to post.: (Tom Dick ANd Harry)
Tibialis Posterior Tendon Flexor Digitorum Longus tendon Posterior Tibial artery Posterior Tibial Nerve Flexor Hallucis Longus tendon
Posterior tibial nerve
is a branch of the sciatic nerve enters the deep posterior compartment of the leg between the two heads of the gastrocnemius. It passes deep to the soleus and travels distally between it and the posterior tibialis muscle. 3 terminal branches in the tarsal tunnel medial plantar nerve - Sensation to the plantar-medial aspect of the foot from the great toe to the medial half of the 4th toe. Motor to the abductor hallucis, flexor brevi & the 1st lumbrical. lateral plantar nerve - Sensation to the 4th & 5th rays & toes. Motor to ADQ, the interossei, adductor hallucis, 2nd to 5th lumbricals. the calcaneal branch - can be of a variable origin. Provides sensation to the heel pad.
Aetiology:
1. An accessory FDL muscle 2. Proliferative synovitis - Rheumatoid 3. Ganglia 4. Varicosities 5. Lipomas 6. Neurilemomas
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Examination:
Insidious onset of symptoms in the sensory distribution of the involved nerves
Pain radiates along the plantar side of the foot
Paresthesias, & atrophy of foot intrinsics
+ve Tinel sign behind medial malleolus
Manual compression for 30 sec. may reproduce symptoms
Investigations:
Nerve Conduction Studies can be useful - sensory conduction studies are more sensitive than motor studies.
MRI - 88% of Tarsal Tunnel Syndrome has shown an abnormality on MR scans.
Differential Diagnoses:
stress fractures (identified on 45 deg medial oblique view) inflammatory arthritides plantar fasciitis PID.
Treatment:
Depends on the aetiology
Rheumatoid synovitis responds well to rest & NSAIDs.
Space occupying lesions respond well to surgical decompression.
Steroid injections are a useful temporizing measure.
Surgery:
Curved incision that follows the nerve posterior to the medial malleolus. The flexor retinaculum is divided from proximal to distal, down to the abductor hallucis fascia. [Picture] The calcaneal branch or branches are protected as they extend posteriorly The medial and lateral plantar nerves are followed and freed beneath the abductor hallucis. The deep fascia of the abductor hallucis should be divided if it is tight.
Deep Peroneal Nerve Entrapment / ANTERIOR TARSAL TUNNEL SYNDROME
Aetiology:
Can occur as the nerve passes under the inferior extensor retinaculum.
Other causes include:
compression against dorsal osteophytes on the tarsal bones shoe wear that is tight over the dorsum of the foot.
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Patients complain of aching over the dorsum of the foot with numbness or pain in the first webspace.
If the lateral branch of the nerve is involved, the extensor brevis will show signs of atrophy.
Medial branch entrapment causes a sensory deficit in the first webspace.
Nonsurgical treatment involves shoe modifications & NSAIDs or steroid injection.
Surgery is indicated for persistent symptoms and is directed toward decompression of the nerve by the release of the tight retinaculum and the removal of any osteophytes.
Superficial Peroneal Nerve Entrapment
The Superficial Peroneal nerve passes through the fascia about 10 cm above the ankle to become subcutaneous. It branches into the medial & intermediate dorsal cutaneous nerves just proximal to the ankle which supply sensation over the dorsum of the foot except for the first webspace.
Entrapment may occur where the nerve passes through the fascia of the lateral compartment.
Sural Nerve Entrapment
A branch of the tibial nerve that accompanies the small saphenous vein.
It provides sensation to the calf, lateral heel, and lateral border of the foot.
Entrapment of the sural nerve is rare, because it is protected over its course by subcutaneous tissue & does not pass under restraining fascial edges or against bones.
It can become entrapped against a fracture fragment of the lateral malleolus, tarsal bones, or fifth metatarsal, or against an adjacent ganglion.
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Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Tendo Achilles Disorders
Achilles Tendinopathy Nomenclature Aetiology Rupture
Treatment Tendon Pain References
Updated by Matt Costa, 2005
Achilles Tendinopathy [Back To Top]
Achilles tendinopathy represents a common and debilitating spectrum of conditions. These range from acute Achilles tendon pain, to chronic painful Achilles tendinosis, to rupture of the tendon. Symptoms from the Achilles tendon result in prolonged periods of absence from work and sporting activity. The incidence of rupture is increasing in the Western World. Despite this fact, there are large areas of Achilles tendon pathology that are poorly understood and most therapeutic interventions are controversial.
Nomenclature [Back To Top]
The term 'tendinitis' should be reserved for acute Achilles tendon pain, usually as a result of trauma. This may have an inflammatory component. It is usually self-limiting and responds to analgesia and modified activity. 'Tendinosis' is the term used for chronic degenerative change within the tendon. There does not appear to be a major inflammatory component to these changes. The condition is common and often asymptomatic. Those patients who have pain are often resistant to treatment. 'Tendinopathy' is probably the safest term for all tendon pathology as it does not imply an aetiology
Aetiology [Back To Top]
In the normal tendon the collagen fibres are arranged in a linear fashion with a characteristic crimp. The tenocytes are 'squashed' into oval shapes between the fibres.
In tendinosis the fibre alignment and structure becomes less well defined and eventually is lost. The tenocytes become more round. The number of tenocytes may decrease (or in cases of painful tendinopathy increase.)
Fig 1. Normal tendon and tendinosis
The aetiology of tendinosis is not fully understood. Repetitive micro-trauma affects all tendons and usually leads to a reparative process. In the Achilles tendon the repair process may fail leading to progressive tendinosis. Why does the process fail?
There appears to be a hypovascular area of the tendon 2 to 6 cm proximal to the insertion into the calcaneus. (The major blood supply of the tendon is through its mesotenon, with the richest supply anteriorly).
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With increasing age this blood supply has been shown to reduce further.
Reduced blood supply appears to be at least partly responsible in some cases. However, there are several reports that suggest that painful tendinosis is actually characterized by increased vascularity.
