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Trauma & Orthopaedics Revision
PAEDIATRIC ORTHOPAEDICS - Go to Main Contents
A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
Some of the psychomotor skill development in a child between the age 1 and 5 are:
Social smile at 2 months of age, head control at 3 months, sitting by 6 months, standing by 10 months, independent walk at 14 months. It is considered abnormal if child is not rolling by 6 months, not sitting by 8 months, no words by 14 months and not walking by 18 months
Skeletal development in a child - femoral epiphyses ossific centre appears by the age of 4 months but at any point up to 11 months may be normal. Tarsal navicular does not ossify until 3 to 4 years of age. Ossification around the elbow can be remembered with a mnemonic CRITOE - stands for Capitellum, Radial Head, Internal Epicondyle, Trochlea, Olecranon and External Epicondyle - CRITOE. Appearances at ages 2, 5, 7, 9, 10,11.
Normal Baumann's Angle at the distal humeral articular surface is 720 +/- 4, which remains uniformly same from 2 to 13 years of age. Cervical spine in children C2/C3 pseudo subluxation should not exceed 3 mm. Odontoid fuses with the body by 3 to 6 years. Atlas-dens interval is normal up to 5mm. in children. Centre of ossification for the vertebral body of Atlas appears some times during the first year after birth. Odontoid fuses with the body between 3 to 6 years of age.
Extremity growth in children - Most growth occurs away from the elbow and at the knee joint.
Individual bone:
HUMERUS -80% of the growth occurs proximally and 20% distally
RADIUS & ULNA - 20% at the elbow and 80% distally
FEMUR - 30% of the growth proximally and 70% at the knee joint
TIBIA & FIBULA - 60% of the growth at the knee joint and 40% at the ankle
Over all length of the extremity, contributions are as follows:
Upper extremity: 40% proximal humerus, 10% distal humerus, 10% proximal radius and ulna and 40% distal radius and ulna.
Lower extremity: 15% proximal femur and 15% at the ankle, 40% distal femur and 30% proximal tibia and fibula. Growth measurement is carried out by Anderson and Green Growth chart, which is curved line graph. Moseley's has modified this as a straight-line graph for predicting limb length inequality. At least three readings at 6 months interval is essential to predict correctly the expected leg length discrepancy on this growth charts. Rough estimation of growth at the knee joint is 15 mm. every year, 9 mm. at the distal femur and 6 mm. at proximal tibia and fibula.
Lower limb ALIGNMENT measurement in children
(1) Femoral anteversion normally it can be as high as 40 degrees at birth and about 15 degrees in adults. Methods to measure femoral anteversion are: Murphy's method using CT measurement or clinical evaluation described by Staheli with patient prone. Anteversion is likely to be present if internal rotation exceeds 70 degrees and external rotation is less than 20 degrees
(2) Coronal plane alignment of the knee - Any genu varum after the age of 2 should be investigated. Physiological genu varum upto 2 is normal. Physiological genu varum changes to excessive valgus by 4 and normal valgus alignment is usually reached by 6 years of age. Normal metaphyseal diaphyseal angle should be less than 120 at the age of 18 months.
(3) Metatarsus adduction is quantified by drawing a line through the heel bisector and noting which toe it intersects and normally the line should intersect between second and third toes. Other things to remember are foot progression angle, thigh foot angle. Normal Foot progression angle at 4 -16 years of age range between - 8 to +16.
(4) Tibial torsion: Trans-malleolar axis will measure the tibial version and at birth normal tibial version is minus 15 degrees. This increases to plus 5 degrees of external rotation by the end of first year, plus 10 degrees by mid childhood and normal lateral rotation in adulthood is 20 - 24 degrees.
X-RAY INTERPRETATION in Paediatric Orthopaedics:
AP pelvis: acetabular index at 1 year less than 30 degrees, 2 years less than 25 and at 3 years less than 20 degrees. Ossific centre of the femoral head appears by 4 months and upto 11 months is normal.
Lines: Line through the triradiate cartilage is Hilgenreiner's line. Ossific nucleus of the femoral head is normally lies medial to Perkin's line. Shenton's line in a normal hip is not broken. Centre edge angle of Wiberg, normal is 200 .
Foot x-rays: AP talo calcaneal angle is called Kite angle, which is 20 to 40 degrees. Dorsiflexed-lateral view is called Turco View, and talocalcaneal angle on the lateral film should be more than 35 degrees.
Some of the definitions to remember
(1) Kinematics is study of motion
(2) Kinetics - forces that produce motion
(3) Cadence - number of steps per unit of time
(4) Stride - one cycle which includes right and left steps
(5) First rocker - It is the first stage of ankle motion in stance phase
(6) Second rocker is the ankle motion when the foot is flat on the ground
(7) Third rocker starts at the heel rise and ends at toe off the ground
(1) Initial contact
(2) Loading response
(3) Midstance
(4) Terminal Stance
(5) Pre Swing
(6) Initial Swing
(7) Mid Swing
(8) Terminal Swing
60% is stance phase and 40% is swing phase.
Gait analysis in three different planes - Sagittal, Coronal and transverse plane, and the most important points to express are
(1) Stability in stance phase
(2) Foot clearance in swing phase
(3) Pre positioning of the foot for initial contact either heel or fore foot, normal or abnormal
(4) Adequate step length
(5) Energy consumption is good enough? Energy onsumption can be measured in the gait lab
DEVELOPMENTAL DYSPLASIAS OF THE HIP
Incidence 1 to 6 per thousand live births.
Risk factors: First born female. Family history: Breech presentation associated torticollis, scoliosis or musculo-skeletal abnormalities.
Theories:
(1) Mechanical theory
(2) Maternal hormone induced theory
(3) Primary dysplasia theory and
(4) Genetic
Diagnosis:
(1) In a new born
(2) 6 to 18 months
(3) Walking age and
(4) After 3
At birth Ortolani Test is for dislocated hips. Barlow's test is a provocative test. Other tests to remember are Galeazzi's sign. Galeazzi's sign is apparent shortening of the dislocated hip.
X-ray evaluation: Hilgenreiner's line, Perkin's line, Shenton's line, Acetabular index, Centre edge angle normal is 200 and delayed ossific nucleus.
Treatment: New born - Pawlik harness. 4 to 6 weeks - if not stabilised in harness, closed reduction and spica. Safe zone of Ramsey needs to be considered while applying the spica. Safe zone of Ramsey is the safe position of hip immobilisation in spica to avoid AVN. Minimum of 20 degrees and 45 degrees of safe zone is preferable. Irreducible hip needs arthrography and open reduction if necessary.
What to look for on Arthrography?
(1) Whether the acetabulum is dysplastic?
(2) Whether the hip is subluxed or dislocated?
(3) Can it reduce?
