http://upload.orthobullets.com/topic/4086/images/CMT_moved.jpg
http://upload.orthobullets.com/topic/4086/images/pes cavus.jpg
http://upload.orthobullets.com/topic/4086/images/hammertoes.jpg
http://upload.orthobullets.com/topic/4086/images/demyelinating.jpg
http://upload.orthobullets.com/topic/4086/images/wallerian.jpg
Introduction
  • A hereditary motor sensory neuropathy (HMSN) that has two forms resulting in muscles weakness and sensory changes
  • Epidemiology
    • most common inherited neurological disease
    • 1:2,500
  • Pathophysiology
    • combination of motor and sensory disturbances as a result of nerve damage
      • motor involvement more profound than sensory
    • affected muscles become weak 
      • peroneus brevis
      • tibialis anterior
      • intrinsic muscles of hand and foot
  • Genetics
    • inheritance
      • autosomal dominant (most common)
      • may also be
        • autosomal recessive
        • X-linked
    • mutations
      • duplication on chromosome 17 
        • codes for peripheral myelin protein 22 (PMP 22
        • X-linked connexin 32
  • Orthopedic manifestations  
    • pes cavus 
    • hammer toes 
    • hip dysplasia 
    • scoliosis
Classification
 
 Classification of CMT
Type I demyelinating condition that slows nerve conduction velocity 
Characteristics:
   1. autosomal dominant
   2. onset in first or second decade of life
   3. most commonly leads to cavus foot
Type II Direct axonal death caused by Wallerian degeneration (not demyelination) 
Characteristics:
   1. Usually less disabled than Type I
   2. onset in second decade of life or later
   3. most commonly leads to flaccid foot
 
Presentation
  • Symptoms
    • lateral foot pain 
    • sensory deficits are variable
    • clumsiness
    • frequent ankle sprains
    • difficulty climbing stairs
  • Physical exam
    • lower extremity
      • rigid cavovarus foot (similar to Freidreich's ataxia) with hammer toes or clawing of toes 
      • atrophied EDB and EHB
      • calf atrophy
      • weak dorsiflexion and eversion due to weak tib ant and peroneals (foot drop during swing phase)
      • lower limb areflexia
      • Coleman block test
        • test to evaluate flexibility of hindfoot
          • flexible hindfoot will correct to neutral when block placed under lateral aspect of foot
          • a rigid hindfoot will not correct into neutral
    • upper extremity
      • intrinsic wasting of hands
Studies
  • EMG
    • low nerve conduction velocities with prolonged distal latencies are noted in peroneal, ulnar, and median nerves
  • Genetic Testing
    • DNA analysis
      • PCR analysis used to detect peripheral myelin protein 22 (PMP22) gene mutations
    • chromosomal analysis
      • duplication on chromosome 17 seen in autosomal dominant (most common) form
Cavus Foot Deformity
  • Introduction
    • plantar flexed 1st ray is initial deformity 
    • cavus caused by peroneus longus (normal) overpower weak tibialis anterior  
    • varus caused by tibialis posterior (normal) overpowering weak peroneus brevis
  • Treatment
    • follows similar treatment principals to cavovarus foot
    • nonoperative
      • stretching, strengthening, and orthotics
        • indications
          • as initial management of a young patient
        • modalities
          • stretching & strengthening
            • should focus on mobilization and strengthening of the weakening muscular units (peroneals, tibialis anterior)
          • orthotics 
            • includes accommodative inserts and orthotic devices for flexible deformity
            • in a flexible deformity the orthosis should post lateral forefoot and the lateral heel   
            • AFOs for foot drop
    • operative
      • plantar fascia release, tibialis posterior or peroneus longus tendon transfer, ± TAL, ± 1st metatarsal dorsiflexion osteotomy
        • indications
          • flexible hindfoot cavus deformities (normal Coleman block test)
          • surgical intervention should be delayed until progression of the deformity begins to cause symptoms and/or weakness of the muscular units, resulting in contractures of the antagonistic muscle units.
        • technique
          • tendon transfer (two method depending on involved muscels)
            • posterior tibialis transfer to dorsum of foot to improve foot drop (augment weak tibialis anterior)   
            • peroneus longus transfer to peroneus brevis (if peroneus longus is normal)
      • calcaneal valgus producing osteotomy
        • indications 
          • rigid hindfoot cavus deformities (abnormal Coleman block test)
        • technique
          • combine with soft tissue procedure discussed above, and dorsiflexion 1st metatarsal osteotomy
      • triple arthrodesis 
        • indications
          • severe rigid deformities
          • may be helpful in select cases but is falling out of favor
      • 1st metatarsal osteotomy and transfer of EHL to neck of 1st MT 
        • indications
          • if there is hallux clawing combined with cavus foot
Claw Toes Deformity
  • Introduction
    • ankle dorsiflexion weakness may result in the recruitment of toe extensors for assistance
      • in the setting of intrinsic muscle weakness, increased toe extensor activity can lead to claw toe deformity
  • Treatment
    • operative
      • Jones procedure 
        • indications
          •  for symptomatic claw toe deformity which has failed non-operative measures
        • technique
          • transfers extensor tendons of the great and lesser toes through the bone into the metatarsal neck
          • goal is to increase contributions to ankle dorsiflexion and decrease clawing in order to relieve pain on the dorsum of the toes
Hip dysplasias
  • Introduction
    • hip dysplasia is sometimes associated with CMT
      • may present during adolescence in ambulatory patients
  • Treatment
    • pelvic osteotomy
      • indications
        • end-stage osteoarthritis
      • outcomes
        • higher rate of sciatic nerve palsy after surgery
Scoliosis
  • Introduction
    • often occurs in children with CMT
    • characteristic left thoracic and kyphotic curve distinguish from idiopathic scoliosis
  • Treatment
    • nonoperative
      • bracing
        • indications
          • bracing rarely effective
    • operative
      • fusion and instrumentation
        • indications
          • progressive deformity
 

