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ClubfootCongenital Talipes Equino Varus
(CTEV)
ClubfootCongenital Talipes Equino Varus
(CTEV)
Definition
Twisting of the scaphoid, os calcis and cuboid around the astragalusCongenital Talipes Equino Varus or club foot has 4 basic deformation:1. fore foot : adduction2. hind foot : inversion or varus3. hind foot : equinus4. mid foot : cavus
Incidence : - (1-2) per 1000 births - male : female = 7:5 - 50% bilateralIncidence : of CTEV in various races
Race Cases perthousand birth
Chinese 0.39Japanese 0.53Malay 0.68Filipino 0.76Caucasian 1.12Puerto Rican 1.36Indian 1.51South African black 3.50Polynesian 6.81
Tachjian, The child foot
ETIOLOGY
Chromosomal theory Embryonic theory Otogenic theory Fetal theory Neurological theory Muscular theory
ETIOLOGY
Chromosomal theorydefect : in unfertilized germ cell (defect exists before fertilization)
ETIOLOGY
Embryonic theorydefect : within fertilized germ cellOccurs : between conception-12 weeks (Irani,
Sherman and Settle)
ETIOLOGY
Otogenic theory (arrest theory)arrest of developmentrelated to a change in genetic factor known as “cronon”Cronon : guide the precise time of the progressive
modification every structure during development
ETIOLOGY
Neurologic theoryMuscular theory
ETIOLOGY
Fetal theory (packing syndrome)Intrauterine packing (mechanical factors)
Schematic illustration of the critical periods in human development. During the first two weeks development, of the embryo is usually not susceptible to teratogens. During these pre-embryonic stages, a teratogen either damages all or most of the cells, resulting in its death, or damages only a few cells, allowing the conceptus to recover and the embryo to develop without birth defects. Red denotes highly sensitive periods when major defects may be produced (e.g. amelia, absence of limbs). Yellow indicates stages that are less sensitive to teratogens when minor defects may be induced (e.g. hypoplastic thumbs)
Etiology
- chromosomal theory polygenic (multi factorial)- defect in unfertilized germ cell : - in family - race (palynesia-Maori)
WeekTERM30128 50
- Embryonic theory (0-12) weeks defect occurs during fertilized germ cell
Otogenic theory -- arrest theory - Cronon : genetic factor which determine the precise time for progression modification during development- Cronon may be changed by certain element (teratogen) abnormal development of the limb- growth arrest : permanent, temporair, slowed growth permanent deformity temporary CTEV, slow – steroid- occur during (7-8) week marked CTEV- occur during (9-12) week moderate to mild CTEVSpecification defect (Hoofnick)limb specification at 5 month (teratogen)- neuromuscular- vascular- bone
CTEV : post specification defect
primary muscleabnormality?
Intra uterine pressure(packing syndrome)
20
Ponseti : genetic, embryonic malformation, collagen over production in ligament, collagen fibres wavy arranged, dense, many cells
PATHOANATOMY
Major deformity• Inward rotation of the whole foot on the talus
Rotation primarily takes place in :• talocalcaneal joint• talonavicular joint• calcaneocuboid joint
PATHOANATOMY
Talocrural (ankle ) joint :• Talus in equinus• Talus in mortise = external rotation (horizontal breach)• Posterior = capsule & ligament contracted
“Horizontal breach” according to the concept of Swann, Lloyd-Roberts, and Catterall
PATHOANATOMY
TALUS Constriction encasement Head & neck : medial & plantar deviation
PATHOANATOMY
TALOCALCANEAL JOINT:Calcaneus :rotation in 3 dimensions :
• Sagittal• Coronal• Horizontal
Pathomechanics of talipes equinovarusA. Posterolateral view of the calcaneus and talus of normal
foot. B. Lateral rotation of the talus, C. The anterior part of the calcaneus is pressed by the head of the talus and forced into plantar flexion, rotation, and varus position. (From Carroll, N., Murphy, R, and Leete, S.F. : The pathoanatomy of congenital clubfoot, Orthop.Clin.N. Amer., 9 : 227, 1978)
The articular relationship of the calcaneus to the talus as seen from the front in the left foot.
