Epiphyseal Growth-Plate Injuries

Surjit Lidder and Manoj Ramachandran

Contents Post-Operative Care and Rehabilitation . . . . . . . . 4665

General Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4654 Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4666
Complete Growth Arrest . . . . . . . . . . . . . . . . . . . . . . . . . . . 4666
Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4654 Partial Growth Arrest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4666
Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4654 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4667
Blood Supply . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4655
Aetiology of Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4656
Iatrogenic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4656
Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4656
Tumour . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4656
Repetitive Stress Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4656
Metabolic Abnormalities . . . . . . . . . . . . . . . . . . . . . . . . . . . 4656
Irradiation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4657
Miscellaneous . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4657
Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4657
Type I Salter- Harris Injury . . . . . . . . . . . . . . . . . . . . . . . . 4657
Type II Salter-Harris Injury . . . . . . . . . . . . . . . . . . . . . . . . 4657
Type III Salter-Harris Injury . . . . . . . . . . . . . . . . . . . . . . . 4658
Type IV Salter-Harris Injury . . . . . . . . . . . . . . . . . . . . . . . 4658
Type V Salter-Harris Injury . . . . . . . . . . . . . . . . . . . . . . . . 4658
Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4660
Indications for Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . 4661
Operative Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4661
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4661
Treatment of Salter-Harris Fractures . . . . . . . . . . . . . . 4663
Special Cases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4664

S. Lidder (*)  M. Ramachandran

Barts and The London NHS Trust and The London
Childrens Hospital, Whitechapel, London, UK

G. Bentley (ed.), European Surgical Orthopaedics and Traumatology, 4653

DOI 10.1007/978-3-642-34746-7_170, # EFORT 2014
4654 S. Lidder and M. Ramachandran

together with the age of the child and time from

Abstract
injury to treatment.
In children, the epiphysis is a unique structure,
The early recognition of these injuries is
which is essential for the normal growth of long
essential as the effect of subtle growth inequal-
bones. Injury to the epiphysis is any form,
ities may not be immediately apparent. The child
whether traumatic, iatrogenic, metabolic or
should be followed up regularly for an adequate
due to infection may lead to long-term sequelae
period to assess limb growth; this may be until
of growth arrest or angular deformity. In this
skeletal maturity is attained. The treatment of
chapter the structure, blood supply to the epiph-
complications following physeal injuries is
ysis, aetiology of injury, together with the com-
often difficult and complex.
mon classification systems used for epiphyseal
We discuss the aetiology, classification, diag-
injuries are described. Diagnosis of injuries
nosis and treatment of epiphyseal injuries
may often be difficult, and after a thorough
together with the management of growth arrest.
history and examination, further imaging, as
adjuncts to orthogonal radiographs may be nec-
essary. For the orthopaedic surgeon, an under-
Epidemiology
standing of the epiphysis is essential in treating
insults to the epiphysis. A fine balance exists
Epiphyseal injuries are common, reported to
between accepting a degree of deformity which
occur in approximately 30 % of paediatric long
over time will correct, to restoring articular
bone fractures [12]. They are twice as likely in
congruence and preventing iatrogenic injury
boys possibly due to a greater degree of risk-
after manipulation. Subtle growth inequalities
taking behaviour. The greatest incidence is
may not be immediately apparent and longer-
found in girls between 9 and 12 years of age and
term follow up may be required for some epiph-
in boys between 12 and 14 years. These peak
yseal injuries.
incidences correspond to the time when the
physis is at its weakest during the growth spurts.
Keywords
There is no tendency for injuries to occur more
Aetiology  Anatomy  Blood supply  Classi-
frequently on one side or the other, nor is there
fication  Complications  Epidemiology 
a link to hand dominance. Injuries to the upper
Epiphysis  Growth arrest  Growth-plate 
limbs are more common than those of the lower
Injuries  Rehabilitaion  Surgical indications 
limbs and the distal epiphyses more than the
Surgical Techniques
proximal epiphysis. The commonest sites of
injury are the phalanges (43.4 %), distal radius
(17.9 %) and distal tibia (11 %) [18].
General Introduction

