The document summarizes a seminar on fracture healing and epiphyseal injuries. It discusses the stages of fracture healing in adults, including inflammation, soft callus formation, hard callus formation, and remodeling. It also discusses differences in fracture healing between cancellous and cortical bone. Additionally, it covers anatomy of the child bone, including the epiphysis, physis, metaphysis and diaphysis. It describes factors influencing bone growth and the phases of fracture healing in children. Finally, it discusses classification systems for epiphyseal injuries including Salter Harris, Poland, Aitken, and Peterson, as well as causes, evaluation, and treatment of physeal injuries.
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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
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
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.
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
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
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.
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
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.
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
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.