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Questions (12)

(OBQ12.248) A mutation of PMP22 located at chromosome 17p12 most likely leads to an initial presentation highlighted by a: Review Topic

QID:4608
1

Weak tibialis posterior

8%

(316/3774)

2

Weak peroneus longus

19%

(713/3774)

3

Strong peroneus brevis

2%

(78/3774)

4

Strong peroneus tertius

1%

(20/3774)

5

Weak tibialis anterior

69%

(2601/3774)

Select Answer to see Preferred Response

PREFERRED RESPONSE 5

Charcot-Marie-Tooth disease (CMT, also known as hereditary motor and sensory neuropathy/HMSN/or peroneal muscular atrophy) comprises a group of disorders caused by a mutation in the genes that affect the normal function of peripheral nerves. CMT is due to a mutation of PMP22 located at chromosome 17p12 and leads to symmetrical, predominantly distal limb-muscle wasting, weakness, and sensory loss, especially in the lower extremities.

The initial presentation is highlighted by a weakened tibialis anterior and peroneus brevis that is overpowered by a stronger peroneus longus/posterior tibialis, resulting in a plantar flexed first metatarsus and pronated forefoot. Hindfoot varus deformity develops secondarily. As the deformities become more fixed, an equinus contracture will often develop as well.

Illustrations A and B are radiographs demonstrating the significant pes cavus associated with Charcot-Marie-Tooth disease.

Incorrect Answers:
Answer 1&2: Peroneus longus and tibialis posterior is relatively stronger in CMT
Answer 3: Peroneus brevis is weakened in CMT
Answer 4: There is no known effect of the peroneus tertius in the pathophysiolgy of CMT

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(OBQ10.56) A 32 year-old male complains of lateral foot pain and a progressively awkward gait. He has a family history of "foot problems" and reports some minor burning and numbness in both feet. He has no other medical problems, and takes no medications. Physical exam reveals bilateral cavus feet with clawing of the toes and intrinsic muscle wasting of the hands. A clinical photograph is shown in Figure A. Which of the following is responsible for the patients initial symptoms and awkward gait? Review Topic

QID:3144
FIGURES:
1

Weak gastrocnemius-soleus complex

2%

(55/2215)

