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Seminar
on
“ Fracture Healing and Epiphyseal injuries”
13 – 10 - 2011

Moderator:

Presenter:

Dr. C B Patil

Dr

Professor
Graduate
VIMS & RC.

Post

Somnath Machani
VIMS & RC
.
Bone healing in adults


Fracture healing can be divided in to two types


Primary- direct healing by internal remodelling



Secondary- Indirect healing by callus



Stages
−
−
−
−

Inflamation
Soft callus
Hard callus
remodelling


Stage of inflamation



1 to 7 days
Hematoma, inflamatory
exudates



Cytokines role



Collagen formation



Necrotic bone removal


Soft callus formation


2- 3 weeks



Decreased pain and swelling



Prone to angulation





Progenitor cells in cambium
layer
Hematoma replaced


Hard callus formation


3 to 4 months



Firmly united by new bone



Enchondral ossification





Bone callus begins at the
periphery of the fracture sitelow strain
Initial bone bridge forms
externally of within medullary
canal and later joins original
cortex


Remodelling




Woven bone replaced by
lamellar bone.
Few months to years till the
meduallary canal is replaced
Difference


Cancellous


Less formation of significant external callus



After inflamatory stage – intramembranous ossification



In unusual cases interfragmentary motion leads to intermediary soft
tissue formation and soon replaced by bone
Need to study child fracture healing


Changing structure and function



Different failure pattern



Fracture after insignificant trauma



15% of childhood fractures are physeal injuries



Physis has longitudinal and diametric growth



Salter harris type 1 MC in infants



Salter harris type 2 to 4 when 2 nd ary ossification centre enlarges
Anatomic regions of child bone


Epiphysis



Physis



Metaphysis



Diaphysis
Epiphysis







@ birth except distal femur
Cartilagenous
chondroepiphysis
2nd ary ossification centre
enlarges until replaced by
bone
Lucent physeal lines






External surface has
perichondrium or articualar
cartilage
Pericondrium has ligament
and muscle attachmentscentrifugal enlargement of the
epiphysis
Thick perichondriummechanical strength to zone
of Ranvier
Physis / growth plate






Rapid longitudinal and
diametric growth
Appreciated by growth of the
secondary centre
Epiphyseal blood vessels
penetrate to reach physis(fig
2)


Vessel damage leads to
uneven growth

Patterns of response to ischemia of the
epiphyseal (A, B) versus metaphyseal (C,
D) circulatory systems. Metaphyseal
ischemia is usually transient; epiphyseal
ischemia is usually severe and permanent.
Histologic section showing an area of central
ischemic growth arrest (arrow). The
infarcted area of cartilage is left behind as
the rest of the physis continues longitudinal
growth.
Metaphysis






Contoured flare at the end of
diaphysis
Less cortical and more
trabecular bone
Te99m scan shows increased
bone turnover

Cortical fenestration (solid arrows) of a
metaphysis. Note the interdigitation of
periosteal (Ps) tissue with the fenestrations.
The periosteum blends into the perichondrium
(Pc). Extensive vascularity is often present in
this region (open arrows). (E, epiphysis; P,
physis; Z, zone of Ranvier; L, ring of Lacroix.)


Fibrovascular connections is
the cause for torus or buckle
fractures

Extensive modeling and remodeling of the
medial (M) versus the lateral (L) cortex of
the distal femur may create irregularities
that have been misinterpreted as fracture,
stress fracture, infection, and tumor. Note
the well-formed subchondral bone at the
periphery of the epiphyseal ossification
center.


Transverse lines of park and
harris

Histologic section (A) and x-ray study (B) of a
distal femur showing a typical Harris line
(arrows). This formed during an acute
illness and chemotherapy for leukemia. The
child then resumed a more normal pattern
of growth until her death from leukemia
about 14 months later.
Diaphysis





Extremely vascualar
Periosteum- thicker in child
and easily elevated
Greater osteogenic potential
and less likely to injure
periosteum

Simulated type 1 epiphyseal (E) displacement from
the metaphysis (M). Note the thick periosteum
(arrow) and its contiguity with the cartilage of
the epiphysis (radiopaque here because of the
cartilage and air contrast). In the body,
however, the similar soft-tissue radiodensities of
cartilage, ligament, muscle, and so forth blend
together, making them radiolucent.
Composition of bone
Composition of Cartilage
Zones of physis
Factors influencing bone growth
Fracture healing in children






Usually associated with
ligament and soft tissue injury
Physis and epiphysis don't
heal by callus formation
Phases


Inflamatory



Reparative



remodelling
Inflamatory phase





Hematoma and local necrosis
Bleeding from periosteum
and bone
Dissects along diaphysis upto
the zone of ranvierPDGF,
VGEF, TGF beta promote
osteoblast recruitment and
activation