The most recent research suggests that tendinosis is linked to a failure of the regulation of the enzymes (metaloproteinases in particular) that breakdown the tendon matrix.
There are several factors that appear to accelerate the development of tendinopathy:
Drugs such as steroids and quinolone antibiotics (such as ciprofloxacin) Repeated trauma due to over-training, the wrong footwear (functional over-pronation) and dysfunction of the triceps surae. Connective tissue disorders
Rupture [Back To Top]
History
The most common mechanism for TA rupture is pushing off with the weight-bearing forefoot while extending the knee (eccentric contraction of the calf muscles). The same effect can also be created by a sudden unexpected dorsiflexion of the ankle as in a fall from a height.
The patient describes a sudden pain (like being hit from behind), but is usually able to weight-bear. This may explain why late presentation is common “ c 40%.
Diagnosis
The easiest way to assess the Achilles tendon is with the patient kneeling on a chair facing away from you.
Acute ruptures are characterized by a palpable tendon defect And a negative calf-squeeze test (Simmonds squeeze test in the UK = Thompson test in USA). Plus an inability to do a toe-raise on the affected side
85% of tendon ruptures occur in the mid-portion of the tendon; 10% at the musculo-tendinous junction (these respond well to non-operative treatment) and 5% at the insertion (these are usually treated surgically and often require augmentation)
Late presentation ruptures may be difficult to assess. Tendon lengthening, as measured by dorsiflexion of the ankle, may be a useful surrogate sign. NB compare to the other side.
In equivocal cases dynamic ultrasound is by far the best investigation.
Treatment [Back To Top]
There are two key decisions about treatment:
Operative versus non-operative How will I rehabilitate the patient?
Operative Non-operative Re-rupture at 1yr 3.5% 12.5% Other complications (mostly 34% 3% wound related) Some evidence of earlier return to Longer period of protected Other factors sports; less calf atrophy, better ankle rehabilitation but avoiding the risks movement and improved gait pattern etc. of surgery
Operative technique:
Open or percutaneous repair
Open repair has a high complication rate, but in more recent papers these are much less frequent than has been reported in earlier articles. This may be due to a better understanding of the soft-tissues or more aggressive post-op rehab regimes.
Percutaneous repair has been shown to reduce the wound complication rate, but there is a relatively high risk of sural nerve damage. The results of accelerated rehabilitation following percutaneous repair have not yet been evaluated.
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There is little evidence (actually, none) that mechanically stronger suture techniques produce better results than more traditional Kessler and Bunnel techniques. Nor is there much evidence to support the use of non-absorbable sutures
There is no evidence that primary reinforcement (with any material) in otherwise uncomplicated cases produces betters results than simple primary suture
6 to 8 weeks of protected mobilization is all that is required.
The knee does not need to be included in the cast / orthosis, (knee position does not affect the tension in the repair when the foot is in equinus and immobilisation of the articular cartilage of the knee is detrimental).
Open repair:
With the patient in the prone position, make a posteromedial longitudinal incision; make it about 1 cm medial to the tendon and end it just proximal to where the shoe counter strikes the heel. Carry the incision sharply through the skin, subcutaneous tissues, and tendon sheath.
Reflect the tendon sheath with the subcutaneous tissue, minimizing subcutaneous dissection.
Approximate the ruptured ends of tendon with a tension suture, using a modified Kessler stitch through the stump 2.5 cm from the rupture “ depending on the degree of tendinosis.
Plantar flex the foot to approximate the ends of the tendon before tying the tension suture.
Percutaneous Repair:
Classic: Ma & Griffith: (Ma GWC and Griffith TG: Clin Orthop 128:247, 1977.)
Uses medial & lateral percutaneous wounds; therefore there is a risk of sural nerve entrapment.
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1. Webb & Banister ( JBJS Br. 1999 Sep;81(5):877-80 )
Can be done under local anaesthesia (with adrenaline)
3 posterior transverse incisions - the middle one at the level of the rupture & the other two 5cm prox. & distal. Make the proximal incision slightly medial (to avoid the sural nerve).
Repair as per diagram - No. 1 Nylon suture on curved needle.
Post-op: - 2wks in BK cast in plantarflexion - 2wks mid-position - 2wks neutral FWBing - 4wks heel raise.
How will I rehabilitate the patient?
Fig. A traditional cast versus an orthotic for this patient with bilateral ruptures?
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Traditional cast immobilization:
2 weeks - the cast is removed, the wound is inspected. Another short leg cast with the foot in 'gravity' equinus (full equinus is detrimental) is applied. The patient is mobilized non-weight-bearing with crutches. The cast is changed sequentially, and the foot is gradually brought to the plantigrade position. 6 to 8 weeks - a short leg walking cast is applied and full weight-bearing is allowed. The cast is then removed.
Weight-bearing mobilization:
An orthosis is applied in theatre (or on the ward when the patient is awake). The heel is lifted into a gravity equinus position with heel wedges within the device. The patient is encouraged to mobilize fully weight-bearing The heel raises are removed over the next 6 to 8 weeks until plantigrade is achieved. The orthotic is then removed. There is some evidence that this leads to faster recovery (A Cochrane review will be published soon).
These techniques can be applied to operative and non-operatively managed patients, although the cast or orthotic is generally worn for 10 to 12 weeks for non- operatively treated patients
Mobile Cast Method ( Cetti ):
Allows for limited active plantarflexion & early weight bearing. Advantages: 1) better plantarflexion strength at 1 year; 2) less calf atrophy; 3) less elongated tendon; 4) less wound problems & scar adhesions; 5) faster recovery & return to work. Method: - 1 week in equinus below knee cast post-op - At 1 week apply cast - patient prone; Hexcelite thermoplastic material; weightbearing stirrup for heel; dorsal foot cover to - position foot in 20deg. plantarflexion. - 6 weeks - remove cast & walk with half steps on injured side; with 1cm heel raise (on both sides). - 8 weeks - normal walking without heel raise. - 10 weeks - resistance exercises begin. - 4 months - jogging - 6 months - normal sports.
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Rehabilitation guide:
Average return to full sporting activity is still in the region of 6 to 9 months “ warn the patients!