(4) Is there any soft tissue inter position
(5) Is there any pooling of dye medially?
(6) Is limbus normal or inverted? Thorn sign is seen in normal hips.
Open reduction - Approaches are
(1) Anterior approach is called Smith Peterson approach. It has been modified by Somerville who has used bikini incision instead of ilioinguinal incision.
(2) Antero-medial approach described by Winstein and Ponseti.
(3) Medial approaches are mainly called Ludloff's or Ferguson approach. Basic difference is going either anterior or posterior to the adductor brevis.
Kalamchi classification of AVN as a complication of the CDH. Simple way to remember -
Type I - Ossific centre not appeared by the age of 1 year
Type II - Damage to the lateral part of the physis resulting in valgus neck
Type III - Damage to the growth plate more centrally resulting in cessation of growth of the femoral neck with relative over growth of greater trochanter
Type IV - Total involvement
Salter's Innominate Osteotomy - Pre-requisites for Salter's Innominate osteotomy
(1) Femoral head level with acetabulum
(2) No fixed flexion or adduction contracture
(3) Head reduced completely & concentrically
(4) Hip joint must be congruous
(5) Good hip range of motion.
(1) Salter's innonimate hinges at the pubic symphysis
(2) Pemberton osteotomy hinges at the tri-radiate cartilage
(3) Steel's triple osteotomy, which osteotomises ileum, pubis as well as ischium and rotates acetabulum
(4) Periacetabular procedures for rotation of the acetabulum described for dysplastic hips are - Dial osteotomy, or Ganz technique in adolescent hips
(5) Salvage procedures in the dysplastic hips are - Staheli's Shelf procedure and Chiari displacement osteotomy
Independently described condition by Leg, Calvé and Perthes.
Aetiology is unknown. (1) Trueta's hypothesis says solitary retinacular blood supply between the age of 4 and 8 years makes the femoral head vulnerable for ischaemia
(2) Caffey's hypothesis - primary thickening and disorganisation of growth plate with intra epiphyseal compression of blood supply to the ossification centre. Incidence 1 in 1200, Age 3 to 12, male to female 4:1, 15% bilateral
Waldenstrom radiographic staging of the disease
(1) Stage of necrosis
(2) Stage of resorption or fragmentation
(3) Stage of re-ossification and
(4) Stage of remodelling. In general necrotic and fragmentation stages lasts approximately six months each, re-ossification stage for one and half years and remodelling stage for three years.
Staging of the Perthes disease:
(1) Catterall classification
(2) Salter's classification
(3) Herring lateral pillar classification
Catterall has 4 groups, Salter has 2 groups and Herring has 3 groups.
Catterall classification:
(1) Central anterior head involved
(2) More than 25% of head involved but medial and lateral columns intact
(3) 75% of femoral head involved but intact medial column
(4) Whole head involved
Salter classification:
(1) Less than half the femoral head involved and intact lateral pillar
(2) More than half of head involved and lateral pillar is involved. Salter classification is based on Crescent sign due to subchondral fractures
Herring lateral pillar classification:
(A) Lateral pillar intact
(B) Lateral pillar collapsed but less than 50% of the normal side
(C) Lateral pillar collapse more than 50% of normal height. Herring classification is done during the stage of fragmentation
Head at risk sign of Catterall:
(1) Lateral calcification
(2) Lateral subluxation
(3) Lucency proximal and distal to lateral physes otherwise called Gage's Sign
(4) Metaphyseal cysts
(5) Horizontal physis
Stulberg Rating System at maturity:
Class 1 - Normal femoral head
Class 2 - Spherical femoral head with short femoral neck and coxa magna
Class 3 - Non-spherical or ovoid femoral head, which is not flat
Class 4 - Flat femoral head as well as flat acetabulum and
Class 5 - Flat femoral head but normal acetabulum. Mose's concentric circles are used
Treatment options of Perthes disease jury is out.
Options available are:
(1) Do nothing or supervised neglect
(2) Ambulation abduction brace or cast
(3) Femoral varus osteotomies
(4) Innominate osteotomies
(5) Epiphysiodesis
Important clinical prognosticator is ROM, especially abduction.
Guidelines by Herring are:
(1) Patient's who are less than 6 years of age no evidence that any form of treatment alters either the growth potential of physis or the outcome, so principle is to treat the symptoms
(2) Patients who are 6,7 or 8 early results suggest that, Group B does better with containment methods and Group C in this age group effect of any treatment is inconclusive
(3) Patient's who are 9 years or older: Group A in this age group needs symptomatic treatment. In group B & C, bracing is difficult, operative treatment has got a stronger argument
Salvage procedures described are:
Shelf Arthroplasty or
Chiari osteotomy for head coverage if hip hinge abduction is seen proximal femoral
Valgus osteotomy has been performed in selected cases to increase abduction
Rarely performed operation is advancement of the relatively enlarged greater trochanter
SLIPPED UPPER FEMORAL EPIPHYSES (SUFE)
More common in black females. Incidence in black females 6 to 7 per 100,000 (hundred thousand) population. Caucasians it is 1 to 3 per 100,000 population.
Aetiological factors to consider:
(1) Certain anatomical and structural features. Retroversion of the femoral head more prevalent among the group who had slipped capital femoral epiphyses (10 degrees more than normal)
(2) Maturation factors- in girls before menarche - increase in thickness of the physis reduces its resistance to shear
(3) There may be structural abnormalities of the physis itself
(4) Endocrine influence - incidence of bilateral SUFE is 70% in patients with endocrinopathy compared to 25% in patients without endocrinopathies
(5) Triggering traumatic event
Clinical classification (1) pre-slip (2) acute slip (3) chronic slip and (4) acute on chronic slip
Dunn has classified the SUFE into
(1) Acute traumatic slip
(2) Chronic slip. Chronic slip is sub-classified as: (a) Acute on chronic (b) Early (c) Late
Severity of the slip is classified as
(1) Grade I or mild slip: one-third of the metaphyses uncovered
(2) Grade II or Moderate slip: two-thirds of the metaphyses uncovered
(3) Grade III or Severe slip that is more than two-thirds of the metaphyses uncovered
Southwick has classified SUFE on the basis of Southwick Angle Difference. Southwick angle difference less than 300 is mild, between 30 and 600 is moderate, and more than 600 is severe slip.
The more recent classification of the SUFE by Loder: Loder has addressed the prognosis of the condition in relation to slip as Stable or unstable SUFE. Clinical presentation of unstable SUFE is when individual is unable to tolerate any kind of weight bearing on the affected hip. Unstable hips have got 47% satisfactory prognosis compared to 96% satisfactory prognosis in the stable group. Incidence of AVN in the stable group is nil; in the unstable group is 50%.