The epiphysis is a unique structure, which is Anatomy

essential for the normal longitudinal growth of
childrens long bones. It is prone to injury from
tension, shear and bending stresses and also by
non-traumatic insults such as thermal energy,
radiation or infection.
Injuries to the epiphysis may often be subtle
and can result in angular deformity, growth arrest
and limitation in the function of the joint. The
clinical sequelae following injury are dependent
upon the initial severity of the injury, the relative
size and anatomical location of the lesion
The epiphysis is the primary centre for skeletal
growth of long bones. It is either pressure (com-
pression) or traction (tensile) responsive. The
primary epiphyses are initially discoid areas
where cartilage rapidly undergoes undulations
during maturation due to increased stress; they
contribute to longitudinal growth [7, 9]. Circum-
ferential expansion also occurs at the level of the
epiphysis in the zone of Ranvier. Continued
growth of cartilage cells occurs towards the side
Epiphyseal Growth-Plate Injuries
Epiphyseal blood vessels
Resting layer
Proliferative
layer
Hypertrophic
layer
Zone of
Calcification
Metaphysis with blood vessels
Fig. 1 Diagram of the zones of the epiphysis (From
Ramachandran [22])
of the epiphysis facing the epiphysis of the long
bone, with cartilage being replaced by bone on
the metaphyseal side. On completion of growth,
epiphyseal resorption occurs with primary can-
cellous bone fusing the epiphysis permanently to
the metaphysis.
The epiphysis is comprised of a highly ordered
layered structure of chondrocytes in an extracel-
lular matrix which histologically on longitudinal
section can be divided into four distinct layers
according to function (Fig. 1). These zones are:
1. The resting or germinal,
2. Proliferative,
3. Hypertrophic and
4. The zone of provisional calcification.
Chondrocytes progress through a sequence of
changes as they move through the zones.
In the resting zone the cells are relatively
small and surrounded by a mechanically strong
thick layer of matrix, which is particularly resis-
tant to shear. Oxygen tension is low and cells
respond to circulating hormones. These cells con-
tribute to growth of the epiphysis and also the
4655
secondary ossification centre. The proliferative
zone is an area of high oxygen tension where
cells appear as thin discs and palissade. The col-
lagen fibres are arranged longitudinally within
the extracellular matrix [22].
In the zone of hypertrophy, chondrocytes
increase in size by up to 10-fold (Hunziker 1987)
and the relative space for extracellular matrix is
decreased along with its strengthening effect. This
is the weakest layer of the epiphysis and the fracture
plane usually occurs through this zone. In the zone
of provisional calcification, metaphyseal vascular
invasion occurs enabling mineralisation of the
matrix and allows osteoblasts and osteoclasts to
enter to form primary cancellous bone with subse-
quent remodelling to secondary cancellous bone.
The peripheral margin of the epiphysis com-
prises two important structures. The zone of
Ranvier, responsible for peripheral growth, con-
tains chondroblasts, osteoblasts and fibroblasts.
The perichondral ring of LaCroix is a fibrous
layer over the zone of Ranvier connecting and
stabilizing the epiphysis to the metaphysis to
provide mechanical integrity [22].
Blood Supply
The blood supply to the epiphysis is supplied
by three sources, namely the epiphyseal,
metaphyseal and perichondral circulations.
The epiphyseal vessels (artery, vein and cap-
illary network) are present throughout the
chondro-epiphysis. Dale and Harris [4] identified
two patterns of blood supply to the epiphysis.
Type A epiphyses are entirely covered by articu-
lar cartilage (e.g., proximal femoral and proximal
humeral epiphysis) and the blood supply enters
from the metaphyseal side of the epiphysis enter-
ing the epiphysis by traversing the perichondrium