8 weeks - normal walking, physiotherapy concentrates on proprioception and gait correction 12 weeks - resistance exercises begin, low impact (cycling and swimming preferred) 4 months - jogging 6-9 months - normal sports.
Neglected Rupture of the TA:
Treatment depends on the patient's physiological age, activity level, and amount of functional impairment. Surgery
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is generally indicated but the risks are high. Some patients do manage to walk without an Achilles tendon but stairs are very difficult
Options:
V-Y advancement of the aponeurosis over the gastrocnemius TA tendon turn-down flap of proximal tendon/aponeurosis Artificial tendon substitutes If there is extensive tendinosis or gross wasting of the triceps surae (any injury over 2 months old will have this) then seriously consider an FHL transfer.
Tendon Pain [Back To Top]
Acute Achilles tendon pain is very common in sportsmen
It is important to identify training errors, incorrect footwear etc in recurrent cases
It can usually be treated effectively with modified/restricted activity and analgesia for 6 to 8 weeks
Chronic tendon pain:
This is associated with an underlying tendinopathy. NB Not all tendinopathies are painful. Inflammation of the peritendinous tissues may occur in association with the tendon problem or as a separate entity The differential diagnoses include a chronic muscular tear proximally, ischaemia, and hindfoot pathology including arthritis, sinus tarsi syndrome and tarsal tunnel syndrome. In cases of insertional pain, rule out a Haglund deformity The patient usually complains of activity related pain but there may also be rest pain in severe cases Classically there is fusiform swelling of the mid-portion of the tendon, although absence of this finding does not exclude tendinosis. Ultrasound is the best investigation to assess the extent of the problem.
Treatment:
The 2001 Cochrane review suggested that there was no RCT evidence to support any non-operative therapy for chronic Achilles pain! Treatment modalities include:
Steroid injection - this has been associated with tendon rupture NSAIDs “ no effect in a placebo controlled trial Shockwave therapy “ no effect in a placebo controlled trial Orthoses to alleviate overpronation “ no effect in a placebo controlled trial
However, since this review there have been 2 trials that support the use of ' heavy eccentric loading exercises' , - these involve the patient stretching the tendon until it becomes painful.
Treatments that address the pathophysiology of the tendon are in development e.g. the injection of sclerosing agents (designed to reduce neo-vascularisation), appear to be beneficial.
Surgery:
If non-operative treatment fails surgical intervention may be necessary. However, the risks of wound complications remain high.
There is limited evidence to support any particular operation
Most surgeons advocate selective stripping of inflamed peritendinous tissues and some form of longitudinal tenotomy.
In more advanced cases, areas of tendinosis may need to be excised. If the area is very large, a tendon transfer may be the only option.
References [Back To Top]
Kannus P, Jozsa L. Histopathological changes preceding spontaneous rupture of a tendon. JBJS 1991; 73-A: 1507-1525.
Astrom M, Rausing A. Chronic Achilles tendinopathy. A survey of surgical and histopathological findings. Clin Orthop 1995;316:151-64.
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Riley G. The pathogenesis of tendinopathy. A molecular perspective. Rheumatology 2004; 43: 131-142.
Surgical interventions for treating acute Achilles tendon ruptures. Kahn R et al. Cochrane Database Syst Rev. 2004;(3):CD003674.
Lim J, Dalal R, Waseem M. Percutaneous vs. open repair of the ruptured Achilles tendon--a prospective randomized controlled study. Foot Ankle Int. 2001 Jul;22(7):559-68.
Tashjian RZ, Hur J, Sullivan RJ, Campbell JT, DiGiovanni CW. Flexor hallucis longus transfer for repair of chronic achilles tendinopathy. Foot Ankle Int. 2003 Sep;24(9):673-6.
Gravare Silbernagel K, Thomee R, Karlsson J. Eccentric overload training for patients with chronic Achilles tendon pain - a randomised controlled study with reliability testing of the evaluation methods. Scand J Med Sci Sports 2001; 11: 197-206.
Alfredson H, Ohberg L. Neovascularisation in chronic painful patellar tendinosis -promising results after sclerosing neovessels outside the tendon challenge the need for surgery. Knee Surg Sports Traumatol Arthrosc. 2005 Mar;13(2):74-80
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Percutaneous repair of the ruptured tendo Achillis [Picture]
J. M. Webb, G. C. Bannister From Southmead Hospital, Bristol, England; J Bone Joint Surg [Br] 1999;81-B:877-80.
Percutaneous repair of the ruptured tendo Achillis has a low rate of failure and negligible complications with the wound, but the sural nerve may be damaged. We describe a new technique which minimises the risk of injury to this nerve.
The repair is carried out using three midline stab incisions over the posterior aspect of the tendon. A No. 1 nylon suture on a 90 mm cutting needle approximates the tendon with two box stitches. The procedure can be carried out under local anaesthesia.
We reviewed 27 patients who had a percutaneous repair at a median interval of 35 months after the injury. They returned to work at four weeks and to sport at 16. One developed a minor wound infection and another complex regional pain syndrome type II. There were no injuries to the sural nerve or late reruptures. This technique is simple to undertake and has a low rate of complications.
Unfavorable effect of knee immobilization on Achilles tendon healing in rabbits. Yasuda T, Kinoshita M, Abe M, Shibayama Y Acta Orthop Scand 2000 Feb;71(1):69-73 Department of Orthopedic Surgery, Osaka Medical College, Takatsuki, Japan.
This study was undertaken to assess the effect of knee immobilization on the treatment of Achilles tendon rupture. After their Achilles tendons were severed, rabbits were divided into 2 groups. In Group A, only the ankle joint was immobilized. In Group B, both the knee and ankle joints were immobilized. At 4 weeks after surgery, both the ultimate tensile force and stiffness of the severed tendons were significantly greater in Group A than in Group B. In Group A, dense collagen fibers were seen in the repaired tendons, and the bundles of collagen fibers were parallel to one another along the axis of the tendons. In contrast, in Group B, dilated veins and capillaries were seen in the repaired tendons, and the proliferation of connective tissue containing collagen fibers was severely reduced around these veins and capillaries and was in general irregular and uneven. These results suggest that knee immobilization retards the healing of a ruptured Achilles tendon without suture, due to congestion and tension deprivation produced by keeping the tendon static.
