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142
D. B. Kraft et al.
• Calcied zone: Metabolically, the matrix has
been readied for the deposition of calcium salts,
and the task of forming the osteoid is left for
this lowest region of the plate. In the adjacent
metaphysis, small vascular twigs can be seen
arborizing toward the basal layers of the plate.
Peripheral Structures ofthePlate
Two histologic regions have been identied with
specic functional roles in skeletal development.
• Zone of Ranvier: Around the circumference of
the plate is an identiable clustering of cells
that are responsible for latitudinal growth of
the plate.
• Perichondral ring of La Croix: As the periosteum is continuous around the margins of the
plate, this brous structure is apparent. Its
function is to provide mechanical support
against translational movement.
Factors Aecting theSkeletal
Growth
Numerous factors, both intrinsic and extrinsic,
affect the way in which the skeleton develops.
Some examples are noteworthy and indicated
below.
• Endocrine
– Hormonal inuences play a signicant tro-
phic or permissive role in the development
of the skeleton. Shortages or excesses,
therefore, will disrupt the way in which the
skeleton matures. Thyroid hormone is a
good example whereby disrupted epiphyseal development is a hallmark of
cretinism.
• Environmental
– Mechanical effects as well as environmen-
tal toxins and drugs can adversely affect
the development of the skeleton. Fetal
alcohol syndrome and the use of illicit narcotics by the mother are just two examples
of the growing compendium of skeletal
aberrations due to externally applied
toxins.
• Coexistent Disease
– Neuromuscular diseases of children, such
as cerebral palsy, polio, and muscular dystrophy, provide good examples of the secondary effects seen in the skeleton due to
extrinsic disease. In these examples, the
nal common pathway in the pathophysiology of the deformities is muscle imbalance; hence, eccentric mechanical loading
and aberrational mechanical loading of the
immature skeleton produce changes such
as joint dislocations and deformities (e.g.,
scoliosis).
• Genetic
– Inborn errors of metabolism (e.g., renal
rickets) as well as chromosomal alterations
(e.g., Down’s syndrome) can cause phenotypic variations in the development of the
skeleton. Abnormal histology, aberrational
growth, and variational development will
affect the ultimate shape and behavior of
the skeleton.
• Nutrition
– Vitamins and proteins are required for nor-
mal skeletal development and without
appropriate levels, abnormalities will be
seen. Rickets, for example, will alter the
shape of the metaphysis, in addition to disrupting normal physical development.
Developmental Variations
inSkeletal Growth
One of the most common reasons that children
are brought to a physician is to evaluate the position of their lower extremities, particularly the
way in which they stand and walk. Intoeing and
toeing-out, as well as knock knees and bowlegs,
are a major preoccupation of parents—and a
major source of orthopedic referrals. The simple
fact is that most of these children—well over
90%—are normal children who are simply
reecting variational growth and development.
Dr. Mercer Rang, a preeminent pediatric orthopedist, has tried to emphasize this important fact by
7 Pediatric Orthopedics
143
referring to these conditions as “non-disease.”
Rang further suggested that the appropriate management for “non-disease” is “non-treatment.” It
is important to recognize the difference between
doing nothing and “non-treatment.” As the physician seeing the child, one must recognize the
variational patterns and differentiate them from
pathologic states. Once that has been
accomplished, the physician may embark on a
program of aggressive “non-treatment” which
might include such things as the following:
• Careful examination of the normal child
• Reassurance of parents and grandparents
• Supply educational information to strengthen
one’s diagnosis and approach
• Offer the option of yearly follow-up “to be
sure that the non-disease is getting better”
Torsional Variations
The skeletal variations in the newborn reect the
intrauterine position and environment. This
“molding” usually, but not always, results in an
internally rotated position of the lower extremities
and the ultimate manifestation of this rotation is
intoeing when the child begins to walk. The two
most typical variations leading to intoeing are
internal tibial torsion and femoral anteversion.
Axial rotation of the tibias can best be identied by examining the child supine with hips and
knees exed and evaluating the transmalleolar
axis at the ankle for its relation to the knee axis.