at the periphery of the epiphysial plate. It is prone
to injury during epiphyseal separation. In type
B epiphyses, which are partly covered by articu-
lar cartilage (e.g., proximal and distal tibia), the
blood vessels enter from the side of the epiphysis
by penetrating the cortex and are theoretically
less susceptible to damage during epiphyseal
separation.
4656
Aetiology of Injuries
Direct skeletal trauma is the commonest cause of
epiphyseal injury, however paediatric fractures
tend to occur at lower energy than adult fractures.
Most are the result of compression, torsion or
bending forces. The epiphysis may also be
injured in subtle ways such as crushing, which
may not be appreciated on initial radiographs and
may in fact be diagnosed later as angular defor-
mity or growth arrest.
Iatrogenic
Care is required when manipulating the epiph-
ysis during closed reduction. Excessive force
during manipulation may damage the blood
supply to the epiphysis and result in growth
arrest. Meticulous soft tissue dissection and
care during subperiosteal dissection adjacent
to the epiphysis is also necessary as injury
adjacent to the perichondral ring of Ranvier
may injure the peripheral part of the epiphysis.
Operative intervention for infection or tumour
excision may require excision of part of the
epiphysis, which will result in growth arrest.
During operative fixation of fractures around
the epiphysis, care should be taken during pin
placement. Epiphyseal closure is more likely
with the use of threaded, multiple and larger
diameter pins. It is also more likely with pins
passing through the centre of the epiphysis,
where metalwork retention is prolonged,
in those that are not perpendicular to the
epiphysis and the use of materials such as
titanium may have bone-bonding properties
that increase the possibility of tethering the
epiphysis [17].
Infection
Localised infection near the epiphysis
(metaphyseal osteomyelitis or septic arthritis) can
result in direct epiphyseal damage causing growth
S. Lidder and M. Ramachandran
disturbance. Systemic infections (meningococcal
septicemia) may cause a vascular insult to the
epiphysis as a result of cardiovascular collapse
resulting in epiphyseal arrest. Long-term follow
up is required as growth arrest may occur some
time after the primary insult.
Tumour
The epiphysis can be damaged by direct
destruction by benign tumours (such as
chondroblastoma and aneurysmal bone cyst) or
malignant tumours (such as osteosarcoma). The
degree of growth arrest is dependent upon the size
and location of the primary lesion and the extent
of treatments including radiotherapy and surgical
intervention.
Repetitive Stress Injury
There are increasing reports in adolescent ath-
letes that repetitive loading of sufficient duration
and intensity can produce chronic epiphyseal
injury. The commonest locations are: the distal
radius and ulna of competitive gymnasts; the
proximal humeral epiphysis of baseball
pitchers; and, the proximal tibia in long distance
runners. Repetitive loading alters metaphyseal
perfusion and interferes with mineralisation of
hypertrophied chondrocytes in the zone of
provisional calcification. This results in widen-
ing in the germinal and proliferative zones.
Additionally localised ischaemia may lead
to osseous necrosis, which may result in
irregularities of physeal growth or growth arrest
([3, 14, 17]).
Metabolic Abnormalities
Chronic illness in childhood can cause impair-
ment of growth-plate chondrogensis and may
result in growth retardation. This is thought to
occur as a result of the interplay of some or all
factors which can be recognised in severe chronic
Epiphyseal Growth-Plate Injuries
Fig. 2 Diagram of Salter-Harris classification of epiphyseal injuries (After Salter and Harris [24], with kind permission)
disease including inflammation, protein/calorie
deprivation, uraemia, metabolic acidosis, gluco-
corticoids and impaired growth hormone secre-
tion [5].
Irradiation
Standard radiographs and CT scans are not
