Running Injuries to the Knee

Stan L. James, MD

Abstract

Approximately one third of serious runners will incur an injury in a given year, Lysholm and Wiklander6 studied
and approximately one third of the injuries will involve the knee. Biomechanical variables in runners’ injuries and
studies on running reveal the tremendous cyclic forces to which the knee is sub- found that a training fault was the
jected. There are several etiologic factors involved, including training errors, cause in 72% of the cases. Such
anatomic and biomechanical variations, and differences in shoes and running sur- training errors involve a sudden
faces. Training errors, particularly rapid transitions in training, are responsible change in the frequency, duration,
for two thirds of injuries. Knee injuries in runners must be approached with a and/or intensity of training. The
thorough review of the training program and a complete examination of the lower most common error is suddenly
extremity. Several conditions can cause anterior knee pain commonly involving increasing mileage or trying to
the extensor mechanism, and these must be differentiated. Most knee injuries can maintain too high a training
be resolved with conservative treatment, but occasionally surgery is indicated. mileage.
After a layoff due to injury or surgery, appropriate rehabilitation, including a Scott and Winter7 calculated the
graduated return to running, is essential to avoid reinjury. patellar tendon force to be around
J Am Acad Orthop Surg 1995;3:309-318 4.7 to 6.9 times body weight. They
also found patellofemoral joint com-
pressive forces to be 7.0 to 11.1 times
body weight in a jogger and two
Distance running is a significant part and Jones3 also found that the knee
middle-distance runners. Peak
of the basic fitness program of many is the most common site of running
loads were associated with the mid-
people. However, “serious” dis- injuries.
support and push-off phases of run-
tance runners (defined as those who
ning, when muscle activity is
run more than 25 miles per week)
maximal. This type of biomechani-
face an injury rate of approximately Biomechanics of Running cal information is consistent with
30% each year. Injuries high knee loads and greater fre-
In their 1985 study, McKenzie et
quency of injury.
al1 reported that the incidence of Leadbetter’s “rule of too’s” (i.e.,
knee injuries in runners had athletes court disaster when they
increased from 18% in studies per- exercise too often, too hard, and too
Dr. James is Courtesy Professor, Department of
formed a few years earlier to 50%. soon and too much after injury and Exercise and Movement Science, University of
They believed that the improved attempt remediation too little and Oregon, Eugene, and is in private practice with
construction of running shoes too late)4 often applies to runner’s Orthopedic & Fracture Clinic of Eugene.
probably played some role in injuries, most of which are attribut-
Reprint requests: Dr. James, Orthopedic & Frac-
reducing the number of leg and able to training errors. The body is
ture Clinic of Eugene, 1200 Hilyard, Suite 600,
foot injuries, but had not been quite a tremendously adaptable mecha- Eugene, OR 97401.
as effective in protecting the knee. nism, but it requires time to accom-
In a review of the epidemiologic lit- modate to new stress levels, which The author or the institutions with which he is
erature in regard to running in the case of the knee can be sig- affiliated have received something of value from a
commercial or other party related directly or indi-
injuries, van Mechelen2 found that nificant. In a study in 1978, James
rectly to the subject of this article.
most running injuries occur in the et al5 reported that training errors
lower extremity, preponderantly in accounted for two thirds of run- Copyright 1995 by the American Academy of
the knee. In another review of data ners’ injuries and that one third of Orthopaedic Surgeons.
on running biomechanics, James the injuries affected the knee.

Vol 3, No 6, November/December 1995 309

Running Injuries to the Knee
Andriacchi et al8 have reported
that the maximum knee-flexion
moment with running is more than
five times the moment that normally
occurs during level walking. That
large increase in knee-flexion
moment during the support phase of
running must be balanced primarily
by the quadriceps mechanism,
which generates significant forces in
the patellofemoral joint. They also
noted a large adduction moment of
the hip and the knee, which stresses
the iliotibial band (ITB) and possibly
contributes to a very common knee
injury, ITB friction syndrome.
History
Because approximately two thirds4,5
of runners’ injuries are related to
training errors, such as sudden
changes in duration, frequency, or
intensity of training, the single most
important aspect of the history is an
analysis of the runner’s training pro-
gram for errors. The examiner must
be able to “speak the language” of
runners. Noakes’s Lore of Running9 is
perhaps the most comprehensive
resource now available; it covers all
aspects of running, including infor-
mation on training as well as physi-
ologic and medical considerations.
The runner’s history must
include the current complaints, past
running injuries, running experi-
ence, training patterns (duration,
frequency and intensity), and run-
ning terrain. Is cross-training used?
What type and how often? Has
there been a sudden increase in
mileage? An increase in miles run
per week of 10% is about the maxi-
mum that can be tolerated safely. It
must be kept in mind that many
complaints are secondary to com-
pensation for a previous injury that
may not, at the time of evaluation,
be the most prominent problem. It
is important to know where and
when the pain occurs in the run. For
310
example, is it worse running uphill
or downhill? Does it vary with the
intensity of the run? Does the pain
occur during the swing phase or the
support phase?
Previous injuries and their treat-
ment should be investigated because
there is a tendency toward reinjury
to a given area. An anecdotal exam-
ple involves a marathon runner with
a history of recurrent Achilles prob-
lems. As he was telling me his his-
tory, he casually mentioned that
every time his weekly mileage got
over 80 miles, he seemed to get
injured. At the time of evaluation, he
was running 110 miles per week. It
was only when I specifically pointed
out what he had just said that he
began to relate mileage to injury.
Finally, it is important to identify
the make and style of running shoe
worn and whether a shoe change or
wearing a particular type of shoe can
be related to an injury. If orthotic
devices have ever been used, it is
helpful to know whether they had
any positive or negative effect on
symptoms.
Physical Examination
The physical examination must
include a thorough assessment of
the entire lower extremity, from
pelvis to toes. It is not uncommon
for the cause of knee pain in runners
to be either distal or proximal to the
knee itself (Fig. 1). One cannot
emphasize enough the importance
of not simply concentrating on the
major complaint at the knee without
a thorough examination of the entire
lower extremity. It must be borne in
mind that gross abnormalities are
not always present on examination,
nor should they be expected.
The lower-extremity examina-
tion should include evaluation of
alignment in the frontal and transverse
planes during stance and walking
and/or running. The level of the
Journal of the American Academy of Orthopaedic Surgeons
iliac wings will give some idea of
whether there is a leg-length dis-
crepancy. Extremity length should
be measured from the anterior supe-
rior iliac spine to the medial malle-
olus. Patellar dynamics should be
assessed with the patient walking to
detect patellar malalignment or
transverse-plane rotational abnor-
malities. The presence of “squinting
patellae” (patellae that incline some-
what to the midline when the feet
are parallel) suggests rotational
malalignment. Ankle dorsiflexion
should be assessed with the knee
extended and flexed. At least 10
degrees of dorsiflexion is required
during the support phase of run-
ning; compensatory foot pronation
is necessary when there is a tight
gastrocsoleus group. The overall
alignment and configuration of both
feet should be noted with the patient
both standing and walking. Muscu-
lar imbalance can often be grossly
detected with muscle testing against
resistance.
Heel-leg alignment and heel-
forefoot alignment should be evalu-
ated. With the subtalar joint in
neutral position, forefoot supina-
tion or pronation is sought. Subta-
lar joint motion normally should
allow approximately 8 degrees of
eversion and 25 degrees of inver-
sion (i.e., a ratio of about 1:3). A dis-
ruption in this ratio is often
associated with compensatory
pronation of the foot secondary to
tibia vara, tightness of the gastroc-
soleus muscles with limited ankle
dorsiflexion, heel varus, or forefoot
supination. Compensatory prona-
tion becomes necessary for the foot
to assume a plantigrade position
during the support phase; to
achieve this, the tibia is held inter-
nally rotated for a longer-than-nor-
mal period of time, which, it has
been speculated, creates rotational
mistiming at the knee.3 Inspection
of the runner’s shoes for wear pat-
terns and distortion of the heel
 Stan L. James, MD

ITB
friction
syndrome

Quadriceps
tendinosis Excessive
lateral
Patellar pressure
Excessive instability syndrome
lateral
pressure Plica
syndrome Popliteal
Patellar tenosynovitis
Fibular tendinosis
collateral
Medial collateral Fibular
ligament
ligament collateral
instability
instability ligament
instability Osteoarthritis
Voschel’s
bursitis
Anterior
Pes anserine cruciate
bursitis ligament
instability
Stress
fracture Meniscal lesion

Anterior View Lateral View

Fig. 1 Sites in the knee affected by conditions commonly seen in the runner.

counter may give a clue to the cause
of lower-extremity malalignment.
It is not uncommon for runners
with knee pain to have several
anatomic variations. A classic exam-
ple of such a combination occurs in
the “miserable malalignment”
group,5 who usually are seen with
the complaint of knee pain associ-
ated with running. Examination
reveals femoral-neck anteversion
with a greater range of internal hip
rotation than external hip rotation,
genu varum, squinting patellae,
excessive Q angle, tibia vara, func-
tional equinus with tight gastroc-
soleus muscle groups, and often
compensatory pronation of the feet.
Finally, a thorough knee exami-
nation must be carried out. Since
many of the problems dealing with
the knee in runners involve anterior
knee pain, the extensor mechanism
must be examined in detail, as
described by Fulkerson.10 Patellar
position, tracking, stability, and
crepitus and areas of tenderness
about the patella should be noted.
Radiographic Examination
Radiographic examination of the
knee includes at least four views: a
weight-bearing anteroposterior
view, a lateral view in 45 degrees of
flexion, a tangential view of the
patella, and a notch view in either
the weight-bearing or the non-
weight-bearing position. Such a
study is not required for an obvious
tendinopathy or other soft-tissue
condition, but if a degenerative con-
dition, patellofemoral malalign-
ment, or a bone abnormality or
injury is suspected, a complete
examination is certainly warranted.
Anterior Knee Pain
Approximately one third of runners’
injuries fall into the category of knee
pain (Table 1). In the 1970s, at the

Vol 3, No 6, November/December 1995 311

Running Injuries to the Knee
Table 1
Causes of Knee Pain in Runners
Anterior knee pain
Excessive lateral pressure syn-
drome
Patellar instability
Quadriceps or patellar
tendinopathy
Pathologic plica
Other conditions
Meniscal lesions
Bursitis
Stress fracture
Osteoarthritis
ITB friction syndrome
Popliteal tenosynovitis
Ligamentous instability
peak of the running boom, the term
“runner’s knee” was prevalent in the
lay literature. This term seems syn-
onymous with chondromalacia in
the professional literature. How-
ever, neither term accurately defines
the range of problems associated
with anterior knee pain. Several
conditions may cause anterior knee
pain and must be specifically diag-
nosed before any attempt at treat-
ment can be considered.
Excessive Lateral Pressure
Syndrome
Excessive lateral pressure syn-
drome11 is characterized by diffuse
anterior knee pain, but usually the
runner will indicate the patella as
being the major site of discomfort.
Clinical examination of patellar
tracking may not reveal anything
particularly remarkable, but palpa-
tion over the lateral retinaculum
often reveals tenderness. There may
be tightness of the lateral retinacu-
lum, which can be identified when
the lateral border of the patella can-
not be brought to the horizontal
plane on examination. This is deter-
mined by stabilizing the medial
patella with the fingers of both
312
hands while using the thumbs to
pull up on the lateral patella and
then observing the degree of mobil-
ity present. If the condition has per-
sisted, there may be crepitus and
tenderness along the lateral patellar
border, which is indicative of possi-
ble degenerative changes in the lat-
eral-facet articular cartilage.
An axial view of the patella, such
as the Merchant view (taken with the
knee flexed 45 degrees and the x-ray
beam projected caudad at a 30-
degree angle from the femoral
plane), will normally show the
patella concentrically positioned in
the sulcus without tilt or subluxa-
tion. Tilt is suspected when the
medial facet is lifted away from the
medial trochlear condyle. Since this
technique is not particularly sensi-
tive for tilt, there are some instances
in which carefully performed com-
puted tomography should be per-
formed, with special emphasis on
patellofemoral joint alignment, 10
particularly when the diagnosis is
not clearly confirmed and surgery is
contemplated.
Once the diagnosis of excessive
lateral pressure syndrome has been
made, a conservative treatment pro-
gram should be initiated (discussed
later in the “Treatment” section). If
6 months of conservative treatment
does not result in reduction of symp-
toms and the diagnosis is clinically
and radiographically confirmed,
surgery may be considered
An arthroscopic or open lateral
retinacular release is thought to be
effective for treatment of patellar tilt,
particularly when there is minimal
or no articular involvement of the
patella. A lateral retinacular release
when there is no evidence of patellar
tilt stands much less chance of being
successful. Although arthroscopic
lateral release may seem relatively
benign, it is important to stress that a
rehabilitation period of 8 to 12 weeks
may be necessary before the patient
can return to running.
Journal of the American Academy of Orthopaedic Surgeons
Patellar Instability
Patellar instability is a condition
associated with anterior knee pain in
runners. A dislocated patella in a
runner is rare, but subtle subluxa-
tion and maltracking are frequent.
Even minor patellar subluxation or
lateral maltracking can alter the nor-
mal distribution of patellofemoral
joint-compression forces, creating
pain with or without actual articular
cartilage damage. Usually the pain
is insidious and gradual in onset;
however, some dramatic alteration
in the runner’s program, such as
incorporating hill workouts, may
trigger pain. Symptoms of giving
way may be present, but anterior
knee pain is the most common com-
plaint.
Physical examination to deter-
mine patellar position, tracking, and
stability should be done along with
appropriate radiographic evalua-
tion. It is important to observe patel-
lar tracking with active knee
extension and flexion. Lateral place-
ment of the patella or lateral
displacement at termination of
extension, termed the J sign, suggests
maltracking. The knee is positioned
in 30 degrees of flexion, lateral pres-
sure is applied to the patella, and the
presence of lateral displacement is
noted. Normally, the patella should
remain secure in the sulcus. A posi-
tive instability test, particularly
when associated with apprehension,
denotes instability. A Q angle of
more than 20 degrees indicates a ten-
dency for the quadriceps to displace
the patella laterally. In cases of patel-
lar instability and maltracking, the
diagnosis can usually be made on the
basis of the history and clinical exam-
ination. Confirmation is by x-ray
examination. Determination of the
congruence angle on a Merchant
view of the patella may reveal patel-
lar subluxation. A lateral radiograph
with the knee in 30 degrees of flexion
will suggest whether there is patella
alta, which is often present with

instability. The normal ratio of patel-
lar length to patellar-tendon length
should be no more than 1:1.2.
Most of the more subtle forms of
maltracking and subluxation can be
managed with quadriceps rehabili-
tation, placing emphasis on closed-
chain exercises. A program directed
by a knowledgeable physical thera-
pist or the physician should be faith-
fully pursued for at least 3 months
before surgical treatment is even
considered. Most runners will
become symptom-free and can
return to training after such a reha-
bilitation program, but continuation
of rehabilitation exercises for an
indefinite period may be necessary
even after there has been a return to
training.
For the small group of patients for
whom surgical intervention is con-
sidered, arthroscopic lateral retinac-
ular release followed by patellar
chondroplasty is the option selected
most often. A lateral release is com-
patible with a return to running and
is preferable to more extensive pro-
cedures. As in the case of patients
who have had this procedure for lat-
eral tilt, 8 to 12 weeks of rehabilita-
tion is required before a return to
running. Distally, medial tibial-
tubercle placement or anteromedial-
ization of the tibial tubercle, as
described by Fulkerson,10 may be
indicated. Proximally, medial reti-
nacular reefing can be carried out,
but this must be done judiciously so
as to avoid creating a tight medial
retinaculum and patellar tilt or rota-
tion. In runners, extensive proximal
and distal realignment of the exten-
sor mechanism has unpredictable
results in terms of the ability to
return to serious running. The sim-
pler the procedure, such as a lateral
release, the more likely are the
prospects for a return to training. In
large part, the result will be deter-
mined by the extent of patello-
femoral joint degenerative changes
or chondral damage from repeated
Vol 3, No 6, November/December 1995
episodes of subluxation or mal-
tracking.
Quadriceps and Patellar
Tendinopathy
Quadriceps tendinosis and patel-
lar-tendon (ligament) tendinosis,
often referred to as “jumper ’s
knee,”12 are frequently encountered
in runners. The latter, by far the
more common, involves the tendon
insertion on the distal pole of the
patella. Excessive stress at the liga-
ment insertion on the patella results
in microruptures and perhaps local
areas of deep tendon degeneration
or tendinosis. The microtears lead to
structural deterioration with partial
tissue failure and, in some instances,
can lead to complete rupture of the
tendon.2 Tendinosis at the tendon
insertion distally on the tibial tuber-
cle is a far less common running
injury.
Quadriceps tendinosis is associ-
ated with pain at the insertion site of
the quadriceps tendon, which is usu-
ally more lateral than medial, on the
proximal pole of the patella. Patellar
tendinosis pain is felt at the distal
pole of the patella. The runner will
usually indicate one or the other area
as the site of maximum discomfort.
He or she may also describe local-
ized swelling when the symptoms
are acute, but generally the com-
plaint is largely of pain at the
involved site, particularly with bent-
knee activities. Typically, pain
comes on gradually during the
course of a run. Initially the symp-
toms may not stop the runner from
training; with time, however, the
pain becomes more persistent and
may eventually lead to cessation of
the sport.
In cases of quadriceps tendinosis,
physical examination reveals ten-
derness directly over the insertion
site of the quadriceps tendon, which
is commonly located proximal and
lateral on the patella. There may be
associated crepitus, particularly if
Stan L. James, MD
there is a prominent lateral epi-
condylar ridge or perhaps even an
osteophyte from some degenerative
patellofemoral joint changes, similar
to that noted with maltracking of the
patella. Squatting places increased
tension on the tendon and is often
painful.
The tenderness associated with
patellar tendinosis is best palpated
with the patient’s knee in full exten-
sion and the quadriceps relaxed.
Pressure is applied to the proximal
pole of the patella to tilt the distal
pole up, so that the patellar tendon
insertion may be easily palpated.
Occasionally, swelling or induration
of the soft tissues is also noted. There
may be an increased Q angle. The Q
angle may be observed to change
dramatically during the support
phase of gait, during which prona-
tion or supination of the foot results
in alteration of tibial rotation. This
dynamic effect on lower-extremity
alignment may aggravate or cause
the problem by placing eccentric
traction on the patellar tendon.
The radiographic findings are
often normal, although the distal
pole of the patella may have an elon-
gated or fragmented tip. Occasion-
ally, ectopic bone or calcific deposits
are noted in the tendon. Ultra-
sonography and magnetic reso-
nance (MR) imaging may delineate
a lesion within the substance of the
tendon. These studies are usually
reserved for cases in which conser-
vative treatment for at least 3
months has failed and surgery is
contemplated. Ultrasonography is
quite specific and less expensive
than MR imaging.
Both patellar and quadriceps
tendinosis can usually be resolved
conservatively with the use of the
treatment protocol that will be dis-
cussed later. Curwin and Stanish13
have described an eccentric rehabili-
tation program for tendinosis with
a success rate approaching 90%.
However, their results were less suc-
313
Running Injuries to the Knee
cessful with patellar tendinosis, with
only 30% of patients experiencing
relief.
In the event of intractable pain
that fails to respond to 3 to 6 months
of conservative treatment, surgical
exploration of the proximal portion
of the patellar tendon and excision of
any abnormal tissue may be consid-
ered. If the tendinous lesion is quite
large, reattachment of the tendon to
freshened bone may be necessary.
Fortunately, in most patients the
area of involvement is relatively
small, and the defect can be closed
by imbrication. The surgical tech-
nique for quadriceps tendinosis is
similar. If an osteophyte or promi-
nent epicondylar ridge is present, it
can be removed to decompress the
involved area.
Pathologic Plica
Another condition that causes
anterior knee pain in runners is
painful plica. Most commonly, a
medial parapatellar plica becomes
fibrotic and rubs or snaps over the
medial femoral condyle with knee
motion. Occasionally, a retained
suprapatellar plica may become
symptomatic as well. Pain usually
comes on gradually with distance
running; however, it can be acute
and associated with a sudden
change in training routine, such as
more intense, shorter-interval work-
outs. Snapping and buckling may be
noted. The patient may also report
that sitting is painful. Pain may be
diffuse, but often the runner can
localize it to the medial retinacular
area or the suprapatellar area.
A common physical finding is
localized tenderness over the
femoral condyle adjacent to the
medial border of the patella. Often a
palpable snap and sometimes crepi-
tus are noted over a tender and pal-
pable medial fibrotic cord. If the
suprapatellar plica is involved, there
may be tenderness and sometimes
crepitus on compression of the
314
patella and quadriceps tendon.
Acute knee flexion may elicit supra-
patellar pain. An effusion is not
usual; if present, other intra-articu-
lar conditions should be considered.
There is a tendency to overdiagnose
this condition, but it is also impor-
tant to remember that a truly patho-
logic plica may mimic many other
conditions in the joint.
The treatment protocol discussed
later in this article should be initi-
ated, but active resistive knee exer-
cises, which may irritate the plica,
must be avoided. Arthroscopic exci-
sion may be necessary in some cases
and usually will entail little down-
time for the runner. If arthroscopic
examination shows that the plica
suspected of causing symptoms is
not thickened, avascular, and
widened (over 12 mm), Ewing14 sug-
gests that it probably is not the
cause of the problem; other causes
should always be diligently sought
by examining the entire joint.
Other Conditions
Meniscal lesions
Meniscal lesions are quite
unusual in younger runners but do
become a problem in middle-aged
and older runners. The diagnosis of
meniscal tears in runners is no dif-
ferent from that in any other athlete
with this condition. In runners, par-
ticularly middle-aged and older run-
ners, the onset of pain is usually
insidious, although there may be an
inciting incident, such as a misstep
or twist. There may be a history of
joint effusion or catching. Locking
episodes are less common in the
older runner.
Physical signs often include a
small effusion, usually joint-line
tenderness. In my experience, the
McMurray test is positive in about
half of patients. Arthrography or
MR imaging may be helpful if the
diagnosis is uncertain, but fre-
Journal of the American Academy of Orthopaedic Surgeons
quently the diagnosis can be made
on the basis of clinical criteria
alone.
This condition readily lends itself
to arthroscopic surgery, generally
with a relatively short interrup-
tion (4 to 6 weeks) in the training-
program. Even so, an appropriate
rehabilitation program must be
supervised.
Bursitis
Medial knee pain has been
reported to most commonly involve
the pes anserine bursa and Voschel’s
bursa deep to the superficial portion
of the medial collateral ligament.15,16
Tenderness with Voschel’s bursitis
is immediately below the joint line
deep to the medial collateral liga-
ment. Pes anserine bursitis is more
distal, with tenderness and perhaps
crepitus over the pes anserine area;
in addition, active knee flexion
against resistance may cause pain.
These two conditions must be differ-
entiated from a medial meniscal
lesion, with which there will be ten-
derness more directly over the joint
line. Both usually respond promptly
to conservative measures. These
conditions are relatively uncom-
mon among runners whom I have
treated.
Stress Fracture
Proximal medial tibial stress frac-
tures are also a consideration but not
very common in runners. Most tib-
ial stress fractures occur in the mid-
dle and distal thirds of the tibia in
runners. They are usually associated
with localized tenderness on palpa-
tion and swelling. A bone scan is the
best early diagnostic tool. Once the
diagnosis has been made, the treat-
ment is rest until the symptoms
abate.
Osteoarthritis
Since running became popular in
the 1970s, there has been a signifi-
cant increase in the number of older