Normally, it should lie 10–30° externally rotated
from that of the knee. Neonates typically have an
internally rotated axis which causes intoeing with
the initiation of walking and spontaneously corrects after about 1year of walking. Tibial external rotation can occasionally be seen but is far
less common. Neither requires any specic treatment other than those recommended for
“non-treatment.”
The plane of the femoral head and neck in the
normal adult lies 15° externally rotated from that
of the transcondylar plane of the distal femur. In
the newborn, this relationship is more extreme:
the head/neck plane is about 45° external to that
of the transcondylar plate, and it corrects spontaneously at a rate of about 2° per year (Fig.7.4).
Persistence of this infantile pattern beyond the
age of walking will cause intoeing as the leg
internally rotates at the hip so that the femoral
head sits properly in the acetabulum. The rate of
correction varies widely, and “non-treatment” is
usually all that is required.
Most believe that external femoral torsion represents the persistence of an infantile external
rotational contracture of the soft tissues posterior
to the hip; despite its etiology, spontaneous correction of this variation can similarly be
anticipated.
When examining the child for femoral rotational patterns, it is best accomplished with the
child prone, hips extended, and knees exed 90°.
Internal and external rotation of the hips can then
be easily estimated using the leg as an angle
guide (Fig.7.5).
Knock knees (genu valgum) and bowlegs
(genu varum) are another common source of
physician referrals. Recognition of the normal
allows relatively easy determination of pathologic states.
Newborns demonstrate 4–10° of genu varus,
which tends to spontaneously correct by
18–24months of age. Thus, a child who presents
with bowlegs would be diagnosed as “physiologic genu varum.” After 18–24months of age, a
child develops knock knees, which increases
until about age 4 or 5 and then begins to improve.
By age 7 or 8, most children have assumed more
of an adult pattern: 5–7° of valgus in males and
7–9° of valgus in females.
Dierential Diagnosis
Recognizing that the vast majority of children
with angular patterns are normal and require
“non-treatment,” it is important to realize that
angular deformities can be a manifestation of
pathologic states.
Physiologic angular deformity is virtually
always symmetric; the nding of asymmetry
should, therefore, suggest a pathologic state and
trigger an appropriate workup (Table7.1).
144
Age (years)
Degrees of anteversion
789
0°
Fig. 7.4 Degree of
normal femoral torsion
in relation to age. The
curve represents the
mean; the vertical lines
represent the standard
deviation. (From
Tachdjian MO.Pediatric
Orthopedics, 6th ed.
Philadelphia, PA:
Herring; 2022.
Reprinted with
permission)
D. B. Kraft et al.
50
45
40
35
30
25
20
15
10
5
0
ab
External
rotation
Internal
rotation
Fig. 7.5 Torsional prole examination with the patient
prone. The examiner can expediently assess the thigh–
foot axis to estimate tibial torsion and examine the shape
of the lateral border of the foot to assess the presence of
12345
6
internal and external rotation of the hip as an indication of
the amount of femoral anteversion (b). (From Tachdjian
MO. Pediatric Orthopedics, 6th ed. Philadelphia, PA:
Herring; 2022. Reprinted with permission)
metatarsus adductus (a) and to determine the amount of
7 Pediatric Orthopedics
145
Table 7.1 Differential for genu valgum and genu varum
Knock knees (genu
valgum) Bowlegs (genu varum)
Physiologic Physiologic
Renal rickets Blount’s disease
Skeletal dysplasias Rickets (nutritional)
Physeal injury Skeletal dysplasias (e.g.,
achondroplasia)
Trauma Physeal injury
Trauma
General Aectations
ofthePediatric Skeleton
There are many diseases that have skeletal manifestations. This makes it impossible in one short
chapter to fully discuss the vast array of pathologic states that have an impact on the musculoskeletal system. Rather, by being introduced to
several specic examples in each disease category, one can appreciate some of the general
ways in which the skeleton will react to various
insults. This chapter will now focus on some of
the vascular, infectious, arthritic, metabolic, and
neurodevelopmental diseases that produce skeletal manifestations. An entire chapter of this book
is devoted to a discussion of tumor and one to
injury; therefore, these will only be mentioned
insofar as their effects are unique to the growing
skeleton.