Local necrosis- supply is
disrupted for a few mm on
either side
Necrosis also releases
growth factors
Initial matrix contains type
1,3,5 collagen
Promotes mineralization and
primary callus
Reparative phase










Osteogenic cells proliferate
from the external callus
10-14 days thick fracture
callus enveloping mass of
peripheral osteogenic tissue
BMP family- mesenchymal
cell differenciation
Till healing goes thro final
stages- fracture is still
biologically plastic
Clinical union
Remodelling







Resorption of unnecessary
and in efficient callus
Trabecular orientation
Cancellous bone- the cells
are never far away from the
blood vessels
Replacement of bone occur
in the trabeculae
Physeal healing


Limted ability to repair



Primarily heals by increased endochondral bone



3 types of chondro osseous healing


I- # thro columns



II - # thro transition zone



III - # injury to all layers of the physis
Mechanism of bone bridge formation
Intramembranous ossification mechanism
for bone bridge formation at the growth
plate injury site. Histologically (Barbara's
histology stain), bony bridge trabeculae
start to appear on day 7 postinjury (A),
and become well-constructed on day 14
with marrow (B). Prior to and during
physeal bar formation, there is no new
cartilage formation, no collagen-X
synthesis (as examined by
immunostaining) at the injury site (C),
and no expansion of chondrocyte
proliferation (as examined by BrdU
labeling) from adjacent physeal cartilage
(D).
Starting from day 3 (E) until day 14, there is
infiltration of marrow-derived fibroblast-like
mesenchymal cells (as examined by
vimentin immunostaining), some of which
are osteoblast precursor cells displaying
positive immunostaining for bone cell
differentiation transcription factor cbf-a1 (F)
and osteoblast/osteoprogenitor maturation
marker alkaline phosphatase (G). During
bone bridge formation, bone matrix protein
osteocalcin is produced by osteoblasts on
bone bridge trabeculae (immunostaining)
(H). *, injury site; block arrow, pointing to
adjacent growth plate cartilage; small arrow,
pointing to bone bridge trabeculae or
immunostained positive cells.
Etiology of Physeal injuries


Infection

Standing anteroposterior lower
extremity x-ray of a 12-year-old
boy with multifocal physeal
disturbance from purpura
fulminans associated with
meningococcemia. X-ray
abnormalities are present in the
left proximal femur; both distal
femoral epiphyses, including
partial arrest of the left distal
femoral physis; and both distal
tibial epiphyses. The patient also
has digital amputations and


Tumours

Valgus deformity of the distal femur
associated with the presence of
an enchondroma of the distal
lateral femur involving the lateral
physis.


Vascular insult

A. The patient's leg was caught under heavy pipes
rolling off a rack, resulting in stripping of the soft
tissues from the distal thigh, open comminuted
fracture of the distal femur, and popliteal artery
injury. B. In follow-up, after arterial and soft
tissue reconstruction, the patient has physeal
growth arrests of the distal femur and proximal
tibia. The mechanism of injury to the proximal
tibial physis was presumed to be vascular,
because of the associated femoral artery injury.


Repetitive stress



Distal radius in gymnast



Proximal tibia in soccer
Classification of epiphyseal injuries


Salter Harris- 1963



Poland 1898



Aitken 1936



Petersons 1970
Salter Harris


Type 1

transphyseal plane


X ray only shows soft tissue
swelling



Diagnosis by MRI and USG



Avoid stress x ray



# line in zone of hypertrophy



Minimal growth disturbance







Type II
Metaphyseal and physeal
component
Thurston holland fragment
sign
Growth disturbance
uncommon


Metaphyseal spike may
damage physis

A. Dorsally displaced type II fracture of the distal
radius. Note the evidence of impaction of the
epiphyseal fragment (with the physis) by the
dorsal margin of the proximal fragment
metaphysis. B. One year later, there is x-ray
evidence of physeal arrest formation in the
distal radial physis.
Type III
 Begins in the epiphysis as a
fracture thro the articular
surface
 2 fragments- small portion of
epiphysis and physis
large with long bone
 Type 3 fracture fixed with
screw








Type IV
Veritical shear
Disrrupt articular cartilage
Metaphyseal and epiphyseal
cross union is common
Reduction and stabilization


Type V



Unrecognized compression



Normal x ray show a
premature physeal closure
later
Poland classification

Poland type I, epiphyseal separation without metaphyseal fragment, or extension into the epiphysis.
Poland type II, physeal fracture line extends into the metaphysis.
Poland type III fracture extends from the articular surface to the physis and continues peripherally through the physis.
Poland type IV, T-condylar fracture of the epiphysis and physis.
Aitken classification