runners. It is not unusual to find
very dedicated runners in the sixth
and seventh decades of life. With
increasing age, the frequency of
osteoarthritic conditions increases,
although there is no evidence to date
in the literature that implicates run-
ning as a cause of degenerative
changes in a normal knee.17 Once
degenerative changes are estab-
lished, the running program must
be carefully customized and moni-
tored.
A frequent question from runners
is whether running will accelerate a
known osteoarthritic condition. The
answer is yes, it probably does to
some extent, depending on the
program. This possibility raises a
difficult problem for runners. Some-
times it is best to first allow them to
try to find a program that their knees
will tolerate. If they are unable to do
so, it may be easier for them to make
the decision to discontinue running
rather than being arbitrarily told
they must stop. With significant
degenerative changes, alternative
low-impact aerobic activities are an
option; these include cross-country
skiing or using ski machines, swim-
ming, doing aerobic water exercis-
es, biking, and race-walking.
Minimal joint debridement with
arthroscopic removal of sympto-
matic osteophytes, degenerative
menisci, and loose bodies may help
symptomatically, but whether this
results in long-term improvement is
debatable. Extensive chondroplas-
ty procedures and abrasion chon-
droplasty procedures are not very
effective in allowing a return to run-
ning.
Iliotibial Band Friction
Syndrome
Iliotibial band friction syndrome9
is the most common problem
involving the lateral aspect of the
knee in runners. It is usually initi-
ated by an extra-long run and is par-
ticularly aggravated by running
Vol 3, No 6, November/December 1995
downhill. The pain is lateral, often
starts a mile or two into the run,
becomes worse for the duration of
the run, and may cease on stopping.
Sometimes it occurs only with
downhill running and running on
the level; participation in other
sports is pain free.
The physical findings are tender-
ness over the distal ITB and the lat-
eral femoral condylar region, with
occasional swelling and sometimes
crepitus. The lateral condyle may be
prominent. The runner frequently
has genu varum and/or tibia vara,
heel varus, forefoot supination, and
compensatory pronation. Examina-
tion of the running shoes often
shows excessive lateral heel wear.
This combination of subtle lower-
extremity malalignments is thought
to cause increased friction between
the ITB and the lateral femoral
condyle due to greater tension on
the lateral structures. It is also
thought that hip abductor weakness
with early muscle fatigue may cause
exaggerated pelvic sag during the
support phase and place increasing
tension on the ITB. This enhances
friction between the ITB and the lat-
eral femoral condyle, which results
in synovitis. Tenderness is typically
present about 2 to 3 cm proximal to
the joint line and over the lateral
femoral condyle and distal portion
of the ITB.
Ober’s test may be positive for
ITB tightness. However, a better test
is performed as follows: With the
patient lying on his or her side with
the affected knee up, pressure is
applied to the lateral femoral
condyle. The knee is then moved
through a range of motion of about
30 to 45 degrees. This positions the
tensed ITB directly over the lateral
femoral condyle, which accentuates
pain.
In addition to the modalities usu-
ally used in the treatment of runners’
injuries in general, a corticosteroid
injection or phonophoresis (ultra-
Stan L. James, MD
sound with topical hydrocortisone)
in the area of involvement may help
resolve the condition, particularly in
the acute phase. Other techniques
include stretching the ITB and
strengthening the abductor muscu-
lature.
Surgery may be indicated in
patients with intractable symptoms.
Before arthroscopy of the joint is
performed, the knee must be care-
fully inspected, particularly the lat-
eral compartment, to rule out a
meniscal lesion or other disorder,
such as synovitis or pathologic lat-
eral plica. If no other cause is iden-
tified, an open procedure similar to
that described by Noble18 is per-
formed to release the posterior 2 cm
of the ITB at the level of the lateral
condyle, where it appears to create
the most tension over the femoral
condyle. This procedure has been
effective in my experience and usu-
ally allows a return to running
within 4 weeks. However, as is the
case for many operations used in the
treatment of runners’ injuries, there
are no well-controlled prospective
clinical studies that unequivocally
show efficacy.
Popliteal Tenosynovitis
Popliteal tenosynovitis also
causes lateral knee pain but in my
practice is not as frequent as ITB fric-
tion syndrome. It involves the
popliteal tendon posterolaterally
and may vary from a transient con-
dition to one that becomes chronic.
The onset is often associated with
downhill running.
Examination reveals tenderness
directly over the popliteal tendon
just posterior to the fibular collateral
ligament. It sometimes is difficult to
differentiate this condition from ITB
friction syndrome or a lateral menis-
cal lesion. The former can be differ-
entiated because tenderness is
located over the ITB at the femoral
condyle; in the latter, tenderness is
directly over the lateral joint line.
315
Running Injuries to the Knee
Treatment is conservative and
similar to that used for ITB friction
syndrome. I have never considered
it necessary to operate on a patient
with this condition.
Ligamentous Instability
Ligamentous instability of the
knee is not a common injury caused
by running, even among com-
petitive runners. However, some
recreational runners may have liga-
mentous instability, particularly
anterior cruciate ligament deficits,
which have been incurred in other
sports. If the menisci remain intact,
there are no recurrent episodes of
instability with swelling and pain,
and the activity of running is con-
fined to good surfaces, the knee
may function well without difficulty.
Treatment
Most knee injuries in runners can
be resolved with the use of conserv-
ative methods.19 Nigg20 suggests that
the most effective biomechanical
strategies to reduce load and stress
on a locomotor system involve the
following factors: (1) the movement,
such as a change in running style;
(2) the surface (i.e., soft versus hard);
(3) the shoe (current shoe designs
provide variability in cushion effect
and motion control of the foot); and
(4) the frequency of repetitive move-
ments (e.g., the mileage, pace, or
duration of running).
A logical treatment protocol that
addresses the elements listed in
Table 2 is adaptable for virtually all
runner’s injuries, including those
involving the knee.
Training Program
The training program must first
be evaluated and modified as neces-
sary. This will often resolve many of
the injuries. Rest is the last bit of
advice runners generally want to
hear, but at times it is necessary.
316
Table 2
Treatment Considerations
Training program
Anatomic and biomechanical
variations
Shoe modifications
Muscle reconditioning and
flexibility
Orthotic devices
Medications and physical therapy
Surgery
Rehabilitation
They generally prefer modification
of the program by reducing the fre-
quency, intensity, and duration of
their running. Running in water
(aqua-jogging) is an excellent form
of non-weight-bearing cross-train-
ing for running during rehabilita-
tion, which allows patients to
maintain a high level of aerobic con-
ditioning as well as lower-extremity
muscle strength and endurance and
joint mobility.
Anatomic and Biomechanical
Variations
Thorough assessment of the
entire lower extremity is mandatory.
As stressed earlier, concentrating on
the site of the injury about the knee
will often lead the examiner to over-
look the etiologic factor actually
causing the pain. Thus, it is impor-
tant to look both distal and proximal
to the knee for anatomic or biome-
chanical variations. It is also impor-
tant to learn how to evaluate foot
function.3,5,21
Shoe Modifications
Shoes generally come in three
classifications: motion control, sup-
port, and cushion. Most running-
shoe manufacturers have shoes
fitting these classifications. A fabricate the devices provide func-
motion-control shoe is for someone
who needs control of subtalar joint
Journal of the American Academy of Orthopaedic Surgeons
motion for compensatory pronation.
The support shoe is for the individ-
ual who does not demand much con-
trol. A cushion shoe is for the runner
with a rigid-type foot requiring
more flexibility and cushioning for
shock absorption. Usually an ortho-
tist or shoe-repair shop can modify
running shoes for special problems,
such as leg-length discrepancies.
Changing the hardness of the mid-
sole and heel wedge and using a
variable-hardness heel wedge can
change foot mechanics by altering
pronation or supination, which then
influences knee function through the
amount of obligatory tibial rotation
during pronation. However, heel-
wedge and midsole cushioning do
little to alter the vertical impact
forces during the support phase.
Muscle Reconditioning and
Flexibility
Restoring the muscle strength,
endurance, and balance of the entire
lower extremity is essential after
injury. If runners do not specifically
restore muscle strength and
endurance to affected muscle
groups, deficits will persist even
after they return to running. Gentle,
sustained stretching is another
aspect of conditioning that must not
be ignored, since tightness of the
hamstring and gastrocsoleus muscle
groups is very common among dis-
tance runners.
Orthotic Devices
By controlling pronation and
supination, orthotic devices are used
to alter foot biomechanics. The pur-
pose of an orthotic device in the shoe
is to allow the subtalar joint complex
to function effectively from the neu-
tral position during the support
phase, reducing the amount and
duration of compensatory prona-
tion. The special materials used to
tional and impact shock absorp-
tion.9,21,22 These devices are most

useful in the treatment of problems
due to subtle patellar maltracking or
the ITB friction syndrome.
Medications and Physical
Therapy
Reducing pain and inflammation
with medications such as non-
steroidal anti-inflammatory agents
is helpful. Physical therapy modali-
ties are also options. Corticosteroid
injection is generally contraindi-
cated in tendons. The most likely
indications for steroid injection are
ITB friction syndrome, popliteal
tenosynovitis, and bursitis, par-
ticularly in the acute phase. Admin-
istering narcotic analgesics or
injecting local anesthetics to allow
running cannot be condoned.
Surgery
Most runner’s injuries can be
managed conservatively, but the
program must be adequately super-
vised so that if conservative means
fail, the runner, the coach, and the
physician will feel comfortable
about considering surgical treat-
ment if indicated.
Surgery is not often required in
runners, and the indications for
surgery are really no different from
those in the general population.
Surgery is reserved as almost a last
resort, particularly in the elite run-
ner, except in the presence of certain
conditions that can be managed
effectively with early arthroscopic
surgery, such as a documented
meniscal lesion or loose body. This
does not necessarily mean unusual
or unwarranted delay, but rather
taking a methodical approach to the
problem. In some situations, it is
important to point out to the runner
that the condition could actually ter-
Vol 3, No 6, November/December 1995
minate running in spite of well-indi-
cated surgery.
Rehabilitation
If surgery has been deemed neces-
sary, the surgeon must direct the post-
operative rehabilitation program with
the athlete, the trainer or physical ther-
apist, and the coach. All too often, the
results of surgery are negated by too
rapid a return to running without ade-
quate and careful rehabilitation. A
program that I have found quite satis-
factory (Table 3), with modification
depending on the individual situa-
tion, emphasizes a graduated return
to running after a layoff from injury or
surgery. The patient should use an
easy, comfortable pace (7 to 10 min-
utes per mile). He or she should also
rest one day each week and not be
concerned about mileage or aerobic
conditioning. The purpose of the pro-
gram is to condition the injured area.
During the course of the graduated
buildup, the patient can hold at a
given level or even drop back a level if
necessary. Aerobic conditioning can
be maintained with cross-training
activities, such as aqua-jogging, swim-
ming, and biking. General strength-
ening and flexibility exercises should
also be used.
Summary
The knee remains the primary loca-
tion for lower-extremity injuries in
runners, being the site of approxi-
mately 30% of all injuries. Anterior
knee pain is the most common knee
complaint. Although many factors
are involved, training errors, particu-
larly rapid transitions in the program
and increases in mileage, are the pri-
mary cause of injury. A comprehen-
Stan L. James, MD
Table 3
Program for Graduated Return to
Running
Week Activity
1 Walk 4 to 8 laps (alternate
50 m fast, 50 m normal)
2 Walk 8 to 12 laps (alter-
nate 100 m fast, 100 m
normal)
3 Jog 10 minutes every
other day at an easy
pace
4 Jog 15 minutes every
other day
5 Jog 15 minutes one day,
25 minutes the next
6 Jog 20 minutes one day,
30 minutes the next
7 Jog 20 minutes one day,
35 minutes the next
8 Jog 20 minutes one day,
40 minutes the next
9 Resume training at an
appropriate mileage
and intensity
sive history of the training program,
a thorough examination of the entire
lower extremity (not just the knee),
and a methodical approach to treat-
ment are essential. Most problems
can be resolved conservatively, but
surgery is occasionally indicated.
After an injury or surgery to the
knee, the physician must supervise
the rehabilitation and the return to
running so as to avoid reinjury.
317
Running Injuries to the Knee
References
1. McKenzie DC, Clement DB, Taunton JE:
Running shoes, orthotics, and injuries.
Sports Med 1985;2:334-347.
2. van Mechelen W: Running injuries: A
review of the epidemiological literature.
Sports Med 1992;14:320-335.
3. James SL, Jones DC: Biomechanical
aspects of distance running injuries, in
Cavanagh PR (ed): Biomechanics of Dis-
tance Running. Champaign, Ill: Human
Kinetics Books, 1990, pp 249-269.
4. Leadbetter WB: Aging effects upon the
repair and healing of athletic injury, in
Gordon SL, Gonzalez-Mestre X, Garrett
WE Jr (eds): Sports and Exercise in
Midlife. Rosemont, Ill: American Acad-
emy of Orthopaedic Surgeons, 1993, pp
177-223.
5. James SL, Bates BT, Osternig LR:
Injuries to runners. Am J Sports Med
1978;6:40-50.
6. Lysholm J, Wiklander J: Injuries in run-
ners. Am J Sports Med 1987;15:168-171.
7. Scott SH, Winter DA: Internal forces of
chronic running injury sites. Med Sci
Sports Exerc 1990;22:357-369.
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8. Andriacchi TP, Kramer GM, Landon
GC: The biomechanics of running and
knee injuries, in Finerman G (ed):
American Academy of Orthopaedic Sur-
geons Symposium on Sports Medicine:
The Knee. St Louis: CV Mosby, 1985,
pp 23-32.
9. Noakes T: Lore of Running, 3rd ed.
Champaign, Ill: Leisure Press, 1991.
10. Fulkerson JP: Patellofemoral pain dis-
orders: Evaluation and management. J
Am Acad Orthop Surg 1994;2:124-132.
11. Ficat RP, Hungerford DS: Disorders of
the Patello-femoral Joint. Baltimore:
Williams & Wilkins, 1977, pp 123-148.
12. Blazina ME, Kerlan RK, Jobe FW, et al:
Jumper’s knee. Orthop Clin North Am
1973;4:665-678.
13. Curwin S, Stanish WD: Tendinitis: Its
Etiology and Treatment. Lexington, Mass:
Collamore Press, 1984, pp 162-163.
14. Ewing JW: Plica: Pathologic or not? J
Am Acad Orthop Surg 1993;1:117-121.
15. Leach R: Running injuries of the knee,
in D’Ambrosia R, Drez D Jr (eds): Pre-
vention and Treatment of Running Injuries.
Journal of the American Academy of Orthopaedic Surgeons
Thorofare, NJ: Charles B. Slack, 1982,
pp 55-75.
16. Rubin BD, Collins HR: Runner’s knee.
Phys Sports Med 1980;8:47-58.
17. Lane NE, Michel B, Bjorkengren A, et al:
The risk of osteoarthritis with running
and aging: A 5-year longitudinal study.
J Rheumatol 1993;20:461-468.
18. Noble CA: The treatment of iliotibial
band friction syndrome. Br J Sports
Med 1979;13:51-54.
19. Taunton JE, Clement DB, Smart GW,
et al: Non-surgical management of
overuse knee injuries in runners. Can J
Sport Sci 1987;12:11-18.
20. Nigg BM: Biomechanics, load analysis
and sports injuries in the lower extrem-
ities. Sports Med 1985;2:367-379.
21. D’Ambrosia RD, Douglas R: Orthotics,
in D’Ambrosia R, Drez D Jr (eds): Pre-
vention and Treatment of Running Injuries.
Thorofare, NJ: Charles B. Slack, 1982,
pp 155-164.
22. Mann RA, Baxter DE, Lutter LD: Run-
ning symposium. Foot Ankle 1981;1:190-
224.
 Scapular Winging

John E. Kuhn, MD, Kevin D. Plancher, MD, and Richard J. Hawkins, MD, FRCS(C)

Abstract
Scapular winging, one of the more common scapulothoracic disorders, is caused (including surgical biopsy of lymph
by a number of pathologic conditions. It can be classified as primary, secondary, nodes in the posterior cervical trian-
or voluntary. Primary scapular winging may be due to neurologic injury, patho- gle3,4 and radical neck dissection).1
logic changes in the bone, or periscapular soft-tissue abnormalities. Secondary After injury to the spinal acces-
scapular winging occurs as a result of glenohumeral and subacromial conditions sory nerve, the patient assumes a
and resolves after the primary pathologic condition has been addressed. Volun- position with the shoulder depressed
tary scapular winging is not caused by an anatomic disorder and may be associ- and the scapula translated laterally
ated with underlying psychological issues. The evaluation and treatment of these with the inferior angle rotated later-
three types are discussed. ally (Fig. 1, A). Patients will attempt
J Am Acad Orthop Surg 1995;3:319-325 to compensate for this deformity by
using muscles of the shoulder girdle,
including the levator scapulae and
the rhomboids. This strain may lead
Scapular winging is one of the most smooth rhythm may become evident to disabling pain and muscle spasm.5
common abnormalities of the scapu- with dynamic testing. The examiner Patients can also have pain due to
lothoracic articulation. Winging may must also look for winging with secondary effects of winging, includ-
be described as primary, secondary, resisted motion, such as may occur ing adhesive capsulitis, subacromial
or voluntary (Table 1). Primary when the patient pushes against a impingement, and radiculitis from
scapular winging is caused by wall or resists forward elevation traction on the brachial plexus. On
anatomic disorders that directly affect with the arms at 30, 90, and 150 examination, patients will have
the scapulothoracic articulation. Sec- degrees. Static, dynamic, or resisted trapezius wasting, will be unable to
ondary scapular winging usually winging may be graded subjectively shrug the shoulder, and will have
accompanies some glenohumeral dis- as mild, moderate, or severe. associated weakness on forward ele-
order and should resolve once that
disorder has been addressed. Volun-
tary winging may have psychological Primary Scapular Winging
Dr. Kuhn is Lecturer, Division of Sports Medi-
overtones and is quite rare.
cine, Section of Orthopaedic Surgery, University
Neurologic Origin of Michigan Medical Center, Ann Arbor. Dr.
Plancher is Assistant Professor, Albert Einstein
Evaluation Trapezius Winging College of Medicine, New York; Attending Sur-
The spinal accessory nerve, which geon, Montefiore Medical Center, New York; and
Hand Consultant, Steadman-Hawkins Clinic,
Patients with scapular winging provides the only innervation to the
Vail, Colo. Dr. Hawkins is Clinical Professor,
should be first observed at rest with trapezius muscle,1 is located in the Department of Orthopedics, University of Col-
the arms at the sides. A static defor- subcutaneous tissue on the floor of orado Medical School, Denver, and Orthopaedic
mity should be sought, as well as the posterior cervical triangle. Its Consultant, Steadman-Hawkins Clinic, Vail.
muscle atrophy. The patient is then superficial location makes it suscep- Reprint requests: Dr. Kuhn, The University of
asked to elevate his arms in the for- tible to injury, which can result in Michigan Shoulder Group, 24 Frank Lloyd
ward plane, and the scapulae are significant deformity as well as Wright Drive, Box 363, Ann Arbor, MI 48106-
observed in relation to the chest painfully disabling alterations in 0363.
wall. The scapulothoracic rhythm scapulothoracic function.2-4 Injury Copyright 1995 by the American Academy of
and the presence of crepitus should can be caused by blunt trauma,4,5 Orthopaedic Surgeons.
be noted; alterations in the normally traction,4 or penetrating trauma

Vol 3, No 6, November/December 1995 319

Scapular Winging

are unlikely to benefit from contin- scapulae substitutes for the upper third of
Table 1 ued conservative treatment, and the trapezius; the rhomboideus major,
Classification of Scapular surgery can be offered. Historically, for the middle third; and the rhom-
Winging a variety of surgical procedures have boideus minor, for the lower third. By
been described for the treatment of moving these muscle insertions laterally,
Primary
spinal accessory nerve paralysis.2,9,10 their mechanical advantage is improved,
Neurologic origin
These can be divided into static and and winging is diminished or eliminated.
Spinal accessory nerve
(trapezius palsy) dynamic procedures. Static stabiliza- The surgical technique involves
Long thoracic nerve tion includes scapulothoracic fusion9 two incisions. The first is along the
(serratus anterior palsy) and any of the many operations that medial scapular border, and the sec-
Dorsal scapular nerve tether the scapula to the spine.2 The ond is over the spine of the scapula.
(rhomboideus palsy) dynamic procedures all involve some The levator scapulae, rhomboideus
Osseous origin form of muscle transfer.5,10,11 Because minor, and rhomboideus major are
Osteochondromas scapulothoracic fusions represent a detached from their origins, taking a
Fracture malunions huge undertaking and may limit small portion of insertional bone
Soft-tissue origin motion significantly, and because fas- from the medial scapula. The rhom-
Contractural winging
cial-sling suspensions tend to fail, boid muscles are advanced laterally
Muscle avulsion or agenesis
causing recurrence of winging in 2 to under the infraspinatus and are
Scapulothoracic bursitis
Secondary 3 years,5 dynamic muscle transfers secured with suture, which is passed
Voluntary have become the procedure of choice through drill holes placed 5 cm lateral
for persistent trapezius winging.5,10-13 to the medial border of the scapula.
The muscle-transfer operation per- The levator scapulae is passed 5 cm
haps most commonly performed for laterally, subcutaneous to the second
vation and abduction of the arm. The trapezius paralysis is the Eden-Lange incision, and is sutured to the scapu-
diagnosis can be confirmed by elec- procedure,5,12,13 in which the levator lar spine through drill holes. Postop-
tromyographic (EMG) examination. scapulae, rhomboideus minor, and eratively, a sling is used for 6 weeks,
Treatment depends on the dura- rhomboideus major muscles are trans- after which passive and then active
tion and severity of symptoms. An ferred laterally (Fig. 2). The levator range-of-motion exercises are used.
initial treatment regimen including
physical therapy is helpful to main-
tain glenohumeral motion and pre-
vent adhesive capsulitis. In patients
in whom spinal accessory nerve
injury is due to blunt trauma, serial
EMG examinations may be per-
formed at 6-week intervals to follow
the returning function of the nerve.
This is usually not begun until 3
months after the injury, because
denervation changes in the muscle
may not be manifest before that
time. In nerve injuries due to pene-
trating trauma, or when there is no
evidence of nerve function on EMG
analysis, neurolysis and/or nerve
grafting can be considered.3,6-8 The
results of these procedures have
been variable. If neurolysis is per-
formed, the success rate seems to be
improved if the procedure is done A B
within 6 months of the injury.5 Fig. 1 Position of the scapula with primary scapular winging due to trapezius palsy (A) and
Patients who have had debilitat- serratus anterior palsy (B).
ing symptoms for more than 1 year