Infection
Osteomyelitis
stasis “catches” bacteria as they are showered
hematogenously from distant sites. Once
entrenched, the bacteria establish a focus of
infection, and the classic case of osteomyelitis
develops. It is important to recognize that the
changes are not simply the result of the damage
the bacteria do to the bone but also the reparative
changes initiated by the bone in an effort to localize the infection.
The result of this activity is a mixture of bony
destruction by the organisms and new bone
formed to wall off the infection and shore up the
areas of damage. The dead and dying bony fragments are referred to as “sequestra,” and the new
viable bone being formed is called “involucrum.”
Clinical Features
One should inquire about a history of trauma, as
well as infections elsewhere, that may have provided a source for the organism. Occasionally, no
such history will be available, and the child presents with pain in a limb and fever. The combination of these two ndings—pain in an extremity
and fever—should be presumed to be infectious
until proven otherwise. In children under 1year
of age, the ndings may be more nonspecic and
poorly localized—e.g., irritability, changes in
feeding habits, and few signs of sepsis.
Pseudoparalysis (failure to use the limb) may be
the only localized nding. Localized physical
ndings such as swelling, heat, localized tenderness, erythema, and signs of systemic sepsis are
frequently seen in the older child.
The pediatric skeleton is a prime location for
bone and joint infections. In part, this is due to
the many bacterial infections that small children
seem to have—hence providing organisms capable of hematogenous spread from skin, ear, and
nasopharynx. In addition, the unique metaphyseal blood supply in the child establishes the
battleeld for the host–organism interaction.
Since the physis creates a barrier to the vessels,
they must double back on themselves, forming
end-loop capillaries and creating an area of stasis
in the bony metaphysis (Fig.7.6). This area of
Diagnosis
Standard laboratory studies will usually show an
elevated white blood cell (WBC) count, sedimentation rate (ESR), and C-reactive protein (CRP).
The ESR and CRP are both acute phase reactants;
however, the latter responds more rapidly to the
presence of infection and, therefore, tends to be a
more sensitive measure of skeletal involvement.
X-rays initially may be negative, since it takes at
least 10days for the pathology to become demon-
146
D. B. Kraft et al.
Fig. 7.6 Metaphyseal
circulation of the long
bones in children. The
nutrient artery
terminates in end
arterioles, which make a
hairpin turn adjacent to
the physis and feed into
larger venous sinusoids.
The resultant turbulent
circulation enables
bacteria to enter the
extravascular space.
(From Tachdjian
MO.Pediatric
Orthopedics, 6th ed.
Philadelphia, PA:
Herring; 2022.
Reprinted with
permission)
Joint
capsule
Epiphysis
Physis
Perichondral
vasculature
Peripheral
physeal
circulation
Physis
Sinusoid
Arteriole
Venule
Central
physeal
circulation
Metaphysis
strable radiographically, they should nevertheless
always be acquired. Bone resorption and new
periosteal bone formation are the characteristic
changes. However, neither of these may be seen
initially. An MRI with contrast is helpful in the
evaluation of these children.
Appropriate cultures are essential. Blood cultures are positive in up to 50% of cases of acute
hematogenous osteomyelitis. The organisms vary
slightly with age, but either Staphylococcus
aureus or Streptococcus species should be antici-
pated. In neonates, one needs to consider the possibility of gram-negative organisms. Management
may involve empiric intravenous antibiotics that
covers the most likely organism, typically based
on the local community acquired S. aureus sensitivities, and dosing is typically two to three times
the standard to ensure peak bactericidal titer. The
duration of intravenous medication varies based
on the severity of the illness and laboratory value
response, such as CRP.If empiric treatment fails,
the next step is either bone aspiration with a large
bore needle or surgical irrigation and debridement with intraoperative culture.
