2. ANATOMY
• A typical long bone, ossifies in three parts; the
two ends and one shaft.
• The ends ossify from secondary centers of
ossification while the shaft ossifies from
primary center of ossification
3. • In a young bone in which the process of
ossification is not complete
• Epiphysis
• Diaphysis
• Metaphyses
• Epiphyseal plate of cartilage
4. • Epiphysis:
• The ends and the tips of a long bone that
ossify from secondary centers are known as
epiphyses. Growth of the epiphysis arises from
two areas: (1) the vascular reserve zone car-
tilage, which is responsible for growth of the
epiphysis toward the joint, and (2) the
epiphyseal plate, which is responsible for
growth in bone length
5. TYPES OF EPIPHYSIS
• Pressure epiphyses: articular & take part in joint formation. These
epiphyses are the weight transmitting epiphyses. Ex -head of the
humerus, lower end of the radius etc.
• Traction epiphyses: provide attachment to tendons of muscles. The
traction epiphyses ossify later than the pressure epiphyses.
Examples of these epiphyses are tubercles of humerus and
trochanters of femur
• Atavistic epiphyses: are phylogenetically independent but they
become fused in man. Examples are coracoid process of scapula
• Aberrant epiphyses: these epiphyses are not always present.
Examples are epiphyses at the head of the first metacarpal bone
and at the base of other metacarpal bones.
6. DEFINITION
• The terms osteochondrosis or epiphysitis is a
self limiting developmental dearrangement of
normal bone growth primarily involving
centres of ossification in the epiphysis
• It is an aseptic ischemic necrosis
• The disorder may be localized to a single
epiphysis or occasionally may involve two or
more epiphyses simultaneously or
successively
7. CHARACTERISTICS
• Predilection of immature skeleton
• Involvement of epiphysis
• Radiographic picture dominated by
fragmentation ,collapse, sclerosis and
reossification of osseous centres
9. SIFFER CLASSIFICATION
• Articular osteochondroses:
– Calvé-Legg-Perthes Disease (hip/femur)
– Köhler's Bone Disease (ankle navicular bone)
– Freiberg's Disease (2nd metatarsal head)
– Panner's Disease (capitulum of humerus)
• Non-articular osteochondroses:
– Osgood-Schlatter Disease (tibial tuberosity)
– Sever's Disease (calcaneus)
– Sinding-Larsen and Johansson Syndrome (inferior tip of patella)
• Epiphyseal osteochrondroses:
– Scheuermann's Disease (vertebral bodies)
10. ARTICULAR OSTE0CHONDROSIS
Legg Calve Perthes Disease
Legg-Calvé-Perthes disease
(LCPD) is the name given to
idiopathic osteonecrosis of the
capital femoral epiphysis in a
child.
12. Blood supply to femoral head
• Upto 4 years
1. Retinacular vessels mainly lateral epiphyseal
vessels
2. Metaphyseal
3. Artery of ligamentum teres
13. Blood supply to femoral head
• By 4 yrs
Epiphyseal plate forms a barrier to metaphyseal
vessels.
• Pre-adolescent
1. After 7 yrs arteries of lig teres become more
prominent and anastomose with the lateral
epiphyseal vessels.
Between 4&7 yrs blood supply is dependent on
retinacular vessels only
14. Incidence
• Male : Female = 4-5:1
• 2.5:1 in India
• Age of onset earlier in females.
• Age –
Range – 2-13 years.
Most common 4-8 years.
Average – 6 years.
• Bilateral in 10-12 %
• Incidence more in Caucasians as compared to Negroid,
mongoloid.
15. Etiology
• Etiology not known.
• Coagulation disorders.
• Altered arterial status of femoral head.
• Abnormal venous drainage.
• Abnormal growth and development.
• Trauma.
• Hyperactivity or attention deficit disorder.
• Genetic component.
• Environmental influences.
• As a sequelae to synovitis.
16. Pathogenesis
• Waldenstrom staged the pathological
process of the disease as
1. Initial or ischaemic stage
2. Resorption or fragmentation stage
3. Reparative stage
4. Remodelling stage
17. Stage of Avascular Necrosis
Ischemia
A part ( anterior) or whole of capital
femoral epiphysis is necrosed.