320 Journal of the American Academy of Orthopaedic Surgeons


Fig. 2 Eden-Lange dynamic transfer, used
to treat trapezius paralysis.5 The levator
scapulae, rhomboideus minor, and rhom-
boideus major muscles are detached from
their origins (inset), taking a small portion of
insertional bone from the medial scapula.
The rhomboid muscles are advanced later-
ally under the infraspinatus and are secured
with suture, which is passed through drill
holes placed 5 cm lateral to the medial bor-
der of the scapula. The levator scapulae is
passed 5 cm laterally and is sutured to the
scapular spine through drill holes.
Bigliani et al5 recently reported
their results with this procedure.
Of 23 patients with trapezius wing-
ing, 87% had good or excellent
results. Significant improvement in
pain was seen in 91% of these
patients, and 87% demonstrated an
improvement in function.
Serratus Anterior Winging
Palsy of the serratus anterior mus-
cle can also cause painful, disabling
scapular winging. The long thoracic
Vol 3, No 6, November/December 1995
nerve originates from the ventral
rami of the C5, C6, and C7 cervical
nerves and travels beneath the
brachial plexus and clavicle over the
first rib. The nerve then travels along
the lateral aspect of the chest wall
superficially, making it susceptible
to injury. Blunt trauma or stretching
of this nerve is particularly common
in athletes and has been reported in
almost every sport.14-16 Repetitive
industrial use of the shoulder has
also been implicated as a cause of ser-
ratus anterior paralysis.17 Penetrat-
ing trauma will rarely cause injury to
this nerve, although surgical proce-
dures such as radical mastectomy,
first-rib resection, axillary lymph-
node dissection, and transaxillary
sympathectomy have been impli-
cated as sources of injury to the long
thoracic nerve.16
The long thoracic nerve can also
be affected by nontraumatic events,
including positioning during anes-
thesia,17 the sequelae of viral ill-
ness,18 inoculations,19 and neuritis
affecting the brachial plexus or the
long thoracic nerve alone.20,21 Even
prolonged bed rest has been
reported to trigger dysfunction of
the long thoracic nerve, particularly
if the arm is abducted while prop-
ping up the head to read.17,22 Since
the long thoracic nerve has its ori-
gin at C7, patients with C7 radicu-
lopathy may also manifest serratus
anterior weakness and scapular
winging.23
With an injury to the long thoracic
nerve, the scapula assumes a posi-
tion of superior elevation and
medial translation, and the inferior
pole is rotated medially (Fig. 1, B).
Patients will complain of pain as the
other periscapular muscles try to
compensate for the serratus weak-
ness. More severe pain may indicate
acute brachial plexus neuritis or Par-
sonage-Turner syndrome, which
may affect the long thoracic nerve
alone.21 The patient will have diffi-
culty with arm elevation above 120
John E. Kuhn, MD, et al
degrees, which will magnify the
degree of winging. Pain may be
increased with this maneuver and
when the head is tilted toward the
contralateral shoulder.
Electromyography is recom-
mended to confirm the diagnosis.
Electromyographic examinations at
3-month intervals have also been
recommended to follow nerve
recovery.22,24
Range-of-motion exercises to
prevent adhesive capsulitis of the
shoulder should be implemented
immediately on diagnosis. Many
types of braces and orthotic devices
have been developed.20 They may
have some role, but often their cum-
bersome nature overshadows symp-
tom relief.22 Most injuries of the long
thoracic nerve recover sponta-
neously within 1 year,15,17,20,22,25 but
recovery may take up to 2 years.26
There is little data in the literature
regarding the results of neurolysis,
nerve grafting, or nerve repair of an
injured long thoracic nerve. Never-
theless, penetrating injuries should
be treated with nerve exploration
and early repair. Neurorrhaphy may
be indicated when the lesion can be
localized.22 Patients with persistent
impairment of the serratus anterior
are often able to compensate, and
most do not require surgical recon-
struction.22 For patients who have
had symptomatic serratus winging
for more than 1 year and whose
EMG studies show total denerva-
tion, surgical options may be offered
to alleviate pain and improve func-
tion.
Like the surgical treatments for
trapezius winging, the operations for
serratus paralysis can be classified
into three types: scapulothoracic
fusions,9 fascial sling suspensions,7
and muscle transfers. A variety of
muscle-transfer operations have
been described; these include the use
of the pectoralis minor, the pec-
toralis major, the sternocostal head
of pectoralis major, the clavicular
321
Scapular Winging

head of the pectoralis major, the

teres major, the rhomboid muscles,
and combinations of these muscles.
Scapulothoracic fusions for serra-
tus winging have been discouraged
by some,20 primarily because of the
associated inherent loss of motion,
as well as the magnitude of the
surgery. Pain relief, however, is a
reasonable expectation.9 Complica-
tions of scapulothoracic fusions are
many and include nonunion and
pneumothorax.9 For these reasons,
as well as the limited expectations
with regard to motion, scapulotho- B
racic fusions have been generally A
reserved for salvage operations after
failure of other techniques and for
treating patients with paralysis of
other shoulder girdle muscles in
addition to the serratus anterior.24
Although controversial, a primary
scapulothoracic fusion may also be
considered for the laborer with
disabling serratus winging who
places heavy demands on the
shoulder.26
Fascial-sling suspensions to cor-
rect serratus winging have been
advocated by some.7,27 However,
there are significant concerns about
sling failure and recurrence of wing- C
ing.10 For these reasons, muscle
D
transfers for dynamic scapular stabi-
lization have gained broader accep-
Fig. 3 Marmor-Bechtol transfer of the ster-
tance. nocostal head of the pectoralis major, used
Of the variety of muscle transfers to treat serratus anterior paralysis.28 A, With
that have been described, transfer of the patient in the lateral decubitus position,
an incision is made, crossing the axilla from
the sternocostal head of the pec- the pectoralis major muscle anteriorly to the
toralis major with a fascia lata graft inferior tip of the scapula. B, The ster-
extension28 (Fig. 3) is probably the nocostal head of the pectoralis major is
released from its insertion on the bicipital
most popular.22,24,25,29 In this tech- groove of the humerus, leaving the clavicu-
nique,24,28,29 the patient is placed in lar head intact. C, A graft of fascia lata mea-
the lateral decubitus position with suring 7 by 2 inches is harvested from the
ipsilateral leg and sutured into a 7-inch-long
use of a beanbag, and the involved tube. Graft is then sutured to the distal por-
arm and forequarter are prepared tion of the freed pectoralis tendon. D, A
and draped. An incision is made, foramen is made in the inferior angle of the
scapula. E, The graft is inserted through this
crossing the axilla from the pectoralis foramen and sutured to itself under moder-
major muscle anteriorly to the infe- ate tension.
rior tip of the scapula. The ster-
nocostal head of the pectoralis major E
is released from its insertion on the
bicipital groove of the humerus,

322 Journal of the American Academy of Orthopaedic Surgeons


leaving the clavicular head intact. A
graft of fascia lata measuring 7 by 2
inches is harvested from the ipsilat-
eral leg and sutured into a 7-inch-
long tube. This graft is then sutured
to the distal portion of the freed pec-
toralis tendon. After the inferior bor-
der of the scapula has been exposed,
a foramen is made in the inferior
angle. The graft is inserted through
this defect and sutured to itself under
moderate tension. Postoperatively,
the arm is placed in a sling, and pas-
sive motion is started after 4 weeks.
Active motion is begun at 6 weeks
and strengthening at 12 weeks.
Although there are few large series in
the literature, results with this tech-
nique have been encouraging, with
70% to 91% success rates, defined on
the basis of normal shoulder motion
and a significant reduction in pain
and winging.16,24,25,29
Rhomboideus Major and Rhomboideus
Minor Winging
Weakness of the greater and
lesser rhomboid muscles is a rare
source of scapular winging. These
muscles are innervated by the dorsal
scapular nerve, which takes its ori-
gin from the C5 nerve root. The dor-
sal scapular nerve passes deep to or,
in some patients, through the levator
scapulae on its way to the rhomboid
muscles. A C5 radiculopathy or an
injury to the dorsal scapular nerve
may produce rhomboid weakness
and scapular winging.30 Patients
may complain of pain along the
medial border of the scapula. The
winging produced by rhomboideus
palsy at rest is usually minimal but
may appear similar to trapezius
winging, with the shoulder slightly
depressed, the scapula laterally
translated, and the inferior angle
rotated laterally.
On physical examination, atro-
phy may be evident along the
medial border of the scapula. Dur-
ing arm elevation, the inferior angle
of the scapula is pulled downward
Vol 3, No 6, November/December 1995
and laterally by the unopposed ser-
ratus anterior muscle.27 With weak-
ness of the rhomboid muscles, the
winging is accentuated when the
arm is slowly lowered from the for-
ward elevated position. The inferior
angle of the scapula is pulled later-
ally and dorsally.30 The patient will
also have difficulty pushing the
elbow backward against resistance
with the hands on the hips.
Treatment of rhomboideus wing-
ing consists of trapezius-strength-
ening exercises. Although no
muscle-transfer operations have
been described for rhomboideus
palsy, the patient with significant
symptoms for whom conservative
therapy has proved a failure may be
helped by a fascial-sling operation,
as described by Dickson.7,27 In this
operation, two fascia lata grafts are
tubularized and used to connect the
lower vertebral border of the
scapula to the spinal muscles and the
inferior angle of the scapula to the
fibers of the latissimus dorsi. This
procedure is thought to be useful in
stabilizing the scapula and partially
arresting the high thoracic scoliosis
that may occur with rhomboideus
and levator scapulae paralysis.27
Osseous Origin
Osteochondromas, the most
common scapular tumors, can be a
cause of “pseudowinging.”14 Rib osteo-
chondromas may also cause the
deformity.14 This type of winging is
structural and may be associated
with scapular crepitus. The winging
may not change when the position
of the arm is varied. The EMG find-
ings will be normal in patients with
such osteochondromas; however,
the lesion can be identified on radio-
graphs obtained tangential to the
plane of the scapula or on computed
tomograms. Winging is alleviated
with resection of the abnormal bone.
Malunions of scapular fractures
have also been implicated as a
source of primary winging. 31
John E. Kuhn, MD, et al
Because muscle function is not
impaired, affected patients may not
be symptomatic.
Muscular Origin
Muscle abnormalities that cause
winging include traumatic ruptures
and congenital absence of periscapu-
lar muscles. In patients with serra-
tus anterior muscle avulsion,
significant trauma has occurred,
which pulls the muscle insertion
from the medial border of the
scapula.17,32-34 Fiddian and King 14
reported the case of a patient in
whom serratus anterior division
occurred during thoracotomy,
which produced symptomatic wing-
ing. In this situation, early nerve-
conduction studies may be normal,
and magnetic resonance imaging
should be considered to assist in the
diagnosis. Surgical reattachment is
recommended in all cases, and excel-
lent results can be expected.17,32,34
However, the combination of ad-
vanced age and systemic disease
may be a contraindication to sur-
gery.33
Congenital absence of the serra-
tus anterior,35 the trapezius,36 and
the rhomboideus major and trapez-
ius muscles36 have all been reported
as causes of scapular winging.
Patients with these congenital anom-
alies seem to function very well
without treatment.36
Bursal Origin
The articulation between the
scapula and the thorax is character-
ized by bursae, which in rare cir-
cumstances may become inflamed,
causing scapular crepitus and pain.
In one study,37 winging was identi-
fied in 50% of patients with a symp-
tomatic snapping scapula and no
bone abnormalities. This type of
winging is presumably related to
subscapular bursitis. With treat-
ment of the bursitis, either by
nonoperative means or surgical bur-
sectomy, the winging resolves.
323
Scapular Winging
Asymptomatic scapulothoracic
crepitus also exists but is usually not
associated with scapular winging.
Secondary Scapular
Winging
Secondary scapular winging orig-
inates from disorders of the
glenohumeral joint that produce
abnormal scapulothoracic dynam-
ics. This phenomenon has not been
thoroughly investigated in the pub-
lished literature.
A thorough evaluation of the
patient with secondary scapular
winging will usually, but not always,
identify the source as a glenohumeral
or subacromial disorder.38 When
examining any patient with a shoul-
der condition, secondary scapular
winging should be sought with the
shoulder at rest, with dynamic for-
ward elevation, and with resisted for-
ward elevation. One would expect a
patient with secondary scapular
winging to have normal findings on
EMG and nerve-conduction exami-
nations of the long thoracic nerve and
serratus anterior muscle, the spinal
accessory nerve and trapezius mus-
cle, and the dorsal scapular nerve and
rhomboid muscles.
In contractural winging, contrac-
tures about the glenohumeral joint
produce secondary scapular winging.
Patients with obstetric shoulder
trauma may develop contractures
due to unbalanced muscle forces with
the humerus abducted and internally
rotated relative to the scapula. When
the arm is forcibly adducted to the
chest wall and externally rotated, the
superior corner of the scapula projects
away from the chest wall at the upper
margin of the trapezius, producing
the “scapular sign of Putti.”39
Contractural winging can also
occur with fibrosis of the deltoid.40
This type of winging decreases when
the arm is raised and increases when
it is lowered. Fibrosis of the deltoid
324
muscle is thought to be either con-
genital41 or related to a history of
injections,42 and is almost always
associated with scapular winging.42
Common disorders involving the
glenohumeral joint can also be a
cause of secondary scapular winging.
The mechanism is thought to be due
to reflex muscle spasm provoked by
some painful condition in the gleno-
humeral or subacromial area. 40
Winging has been associated with
rotator cuff tears,40 nonunion of
acromion fractures,15 malunion of
clavicular fractures,14 fractures of the
glenoid, 14 osteonecrosis of the
humeral head, 15 acromegalic ar-
thropathy of the shoulder,14 acromio-
clavicular joint disorders,14,38 and
shoulder instability.14,38 In our prac-
tice, we have observed secondary
scapular winging in patients with
adhesive capsulitis, the impingement
syndrome, anterior shoulder instabil-
ity, posterior shoulder instability,
and multidirectional shoulder insta-
bility. We have also encountered sec-
ondary impingement due to subtle
shoulder instability in throwing ath-
letes.
Winging frequently accompanies
the asynchronous shoulder motion
seen in patients with voluntary pos-
terior shoulder subluxation. If the
scapula is forcibly held against the
chest wall, preventing winging, the
patient may have difficulty sublux-
ating the shoulder.
Patients with painful shoulders
may reflexively limit glenohumeral
motion. This forces the periscapular
muscles to work in excess, because
scapulothoracic motion must in-
crease to compensate for the limited
glenohumeral motion. With fatigue
of the periscapular muscles, particu-
larly the serratus anterior, trapezius,
and rhomboid muscles, secondary
scapular winging occurs. As has
been shown,38,40 treatment of the pri-
mary glenohumeral disorder will
alleviate the scapular winging; con-
versely, scapular winging is unlikely
Journal of the American Academy of Orthopaedic Surgeons
to improve until the primary prob-
lem is addressed.38 Nevertheless, in
every patient with secondary scapu-
lar winging, a scapular rehabilita-
tion program should be added to the
treatment of the primary gleno-
humeral disorder to facilitate re-
covery.
Voluntary Scapular
Winging
Voluntary scapular winging is very
rare.14,15,38,43 In fact, the largest series
is Rowe’s report of four cases.43 The
patients were reassured and in-
structed on the normal muscle-firing
patterns of the shoulder, with
“instructions not to tighten or con-
tract their shoulder muscles when
elevating the arm.” All four recov-
ered after this coaching. In another
report, Gregg et al15 described
asymptomatic bilateral voluntary
scapular winging in an orthopaedic
resident. It is important to appreciate
that patients with voluntary scapular
winging who seek medical attention,
like patients with voluntary subluxa-
tion of the shoulder, may have unad-
dressed psychological issues that
complicate their care.
Summary
A variety of disorders can cause
scapular winging. An understand-
ing of these disorders and an appre-
ciation of the physical examination
findings will prevent misdiagnosis
and assist in directing treatment.
For most patients, conservative
treatment, which includes scapular
rehabilitation emphasizing range of
motion and periscapular muscle
strengthening, will alleviate symp-
toms. If symptoms persist despite
adequate time and conservative
treatment, one should consider the
surgical options, which are capable
of resolving pain and winging.

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325
 Genu Varum in Children: Diagnosis and Treatment

Werner C. Brooks, MD, and Richard H. Gross, MD

Abstract

Genu varum is a relatively common finding in children. Physiologic bowing, amined in the frontal and sagittal
which is seen most often, has a well-documented favorable natural history. Idio- planes for asymmetry and align-
pathic tibia vara is the most common of the pathologic conditions that are associ- ment. It should then be determined
ated with bowed legs; treatment strategies vary with the patient’s age and the stage whether the deformity is a gradual
of disease and deformity. Genu varum may also accompany systemic conditions, bowing or an abrupt angulation. If
such as achondroplasia, vitamin D–resistant rickets, renal osteodystrophy, and the deformity is angular, its loca-
osteogenesis imperfecta—all of which can result in short stature. Indications for tion is identified in the distal femur,
intervention are not always well defined. A rare disorder, focal fibrocartilaginous the knee, or the proximal tibia.
dysplasia, usually requires no treatment. Standing radiographs of the entire lower Obliquity of the popliteal crease, if
limbs are necessary for surgical planning, as the deformity can sometimes affect present, is a useful sign; distal
the distal femur rather than the proximal tibia. Restoration of the mechanical axis femoral varus will produce obliq-
of the limb is the principal goal of treatment; the particular type of internal fixa- uity of the popliteal crease, while
tion is of secondary importance. deformity more distal in the ex-
J Am Acad Orthop Surg 1995;3:326-335 tremity will not.
Passive rotation of the hips and
motion of the knee are noted. Liga-
mentous stability of the knee is as-
Genu varum, known colloquially as may be a good source for this infor- sessed, with particular attention to
bowlegs, is relatively common in mation. The ages at attainment of the lateral ligamentous complex. A
children and is a frequent cause of various developmental milestones, dynamic component of the defor-
parental concern. In the vast major- such as sitting independently, mity or lateral thrust at the knee dur-
ity of cases, genu varum will correct pulling to stand, and walking, ing the stance phase of gait indicates
with growth. A small number of should be determined. It is useful to laxity of the lateral ligamentous
children have pathologic conditions establish whether the parents con- complex. Torsion of the tibia should
that may result in functional and sider the deformity to be progres- also be routinely assessed; determi-
cosmetic problems if left untreated. sive. The positional sleeping and nation of the thigh-foot angle and
In this article, we will review perti- sitting habits of the child are also of evaluation of the bimalleolar axis, as
nent factors in the assessment of interest. described by Staheli et al,1 are useful
genu varum, associated conditions,
and treatment options. Physical Examination
After routine documentation of Dr. Brooks is a Resident in the Department of Or-
the height and weight and determi- thopaedic Surgery, Medical University of South
Carolina, Charleston. Dr. Gross is Professor of
Assessment nation of their percentiles for age,
Orthopaedic Surgery and Pediatrics, Medical
the patient’s pelvis, knees, and feet University of South Carolina.
History should be examined carefully.
A thorough history will often dis- Shortening of the limbs relative to Reprint requests: Dr. Gross, Department of Or-
tinguish the relatively infrequent the trunk, especially rhizomelic thopaedic Surgery, Medical University of South
pathologic genu varum from the shortening, suggests a dwarfing Carolina, 171 Ashley Avenue, Charleston, SC
condition. In ambulatory children, 29425.
much more common physiologic va-
riety. A family history of short the appearance while standing and
Copyright 1995 by the American Academy of Or-
stature or similar varus alignment during gait provides the most infor- thopaedic Surgeons.
should be sought; the grandparents mation. Both limbs should be ex-