Radiological findings SUFE:
(1) Decreased height of the epiphyses
(2) Metaphyseal blanch sign
(3) Trethowen's line otherwise called Klein's line
Radiological diagnosis of chondrolysis - decrease in the width of the joint space more than 2 mm. compared to the contralateral hip is suggestive of chondrolysis.
Treatment options:
Mild & moderate slips pinning in situ.
Principles of treatment are to
(1) Prevent further slip and
(2) To promote closure of physes
In severe slip gentle manipulation before any surgical intervention is controversial. Ponseti and Winstein have suggested five pound traction before pinning.
Surgical options are:
(1) Pinning in situ which can be technically demanding if there is significant displacement
(2) Gentle reduction and pinning in situ in severe slips, controversial
(3) Bone graft epiphyseodesis
(4) Osteotomies in grade III SUFE:
(a) subcapital osteotomy described by Dunn
(b) extra capsular base of the neck osteotomy
(c) Southwick described an inter-trochanteric osteotomy
(d) Sugioka rotational osteotomy of the femoral neck - technically difficult.
All osteotomies are fixed with internal fixation.
Main Complications in SUFE:
(1) Chondrolysis (2) AVN
Rubin says - Dysplasia refers to deformities caused by intrinsic bone disturbance. Dystrophy is the deformities caused by the metabolic or nutritional deficiencies like mucopolysaccharidosis Diastosis is the term when there is underlying mesodermal or ectodermal abnormalities for e.g. Diastrophic dysplasia.
Rubin's classification of bone dysplasias - He described 4 categories:
(1) Epiphyseal dysplasia
(2) Physeal dysplasias
(3) Metaphyseal dysplasias
(4) Diaphyaseal dysplasias
Each of these groups is sub-grouped:
(A) Hypoplasias and
(B) Hyperplasias
Rubin's classification
(1) Epiphyseal dysplasias -
a. Epiphyseal hypoplasia - (i) failure of articular cartilage, spondylo epiphyseal dysplasia
(ii) failure of ossification centre i.e. multiple epiphyseal dysplasias
b. Epiphyseal hyperplasia - excessive articular cartilage, dysplasia epiphysealis hemimelica otherwise called Trevor's disease.
(2) Physeal dysplasias -
a. Cartilage hypoplasia (i) failure of proliferation of cartilage which is achondroplasia (ii) failure of hypertrophic cartilage otherwise metaphyseal dysostosis, cartilage hair hypoplasia
b. Cartilage hyperplasia - (i) excess cartilage proliferation, hyper-chondroplasia, Marfan's syndrome (ii) excess of hypertrophic cartilage is enchondromatosis.
(3) Metaphyseal dysplasias -
a. Metaphyseal hypoplasia - (i) failure to form primary spongiosa i.e. hypophophatasia (ii) failure to absorb primary spongiosa i.e. osteopetrosis (iii) failure to absorb secondary spongiosa i.e. cranio-metaphyseal dysplasia
b. Metaphyseal hyperplasias- (i) excessive spongiosa formation is multiple exostosis
(4) Diaphyseal dysplasias
a. Diaphyseal hypoplasias - (i) failure of periosteal bone formation or osteogenesis imperfecta (ii) failure of endosteal bone formation which is idiopathic osteoporosis, congenita and tarda
b. Diaphyseal hyperplasia - (i) excessive periosteal bone formation i.e Engelmann's disease, progressive diaphyseal dysplasia (ii) excessive endosteal bone formation i.e hyperphospataemia, Including juvenile Paget's disease and VanBucheum's disease
(Proportionate dwarfism is decrease both in trunk and limb length, Disproportionate dwarfism can be (1) short trunk or (2) short limb. Short limb dwarfism is subclassified as: Rhizomelic i.e proximal limb shortening Mesomelic i.e middle limb shortening or Acromelic which is distal limb shortening)
SOME OF THE DYSPLASIAS
Autosomal dominant with frequent new mutation. It is the most common skeletal dysplasia.
Clinical features: Macrocephaly, frontal bossing, saddle nose, maxillary hypoplasia and mandibular prognathism, small mandible, trident hands, lumbar lordosis, genu varum, spinal stenosis, rhizomelic dwarfism. Life expectancy is normal.
Orthopaedic interventions in achondroplasia are mainly due to -
(1) Limb lengthening procedures
(2) Thoraco lumbar kyphosis, which is usually, self corrected but if it remains greater than 400 by 5 to 6 years of age associated with a single wedge shaped apical vertebra, surgery is indicated
(3) Cervical and/or lumbar lordosis if symptomatic which is very rare
(4) Lumbar canal stenosis is congenital stenosis. This may need decompression if symptomatic, especially cuada-equina syndrome.
Autosomal dominant. Clinical findings are similar to those of mild achondroplasia.
Autosomal dominant or recessive, both forms are encountered. Clinical features: This is also rhizomelic shortening of extremities but facial features are absent. C1/C2 instability may be present and no stenosis.
Autosomal recessive. Clinical features: cauliflower ear, rhizomelic shortening. Hitchhikers thumb cervical spina bifida, kyphosis, and scoliosis of the thoraco lumbar spine.
SPONDYLO EPIPHYSEAL DYSPLASIA CONGENITA
Autosomal dominant. Clinical features: Odontoid hypoplasia with instability, platy-spondyly, scoliosis, and coxa-vara deformity.
Spondylo epiphyseal dysplasia tarda -X linked recessive condition. Clinical features - hip resembling Perthes disease, scoliosis, and occasional cervical instability.
Autosomal dominant. Clinical features- irregular epiphyseal ossification with deformity, hips, knees and ankle most commonly involved, usually presents in late childhood, spine normal.
MULTIPLE OSTEO-CARTILAGINOUS EXOSTOSIS (DIAPHYSEAL ACHALESIA)
(1) Autosomal dominant
(2) Clinical features: short stature, multiple lumps, asymmetric growth at the knees and ankles may lead to deformities, leg length inequality usually about 4 cms and there is 1% to 20% risk of malignant degeneration.
(3) Radiological features:
a. Sessile or pedunculated
b. Lesions usually close to the metaphyses
c. Cortex of the lesion continues with the cortex of the bone with a homogeneous continuation of the medulla.
DYSPLASIA EPIPHYSEALIS HEMIMELICA OR TREVOR'S DISEASE
These are basically osteochondromas arising in the epiphyses thus involving the joint. They are usually restricted to one side of the limb either medial or lateral and involve one of the limbs, this is why it is called hemimelica - one side of the epiphyses - lateral or medial.
OLLIER'S DISEASE (Multiple enchondromas)
Clinical presentations are usually angular deformities, bony irregularities and limb length problems. Located in the
Autosomal dominant. Hypoplasia or aplasia of the clavicle with wide symphysis pubis, short middle phalanx of fifth finger.