2

Peroneus brevis overpowering the posterior tibial tendon

5%

(119/2215)

3

Tibialis anterior overpowering the peroneus longus

32%

(712/2215)

4

Plantar flexion of the first ray

57%

(1264/2215)

5

Clawing of the toes

3%

(59/2215)

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PREFERRED RESPONSE 4

This patient is presenting with the history and clinical findings of Charcot-Marie-Tooth disease. Symptoms can vary, but the development of cavovarus deformity as seen in the clinical radiograph is common. The initial deforming force is the result of a weak anterior tibialis being overpowered by the unaffected peroneus longus, bringing the first ray into a plantarflexed position. This forces the hindfoot into varus position leading to lateral column overload and pain. The weakened tibialis anterior can also lead to a foot-drop deformity, and compound the gait difficulties. The reference by Ward et al listed below shows improved outcomes in treatment of flexible cavovarus foot deformities with soft-tissue and osteotomy procedures compared to triple arthodesis at an average of 26 years post-operatively.


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(OBQ10.129) The PMP22 (peripheral myelin protein 22) is found at the cytogenetic location found in Figure A. What pediatric congenital disorder is associated with a mutation of this gene? Review Topic

QID:3222
FIGURES:
1

Duchenne's/Becker's muscular dystrophies

9%

(181/2086)

2

Limb-girdle dystrophies

1%

(31/2086)

3

Myotonic dystrophy

4%

(74/2086)

4

Charcot-Marie-Tooth disease

79%

(1644/2086)

5

Spinal muscular atrophy

7%

(146/2086)

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PREFERRED RESPONSE 4

Charcot-Marie-Tooth disease is a sensory motor demyelinating neuropathy that is autosomal dominant and is often due to a mutation of PMP22 (peripheral myelin protein 22) located at Chromosome 17p12. Orthopaedic manifestations include progressive distal muscle wasting/weakness (especially peroneal muscles), areflexia, hammertoes, hip dysplasia, and cavovarus foot deformities. Low nerve conduction velocities with prolonged distal latencies are noted in the peroneal, ulnar, and median nerves. Nerve pathology can show simultaneous demyelinization and remyelinization. There are several subtypes of the disease, but diagnosis is made commonly by DNA testing for a duplication of a portion of chromosome 17. Other pediatric congenital disorders and their associated genetic defect include Duchenne's/Becker's muscular dystrophies (dystrophin), Limb-girdle dystrophies (sarcoglycan and dystroglycan complex), myotonic dystrophy (myotonin), and spinal muscular atrophy (Survival motor neuron protein).


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(OBQ10.224) A 22-year-old woman is concerned about frequent ankle sprains and an awkward gait. Lower extremity nerve conduction velocities show prolonged distal latencies in the peroneal nerves. DNA testing shows a duplication on chromosome 17. Which of the following images is most likely the radiograph of this patient? Review Topic

QID:3323
FIGURES:
1

Image A

2%

(38/1828)

2

Image B

15%

(272/1828)

3

Image C

67%

(1230/1828)

4

Image D

4%

(82/1828)

5

Image E

11%

(199/1828)

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PREFERRED RESPONSE 3

Charcot-Marie-Tooth disease (CMT), or Hereditary Motor Sensory Neuropathy, is a demyelinating disorder of the peripheral nervous system. Manifestations in the foot include pes cavovarus, claw toes, and frequent ankle sprains. The cause of the foot deformities in CMT is an imbalance of distal musculature, with the peroneus brevis and tibialis anterior being relatively overpowered by the peroneus longus.

The paper by Alexander et al. discussed the difficulties reconstructing cavovaus feet of CMT, with special focus on muscle imbalance causing the deformity.

Paulos et al studied over twenty patients with CMT who underwent plantar tissue releases and tendon transfers. With at least two year follow up, 85% were found to have acceptable results. Other described techniques include osteotomies as well.

Image C shows a high arched foot of a person with CMT.

Incorrect Answers:
Image A shows an accessory navicular.
Image B shows a calcaneonavicular coalition.
Image D shows a foot without pathology
Image E shows a ball-and-socket ankle, which can be associated with fibular hemimelia.