326 Journal of the American Academy of Orthopaedic Surgeons


in torsional assessment. Serial pho-
tographs of the standing child at the
initial and follow-up evaluations
serve as an inexpensive method of
documenting any progression of the
deformity.
Radiographs
We believe radiographs are un-
necessary in a young child of normal
stature with physical findings com-
patible with physiologic bowing.
When there is a localized deformity
or the child is short, full-length
standing radiographs (hip to ankle)
should be obtained with the knees
pointing straight forward. When in-
ternal tibial torsion is present, the
technician often attempts to exter-
nally rotate the leg (and the knee) to
point the foot straight forward;
however, rotation affects the
tibiofemoral and metaphyseal-dia-
physeal angles and tends to minimize
the degree of deformity.2 In addition
to the angular deformity present, the
physes of the femur and tibia should
be carefully assessed.
Physiologic Genu Varum
Physiologic genu varum is by far the
most common cause of bowlegs in a
toddler. The natural history of the
changing angular relationship be-
tween the femur and the tibia in chil-
dren is required knowledge for any
orthopaedist with a pediatric prac-
tice. Development of the tibio-
femoral angle follows a predictable
sequential pattern. Infantile genu
varum progresses to excessive genu
valgum, followed a gradual correc-
tion to adult physiologic valgus
alignment (Fig. 1). Genu varum is
greatest at 6 months of age. Correc-
tion to neutral alignment is often
complete by 18 months of age.
Heath and Staheli3 report that per-
sistence of genu varum beyond 2
years of age is abnormal, and Sale-
nius and Vankka4 state that neutral
Vol 3, No 6, November/December 1995
Werner C. Brooks, MD, and Richard H. Gross, MD
+20°
+15°
Varus
+10°
+5°
0°
-5°
Valgus
-10°
-15°
1 2 3 4 5 6 7 8 9 10 11 12 13
Age, yr
Fig. 1 Graph illustrating the development of the tibiofemoral angle in children during
growth, based on measurements from 1,480 examinations of 979 children. Of the lighter lines,
the middle one represents the mean value at a given point in time, and the other two repre-
sent the deviation from the mean. The darker line represents the general trend. (Adapted
with permission from Salenius P, Vankka E: The development of the tibiofemoral angle in
children. J Bone Joint Surg Am 1975;57:259-261.)
alignment may not be reached until bowing without an acute angular
22 to 24 months of age. Even pro- component. The physis will appear
nounced physiologic genu varum normal without medial physeal
greater than 30 degrees can correct changes. There may be equal
with continuing growth.3 Overcor- beaking of both the distal femoral
rection to excessive genu valgum is and the proximal tibial metaphyses.
maximal at 4 years of age; the valgus The treatment of physiologic
angulation averages 8 degrees. Cor- genu varum is periodic observation
rection to physiologic valgus is usu- and examination, together with edu-
ally complete by 5 or 6 years of age.4 cation and reassurance of the par-
Early walking has been docu- ents. Occasionally, spontaneous
mented in black children,5 and this correction of the physiologic genu
may be a factor in a tendency toward varum will be delayed. We believe
increased physiologic bowing. In- this happens more often in children
ternal tibial torsion is frequently who habitually sleep or sit with their
found in association with physio- legs rotated beneath them, as this
logic genu varum; if physiologic, it seems to counteract the normal un-
corrects concomitantly with the winding effect of weight-bearing in
genu varum. correcting tibial torsion and genu
Radiographically, physiologic varum.
genu varum is characterized by Reassurance of anxious parents
bowing of the entire limb. On the or other relatives of a child with
standing anteroposterior radio- physiologic bowing is not always
graph, both the distal femur and the easy to achieve. We find that giving
proximal tibia will have some varus a copy of a graph depicting the nor-
327
Genu Varum in Children
mal progression of genu varum to
genu valgum in early childhood,
along with the orthopaedist’s expla-
nation of the graph, is extremely
helpful. The parents can then show
the graph to other concerned rela-
tives. In addition, the American
Academy of Orthopaedic Surgeons
has produced a video on common
lower-limb problems in children
(“Growing Out of It: Torsional De-
formities in Children” [No. 29-074]),
which can be viewed independently
by the family.
Tibia Vara
History
Tibia vara, often referred to as
Blount’s disease, is characterized by
an abrupt varus deformity of the
proximal tibia. It is the most fre-
quent cause of pathologic genu
varum. Unlike physiologic genu
varum, Blount’s disease is progres-
sive and rarely corrects sponta-
neously. There are two predominant
types of tibia vara—infantile and
late-onset, or adolescent—which are
distinguished by the age at onset
and the distinctive clinical presenta-
tion. While the two types are simi-
lar in the histologic appearance of
the proximal tibial physes, the exact
etiologies remain somewhat un-
clear.
Tibia vara is classified as infantile
when the onset occurs before 5 years
of age. Idiopathic infantile tibia vara
is more often seen in black, female,
and obese children and in children
who begin to walk earlier than
usual. Involvement is bilateral in
80% of patients and is associated
with a greater degree of internal tib-
ial torsion than in the adolescent
form. There may be difficulty in dis-
tinguishing early infantile tibia vara
from physiologic genu varum.
Children in whom significant
tibia vara develops after 6 years of
age are thought to have the late-onset
328
form, which is less common than the
infantile type. Late-onset tibia vara
is more often unilateral and has a
greater prevalence in black, male,
and obese children and teenagers. In
his study of the natural history of
tibia vara in Finnish children, Lan-
genskiöld6 reported more rapid pro-
gression of the varus deformity in
the infantile type than in the late-onset
type. The prevalence of morbid obe-
sity in adolescents has increased in
the United States,7 and there appears
to be an associated increase in the in-
cidence of late-onset tibia vara.
Children in whom pathologic
tibia vara later develops are born
with normal alignment of the femur
and tibia; the deformity results from
a subsequent growth disturbance of
the proximal tibia. Tibia vara does
not occur in children who do not
walk. While the exact etiology of in-
fantile tibia vara remains unclear, an
association between tibia vara and
walking at an early age and obesity
in infancy suggests that mechanical
forces are at least partially causative.
Early weight-bearing and obesity re-
sult in greater compressive forces
across the medial tibial physis than
in infants who are not obese and
who begin walking at about 1 year of
age. The compressed posteromedial
physis responds with slower growth
in this region, producing a progres-
sive varus deformity of the proximal
tibia.
In the late-onset type, there is
usually a mild preexisting varus de-
formity, which is thought to be a
factor in the development of a pro-
gressive varus deformity. When
mild genu varum persists into ado-
lescence, increased body weight and
physical activity repetitively trau-
matize the posteromedial physis,
causing medial growth suppres-
sion.8
Cook et al9 performed a two-di-
mensional finite-element analysis of
the effect of varus angulation and in-
creased body weight on resultant
Journal of the American Academy of Orthopaedic Surgeons
forces on the medial proximal tibial
physis and found that in older chil-
dren, lesser degrees of varus were
necessary to produce medial phy-
seal growth retardation. In a 2-year-
old, 20 degrees of varus could
produce medial tibial physeal
growth inhibition; in a 5-year-old of
normal weight, as little as 10 degrees
of varus angulation could result in
growth inhibition.
Assessment
Examination of the child with
tibia vara is notable for an angular
varus deformity discernible just be-
low the knee. In morbidly obese
children, the acute angulation of the
tibia may be hidden by their exces-
sive soft tissue. In contrast, the
young child with physiologic genu
varum will have a more gentle cur-
vature of the entire extremity. An in-
wardly directed thigh-foot angle
due to internal tibial torsion may ac-
company either of these conditions,
but is more severe in infantile tibia
vara. A lateral thrust, indicating lax-
ity of the lateral ligamentous com-
plex, may be seen in children over
the age of 3 with tibia vara. This lax-
ity is thought to exacerbate the dy-
namic forces across the physis
during gait and is not seen in physi-
ologic bowing.
Pathology
The histopathologic findings in the
physes are the same whether the child
has infantile or late-onset tibia vara.8,10
The physeal disruption is similar to
that found in slipped capital femoral
epiphysis, which may suggest a com-
mon etiology. Disorganized physeal
cartilage is present, with disruption of
the normal columnar architecture of
the physis, which is most evident in
the resting zone. Islands of densely
packed, unusually hypertrophic carti-
lage cells are seen. Both fibrovascular
and cartilaginous reparative tissue
can be found at the physeal-metaphy-
seal junction.
 Werner C. Brooks, MD, and Richard H. Gross, MD

Radiographs
The characteristic radiographic
appearance of tibia vara is not usu-
ally present until the age of 2 years.
The radiographic classification de-
veloped by Langenskiöld6 is most of-
ten used to stage the infantile forms
of the disease (Fig. 2). The potential
for recovering growth after treat-
ment is thought to be directly related
to the stage of the disease, although
this staging may be more pertinent
in a retrospective review than
prospectively.
Medial fragmentation of the
proximal tibial metaphysis is the
earliest abnormal radiographic find-
ing. Later, medial physeal depres-
sion and varus angulation of the
metaphysis develop, with beaking
of the proximal tibial metaphysis. In
very late stages of Blount’s disease,
the medial physis develops an os-
seous bridge between the epiphysis
and the metaphysis.
As with the use of many classifi-
cation systems, there is considerable
interobserver variation, and the
staging is not precise. However, the
system does provide the user with
some notion of the natural history of
progression of the condition.
Whether a given tibia demonstrates
stage III or stage IV changes is less
important than is the recognition
that tibia vara is well established and
the treatment that might be appro-
priate for stage I or II is no longer
appropriate.
In late-onset tibia vara, the radi-
ographic changes are less dramatic.
The growth plate shows less irregu-
larity and rarely forms the physeal
bone bridge that may be seen in the
infantile form. The epiphysis is less
deformed, producing less articular
incongruity. Overgrowth of the lat-
eral femoral condyle is common,
and distal femoral varus may be pre-
dominant.11
Levine and Drennan12 have popu-
larized measurement of the metaph-
yseal-diaphyseal angle of the
proximal tibia for the early differen-
tiation of infantile tibia vara from
physiologic genu varum. This angle
is formed by a line drawn perpen-
dicular to the tibial diaphysis and a
line drawn between the medial and
lateral aspects of the tibial metaph-
ysis (Fig. 3). A metaphyseal-diaphy-
seal angle greater than 11 degrees is
strongly associated with subsequent
development of tibia vara. In their
study, Levine and Drennan found
that 29 of 30 affected limbs with a
metaphyseal-diaphyseal angle over
11 degrees developed advanced
radiographic changes consistent
with the diagnosis of tibia vara, with
a false-positive rate of only 3%. In
contrast, tibia vara developed in
only 3 of 59 limbs with metaphyseal-
diaphyseal angles of less than 11 de-
grees.
Feldman and Schoenecker 2
found the metaphyseal-diaphyseal
angle to be somewhat less reliable
in younger patients. On linear-
regression analysis of the use of a
metaphyseal-diaphyseal angle of 11
degrees or more as a basis for de-
ciding treatment, they found a
false-negative rate of 9% and a
false-positive rate of 33%.
With increasing age, the metaph-
yseal-diaphyseal angle is more reli-

Fig. 2 The six stages of tibia vara, as described by Langenskiöld.6 Stage I (seen in children up to age 3 years) is characterized by medial and
distal beaking of the metaphysis and irregularity of the entire metaphysis. Stage II (seen in children aged 21⁄2 to 4 years) is characterized by a
sharp lateromedial depression in the ossification line of the wedge-shaped medial metaphysis. Complete restoration is common in this stage.
Stage III (seen from ages 4 to 6 years) is characterized by deepening of the metaphyseal beak, which gives the appearance of a step in the me-
dial metaphysis. Stage IV (seen from ages 5 to 10 years) is characterized by enlargement of the epiphysis, which occupies the medial me-
taphyseal depression. Restoration is still possible in this stage. Stage V (seen from ages 9 to 11) is characterized by a cleft in the epiphysis,
which gives the appearance of a double epiphysis; the articular surface of the medial tibia is deformed, sloping distally and medially from
the intercondylar region. Stage VI (seen from ages 10 to 13) is characterized by closure of the medial proximal tibial physis, with a normal
lateral physis. Langenskiöld described his findings on the basis of his observations of Finnish children; changes in African-American chil-
dren tend to occur at a younger age.

Vol 3, No 6, November/December 1995 329

Genu Varum in Children
CALLOUT NEEDED
Fig. 3 Determination of the metaphyseal-
diaphyseal (MD) and tibial-femoral (TF) an-
gles.
able, since it tends to increase in
magnitude in patients who have
Blount’s disease and decrease in
magnitude in patients with physio-
logic genu varum. Rotation can
have a small but significant effect on
the radiographic measurement of
the metaphyseal-diaphyseal angle.
Henderson et al13 compared radio-
graphs obtained with and without
rotation and found a difference of 2.8
± 1.2 degrees in the metaphyseal-
diaphyseal angles that were measured.
When attempting to distinguish
physiologic genu varum from tibia
vara in young patients, this amount
of measuring error can be mislead-
ing if one is relying on the metaphy-
seal-diaphyseal angle alone for the
diagnosis. If there is doubt regard-
ing the radiographic findings, we be-
lieve a further period of observation
is indicated, rather than initiating
treatment on the basis of blind ad-
herence to arbitrary radiographic
measurements.
Treatment
There are still no generally ac-
cepted criteria for initiation of treat-
ment in infantile tibia vara.
330
Although Levine and Drennan12 re-
ported that a metaphyseal-diaphy-
seal angle of 11 degrees could be
used as a basis for treatment, others
have recommended observation of
children aged less than 24 months
with metaphyseal-diaphyseal angles
of as much as 16 degrees.2 Persistent
internal tibial torsion, lateral thrust
during stance phase in gait, and pos-
terolateral instability are additional
findings that may influence a deci-
sion to initiate early treatment.
There is certainly a place for ob-
servation of the young child with ab-
normal clinical and radiographic
findings before initiating brace or
surgical treatment. A child with a
metaphyseal-diaphyseal angle of
less than 9 degrees is obviously at
minimal risk for tibia vara. If the an-
gle is greater than 16 degrees, treat-
ment probably should be initiated.
Children with metaphyseal-diaphy-
seal angles between 9 and 16 degrees
are generally treated if there has
been no tendency toward correction
after 24 months of age.
While early tibia vara will correct
without bracing in some children
(Fig. 4), bracing has often been rec-
ommended as the initial treatment of
children with Langenskiöld stage I or
II tibia vara. The device usually pre-
scribed is a knee-ankle-foot orthosis
with a single medial upright secured
at the upper thigh and ankle. A knee
hinge is not used, but this does not
prevent the child from sitting. The
ankle is left free. A strap at the knee
applies a corrective valgus force. The
brace is worn nearly full-time, espe-
cially during walking, to minimize
the valgus stress at the knee. The ef-
fectiveness of the brace is thought to
be related to the relief of weight-
bearing stresses on the medial phy-
seal region of the proximal tibia.
Brace treatment is reported to be suc-
cessful in 50% to 80% of the patients
treated.14,15 The brace is worn until
the deformity has been corrected and
reconstitution of medial physeal
Journal of the American Academy of Orthopaedic Surgeons
growth is present on radiographs,
which usually takes about 1 year.
Thus, bracing is usually not a viable
option for children over the age of
3.16 Factors such as patient age, stage
of the disease, family compliance,
and brace fit can have an effect on the
success of bracing. Studies control-
ling for all these variables have not
yet been reported. However, it
seems that bracing is a reasonable
first treatment option when a deci-
sion is made to start treatment of
early tibia vara in a 2- or 3-year-old
child.
Children who are too old for brac-
ing and children in whom tibia vara
has progressed despite bracing are
best treated with a proximal tibial
valgus osteotomy. The goal of the
osteotomy is to restore the mechani-
cal axis of the lower extremity. The
osteotomy is performed below the
tibial tubercle apophysis and is com-
bined with a fibular osteotomy.
Ideally, the osteotomy is done be-
fore the child is 4 years old. Residual
internal tibial torsion can be cor-
rected at the same time. If os-
teotomies are first done in older
children, repeat osteotomies are
more often needed. Ferriter and
Shapiro17 retrospectively analyzed
factors affecting the outcome of 77
proximal tibial osteotomies per-
formed on 25 patients with tibia vara
and found a 76% rate of deformity
recurrence in children operated on
after the age of 4.5 years. In younger
children, the rate of recurrence of
varus deformity was 31%.
Loder and Johnston14 reported
lower rates of recurrent deformity
after valgus tibial osteotomy. Prog-
nostic factors associated with a
higher rate of recurrence in their
older patients included morbid obe-
sity and more severe disease (Lan-
genskiöld stages IV, V, or VI).
Efforts to improve the results of
tibial osteotomy as treatment of in-
fantile tibia vara in children older
than 4 years include physeal-bar re-

A B
D E
section and lateral proximal tibial
hemiepiphysiodesis (Fig. 5). These
procedures were developed with an
understanding that recurrence of the
deformity is largely due to the lack
of reconstitution of growth of the
medial proximal tibial physis.
Physeal bridges are more com-
mon in children with infantile tibia
Vol 3, No 6, November/December 1995
Werner C. Brooks, MD, and Richard H. Gross, MD
vara who are older than 5 years. The
presence of a physeal bridge may be
impossible to ascertain on routine
radiographs. Computed tomogra-
phy or magnetic resonance imaging,
with thin sections obtained through
the physis, can be helpful in detect-
ing the presence and size of the os-
seous bridge.
C
Fig. 4 A, Clinical appearance of a healthy
boy, aged 1 year 9 months, being evaluated
for infantile tibia vara. B, Initial radiograph
shows medial tibial physeal beaking and me-
taphyseal-diaphyseal angles of 17 degrees
on the left and 12 degrees on the right. Ob-
servation without bracing was elected at that
time. C, Radiograph obtained at age 2 years
3 months shows persistent medial tibial
beaking and irregularity of the proximal tib-
ial physes, greater on the left than the right.
D, Normal tibial alignment was seen at age 4
years 10 months. E, Clinical appearance at
age 4 years 10 months.
Physeal-bridge resection is a diffi-
cult operative procedure due to the
deformity of the physis, and the poor-
est results have been associated with
involvement of more than 30% of the
physis.16 Fat, cartilage, Silastic, and
methylmethacrylate have all been
used as spacers to prevent bridge re-
currence after surgical resection. Fa-
331
Genu Varum in Children

A B C

Fig. 5 A, Radiograph of a 7-year-old girl with unilateral varus deformity and severe depression of the medial tibial physis. B, A corrective
closing-wedge proximal tibial osteotomy was performed, with stapling of the lateral proximal tibial physis. C, On radiograph obtained at 2-
year follow-up examination, alignment is normal, with minimal leg-length discrepancy.

vorable outcomes in small series of
patients have been reported.14,18 Ac-
tual growth, however, is difficult to
determine from the published radio-
graphs, and our personal experience
with this procedure has been poor. A
rim of viable physis surrounding the
excised portion is necessary if growth
is to recover after partial physeal re-
section. It may not be possible to de-
termine on gross examination at the
time of surgery whether the remain-
ing physeal rim is biologically active.
The use of lateral hemiepiphys-
iodesis of the proximal tibial physis
is an attractive treatment alternative
in the older child with tibia vara at
risk for redevelopment of varus de-
formity after proximal tibial os-
teotomy alone. A formal ablation of
the lateral tibial physis or simple sta-
pling can be done (Fig. 5). When
done unilaterally, a limb-length dis-
crepancy is predictable in younger
patients; however, treatment of this
inequality may not be needed.15
In advanced forms of infantile
tibia vara (Langenskiöld stage IV or
greater), resultant deformity of the
tibial epiphysis, as well as the physis,
produces articular incongruity.
Restoration of normal articular
anatomy by elevation of the de-
pressed medial epiphysis and physis
has been reported to reconstruct the
joint architecture, generally in com-
bination with a valgus tibial os-
teotomy to restore the alignment of
the lower limb.19 Medial elevation
combined with proximal tibial os-
teotomy (and occasionally distal
femoral osteotomy) has been utilized
with success by Schoenecker et al.15
For patients with late-onset tibia
vara, the indication for treatment has
been defined arbitrarily as varus
alignment greater than approxi-
mately 10 degrees. The goal of
surgery is correction of the mechani-
cal axis to prevent the development of
medial knee-compartment osteo-
arthrosis. Young adults with tibia
vara have a high incidence of acceler-
ated symptomatic degenerative
changes of the knee, which is related
to the degree of varus malalignment.20
Treatment of the adolescent with
tibia vara often involves increased
technical problems due to morbid
obesity. Complications are more
common than in the treatment of in-
fantile tibia vara. These complica-
tions include difficulty in the
exposure and performance of the os-
teotomy and failure of osteotomy
fixation. For these reasons, Hender-
son et al21 have proposed lateral
proximal tibial hemiepiphysiodesis
as a primary procedure, reserving
osteotomy for those cases in which
more conservative procedures have
failed. The importance of standing
radiographs of the entire lower
limbs has recently been empha-
sized.11 We believe such radio-
graphs are necessary for proper
preoperative planning and postop-
erative assessment. The literature is
replete with techniques for the per-
formance of the tibial osteotomy in
late-onset tibia vara, including vari-
ous types of internal and external
fixation. Regardless of the method
of fixation chosen, the goals of