DIAPHYSEAL DYSPLASIA (Camurati-Englemann syndrome)
Autosomal dominant, thickened diaphyses with narrowing of the medullary cavity, fusiform shaped long bones. Bone changes persist in adulthood.
APERT'S SYNDROME (Acrocephalo syndactyly)
Autosomal dominant condition, skull has short antero-posterior diameter, high full forehead and flat occiput, craniosynostosis is present mainly coronal sutures affected.
It is a condition resulting from lysozomal enzyme deficiency.
Mainly there are four types:
Type I Hurler's: Urine excretes dermatan sulphate and heparan sulphate
Type II Hunter's: Urine shows dermatan sulphate and heparan sulphate
Type III Sanfilippo's Syndrome: Most common mucopolysaccharidoses, excretes excess heparan sulphate
Type IV Morquio's Syndrome: Secretes excessive keratin sulphate in the urine
Type II is X linked recessive and rest of the three are autosomal recessive conditions.
Autosomal dominant, Features:
(1) Nails are grooved, small or absent especially on the thumb
(2) Knee anomalies, patella bipartite, small or absent patella, femoral condyles can be hypoplastic, osteochondritis dessicans of femur or talus
(3) Elbow abnormalities capitellar hypoplasias, cubitus valgus, flexion contractures, dislocated radius
(4) Pelvis - Iliac horns
Benign sporadic pathologic condition that affects skeletal development. It can be mono-ostotic or polyostotic affecting multiple bones. This is often referred to as McCune Albright Syndrome. (Albright Osteodystrophy is pseudo hyperparathyroidism). Fibrous dysplasia typical X-ray appearance of Shepherd Crook deformity, café-au-lait pigmentation can be seen.
FIBRO DYSPLASIA OSSIFICANS PROGRESSIVA
(Myositis Ossificans Progressiva) which presents with multiple soft tissue ossification.
Disorders causing increased bone density:
Melorheostosis
Osteopoikilosis
Osteopetrosis
(1) Marfan's syndrome
(2) Homocysteinuria
(3) Congenital contractural arachnodactyly
(4) Achard syndrome
(5) Stickler syndrome otherwise called Hereditary Arthro-opthalmopathy.
Systems involved are (i) skeletal (ii) ocular (iii) cardiovascular (iv) pulmonary (v) skin (vi) central nervous system.
Diagnostic criteria - Positive family history or skeletal involvement and involvement of two other systems. At least one must be a major manifestation.
Skeletal features: anterior chest deformity, long narrow limbs, arachnodactyly, vertebral deformity, tall stature, high narrowed arched palate, increased appendicular joint hyper mobility, protrusio acetabuli.
Arthrogryposis multiplex congenita - It is the classic arthrogryposis.
Aetiology is unknown.
What is Arthrogryposis?
Arthrogryposis is a non-specific term describing conditions characterised by congenital, non-progressive limitation of movement due to soft tissue contractures affecting two or more joints.
Sub-groups:
(1) Arthrogryposis multiplex congenita
(2) Larsen's Syndrome
(3) Freeman Sheldon Whistling face Syndrome
(4) Mobius Syndrome
(5) Pterygium Syndrome
Arthrogryposis multiplex congenita: Hips are usually dislocated, knees flexed, clubfoot can be present with vertical talus, and upper extremity deformities are similar to Erb's palsy deformity.
Larsen Syndrome presents with multiple joint dislocations mainly hips, hyper extended and dislocated knees.
(1) Klippel-Trenaunay-Weber Syndrome consists of vascular anomalies, haemangiomas with hemihypertrophy of the limbs
(2) Mafucci Syndrome consists of multiple enchondromas (Olier's Syndrome) with cutaneous haemangiomas. Very high risk of malignancy
(3) Sturge Weber Syndrome mainly haemangiomas with neurological sequelae and meningeal haemangiomas
(4) Blue Rubber Blebnevuas Syndrome
This is the most prevalent skeletal disorder to be caused by a single gene defect. There are two types. Neurofibromatosis Type I & Type II Neurofibromatosis Type I is Von Recklinghausen's Disease- Incidence 1 in 4000, autosomal dominant, chromosome 17 gene locus.
Diagnostic criteria's- more than two of the following:
(i) More than 5 café-au-lait spots (more than 5mms in a child and more than 15mms in an adult)
(ii) More than two neurofibromas or one plexiform neurofibroma
(iii) Axillary or inguinal freckles
(iv) More than two iris hemartomas (lisch nodules)
(v) Osseous lesions like long bone pseudo arthrosis, dystrophic curve of spine, sphenoid abnormalities
(vi) First degree relative affected with neurofibromatosis and
(vii) Optic glioma
Neurofibromatosis Type II: is central one with chromosomal 22 locus. CNS manifestations.
Orthopaedic manifestations of Neurofibromatosis type I:
(1) Scoliosis
(2) Over growth of bone
(3) Pseudoarthrosis
(4) Cystic lesions in the bone
(5) Metaphyseal fibrosis
(6) Pressure erosions of the bone
(7) Over growth of the extremity
Scoliosis in Neurofibromatosis can be dystrophic or non-dystrophic.
Non-dystrophic is like idiopathic. Dystrophic has got severe degree of apical rotation with platy-spondyly as well as vertebral scalloping. Dystrophic spinal curves are aggressive and if it is more than 300 anterior and posterior fusion is considered.
Rate of non-union is high in scoliosis surgery for Neurofibromatosis.
These are group of disorders with Type I collagen abnormalities causing bone fragility.
Sillence Classification:
Type I to Type IV.
Type I & IV are autosomal dominant; Type II & III are autosomal recessive. Autosomal dominant types are less severe. Type II is usually not compatible with life; Type III is the one, which is most often seen with a severe degree of osteogenesis imperfecta in the clinical practice.
Type I & II have blue sclera,
Type III & IV do not have blue sclera.
Spectrum ranging from hypoplasia to complete absence of pre-axial parts associated with
(1) Blood dyscrasias like Fanconi's syndrome or TAR's syndrome (Thrombocytopenia Absent Radius syndrome)
(2) Congenital heart Defects like Holt oram syndrome
(3) Cranio-fascial anomalies Nager's syndrome
(4) Congenital scoliosis in VATER, VACTERL syndrome or Klippel feil syndrome
This is a clinical syndrome of low hairline, short neck and decreased range of neck movements. Cervical spine fusion may be associated with instability or stenosis. Associated skeletal anomalies are scoliosis (60% of the patients) sprengel's deformity (30%), Upper extremity or hand anomalies. Non skeletal associations may be genito urinary, hearing, cardiac or fascial asymmetry.