thought to cause growth disturbance at the epiph-
ysis. Therapeutic irradiation alters chondroblastic
activity and has an inhibitory effect upon the
epiphyseal growth. The extent of inhibition of
growth is dependent upon the age of the patient
at commencement of therapy, field size, site,
delivered dose and growth potential of the
epiphysis.
Miscellaneous
Rare causes of epiphyseal injury include vascular
injury to the limb or other causes of ischaemic
insult and thermal injury such as frostbite or
burns (including electrical), resulting in premature
closure of the epiphysis.
Classification
Several classification systems have been devel-
oped to describe epiphyseal injuries. These
include those of Salter and Harris [24], Foucher
[6], Poland [21] and Aitken [1]. The most widely
4657
used classification system in daily practice is that
of Salter and Harris, described in 1963 (Fig. 2).
This is based on the mechanism of injury and
relationship of the fracture line to the epiphysis
and metaphysis. Although scoring systems were
originally thought to allow predication of prog-
nosis, it is now recognised that even seemingly
innocuous injuries around the metaphysis may
lead to growth arrest [2, 3, 13, 14].
Five fracture patterns are described in the
Salter-Harris classification:
Type I Salter- Harris Injury
A transepiphyseal fracture occurs through the
hypertrophic zone, which separates the epiphysis
from the metaphysis. This often results from
a shearing or avulsion force and is more common
in birth injuries and during early childhood when
the epiphyseal plate is relatively thick. As the
resting zone remains within the epiphysis, the
blood supply remains undamaged and prognosis
is good; however complete or partial growth
arrest may occur with displaced fractures.
Type II Salter-Harris Injury
This is the most common epiphyseal injury in
which a transepiphyseal fracture extends for a
variable length and exits through the metaphysis
(Fig. 3). The metaphyseal fragment, known as the
Thurston-Holland sign on radiographs, is present
4658
Fig. 3 Lateral and AP
radiographs of little finger
showing a Salter Harris
type II injury of the middle
phalanx
on the compression side of the fracture. The peri-
osteal hinge remains intact on the side of the
metaphyseal fragment and provides stability
once the fracture has been reduced. The progno-
sis is good as the resting layer is intact and growth
disturbance is rare.
Type III Salter-Harris Injury
This is an uncommon injury that is due to
a shearing force causing an intra-articular frac-
ture. The transphyseal fracture extends through
the epiphysis into the joint. Prognosis is guarded
as partial growth arrest and angular deformity
may occur and if intra-articular displacement is
present, anatomical reduction is necessary which
may require an open approach.
Type IV Salter-Harris Injury
This is an intra-articular fracture where the frac-
ture traverses the epiphysis, and exits through
the metaphysis through all four zones. The
S. Lidder and M. Ramachandran
commonest example of this injury is a lateral
condyle fracture of the humerus. Anatomical
reduction is necessary to prevent articular
incongruity and osseous bridging across the
epiphysis.
Type V Salter-Harris Injury
This is a crush injury at the epiphysis occurring
in uniplanar joints such as the knee and ankle.
Diagnosis is often delayed and made retrospec-
tively as there are few radiographic changes.
Prognosis is poor as growth arrest and partial
physeal closure are common.
Some epiphyseal injuries do not fit into
the Salter-Harris classification scheme. Rang
[23] described injury to the perichondral ring
of LaCroix resulting in angular deformity
and named it a type VI injury [23]. Ogdens
classification included peri-epiphyseal frac-
tures that radiologically do not appear to
involve the epiphysis but may interfere with
epiphyseal blood supply and result in growth
disturbance [15].
Epiphyseal Growth-Plate Injuries 4659