332 Journal of the American Academy of Orthopaedic Surgeons


surgery are unchanged: correction of
the mechanical axis and leveling of
the knee joints.
Differential Diagnosis
Vitamin D–Resistant Rickets
Progressive genu varum often de-
velops in children with untreated
hypophosphatemic rickets, a sex-
linked inherited disorder due to vit-
amin D resistance that results in
defective bone mineralization. Chil-
dren with this disorder typically
present with bilateral lower-limb an-
gular deformities. The diagnosis
should be considered if the child is
relatively short, because height in af-
fected children is usually in the
lower 10th percentile. The bowing is
due to a combination of varus of the
distal femur and varus of the proxi-
mal tibia.
Medical treatment of this type of
rickets includes oral phosphates and
some form of vitamin D replacement.
Surgical measures to correct the de-
formity are often unsuccessful when
adequate medical control of the rick-
ets has not been achieved before
surgery. In that situation, it may be
best to wait until skeletal maturity to
realign the mechanical axis.22 When
only partially treated, this condition
may be difficult to distinguish from
physiologic bowing, but children
with rickets typically are older. Mas-
sive doses of a vitamin D preparation
can restore a normal radiographic
appearance to the epiphysis; how-
ever, normal growth will not be
restored unless phosphate replace-
ment is also adequate. Phosphate re-
placement therapy has to be
administered at regular intervals,
and patient compliance with this
strict dosage schedule may be poor.
Renal Failure and Renal
Osteodystrophy
Children who are in renal failure
or who have renal osteodystrophy
Vol 3, No 6, November/December 1995
Werner C. Brooks, MD, and Richard H. Gross, MD
have a high incidence of growth dis-
turbance in both the proximal and
distal ends of the tibia. The physes
in these children have been shown to
exhibit many of the same pathologic
changes found in tibia vara and
slipped capital femoral epiphysis,
particularly disorganized growth
plates at the physeal-metaphyseal
junction.23 Deformity results when
eccentric forces occur across the
weakened physis. Because renal
failure occurs more commonly in
older children who have already
achieved physiologic valgus align-
ment, valgus deformity is encoun-
tered most often at the knee.
Younger children who have retained
physiologic varus alignment may
undergo exaggeration of preexisting
genu varum. Deformities secondary
to renal disease are usually bilateral,
with a gentle curve of the extremity
due to simultaneous involvement of
both the distal femoral and proximal
tibial physes.
Rickets and renal osteodystrophy
may be easily distinguished from
tibia vara on the basis of their radio-
graphic appearance. In both, phy-
seal cupping and widening occur at
both the distal femoral and proximal
tibial physes. Marked osteopenia
and thinning of cortical bone are also
present.
Orthopaedic treatment of angular
lower-limb deformities resulting
from renal disease is wisely post-
poned until the renal status has sta-
bilized in response to medical
treatment or renal transplantation.
Correction of genu varum or valgum
with osteotomy will be short-lived
unless the abnormal bone metabo-
lism resulting from the renal disease
has been reversed.
Metaphyseal Chondrodysplasia
Metaphyseal chondrodysplasia,
which results from abnormal chon-
droblast function and chondroid
production, is a very rare cause of
genu varum. A number of metaph-
yseal dysplasias can lead to bowing,
among them the Jansen and Schmid
types. The more severe Jansen type
has an autosomal-dominant inheri-
tance and is characterized by mental
retardation, short-limb dwarfism,
exophthalmia, hypercalcemia, and
long-bone bowing. The more mild
Schmid type, which is also transmit-
ted by autosomal-dominant inheri-
tance, is characterized by normal
intellect and normal laboratory find-
ings. As lower-extremity bowing
does occur with this condition, it
may be difficult to distinguish from
rickets. Even though the physes are
widened and cupped in the Schmid
type, the epiphyses are normal, and
the presence of short stature should
be helpful in arriving at the correct
diagnosis.
Achondroplasia
Genu varum is a frequent finding
in achondroplasia, a rhizomelic
dwarfing condition due to abnormal
endochondral bone formation. At
birth, lower-limb alignment is rela-
tively normal. However, with
growth, the spontaneous correction
to genu valgum does not occur. In-
stead, genu varum tends to increase
throughout childhood and adoles-
cence, largely due to overgrowth of
the fibula in relation to the tibia. In
addition, the growth of the proximal
tibial metaphysis may be asymmet-
rical. Radiographically, the proxi-
mal fibular physis is superior to the
proximal tibial physis. Although the
tibial metaphysis is enlarged, the
epiphysis remains normal.
Children with achondroplasia
rarely have knee pain, and function-
al indications for surgical correc-
tion of bowlegs are not well defined.
Treatment options include proximal
fibular epiphysiodesis and tibial os-
teotomy. A fibular epiphysiodesis
must be done early in childhood to
prevent the development of progres-
sive genu varum. For established
genu varum, proximal tibial valgus
333
Genu Varum in Children
osteotomy is most often used. An
accompanying distal tibial os-
teotomy and concomitant tibial
lengthening have also been advo-
cated by some. The role of lengthen-
ing of short limbs in this condition is
still unsettled. Bracing is ineffective,
in part because of the joint laxity
commonly present.
Osteogenesis Imperfecta
Osteogenesis imperfecta results
from a defect in type I collagen and
produces varying degrees of skeletal
fragility. In the more severe forms,
multiple fractures of the lower ex-
tremities are common. The femur is
most frequently fractured, followed
by the tibia. Repeated fractures of-
ten lead to bowing and torsional de-
formities of the lower extremity. The
distal third of the femur is a common
location of these fractures, usually
associated with anterolateral angu-
lation at the fracture site. Residual
deformity after fracture is common,
and the varus angulation often in-
creases as a result of repeated frac-
tures. Radiographs demonstrate
diffuse osteopenia, occasionally ac-
companied by evidence of fracture
healing at multiple locations.
In cases of mild deformity, bracing
can be used for support and prophy-
laxis against repeat fractures. Occa-
sionally in more severe cases,
pronounced bowing is present from
birth, and ambulation will not be pos-
sible unless correction is undertaken
early. There are a number of options
for the surgical management of varus
deformity secondary to osteogenesis
imperfecta; selection is dependent on
the age of the patient and the nature
of the anatomic deformity.
Focal Fibrocartilaginous
Dysplasia
Focal fibrocartilaginous dyspla-
sia is a rare cause of unilateral genu
varum.24,25 It affects the proximal
medial tibia, and the resultant de-
334
formity is more properly termed
tibia vara. The deformity is usually
apparent to the parents before the
child is 18 months of age. Radio-
graphs show a characteristic cortical
lucency with surrounding sclerosis
in the proximal medial tibial me-
taphysis and varus angulation. The
condition usually corrects by age
4 with growth. Surgical correction
of the deformity is usually not
needed.25
Less Common Causes
Any disorder that can affect the
proximal tibial or distal femoral
growth plate has the potential for
causing genu varum. For example,
infantile osteomyelitis with abscess
formation can generate uneven sub-
sequent growth, with resultant de-
formity. Another such disorder is
physeal growth disturbance sec-
ondary to trauma or sepsis. The dis-
tal femur is a relatively common site
of growth disturbance following
physeal fracture. Physeal fractures
of the proximal tibia are much less
common. Management of physeal
growth disturbances is complex and
is beyond the scope of this article.
Principles of Evaluation
and Treatment
The following are a few principles
that will help the orthopaedist in the
evaluation and treatment of the
child with genu varum:
(1) Genu varum is physiologic
until the age of 18 to 24 months, and
treatment is unnecessary.
(2) In a child with normal stature
and findings compatible with physi-
ologic bowing, radiographic docu-
mentation is unnecessary. If
documentation of the condition is
desired, photographs are less expen-
sive and just as valuable.
(3) If radiographs are deemed
necessary, full-length standing films
Journal of the American Academy of Orthopaedic Surgeons
of the entire lower limbs are required
for the evaluation of the mechanical
axis and the site of deformity.
(4) Shortness of stature should
signal the likelihood that a constitu-
tional disorder is the cause of genu
varum.
(5) Idiopathic tibia vara is the
most common pathologic cause of
bowlegs in the child. Bracing may be
effective in the early stages, but this
has not been established by prospec-
tive controlled clinical trials.
(6) Surgical correction of tibia
vara can be guided by the principle
that reestablishing a normal me-
chanical axis in the early stages will
allow normal growth to occur. In
older children, resumption of nor-
mal growth cannot be assumed, and
measures to slow later tibial physeal
growth may also be needed.
(7) There are various types of in-
ternal and external fixation, all of
which are satisfactory. The particu-
lar type of fixation used for surgical
treatment of tibia vara is less impor-
tant than reestablishment of the me-
chanical axis.
(8) Treatment of genu varum sec-
ondary to constitutional disorders
must be tailored on an individual
basis.
Conclusion
Although genu varum is fairly com-
mon in children, considerable
changes in evaluation and treat-
ment approaches have occurred
over the past decade. Further re-
finements can be expected in the
coming years, perhaps including a
clearer concept of the etiology of
tibia vara, a better grasp of the role
of bracing in infantile tibia vara,
and a more complete understand-
ing of the effects of treatment (both
positive and negative) in consti-
tutional disorders such as achon-
droplasia.

References
1. Staheli LT, Corbett M, Wyss C, et al:
Lower-extremity rotational problems in
children: Normal values to guide man-
agement. J Bone Joint Surg Am 1985;
67:39-47.
2. Feldman MD, Schoenecker PL: Use of
the metaphyseal-diaphyseal angle in
the evaluation of bowed legs. J Bone
Joint Surg Am 1993;75:1602-1609.
3. Heath CH, Staheli LT: Normal limits of
knee angle in white children: Genu
varum and genu valgum. J Pediatr Or-
thop 1993;13:259-262.
4. Salenius P, Vankka E: The development
of the tibiofemoral angle in children. J
Bone Joint Surg Am 1975;57:259-261.
5. Illingworth RS (ed): The Development of
the Infant and Young Child: Normal and
Abnormal, 9th ed. Edinburgh: Churchill
Livingstone, 1987.
6. Langenskiöld A: Tibia vara: Osteochon-
drosis deformans tibiae—Blount’s dis-
ease. Clin Orthop 1981;158:77-82.
7. Henderson RC, Kemp GJ, Hayes PRL:
Prevalence of late-onset tibia vara. J Pe-
diatr Orthop 1993;13:255-258.
8. Wenger DR, Mickelson M, Maynard JA:
The evolution and histopathology of
adolescent tibia vara. J Pediatr Orthop
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9. Cook SD, Lavernia CJ, Burke SW, et al: A
biomechanical analysis of the etiology of
tibia vara. J Pediatr Orthop 1983;3:449-454.
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Werner C. Brooks, MD, and Richard H. Gross, MD
10. Carter JR, Leeson MC, Thompson GH,
et al: Late-onset tibia vara: A histo-
pathologic analysis—A comparative
evaluation with infantile tibia vara and
slipped capital femoral epiphysis. J
Pediatr Orthop 1988;8:187-195.
11. Kline SC, Bostrum M, Griffin PP:
Femoral varus: An important compo-
nent in late-onset Blount’s disease. J Pe-
diatr Orthop 1992;12:197-206.
12. Levine AM, Drennan JC: Physiological
bowing and tibia vara: The metaphy-
seal-diaphyseal angle in the measure-
ment of bowleg deformities. J Bone Joint
Surg Am 1982;64:1158-1163.
13. Henderson RC, Lechner CT, DeMasi
RA, et al: Variability in radiographic
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494.
14. Loder RT, Johnston CE II: Infantile tibia
vara. J Pediatr Orthop 1987;7:639-646.
15. Schoenecker PL, Meade WC, Pierron
RL, et al: Blount’s disease: A retrospec-
tive review and recommendations for
treatment. J Pediatr Orthop 1985;5:181-
186.
16. Greene WB: Infantile tibia vara. J Bone
Joint Surg Am 1993;75:130-143.
17. Ferriter P, Shapiro F: Infantile tibia
vara: Factors affecting outcome following
proximal tibial osteotomy. J Pediatr Or-
thop 1987;7:1-7.
18. Beck CL, Burke SW, Roberts JM, et al:
Physeal bridge resection in infantile
Blount disease. J Pediatr Orthop 1987;
7:161-163.
19. Siffert RS: Intraepiphyseal osteotomy
for progressive tibia vara: Case report
and rationale of management. J Pediatr
Orthop 1982;2:81-85.
20. Hofmann A, Jones RE, Herring JA:
Blount’s disease after skeletal maturity.
J Bone Joint Surg Am 1982;64:1004-1009.
21. Henderson RC, Kemp GJ Jr, Greene WB:
Adolescent tibia vara: Alternatives for
operative treatment. J Bone Joint Surg
Am 1992;74:342-350.
22. Evans GA, Arulanantham K, Gage JR:
Primary hypophosphatemic rickets: Ef-
fect of oral phosphate and vitamin D on
growth and surgical treatment. J Bone
Joint Surg Am 1980;62:1130-1138.
23. Oppenheim WL, Shayestehfar S,
Salusky IB: Tibial physeal changes in
renal osteodystrophy: Lateral Blount’s
disease. J Pediatr Orthop 1992;12:774-
779.
24. Olney BW, Cole WG, Menelaus MB:
Three additional cases of focal fibrocar-
tilaginous dysplasia causing tibia vara.
J Pediatr Orthop 1990;10:405-407.
25. Bradish CF, Davies SJM, Malone M:
Tibia vara due to focal fibrocartilagi-
nous dysplasia: The natural history. J
Bone Joint Surg Br 1988;70:106-108.
335
 Paget's Disease of Bone: Pathophysiology,
Diagnosis, and Management

Frederick S. Kaplan, MD, and Frederick R. Singer, MD

Abstract

Paget’s disease of bone is a common geriatric disorder of skeletal remodeling, Pathology

which may have a viral etiology. Safe and effective treatments are now available
for associated complications of symptomatic involvement. The orthopaedic sur- Paget’s disease is a focal disorder of
geon should have a fundamental understanding of the complications of Paget’s skeletal remodeling in which the pri-
disease and should be familiar with the indications for treatment, as well as avail- mary cellular abnormality is an
able medical and surgical therapies. increase in osteoclastic resorption of
J Am Acad Orthop Surg 1995;3:336-344 bone (Fig. 1). Increased bone resorp-
tion leads to a compensatory
increase in bone formation. The
The orthopaedic surgeon is often The prevalence has been reported to overall rate of bone remodeling is
involved with family practitioners, be 10% to 15% by the ninth decade of accelerated, resulting in a predomi-
general internists, endocrinologists, life. The disorder is rarely recog- nance of highly vascular bone that is
and rheumatologists in the diagno- nized before age 40. structurally weak and prone to
sis and care of patients who have Several members of a family may deformities and pathologic frac-
Paget’s disease of bone. The ortho- manifest Paget’s disease. As many tures.1,2,4,5
paedic surgeon may be recruited to as 25% of patients have one or more Pagetic osteoclasts are more
render a definitive diagnosis, to par- family members who also have the numerous and larger than normal
ticipate in patient education, to pre- disorder. The cumulative incidence osteoclasts and may contain as many
scribe medical or physical therapy, of Paget’s disease to age 90 is as 100 nuclei per cell. These bone-
or to perform a surgical procedure. approximately four times greater in resorbing cells often contain nuclear
Accordingly, the orthopaedic sur- relatives of patients with the condi- and cytoplasmic inclusions, which
geon should be familiar with all tion than in relatives of control sub-
aspects of diagnosis and available jects. In many families, genetic
medical and surgical treatments for susceptibility is also suggested by Dr. Kaplan is Associate Professor of Orthopaedic
Surgery and Medicine and Chief, Division of
patients who have Paget’s disease. the finding of a linkage between the Metabolic Bone Diseases and Molecular
This article will review the epidemi- HLA-DQW1 haplotype and the Orthopaedics, University of Pennsylvania
ology, pathology, etiology, patho- presence of Paget’s disease. These School of Medicine, Philadelphia. Dr. Singer is
physiology, diagnosis, and medical data do not establish a genetic basis Director, Endocrine-Bone Disease Program,
management of Paget’s disease of for the disease, but rather define John Wayne Center Institute at St. John’s Hospi-
tal and Health Center, Santa Monica, Calif, and
bone. familial characteristics that have Clinical Professor of Medicine, University of Cal-
been observed in a large number of ifornia at Los Angeles School of Medicine.
affected patients.3
Epidemiology There is a striking geographic dis- Reprint requests: Dr. Kaplan, Department of
tribution of Paget’s disease. The dis- Orthopaedic Surgery, University of Pennsylva-
Paget’s disease of bone, or osteitis ease is most prevalent in England, nia School of Medicine, 3400 Spruce Street,
Philadelphia, PA 19104-4283.
deformans, is a common geriatric western Europe, the United States,
problem, occurring in 3% to 4% of Australia, and New Zealand, but is Copyright 1995 by the American Academy of
the population over 50 years of age.1 uncommon in Scandinavia, China, Orthopaedic Surgeons.
It is slightly more common in men.2 Japan, and India.4

336 Journal of the American Academy of Orthopaedic Surgeons


A B
Fig. 1 Light- and electron-microscopic findings in Paget’s disease. A, Section of bone shows
intense osteoclastic and osteoblastic activity and mosaic of lamellar bone. B, Electron-micro-
scopic view of multinucleated osteoclast with nuclear inclusions that may be viruses
(arrows). N = nuclei; C = cytoplasm. (Reproduced with permission from Netter FH: The
CIBA Collection of Medical Illustrations. Summit, NJ: CIBA-Geigy Corp, 1987, vol 8, pt I, p 238.)
resemble nucleocapsids of the
Paramyxoviridae family of viruses.6
The pathologic process in Paget’s
disease may be divided into active
and inactive phases. Early in the
active phase, intense osteoclastic
bone resorption prevails (lytic
phase). Later, compensatory bone
formation is apparent (mixed
phase). Very late in the active phase,
osteoblastic bone formation pre-
dominates (sclerotic phase). Occa-
sionally, the disease may reach an
inactive phase in which a sclerotic
lesion may remain in the absence of
excessive bone-cell activity. In such
a lesion, the adjacent marrow con-
sists predominantly of fat cells with
few areas of hematopoietic or
fibrovascular elements.5
Pagetic bone is usually lamellar
and fully mineralized. In very active
lesions, however, immature woven
bone may be present in regions of
poorly mineralized osteoid. The
affected bone has a characteristic
mosaic pattern with irregularly
shaped areas of lamellar bone and an
Vol 3, No 6, November/December 1995
Frederick S. Kaplan, MD, and Frederick R. Singer, MD
erratic pattern of cement lines. This
mosaic pattern is a consequence of
accelerated bone resorption and for-
mation.5
Etiology
A number of hypotheses have been
proposed to explain the genesis of
Paget’s disease. The most likely
cause is a slow viral infection of
bone,7 perhaps with an underlying
familial predisposition.
Immunohistologic studies of
pagetic osteoclasts have revealed
the antigens of paramyxoviruses,
particularly the measles and respi-
ratory syncytial viruses. Further
support of a viral etiology is pro-
vided by the finding of the mRNA
of paramyxoviruses in some patho-
logic material. Although an infec-
tious virus has not yet been isolated
from long-term cultures of pagetic
bone cells, this does not eliminate
a viral etiology, because the puta-
tive virus is highly defective4,6 and
therefore no longer capable of being
cultured.
Current data suggest that Paget’s
disease may be caused by hematoge-
nous infection with one of several
possible paramyxoviruses and that
following an acute viremia, osteo-
clasts or their precursors become
chronically infected. According to
this hypothesis, the virus mutates
rapidly and loses its infectivity but is
able to stimulate osteoclast prolifera-
tion and activity, possibly by
cytokine production. This may
induce dramatic local osseous
effects.7,8 Various familial and
genetic factors may be involved in
susceptibility and immunologic reac-
tivity to the putative infectious agent,
which would likely influence the clin-
ical expression of the disease.3,5,6,9
Clinical Manifestations and
Complications
Paget’s disease may affect any bone
and may be monostotic or polyos-
totic. Clinical manifestations vary,
depending on the sites and severity
of lesions (Tables 1 and 2). Many
individuals with radiologic evidence
of the disease have no symptoms and
may not require treatment.1,2,4 In fact,
because Paget’s disease is usually
asymptomatic, it most often is
detected incidentally on radiographs
obtained for other purposes or is sug-
gested by the unexpected elevation
of serum alkaline phosphatase activ-
ity on a routine serum chemistry
screening panel.
In symptomatic patients, bone
pain can be mild to severe and is
usually unrelated to physical activi-
ty. Acute pain may develop as a
consequence of pathologic fractures
of affected bone. A variety of other
local and general signs and symp-
toms may also occur.
The characteristic bone enlarge-
ment that occurs with Paget’s dis-
ease may cause spinal stenosis,
337
Paget’s Disease of Bone
Table 1
Common Diagnostic Features of
Paget’s Disease of Bone
History
Rare before 40 years of age
Insidious onset of symptoms
(pain, deformity, headache)
Often asymptomatic
Physical findings
Bone deformity and enlargement
Increased heat (due to increased
blood flow) over affected bone
Bone tenderness
Asymmetric limb involvement
Associated neurologic involve-
ment
Associated pagetic arthritis
Biochemical findings
Increased serum alkaline phos-
phatase level
Increased urinary excretion of
pyridinoline cross-links
Radiologic findings
Metaphyseal involvement
Sclerotic and lytic changes in
same bone
Coarse, thick trabeculae
Enlargement of bone
Associated arthritic changes
(late)
Increased radionuclide uptake
on technetium-99m methylene
diphosphonate bone scan
Bone pathology findings (often
from surgical specimens)
Disordered remodeling
Increased osteoclastic and
osteoblastic activity
Giant osteoclasts
Mosaic pattern of lamellar bone
Presence of woven bone
Virus-like inclusions in nuclei
and cytoplasm of osteoclasts
on electron microscopy
resulting in spinal radiculopathy or
cauda equina syndrome.10 Increased
blood flow to the highly vascular
pagetic bone has been thought to
provoke the “steal syndrome.” In
this situation, blood is shunted
away from the neural elements,
338
exacerbating the neurologic symp-
toms and signs accompanying the
stenosis.10
The function of the cranial nerves
may also be affected. Pagetic in-
volvement of the temporal bone is a
common cause of conductive hear-
ing loss in this condition. Less com-
monly, involvement of the cochlea
results in mixed sensory and con-
ductive deafness. Extreme thicken-
ing and enlargement of the skull
may result in platybasia and, in rare
instances, impaired cerebrospinal
fluid flow and hydrocephalus.9
Painful fissure fractures, pseudo-
fractures (transverse radiolucent
areas on the convex side of a long
bone), and complete pathologic frac-
tures (transverse “chalk-stick” frac-
tures) may occur in areas of high
stress, particularly in the weight-
bearing bones of the lower limbs.
Fracture healing may be impaired,
resulting in delayed union or
nonunion. This complication is most
common with fractures of the
femur.1,4,5
Articular disorders commonly
associated with Paget’s disease of
bone are degenerative arthritis, cal-
cific periarthritis, and gout. 11,12
Degenerative arthritis in joints con-
tiguous with pagetic bone is likely to
occur because of accelerated remod-
eling of the affected bone, which
results in juxta-articular bone
enlargement, abnormal joint biome-
chanics, and altered subchondral
support. When the hip is affected,
acetabular protrusion along with
medial joint-space narrowing may
result.1,2,4 The association of gout
with Paget’s disease may be sec-
ondary to hyperuricemia due to
accelerated nucleic acid turnover in
subjacent bone.11,12
Metabolic complications of
Paget’s disease are uncommon but
include hypercalciuria and hyper-
calcemia.1,4 These complications are
seen in only the most severely
involved (polyostotic Paget’s dis-
Journal of the American Academy of Orthopaedic Surgeons
ease) and immobilized patients.
The association of mild hyperparathy-
roidism and Paget’s disease has been
reported, but its significance is
unclear and may be coincidental.1,4
The most serious complication of
Paget’s disease is the development
of a malignant bone tumor.13
Osteosarcomas, chondrosarcomas,
fibrosarcomas, and tumors of mixed
histologic characteristics may
develop, almost always in a preex-
isting pagetic lesion. Primary giant
cell tumors and secondary meta-
static spread of carcinoma to pagetic
bone are also quite common.
Paget’s sarcoma, a rare complica-
tion, occurs in fewer than 1% of
affected patients and is rare before
70 years of age.13 A marked and sus-
tained increase in pain in an area of
long-standing Paget’s disease in an
elderly patient suggests this serious
sequela. Other manifestations are
night pain and radiographic evi-
dence of bone destruction. Serum
alkaline phosphatase activity may
be unaltered and thus is not a useful
test. Rapid worsening of bone pain
or deformity should indicate the
need for radiologic evaluation, fol-
lowed by bone biopsy if suspicion of
a tumor remains. Magnetic reso-
nance imaging and computed
tomography are particularly helpful
in delineating the presence of bone
tumors. Despite recent advances in
the treatment of malignant bone
tumors, the prognosis remains very
poor in patients who have Paget’s
disease.13 There are currently no
data to support the preventive
effects of chronic suppressive med-
ical therapy on the risk of pagetic
sarcoma.
Diagnostic Evaluation
The initial evaluation of a patient
with Paget’s disease should include
a complete history and physical
examination, a radionuclide bone
 Frederick S. Kaplan, MD, and Frederick R. Singer, MD