Type 1 – SH2
Type 2 – SH 3
Type 3 – SH 4
Petersons Classification


Does not accept SH 5



Peterson 2 to 5 like SH 1 to 4





Peterson 1- transverse
metaphyseal fracture with
longitudinal extension into
physis
Peterson 6- partial physeal
loss
Evaluation of physeal injury


Xray



CT



MRI



USG



Arthorgraphy to assess the congrugency of articular surface
Treatment


Stabilize first



General principles


Children # heal rapidly



Cast immobilization



Accurate reduction



Complication – growth disturbance, neurovascular compromise
Physeal growth disturbance


Etiology





Blounts disease





Peterson type 6, Infection, Cyst
Purpura fulminans

Evaluation- serial x rays
Loss of physeal contour,
radiolucency between
physeal and metaphyseal
bone

Asymmetric growth arrest line that does not taper to the
physis is a strong indication of the presence of physeal
growth disturbance without frank physeal arrest. In this case,
the asymmetric growth arrest line is noted in the proximal
tibial metaphysis on computed tomography scan.
Harris growth arrest line tapering to the physis
at the level of the growth arrest can serve as
an excellent x-ray confirmation of the
presence of the true growth arrest. Although
most commonly noted on plain x-rays, these
arrest lines can be seen on computed
tomography (CT) scans and magnetic
resonance images as well. A.
Anteroposterior x-ray of the distal tibia after
Salter-Harris type IV fracture demonstrates
a Harris growth arrest line tapering to the
medial distal tibial physis, where a partial
physeal arrest has formed. B. Harris growth
arrest line as noted on CT. CT scans with
coronal (C) and sagittal (D) reconstructions
corrected for bone distortion provide
excellent images of the location and size of
arrest.
Magnetic resonance imaging scan of a
patient with traumatic lateral distal
femoral partial growth arrest. Note
Harris arrest line tapering to the site
of the arrest.
Magnetic resonance imaging scan (threedimensional spoiled recalled gradient
echo images with fat saturation)
provides excellent visualization of the
affected area and some sense of the
integrity of the residual physis. This
patient has infantile Blount disease.
Physeal arrests
Potential Causes
Traumatic vascular disruption
Transphyseal infection
Vascular collapse associated with infection (purpura
fulminans)
Infantile Blount's disease
Irradiation
Unicameral bone cyst
Enchondroma
limb shortening, angular deformity, and epiphyseal
distortion, depending on the duration of the arrest, the
physis affected, and the size of the arrest. A long,
standing film of the lower extremities with the hip,
knee, and ankle joints included provides an overall
assessment of angular deformity and shortening.
Classification of physeal arrests
Central arrests are surrounded by a perimeter
of normal physis.
Peripheral arrests are located at the perimeter
of the physis.
Linear arrests are through-and-through
lesions with normal physis on either side of
the arrest area.
Management





Prevention of arrest formation
Gentle anatomic and secure
reduction
Fat grafting

NSIAD's ??
Physiolysis




Partial physeal arrest
resection
Principle- to remove bone
between metaphysis and
physis and fill defect with
bone reformation retardant
Physeal distraction






External fixator is used to
span the arrest .
Gradual distraction until
arrest separates
Distraction injury may cause
complete cessation of normal
physeal growth
Repeated osteotomies




Corrective osteotomy of adjacent metaphysis to correct angular
deformity
Completion of epiphysisodesis and management of resulting
limb length discrepancy



Epiphysiodesis prevents angular deformtiy



Limb lengthening can be considered
Physeal arrest resection


Etiology- trauma/ blounts- good prognosis
infection / tumour- unlikely to show growth