While other radiographic choices could represent a patient with frequent ankle spains, none of them except a patient with CMT would have abnormal nerve conduction studies.


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(OBQ08.29) A 5-year-old boy has bilateral cavus feet and genetic testing reveals duplication of the PMP (peripheral myelin protein) gene on chromosome 17. What is the most likely diagnosis? Review Topic

QID:415
1

Myelodysplasia

3%

(32/962)

2

Ewings Sarcoma

0%

(3/962)

3

Charcot-Marie-Tooth Disease

95%

(917/962)

4

Cerebral Palsy

1%

(6/962)

5

Poliomyelitis

0%

(1/962)

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PREFERRED RESPONSE 3

Charcot-Marie-Tooth disease, a group of diseases that affect the peripheral nerve, is moderately common, with an incidence of 1 in 2500 individuals. All forms of the disease manifest as distal weakness primarily in the foot and ankle; somewhat later in life the hand may be affected as well. Most patients usually present toward the end of the first decade with progressive cavovarus deformities of the feet associated with dorsiflexion of the toes during the swing phase of gait and contracture of the plantar fascia. There are 30 genes that now have been described in association with the different forms of HMSN, CMT disease. 70% of patients show a duplication of the peripheral myelin protein (PMP) gene on chromosome 17

Authors:

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(OBQ06.75) Plantar flexion of the first ray is the initial deformity seen in which condition? Review Topic

QID:186
1

Oblique talus

2%

(21/957)

2

Kohler's disease

2%

(20/957)

3

Charcot-Marie-Tooth

89%

(854/957)

4

Calcaneovalgus foot

4%

(43/957)

5

Juvenile hallux valgus

2%

(17/957)

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PREFERRED RESPONSE 3

Charcot-Marie-Tooth (CMT) disease is a hereditary motor sensory neuropathy. These patients often develop a pes cavovarus deformity (Illustration A) with the intial stage being plantar flexion of the 1st ray.

A weakened tibialis anterior / peroneus brevis is overpowered by a stronger peroneus longus / posterior tibialis and results in a plantar flexed first metatarsal and pronated forefoot as described in the article by Mosca. Hindfoot varus deformity develops secondarily. As the deformities become more fixed, an equinus deformity can also develop.

Coleman block testing as described in CORR from 1977 can help determine if the hindfoot varus deformity is fixed or flexible. Hindfoot flexibility is noted by placing the lateral foot on a block to remove the plantar flexed first ray from contributing to the deformity and observing the hindfoot moving to a more neutral position.

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(OBQ06.83) A 42-year-old woman with Charcot-Marie-Tooth disease complains of longstanding foot pain. Orthotics, bracing, and NSAIDs no longer provide relief. She has cavovarus hindfoot deformity that does not correct with Coleman block testing. Radiographs are notable for degenerative changes within the talocalcaneal and calcaneocuboid joints. Which of the following is the most appropriate treatment? Review Topic

QID:194
1

Split tibialis posterior transfer

1%

(2/296)

2

Triple arthrodesis

80%

(238/296)

3

Lateral closing wedge calcaneal osteotomy with peroneus longus to brevis transfer

15%

(44/296)

4

First metatarsal dorsal closing wedge osteotomy

2%

(5/296)

5

Achilles tendon lengthening

2%

(5/296)

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PREFERRED RESPONSE 2

Charcot-Marie-Tooth disease is also known as hereditary motor sensory neuropathy. Characteristic deformity occurs when the weakened peroneal brevis and anterior tibalis succumb to the stronger posterior tibialis and peroneus longus resulting in a cavovarus foot. Coleman block testing is used to determine whether the deformity is flexible or rigid. An example of a correctable deformity is provided in Illustration A. Once the foot has become rigid and begins developing arthritic changes, triple arthrodesis is indicated. Flexible deformities without arthritic changes may be amenable to tendon transfers and dorsiflexion osteotomy of the first ray. Holmes et al reviews the evaluation, diagnosis, and treatment of the cavovarus foot in Charcot-Marie-Tooth disease.