On X-ray –
– The ossific nucleus looks smaller
– Classically of Perthes’, looks
dense
– The articular cartilage remains
viable & becomes thicker than
normal
– increased joint space.
PATHOGENESIS
18. PATHOGENESIS
Stage of REVASCULARIZATION / FRAGMENTATION
• Ingrowths of highly vascular & cellular connective tissue.
• Necrotic trabecular debris is resorbed & replaced by vascular
fibrous tissue the alternating areas of sclerosis and
fibrosis appear on X- ray as fragmentation of epiphysis.
• New immature bone laid on intact
necrosed trabeculae by creeping
substitution further increases
the density of ossific nucleus on
X-ray.
19. PATHOGENESIS
Stage of Ossification / Healing
New bone starts forming and epiphyseal
density increases in the lucent portions of
the femoral head.
20. • Remodeling / Residual stage
This is the stage of remodeling and there is no
additional change in the density of the femoral
head.
Depending on the severity of the disease the
residual shape of the head may be spherical
or distorted.
PATHOGENESIS
21. Remodelling stage
(replacement by biologically plastic
bone)
If treated
• Femoral head is
congrous
If untreated
• Subluxation and deformity
22. CLINICAL FEATURES
• Classic portrait of the child with Legg-Calvé-
Perthes disease—small, often thin, extremely
active, constantly running and jumping, and
limping after strenuous physical activities
23. • Often insidious onset of a painless limp,
excaberated by activity.
• C/O pain in groin, thigh, knee
• Few relate trauma hx
• Can have an acute onset
Presentation
24. • Tredelenburg with antalgic
gait
• Trendelenburg test often
positive
• Muscular atrophy of
thigh/buttock/calf
• Limb length discrepency
• Decreased ROM, especially
abduction and internal
rotation: initially due to
muscle spasm
Physical Exam
25. Imaging – Radiographic Feature
• Widening of the joint space and minor subluxation
• Sclerosis
• Fragmentation and focal resorption
• Loss of height
• Metaphyseal cyst formation
• Widening of the femoral neck & head (Coxa Magna)
• Lateral uncovering of the femoral head
• Sagging rope sign
• Acetabular remodelling
28. Caffey’s sign
• As the disease progresses, a
subchondral # may occur in the
anterolateral aspect of the
femoral capital epiphysis.
• Is an early radiographic feature
best seen on the frog-lateral
projection.
• This produces a crescentic
radiolucency known as the
crescent, Salter’s or Caffey’s
sign
30. Stages of radiological changes in
Perthe's disease: cont…
Late Stage–
Coxa magna
High-riding trochanter
Flattened femoral head
Irregular articular surface
31. ‘Sagging Rope Sign’
• This a curvilinear sclerotic
line running horizontally
across the femoral neck.
• It is confirmed by 3D CT
studies.
• It is a finding in AP
radiograph in a mature
hip with Perthes’ disease.
32. Workup
• Technetium 99 bone scan -
Helpful in delineating the
extent of avascular changes
before they are evident on
plain radiographs.
– The sensitivity of
radionuclide scanning in the
diagnosis of LPD is 98%, and
the specificity is 95%.
• Avascular areas show cold
spots
33. Ultrasound features
• Effusion, especially if persistent
• Synovial thickening
• Cartilaginous thickening
• Atrophy of the ipsilateral quadriceps muscle
• Flattening, fragmentation, irregularity of the
femoral head
• New bone formation
• Revascularisation with contrast enhanced power
Doppler
34. CT Scan
• Staging determined by
using plain radiographic
findings is upgraded in 30%
of patients.
• Not as sensitive as nuclear
medicine or MRI.
• CT may be used for follow-
up imaging in patients with
LPD.
35. Arthrography
• Shows configuration of the femoral head and
its relation with the acetabulum.
• Containment
• Congruity
• Not routinely used .
36. MRI
• It allows more precise
localization of involvement
than conventional
radiography.
• MRI is preferred for
evaluating the position, form,
and size of the femoral head
and surrounding soft tissues.
• MRI is as sensitive as isotopic
bone scanning.
37. Morphological classifications of the
extent of the lesion
• Classification according to Catterall (Common)
• Classification according to Salter &
Thompson
• Classification according to Herring
38. • Legg, who identified two types of femoral
heads—a “cap” and a “mushroom.”