Central and linear arrest regrowth more likely
Proximal humeral and femoral leisions more difficult to exposeadequate resection unlikely
Arrests affecting >25% of total surface area are unlikely to grow
Preoperative planning
extent and location of the arrest relative to the rest
of the physis must be carefully documented
evaluate an arrest is with reconstructed sagittal and
coronal CT images to provide views orthogonal
to the affected physis
estimation of the affected surface area can be
computed with the assistance of the radiologist
using a modification of the method of Carlson
and Wenger
Reconstructed magnetic resonance images allow
estimation of the percentage of surface area of
the physis affected by a growth arrest. This
workstation reconstruction delineates the
perimeter of normal physis (border 2) and that of
the physeal arrest (border 1). Surface area
affected can be calculated from these
reconstructions.
The arrest must be resected in a manner that
minimizes trauma to the residual physis.
Central lesions should be approached
through either a metaphyseal window or
through the intramedullary canal after a
metaphyseal osteotomy. Peripheral lesions
are approached directly, resecting the
overlying periosteum to help prevent
reformation
Fluoroscopy is needed to keep the surgeon
oriented properly to the arrest and the
residual healthy physis.
A high-speed burr worked in a gentle to-andfro movement perpendicular to the physis
usually is the most effective way to
gradually remove the bone composing the
arrest and expose the residual healthy
physis
By the end of the resection, all of the
bridging bone between the metaphysis
and epiphysis should be removed,
leaving a void in the physis where the
arrest had been, and the perimeter of
the healthy residual physis should be
visible circumferentially at the margins of
the surgically created cavity
Prevent Re-forming of Bridge between Metaphysis and Epiphysis
A bone-growth retardant or a spacer material
should be placed in the cavity created by
the arrest resection to prevent re-forming of
the bony bridge between the metaphysis
and epiphysis.
Four compounds have been used for this
purpose either clinically or experimentally:
autogenous fat , methylmethacrylate ,
silicone rubber , and autogenous cartilage.
Silione and cartilage not used anymore
Methlymethacrylate is inert but gives structural
stability in large resection and in weight
bearing areas (tibia in blounts disease)
Metallic markers should implanted in the
epiphysis and metaphysis at the time of
arrest resection to allow reasonably
accurate estimation of the amount of
longitudinal growth that occurs across the
operated physis, as well as to identify the
deceleration or cessation of that growth
Resumption of longitudinal growth may not
occur despite technically adequate arrest
resection in patients with good clinical
indications.
The treating surgeon be alert to those
developments, so that proper intervention
can be instituted promptly. Embedded
metallic markers serve these purposes
Treatment recommendations
On average, approximately 60% of physeal arrests demonstrate clear x-ray evidence of
resumption of longitudinal growth of the affected physis after physeal arrest resection.
There is a correlation between the amount of surface area of the physis affected and the
prognosis for subsequent longitudinal growth after arrest resection. Physeal arrests affecting
less than 10% of the surface area of the physis have a better prognosis than larger arrests.
Langenskiod stage VI infantile Blount disease has results comparable to post-traumatic physeal
arrests.
Etiologies other than post-traumatic and infantile Blount disease have poor prognoses for
subsequent growth.
Central and peripheral arrests have equivalent prognoses with respect to resumption of growth.
Early growth resumption may be followed by cessation of longitudinal growth before skeletal
maturity. As a consequence, patients must be evaluated regularly until skeletal maturity with
some reliable method (such as metaphyseal and epiphyseal x-ray markers) to detect such
development as promptly as possible.
Growth Deceleration Without Arrest
growth deceleration without frank cessation of growth
is characterized by x-ray abnormality of the
appearance of an injured physis
clinical or x-ray deformity if the disturbance is severe
and long-standing, but without complete cessation
of growth in the affected area
The concept of growth deceleration without arrest is
most readily appreciated in patients with
adolescent Blount disease and the milder stages of
infantile Blount disease, infection and physeal
fracture
there is no sclerotic area of arrest on plain x-rays
A growth arrest line, if present, may be asymmetric
but will not taper to the physis, thereby suggesting
growth asymmetry but not complete arrest.
Management
The diagnosis of physeal growth disturbance usually is made
incidentally by noting physeal abnormality on x-rays during
physeal fracture follow-up or after a diagnosis of frank physeal
arrest has been excluded during the evaluation of a patient with
angular deformity and physeal abnormality on plain x-rays.
Assess extent of limb length inequality and the calculated amount
of potential growth remaining for the affected physis.
If angular deformity is present or progressive, treatment options
include hemiepiphysiodesis or stapling and corrective
osteotomy, with or without completion of the epiphysiodesis.
Hemiepiphysiodesis or stapling of the affected physis on the convex side of the deformity
may result in gradual correction of the deformity. If correction occurs, options include
completion of the epiphysiodesis (with contralateral epiphysiodesis if necessary to
prevent the development of significant leg length deformity) or removal of staples with
careful longitudinal observation for recurrence or overcorrection of deformity.
Corrective osteotomy is the other option for the management of growth disturbance with
established angular deformity.
Treating surgeon must decide whether to perform epiphysiodesis of the affected physis
(with contralateral epiphysiodesis, if appropriate) to prevent recurrence or to ensure
careful longitudinal observation of the growth performance of the affected physis until
skeletal maturity.
Conclusion
Physeal injuries are common
Gentle and expert management to maximize restoration of
normal limb function and longitudinal growth
Follow up with serial x rays to identify physeal arrest
References