Fig. 4 Peterson classification of epiphyseal injuires (After Petersen [17])

Fig. 5 AP and lateral radiographs of Peterson Type I injury (metaphyseal fracture with extension into physis)

Peterson [19] later introduced a new classifica-
tion of epiphyseal injuries based upon an epidemi-
ological study of 951 fractures (Fig. 4). Peterson
retained Salter-Harris type I through to type IV
injuries as Peterson type II to V, and added two
new types. The Peterson Type I injury is
a transverse metaphyseal fracture with extension
to the epiphysis (Fig. 5) and subdivided into four
types based on fracture pattern and extent of
metaphyseal comminution. In the Peterson type
4660
VI fracture, he described an open injury with par-
tial epiphyseal loss requiring emergency debride-
ment and requiring complex reconstructive
surgery. With the Peterson classification, there is
an increase in the amount of epiphyseal cartilage
damage from type I to type VI fractures. The rates
of both initial surgery to treat the fracture and later
surgery to treat complications gradually progresses
from type I fractures, for which surgery is rarely
necessary, to type VI fractures for which surgery is
always necessary [19].
Diagnosis
A thorough history of the traumatic event is neces-
sary, either from the child themselves or the carers.
The child will have focal pain, localised swelling,
deformity and impaired function, which will vary
depending on the severity of the injury and degree
of fracture displacement. When no antecedent trau-
matic event is described, the history should attempt
to elucidate the possibility of other aetiologies such
as infection, neoplasia or metabolic causes. The
clinical signs of an upper limb injury may include
reduced range of movement and for lower limb
injuries, the child may be unable to weight-bear
through the affected limb. Examination of the
entire limb should be performed and findings
compared with the contralateral side. The
neurovascular status of the limb should be assessed
and documented contemporaneously.
True orthogonal radiographs, commonly
anteroposterior and lateral, centred over the
injury are required to decrease parallax. The
joint proximal and distal to the injury should
also be imaged. Where irregularity of the epiph-
ysis makes diagnosis difficult such as in the distal
humerus, additional oblique views may be useful
in the assessment of minimally displaced frac-
tures. Radiographs of the contralateral side may
also be necessary for comparison to aid in the
diagnosis of non-displaced fractures or to delin-
eate normal ossification patterns.
Occasionally diagnosis on plain radiographs is
difficult for subtle injuries. Stress views under
sedation performed for uni-planar joints such as
the elbow, knee and ankle may show gapping
S. Lidder and M. Ramachandran
between the epiphysis and metaphysis; however
they are not recommended because of the risk of
iatrogenic epiphyseal injury and discomfort to the
patient. Magnetic resonance imaging (MRI) or
repeat radiographs following a period of
immobilisation for 10 days may aid in diagnosis
but with less discomfort.
Modalities available for further evaluation
include ultrasound, MRI, computer tomography
(CT) and arthrography. Ultrasound is helpful in
evaluating soft tissue involvement, epiphyseal sep-
aration in infants and for proximal and distal
humerus epiphysis fractures in neonates where no
ossification centres are present. Arthrography aids
diagnosis in areas where there is a high volume of
cartilage such as the distal humerus. MR can sensi-
tively demonstrate soft tissue lesions. CT provides
better detail for assessing intra-articular displace-
ment (Salter Harris Type III and Type IV fractures),
highly comminuted fractures and complex injuries
(Tillaux or tri-plane fractures) (Fig. 6).
Injuries caused by non-accidental injury (NAI)
constitute a relatively small proportion of childhood
fractures; however one must be aware of these pre-
sentations from the salient features obtained during
history and examination. No fracture in isolation
can be said to be pathognomonic of NAI; however
specific abuse-related injuries include metaphyseal
corner and bucket-handle fractures [10]. The care
of such patients should be shared from the earliest
opportunity with the paediatric multidisciplinary
team ensuring early recognition of child protection
issues.
Previous injuries to the epiphysis causing
slowing or cessation of growth may be evident
by the presence of Harris growth arrest lines [8]
on radiographs (Fig. 7). These are transverse stri-
ations in the metaphysis that may be present in
a long bone after traumatic insult or in all long
bones following a systemic illness. Following an
insult, if the Harris growth lines continue to grow
parallel to the epiphysis, then normal resumption
of growth is presumed. When these lines are
asymmetrical or oblique, partial arrest may have
occurred. With complete arrest occurs, no growth
lines are present. The assessment of bony bars
following growth arrest can be made using MRI
[11] and CT.
Epiphyseal Growth-Plate Injuries
Indications for Surgery
The indications for surgery are dependent upon
the anatomical location of the injury, severity,
age of the child, time since injury and degree of
deformity. The aim is to obtain and then maintain
anatomical alignment of the growth- plate. In
children, there is rapid healing compared with
adults. In the young, injuries may be stable within
34 weeks.
In Salter- Harris type I and II injuries, reduc-
tion should be achieved early. If delay is greater
than 7 days, then it is safer to perform an
osteotomy later than to cause iatrogenic injury
during delayed reduction. This does however
depend on location and degree of deformity.
Intra-articular injuries (Salter Harris types III
and IV) require anatomical reduction. This is to
restore the congruency of the articular surface
a b
Fig. 6 (continued)
4661
and to minimize epiphyseal bar formation. Open
reduction and internal fixation to maintain posi-
tion should be performed on fractures that are
open, unstable or are displaced intra-articularly.
Injuries with associated neurovascular injury or
compartment syndrome should be treated on an
emergency basis.
Operative Technique
General
The child should be fully assessed using the pae-
diatric ATLS protocol. Life- and limb-
threatening injuries need to be identified and
treated first. The primary aim of treating epiphy-
seal injuries is to maintain an acceptable reduc-
tion by closed or open means without causing
further iatrogenic injury during manipulation.
4662 S. Lidder and M. Ramachandran