In contrast to acute osteomyelitis, subacute
osteomyelitis often lacks signs of systemic infection with normal labs and negative cultures.
Treatment
Diagnosis is critical prior to initiating antimicrobial treatment. All too often broad-spectrum antibiotics are given before a bacteriologic
diagnosis is made. The result is a “partially
treated osteomyelitis.” These children present
7 Pediatric Orthopedics
147
a challenging problem since the classical
physical findings tend to be dampened or eradicated completely. The problem, however, is
that the organisms are frequently not killed—
they only await antibiotic withdrawal before
initiating a new wave of bony destruction. The
principles of management have been established for many years and are best summarized
as follows: (1) complete bacteriologic diagnosis, (2) appropriate antibiotic selection, (3)
antibiotic delivery by the appropriate route
and for the appropriate duration, (4) immobilization to decrease the risk of pathologic fracture, and (5) surgical drainage of any abscesses.
For many years, the tradition of intravenous
(IV) antibiotic delivery has been accepted as
essential. Although some would argue that the
oral route is adequate, the IV route is still considered by most to be the standard mode of
ab
delivery despite the inconvenience caused to
child, family, and physician. The traditional
duration of 6weeks has been altered in some
protocols to 3weeks intravenous and 3weeks
oral, based on clinical response and the isolated organism. The indication for surgical
drainage is the presence of loculated pus or
infection resistant to antibiotics.
Typically, purulent loculations will be seen
within the metaphysis and/or under the periosteum (Fig. 7.7). These subperiosteal abscesses
typically follow breakthrough of the thin cortical
bone in the metaphyseal region. As these subperiosteal collections strip the periosteum from the
underlying cortex, the cortex is devascularized
and segments become avascular. In severe cases
of acute hematogenous osteomyelitis, it is not
uncommon to see sequestration of the entire bony
diaphysis.
Fig. 7.7 Vascular anatomy of the proximal femur. (a) In
the neonate, the entire epiphysis shares a blood supply
with the metaphysis. Thus, infection in the metaphysis
can spread into the epiphysis and can produce devastating
osteonecrosis of the proximal femur. (b) After development of the secondary ossication center, the epiphysis
and metaphysis have separate blood supplies. Thus, in the
older child, the physis prevents the spread of infection into
the epiphysis. However, the metaphysis remains intraarticular, and infection may decompress into the joint and
produce septic arthritis. (From Tachdjian MO. Pediatric
Orthopedics, 6th ed. Philadelphia, PA: Herring; 2022.
Reprinted with permission)
148
D. B. Kraft et al.
Septic Arthritis
Infection of a child’s joint typically results from
one of the three pathologic mechanisms:
1. Hematogenous spread: Just as in osteomyelitis, organisms can localize in the joint nding
the highly vascular synovium a favorable
location for replication.
2. Breakthrough from a metaphyseal osteomyelitis: This occurs in specic joints where a
portion of the metaphysis is intraarticular.
Anatomically, the synovial reection extends
beyond the physis and includes a portion of
metaphyseal cortical bone. The transverse
Volkmann’s canals provide a conduit for pus
in the metaphysis to access the joint. In doing
so, a secondary septic arthritis results. This
phenomenon of breakthrough is most typical
in the hip but can also occur in the elbow,
where the radial head is intraarticular, the
shoulder, and the ankle, where the bular physis is intraarticular.
3. Penetrating trauma: This results in joint sepsis
when organisms are directly injected into the
joint.
Clinical Features
Joint swelling and redness are the typical physical ndings that one would expect. Systemic
signs of sepsis are also usually readily apparent.
In contradistinction to acute hematogenous
osteomyelitis, children affected with septic
arthritis tend to be more toxic, exhibiting high
fevers, listlessness, and poor feeding. In addition,
these children will resist any attempt to move the
involved joint.