Rockwood and wilkins fractures in children



AO trauma manual
Thankyou

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Epiphyseal injury

  • 1. Seminar on “ Fracture Healing and Epiphyseal injuries” 13 – 10 - 2011 Moderator: Presenter: Dr. C B Patil Dr Professor Graduate VIMS & RC. Post Somnath Machani VIMS & RC .
  • 2. Bone healing in adults  Fracture healing can be divided in to two types  Primary- direct healing by internal remodelling  Secondary- Indirect healing by callus  Stages − − − − Inflamation Soft callus Hard callus remodelling
  • 3.  Stage of inflamation   1 to 7 days Hematoma, inflamatory exudates  Cytokines role  Collagen formation  Necrotic bone removal
  • 4.  Soft callus formation  2- 3 weeks  Decreased pain and swelling  Prone to angulation   Progenitor cells in cambium layer Hematoma replaced
  • 5.  Hard callus formation  3 to 4 months  Firmly united by new bone  Enchondral ossification   Bone callus begins at the periphery of the fracture sitelow strain Initial bone bridge forms externally of within medullary canal and later joins original cortex
  • 6.  Remodelling   Woven bone replaced by lamellar bone. Few months to years till the meduallary canal is replaced
  • 7. Difference  Cancellous  Less formation of significant external callus  After inflamatory stage – intramembranous ossification  In unusual cases interfragmentary motion leads to intermediary soft tissue formation and soon replaced by bone
  • 8. Need to study child fracture healing  Changing structure and function  Different failure pattern  Fracture after insignificant trauma  15% of childhood fractures are physeal injuries  Physis has longitudinal and diametric growth  Salter harris type 1 MC in infants  Salter harris type 2 to 4 when 2 nd ary ossification centre enlarges
  • 9. Anatomic regions of child bone  Epiphysis  Physis  Metaphysis  Diaphysis
  • 10. Epiphysis     @ birth except distal femur Cartilagenous chondroepiphysis 2nd ary ossification centre enlarges until replaced by bone Lucent physeal lines
  • 11.    External surface has perichondrium or articualar cartilage Pericondrium has ligament and muscle attachmentscentrifugal enlargement of the epiphysis Thick perichondriummechanical strength to zone of Ranvier
  • 12. Physis / growth plate    Rapid longitudinal and diametric growth Appreciated by growth of the secondary centre Epiphyseal blood vessels penetrate to reach physis(fig 2)
  • 13.
  • 14.  Vessel damage leads to uneven growth Patterns of response to ischemia of the epiphyseal (A, B) versus metaphyseal (C, D) circulatory systems. Metaphyseal ischemia is usually transient; epiphyseal ischemia is usually severe and permanent. Histologic section showing an area of central ischemic growth arrest (arrow). The infarcted area of cartilage is left behind as the rest of the physis continues longitudinal growth.
  • 15. Metaphysis    Contoured flare at the end of diaphysis Less cortical and more trabecular bone Te99m scan shows increased bone turnover Cortical fenestration (solid arrows) of a metaphysis. Note the interdigitation of periosteal (Ps) tissue with the fenestrations. The periosteum blends into the perichondrium (Pc). Extensive vascularity is often present in this region (open arrows). (E, epiphysis; P, physis; Z, zone of Ranvier; L, ring of Lacroix.)
  • 16.  Fibrovascular connections is the cause for torus or buckle fractures Extensive modeling and remodeling of the medial (M) versus the lateral (L) cortex of the distal femur may create irregularities that have been misinterpreted as fracture, stress fracture, infection, and tumor. Note the well-formed subchondral bone at the periphery of the epiphyseal ossification center.
  • 17.  Transverse lines of park and harris Histologic section (A) and x-ray study (B) of a distal femur showing a typical Harris line (arrows). This formed during an acute illness and chemotherapy for leukemia. The child then resumed a more normal pattern of growth until her death from leukemia about 14 months later.
  • 18. Diaphysis    Extremely vascualar Periosteum- thicker in child and easily elevated Greater osteogenic potential and less likely to injure periosteum Simulated type 1 epiphyseal (E) displacement from the metaphysis (M). Note the thick periosteum (arrow) and its contiguity with the cartilage of the epiphysis (radiopaque here because of the cartilage and air contrast). In the body, however, the similar soft-tissue radiodensities of cartilage, ligament, muscle, and so forth blend together, making them radiolucent.
  • 23. Fracture healing in children    Usually associated with ligament and soft tissue injury Physis and epiphysis don't heal by callus formation Phases  Inflamatory  Reparative  remodelling
  • 24. Inflamatory phase    Hematoma and local necrosis Bleeding from periosteum and bone Dissects along diaphysis upto the zone of ranvierPDGF, VGEF, TGF beta promote osteoblast recruitment and activation
  • 25.     Local necrosis- supply is disrupted for a few mm on either side Necrosis also releases growth factors Initial matrix contains type 1,3,5 collagen Promotes mineralization and primary callus
  • 26. Reparative phase      Osteogenic cells proliferate from the external callus 10-14 days thick fracture callus enveloping mass of peripheral osteogenic tissue BMP family- mesenchymal cell differenciation Till healing goes thro final stages- fracture is still biologically plastic Clinical union