c d

Fig. 6 (a) Lateral and (b) AP radiographs of a Salter Tillaux fracture demonstrating clearly intra-articular
Harris type III injury of the distal tibia (Tillaux fracture). displacement
(c) Sagittal (d) coronal (e) axial CT images of the same
Epiphyseal Growth-Plate Injuries
Fig. 7 AP and lateral radiographs showing Harris growth arrest lines in the distal tibia (and disuse osteopenia
of the foot)
Treatment of Salter-Harris Fractures
Salter-Harris Type I Fractures
These are treated by closed reduction and immo-
bilization with a cast. Healing is usually rapid,
taking approximately 3 weeks.
Salter-Harris Type II Fractures
The intact periosteum hinge present with the
metaphyseal (Thurston-Holland) fragment aids
closed reduction. When the reduction cannot be
maintained, either screws or K-wires can be used
to maintain reduction of the metaphyseal frag-
ment. The epiphysis should be avoided. When
the metaphyseal fragment is small, smooth pins
can be used to cross the epiphysis; however mul-
tiple attempts at reduction should be avoided.
4663
Salter-Harris Type III Fractures
Anatomical reduction by means of open reduc-
tion to visualise the articular surface and stabili-
zation is required in Salter-Harris III fractures
(Fig. 8). The fragment may be pinned to the
epiphysis or across the fracture site parallel to
the epiphysis.
Salter-Harris Type IV Fractures
Again, with this intra-articular fracture, anatomical
reduction of the articular surface is necessary by
open reduction and internal fixation. Follow-up is
needed for at least a year as growth arrest is likely.
Salter-Harris Type V Fractures
These injuries are rarely diagnosed acutely
and treatment is delayed until growth arrest
4664
is evident. Epiphyseal injuries may be difficult
to diagnose in certain anatomical locations
and growth disturbance is more likely to
occur at some epiphyses compared with
others. Also, some epiphyseal sites will more
commonly require open reduction and internal
fixation.
Special Cases
Proximal Humerus
Salter-Harris type II injuries are most common
and occur in younger children. In rare cases, they
require open reduction and internal fixation when
soft tissue interposition at the fracture site is
present.
Fig. 8 (continued)
S. Lidder and M. Ramachandran
Distal Humerus and Proximal Ulna
Care is required to differentiate epiphyseal frac-
tures from normal secondary ossification centres
of the olecranon and also fracture separation of
the distal humerus from dislocations of the elbow
or lateral condyle fractures.
Distal Radius and Ulna
Most distal radius and ulna Salter-Harris type
I and II injuries can be treated with closed manip-
ulation and casting. Care should be taken not to
cause iatrogenic injury during manipulation and
due to the late ossification of the distal ulna
epiphysis, these concomitant injuries should not
be missed. Open reduction and internal fixation
may be required when the periosteal flap may
become interposed at the fracture site preventing
reduction.
Epiphyseal Growth-Plate Injuries
Proximal Femur
Avascular necrosis may occur following epiphy-
seal separation of the proximal femur. Closed
reduction and pinning can be performed.
Distal Femur
Significant angular deformity and shortening can
occur with at the distal femoral epiphysis. Premature
closure can occur even in Salter-Harris type II inju-
ries due to the undulating nature of the epiphysis.
Proximal Tibia
Salter-Harris type III injuries may result in varus
or valgus deformity due to premature epiphyseal
closure if unrecognised.
Distal Tibia
High rates of growth disturbance have been
reported at the distal tibia. The two distinct
types of fractures here are the tri-plane and
Tillaux fracture. In tri-plane fractures, there are
Fig. 8 (continued)
4665
two types of fracture: a two-part fracture which is
a Salter-Harris Type IV injury occurring at the
medial malleolus and a three-part fracture which
is a combination of a Salter-Harris type II and III
fractures that occur when the central part of the
distal tibial epiphysis is closed.
Tillaux fractures are Salter-Harris type III
fractures involving avulsion of the anterolateral
tibial epiphysis. Treatment of displaced S-H III
and S-H IV fractures of the distal tibia involves
open reduction.
Post-Operative Care and
Rehabilitation
In children, epiphyseal injuries heal rapidly.
A weekly follow-up is necessary for the first
3 weeks to ensure that displacement has not
occurred and to allow time for a further reduction
if required. Follow-up at six months allows for
4666 S. Lidder and M. Ramachandran