Diagnosis
A workup like that for osteomyelitis should be
carried out and at the risk of appearing repetitious, one cannot seriously consider this diagnosis in the differential without having made an
attempt to retrieve organisms from the joint. It is
important to be sure that the joint is, indeed,
being aspirated and this frequently will require
uoroscopic control, especially if the joint in
question is the hip. The pediatric hip is often difcult to enter under the best of circumstances and
radiographic control using an arthrogram or
ultrasound is recommended.
The most common organism retrieved in the
child is S. aureus. As is the case with osteomyelitis, neonates should be suspected of having
unusual organisms, including gram negatives. In
the adolescent patient, one must never forget the
common cause of septic arthritis: Neisseria
gonorrhoeae.
Treatment
Septic arthritis, unlike acute hematogenous
osteomyelitis, is a surgical emergency. It is
imperative that the pus be removed from the
joint as soon as possible. The articular cartilage is extremely vulnerable and easily damaged by enzymes—both those produced by the
microorganisms and those produced by the
white cells. It is, therefore, NOT enough to
simply kill the organisms in the joint. The joint
must be rid of all WBCs, bacterial byproducts,
and enzymes. In most young children, this
requires an arthrotomy. Occasionally, in the
older child, arthroscopy is an appropriate technique for cleaning out a more accessible joint,
such as the knee.
Repeated needle aspirations are rarely effective in cleaning the inamed joint. In addition,
repetitive aspiration in the child is yet another
example of “man’s inhumanity to man.” Antibiotic management is similar to that for osteomyelitis regarding the choice of antibiotic and
the route of delivery. The duration of administration, however, is frequently shortened. The
prognosis for septic arthritis in a child depends
on early diagnosis, aggressive drainage, and
appropriate antibiotic management. Delay in
diagnosis or delay in adequate surgical drainage can have disastrous long-term effects on
the joint, typically producing irreversible
changes (Fig.7.8).
7 Pediatric Orthopedics
149
a
c
b
d
ef
Fig. 7.8 This 11-year-old boy with a 2-week delay in
presentation developed septic arthritis of the right hip and
osteomyelitis of the proximal femur. Plain radiographs (a
and b) after nine surgical procedures for irrigation and
débridement (c and d) demonstrate involucrum associated
with the proximal femur and a cortical window used for
Complications ofBone andJoint
débridement. Radiographs taken 6months later (e and f)
demonstrate autolytic destruction of the femoral head and
loss of the proximal femur. (From Tachdjian MO.Pediatric
Orthopedics, 6th ed. Philadelphia, PA: Herring; 2022.
Reprinted with permission)
Septic Joint Destruction
Infections
Loss of articular cartilage and arthrobrosis ulti-
Long-term sequelae can result from bacterial damage to these relatively vulnerable tissues. In addition to the bone and articular cartilage, the child has
a physis, which is likewise exposed to the insult.
mately result in joint contracture, deformity, and
occasionally bony ankylosis (fusion). Salvage of
the irreparably damaged articulations is difcult
at best and frequently impossible.
150
D. B. Kraft et al.
Physeal Damage
Injury to the growth plate can have long-term
effects, especially when it occurs in a very young
child with signicant growth remaining.
Complete arrest and subsequent limb-length
inequality or partial physeal arrest and the resultant angular deformity are the two standard patterns of postinjury deformity.
Pathologic Fracture
Although infected bone will frequently look
denser (i.e., sclerotic) on X-ray, it should not be
assumed that it is mechanically stronger. The
dense bone is disorganized, its lamellar pattern
disrupted, and, therefore, it is mechanically
weaker. Pathologic fracture can occur even in the
immobilized limb, although the risk is decreased.
Chronic Infection
Despite aggressive treatment, some infections are
not completely eradicated, and a “stalemate” is
established between the host and the organism.
Occasionally, at times of physiologic stress, the
infection will reactivate and cause additional
damage.