Pefloxacin-induced achilles tendon toxicity in rodents: biochemical changes in proteoglycan synthesis and oxidative damage to collagen.
Antimicrob Agents Chemother 2000 Apr;44(4):867-72
Simonin MA, Gegout-Pottie P, Minn A, Gillet P, Netter P, Terlain B
Department of Pharmacology, UMR 7561, CNRS-Universite Henri Poincare-Nancy I "Physiopathologie et Pharmacologie Articulaires," Faculte de Medecine, Vandoeuvre-les-Nancy, France.
Despite a relatively low incidence of serious side effects, fluoroquinolones and the fluoroquinolone pefloxacin have been reported to occasionally promote tendinopathy that might result in the complication of spontaneous rupture of tendons. In the present study, we investigated in rodents the intrinsic deleterious effect of pefloxacin (400 mg/kg of body weight) on Achilles tendon proteoglycans and collagen. Proteoglycan synthesis was determined by measurement of in vivo and ex vivo radiosulfate incorporation in mice. Collagen oxidative modifications were measured by carbonyl derivative detection by Western blotting. An experimental model of tendinous ischemia (2 h) and reperfusion (3 days) was achieved in rats. Biphasic changes in proteoglycan synthesis were observed after a single administration of pefloxacin, consisting of an early inhibition followed by a repair-like phase. The depletion phase was accompanied by a marked decrease in the endogenous serum sulfate level and a concomitant increase in the level of sulfate excretion in urine. Studies of ex vivo proteoglycan
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synthesis confirmed the in vivo results that were obtained. The decrease in proteoglycan anabolism seemed to be a direct effect of pefloxacin on tissue metabolism rather than a consequence of the low concentration of sulfate. Pefloxacin treatment for several days induced oxidative damage of type I collagen, with the alterations being identical to those observed in the experimental tendinous ischemia and reperfusion model. Oxidative damage was prevented by coadministration of N-acetylcysteine (150 mg/kg) to the mice. These results provide the first experimental evidence of a pefloxacin-induced oxidative stress in the Achilles tendon that altered proteoglycan anabolism and oxidized collagen.
The effect of knee and ankle position on displacement of Achilles tendon ruptures in a cadaveric model. Implications for nonoperative management.
Sekiya JK, Evensen KE, Jebson PJ, Kuhn JE
Am J Sports Med 1999 Sep-Oct;27(5):632-5
Section of Orthopaedic Surgery, The University of Michigan Medical Center, Ann Arbor, USA.
Using a cadaveric model, we evaluated the effect of knee and ankle position on the displacement of the severed ends of an Achilles tendon transected at three different points. In six cadaveric legs the Achilles tendon was severed transversely, then marked with radiopaque wire suture. The distance between the wire markers was measured on radiographs taken in different positions of ankle and knee flexion. Ankle plantar flexion had a statistically significant effect on decreasing the gap between the severed ends of the Achilles tendon. This effect was clinically significant as, on average, the tendon edges were separated more than 20 mm when the ankle was in the neutral position and were apposed when the ankle was in 60 degrees of plantar flexion. With the ankle fixed in 60 degrees of plantar flexion, knee position had no significant effect on the displacement of the severed ends of the Achilles tendon. Overall, the effect of knee flexion was neither statistically significant nor clinically significant, as the increase in displacement of the severed ends of the Achilles tendon was only 3 mm from 0 degrees to 120 degrees of knee flexion. These results suggest that the nonoperative treatment of Achilles tendon ruptures requires immobilization in maximal ankle plantar flexion, and that immobilization of the knee may not be necessary to achieve tendon-edge apposition.
The effect of knee and ankle position on displacement of Achilles tendon ruptures in a cadaveric model. Implications for nonoperative management.
Sekiya JK, Evensen KE, Jebson PJ, Kuhn JE
Am J Sports Med 1999 Sep-Oct;27(5):632-5
Section of Orthopaedic Surgery, The University of Michigan Medical Center, Ann Arbor, USA.
Using a cadaveric model, we evaluated the effect of knee and ankle position on the displacement of the severed ends of an Achilles tendon transected at three different points. In six cadaveric legs the Achilles tendon was severed transversely, then marked with radiopaque wire suture. The distance between the wire markers was measured on radiographs taken in different positions of ankle and knee flexion. Ankle plantar flexion had a statistically significant effect on decreasing the gap between the severed ends of the Achilles tendon. This effect was clinically significant as, on average, the tendon edges were separated more than 20 mm when the ankle was in the neutral position and were apposed when the ankle was in 60 degrees of plantar flexion. With the ankle fixed in 60 degrees of plantar flexion, knee position had no significant effect on the displacement of the severed ends of the Achilles tendon. Overall, the effect of knee flexion was neither statistically significant nor clinically significant, as the increase in displacement of the severed ends of the Achilles tendon was only 3 mm from 0 degrees to 120 degrees of knee flexion. These results suggest that the nonoperative treatment of Achilles tendon ruptures requires immobilization in maximal ankle plantar flexion, and that immobilization of the knee may not be necessary to achieve tendon-edge apposition.
A new treatment of ruptured Achilles tendons. A prospective randomized study.