Sprengel's deformity: Cavendish classification of sprengel's deformity:
(1) Very mild, shoulder level
(2) Mild, lump visible
(3) Moderate, shoulder elevated
(4) Severe, Scapula close to occiput
Woodward procedure for sprengel deformity is the transfer spinal attachment of trepezius muscle distally.
Main problems are - growth disturbances. CNS dysfunction, dysmorphic face.
Orthopaedic problems: contractures, synostosis, hip dislocations, club feet, congenital cervical fusion.
SOME CHROMOSOMAL ABNORMALITIES
(a) Down's Syndrome
(b) Turner's Syndrome
(c) Noonan's Syndrome
(d) Klinefelter's Syndrome
(e) Cridu-chat-syndrome
Mental retardation with trizomy 21
Orthopaedic problems:
(1) Delayed walking
(2) Lax ligaments
(3) C1/C2 instability
(4) Idiopathic scoliosis
(5) Hip dislocations
(6) Slipped capital femoral epiphyses
(7) Perthes disease
(8) Patellar subluxation or dislocation
(9) Metatarsus adductus or hallux valgus
MUSCULAR DYSTROPHY AND NEURO MUSCULAR DISORDERS
Broad categories are
Myopathies and Neuropathies.
Myopathies have abnormalities in the muscle; Neuropathies - muscle changes are secondary to abnormalities or disorders of the neuromuscular junction, peripheral nerve or anterior horn cell.
Investigation and Evaluation:
(1) History
(2) Physical examination look for Gower's sign
(3) Serum CPK: More than 20 times in Duchenne's and Becker's muscular dystrophies, mildly raised with other dystrophies
(4) Dystrophin immuno-blot differentiates Duchenne's from Becker's dystrophy
(5) DNA mutation analysis
(6) Electromyogram
(7) Nerve conduction studies abnormally slow nerve conduction in the peripheral nerve diseases and normal conduction velocities in spinal muscular atrophy
(8) Muscle biopsy - Rectus femoris is used for proximal myopathies and gastrocnemius for distal
(9) Nerve biopsy - sural nerve is the most commonly used
(10) Electro cardiogram to look for abnormalities in Duchenne's muscular dystrophy, Friedriech's ataxia and dystrophia myotonia
Classification of spinal muscular atrophy: Type I, II, III and IV
Type I (Werdnig Hoffmann Syndrome) diagnosed before 6 months of age
Type II is diagnosed between 6 to 12 months of age
Type III is diagnosed between 12 months to 3 years of age and
Type IV (Kugelberg Walander Syndrome) is diagnosed after 3 years of age. These are all autosomal recessive gene defect on chromosome 5. Mainly affected organ is anterior horn cell in spinal muscular atrophy. Type I is not compatible with life
Friedreich's ataxia is spino-cerebellar degeneration. Pes-cavus and scoliosis are orthopaedic problems.
HEREDITARY MOTOR AND SENSORY NEUROPATHIES
Classified as
Type I - Roussy levy or hypertrophic charcot marie tooth
Type II - is otherwise called Charcot marie tooth disease neuronal form
Type III hereditary sensory motor neuropathy or Dejerine sottas syndrome
Type IV is otherwise called Refsum's disease.
Main manifestations of these conditions are progressive equino cavo varus feet, clawing of toes, gait abnormalities, hip dysplasias, and scoliosis. Life expectancy with hereditary sensory neuropathy is normal.
To sum it all
(1) Neuropathies can be:
(a) Spinal muscular dystrophy
(b) Charcot marie tooth disease
(c) Viral neuropathies
(2) Myopathies can be:
(a) Duchenne's muscular dystrophy
(b) Becker's muscular dystrophy
(c) Fascio-scapulo-humeral dystrophy
(d) Limb girdle dystrophy
(e) Emery Dreifuss muscular dystrophy
(f) Myotonic dystrophy and
(g) Congenital myopathy
Classification of cerebral palsy - It is difficult to classify cerebral palsy under one group as such because of mixed involvement but the gross categories can be
(1) Spastic
(2) Athetoid
(3) Motion disorders
Another classification is according to the distribution of cerebral palsy
(1) Quadriplegia
(2) Diplegia
(3) Hemiplegia
(4) Total global involvement
Hoffer classifies ambulation potential:
(1) Community ambulator
(2) House hold ambulator
(3) Therapeutic ambulator or ambulation as a physiotherapy measure
(4) Non-ambulators
Deformities in the cerebral palsy's are mainly (1) Dynamic deformities (2) Fixed contractures (3) Fixed contractures with joint subluxation or dislocation
Assessment of a child begins with the ambulation potential as well as level of intelligence. Deformities should be noted as well as if necessary gait analysis performed before any surgical intervention.
Procedures available are:
(1) Multiple simultaneous surgeries
(2) Botulinum toxins
(3) Dorsal rhizotomy
Deformities to look for:
(1) Pelvic obliquity and scoliosis. Whatever is the reason for pelvic obliquity that should be dealt with, before hips are tackled
(2) Lower limb problems Hip subluxation and dislocation: Non ambulators have higher chance of subluxing or dislocating the hip, which is about 50%, whereas ambulators have less chance of having hip subluxation.
Radiographic monitoring:
(1) Centre edge angle CE angle of Wiberg, Normal 200 or
(2) Migration percentage of Rheimer or Rheimer's index. Hip tends to dislocate rapidly when migration percentage exceeds 50 and the general consensus is that if the migration percentage is less than 50% soft tissue procedures are often successful and if the migration percentage is more than 50% bony procedures may be needed.
Dislocated hip surgical indications in CP:
(1) Perineal hygiene
(2) High prevalence of fractures of the lower extremities
(3) Pain if left untreated. Prevention is better than cure. Only reliable screening test described is x-ray films at a regular interval
Procedures available:
Adductor release (close or open)
Flexor Iliopsoas release
Knee contractures: hamstring release, Femoral derotation varus osteotomies, Pelvic osteotomies
Salvage procedure: Chiari osteotomy
Treatment of extended knee deformities: Quadricepsplasty. Popliteal angle is the angle of the leg to the vertical axis with a patient supine, hip flexed to 900 and knee extended. Normal popliteal angle is about 200 and more than 400 popliteal angle will probably need surgical hamstring release.
Rectus Femoris transfer - Normal action of rectus femoris is biphasic. During swing phase of gait cycle, concentric contraction of the proximal rectus flexes the hip joint and eccentric contraction of the distal rectus flexes the knee joint. Thus foot is cleared from the ground during swing phase.
In cerebral palsy this dual action is taken away in some patients resulting in simultaneous contraction at the hip as well as at the knee joint, resulting in extension of the knee joint during swing phase. Gait analysis and ENMG studies are done to confirm the pathology. In this situation Rectus femoris transfer to the knee flexors is carried out to clear the foot from the ground during the swing phase.