Fig. 8 AP and lateral radiographs of (a) Salter-Harris type III injury of the distal tibia, (b) with open reduction and
internal fixation and (c) after removal of metalwork 1 year post injury

assessment of any deformity, growth arrest or In a younger patient, limb length inequality is
other complications. A longer follow-up may be more likely however when complete growth
required for more severe injuries. arrest is present, no angular deformity occurs.

Complications Partial Growth Arrest

All fractures can be complicated by non-union,
malunion, infection and neurovascular injury.
This is also true for physeal injuries; however
there is the added potential for growth arrest.
Generally as the severity of injury increases, the
likelihood of growth arrest also increases.
Complete Growth Arrest
The significance of complete growth arrest
depends upon the site and the age of the patient.
This is where there is formation of a bridge of
bone across the epiphysis from the epiphysis to
the metaphysis. The unaffected side continues
to grow causing an angular deformity. The degree
of deformity is dependent upon the location,
size and duration of the bony bar. Partial arrest
can be classified into peripheral, central and
combined [16].
Peripheral (type I) bars involve the margin of
the epiphysis. Severe deformity may be produced
over a short time. Central (type II) arrest is more
difficult to treat with surgery and more severe.
Epiphyseal Growth-Plate Injuries
A variable sized osseous bridge forms with the
central portion of the epiphysis surrounded by
normal epiphysis. Longitudinal growth is
affected. In combined (type III) bars, the osseous
bar extends across the epiphysis connecting two
separate segments of the periphery of the epiph-
ysis. This is common at the medial malleolus and
angular deformity may be significant.
Epidemiology
Growth arrest in boys is twice as common than
in girls. Sixty percent of partial growth arrest
occurs at the periphery. The commonest cause is
previous fracture and the most frequently
affected physes are that of the distal femur and
proximal tibia. Long-term follow-up should be
considered for children felt to be at risk of
physeal bars as they may not be evident until
years afterwards.
Clinical Assessment
A bony bridge may become clinically evident
following angular deformity of limb length
discrepancies. A thorough history may localise
the exact epiphysis involved followed by exami-
nation and plain radiographs. The degree of
limb-length discrepancy, joint motion, angular
deformity and functional impairment should be
documented.
Investigations
Orthogonal radiographs of the involved epiphysis
are required. Harris growth arrest lines especially
if oblique or asymmetrical to the epiphysis indi-
cate growth arrest. Further imaging such as
tomography, CT and MRI can help delineate the
exact nature and location of the epiphyseal bar
and help in pre-operative planning.
Treatment
The treatment of complete growth arrest is
dependent upon the age at which growth arrest
occurs and the location of the arrest. The limb
length inequality in children that are nearing
skeletal maturity is minimal and often no inter-
vention is required. For the lower limb, options
include a shoe raise, surgical epiphysiodesis of
the contralateral side, bone lengthening of the
4667
involved bone or a combination of these modal-
ities. In partial growth arrest, the treatment of
bony bars again is dependent upon the age of
the child and the involvement of the specific
epiphysis. No treatment may be required for chil-