• Goff also identified three types of femoral
heads—spherical, cap, and irregular—that
correlated with disease outcome.
39. Classification of extent of lesion - (Acc to
Catterall)
Grade Characteristics
I Only anterolateral quadrant affected
II Anterior third or half of the femoral head
III
Up to 3/4 of the femoral head affected,
only the most dorsal section is intact
IV Whole femoral head affected
40. Grade – I
• Only anterolateral quadrant affected
41. Grade - II
• Anterior third or half of the femoral head
42. Grade – III
• Up to 3/4 of the femoral head affected,
• only the most dorsal section is intact
44. Classification according to Salter &
Thompson
Group Characteristics
A Subchondral # involving <50% of the femoral dome
B Subchondral # involving >50% of the femoral dome
45. Classification according to Herring
Group Characteristics
A Lateral pillar not affected
B
>50% of height of lateral
pillar preserved
C
<50% of height of lateral
pillar preserved
49. Prognostic Factors
1. Age at diagnosis
<6 yrs – good
6 – 9 yrs – fair
>9 yrs - poor
1. Extent of involvement
2. Sex
3. Catterall “head at risk” signs
50. Catterall “head at risk” signs
• Clinical
1. Progressive loss of hip motion more so
abduction.
2. Fixed flexion deformity and adduction
deformities of hip
3. Obese child
4. Age on higher side
51. • Radiographic
1. Gage sign
2. Calcification lateral to epiphysis
3. Diffuse metaphyseal rarefaction
4. Lateral extrusion of femoral head
5. Growth disturbance of physis
56. Classification of End Results
MOSE CLASSIFICATION
• The Mose classification system is based on fitting
the contour of the healed femoral head to a
template of concentric circles.
• In good outcomes, the shape of the femoral
head deviates no more than 1 mm from a given
circle on both AP and frog-leg lateral radiographs.
• If the shape falls within 2 mm, it is considered a
fair outcome.
• If the deviation is greater than 2 mm, it is a poor
outcome.
57. Stulberg classificaton
• Class I – Shape of the femoral head was
basically normal.
• Class II – Loss of head height but within 2 mm
to a concentric circle on AP and frog
leg X-Ray
• Class III – Deviates more than 2 mm and
acetabulum contour matches
the head contour
• Class IV – Head Flattened, Flattened area
<1cm. Acetabulum contour matches
the head contour
• Class V – Collapse of femoral head, Acetabular
contour does not change
58. Stulberg classificaton
• Class I & II – Spherically congruent.
• Class III & IV – Congruous Incongruity
OR
Aspherical congruity.
• Class V – Incongruous incongruity
OR
Aspherically incongruent.
59. Treatment
• Goals of treatment
– Achieve and maintain ROM
– Relieve weight bearing
– Containment of the femoral epiphysis within the
confines of the acetabulum
– Prevent secondary degenerative arthritis of the
hip
60. Treatment
• Caterall group 1 and
group 2 ( < 7 years)
No
• Herring group 1 & Treatment
group 2 (< 6 years)
61. Treatment
Treatment is divided into 3 phases
• Initial Phase – restore & maintain mobility
• Active Phase – Containment and maintainance
of full mobility.
• Reconstructive phase – correct residual
deformities.
62. Treatment ( Initial Phase )
• Physiotherapy – active and passive range of
motion exercises to restore motion
• Traction – B/L skin traction and gradually
abducting over 1-2 weeks till full abduction
isregained.
63. Treatment ( Active Phase )
• Consists of containment of the femoral head
within the acetabulum. This can be achieved
by
orthosis
or by
surgery
64. Treatment (Orthosis)
• Non Ambulatory weight releiving
1. Abduction broomstick plaster cast
2. Hip spica cast
• Ambulatory Both limbs included
1. Petrie Abduction cast
2. Toronto orthosis
3. Newington orthosis
4. Birmingham brace
5. Atlanta Scotish Rite Brace
71. Treatment (Orthosis)
• Orthotic treatment is discontinued when the disease
enters the reparative phase and healing is established.
72. • The radiographic evidence of healing are
1. Appearance of irregular ossification in the femoral head.
2 . Increased density of femoral head should disappear.
3 . Medial segment of femoral head should increase in size
and height.