  • 27. Remodelling     Resorption of unnecessary and in efficient callus Trabecular orientation Cancellous bone- the cells are never far away from the blood vessels Replacement of bone occur in the trabeculae
  • 28. Physeal healing  Limted ability to repair  Primarily heals by increased endochondral bone  3 types of chondro osseous healing  I- # thro columns  II - # thro transition zone  III - # injury to all layers of the physis
  • 29. Mechanism of bone bridge formation Intramembranous ossification mechanism for bone bridge formation at the growth plate injury site. Histologically (Barbara's histology stain), bony bridge trabeculae start to appear on day 7 postinjury (A), and become well-constructed on day 14 with marrow (B). Prior to and during physeal bar formation, there is no new cartilage formation, no collagen-X synthesis (as examined by immunostaining) at the injury site (C), and no expansion of chondrocyte proliferation (as examined by BrdU labeling) from adjacent physeal cartilage (D).
  • 30. Starting from day 3 (E) until day 14, there is infiltration of marrow-derived fibroblast-like mesenchymal cells (as examined by vimentin immunostaining), some of which are osteoblast precursor cells displaying positive immunostaining for bone cell differentiation transcription factor cbf-a1 (F) and osteoblast/osteoprogenitor maturation marker alkaline phosphatase (G). During bone bridge formation, bone matrix protein osteocalcin is produced by osteoblasts on bone bridge trabeculae (immunostaining) (H). *, injury site; block arrow, pointing to adjacent growth plate cartilage; small arrow, pointing to bone bridge trabeculae or immunostained positive cells.
  • 31. Etiology of Physeal injuries  Infection Standing anteroposterior lower extremity x-ray of a 12-year-old boy with multifocal physeal disturbance from purpura fulminans associated with meningococcemia. X-ray abnormalities are present in the left proximal femur; both distal femoral epiphyses, including partial arrest of the left distal femoral physis; and both distal tibial epiphyses. The patient also has digital amputations and
  • 32.  Tumours Valgus deformity of the distal femur associated with the presence of an enchondroma of the distal lateral femur involving the lateral physis.
  • 33.  Vascular insult A. The patient's leg was caught under heavy pipes rolling off a rack, resulting in stripping of the soft tissues from the distal thigh, open comminuted fracture of the distal femur, and popliteal artery injury. B. In follow-up, after arterial and soft tissue reconstruction, the patient has physeal growth arrests of the distal femur and proximal tibia. The mechanism of injury to the proximal tibial physis was presumed to be vascular, because of the associated femoral artery injury.
  • 34.  Repetitive stress  Distal radius in gymnast  Proximal tibia in soccer
  • 35. Classification of epiphyseal injuries  Salter Harris- 1963  Poland 1898  Aitken 1936  Petersons 1970
  • 36. Salter Harris  Type 1 transphyseal plane  X ray only shows soft tissue swelling  Diagnosis by MRI and USG  Avoid stress x ray  # line in zone of hypertrophy  Minimal growth disturbance
  • 37.     Type II Metaphyseal and physeal component Thurston holland fragment sign Growth disturbance uncommon
  • 38.  Metaphyseal spike may damage physis A. Dorsally displaced type II fracture of the distal radius. Note the evidence of impaction of the epiphyseal fragment (with the physis) by the dorsal margin of the proximal fragment metaphysis. B. One year later, there is x-ray evidence of physeal arrest formation in the distal radial physis.
  • 39. Type III  Begins in the epiphysis as a fracture thro the articular surface  2 fragments- small portion of epiphysis and physis large with long bone  Type 3 fracture fixed with screw 
  • 40.      Type IV Veritical shear Disrrupt articular cartilage Metaphyseal and epiphyseal cross union is common Reduction and stabilization
  • 41.  Type V  Unrecognized compression  Normal x ray show a premature physeal closure later
  • 42. Poland classification Poland type I, epiphyseal separation without metaphyseal fragment, or extension into the epiphysis. Poland type II, physeal fracture line extends into the metaphysis. Poland type III fracture extends from the articular surface to the physis and continues peripherally through the physis. Poland type IV, T-condylar fracture of the epiphysis and physis.
  • 43. Aitken classification    Type 1 – SH2 Type 2 – SH 3 Type 3 – SH 4
  • 44. Petersons Classification  Does not accept SH 5  Peterson 2 to 5 like SH 1 to 4   Peterson 1- transverse metaphyseal fracture with longitudinal extension into physis Peterson 6- partial physeal loss
  • 45.
  • 46. Evaluation of physeal injury  Xray  CT  MRI  USG  Arthorgraphy to assess the congrugency of articular surface
  • 47. Treatment  Stabilize first  General principles  Children # heal rapidly  Cast immobilization  Accurate reduction  Complication – growth disturbance, neurovascular compromise
  • 48. Physeal growth disturbance  Etiology    Blounts disease   Peterson type 6, Infection, Cyst Purpura fulminans Evaluation- serial x rays Loss of physeal contour, radiolucency between physeal and metaphyseal bone Asymmetric growth arrest line that does not taper to the physis is a strong indication of the presence of physeal growth disturbance without frank physeal arrest. In this case, the asymmetric growth arrest line is noted in the proximal tibial metaphysis on computed tomography scan.