radioisotope scanning. Localization

Table 2 of the bone-seeking agent Tc-99m
Manifestations of Paget’s Disease of Bone
methylene diphosphonate is depen-
dent on the relative vascularity of
Nonskeletal the bone and the extent of hydroxy-
Neurologic
apatite crystal surface available for
Hearing loss and, less commonly, other cranial nerve deficits
binding of the compound. Bone
Spinal-cord or nerve-root compression
Cardiovascular scans are far more sensitive than
Increased cardiac output due to increased bone vascularity radiographs in detecting occult
Possible high-output congestive heart failure pagetic lesions, although inactive
Metabolic sclerotic lesions may be missed.
Hypercalcemia, hypercalciuria, and urolithiasis in immobilized patients The diagnosis of Paget’s disease is
Hyperuricemia and gout usually established on the basis of
Primary hyperparathyroidism (possibly coincidental) the characteristic radiographic
Dental appearance of the lesions. The earli-
Poor occlusion est lesions of Paget’s disease are
Tooth loosening and loss
osteolytic and are most readily
Oncologic
observed in the skull and long bones
Pagetic osteosarcoma
Pagetic chondrosarcoma (Fig. 3). In the skull, discrete oval or
Pagetic fibrosarcoma round areas of osteolysis are termed
Tumors of mixed histologic characteristics osteoporosis circumscripta. In the
Primary giant cell tumors limbs, the disease usually begins as
Skeletal localized metaphyseal involvement.
Axial skeleton The osteolytic lesion usually has a V
Back pain due to vertebral body involvement or arrowhead shape at its advancing
Osteoarthritis of facet joints edge. Lesions have been observed to
Diskogenic disease secondary to vertebral involvement and alteration of progress slowly toward the opposite
nourishment to disk
end of the affected long bone at a rate
Spinal stenosis (due to vertebral body enlargement)
of approximately 1 cm/yr in un-
Spinal-artery steal syndrome with paraparesis and/or paraplegia
Compression fractures of vertebral bodies treated patients.2,4
Neoplastic degeneration As the osteolytic process pro-
Appendicular skeleton gresses to involve much of the long
Bone pain and tenderness bone or skull, the more familiar
Progressive deformity osteosclerotic lesions of Paget’s dis-
Secondary osteoarthritis ease replace the earlier osteolytic
Pathologic fractures with high rate of delayed union, nonunion, or regions. Over a period of years to
malunion decades, the bone becomes chaotic
Neoplastic degeneration in structure and thickened. The
overall bone size may increase
remarkably.
In the lower limbs, bowing, pseu-
scan, appropriate radiographs, and dence of the disease (Fig. 2). A bone dofractures, and complete transverse
baseline laboratory tests (serum scan should be performed when pathologic fractures are common.
alkaline phosphatase, calcium, there is a question about the meta- The latter chalk-stick fractures (Fig. 4)
phosphorus, and albumin determi- bolic activity of a specific region of can also be seen in osteomalacia or
nations).2,4 the skeleton or when it is desirable to fibrous dysplasia. Subchondral bone
document the full extent of the dis- involvement in the metaphysis on
Radiologic Studies ease. A complete radiographic exam- one side of a diarthrodial joint may
Radioisotope studies should be ination should be obtained, including lead to joint incongruity and subse-
performed to evaluate the metabolic all skeletal sites that demonstrate an quent arthritis.
activity of a pagetic lesion, as well as increase in radionuclide uptake.2,4 In patients with back pain, mag-
to assess the total skeletal involve- Technetium-labeled bisphospho- netic resonance imaging and com-
ment in a patient who has focal evi- nates are most commonly used in puted tomography have been

Vol 3, No 6, November/December 1995 339

Paget’s Disease of Bone

A B C

D E F

Fig. 2 Images of a patient with Paget’s disease. A, Bone scan shows areas of increased isotope uptake. B, Proximal humerus appears thick-
ened and coarsely trabeculated, with patchy rarefaction. C, Proximal femur shows typical manifestations of the disease, including osteoscle-
rotic and osteolytic areas, bone enlargement, and metaphyseal involvement with coarse trabeculation. D, Disease involvement can be seen
throughout the pelvis and the proximal femurs, with involvement of the hip joints. E, The body of L3 appears enlarged, with increased den-
sity. F, Myelogram shows obstruction of the vertebral canal at L3. (Reproduced with permission from Netter FH: The CIBA Collection of Medi-
cal Illustrations. Summit, NJ: CIBA-Geigy Corp, 1987, vol 8, pt I, p 237.)

particularly useful in defining the
extent of degenerative arthritis,
spinal stenosis, and nerve-root
impingement.10 An increase in the
size of a vertebral body is one of the
radiographic hallmarks of Paget’s
disease of the spine, which can be
particularly helpful in differentiat-
ing Paget’s disease from lymphoma
or metastatic carcinoma.
Biochemistry
The measurement of serum alka-
line phosphatase activity is the most
useful biochemical test for Paget’s
disease. The activity of this enzyme,
which is located in the plasma mem-
brane of osteoblasts, reflects the num-
ber and functional state of osteoblasts
in patients who have bone disease. In
Paget’s disease, the level of alkaline

340 Journal of the American Academy of Orthopaedic Surgeons

 Frederick S. Kaplan, MD, and Frederick R. Singer, MD

and inexpensive biochemical index of benefit is commonly overlooked in

disease activity. In selected patients,
new assays specific for bone alkaline
phosphatase may be helpful.
Urinary excretion of pyridinoline
cross-links, a biochemical index of
bone-matrix collagen resorption, is
measured over 24 hours. As with
serum alkaline phosphatase activity,
urinary excretion of pyridinoline
cross-links correlates well with the
extent of pagetic involvement. 14
Because of the expense and inconve-
nience, this test is not generally used
routinely in the assessment or follow-
up of a patient with Paget’s disease.1,2,4
Due to tight metabolic coupling
between bone resorption and bone
formation, calcium levels in the
serum and urine are usually normal
except when there is concurrent gen-
eralized immobilization, hyperthy-
roidism, hyperparathyroidism, or
malignancy.1,2,4
practice. Narcotic agents should be
avoided, if possible, particularly in
the older population.
A cane can be a very important
therapeutic device for patients with
Paget’s disease of the lower limbs.
Because of the benefits of increased
stability, prevention of falls, and
load-sharing capability, the use of a
cane makes good sense and should
be standard treatment for the elderly
patient.
The most important indications
for treatment of Paget’s disease
include bone pain, neurologic
involvement, high-output cardiac
failure, prevention of fracture or
skeletal deformity in young patients

General Diagnostic and

Treatment Considerations

Not everyone with Paget’s disease

Fig. 3 Characteristic early lesions of Paget’s
disease. Top, Lateral radiograph shows
patchy density of the skull, with areas of
osteopenia (osteoporosis circumscripta
cranii). Bottom, Radiographic findings in
the tibia include thickening, bowing, coarse
trabeculation, and an advancing radiolucent
wedge. (Reproduced with permission from
Netter FH: The CIBA Collection of Medical
Illustrations. Summit, NJ: CIBA-Geigy Corp,
1987, vol 8, pt I, p 236.)
phosphatase activity correlates
roughly with the extent of skeletal
involvement as established by
radioisotope bone scanning. Serial
alkaline phosphatase determinations
generally provide a useful, simple,
will require treatment. In many
cases, the symptoms that cause the
patient to seek care are due to an
associated disorder. Therefore, a
careful consideration of the symp-
toms and the physical and radio-
graphic findings is necessary to
determine whether treatment of
Paget’s disease is indicated.
Nonsteroidal anti-inflammatory
medications and aspirin continue to
have an important role in treating
the arthritis associated with joint
destruction in Paget’s disease. Rou-
tinely, patients with end-stage
Paget’s disease have low alkaline
phosphatase levels, limited disease
activity, and moderate joint degen-
eration, which can be symptomati- Fig. 4 Healing chalk-stick fracture. (Repro-
cally controlled with non-steroidal duced with permission from Netter FH: The
CIBA Collection of Medical Illustrations. Sum-
anti-inflammatory agents. The mit, NJ: CIBA-Geigy Corp, 1987, vol 8, pt I,
direct analgesic effects of these med- p 236.)
ications are also important, but this

Vol 3, No 6, November/December 1995 341

Paget’s Disease of Bone
with active disease, and preparation
for orthopaedic surgery (Table 3).4,15
Before considering the use of spe-
cific therapy for Paget’s disease, a
thorough explanation of the disease
should be offered to the patient.
Treatments should be discussed in
the context of arresting progression
of the disease. In all discussions and
planning, relief of pain and restora-
tion of function should be empha-
sized. The need for long-term
follow-up should also be stressed.
All patients should be reexam-
ined at least annually, and the alka-
line phosphatase level should be
determined at these visits. Careful
questioning, examination, and cor-
relation with changes in alkaline
phosphatase levels will often reveal
subtle symptoms and signs of dis-
ease activity or progression that
might be amenable to therapy.
Radiographs may be obtained peri-
odically, as dictated by symptoms.
Repeat bone scans are not obtained
routinely unless bone pain occurs at
a new site or new symptoms arise.
The home environment of the
patient should be discussed with the
goal of preventing accidents that
could lead to pathologic fractures.
In patients who have auditory
Table 3
Indications for Drug Therapy in
Paget’s Disease
Bone pain
Preparation for orthopaedic
surgery
Treatment of medical complica-
tions, including hearing loss,
spinal stenosis with nerve
dysfunction, and high-output
congestive heart failure
Prevention of fracture or skeletal
deformity in patients with
rapidly progressive osteolytic
lesions or in young patients with
active disease
342
deficits due to Paget’s disease, atten-
tion to auditory acuity may be help-
ful to detect subtle changes. 9
Patients with maxillary or mandibu-
lar involvement should be referred
for dental evaluation.9
The Paget Foundation (200 Varick
Street, New York, NY 10014) can be
helpful in providing patient infor-
mation on the disease.
Medical Treatment
The two major types of therapeutic
agents currently used in the treat-
ment of symptomatic Paget’s disease
are calcitonin and the bisphospho-
nates.1,15 The treatment schedules
and special characteristics of each
agent are presented in Table 4. The
observed benefits of long-term calci-
tonin therapy include relief of bone
pain, a reduction of increased car-
diac output, reversal of certain neuro-
logic deficits, stabilization of hearing
loss, healing of osteolytic lesions,
and reduction in complications of
orthopaedic surgery, such as exces-
sive bleeding.
Calcitonin is a safe and highly
effective treatment for Paget’s dis-
ease. Most patients are able to self-
administer daily subcutaneous
injections. Side effects (usually
minor) occur in about 20% of patients
treated with either salmon calcitonin
or human calcitonin. These include
nausea, facial flushing, and polyuria.
In approximately 20% of patients,
resistance to chronic salmon calci-
tonin therapy develops after a suc-
cessful initial treatment period. If
long-term treatment with salmon
calcitonin or human calcitonin is dis-
continued, exacerbation of biochem-
ical abnormalities and symptoms
may occur within 1 year.15
Another class of drugs useful in
treating Paget’s disease is the bis-
phosphonates (formerly diphospho-
nates). These compounds are
pyrophosphate analogues, which
Journal of the American Academy of Orthopaedic Surgeons
are potent inhibitors of bone resorp-
tion. They bind to the hydroxyap-
atite crystals in bone and may
remain in bone for a prolonged time
after the discontinuation of treat-
ment.15
Etidronate disodium was the
original bisphosphonate approved
for routine clinical use. The advan-
tage of this drug is that it can be
used orally. After absorption, the
drug localizes to bone or is
excreted unchanged in the urine.
The recommended dose of etidro-
nate (5 mg/kg of body weight
daily for 6 months) produces sup-
pression of disease activity and
symptoms similar to that which
occurs with calcitonin. Because
absorption of the drug is poor and
variable, it should be taken once
daily on an empty stomach at least
2 hours remote from any other
food; the medication may be taken
with a glass of water. Etidronate
should not be used in the treatment
of patients with osteolytic pagetic
lesions, for whom calcitonin is
preferable.
Side effects appear to be less com-
mon with etidronate than with calci-
tonin; loose bowel movements and
nausea may occur but are infrequent.
Hyperphosphatemia is sometimes
observed, particularly if higher-than-
recommended doses are given; the
dose should be reduced if this is
found. High doses or long-term
uninterrupted use also produce a
mineralization defect and might pre-
dispose to pathologic fractures.1,2,15
After the recommended 6-month
treatment course, biochemical and
symptomatic remissions may persist
for months or, occasionally, for years.
In most patients, biochemical indices
return toward pretreatment levels
within a year. When symptoms
recur, repeat 6-month treatment
courses often will produce biochemi-
cal and symptomatic improvement
similar to that achieved with the ini-
tial treatment course. However,
 Frederick S. Kaplan, MD, and Frederick R. Singer, MD

Table 4
Drug Treatment of Paget’s Disease

Drug Dosage Special Characteristics

Salmon calcitonin 50-100 international units subcuta- Anti–salmon calcitonin antibodies

neously daily; after symptomatic develop in 60% of patients;
improvement, may reduce to 3 clinical resistance in >20%
times weekly

Human calcitonin 0.5 mg subcutaneously daily; after Effective in salmon calcitonin–resistant

symptomatic improvement, may patients with high antibody titers
reduce to 3 times weekly

Etidronate disodium
5 mg/kg of body weight orally for
6 months; may repeat after recur-
rence of symptoms or biochemical
exacerbation, but not sooner than
6 months
Remission for years may occur after
6 months of therapy; some patients
experience transient increased bone
pain; osteolytic lesions rarely heal;
osteomalacia occurs at high doses

Pamidronate disodium
30 mg intravenously slowly over 31⁄2
to 4 hr; repeat daily for 3 consecu-
tive days; repeat as needed; patients
with more severe disease may need
60 mg monthly or quarterly for
variable periods
New bisphosphonate with potent
antiresorption effects; transient
fever (< 24 hr) is common side
effect

resistance to repeated courses of
treatment is common.
Second-generation bisphospho-
nates that are more potent than
etidronate have been developed.
These agents do not impair mineral-
ization. The most widely evaluated
is pamidronate disodium,16 which
has recently been approved by the
Food and Drug Administration for
use in Paget’s disease. The medica-
tion is administered intravenously
because of its poor gastrointestinal
absorption. The approved treatment
regimen is 30 mg/day by slow
(duration, 31⁄2 to 4 hours) intravenous
infusion for 3 consecutive days; the
regimen may be repeated as needed.
The drug can also be administered in
a 60-mg single dose or in a weekly,
monthly, or quarterly regimen,
depending on the severity of the dis-
ease and the response of the patient.
A brief postinfusion fever or acute
pain flare may occur. Short courses
of treatment with pamidronate can
produce long-term remissions of the
disease. Oral preparations of some
of the newer bisphosphonates will
likely be available in the near future.
Thus, it is likely that new-generation
bisphosphonates will become the
most commonly used and effective
therapy for Paget’s disease.16
Surgery
Some indications for surgical inter-
vention in Paget’s disease include
femoral fractures and severe arthritis
that is refractory to medical treat-
ment. Malalignment of the major
weight-bearing bones or impending
fractures may be treated with
orthoses or with surgery. Preopera-
tive medical treatment with bisphos-
phonates or calcitonin decreases
intraoperative bleeding. Spinal
decompression for spinal stenosis is
an important consideration, but
there are meager data on the man-
agement of this complication. Spinal
surgery should be avoided until all
nonsurgical options have been dili-
gently tried. Assiduous attention
must be paid to the surgical
approach in order to preserve spinal
stability.
Surgical intervention in Paget’s
disease is most often sought when
degenerative arthritis of the hip or
knee produces severe pain on weight-
bearing and impaired mobility.17,18
Anti-inflammatory agents usually
produce little relief of symptoms in
this setting. Diagnostic intra-articular
injections with a local anesthetic often
confirm that the pain is primarily
articular, rather than osseous. Total
hip replacement is highly effective in
relieving hip pain and restoring
mobility.18 Tibial osteotomy is
equally effective in relieving knee
pain in patients who have severe tib-

Vol 3, No 6, November/December 1995 343

Paget’s Disease of Bone
ial bowing if the associated articular
degeneration is not too advanced.19
Before any operative orthopaedic
procedure is performed, it is desir-
able, if possible, to reduce disease
activity with drug therapy in order
to prevent excessive blood loss. A
reduction in serum alkaline phos-
phatase activity to approximately
50% of pretreatment levels is proba-
bly adequate preoperative control.
In elective cases, it is therefore desir-
able to begin antipagetic medication
at least 6 weeks before surgery.2
When osteotomy followed by bone
References
1. Kaplan FS, Singer FR: Paget’s disease,
in Morley JE, Korenman SG (eds):
Endocrinology and Metabolism in the
Elderly. Boston: Blackwell Scientific
Publications, 1992, pp 230-240.
2. Merkow RL, Lane JM: Paget’s disease of
bone. Orthop Clin North Am 1990;21:171-
189.
3. Siris ES, Ottman R, Flaster E, et al:
Familial aggregation of Paget’s disease
of bone. J Bone Miner Res 1991;6:495-500.
4. Kaplan FS, Singer FR: Paget’s disease of
bone: Pathophysiology and diagnosis.
Instr Course Lect 1993;42:417-424.
5. Teitelbaum SL: The pathology of
Paget’s disease, in Singer FR, Wallach S
(eds): Paget’s Disease of Bone: Clinical
Assessment, Present and Future Therapy.
New York: Elsevier, 1991, pp 29-43.
6. Mills BG, Singer FR: Critical evaluation
of viral antigen data in Paget’s disease of
bone. Clin Orthop 1987;217:16-25.
7. Hoyland JA, Freemont AJ, Sharpe PT:
Interleukin-6, IL-6 receptor, and IL-6
nuclear factor gene expression in
Paget’s disease. J Bone Miner Res
1994;9:75-80.
344
healing is planned, calcitonin and
pamidronate are the drugs of choice.
When total joint replacement is
performed, long-term suppression
of disease activity through use of cal-
citonin or pamidronate may be
desirable to diminish excessive
bone-remodeling activity and pre-
vent loosening of prosthetic compo-
nents. 17,18 In all circumstances
requiring surgery, the patient must
be aware that delayed bone healing
may occur and that a lengthy reha-
bilitation program may be neces-
sary.
8. Ralston SH, Hoey SA, Gallacher SJ, et al:
Cytokine and growth factor expression
in Paget’s disease: Analysis by reverse-
transcription/polymerase chain reac-
tion. Br J Rheumatol 1994;33:620-625.
9. Kaplan FS, Haddad JG, Singer FR:
Paget’s disease: Complications and con-
troversies [editorial]. Calcif Tissue Int
1994;55:75-78.
10. Hadjipavlou A, Lander P: Paget disease
of the spine. J Bone Joint Surg Am
1991;73:1376-1381.
11. Krane SM, Kroop SF: Arthritis and
Paget’s disease of bone, in Singer FR,
Wallach S (eds): Paget’s Disease of Bone:
Clinical Assessment, Present and Future
Therapy. New York: Elsevier, 1991, pp
191-199.
12. Franck WA, Bress NM, Singer FR, et al:
Rheumatic manifestations of Paget’s
disease of bone. Am J Med 1974;56:592-
603.
13. Huvos AG, Butler A, Bretsky SS:
Osteogenic sarcoma associated with
Paget’s disease of bone: A clinicopatho-
logic study of 65 patients. Cancer
1983;52:1489-1495.
Journal of the American Academy of Orthopaedic Surgeons
Summary
Paget’s disease is a common con-
dition in the elderly, and its com-
plications are a common source of
skeletal morbidity and symp-
toms. Orthopaedic physicians
should be aware of the disorder
and its myriad manifestations.
Although a cure is currently
unavailable, a wide array of med-
ical and surgical therapeutic
options offer much hope to those
afflicted by symptomatic compli-
cations.
14. Delmas PD, Gineyts E, Bertholin A, et al:
Immunoassay of pyridinoline crosslink
excretion in normal adults and in
Paget’s disease. J Bone Miner Res 1993;8:
643-648.
15. Bockman RS, Weinerman SA: Med-
ical treatment for Paget’s disease of
bone. Instr Course Lect 1993;42:425-
433.
16. Siris ES: Perspectives: A practical guide
to the use of pamidronate in the treat-
ment of Paget’s disease. J Bone Miner Res
1994;9:303-304.
17. Gabel GT, Rand JA, Sim FH: Total knee
arthroplasty for osteoarthrosis in
patients who have Paget disease of bone
at the knee. J Bone Joint Surg Am
1991;73:739-744.
18. Ludkowski P, Wilson-MacDonald J:
Total arthroplasty in Paget’s disease of
the hip: A clinical review and review of
the literature. Clin Orthop 1990;255:160-
167.
19. Meyers MH, Singer FR: Osteotomy for
tibia vara in Paget’s disease under cover
of calcitonin. J Bone Joint Surg Am
1978;60:810-814.
 Thoracolumbar Spine Trauma:
I. Evaluation and Classification