Cetti R, Henriksen LO, Jacobsen KS Department of Orthopaedic Surgery, Bispebjerg University Hospital, Copenhage, Denmark. Clin Orthop 1994 Nov;(308):155-65
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Sixty patients with acute rupture of the Achilles tendon were included in a prospective study and assigned randomly for operative treatment using a 4-string suture with either a new mobile cast (30) or a rigid below-knee cast (30). All patients were evaluated clinically for 1 year after surgery. During surgery, a radiographic monitor was placed in the Achilles tendon above and beneath the site of rupture. Radiographic evaluation of tendon behavior during healing was also performed on all patients for 1 year. Major complications were 1 rerupture in the mobile cast group and 2 reruptures and 1 infection in the rigid cast group. There were fewer minor complications in the mobile cast group. More patients in the mobile cast group resumed sports activities at the same level as before the rupture than in the rigid cast group. They also had better recovery of normal ankle movement plus faster and better recovery of plantar flexion strength. Fewer patients in the mobile cast group had calf atrophy, and fewer had problems 1 year after the accident. Furthermore, patients treated with the mobile cast had a statistically significant shorter sick leave. Radiographic evaluation of the tendon monitor showed significantly less elongation of the tendon 1 year after rupture for patients in the mobile cast group. Operative treatment with a 4-string suture and use of a postoperative mobile cast proved safe and convenient and preferable to treatment with the traditional rigid below-knee cast.
Ruptured Achilles tendon--preliminary results of a new treatment. Br J Sports Med 1988 Mar;22(1):6-8 Cetti R
Bispebjerg University Hospital, Department of Orthopaedic Surgery, Copenhagen, Denmark.
The preliminary results of a new treatment of ruptured Achilles tendons are presented. The new treatment consists of a new tendon suture and a new post-operative cast in which it is possible to make non-weight bearing movements of the ankle immediately after the operation. This makes it possible to walk the day after the operation, causes very little discomfort during the time in a cast, gives a quick return to normal mobility with normal plantar flexion strength and makes it possible to resume sport at the same level as before the injury.
Complication-free Achilles tendon repair. Br J Sports Med 1982 Dec;16(4):230-5 Cetti R
Fifty-one patients with subcutaneous rupture of the tendo calcanei Achillis were consecutively operated on with simple end-to-end suture using Bunnell's technique. The operation was performed under local anaesthesia. All patients were seen at follow-up four months after the operation. The complication rate was low compared to the ones reported in the current literature. It is concluded that operative treatment of Achilles tendon rupture performed under local anaesthesia is safe, economical and acceptable to patients.
Functional bracing for rupture of the Achilles tendon. Clinical results and analysis of ground-reaction forces and temporal data.
McComis GP, Nawoczenski DA, DeHaven KE, University of Rochester Medical Center and Ithaca College Department of Physical Therapy, New York 14623, USA. [email protected] J Bone Joint Surg Am 1997 Dec;79(12):1799-808 Fifteen patients who had sustained a rupture of the Achilles tendon were managed non-operatively with use of a functional bracing protocol, and clinical and functional performance measures were assessed after a mean duration of follow-up of thirty-one months (range, twenty-four to forty-five months). An age and gender-matched group of fifteen subjects was assessed to provide normative data for the comparison of side-to-side differences. Numerical scores were generated on the basis of subjective responses to a questionnaire, clinical measurements of the range of motion of the ankle and the circumference of the calf, and the results of the Thompson squeeze test and a single-limb heel-rise test. A 100-point scoring system was used to categorize the outcome as excellent, good, fair, or poor. In addition, ground-reaction forces and temporal data were assessed during functional dynamic activities that included walking, a single-limb power hop, and a thirty-second single-limb heel-rise endurance test. The result was graded as excellent for three patients, good for nine, fair for two, and poor for one. An increase in passive dorsiflexion of the treated ankle was the only clinical measure that was significantly different
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between the groups (p = 0.02). This increase in dorsiflexion was positively correlated with vertical force output between the mid-stance and terminal-stance phases of gait (r = 0.40, p = 0.05). With the numbers available, we could detect no significant differences between the groups with regard to the kinetic or temporal variables that were measured during functional dynamic activities. Patients who generated less peak vertical force and vertical height during the single-limb power-hop test tended to have poorer clinical scores. We believe that non-operative functional bracing may prove to be a viable alternative to operative intervention or use of a plaster cast for the treatment of acute ruptures of the Achilles tendon. The goals of treatment are to prevent the musculoskeletal changes that are associated with immobilization, to reduce the time needed for rehabilitation, and to facilitate an early return to work and to preinjury activities.
Early motion of the ankle after operative treatment of a rupture of the Achilles tendon. A prospective, randomized clinical and radiographic study.
Mortensen HM, Skov O, Jensen PE; Department of Orthopaedics, Odense University Hospital, Denmark. [email protected] J Bone Joint Surg Am 1999 Jul;81(7):983-90 BACKGROUND: Different regimens of early motion of the ankle after operative treatment of a ruptured Achilles tendon have been suggested since the late 1980s. However, as far as we know, no controlled studies comparing these regimens with conventional immobilization in a cast have been reported. METHODS: In a prospective study, seventy-one patients who had an acute rupture of the Achilles tendon were randomized to either conventional postoperative management with a cast for eight weeks or early restricted motion of the ankle in a below-the-knee brace for six weeks. The brace was modified with an elastic band on the posterior surface, in a manner similar to the principle of Kleinert traction. Metal markers were placed in the tendon, and the separation between them was measured on serial radiographs during the first twelve weeks postoperatively. The patients were assessed clinically when the cast or brace was removed, at twelve weeks postoperatively, and at a median of sixteen months postoperatively. RESULTS: The separation between the markers at twelve weeks postoperatively was nearly identical in the two groups, with a median separation of 11.5 millimeters (range, zero to thirty-three millimeters) in the patients managed with early motion of the ankle and nine millimeters (range, one to forty-one millimeters) in the patients managed with a cast. The separation was primarily correlated with the initial tautness of the repair (r[S] = 0.45). No patient had excessive lengthening of the tendon. The patients managed with early motion had a smaller initial loss in the range of motion, and they returned to work and sports activities sooner than those managed with a cast. Furthermore, there were fewer visible adhesions between the repaired tendon and the skin in the patients managed with early motion, and these patients were subjectively more satisfied with the overall result. The patients in both groups recovered a median of 89 percent of strength of plantar flexion compared with that of the noninjured limb, as measured with an isometric strain-gauge at 15 degrees of dorsiflexion. The heel-rise index was similar for both groups: 0.88 for the patients managed with early motion and 0.89 for those managed with a cast. CONCLUSIONS: Early restricted motion appears to shorten the time needed for rehabilitation. There were no complications related to early motion in these patients. However, early unloaded exercises did not prevent muscle atrophy.