Foot deformities in CP:
(1) Equinus deformity
(2) Equino varus deformity
(3) Valgus deformity
(4) Calcaneo valgus deformity
Surgical procedures for foot deformities in CP:
(1) Equinus deformity - gait electromyography is essential to look for proximal limb abnormalities, which may need dealing with before correcting the equinus
(2) Equino varus - fixed or dynamic. Dynamic deformity may require split anterior tibial tendon transfer and fixed deformity, soft tissue release with bony procedures may be necessary
(3) Valgus deformity and calcaneo valgus feet Grice Hind Foot stabilisation is extra articular subtalar arthrodesis
Gait analysis in cerebral palsy - Same principles applies - (1) Stability in stance (2) Foot clearance in swing (3) Normal initial contact (4) Step length and (5) Energy conservation
SPINA-BIFIDA AND MYELOMENINGOCELE
Myelomeningocele are - congenital defects of the vertebrae and neural element.
Myelomeningocele can be
(1) Spina bifida occulta
(2) Meningocele
(3) Myelomeningocele
(4) Lipomeningocele
Spinal dysraphism is a term that categorises congenital defects of the neural tube.
Commonly associated anomalies - Arnold Chiari malformation, hydrocephalus, hydromyelia, diastematomyelia and spinal cord tethering.
Deformities develop in meningomyelocele because of:
(1) Muscle imbalance
(2) Intra-uterine positioning deformities
(3) Postural contractures developed during growth
(4) Spasticity secondary to neurological problems like hydrocephalus or Chiari malformation
(5) Progressive deformities during growth associated with muscle imbalance leading to hip subluxation and dislocation.
Management depends on
(1) Ambulation potential
(2) Spasticity
(3) Associated neurologic problem
(4) Intelligence level
(5) Fractures, joint stiffness and deformities
(6) Obesity
Functional level in Myelomeningocele is classified as:
(1) Thoracic level - No function in the voluntary muscles crossing the hip joint - so hip joints are usually not dislocated. They are ambulators only with high standing brace HKAFO orthosis. Major problem - scoliosis
(2) High lumbar level - i.e. L1/L2 - Hip flexion and adduction is present. Common orthopaedic problem is dislocation of the hip. Treatment of hip dislocation depends on ambulation potential of the patient
(3) Low Lumbar level i.e. L4/5 - Hips not significantly affected. Common orthopaedic problem is calcaneus deformity of the ankle and foot ulceration. Patient is usually mobile with KAFO
(4) Sacral level - Patients are community ambulators. Common orthopaedic problems are foot problems, claw toes and cavus deformities. May require shoe supports and all of these patients will be community ambulators
Hoffer classification of ambulation potential
(1) Community ambulators
(2) House hold ambulator
(3) Therapeutic ambulator
(4) Non-ambulators
Manelaus has summarised the principles in meningomyelocele
(1) Surgery directed to the anticipated adult need
(2) Single surgical procedure and a least possible surgical procedure to correct the deformity
(3) Single session surgery and early weight bearing, single session anaesthesia
(4) Muscle imbalance should be corrected.
Latex allergy is well known in patient with meningomyelocele.
Pathologies to deal:
(1) Pelvic obliquity and scoliosis
(2) Hip contractures: Iatrogenic abduction contractures may result from prolonged abduction splinting in these patients. Ober-yount procedure is release of tight ilio tibial band in abduction contractures. Unilateral dislocation in patients with low lumbar or sacral level deficits should be treated. High bilateral dislocations are best left alone with high myelomeningocele. Surgical techniques: (1) Soft tissue releases (2) Soft tissue transfer (3) Bony procedure Soft tissue releases for adduction and flexion contractures. Muscle transfers to supplement weak abductors. Low lumbar and sacral roots supply abductors. They are usually paralysed in the lumbar myelomeningocele. Sharrard's Procedure - Iliopsoas muscle transfer to greater tuberosity through the ilium aids abduction. Bony procedures are femoral varus osteotomies, pelvic osteotomies or combined procedures.
(3) Knee deformities - Principles are the same - Orthotics & joint mobilisation, soft tissue procedures to release flexion or extension contractures of the knee.
(4) Torsional deformities of the lower extremities in myelomeningocele are: (a) External torsional deformity treated with either Twister cable or surgical management. External rotational deformity of the tibia due to iliotibial band contracture will need release of the contracture (b) Internal torsional deformities can be treated with twister cables and in older child surgical management either muscle transfers or bony procedures
(5) Foot deformities are managed depending on the type of deformity and applying the principles. Deformities are equinus, equino-varus, valgus, vertical talus, cavus, or calcaneo-valgus feet. Special care is needed for the trophic ulcers associated with myelomeningocele patients
There are various classifications described for this condition. Focal femoral deficiency is characterised by reduction in the osseous material of the bone producing leg length discrepancy in the femur. There are 2 main groups:
(1) Total
(2) Partial deficiency.
PFFD can be associated with: coxa vara or fibular hemimelia in 50% of the patients, knee ligamentous laxity, abnormal posterior cruciate as well as anterior cruciate ligaments, may be absent.
Aiken's classification: A, B, C, D
(1) A&B femoral head is present, C&D femoral head is absent
(2) Femoral segment in A is short B is short with proximal bony tuft C is short usually proximally tapered and D is short and deformed
(3) Acetabulum in A. is normal B. is adequate C. is severely dysplastic D. is absent
(4) Connection between the segments of the femur
A. Connected
B. No connection between head & shaft
C. No articular relation
D. Absent hip
In brief: femoral head in A and B is present, femoral head in C and D is absent. Acetabulum is normal in A, adequate in B, severely dysplastic in C and absent in D
Treatment depends on whether the hip is stable or whether the hip is unstable. If the hip is unstable various procedures are described to create hip joint using the knee joint. Minor degree of PFFD will require leg-lengthening procedures. Van-Nes Rotationplasty is one of the techniques described to treat associated fibular hemimelia.
Weinstein has classified the coxa vara in five groups
(1) Coxa vara associated with hypoplastic femur or focal femoral deficiency
(2) Coxa vara associated with congenital skeletal dysplasias like multiple epiphyseal dysplasia or spondylometaphyseal dysplasia or achondroplasia
(3) Acquired coxa vara either traumatic or metabolic diseases like rickets or may be secondary to Perthes
(4) Adolescent Coxa vara in association with SUFE
(5) Idiopathic infantile coxa vara.
Incidence - 1 in 25,000 births. Aetiology may be a vascular abnormality. Triangular piece of bone is noted in the inferior portion of the neck associated with the increasing varus deformity. This metaphyseal fragment of bone seems to reflect abnormal metaphyseal bone formation by the medial physis after it has assumed the more vertical orientation associated with the increasing varus.
Clinical presentation:
70 % of patients present with a limp
25% bilateral (will have Waddling gait). 5% present with back and leg pain. Rarely leg length discrepancy.