4 . Metaphyseal rarefaction involving the lateral cortex of the
metaphysis should ossify.
5 . There should be intact lateral column.
73. • If non-op tx cannot maintain containment
• Surgically ideal pt:
– 6-9years
– Catterral II-III
– Good ROM
– In collapsing phase
Operative Tx
75. • varusderotation osteotomy :-
– INDICATIONS- patients with a spherical femoral head,
– little or no acetabular dysplasia (center-edge angle of at least
15 to 20 degrees),
– lateral overloading, and
– a valgus neck-shaft angle of more than 135 degrees.
78. DISADVANTAGES-
varus angulation that may not correct with growth (especially in a
older child),
further shortening of an already shortened extremity,
the possibility of a gluteus lurch produced by decreasing the leng
of the lever arm of the gluteal musculature,
the possibility of nonunion of the osteotomy,
requirement of a second operation to remove the internal fixatio
79. • ADVANTAGE-
• Anterolateral coverage of the femoral head,
• lengthening of the extremity (possibly shortened by the
avascular process), and
• avoidance of a second operation for plate removal
INNOMINATE OSTEOTOMY
80. • DISADVANTAGES-1)inability sometimes to
obtain proper containment of the femoral head,
especially in older children;
• 2)an increase in acetabular and hip joint
pressure that may cause further avascular
changes in the femoral head;
• 3)an increase in leg length on the operated side
compared with the normal side that may cause a
relative adduction of the hip and uncover the
femoral head.
81. • Valgus extension osteotomy
indication -hinge abduction of hip
• Cheilectomy
indication – malformed femoral head
• Chiari osteotomy
indication – malformed femoral head with lateral
subluxation
• Trochanteric advancement or Greater trochanteric
epiphysiodesis
indication – premature capital femoral physeal arrest
• Shelf augmentation procedure
indication – coxa magna & lack of acetabular
coverage
TREATMENT
Reconstructive procedures
82. FREIBERG INFRACTION
• Osteochondritis of the second metatarsal head.
But may also involve 1st 3rd and 4th metatarsal
heads
• Usually occurs following trauma.
• A misshapen metatarsal head frequently is an
incidental radiographic finding, and careful
questioning of the patient often reveals a
period during adolescence when pain was
noted in the forefoot.
83. PATHOPHYSIOLOGY
• The second toe is the longest and the second
ray the least mobile, excessive pressure on the
metatarsal head on weight bearing cause
repetitive microfractures,
loss of blood supply to subchondral bone,
collapse of this cancellous bone, and cartilage
deformation.
84. • Synovitis accompanies the process, and if it is
prolonged and severe, limitation of motion,
especially in extension, results.
• With this loss of extension of the
metatarsophalangeal joint, weight bearing
causes abnormal stress to be applied to the
metatarsal shaft, which becomes widened
from bicortical thickening.
85. PRESENTATION
-Pain around the involved metatarsophalangeal
joint primarily on weight bearing, local
tenderness around the metatarsophalangeal
joint, and limitation of motion.
-If a synovitis is present, swelling becomes
apparent
86. Irregular ossification of the primary ossification center of the
metatarsal head,widening of the metatarsal shaft,and osteochondral
fragmentation
87. TREATMENT
• Modification of activities, semirigid orthoses,
and metatarsal bars.
• A short leg walking cast with a toe extension
may be needed if other non operative
treatment fails.
• Occasionally, crutches are needed to rest the
painful foot completely.
88. TREATMENT
• If conservative management fails, surgical treatments
include (1) Resection of the metatarsal head
• (2) Elevation of the depressed fragment of the
metatarsal head and bone grafting of the defect
(Smillie procedure)
• (3) Resection of the base of the proximal phalanx with
syndactylization of the second and third toes
• (4) Dorsal closing wedge osteotomy of the metatarsal
head
• (5) Joint débridement and metatarsal head remodeling
89. KOHLER’S DISEASE
• Osteochondritis of tarsal navicular
• The aetiology of Köhler's disease is unknown.
Theories have included vascular trauma and
retarded bone
• It commonly affects children aged 3 to 5 years
old, but is seen any time between age 2 and 10
years.