Jeffrey M. Spivak, MD, Alexander R. Vaccaro, MD, and Jerome M. Cotler, MD

Abstract

A timely and thorough evaluation of thoracolumbar injuries and rational treat- fluid collection, crepitus, and in-
ment based on a complete understanding of the mechanism of bone, soft-tissue, creased interspinous distance, which
and nerve injury is essential for maximizing the patient’s neurologic and func- signal injury to the posterior ele-
tional recovery and minimizing associated complications, the time to recovery, ments. Areas of localized tenderness
and the problems of long-term pain and deformity. The initial evaluation includes noted in the awake patient should be
both clinical and radiologic assessment. Clinical evaluation includes the general remembered for later scrutiny on
trauma examination as well as a detailed spinal and neurologic examination to de- radiographic examination.
termine the level (or levels) of spinal injury. Radiologic evaluation includes both
plain radiography and the appropriate use of advanced imaging modalities. A re- Neurologic Evaluation
view of the evolution of thoracolumbar injury classifications is presented. The neurologic examination for
J Am Acad Orthop Surg 1995;3:345-352 thoracolumbar trauma includes der-
matomal sensory testing, assessment
of lumbar- and sacral-root motor
function, and a detailed reflex exami-
Proper management of thoracolum- ing, circulation) evaluation that is nation (Table 1). “Spinal shock”
bar spine injuries is predicated on a standard for all trauma patients. refers to flaccid paralysis due to a
thorough understanding of the in- The spinal examination includes in- physiologic disruption of all spinal
volvement of the structural and spection and palpation of the spine cord function. This occurs commonly
neural tissues. Initial evaluation in- and a careful and complete neuro- below the anatomic level of an injury
cludes a complete and thorough logic evaluation. A high degree of to the cord. Sensory and motor func-
clinical examination. Appropriate suspicion of other injuries fre-
use of radiologic modalities pro- quently associated with thoracolum-
vides additional information, allow- bar trauma, including chest injury Dr. Spivak is Associate Chief of Spine Surgery,
ing classification of the spinal injury, and intra-abdominal injury, should Department of Orthopaedic Surgery, Hospital
assessment of spinal stability, and prompt serial chest and abdominal for Joint Diseases Orthopaedic Institute, New
York, and Assistant Professor of Orthopaedic
prognosis of recovery of neurologic examinations when significant
Surgery, New York University School of Medi-
deficits. This comprehensive initial spinal trauma is diagnosed. cine, New York. Dr. Vaccaro is Assistant Pro-
evaluation facilitates selection With a cervical collar in place and fessor, Department of Orthopaedic Surgery,
among the various surgical and non- extremity injuries splinted, the pa- Jefferson Medical College of Thomas Jefferson
surgical management options avail- tient is carefully log-rolled onto his University, Philadelphia. Dr. Cotler is Everett J.
and Marian Gordon Professor of Orthopaedic
able. or her side as a physician stabilizes
Surgery, Jefferson Medical College of Thomas Jef-
the neck in a neutral position. Abra- ferson University.
sions and deep lacerations are sug-
Initial Evaluation gestive of underlying spinal column Reprint requests: Dr. Spivak, Department of Or-
injury. Open spinal injuries are in- thopaedic Surgery, Hospital for Joint Diseases
Clinical Examination frequent but do occur, and failure to Orthopaedic Institute, 301 East 17th Street, New
York, NY 10003.
The specific directed examination diagnose an open injury due to an in-
of a patient with suspected thora- complete examination must be
Copyright 1995 by the American Academy of Or-
columbar injury begins only after avoided. Palpation of all spinous thopaedic Surgeons.
the typical “ABC” (airway, breath- processes is done, feeling for areas of

Vol 3, No 6, November/December 1995 345

Thoracolumbar Spine Trauma: I. Evaluation and Classification
Table 1
Reflex Testing in Thoracolumbar Injuries
Reflex
Superficial abdominal (above umbilicus)
Superficial abdominal (below umbilicus)
Cremasteric reflex
Knee jerk
Ankle jerk
Anal wink
Bulbocavernosus reflex
Plantar response
tion are absent, as are all reflexes me-
diated by the spinal cord levels in-
volved (Fig. 1). An accurate
assessment of the patient’s neuro-
logic status can be made only when
the patient has recovered from spinal
shock, which resolves within 48
hours in more than 99% of cases. The
absence of spinal shock is confirmed
by the presence or return of cord-
mediated reflexes below the anatomic
area of injury. The bulbocavernosus
Ascending Posterior
(Sensory)
Tracts
Dorsal column
(position, vibration
sense; light touch
Lateral spinothalamic
tract (pain, temperature)
Anterior spinothalamic
tract (pain, temperature)
Anterior
Fig. 1 Schematic drawing of a transverse section of the spinal cord at the thoracic level,
showing the anatomic organization of the corticospinal tract and the posterior column (L =
lumbar, S = sacral, T = thoracic).
346
Level Tested
T7-T10
T11-L1
T12-L1
L3-L4
S1
S2-S4
S3-S4
Brain/cord continuity
reflex is the lowest cord-mediated re-
flex and is therefore the first to return.
A “complete” neurologic injury is
marked by a total absence of sensory
and motor function below the
anatomic level of injury in the ab-
sence of spinal shock. In an incom-
plete neurologic lesion, residual
spinal cord and/or nerve root func-
tion exists below the anatomic level
of injury. A complete cord lesion
with lumbar-root sparing is the most
Descending
(Motor)
Tracts
Lateral corticospinal
tract (voluntary
motor)
Anterior corticospinal
tract
Journal of the American Academy of Orthopaedic Surgeons
common type of incomplete neuro-
logic injury associated with injury at
the thoracolumbar junction.
An incomplete spinal cord lesion
can be confirmed only on the basis of
sensory or voluntary motor function
emanating from a cord segment be-
low the anatomic level of injury; as
defined by the American Spinal In-
jury Association, this must include
the lowest sacral segments.1 Low
sacral sensation includes perianal
and deep anal sensation, and motor
function is tested by voluntary con-
traction of the external anal sphincter
on digital examination. For injuries
at L2 and below, sacral sensory or
motor function reflects lower motor
integrity, as the spinal cord termi-
nates above that anatomic level.
An incomplete spinal cord lesion
may follow one of four described
classic patterns, or syndromes,
based on the location of neural dam-
age within the spinal cord (Fig. 2).
The central cord syndrome is the
most common incomplete spinal
cord injury pattern. Since the spatial
orientation of the long tracts in the
spinal cord maintains lumbar func-
tion more centrally and sacral func-
tion more peripherally, a central
cord syndrome of the thoracolumbar
spine results in greater loss in upper
lumbar motor functions (hip flexion
and adduction and knee extension),
with relative sparing of lower sacral
motor functions. Functional motor
recovery can be expected in 75% of
cases. In the anterior cord syn-
drome, only the dorsal columns re-
main intact, with preservation of
proprioception, vibration, and light
touch and complete loss of motor
function and deep pain and temper-
ature sensation. Unfortunately, in
this relatively common injury pat-
tern, functional recovery is seen in
only 10% of cases. The posterior
cord syndrome is very uncommon,
with isolated loss of vibration, pro-
prioception, and light-touch sensa-
tion. A unilateral hemi–spinal cord
 Jeffrey M. Spivak, MD, et al

genic shock or hypovolemia due to

chest, abdominal, or extremity in-
jury with local hemorrhage. In one
series,3 neurogenic shock was the
cause of hypotension in 69% of pa-
tients with cervical spine injury. The
percentage is probably similar in pa-
tients with upper thoracic injuries.
In patients with thoracolumbar junc-
tion and lumbar injuries, however,
A B sympathetic tone is maintained to a
Ipsilateral large extent, and neurogenic shock is
Ipsilateral less common.

Radiologic Evaluation

Radiography
The radiologic evaluation of the
patient with suspected thoracolum-
Contralateral bar spine trauma begins with plain-
radiographic examination of each
C D
vertebral level (both anteroposterior
Fig. 2 Types of spinal cord injury (shaded zones) that produce the four main incomplete in- and lateral views). This complete
jury patterns seen clinically. A, Central cord syndrome. B, Anterior cord syndrome. C, Pos-
terior cord syndrome. D, Brown-Séquard syndrome.
evaluation is particularly important
in patients who cannot communi-
cate about areas of pain or who are
uncooperative because of head
injury is responsible for the Brown- upper urinary tract, and hepatic, trauma, cervical trauma with neuro-
Séquard syndrome, an uncommon splenic, and pancreatic lacerations, logic deficit, or alcohol or drug in-
injury pattern characterized by ipsi- is frequently associated with flexion- toxication.
lateral loss of motor function, light distraction injuries and fracture-dis- The chest radiograph, part of the
touch, proprioception, and vibration locations of the thoracolumbar standard trauma series, must be
sense and contralateral loss of deep junction and lumbar spine. carefully examined for evidence of
pain and temperature sense. Func- mediastinal widening. Suspicion of
tional motor recovery is seen in over Vital Signs fullness in the mediastinum must be
90% of patients with this injury pat- Hypotension in patients with evaluated with computed tomogra-
tern. multiple trauma and thoracolumbar phy (CT). An aortogram may be in-
spinal injuries is commonly due to dicated to rule out a traumatic aortic
Chest and Abdominal Examination “neurogenic shock,” a state of rela- dissection, even if thoracic spinal
The final aspect of the clinical tive hypovolemia due to a sudden trauma and paraspinal hematoma
evaluation of the thoracolumbar increase in the available circulatory are clearly visible.
trauma patient involves the exami- space caused by a loss of sympa-
nation for and recognition of associ- thetic tone in the thoracolumbar Plain Tomography and CT
ated internal injuries in the chest and region with unopposed vagal para- Computed tomography has
abdomen. Significant intrathoracic sympathetic vasodilatation. Neuro- proved invaluable in the evaluation
trauma, including hemopneumo- genic shock is characterized by of thoracolumbar injuries, especially
thorax, major vessel injury, and dia- bradycardia despite the hypoten- in assessing the integrity of the pos-
phragmatic rupture, may be seen in sion, which is also the result of un- terior aspect of the vertebral body
more than a third of patients with opposed vagal output. In patients and posterior osseous elements (Fig.
thoracic spine fractures and a neu- with hypotension and tachycardia, 3). Computed tomography is indi-
rologic deficit. 2 Intra-abdominal the physical examination should cated in all cases of suspected injury
trauma, including bowel rupture, seek another cause for the circula- to the posterior elements and poste-
major vessel injury, injuries to the tory compromise, such as cardio- rior vertebral body. Retropulsion of

Vol 3, No 6, November/December 1995 347

Thoracolumbar Spine Trauma: I. Evaluation and Classification
Fig. 3 Transverse CT section shows bone
retropulsion from the posterior vertebral
body of L5 into the spinal canal and a frac-
ture of the lamina on the right.
bone fragments into the spinal canal
can be clearly seen on transverse sec-
tions. Sagittal and coronal recon-
structions can be very helpful in
evaluating the alignment of the
spinal canal. Both CT and plain to-
mography are useful for imaging ar-
eas of suspected injury seen on plain
films and areas not well visualized
by plain radiography, such as the
cervicothoracic junction. Tomogra-
phy offers the benefit of direct imag-
ing in the sagittal and coronal
planes, but is becoming less and less
available as an imaging modality.
Magnetic Resonance Imaging
Magnetic resonance (MR) imaging
provides direct visualization of the
spinal cord and allows evaluation of
intervertebral disk trauma. It is indi-
cated in all cases with neurologic
deficit to assess for both intrinsic and
extrinsic cord injuries. We also use
MR imaging for a more thorough pre-
operative evaluation of the spinal
canal in all cases in which surgical
treatment is planned (even those in
which there is no neurologic deficit).
Magnetic resonance imaging can dif-
ferentiate among the various types of
intrinsic cord injuries, such as edema,
hematoma, and the much less fre-
348
quent transection. Edema is seen as myelogram CT scanning is also use-
fusiform enlargement of the spinal ful in the postoperative evaluation of
cord with increased signal intensity possible persistent spinal cord com-
on T2-weighted images. Hematoma pression, especially when ferromag-
is characterized by decreased signal netic instrumentation has been used
intensity on T2 images acutely, and is posteriorly for the indirect reduction
often surrounded by a halo of T2 en- of intracanal bone fragments.
hancement from adjacent edema.
Edema extending more than two ver- Noncontiguous Spinal Injuries
tebral levels and the presence of It must be reemphasized that the
hematoma within the spinal cord are entire spine must be imaged in any
considered poor prognostic signs for patient with blunt trauma to rule out
functional motor recovery. Extrinsic additional spinal injuries that might
cord compression secondary to be unstable and that, if missed, could
spinal canal compromise by osseous lead to the development or progres-
elements, soft tissue, or fluid collec- sion of neurologic injury. Multilevel
tion is readily identified with MR noncontiguous spinal injuries have
imaging (Fig. 4). been reported in up to 16.7% of
Magnetic resonance imaging is cases.4-6
also useful in the evaluation of In the series of Calenoff et al,4
“spinal cord injury without radio- noncontiguous multilevel injuries
graphic abnormalities,” which is were found in 4.5% of cases. These
more commonly seen in children. In injuries were originally missed in
patients with this entity, as well as in 50% of those cases, with the delay in
patients with significant bone injury,
MR imaging can be used to evaluate
the extent of intradiskal injury and
posterior ligamentous injury. In our
experience, true acute disk hernia-
tions are much less common in tho-
racolumbar injuries than in cervical
injuries, but are occasionally found.
The use of MR imaging for diagnosis
of acute soft-tissue injury may have
a significant impact on the decision
to perform early surgical stabiliza-
tion. Magnetic resonance imaging
may also be useful in the postinjury
period in cases of late development
or worsening of a preexisting neuro-
logic injury. In these clinical situa-
tions, a treatable posttraumatic cyst
or syrinx can often be diagnosed.
Myelography
Myelography may be used for
many of the same indications as MR
imaging, but it is invasive and does
not depict the intrinsic anatomy of Fig. 4 T2-weighted MR image demon-
strates a vertical compression injury at T8
the spinal cord. It is indicated in with bone retropulsion resulting in spinal
cases of progressive neurologic canal compromise and spinal cord edema
deficit when MR imaging is not and compression.
available. Myelography with post-
Journal of the American Academy of Orthopaedic Surgeons

diagnosis averaging more than 52
days. Three common injury patterns
and one subpattern were described,
which accounted for 77% of the
cases. Upper thoracic injuries were
found to be common among patients
with multilevel noncontiguous in-
juries, occurring in 46.7% of cases.
In a more recent series,6 noncon-
tiguous injuries were found in 10% of
cases of spinal column injury, with
only 25.6% falling into the injury pat-
terns described by Calenoff et al.4
This series also documented a con-
tinuing problem with failure of diag-
nosis of noncontiguous injuries; in
31% of patients, the secondary injury
was missed initially, with an average
delay in diagnosis of 7.1 days. In 25%
of these missed injuries, a neurologic
deficit developed or progressed due
to improper initial immobilization.
Classification Schemes
Most patients with thoracolumbar
injuries are still treated nonopera-
tively with cast or brace immobiliza-
tion and early ambulation. More
aggressive treatment is guided by
the use of classification systems that
detail the mechanisms of injury, the
effects on compromised spinal struc-
tures, and the potential for late me-
chanical instability or neural injury.
The Spine as Two Columns
In 1963, Holdsworth7 described a
mechanistic classification of thora-
columbar fractures, including flexion,
flexion-rotation, extension, and com-
pression injuries. He felt that stability
was based on the intactness of the
“posterior ligament complex” (the
supraspinous and interspinous liga-
ments, the facet joint capsule, and the
ligamentum flavum). Wedge com-
pression fractures and compression
burst fractures were considered stable
injuries. Extension injuries and rota-
tional fracture-dislocations were con-
sidered unstable until healed and to
Vol 3, No 6, November/December 1995
be in need of temporary external sta-
bilization. Dislocations were also con-
sidered unstable, but the ligamentous
disruption was thought to require op-
erative fusion for stabilization.
In 1968, Kelly and Whitesides8
put forth a two-column theory of
spinal stability, believing that the an-
terior vertebral column provided a
primary weight-bearing function,
while the posterior neural arch col-
umn primarily resisted tension (Fig.
5). Stability was considered to be
based on the intactness of the poste-
rior column, which they felt was
strong enough to bear weight if the
anterior column was compromised.
The Spine as Three Columns
In 1983, Denis9,10 devised a new
classification of thoracolumbar in-
juries based on a three-column the-
ory of spinal stability (Fig. 5). The
anatomic spine was divided into
three sections, or columns, with
radiographs and CT scans being
used to assess the integrity of each.
The anterior column consists of the
anterior longitudinal ligament and
the anterior two thirds of the annu-
lus and vertebral body. The middle
column consists of the posterior
third of the vertebral body and an-
nulus and the posterior longitudinal
ligament. The posterior column con-
sists of the osseous neural arch, the
interspinous and supraspinous liga-
ments, and the ligamentum flavum.
On the basis of a radiographic re-
view, 412 thoracolumbar injuries
were divided into minor and major
injuries. Minor injuries, which ac-
counted for over 15% of fractures, in-
cluded fractures of the spinous and
transverse processes, the pars inter-
articularis, and the facet articula-
tions. Major spinal injuries were
divided into compression fractures,
burst fractures, seat-belt injuries,
and fracture-dislocations.
Compression fractures repre-
sented 47.8% of all thoracolumbar
spinal injuries in Denis’ series. They
Jeffrey M. Spivak, MD, et al
are defined as a compression failure
of the anterior column with an intact
middle column and a posterior col-
umn that is intact or disrupted in
tension. Failure of the posterior col-
umn occurs when there is more than
40% to 50% loss of anterior vertebral-
body height. In burst fractures,
compression failure occurs in the an-
terior and middle columns, often
with retropulsion of middle-column
bone into the spinal canal. Seat-belt
injuries are flexion injuries about an
axis near the anterior longitudinal
ligament, with tension failure of the
posterior and middle columns
through bone or soft tissue. The an-
terior longitudinal ligament remains
intact, but there may be compression
failure of the anterior column. Frac-
ture-dislocations include flexion-ro-
tation, shear, and flexion-distraction
subtypes. In each type, all three
columns fail in compression, ten-
sion, rotation, or shear. Vertebral
translation causes narrowing of the
spinal canal at the site of injury and
a high incidence of neurologic
deficits.
Also in 1983, McAfee et al11 de-
scribed a classification of six fracture
types based on the failure mode of the
middle column. Compression frac-
tures have only anterior column com-
pression failure, while stable burst
fractures have both anterior- and
middle-column compression failure.
In the unstable burst fracture, ante-
rior- and middle-column compres-
sion failure occurs along with failure
of the posterior column, either in
compression, lateral flexion, or rota-
tion. Factors such as a progressive
neurologic deficit, progression of
kyphosis by more than 20 degrees,
more than 50% loss of vertebral body
height, and free bone fragments
within the spinal canal are indicative
of instability in compression burst
fractures. The Chance fractures de-
scribed in this system resemble the
flexion-distraction injuries of Denis,
and the flexion-distraction injuries
349
Thoracolumbar Spine Trauma: I. Evaluation and Classification
Anterior
column
Anterior longitudinal
ligament
Intervertebral disk
Posterior longitudinal
ligament
Anterior longitudinal
ligament
Supraspinous ligament
Fig. 5 Left, The two columns of the spine, as described by Kelly and Whitesides.8 Right, The three columns of the spine, as described by
Denis.9,10
are similar to Denis’ seat-belt injuries,
with compression failure of the ante-
rior column and distraction failure of
the middle and posterior columns.
Translational injuries are failures in
shear or rotation, which primarily oc-
cur in combination with the other in-
jury types.
Mechanistic Classification
In 1984, Ferguson and Allen12 pre-
sented a mechanistic classification of
thoracolumbar injuries, describing
seven injury patterns. This system
categorizes injuries by the forces that
create them and is therefore useful in
guiding nonoperative and operative
stabilization.
350
Lateral Views
Posterior
column
Ligamentum
flavum
Facet joint
Interspinous
ligament
Supraspinous
ligament
Transverse Views
Posterior longitudinal
ligament
Anterior column
Posterior column
Facet joint
In compressive flexion injuries,
three types are described, all having
in common compression failure of
the anterior column. Type I injuries
involve only anterior column failure
in compression. Type II compres-
sive flexion injuries involve com-
pression failure of the anterior
column combined with tension fail-
ure of the posterior column, with the
axis of rotation being within the
middle column. In type III injuries,
the middle column fails as well, ro-
tating back into the spinal canal due
to either tension or “hydraulic
blowout” (Fig. 6, A). With this
mechanism, the middle-column
height is maintained or increased. In
Journal of the American Academy of Orthopaedic Surgeons
Anterior Middle Posterior
column column column
Anterior column
Middle column
Posterior column
one series of surgically treated tho-
racolumbar fractures, this injury
mechanism was most common, seen
in 48% of cases.13
Distractive flexion injuries repre-
sent tension failure of all three
columns due to flexion about an
axis at or anterior to the anterior
longitudinal ligament. This cate-
gory includes flexion-distraction
fracture-dislocations and the seat-
belt injuries described by Denis
(Fig. 6, B).
Lateral flexion injuries are seen in
two patterns, the first being unilat-
eral compression failure of the ante-
rior and middle elements. In the
second pattern, the posterior ele-