Radiographic Assessment: Hilgenreiner-Epiphyseal HE Angle- If HE angle is greater than 600 corrective surgery is considered. If HE angle less than 450 spontaneous correction will occur and between 45 and 600 outcome is uncertain.
Principles of surgery:
(1) Is to correct the deformity and
(2) Corrective varus as well as femoral retroversion and
(3) Promote ossification.
Pauwel's 'Y' Osteotomy:
ROTATIONAL DEFORMITIES OF THE LOWER EXTREMITY IN CHILDREN
Normal anteversion: 400 at birth, 240 at ten years of age, 160 by mid to late adolescent.
Clinical femoral version analysis can be done with patient prone knees flexed to 900 palpating the greater trochanter and when the greater trochanter is most prominent, neck of the femur is horizontal to the ground that is the anteversion angle.
Trans-malleolar axis will measure the tibial version and at birth normal tibial version is minus 150. This increases to plus 50 of external rotation by the end of first year; +100 by mid childhood and normal lateral rotation in adulthood is 20 - 240
Foot progression angle - Average foot progression angle 4 -16 yrs of age is +4.20 (Normal - 8 to +160).
Toeing in deformity may be due to increased femoral anteversion, genu varum, internal tibial torsion or foot deformities like metatarsus adductus.
Toeing out deformity - Normal toeing out for a child of 4-5 years is 2.80 and increases to 7.30 at age 16.
Treatment: Less than 1% of the cases will require surgical correction (Staheli). Orthosis have no effect.
Causes:
(1) Post infectious
(2) AVN of the femoral head
(3) Post traumatic
(4) Congenital anomalies or focal deficiencies.
Evaluation:
(1) Tape measurement or block method
(2) Radiographic evaluation with AP and lateral views with a metal ruler.
(3) CT scanogram with wrist bone age films. Beware of FFD of the knee. At least 3 evaluations are required separately with an average gap of 6 months to predict accurately the leg length discrepancy at puberty. Wrist films for skeletal age are read using Greulich and Pyle atlas. Growth charts are Green and Anderson tables or a straight-line chart by Moseley.
(4) Tomogram or computed tomography to evaluate growth plate bars.
Treatment:
(1) Observation and wait to correct spontaneously, No intervention if LLD less than 2 centimetres
(2) Shoe lifts
(3) Epiphysiodesis
(4) Limb lengthening initially introduced by Wagner modified by Debastiani using orthofix and present best technique is Ilizarov
(5) Chondrodiastasis may gain some leg length. High chances of epiphyseal fusion after chodrodiastasis and this should be reserved at the end of the growth period.
Epiphysiodesis can be either percutaneous or open. Phemister technique is an open technique. More popular technique is percutaneous.
Physeal Bars
(1) Peripheral bridge - SH II #
(2) Linear bridge extend from one part of metaphyses to another
(3) Central bar - Infection
OSTEOCHONDRITIS DESSICANTS OF THE KNEE
Defined as the impending or actual separation of osteochondral fragments from the cartilaginous surface.
Aetiology is unknown. Combination of trauma and blood supply has been blamed. Fragmentation leads to OA.
Diagnosis: Arthroscopic or X-rays. Key X-ray view is tunnel view. In 25% of the cases only tunnel view shows the pathology. Lesions with bad prognosis are classically anterior to Blumensaat's line. Blumensaat's line is a radiographic shadow produced by the roof of the intercondylar notch.
Site: Intercondylar aspect of the medial femoral condyle 75%, Weight bearing surface of the medial femoral condyle 10%, weight bearing surface of the lateral femoral condyle 10% and anterior intercondylar groove of patella 5%.
Pappas has classified the categories according to the age on detection - Category I: below the age of 12, excellent prognosis
Category II between age 12 and 20 years and
Category III above 20 years of age
Management in the
Category I: Non-operative
Category II & III: Observation and intervention if symptomatic.
Guhl has done arthroscopic classification
(1) Intact lesion 1 to 3 centimetre
(2) Early signs of separation and
(3) Partially detached and
(4) Crater filled with fibrous tissue.
Treatment options: After failed conservative management mainly in Guhl's category III drilling of the lesion, drilling and bone grafting, Grade IV lesions will need autologous chondrocytes culture transfer.
PAEDIATRIC LEG DEFORMITIES
Genu varum: There are 2 types of blount's disease.
(1) Infantile variety less than 3 years of age and
(2) Adolescent variety or late onset if the age of onset is more than 4 years.
Infantile tibia vara or Blount's disease
Multifactorial aetiology. 60% have bilateral involvement.
Differential diagnosis:
(1) Physiological bowleg usually disappears by the age of two. Decreasing metaphyseal diaphyseal angle in serial X-rays is the best indicator of better prognosis of this condition.
(2) Skeletal dysplasia
(3) Metabolic conditions like renal osteodystrophy, dietary, hypophosphataemic rickets
(4) Infection
(5) Trauma and
(6) Tumours
Classification for Blount's disease is by Langenskiold and Riska: I to VI:
Type I- Medial metaphyseal beaking
Type II- Cartilage filled depression in the metaphyseal beaking with medial epiphyseal wedging
Type III- Ossification at the inferomedial corner of epiphyses & type II
Type IV- Epiphyseal ossification fill the metaphyseal depression
Type V- Double epiphyseal plate
Type VI- Medial physeal closure
Upto type IV restoration is possible.
Treatment:
Under 3 years - conservative.
Over 4 years- correction of the deformity is indicated if it is worse than Type IV deformity. Various types of osteotomies or Ilizarov external fixator can be used.
TIBIAL BOWING - 3 TYPES
(1) Postero medial bowing which is relatively benign variety and main problem with this is progressive leg length discrepancy in 33% of these patients
(2) Antero-lateral bowing of the tibia and fibula is ominous sign suggestive of pre-pseudo arthrosis or pseudoarthrosis of tibia. Tibial hemimelia also presents as antero lateral bowing
(3) Antero medial bowing: commonest disorder is fibular hemimelia, which is the commonest long bone deficiency encountered in the paediatric age group
Is classified by Boyd's:
Type I - born with a defect
Type II - born with a hour glass constriction, spontaneous fractures are possible
Type III- bone cysts
Type IV- sclerotic segment without diaphyseal narrowing
Type V- associated with dysplastic fibula and
Type VI- intra-osseous neurofibroma or schwannoma
(Type II and Type VI are associated with neurofibromas)
Treatment:
Prophylactic: bracing.
Establish non-unions:
(i) Resection, intramedullary rod and bone grafting (Williams or Sheffield Rod)
(ii) Resection and vascularised fibula bone graft and
(iii) Ilizarov fixator, excision of the abnormal segment and bone transport
Amputation is an acceptable functional salvage. Should never be performed through pseudoarthrosis. Most commonly performed is Symes or Boyd type of amputation.