• It is more common in boys; however, girls with
this condition are often younger than boys with
the disease
90. • Children present with a unilateral antalgic gait (a
limp, avoiding putting weight on painful
structures)
• Local tenderness of the medial aspect of the foot,
over the navicular bone
• The child is able to walk by taking the majority of
their weight on the lateral aspect of the foot.
Frequently, there is swelling and redness of the
soft tissues
91. • Plain X-ray -The navicular bone is initially
flattened and sclerotic. Later it becomes
fragmented and then re-ossifies.[4]
• The lateral view shows a flat tarsal
scaphoid.
• The space between the talus and the
cuneiforms is preserved.
92. Rest ,avoiding excessive weight bearing
,analgesia & immobilisation in a short leg cast
moulded under the longitudinal arch for at least
6 weeks is recommended.
If pain persists after a 6-week period of casting,
a new cast must be applied for 6 supplementary
weeks
• The course is chronic, but rarely lasts longer
than 2 year
93. • Arthrodesis is the only operation of value, and
the midtarsal joints (talonavicular and
calcaneocuboid) can be arthrodesed.
• Here arthrodesis is difficult to secure; metallic
internal fixation and inlay grafts of autogenous
cancellous bone are helpful.
94. PANNER’S DISEASE
• OSTEOCHONDRITIS OF CAPITELLUM
• Panner's disease affects the dominant elbow
of children, mainly boys, between the ages of
five and 10.
95. PATHOPHYSIOLOGY
• Interference in blood supply to growing
epiphysis, which results in resorption & eventual
repair & and replacement of the ossification
center
• In patients under 20 years of age, capitellum is
only supplied by end arteries entering
posteriorly;
96. • - inciting causes:
- chronic repetitive trauma, congenital
and hereditary factors, embolism (fat), and
endocrine disturbances;
97. Clinical manifestations
• Intermittent pain and stiffness in the affected
elbow that lasts for several months
•
Symptoms are relieved by rest and aggravated by
activity
• local tenderness over capitellum, limited extension is
typical, lacking 20 to 30 deg of full extension
• There may be slight loss of pronation and supination
w/ tenderness
98. RADIOLOGY
• An irregular surface on the capitellum. The
entire growth plate may appear fragmented
and transparent. The capitellum may appear
flattened out, which means that the bone has
coapsed
• The MRI can give a better view of bone
irregularities. The MRI can also detect
swelling.
99. TREATMENT
• Children may need to stop sports activities for a
short time. This reduces the pain and
inflammation
• NSAIDS to help reduce pain and swelling. Physical
therapy such as heat, ice, and ultrasound may be
used to ease pain and swelling.
• In severe cases, when regular treatment is not
effective, doctors may recommend that the child
wear a long-arm splint or cast for three to four
weeks.
101. Osgood Schlatters disease is a very common cause of
knee pain in children and young athletes.
It occurs during the period of rapid growth, due to a
combined high level of sporting activity who play
soccer, basketball, and volleyball, and who participate
in gymnastics
It occurs more frequently in boys than in girls, with
reports of a male-to-female ratio ranging from 3:1 to as
high as 7:1. [1]
102. PATHO-MECHANICS
Following an adolescent growth spurt, repeated stress
from contraction of the quadriceps is transmitted through
the patellar tendon to the immature tibial tuberosity.
This can cause multiple sub-acute avulsion fractures along
with inflammation of the tendon, leading to excess bone
growth in the tuberosity and producing a visible lump
which can be very painful when hit.
Activities such as kneeling may irritate the tendon further.
104. What Makes OSD Worse?
o squatting
o running
o walking up or down stairs
o cycling
o forceful contractions of the quadriceps muscle
o jumping (basketball, volleyball)
o kneeling
o repetitive hard landings
Anything that puts excessive stress on the insertion of the
patellar tendon
105. Symptomso Main symptom - painful swelling over a bump on the
tibia on one or both sides
o Pain: mild and intermittent initially.
o Later stages- the pain is severe and continuous
in nature.
o Pain usually resolve with treatment but may recur for
12–24 months before complete resolution at skeletal
maturity, when the tibial epiphysis fuses.
Palpation: The area is tender to pressure, and swelling
ranges from mild to very severe.