Pathoanatomy
Talonavicular joint : Navicular : displaced medial & plantarward Tib.posterior tendon Tibio-navic. Ligament (deltoid lig.) Calcaneo-navic.lig. (spring lig.) Talo-navic. Ligament Bifurcate ligament Cubonavic. Oblique ligament All navicular ligament
contracted
PATHOANATOMY
Calcaneo-cuboid joint: Cuboid displaced medially on calcaneus and under navicular &
cuneiform All ligaments : contracted Forefoot : supination and adduction Calcaneo-cuboid joint corrected nicely if other 2 subtalar complex
are corrected except in resistant CTEV
PATHOANATOMY
Muscles Imbalance between agonist and antagonist Muscles tonus determined by the amount of muscle
fibres type I & II All muscle below knee in CTEV fibre Type I > II [similar
with L.M.N lesion : AMC, sacral agenesis, Charcot-Marie, post poliomyelitis]
Some CTEV tendency to be recurrent
PATHOANATOMY VascularBy Doppler Technique : In normal population : a.dorsalis pedis 2.2.% absent In mild & moderate CTEV : a.dorsalis pedis = normal In severe CTEV : a.dorsalis pedis = 6.7% absent
MECHANISM of the CTEV
Fetal posture abnormality : foot in equinovarus
Muscle imbalance : tib. post. contracted
Factors determine the severity of the CTEV
Intrauterine position. The hips are always flexed and externally rotated, while the knees are usually flexed and the feet turned inward
EXAMINATION
History Physical examination Radiologic examination
Radiology : age more than (4-5) months
N : AP : talo-calcaneal angle : (200-400), CTEV < 200
Lat : talo-calcaneal angle : (350-500), CTEV<350
DIAGNOSIS
1. Non rigid type (packing syndrome)2. Rigid type :
• Moderate• Severe
3. Resistance rigid type :• AMC• Myelomeningocele• Constriction band
DIFFERENTIAL DIAGNOSIS
1. Constriction bands (Streeter disease)2. A.M.C3. Myelomeningocel4. Sacral agenesis5. Tibial agenesis6. Charcot-Marie disease
Constriction bands
Arthrogryposis Multiplex Congenita
Spina bifida
Sacral agenesis
Tibial agenesis
Charcot-Mary disease
TREATMENT
The goal of treatment :• Realign the os calcis, scaphoid and cuboid
around the astragalus by correcting the varus, adduction, varus and equinus
• Maintain the correction until stable normal function, no pain, plantigrade, good mobility, no callus formation, wearing normal shoe
HISTORY
Egyptian : tomb painting India (1.000 BC) : Tx Hippocrates (400 BC) : manipulative Tx,
early Tx Indian (Aztecs) Pre Columbian American
Tx : splint with cactus leaves
HISTORY : 20th century
Hugh Owen Thomas (1834 -1891)
Wrench
W.H. Trethewan (1882-1934) :
Thomas Wrench is a barbarous weapon
TREATMENT
1. Conservative2. Operative
Conservative treatment
Golden period:• 1st week• laxity :estrogen
1. Serial plastering2. Stretching Dennis Brown splint3. Adhesive strapping4. Physiotherapy
HIRAM KITE : Brought Hippocrates’ view info focus :Stressing slow, gentle, manipulative correction of the adduction, varus and equinus with minimal surgery
Three magic words for the successful and enthusiasm carrying out his treatment : knowledge,patience andenthusiasm
Ponseti :
Concept biomechanical understanding
SURGERY is the wrong approach for the treatment of the clubfoot. Ponseti
Ponseti
Based on kinematic of the subtalar joint.1st concept : the whole foot moves under the talus “calcaneo- pedis block”2nd concept : fore foot and hind foot are corrected simultaneously by abductionEquinus correction :
• mostly close tenotomy• tendo achilles non stretchable collagen, thick and stiff
COMPARISON KITE and PONSETI treatment
Clubfoot
1. Adduction2. Varus3. Equinus
KITE
Fulcrum : calcaneo cuboidCorrection by serial plastering :
PONSETI
1. Adduction Abduction2. Varus valgus
4 Cavus and pronation
Rigid 3 Equinus tenotomy
Fulcrum : head talus
Correction by serial plastering :
Surgery no yes
plastering
(10-11) months Shoe Denis-Brown splint
(3-4) years Evaluation
3 Equinus Rigid close tenotomy 90%
12 weeks
no =5% yes=95% Surgery
plastering
Shoe splint
(3-4) years Evaluation
4. Cavus and pronation (realign cavus by supination) to “unlock” subtalar movement1. Adduction Abduction 600-750
2. Varus : will be corrected by 4 & 1
6 weeks
Abduction of fore foot in pronation the cavus becomes more severe, calcaneus locked (jammed) under the head of talus; mid foot and forefoot are twisted eversion
Kite Clubfoot correction
Kite
Calcaneo-cuboid is used as fulcrum which is pressed medial ward while fore foot is moved lateral ward (abduction); calcaneus will not move lateral ward (no abduction) that is why the varus will not be corrected; only naviculare and fore foot will move lateral ward. To press the posterior part of calcaneus to correct varus is a big mistake
Kite
Clubfoot correction
a. realign cavus : forefoot supinated (3,4)b. fulcrum : caput tali – stabilisator (5)c. forefoot in supination – abduction (6)d. maximal abduction of forefoot (7)e. dorso flexion of the ankle (+TAL)
Process of a,b,c,d (5-6) x each (5-7) days.Plaster cast above knee (groin), knee
flexion 900
Ponseti
Ponseti (Clubfoot correction)
Ponseti
TAL
After 6x plastering TAL (close), local anaesthesia Plaster 3 weeks bracing for 3 months (24hours)
(2-4) hours day time, 12 hours at nigh (3-4) years night splint Ponseti success = 90%
Pre ATL
Pre ATL
Daffa pre ATL
Daffa Post ATL
Daffa
Common errors
1. Forefoot still in pronation during correction of adduction to abduction
2. Not using head of talus as fulcrum
3. Calcaneus is pressed lateral ward to correct varus
4. Equinus is corrected before adduction and varus are corrected Rocker bottom foot
5. Plaster immobilisation below knee
BK plastering High heel
Post posterior release ATL & capsulotomy
Plaster correction complication
1. Neuromuscular2. Pressure necrosis
Plaster correction complication
3. Rocker bottom foot
Plaster correction complication
4. Flat top talus
Plaster correction complication
5. Increase cavus deformity6. Longitudinal breach7. Stiff joint
Operative treatment
Indication1. Conservative Tx—fail Ponseti + 10%2. Neglected
Postero medial release (Turco)
Cincinati
Ilizaroff
Tripple arthrodesis (adult)
Surgical complication
1. Infection2. Bad scar3. Stiff joint4. Over/under correction5. Navicular dislocation6. Flattening or beaking talar head7. Talar necrosis8. Weakening of the muscles 9. Skew foot (severe valgus of the heel and adduction
of the fore foot)10. Main artery injury foot necrosis
Out patient clinic
RSUD.Dr.Soetomo