dren reaching skeletal maturity; however
a number of options are available for younger
children with a significant angular deformity.
The surgical options include the use of a shoe
raise, arresting the remaining growth of the
injured epiphysis, a combination of epiphyseal
arrest with opening or wedge osteotomy without
epiphyseal arrest, lengthening or shortening of
the involved bone or resection of the bony bar
and insertion of interposition material such as fat
or plastic.
Acknowledgments The authors would like to thank
Dr. Sujit Vaidya, Consultant Radiologist, The Royal London
Hospital for help in the sourcing of suitable images.
References
1. Aitken AP. Fractures of the epiphyses. Clin Orthop
Relat Res. 1965;41:1923.
2. Barmeda A, Gaynor T, Mubarak SJ. Premature closure
following distal tibia physeal fractures. J Pediatr
Orthop. 2003;23:7339.
3. Caine D, DiFiori J, Maffulli N. Physeal injuries in
childrens and youth sports: reasons for concern? Br
J Sports Med. 2006;40:74960.
4. Dale G, Harris W. Prognosis of epiphyseal separa-
tions: an experimental study. J Bone Joint Surg Br.
1958;40:11622.
5. De Luca F. Impaired growth plate chondrogenesis in
children with chronic illnesses. Pediatr Res.
2006;59:6259.
6. Foucher M. De la divulsion des epiphyses. Congr Med
France (Paris). 1863; 1:63.
7. Greco F, de Palma L, Specchia N, et al. Growth- plate
cartilage metabolic response to mechanical stress.
J Pediatr Orthop. 1989;9:5204.
8. Harris HA. Lines of arrested growth in the long bones
in childhood: the correlation of histological and radio-
graphic appearances in clinical and experimental con-
ditions. Br J Radiol. 1931;4:56188.
9. Hunziker EB, Schenk RK, Cruz-Orive LM. Quantita-
tion of chondrocyte performance in growth- plate car-
tilage during longitudinal bone growth. J Bone Joint
Surg Am. 1987;69:16273.
10. Jayakumar P, Barry M, Ramchandran M. Orthopaedic
aspects of paediatric non-accidental injury. J Bone
Joint Surg Br. 2010;92(2):18995.
4668
11. Lohman M, Kivisaari A, Vehmas T, et al. MRI in the
assessment of growth arrest. Pediatr Radiol.
2002;32:415.
12. Mann DC, Rajmaira S. Distribution of physeal and
nonphyseal fractures in 2,650 long-bone fractures in
children aged 016 years. J Pediatr Orthop.
1990;10:7136.
13. Oh WH. Type II, epiphyseal fractures may also be
responsible for bone growth distortions. Orthop Rev.
1977;7:958.
14. Ogden JA. Skeletal injury in the child. New York:
Springer; 2000.
15. Ogden JA. Injury to the growth mechanisms of the
immature skeleton. Skeletal Radiol. 1981;6(4):23753.
16. Ogden JA. The evaluation and treatment of partial
physeal arrest. J Bone Joint Surg Am. 1987;69:1297302.
17. Peterson HA. Epiphyseal growth plate fracutures.
Heidelberg: Springer; 2007.
S. Lidder and M. Ramachandran
18. Peterson HA, Madhok R, Benson JT, et al. Physeal
fractures. I. Epidemiology in Olmsted County, Min-
nesota, 19791988. J Pediatr Orthopedics. 1994;14:
42330.
19. Peterson HA. Physeal fractures. II. Two previously
unclassified types. J Pediatr Orthop. 1994;14:4318.
20. Peterson HA. Physeal fractures. III. Classification.
J Pediatr Orthop. 1994;14:43948.
21. Poland J. Traumatic separation of the epiphysis.
London: Smith, Elder & Company; 1898.
22. Ramachandran M. Basic orthopaedic sciences: the
stanmore guide. London: Hodder Arnold; 2007.
23. Rang M. Injuries of the epiphyses, the growth plate,
and the perichondral ring. In Rang M. ed. Childrens
Fracture. 2nd edn. Philadelphia: JB Lippincott; 1983;
1025.
24. Salter RB, Harris WR. Injuries involving the epiphyseal
plate. J Bone Joint Surg Am. 1963;45:587622.