Syme's amputation is suturing the calcaneal periosteum to the distal tibia and Boyd's amputation retains part of the calcaneus as a weight bearing support, which is fixed to the distal tibia.
Autosomal dominant or recessive.
Associated anomalies: are Scoliosis, Hip dysplasia, bifurcation of the femur, adduction or polydactyly of the feet, cardiac genito-urinary and gastro-intestinal systems abnormalities. Tarsal coalition especially talo calcaneal coalition exists universally in this condition
Classification is by Kalamchi:
Type I- More than 450 of fixed flexion and initial radiographs show absent tibia
Type II- 25 to 450 of knee flexion contracture with initial radiographs revealing proximal tibia
Type III- Most of the tibia is present with distal tibio-fibular diastasis
TREATMENT:
Type I - Early knee disarticulation and pylon type prosthesis
Type II deformity - Proximal tibio fibula fusion later on Syme's amputation
Type III deformities - Reconstructive procedures are possible
Antero medial bowing with a skin dimple over the apex of the dissociated tibia. Leg length discrepancy is always present.
Kalamchi and Achterman's classification:
Type I - Partial absence of fibula Type II - Entire fibula is absent
Type III (by Coventry) - Bilateral
Other classification by Lett is -
Type A - Unilateral (expected leg length discrepancy at maturity is less than 6 cm)
Type B - Unilateral (expected LLD at maturity 6 to 10 cm)
Type C - Unilateral (expected LLD more than 10 cm)
Type D - Bilateral
TREATMENT address to:
(1) Leg length discrepancy: Illizarov's method is used if predicted leg length discrepancy is greater than 20 centimetres
(2) Syme's or Boyd's amputation is preferred
(3) Ankle and foot deformities
PAEDIATRIC FOOT DEFORMITIES
Incidence is 1.24 per 1000 live births. Incidence in first degree relatives is 2.4 per 1000.
Theories of pathogenesis are:
- Germplasm defect
- Developmental arrest theory
- Foetal theory i.e. mechanical block
- Neurogenic theory defect in the nerve supply to the muscles
- Myogenic theory primary defect in the muscle
- Vascular theory diminution of the arterial supply
- Theory of retracting fibrosis
Pathoanatomy:
The deformities are:
(1) Equinus
(2) Heel varus
(3) Fore foot adductus and supination
(4) Cavus deformity
Goal of treatment of congenital clubfoot is a functional, pain free, plantigrade foot, with good mobility and without calluses, that does not necessitate the wearing of modified shoes. - Ponseti
Treatment options:
- Manipulation and casting
- Operative treatment
- Treatment of the residual deformities
Radiographic assessment -
(1) Dorsiflexed lateral Turco view:
Talo- calcaneal angle normal is 350
(2) Antero posterior Kite view:
Talo-calcaneal angle (normal 20 to 400) and less than 200 in club foot.
Talus-first metatarsal angle (normal 0 to 200) is negative in clubfoot
Principles of Surgical intervention:
Plantigrade foot before walking age. Surgical intervention at about 9 to 12 months of age. Some people do advocate early surgeries.
Dimeglio's classification of clubfoot:
Stiff - irreducible
Severe - slightly reducible
Mild - partially reducible
Postural - totally reducible
Harris and Walker classification
Grade I - Equinus less than 100
Grade II - Equinus 15 to 200
Grade III equinus more than 200
Structures to release at surgery depend on the deformities to correct.
(1) Equinus correction - Achilles, ankle capsule, subtalar capsule, posterior talo fibular ligament, flexor hallucis, flexor digitorum, tibialis posterior and Henry's knot
(2) Heel varus - the entire above structures and calcaneo fibular ligament
(3) Fore foot adduction - talo navicular and calcaneo cuboid joints, adductor hallucis with rest of the long tendons
(4) Cavus deformity - Release plantar ligament along with tight tendon
Operative technique:
(1) Incision (2) Soft tissue release
Incisions are either Turco's postero medial incision or Cincinnati incision or two-incision technique medial and lateral. Most popular is Cincinnati.
Principles of surgical releases:
(1) Turco advocated postero medial release retaining subtalar joint interosseous ligament and postero-lateral structures.
(2) Mackey's extensive postero medial and postero lateral releases done either with Cincinnati approach or two-incision approach. He releases subtalar joint, ankle joint as well as lateral structures of the ankle joint. Retain deep deltoid ligament.
How to avoid overcorrecting?
(1) Retain deep Deltoid ligament
(2) Retain interosseous talo calcaneal ligament and clinical judgement
(3) Avoid over displacement of the navicular bone
(4) Avoid over lengthening Achilles and tibialis posterior
(5) Avoid over correction in the cast after extensive release
Residual deformities can be
(1) Dynamic deformities
(2) Fixed deformities or
(3) Fore foot deformities
Treatment for Residual deformities - Shortening the lateral column of the foot or lengthening the medial column of the foot
Dynamic deformities - tendon transfer operations, tibialis anterior or tibialis posterior split transfers
Fixed deformities - Over the age of 3 to 4 years usually need bony procedures with soft tissue releases.
Popular bony procedures are:
(1) Dwyer's Osteotomy
(2) Dilwyn Evans procedure
(3) Lichtblau's procedure
(4) Ilizarov lengthening and correction
Bony osteotomies in Dwyer's procedure is Calcaneal osteotomy, Dilwyn-Evan is excision of calcaneo cuboid joint, Lichtblau procedure is wedge excision of the lateral calcaneus proximsl to calcaneo-cuboid joint.
Fore foot deformities are addressed by
(1) Bony procedures described by Bermann-Gartland or soft tissue procedures of tarso metatarsal joint described by Heyman-Herndon
(2) Salvage techniques are triple arthrodesis either Naughton-Dunn or Dennyson Fulford or Lambrinudi's technique Talectomy is also one of the salvage procedure.
Other complications to remember after corrective surgical procedures of the clubfoot are Rocker bottom foot and skew foot.
Skew foot is valgus hind foot with various fore foot deformities.
Defined as - Fixed equinus deformity of the forefoot on the hindfoot Coleman block test assesses the 1st metatarsal equinus. Most important disorder to consider is Charcot-Marie-tooth disease. Other causes are spina bifida and tethered cord syndrome. Benign physiological cavus foot is a diagnosis of exclusion
Treatment depends on whether it is flexible or rigid.
Options:
(1) Plantar fascia release
(2) Robert Jones Procedure, which is transfer of extensor hallucis longus to the first metatarsal and fusion of IPJ
(3) Bony procedures i.e. Calcaneal and metatarsals osteotomies
(4) Flexible deformities, tendon transfers are described