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(OBQ05.47) Lateral forefoot and heel posts would be the appropriate orthotic for the foot deformities associated with which of the following conditions? Review Topic

QID:83
1

Charcot-Marie-Tooth disease

67%

(266/396)

2

Stage II posterior tibial tendon insufficiency

24%

(96/396)

3

Stage III posterior tibial tendon insufficiency

5%

(20/396)

4

Charcot arthropathy

1%

(5/396)

5

Hallux rigidus

2%

(6/396)

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PREFERRED RESPONSE 1

Lateral forefoot and heel posts are most appropriate for cavovarus foot deformities. This deformity is typical of Charcot-Marie-Tooth (CMT) disease. Posting the lateral forefoot allows for flexion of the first metatarsal (correcting the forefoot driven, hindfoot varus deformity commonly seen in CMT), and posting the lateral heel corrects the varus hindfoot.

Cavovarus deformity can also be caused by poliomyelitis and cerebral palsy.

Schwend et al. reviewed cavus foot deformity in children. The goal of surgical management is to obtain a mobile plantigrade foot with correction of the cavus deformity.


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(OBQ05.87) The cavus deformity in Charcot-Marie-Tooth disease is caused by what muscular imbalance? Review Topic

QID:973
1

Peroneus brevis overpowering peroneus longus

2%

(27/1128)

2

Tibialis anterior overpowering tibialis posterior

13%

(143/1128)

3

Achilles overpowering tibialis anterior

4%

(41/1128)

4

Extrinsic toe flexors overpowering intrinsics

7%

(79/1128)

5

Peroneus longus overpowering tibialis anterior

74%

(835/1128)

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PREFERRED RESPONSE 5

The etiology of the abnormal foot posture in Charcot-Marie-Tooth disease usually results from peroneus longus overpowering tibialis anterior. The peroneus longus acts to plantarflex the first metatarsal raising the arch height and tilting the hindfoot into varus. Thus the Coleman block test allows one to check the hindfoot flexibility by eliminating the effect of the plantarflexed 1st ray and observing its effect on the hindfoot.

Additionally, the peroneus brevis is weak, allowing it to be over-powered by the posterior tibialis resulting in adduction of the foot and varus.

Bilateral pes cavovarus is the most common pathologic foot deformity seen with Charcot-Marie-Tooth disease. A passively correctable, and thus flexible, cavovarus foot may be appropriately treated with plantar fascial release, dorsal closing wedge osteotomy of the first metatarsal, and peroneus longus to peroneus brevis tendon transfer. A calcaneal osteotomy may also be indicated.

Holmes and Hansen present a Level 5 review of Charcot-Marie-Tooth disease. They report that the specific components of the disease process includes hindfoot varus, anterior or forefoot cavus, and often clawtoes. The study by Ward looks at long-term follow up of Cavovarus foot correction with (in part) peroneus longus to brevis transfer to eliminate that muscle imbalance.


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(OBQ05.254) A 17-year-old male complains of a foot deformity that has progressed over the past 1 year. He has pain along the lateral border of his foot with walking. His father has had similar problems with both feet throughout his life. A clinical photograph of the foot is provided in Figure A. Proper management of this patient should include evaluation for which of the following findings? Review Topic

QID:1140
FIGURES:
1

Acetabular dysplasia

56%

(362/649)

2

Cervical stenosis

25%

(161/649)

3

Uveitis

8%

(55/649)

4

Hypoplastic thumb

4%

(25/649)

5

Thrombocytopenia

6%

(41/649)

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PREFERRED RESPONSE 1

The patients clinical presentation is consistent with Charcot-Marie-Tooth disease (CMT), also known as hereditary motor sensory neuropathy. The cavovarus foot is secondary to peroneus brevis and anterior tibialis weakness. Acetabular dysplasia is known to occur in association with CMT.

Fuller et al review 4 familial cases of CMT. The patients demonstrated cavovarus foot deformities, decreased conduction velocities, acetabular dysplasia, and Trendelenburg gait.

Schwend et al review the evaluation, diagnosis, and treatment of cavus foot deformity in children. Management of the deformity is predicated upon proper diagnosis of the etiology for the cavus foot.