Arthritis inChildhood
suffering from the pauciarticular form of the disease present with an isolated chronically swollen
joint. This nding should trigger a diagnostic
workup. Diagnostic blood studies are usually
negative (rheumatoid factor is positive in only
15% of cases). X-rays usually only show juxta-
articular osteopenia, and frequently, a synovial
biopsy may be needed. The histology of the
synovium is like that of the adult disease—namely,
hyperplasia and villous hypertrophy of the
synovium. It is imperative to recognize that JIA is
the leading cause of blindness in children due to
the destructive iridocyclitis that can accompany
the joint disease. All children with JIA should be
under the care of an ophthalmologist since eye
involvement does NOT parallel the degree of joint
involvement; those with minimal joint disease can
have the most severe eye changes.
Still’s disease is acute onset JIA and the
most common connective tissue disease in children. Children have systemic symptoms—
fever, rash, hepatosplenomegaly—and develop
polyarticular arthritis. This is the most virulent
and destructive form of the disease and leaves
multiple destroyed joints in its wake (Fig.7.9).
It typically occurs in ages 5–10years and has
no gender predilection.
Treatment should be directed toward control
of the synovitis with medications, physical therapy to maintain joint motion, psychologic support for chronically impaired children, and
ultimately arthroplasties or fusions for those
joints most severely involved.
Juvenile Rheumatoid Disease
The polyarticular form of the juvenile idiopathic
arthritis (JIA), as the name implies, takes its toll on
the joints but is not associated with systemic ndings. The hands and wrists are frequently involved,
over 5 joints are affected, and is typically symmetric. Polyarticular JIA has a 60% remission rate.
Pauciarticular JIA is the most common and
benign form of the disease. Typically, it is a monoarticular arthritis, with the knee, elbow, and ankle
most commonly involved. Frequently, children
Hemophilia
Children with bleeding dyscrasias frequently have
repeated hemarthroses. Initially, the blood in the
joint simply distends the capsular structures and
causes a mild synovitis. With repeated bleeds, the
synovium becomes hyperplastic and ultimately
pannus formation is seen. At this point, the joint
changes appear very similar to those seen in rheumatoid disease—e.g., osteopenia, enzymatic cartilage degradation, bony erosions, and lysis.
7 Pediatric Orthopedics
Fig. 7.9 Radiographic
changes of juvenile
idiopathic arthritis of the
wrist. Carpal destruction
and volar subluxation
are common ndings.
(From Tachdjian
MO.Pediatric
Orthopedics, 6th ed.
Philadelphia, PA:
Herring; 2022.
Reprinted with
permission)
151
Lyme Disease
In the endemic regions of the Northeast and
Middle Atlantic states, the child who presents
with a swollen knee needs to be considered as a
potential victim of Lyme disease. This infectious
arthritis is due to a specic spirochete, Borrelia
burgdorferi. The organism is transmitted to the
human host by the bite of a deer tick. These ticks
are signicantly smaller than the common wood
tick, and they are barely visible with the naked
eye. Unfortunately, a history of a bite is rare and
usually the diagnosis is reached by a high index of
suspicion in a susceptible host. The combination
of endemic region, erythematous annular skin
lesions, and monoarticular arthritis should lead
the physician to order a Lyme titer. Treatment is
generally successful if begun early. Occasionally,
despite adequate treatment, the arthritis can progress to chronic joint destruction mandating further
care. Treatment is usually oral antibiotics.
Metabolic Disease
The classic metabolic disease to affect the pediatric skeleton is rickets (Fig.7.10). The etiologies of rickets are multiple (Table7.2), but the
important pathophysiologic step is a relative
paucity of vitamin D.Vitamin D is essential for
normal progression of physeal bone development, and without it, provisional calcication
will not occur in the deepest layer of the growth
plate. As a result, physeal disorganization can be
anticipated with subsequent physeal widening,
trumpeting of the metaphysis, and aberrant
enchondral bone growth. The clinically apparent
changes of knobby joints, beading of the costochondral joints, and genu varum are all phenotypic reections of the underlying histologic
disruption of bone formation. Depending on the
etiology of the rickets, the histologic pattern will
vary slightly, but the overall skeletal changes
remain relatively constant.