Imaging in chronic achilles tendinopathy: a comparison of ultrasonography, magnetic resonance imaging and surgical findings in 27 histologically verified cases.
Astrom M, Gentz CF, Nilsson P, Rausing A, Sjoberg S, Westlin N; Department of Orthopaedics, Malmo University Hospital, Sweden.
Skeletal Radiol 1996 Oct;25(7):615-20 OBJECTIVE: To compare information gained by ultrasonography and magnetic resonance imaging (MRI) in chronic achilles tendinopathy with regard to the nature and severity of the lesion. DESIGN: Imaging of both achilles tendons with ultrasonography and MRI was performed prior to unilateral surgery. Operative findings and histological biopsies together served as a reference. PATIENTS: Twenty-seven patients (22 men, 5 women; mean age 44 years; 21 athletes) suffering from chronic achilles tendinopathy participated in the study. Eighteen patients had unilateral and 9 had bilateral symptoms. RESULTS AND CONCLUSIONS: Surgical findings included 4 partial ruptures, 21 degenerative lesions and 2 macroscopically normal cases. Microscopy revealed tendinosis (degeneration) in all tendon biopsies, including cases with a partial rupture, but only slight changes in the paratendinous tissues (paratenon). Ultrasonography was positive in 21 of 26 and MRI in 26 of 27 cases. Severe intratendinous abnormalities and a sagittal tendon diameter > 10 mm suggested a
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partial rupture. In tendons with a false negative result histopathological changes were mild and a tendency towards a better clinical outcome was noted in the sonographic cases. Assessment of the paratenon was unreliable with both methods. Ultrasonography and MRI give similar information and may have their greatest potential as prognostic instruments.
Achilles tendon injuries in athletes.
Kvist M; Sports Medical Research Unit, Paavo Nurmi Centre, University of Turku, Finland.
Sports Med 1994 Sep;18(3):173-201 Two-thirds of Achilles tendon injuries in competitive athletes are paratenonitis and one-fifth are insertional complaints (bursitis and insertion tendinitis). The remaining afflictions consist of pain syndromes of the myotendineal junction and tendinopathies. The majority of Achilles tendon injuries from sport occur in males, mainly because of their higher rates of participation in sport, but also with tendinopathies a gender difference is probably indicated. Athletes in running sports have a high incidence of Achilles tendon overuse injuries. About 75% of total and the majority of partial tendon ruptures are related to sports activities usually involving abrupt repetitive jumping and sprinting movements. Mechanical factors and a sedentary lifestyle play a role in the pathology of these injuries. Achilles tendon overuse injuries occur at a higher rate in older athletes than most other typical overuse injuries. Recreational athletes with a complete Achilles tendon rupture are about 15 years younger than those with other spontaneous tendon ruptures. Following surgery, about 70 to 90% of athletes have a successful comeback after Achilles tendon injury. Surgery is required in about 25% of athletes with Achilles tendon overuse injuries and the frequency of surgery increases with patient age and duration of symptoms as well as occurrence of tendinopathic changes. However, about 20% of injured athletes require a re-operation for Achilles tendon overuse injuries, and about 3 to 5% are compelled to abandon their sports career because of these injuries. Myotendineal junction pain should be treated conservatively. Partial Achilles tendon ruptures are primarily treated conservatively, although the best treatment method of chronic partial rupture seems to be surgery. Complete Achilles tendon ruptures of athletes are treated surgically, because this increases the likelihood of athletes reaching preinjury activity levels and minimises the risk of re-ruptures. Marked forefoot varus is found in athletes with Achilles tendon overuse injuries, reflecting the predisposing role of ankle joint overpronation. Athletes with the major stress in lower extremities have often a limited range of motion in the passive dorsiflexion of the ankle joint and total subtalar joint mobility, which seems to be predisposing factor for these injuries. Various predisposing transient factors are found in about one-third of athletes with Achilles tendon overuse injuries; of these, traumatic factors (mostly minor injuries) predominate. The typical histological features of chronically inflamed paratendineal tissue of the Achilles tendon are profound proliferation of loose, immature connective tissue and marked obliterative and degenerative alterations in the blood vessels. These changes cause continuing leakage of plasma proteins, which may have an important role in the pathophysiology of these injuries. The chronically inflamed paratendineal tissues of the Achilles tendon do not seem to have enough capacity to form mature connective tissue.
Long-term results after surgical management of partial Achilles tendon ruptures.
Morberg P, Jerre R, Sward L, Karlsson J; Department of Orthopaedics, Ostra University Hospital, Institution for Surgical Sciences, Goteborg, Sweden.
Scand J Med Sci Sports 1997 Oct;7(5):299-303 Although Achilles tendon injuries are common overuse injuries in sports, the exact incidence is unknown, primarily as a result of varying definitions and diagnoses of the underlying pathological changes. Despite numerous studies of treatment of the Achilles tendon injuries, the long-term results are not well known. The results after surgical treatment of chronic partial Achilles tendon ruptures in 64 patients with a follow-up of 6 (1.5-11) years were evaluated in a retrospective study. The ruptures were divided into three groups: (I) proximal (more than 3 cm above the calcaneus), (II) distal and (III) combined (proximal and distal). All patients underwent an operation involving the excision of the devitalized tendon tissue and, in groups (II) and (III), also the excision of the deep Achilles bursa and removal of the dorsal corner of the calcaneus. The functional results were satisfactory in 43 (67%) patients and unsatisfactory in 21 (33%). The results were better in patients with proximal ruptures than in patients with either distal or combined ruptures. Males experienced better results than females. Post-operative immobilization in a plaster cast had no significant influence on the final result. Nine (14%) patients with either a distal or a combined rupture were re-operated
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on and in seven of them the final result was satisfactory. The conclusion of this study is that partial Achilles tendon ruptures are often difficult to treat and only two out of three patients can be expected to obtain satisfactory results after surgical treatment.
Tendon pathology in long-standing achillodynia. Biopsy findings in 40 patients.