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(SBQ04.2) A 14-year-old male child presents with the increasing foot deformity shown in Figure A. On physical exam, it is noted that he is unable to walk on his heels and has decreased Achilles reflexes bilaterally. Coleman block testing reveals correctable hindfoot deformity. Which procedure is associated with improved clinical outcomes in patients with the above described condition? Review Topic

QID:2187
FIGURES:
1

Transfer of peroneus brevis to peroneus longus

9%

(26/292)

2

Split anterior tibial tendon transfer to lateral column

23%

(68/292)

3

Triple arthrodesis

1%

(2/292)

4

Posterior tibial tendon transfer through the interosseous membrane to dorsum of the foot

58%

(169/292)

5

Lateral column lengthening calcaneal osteotomy

9%

(26/292)

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PREFERRED RESPONSE 4

The physical exam and clinical photo are consistent with a cavovarus foot deformity associated with Charcot-Marie-Tooth (CMT) disease. The Coleman block test reveals a flexible hindfoot deformity, which suggests that soft-tissue transfers and not osteotomies can correct the deformity. The posterior tibial tendon retains its strength in CMT and can aid in decreasing hindfoot varus while providing ankle dorsiflexion when transferred to the dorsum of the foot.

Wetmore and Drennan evaluated long-term outcomes in patient with CMT who had undergone triple arthrodesis. Nearly fifty-percent of patients had poor outcomes with only 24% having good and excellent results. This led to the recommendation that triple arthrodesis be reserved for a salvage procedure only in patients with CMT.

Roper and Tibrewal reviewed long term outcomes in patients with CMT undergoing a variety of soft-tissue procedures. At an average of 14 year follow-up, all 18 feet had avoided the need for triple arthrodesis while continuing to have satisfactory results.

Illustration A shows an example of the Coleman block test. This test is used to evaluate for flexibility of the hindfoot varus deformtiy. The illustration shows a flexible deformity with correction of the hindfoot varus.

Incorrect Answers:
Answer 1: Peroneal longus to brevis transfer can be utilized due to the fact that PL is typically preserved while PB is weakened in CMT.
Answer 2: The anterior tibial muscle is weakened and therefore transfer provides no benefit and can actually worsen the deformity.
Answer 3: Wetmore and Drennan revealed that poor outcomes are associated with triple arthrodesis in CMT.
Answer 5: Lateral column lengthening is used in pes planovalgus foot deformities.

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(OBQ04.211) A 24-year-old male with hereditary motor sensory neuropathy complains of worsening bilateral foot pain with ambulation and limited walking tolerance. Clinical photographs are shown in Figures A and B. The deformity corrects with Coleman block testing. Radiographs of the left foot are provided in Figures C-E. Which of the following is the best initial management for this patient? Review Topic

QID:1316
FIGURES:
1

Custom orthotics with posting of the lateral forefoot and lateral heel

71%

(499/703)

2

Custom orthotics with posting of the medial forefoot and medial heel

8%

(56/703)

3

Custom orthotics with medial heel posting and lateral forefoot recession

7%

(51/703)

4

Gastrocnemius slide followed by dorsiflexion casting

1%

(8/703)

5

Dorsal first metatarsal osteotomy with calcaneal slide osteotomy

12%

(87/703)

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PREFERRED RESPONSE 1

The clinical presentation and photographs demonstrate a patient with bilateral cavovarus feet. The deformity is flexible as evidenced by correction with Coleman block testing. Illustration A provides an example of Coleman block testing. Radiographs demonstrate a high calcaneal pitch, but no arthritic changes. A flexible cavovarus foot can be passively corrected by posting of the lateral forefoot and lateral heel. Surgical interventions should be reserved for fixed deformities and failure of conservative treatment. Sammarco et al reviewed 21 feet with severe symptomatic cavovarus deformity who underwent lateral slide calcaneal osteotomy and dorsal closing wedge osteotomies of the metatarsal(s). The only complications encountered were delayed union and nonunion of the metatarsal osteotomy. Overall, patients did very well with pain reduction, preservation of motion, and enhanced ambulation.

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