109. Conservative Management
o Regular stretching, both before and after exercise and
athletics, can help prevent injury
o NSAIDS for pain relief &rest (3 days) and decreasing
activity (1-2 weeks)
o Ice - over the painful area, 2 to 3 times a day, 20 to 30
minutes at a time,
o Bracing, Orthopedic casting
o Infra patellar strap – 6 to 8 weeks
110. Surgical Management
• Surgery may be considered if
symptoms are persistent and severely
disabling & include -Excision of intra-
tendon ossicles
-Tibial sequestrectomy
111. SEVERE’S DISEASE
• Inflammation of the calcaneal apophysis
which occurs in children and adolescents due
to repeated 'microtrauma' at the site of the
attachment of the Achilles tendon to the
apophysis of the heel, often result of sporting
activities
112. AETIOLOGY
• The line of ossification in the calcaneal
apophysis is thought to develop
microfractures due to recurrent stresses on
the heel, combined with the growth spurt of
puberty. It is caused by decreased resistance
to shear stress at the bone-growth plate
interface.
113. CLINICAL FEATURES
• Heel pain, usually in young physically active individuals,
which is gradual in onset, and worse on exercise,
especially running or jumping relieved by rest. Often
bilateral.
• Tenderness on palpation of the heel - particularly on
deep palpation at the Achilles tendon insertion.
• Pain on dorsiflexion of the ankle - particularly when
doing active toe raises; forced dorsiflexion of the ankle
is also uncomfortable.
• Swelling of the heel - usually mild.
• Calcaneal enlargement - in long-standing cases
114. • X-ray of the heel may show increased sclerosis
and fragmentation of the calcaneal apophysis
– but these features are nonspecific and it
may be normal
• CT or MRI scan may be useful to exclude
osteomyelitis or fusion of the small bones of
the hindfoot.
115. TREATMENT
• Physiotherapy and exercises
• Soft orthotics or heel cups.
• Advice on suitable athletic footwear. In severe
cases: temporarily limiting activity such as
running and jumping.
• Ice and non-steroidal anti-inflammatory drugs
(NSAIDs), which can reduce pain
• In very severe cases, a short period of
immobilisation (eg 2-3 weeks in a case in mild
equinus position)
117. • The mechanism in Sinding-Larsen Johansson
disease is thought to be persistent traction at
the cartilaginous junction of the patella and
the patellar ligament/tendon
It is essentially a chronic stress injury with
overuse of the patella-patellar tendon junction
118. • Knee X-ray: can show calcification or
ossification at the junction between the
patella and the patella ligament
• Physiotherapy is the mainstay of treatment,
including quadriceps strengthening exercises
119. KIENBOCK DISEASE
• Avascular Necrosis of Lunate
• First Described by Robert Kienbock in 1910; as
“traumatic softening” of Lunate bone
120. AETIOLOGY
• Aetiology = unknown, but several cause have been
proposed
• Vascular compromise from repetitive trauma causes
microfracture & excessive stress on microscopic
architecture (sports injury)
• Ulnar minus variant:- Individual having ulnar minus
variance are at increased risk. Short Ulna
increases shear force across the lunate Causes
vascular insufficiency
123. CLINICAL FEATURE
• There may be history of trauma with wrist in severe
dorsiflexion
The lesion presents with
1. Dorsal wrist pain:- Pain may be produced in lunate
region by axial strike/injury at distal end of middle
finger
2. Swelling
3. Decreased Grip strength
4. Decreased range of motion; particularly in extension.
In later stage movement may be painful
124. IMAGING
• X-ray at first show no abnormality but
• Bone scan may reveals increased activity
• Later x-ray may show either mottled or diffuse
density of bone – to – osteoarthritic changes
in wrist
• MRI Most reliable way of detecting the early
change
125.
126. TREATMENT
A Conservative
Casting of wrist for several wks ; for early
stages of disease ( St I or II, before sclerosis,
fragmentation or collapse)
But- Unacceptable & Ineffective
B Operative
• Surgery is only definitive treatment
127. Early Disease Stage I & II
• Unloading the Lunate*
• 1. Ulnar lengthening
• Transverse osteotomy at distal ulna
Distraction Cortical iliac graft Tightening
of plate screw
128. Early Disease Stage I & II
2. Radial Shortening
Indication
– Negative ulnar variance
– Lunate compression fracture without fragmentation or
flattening
Procedure
Transverse osteotomy 3”
proximal to distal
articulating surface
shortening of radius by 2
cm
fixing the bone with
compression plate
129. • Vascularized grafts include the distal radius
based on the pronator quadratus, the pisiform
as a pedicle graft, and various other grafts
from the distal radius, second metacarpal, and
pisiform.