Movin T, Gad A, Reinholt FP, Rolf C; Department of Orthopaedic Surgery, Huddinge University Hospital, Sweden.
Acta Orthop Scand 1997 Apr;68(2):170-5 We evaluated biopsy specimens from the Achilles tendon in 40 patients with long-standing achillodynia and an ultrasonographic widened tendon with hypoechogenic areas. We used a standardized protocol to assess the general tendon pathology score of paraffin-embedded specimens stained with HE. Stereologic measurement of the volume density of glycosaminoglycan (GAG)-rich areas, stained with the Alcian blue (pH 2.5)/periodic acid Schiff method (AB/PAS) was performed. 14 specimens obtained at autopsy served as reference material. Abnormal fiber structure and arrangement, focal variations in cellularity, rounded nuclei, decreased collagen stainability and increased non-collagenous extracellular matrix were seen in all biopsy specimens. Slight histopathological changes were noted in half of the controls. Increased vascularity was present in two thirds of the patient specimens and in one third of the controls, and signs of perivascular hemorrhage, as evidenced by hemosiderin deposition in 6/40 of the patients, but in none of the controls. The volume density of GAG-rich areas was higher in the patients 0.47 (0-0.86) than in the controls 0 (0-0.07). Changes in the fiber structure and arrangement, as well as increased amounts of interfibrillar GAG, appear to be characteristic morphological features in Achilles tendons with long-standing achillodynia and ultrasonographic widening. These findings may indicate that achillodynia is due to local disturbances in connective tissue metabolism or circulation or to both.
Surgical treatment of chronic Achilles tendinitis.
Nelen G, Martens M, Burssens A; Department of Orthopaedic Surgery, University Hospital, Pellenberg, Belgium.
Am J Sports Med 1989 Nov-Dec;17(6):754-9 Between 1977 and 1985, 170 patients suffering from chronic Achilles tendinitis were treated surgically. Ninety-one patients with 143 tendons returned for followup. The duration of preoperative symptoms averaged 18 months. In all cases, conservative treatment was first attempted but failed to alleviate symptoms. Only those patients whose lesions and symptoms were confined to the Achilles tendon segment 2 to 6 cm proximal of the insertion were included in this study. All athletes who had an insertion tendinopathy or a lesion at the musculotendinous junction were excluded from this study. The surgical procedure depended on the lesion. For 93 tendons exhibiting pure peritendinitis, treatment consisted of a simple release of the fascia cruris and the peritenon. For the 50 tendons with tendinosis, a resection of diseased tendon tissue was performed. The defect could be sutured side to side in 26 cases but in the other 24 cases, reinforcement with a turned down tendon flap was necessary because of the extensive debridement. Of the 93 cases in which only dorsal release was performed, results were considered excellent in 54 cases, good in 28, fair in 8, and poor in 3 cases. Of the 26 cases in which side-to-side suture was performed, 15 cases were rated as having excellent results, 4 as good, 4 as fair, and 3 as poor. For the 24 cases in which a turned down tendon flap procedure was performed, the result was excellent in 12 cases, good in 9, fair in 2, and poor in 1 case.(ABSTRACT TRUNCATED AT 250 WORDS)
Structure and histopathology of the insertional region of the human Achilles tendon.
Rufai A, Ralphs JR, Benjamin M; Department of Anatomy, University of Wales College of Cardiff, Wales, Great Britain.
J Orthop Res 1995 Jul;13(4):585-93 The Achilles tendon inserts onto the calcaneus, and the retrocalcaneal bursa intervenes between it and the bone immediately proximal to the enthesis. The enthesis, the bursa, and the bursal walls form a complex insertional region protecting against wear and tear. We examined the structure and histopathology of the insertional region in 50 tendons from cadavers (age at time of death, 57-96 years). The enthesis contained fibrocartilage typical of attachment sites. In specimens with a prominent superior tuberosity (the majority), the walls
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of the bursa also were fibrocartilaginous. On the anterior wall, fibrocartilage replaced the calcaneal periosteum; on the posterior wall, there was a sesamoid fibrocartilage in the deep part of the tendon. When the tuberosity was not prominent, the bursal fibrocartilages were absent. Histopathological features were observed in 31 entheses. Bone spurs extended from the calcaneus into the tendon and probably formed by endochondral ossification of enthesial fibrocartilage. Longitudinal fissures were splits in the fibrocartilage along the lines of the endotenon, and small transverse tears occurred at the tendon-bone junction. Longitudinal fissures showed evidence of repair; they were filled with amorphous material and surrounded by clusters of cells. In the bursal walls, calcification or degradation, or both, were observed in 37 specimens and usually involved both sesamoid and periosteal fibrocartilages. These fibrocartilages could therefore be implicated in retrocalcaneal bursitis.
Surgical management of Achilles tendon overuse injuries. A long-term follow-up study.
Schepsis AA, Wagner C, Leach RE; Department of Orthopaedic Surgery, Boston University Medical Center/University Hospital, Massachusetts.
Am J Sports Med 1994 Sep-Oct;22(5):611-9 We studied 79 cases of surgically treated Achilles tendon overuse injuries in 66 patients. Fifty-three (80%) of these patients were competitive or serious recreational runners operated on between 1978 and 1991. There were 49 men and 17 women with a mean age of 33 years (range, 17 to 59). The cases were divided into surgical subgroups based on their site of primary symptoms and abnormalities: paratenonitis (23), tendinosis (partial rupture or degeneration) (15), retrocalcaneal bursitis (24), insertional tendinitis (7), and combined abnormalities (10). Followup included a comprehensive patient questionnaire and office examination. There were 79% satisfactory (51% excellent, 28% good) and 21% unsatisfactory (17% fair, 4% poor) results. The percentages of satisfactory results in the paratenonitis group (87%) were best and those in the tendinosis group were the worst (67%). Satisfactory results were obtained in 75% of the patients with retrocalcaneal bursitis and 86% with insertional tendinitis. Seven of the 45 cases with longer than 5-year followup with initially satisfactory results deteriorated with time and required reoperation (16%). Of these, 4 were in the tendinosis group, 2 had retrocalcaneal bursitis, and 1 had paratenonitis. One of the 34 patients followed less than 5 years required reoperation.