  • 49. Harris growth arrest line tapering to the physis at the level of the growth arrest can serve as an excellent x-ray confirmation of the presence of the true growth arrest. Although most commonly noted on plain x-rays, these arrest lines can be seen on computed tomography (CT) scans and magnetic resonance images as well. A. Anteroposterior x-ray of the distal tibia after Salter-Harris type IV fracture demonstrates a Harris growth arrest line tapering to the medial distal tibial physis, where a partial physeal arrest has formed. B. Harris growth arrest line as noted on CT. CT scans with coronal (C) and sagittal (D) reconstructions corrected for bone distortion provide excellent images of the location and size of arrest.
  • 50. Magnetic resonance imaging scan of a patient with traumatic lateral distal femoral partial growth arrest. Note Harris arrest line tapering to the site of the arrest.
  • 51. Magnetic resonance imaging scan (threedimensional spoiled recalled gradient echo images with fat saturation) provides excellent visualization of the affected area and some sense of the integrity of the residual physis. This patient has infantile Blount disease.
  • 52. Physeal arrests Potential Causes Traumatic vascular disruption Transphyseal infection Vascular collapse associated with infection (purpura fulminans) Infantile Blount's disease Irradiation Unicameral bone cyst Enchondroma limb shortening, angular deformity, and epiphyseal distortion, depending on the duration of the arrest, the physis affected, and the size of the arrest. A long, standing film of the lower extremities with the hip, knee, and ankle joints included provides an overall assessment of angular deformity and shortening.
  • 53. Classification of physeal arrests Central arrests are surrounded by a perimeter of normal physis. Peripheral arrests are located at the perimeter of the physis. Linear arrests are through-and-through lesions with normal physis on either side of the arrest area.
  • 54. Management    Prevention of arrest formation Gentle anatomic and secure reduction Fat grafting NSIAD's ??
  • 55. Physiolysis   Partial physeal arrest resection Principle- to remove bone between metaphysis and physis and fill defect with bone reformation retardant
  • 56. Physeal distraction    External fixator is used to span the arrest . Gradual distraction until arrest separates Distraction injury may cause complete cessation of normal physeal growth
  • 57. Repeated osteotomies   Corrective osteotomy of adjacent metaphysis to correct angular deformity Completion of epiphysisodesis and management of resulting limb length discrepancy  Epiphysiodesis prevents angular deformtiy  Limb lengthening can be considered
  • 58. Physeal arrest resection  Etiology- trauma/ blounts- good prognosis infection / tumour- unlikely to show growth    Central and linear arrest regrowth more likely Proximal humeral and femoral leisions more difficult to exposeadequate resection unlikely Arrests affecting >25% of total surface area are unlikely to grow
  • 59. Preoperative planning extent and location of the arrest relative to the rest of the physis must be carefully documented evaluate an arrest is with reconstructed sagittal and coronal CT images to provide views orthogonal to the affected physis estimation of the affected surface area can be computed with the assistance of the radiologist using a modification of the method of Carlson and Wenger Reconstructed magnetic resonance images allow estimation of the percentage of surface area of the physis affected by a growth arrest. This workstation reconstruction delineates the perimeter of normal physis (border 2) and that of the physeal arrest (border 1). Surface area affected can be calculated from these reconstructions.
  • 60. The arrest must be resected in a manner that minimizes trauma to the residual physis. Central lesions should be approached through either a metaphyseal window or through the intramedullary canal after a metaphyseal osteotomy. Peripheral lesions are approached directly, resecting the overlying periosteum to help prevent reformation Fluoroscopy is needed to keep the surgeon oriented properly to the arrest and the residual healthy physis.
  • 61. A high-speed burr worked in a gentle to-andfro movement perpendicular to the physis usually is the most effective way to gradually remove the bone composing the arrest and expose the residual healthy physis
  • 62. By the end of the resection, all of the bridging bone between the metaphysis and epiphysis should be removed, leaving a void in the physis where the arrest had been, and the perimeter of the healthy residual physis should be visible circumferentially at the margins of the surgically created cavity
  • 63. Prevent Re-forming of Bridge between Metaphysis and Epiphysis A bone-growth retardant or a spacer material should be placed in the cavity created by the arrest resection to prevent re-forming of the bony bridge between the metaphysis and epiphysis. Four compounds have been used for this purpose either clinically or experimentally: autogenous fat , methylmethacrylate , silicone rubber , and autogenous cartilage. Silione and cartilage not used anymore Methlymethacrylate is inert but gives structural stability in large resection and in weight bearing areas (tibia in blounts disease)