• These procedures also are effective in
relieving pain and improving function in
approximately 90% of patients
130. In stage III
1. Ulnar lengthening
2. Silicon prosthesis
- silicon synovitis
- foreign body cyst
3. Interacarpal fusion
4. Lunate excision
5. Arthrodesis Tri scaphe
Scaphocapitate
131. In stage IV
• Proximal carpal row resection
• Wrist arthrodesis
132. ISELIN DISEASE
• Traction epiphysitis of the base of the fifth
metatarsal occurring in young adolescents at
the time of appearance of the proximal
epiphysis of the fifth metatarsal
• This bone is located within the cartilaginous
flare onto which the peroneus brevis inserts
133. PRESENTATION
• Tenderness over a prominent proximal fifth
metatarsal.
• Weight bearing produces pain over the lateral
aspect of the foot.
• The affected area over the tuberosity is larger on
the involved side, with soft-tissue edema and
local erythema.
• The area is tender to palpation at the insertion of
the peroneus brevis, and resisted eversion and
extreme plantar flexion and dorsiflexion of the
foot elicit pain.
134. • Oblique radiographs- enlargement and
fragmentation of the epiphysis and widening
of the cartilaginous-osseous junction.
• Technetium-99m bone scanning-incresed
uptake
136. TREATMENT
• For mild symptoms, limitation of sports
activity, application of ice, and administration
of NSAIDS
• For severe symptoms, cast immobilization
may be required. Internal fixation of the
epiphysis is not indicated.
137. SCHEUREMANN’S DISEASE
• It is essentially osteochondrosis of the
vertebrae
• It affects the thoracic or thoracolumbar spine
causing increased kyphosis, poor posture and
possible backache. It is the most common
cause of structural kyphosis in adolescents.
138. PATHOPHYSIOLOGY
• A defect in the secondary ossification centres
of the vertebral bodies. A few vertebral bodies
may be involved or the whole thoracolumbar
spine.
• Hereditary factors are thought to play a part
• Taller height, as well as an association with
increased levels of growth hormone, have also
been suggested
• Mechanical factors and trauma
140. Presentation
• Poor posture with increased kyphosis (usually
noticed by parents).
• Pain is a more common presentation if the
disease affects the lumbar spine. Pain is usually
dull aching worse on activity and relieves on rest
• Neurological symptoms may rarely be the
presenting feature
• Cardiorespiratory symptoms can also rarely occur.
141. Examination
• It is normal to have a degree of kyphosis. Any degree of
kyphosis of more than 40° is considered abnormal
• Kyphotic deformity may be progressive.
• Upper thoracic kyphosis is best seen in the forward
flexed position; lower thoracic kyphosis may be seen at
the thoracolumbar junction.
• There is reduced flexibility of the spine.
• There may be tenderness above and below the apex of
the kyphosis.
• Scoliosis may also be present
• Neurological signs are rare.
142. RADIOGRAPHY
• Wedge-shaped vertebral bodies
• Rigid kyphosis
• Narrow intervertebral disc spaces with
calcifications
• Prominent irregularities of the vertebral
surfaces
• Vertebral plates that are poorly formed and
that develop multiple herniations of the
nucleus pulposus known as Schmorl nodes
143. TREATMENT
• Mild, nonprogressive disease can be treated
by reducing weight-bearing ,stress and
avoiding strenuous activity
• For severe kyphosis , recommendations
include casting, a spinal brace, or rest and
recumbency on a rigid bed. Orthotic Mx
usually requires 12-24 months of treatment.
• Non-steroidal anti-inflammatory drugs may be
used for pain relief
144. • Surgery ,if there is neurological deficit,
uncontrolled pain, unacceptable cosmetic
appearance or documented progression
• Cord decompression for neurological deficit
and
• Spinal fusion techniques for kyphosis
correction and pain control.
145. Complications
• Chronic back pain.
• Progressive and permanent deformity.
• Neurological deficit.
• Cardiorespiratory problems.