Eccentric exercise in chronic tendinitis.
Stanish WD, Rubinovich RM, Curwin S
Clin Orthop 1986 Jul;(208):65-8 Chronic tendinitis, particularly of the Achilles tendon, frequently outwits traditional programs of therapy including surgery and/or prolonged immobilization. A hypothesis proposes that disruption of the tendon, micro or macro, occurs under specific conditions of eccentric loading. In order for the healing tendon to be adequately rehabilitated, the treatment program must include specific eccentric strength rebuilding exercises.
Operative management of Haglund's deformity in the nonathlete: a retrospective study.
Sammarco GJ, Taylor AL; University of Cincinnati Medical Center, Ohio, USA.
Foot Ankle Int 1998 Nov;19(11):724-9 Haglund's deformity, or "pump bump," is a common cause of posterior heel pain. Management of the condition usually consists of nonoperative therapy. This study presents a retrospective study of 65 cases (53 patients), with symptomatic Haglund's deformity in nonathletes (13 male and 40 female), who presented during a 4-year period (1989-1994). Sixty-five percent (39 heels) of these patients failed to respond to nonoperative therapy for an average of 62 weeks, (range, 4-260 weeks). This group of patients went on to operative treatment. Surgical management consisted of excision of the posterior calcaneal tuberosity through a medial longitudinal incision with debridement, reattachment of the Achilles tendon using bone anchors, and 4 weeks of postoperative immobilization. Thirty-nine patients (74%) were contacted for follow-up. The average follow-up period for these patients was 155 weeks, (range, 92-335 weeks). There were 50% excellent results, 47% good results, 3% fair results (1 patient), and no poor results. The Maryland Foot Score for operated heels was an average of 67/100 preoperative and an average of 92/100 postoperative. On unoperated heels the score was an average of 81/100 at first evaluation and an average of 86/100 at final evaluation. Complications included one recurrence of painful prominence, one wound infection, and one incisional neuroma. The outcome of these cases demonstrated that in
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those patients who fail nonoperative treatment, surgical treatment of Haglund's deformity produces a predictably good surgical result when performed using the technique described.
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Printout from Orthoteers.com website, member id 1969. © 2007 All rights reserved. Please refer to the site policies for rules on diseminating site content. Tendon Disorders
TIBIALIS POSTERIOR INSUFFICIENCY
Adapted from the Foot & Ankle Hyperbook
Commonest cause of adult acquired flat foot
Tears occur in the hypovascular zone 3-5 cm proximal to insertion
Causes
trauma chronic flat foot inflammatory arthropathy degenerative tendonopathy
Myerson described two groups:
younger patients aged 30-40 with inflammatory arthropathy older, typically female patients 50-60 years old with degenerative tears
Complaints
post-malleolar pain arch pain + aching progressive flat foot forefoot problems: progressive hallux valgus, metatarsalgia, lesser toe deformities rarely, tarsal tunnel syndrome
Examination
gait planovalgus foot heel remains in valgus on double foot tiptoe standing post-malleolar tenderness/swelling with no palpable tendon on resisted plantar flexion/inversion single foot tiptoe test: cannot stand on tiptoe on single foot if tibialis posterior not functioning tight TA in hindfoot neutral hindfoot/forefoot malalignment and its degree of correctability
Differential diagnosis
longstanding flat foot made symptomatic, usually by minor trauma sequelae of other injuries joint instability or destruction due to inflammatory arthritis neuropathic foot collapse
Imaging
Standing hindfoot alignment view: shows where the valgus is Standing lateral footà ¼ both show talonavicular Standing AP forefootà ¾ and talometatarsal alignment MR: best technique for assessing tendons
The first three are known in Blackburn as a "deformity series" (they are also employed in other generalised foot deformities such as pes cavus). They also demonstrate joint alignment and degeneration.
Pathology: staging systems
Classification after Johnson (1989), indicating findings and treatment
Stage I Stage II Stage III
Tendon condition peritendonitis/ elongation elongation
degeneration
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Hindfoot mobile, normal mobile, valgus mobile, fixed
Pain medial, focal medial, along tendon medial + sinus tarsi/lat ankle
Single heel rise test mild weakness marked weakness marked weakness
"Too many toes" sign normal positive positive
Pathology synovitis/ degeneration degeneration
degeneration
Treatment conservative/ FDL=>tib post transfer subtalar arthrodesis
debridement
Dereymaeker and Wouters extended the classification at both ends to produce five stages:
Stage I Stage II Stage III Stage IV Stage V
Tendon condition Biomechanical Peritendonitis/ Elongation/ Disrupted Disrupted predisposition degeneration rupture
Hindfoot Mobile Mobile Mobile Fixed Fixed
Forefoot-hindfoot Normal Normal Valgus Valgus Valgus
alignment
Pain None/after activity Mild/moderate Moderate/ Sinus tarsi Ankle
severe Arthritic
Their treatment recommendations:
Stage I: correct biomechanical defect
Stage II: synovectomy - tendon debridement
Stage III: tibialis posterior reconstruction by tendon transfer
Stage IV: triple arthrodesis
Stage V: pantalar arthrodesis
Neither of these classifications take much notice of hindfoot/forefoot malalignment (Johnson & Strom denied it exists), and Johnson classification is difficult to apply to patients with pre-existing flat foot. I subclassify the Johnson stages II and III according to the absence(A) or presence(B) of fixed hindfoot/forefoot malalignment >10deg
Blackburn treatment protocol
clinical diagnosis MRI if will affect management cast orthosis from podiatrist physio if significant tendonitis/ muscle problems / contracture surgery for non-operative failures, if patient of reasonable weight for height
stage I: debridement
stage IIA: calcaneal osteotomy + FDL=>TP transfer
stage IIB: talonavicular/double fusion
stage IIIA: subtalar fusion
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stage IIIB - heavy/high demand patient: triple fusion
stage IV: extended hindfoot fusion
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