  • 64. Metallic markers should implanted in the epiphysis and metaphysis at the time of arrest resection to allow reasonably accurate estimation of the amount of longitudinal growth that occurs across the operated physis, as well as to identify the deceleration or cessation of that growth Resumption of longitudinal growth may not occur despite technically adequate arrest resection in patients with good clinical indications. The treating surgeon be alert to those developments, so that proper intervention can be instituted promptly. Embedded metallic markers serve these purposes
  • 65. Treatment recommendations On average, approximately 60% of physeal arrests demonstrate clear x-ray evidence of resumption of longitudinal growth of the affected physis after physeal arrest resection. There is a correlation between the amount of surface area of the physis affected and the prognosis for subsequent longitudinal growth after arrest resection. Physeal arrests affecting less than 10% of the surface area of the physis have a better prognosis than larger arrests. Langenskiod stage VI infantile Blount disease has results comparable to post-traumatic physeal arrests. Etiologies other than post-traumatic and infantile Blount disease have poor prognoses for subsequent growth. Central and peripheral arrests have equivalent prognoses with respect to resumption of growth. Early growth resumption may be followed by cessation of longitudinal growth before skeletal maturity. As a consequence, patients must be evaluated regularly until skeletal maturity with some reliable method (such as metaphyseal and epiphyseal x-ray markers) to detect such development as promptly as possible.
  • 66. Growth Deceleration Without Arrest growth deceleration without frank cessation of growth is characterized by x-ray abnormality of the appearance of an injured physis clinical or x-ray deformity if the disturbance is severe and long-standing, but without complete cessation of growth in the affected area The concept of growth deceleration without arrest is most readily appreciated in patients with adolescent Blount disease and the milder stages of infantile Blount disease, infection and physeal fracture there is no sclerotic area of arrest on plain x-rays A growth arrest line, if present, may be asymmetric but will not taper to the physis, thereby suggesting growth asymmetry but not complete arrest.
  • 67. Management The diagnosis of physeal growth disturbance usually is made incidentally by noting physeal abnormality on x-rays during physeal fracture follow-up or after a diagnosis of frank physeal arrest has been excluded during the evaluation of a patient with angular deformity and physeal abnormality on plain x-rays. Assess extent of limb length inequality and the calculated amount of potential growth remaining for the affected physis. If angular deformity is present or progressive, treatment options include hemiepiphysiodesis or stapling and corrective osteotomy, with or without completion of the epiphysiodesis.
  • 68. Hemiepiphysiodesis or stapling of the affected physis on the convex side of the deformity may result in gradual correction of the deformity. If correction occurs, options include completion of the epiphysiodesis (with contralateral epiphysiodesis if necessary to prevent the development of significant leg length deformity) or removal of staples with careful longitudinal observation for recurrence or overcorrection of deformity. Corrective osteotomy is the other option for the management of growth disturbance with established angular deformity. Treating surgeon must decide whether to perform epiphysiodesis of the affected physis (with contralateral epiphysiodesis, if appropriate) to prevent recurrence or to ensure careful longitudinal observation of the growth performance of the affected physis until skeletal maturity.
  • 69. Conclusion Physeal injuries are common Gentle and expert management to maximize restoration of normal limb function and longitudinal growth Follow up with serial x rays to identify physeal arrest
  • 70. References  Rockwood and wilkins fractures in children  AO trauma manual

Editor's Notes

  1. In 1989, Siliski, Mahring, and Hofer evaluated 52 intercondylar femoral fractures (AO type C) treated predominantly with blade plates. Three quarters of the fractures were caused by high-energy mechanisms, and 39% were open fractures. Overall, good or excellent results were obtained in 81% of fractures, and range of motion averaged 107 degrees. Results were better in type C1 fractures (92% good or excellent results) than in type C2 and type C3 fractures (77% good or excellent results). Only three (5.8%) fractures had malalignment in the sagittal plane; however, shortening of 1 to 3 cm occurred in 15 patients. Shortening was intentional to improve stability in 11 older patients (average age 60 years), but it was unintentional in four younger patients (average age 30 years). Infection occurred in four patients (7.7%) and accounted for three of the four poor results. Two fractures complicated by infection required amputation, and one required arthrodesis to treat the infection. Perioperative antibiotics were not used in closed and type I open fractures.