A B
Fig. 6 Lateral injury radiographs. A, Ferguson-Allen type III compressive flexion injury. B, Distractive flexion injury. C, Translational in-
jury (primarily anteroposterior translation in combination with
ments are disrupted as well, with ip-
silateral compression failure and
contralateral tension failure, includ-
ing unilateral facet dislocations.
Translational injuries are the re-
sult of anterior-posterior or lateral
shear forces. They are uncommon as
isolated injuries but are often associ-
ated with other injury mechanisms
(Fig. 6, C). In torsional flexion in-
juries, the anterior column fails in
compression and rotation, and the
posterior elements fail in tension
and rotation, commonly with mid-
dle-column involvement as well.
These and translational injuries are
the most unstable thoracolumbar in-
juries and have the highest propen-
sity to cause paraplegia.
Vertical compression injuries are
characterized by anterior- and mid-
dle-column compression failure
with vertebral-body shortening.
Middle-column failure is osseous,
not ligamentous, and the posterior
Vol 3, No 6, November/December 1995
bony elements may also fail in com-
pression.
Distractive extension, the final in-
jury mechanism, is rare in the thora-
columbar spine. This mechanism is
characterized by tension failure of
the anterior column and compres-
sion failure of the posterior elements.
Neurologic Injury and Recovery
In 1988, Dall and Stauffer14 classi-
fied burst fractures of the thora-
columbar junction by the degree of
regional kyphosis and the location of
maximal canal compromise in order
to correlate fracture pattern with
neurologic injury and recovery. The
severity of neurologic injury did not
correlate with the fracture pattern or
the amount of spinal canal compro-
mise. Neurologic recovery was
greatest in patients with more than
15 degrees of initial kyphosis and
least in patients with less than 15 de-
grees of initial kyphosis and maxi-
Jeffrey M. Spivak, MD, et al
C
mal canal compromise at the level of
the bony posterior neural arch.
Summary
Successful management of thora-
columbar spine injuries depends on a
thorough knowledge of spinal anat-
omy and an understanding of the in-
jury mechanism and the resultant
compromise of bone and soft-tissue
structures. A complete classification
scheme for thoracolumbar fractures
that incorporates the mechanism of
injury, a description of osseous and
ligamentous destruction, and the de-
gree of neurologic damage is still
lacking. Such a classification system
would enable the treating physician
to identify an unstable thoracolum-
bar injury, make a prognosis as to
neurologic recovery, and direct the
choice of nonoperative or operative
management.
351
Thoracolumbar Spine Trauma: I. Evaluation and Classification
References
1. Ditunno JF Jr (ed): International Stan-
dards for Neurological and Functional Clas-
sification of Spinal Cord Injury. Chicago:
American Spinal Injury Association,
1992.
2. Bohlman HH, Freehafer A, Dejak J:
The results of treatment of acute in-
juries of the upper thoracic spine with
paralysis. J Bone Joint Surg Am 1985;67:
360-369.
3. Soderstrom CA, McArdle DQ, Ducker
TB, et al: The diagnosis of intra-ab-
dominal injury in patients with cervical
cord trauma. J Trauma 1983;23:1061-
1065.
4. Calenoff L, Chessare JW, Rogers LF, et
al: Multiple level spinal injuries: Impor-
tance of early recognition. AJR Am J
Roentgenol 1978;130:665-669.
352
5. Henderson RL, Reid DC, Saboe LA:
Multiple noncontiguous spine fractures.
Spine 1991;16:128-131.
6. Vaccaro AR, An HS, Lin S, et al: Non-
contiguous injuries of the spine. J Spinal
Disord 1992;5:320-329.
7. Holdsworth FW: Fractures, disloca-
tions, and fracture-dislocations of the
spine. J Bone Joint Surg Br 1963;45:6-20.
8. Kelly RP, Whitesides TE Jr: Treatment
of lumbodorsal fracture-dislocations.
Ann Surg 1968;167:705-717.
9. Denis F: The three column spine and its
significance in the classification of acute
thoracolumbar spinal injuries. Spine
1983;8:817-831.
10. Denis F: Spinal instability as defined by
the three-column spine concept in acute
spinal trauma. Clin Orthop 1984;189:65-76.
Journal of the American Academy of Orthopaedic Surgeons
11. McAfee PC, Yuan HA, Fredrickson
BE, et al: The value of computed to-
mography in thoracolumbar frac-
tures: An analysis of one hundred
consecutive cases and a new classifi-
cation. J Bone Joint Surg Am 1983;65:
461-473.
12. Ferguson RL, Allen BL Jr: A mechanis-
tic classification of thoracolumbar
spine fractures. Clin Orthop 1984;189:
77-88.
13. Cotler JM, Vernace JV, Michalski JA:
The use of Harrington rods in thora-
columbar fractures. Orthop Clin North
Am 1986;17:87-103.
14. Dall BE, Stauffer ES: Neurologic injury
and recovery patterns in burst fractures
at the T12 or L1 motion segment. Clin
Orthop 1988;233:171-176.
 Thoracolumbar Spine Trauma:
II. Principles of Management

Jeffrey M. Spivak, MD, Alexander R. Vaccaro, MD, and Jerome M. Cotler, MD

Abstract

The care of patients with thoracolumbar spine trauma with or without neurologic or preventing the secondary cord in-
deficits has evolved dramatically over the past 20 years with the emergence of ter- jury caused by edema and ischemia.
tiary-care spinal injury centers and the development of more effective spinal in- Intravenous methylprednisolone is
strumentation and anesthesia techniques. Despite these advances, the majority of routinely administered in all cases of
patients with thoracolumbar injuries are still treated nonoperatively with cast or blunt spinal cord injury, in accor-
brace immobilization and early ambulation. More aggressive treatment is guided dance with the protocol established
by the use of classification systems that detail the mechanism of injury, the degree by Bracken et al1 (bolus of 30 mg/kg
of compromise of spinal structures, and the potential for late mechanical instabil- of body weight, followed by 5.4
ity or neural injury. The goal of treatment remains attainment of spinal stability mg/kg/hr by continuous infusion
with protection or improvement of the patient’s neurologic status, allowing rapid for a total of 23 hours). Its efficacy
and maximal functional recovery. has been established only in situa-
J Am Acad Orthop Surg 1995;3:353-360 tions in which treatment is started
within 8 hours of injury and in cases
of blunt spinal cord injury. The effi-
cacy of corticosteroid use has not
There are a variety of issues to be rolling of the patient or miscommu- been shown for pure root injuries.
considered in the management of nication concerning the patient’s The complications of steroid use, in-
patients with thoracolumbar spine spinal stability and activity level. An cluding a higher rate of postopera-
trauma. Initial management issues oscillating bed is useful for shifting tive infection and gastric ulcers,
include immobilization, medical sta- the patient’s body weight without
bilization, and achievement of spinal moving the patient. If traction is
alignment. Definitive management deemed desirable, this is an effective
decisions are based on spinal stabil- means of providing spinal immobi- Dr. Spivak is Associate Chief of Spine Surgery,
ity at the injury site and the need for lization. Department of Orthopaedic Surgery, Hospital
decompression of neural elements, for Joint Diseases Orthopaedic Institute, New
followed by appropriate rehabilita- York, and Assistant Professor of Orthopaedic
tion to maximize the patient’s func- Medical Stabilization Surgery, New York University School of Medi-
cine, New York. Dr. Vaccaro is Assistant Pro-
tional outcome. fessor, Department of Orthopaedic Surgery,
Medical stabilization of the trauma Jefferson Medical College of Thomas Jefferson
patient with a thoracolumbar injury University, Philadelphia. Dr. Cotler is Everett J.
Immobilization is of paramount importance. Hy- and Marian Gordon Professor of Orthopaedic
potension secondary to neurogenic Surgery, Jefferson Medical College of Thomas Jef-
ferson University.
Immobilization has been shown ex- shock or hemorrhagic shock must be
perimentally to help limit further reversed through fluid and/or Reprint requests: Dr. Spivak, Department of Or-
damage to the injured spinal cord blood replacement, with or without thopaedic Surgery, Hospital for Joint Diseases
and is often beneficial in controlling the use of vasopressors. Critical or- Orthopaedic Institute, 301 East 17th Street, New
the pain associated with a spinal col- gan systems must be evaluated and York, NY 10003.
umn injury. Simple bed rest with treated as needed.
log-rolling can be used, but prob- Medical treatment of the injured Copyright 1995 by the American Academy of Or-
thopaedic Surgeons.
lems may occur with improper log- spinal cord is directed at minimizing

Vol 3, No 6, November/December 1995 353

Thoracolumbar Spine Trauma: II. Principles of Management
must be considered. Although the
study by Bracken et al has been crit-
icized for methodologic flaws, their
protocol is currently considered by
many to be the standard of care in
acute spinal cord injury and should
be followed. Newer pharmacologic
agents, such as b-glycosides and
growth factors, are currently being
evaluated prospectively in major
spinal cord injury centers.
Thromboembolic disease remains
a considerable problem in acutely
traumatized patients, and patients
with spinal injuries are no excep-
tion.2 We aggressively employ me-
chanical prophylaxis (intermittent
external pneumatic compression de-
vices) for lower-extremity deep-vein
thrombosis and the more serious
pulmonary embolism in all cases of
significant spinal trauma. Routine
prophylaxis also includes subcuta-
neous heparin in a dosage of 5,000
units every 12 hours. The use of in-
travenous low-molecular-weight
heparin is currently being investi-
gated. Deep-vein thrombosis is di-
agnosed with the use of real-time
B-mode ultrasonography. Venogra-
phy is used if the ultrasound results
are unclear. The presence of pul-
monary embolism is assessed with
ventilation-perfusion scanning and,
if needed, pulmonary angiography.
Treatment includes heparin or war-
farin if the patient clearly does not
have an operative problem. If
surgery is required, the thromboem-
bolic problem is treated by percuta-
neous placement of an inferior vena
cava filter.
Alignment
Various means have been employed
to improve spinal alignment in the
peri-injury period. Postural reduc-
tion with simple bed rest and place-
ment of a small padded bolster at the
apex of a spinal deformity may be ef-
fective in certain injury patterns. If
354
the desire is to improve anterior ver-
tebral column height and reduce the
degree of kyphosis, Gardner-Wells
tong–bifemoral skeletal traction may
be a useful adjunct. This form of im-
mobilization certainly ensures pa-
tient compliance in terms of bed rest.
The skin beneath any padded bolster
must be examined daily for evidence
of skin breakdown, which could sig-
nificantly compromise a posterior
surgical site.
Evaluation of Spinal
Stability
In determining the optimal treat-
ment in cases of spine trauma, the
stability of the particular spinal in-
jury must be carefully assessed fol-
lowing a complete clinical and
radiographic evaluation. In the
most general sense, the spinal col-
umn is considered stable if it is able
to withstand normally applied phys-
iologic loads without the develop-
ment of neural irritation or damage,
unacceptable deformity, or chronic
pain due to abnormal motion.
Early reports assessing the degree
of spinal stability focused on the in-
tegrity of the posterior elements.
More recent analysis considers the
degree of osseous and ligamentous
destruction in conjunction with the
degree of canal compromise, defor-
mity, and neurologic deficit.
In 1983, Denis used computed to-
mographic analysis of thoracolum-
bar fractures and dislocations in the
development of the three-column
theory of spinal stability,3,4 as de-
scribed in the accompanying article.
The spine is considered to be un-
stable if two or more columns are
injured. Denis described three
categories of instability. Mechanical
instability includes severe compres-
sion fractures, in which posterior el-
ements are injured in distraction and
late kyphotic collapse is possible.
Cases of neurologic instability in-
Journal of the American Academy of Orthopaedic Surgeons
clude burst fractures without neuro-
logic deficit, in which the late onset
of neurologic deficits is sometimes
seen. The most unstable injuries,
those characterized by mechanical
and neurologic instability, include
burst fractures with neurologic
deficit and fracture dislocations.
White and Panjabi5 have devised
a clinical checklist for thoracic and
lumbar instability. In their system,
they consider radiographic criteria
(subluxation, segmental angulation)
and the degree of neural injury, as
well as anticipated dangerous load-
ing, to determine the degree of
spinal instability.
At our institutions, we use Denis’
definition as a broad guideline for
the assessment of stability of a thora-
columbar injury. Spinal injuries
with any associated neurologic
deficit are considered to be unstable.
These injuries usually require opera-
tive stabilization to adequately im-
mobilize the injured segments and
protect the injured and at-risk neu-
rologic structures.
Nonoperative Treatment
Nonoperative treatment in thora-
columbar trauma is reserved for
those injuries that are considered to
be stable without the potential for
progressive deformity or neural
compression with ambulatory treat-
ment and external immobilization.
In 1992, Gertzbein6 reported the
findings from the Scoliosis Research
Society multicenter prospective
study of 1,109 patients with spinal
fractures. At the 2-year follow-up,
patients with a kyphotic deformity
of more than 30 degrees had an in-
creased incidence of significant back
pain.
One-column injuries are stable by
definition; these include wedge
compression fractures and fractures
of the posterior elements. These in-
juries will heal well when treated in

an ambulatory fashion with external
immobilization by means of a plas-
ter cast or orthosis. The form of im-
mobilization chosen should provide
a force vector opposite to the initial
major injury force, such as an exten-
sion cast or an orthosis for a com-
pressive flexion injury. For injuries
above T7, an occipitocervicothoracic
orthosis is used until healing, which
is expected in 8 to 12 weeks. For le-
sions at T7 or below, a thoracolum-
bosacral orthosis is prescribed, and
healing is expected in 12 to 16 weeks.
In low lumbar injuries, the cast or
orthosis should include one thigh for
the first 6 to 12 weeks in order to sta-
bilize the pelvis.
Nonoperative treatment is also an
option for certain isolated injuries
with bone instability and no neuro-
logic deficits. For example, flexion-
distraction injuries through bone
(Chance fractures) will heal when
immobilized in an extension cast or
a custom-molded orthosis. Certain
vertical compression fractures (sta-
ble burst fractures) with minimal or
no middle-column comminution or
shortening and minimal kyphosis
can also be treated in an extension
cast or a custom-molded brace.
Operative Treatment
Surgical Indications
Operative management of thora-
columbar injuries is indicated for le-
sions that are considered to be
unstable and to have the potential
for further compromise to the neuro-
logic elements. Even in patients
with complete neurologic lesions,
surgical stabilization can allow more
rapid mobilization and earlier com-
mencement of physical rehabilita-
tion. Controversy exists as to the
treatment of unstable spinal column
injuries in patients without neuro-
logic injury. Proponents of initial
nonoperative treatment believe that
good results can be obtained in most
Vol 3, No 6, November/December 1995
cases and that late neurologic
deficits, bone deformity, and insta-
bility can be corrected if they occur.
We agree with others who believe
that surgical stabilization facilitates
the most rapid functional return and
reintegration into society for pa-
tients with unstable fractures. This
approach also prevents the late com-
plications of neurologic injury, de-
formity, and painful instability. The
surgical methods needed to correct
the sequelae of late instability and
fixed deformity are quite complex
and fraught with significant mor-
bidity.
In cases of middle-column dis-
ruption, decompression of persis-
tent spinal canal compromise is
often indicated, even in the presence
of complete neurologic lesions, in
the hope of additional root recovery.
This is most important in the case of
trauma at the thoracolumbar junc-
tion and in the upper lumbar spine,
where recovery of an additional root
level may have tremendous func-
tional significance.
Decompression
Spinal canal intrusion by bone or
soft-tissue fragments may require
surgical decompression. Most often,
compression occurs anteriorly in the
spinal canal due to retropulsion of
bone or disk fragments from the mid-
dle column. Posterior compression
by lamina fragments can also occur.
In cases of significant spinal canal
compromise with an incomplete neuro-
logic deficit, persistent neural com-
pression should be assumed to
necessitate spinal decompression. In
the case of complete lesions of the
thoracolumbar junction and lumbar
spine, additional root recovery may
provide important functional bene-
fits; decompression may be indicated
if significant canal compromise ex-
ists. In cases without neurologic
deficit, canal decompression may not
be indicated as long as spinal stability
can be ensured due to eventual re-
Jeffrey M. Spivak, MD, et al
modeling of retropulsed bone frag-
ments.
Decompression of the spinal col-
umn can be done via an anterior, a
posterolateral, or a posterior ap-
proach. Anterior decompression
by means of a vertebrectomy is use-
ful for spinal canal compromise
due to retropulsion of bone and
disk fragments from the middle col-
umn in the thoracic spine and tho-
racolumbar junction. The vertebral
body is commonly reconstructed
with the use of an autogenous ante-
rior iliac-crest strut graft. Anterior
decompression and vertebral re-
construction require additional
stabilization, which can be accom-
plished by means of external
immobilization, anterior instru-
mentation, or posterior instrumen-
tation and fusion.
Posterolateral decompression in
the thoracolumbar spine can be per-
formed with the use of a modified
costotransversectomy approach by
removal of the transverse process
and pedicle. Although posterior
spinal stabilization can be per-
formed through the same incision,
structural grafting of the anterior
column is difficult via this approach
because of the limited exposure.
Another method of posterolateral
decompression that can be em-
ployed at the level of the conus
medullaris involves removing the
medial half of the pedicle at the level
of injury, undercutting anterior to
the retropulsed fragment, and im-
pacting the fragment back into the
vertebra without retraction of the
dura. We have no experience with
this technique and prefer anterior
decompression in these situations
for more complete visualization of
the compressed dural sac.
Posterior decompression of the
retropulsed middle column can be
done either directly or indirectly.
We use direct posterior decompres-
sion only below the conus medul-
laris in the region of the cauda
355
Thoracolumbar Spine Trauma: II. Principles of Management
equina. Retraction of the dural sac
may be necessary for direct posterior
decompression; this can cause dam-
age to the spinal cord and conus
medullaris. The safe region is typi-
cally at the level of L2 and more cau-
dally. This can be easily confirmed
with a preoperative magnetic reso-
nance imaging study.
Indirect posterior decompression
through the use of distraction and
lordosis forces can be useful in the
thoracic spine and at the thora-
columbar junction. Distraction in-
strumentation has been shown to be
effective in reducing retropulsed
middle-column fragments in the
spinal canal, especially when done
within 2 days of injury. Transpe-
dicular screw constructs that allow
distraction and lordosing force ap-
plications can also be used for indi-
rect canal decompression. It has
been shown experimentally that in-
direct reduction results from the in-
sertion of the posterior annulus
fibrosus into the superior vertebral
endplate, not the posterior longitu-
dinal ligament.7 Distraction, not lor-
dosis, was shown to be the major
reduction force, and a combination
of distraction and lordosis was
found to provide the optimal indi-
rect reduction forces necessary for
spinal realignment.
Laminectomy alone as a decom-
pressive procedure has been shown
to be ineffective in alleviating ante-
rior spinal canal compression.
Laminectomy is indicated in pa-
tients with neurologic deficits and
laminar fractures, to allow inspec-
tion for trapped neural elements and
dural tears. In all cases in which a
laminectomy is performed, the
spinal column is further destabi-
lized, and fusion with instrumenta-
tion is mandatory.
Timing of Surgery
We believe that surgical decom-
pression, if needed, and stabilization
of thoracolumbar injuries should be
356
done on an urgent, not emergent, ba-
sis. Patients are medically stabilized
as active fracture bleeding abates,
and hematoma is allowed to form,
minimizing surgical blood loss, es-
pecially with anterior decompres-
sive procedures. The only emergent
indications for surgery in cases of
thoracolumbar trauma are a pro-
gressive neurologic deficit and an
incomplete neurologic deficit associ-
ated with an irreducible dislocation,
both of which are uncommon. No
studies have documented improved
neurologic outcomes with emergent
stabilization of unstable thora-
columbar injuries with or without
neural decompression. Studies have
shown, however, that even late de-
compression of persistent thora-
columbar spinal cord compression
can be beneficial in terms of im-
proved neurologic status.8
Posterior Instrumentation
The choice of posterior instru-
mentation and the selection of the
method of application are based on a
number of factors. The mechanism
of injury and the resultant fracture
pattern determine the force applica-
tion that must be supplied by the in-
strumentation system. In general,
distraction instrumentation is used
for compression injuries with intact
posterior elements. Distraction and
lordosing constructs are also useful
for indirect decompression of spinal
canal compromise due to middle-
column compression. Distraction
can be achieved with either hook,
pedicle-screw, or hybrid constructs
connecting longitudinal rods. Com-
pression constructs are used for flex-
ion-distraction injuries if the middle
column is not comminuted and the
facets are intact. Segmental stabi-
lization with hooks, sublaminar
wires, and transpedicular screws is
used in the highly unstable flexion-
rotation and translational injuries
and can be used in conjunction with
compression or distraction forces if
Journal of the American Academy of Orthopaedic Surgeons
needed. In cases of posterior stabi-
lization after anterior decompres-
sion and strut-graft stabilization of
the anterior and middle columns,
compression instrumentation cre-
ates the most stable overall con-
struct.
Treatment of Specific Injuries
Middle-Column Disruption With
Canal Compromise
We agree with others that ante-
rior decompression is the most reli-
able method of achieving a complete
decompression and is preferred for
cases of anterior canal compromise
with incomplete neurologic deficits.
Direct posterior decompression is
used for injuries below the conus
medullaris. In cases without neuro-
logic deficit in which stabilization is
required, indirect posterior decom-
pression is performed. In cases of
complete injury, if one is attempting
decompression for added functional
root recovery, we prefer either ante-
rior decompression at or above the
conus level or direct posterior de-
compression below the conus level;
if not, stabilization is accomplished
posteriorly, with indirect reduction
of the spinal canal.
After anterior decompression, we
utilize an autologous tricortical ante-
rior iliac-crest strut graft, placed be-
tween the superior endplate of the
vertebral body above and the infe-
rior endplate of the vertebral body
below, with the anterior column un-
der distraction. This is followed by
posterior fusion with compression
instrumentation with use of a rod-
hook system or a rigid pedicle
screw-rod construct.
Anterior instrumentation systems
can obviate the need for posterior
surgery. While certain older anterior
systems were associated with late in-
jury to the great vessels, newer sys-
tems present a lower profile and are
placed along the lateral aspect of the
vertebral body. These have been

used safely to stabilize vertebral re-
constructions for trauma and tumor
surgery. If anterior instrumentation
is used, the bone graft is sized to fit
between the inferior endplate of the
cranial vertebra and the superior
endplate of the caudal vertebra, to al-
low fixation into undisturbed verte-
bral bone. We remain reluctant to
use hardware anteriorly at L5 and
the sacrum, because of the potential
for late injury to the great vessels.
Middle-Column Disruption and
Posterior-Element Fractures
Posterior surgery is an integral
part of the operative treatment of
vertical compression or burst frac-
tures with associated laminar frac-
tures and neurologic deficits. A
number of reports have documented
dural tears and entrapment of neural
elements with laminar fractures. It is
hypothesized that the initial splay-
ing of the pedicles and the posterior-
element displacement are followed
by the recoiling to the stable position
that is seen on radiographic evalua-
tion.9 The dura and neural elements
become trapped within the frac-
tured posterior elements and injured
during the recoil. Recognition of
trapped neural elements and their
decompression can be accomplished
only through posterior exploration.
Special care must be taken during
the approach. Because the dura and
neural elements can be encountered
before reaching the lamina, expo-
sure of the lamina above and below
the injury level is done first. The in-
jury level is then exposed by careful
blunt dissection. Visualization of
the dura or nerve roots is an indica-
tion for hemilaminectomy to explore
the surrounding dura for tears,
which are repaired if possible.
Hemilaminectomy and explo-
ration may also benefit patients with
laminar fractures without posteri-
orly visible neural elements, as
neural entrapment along the anterior
aspect of the lamina is possible. This
Vol 3, No 6, November/December 1995
might be particularly useful in pa-
tients with neural deficits and only a
small amount of anterior compres-
sion, in whom occult neural injury
secondary to laminar entrapment is
more likely.
Thoracic Spine (T1-T10)
In the thoracic spine, we treat Fer-
guson-Allen type I compressive flex-
ion injuries10 with an extension cast
and early ambulation. Type II and
type III compressive flexion injuries
with or without neurologic deficit
are generally stabilized with seg-
mental instrumentation with the use
of a hook-and-rod construct. In the
presence of a complete spinal cord
injury, sublaminar wires can be uti-
lized in addition to a hook-rod con-
struct. Alternatively, one may use
an inexpensive rectangular Luque
rod with sublaminar wires (Fig. 1).
The Luque rectangle is prebent in
mild hypokyphosis to reduce the
segmental kyphosis at the level of in-
jury. The instrumentation generally
incorporates three levels above and
two to three levels below the injury.
Other acceptable instrumentation
constructs include standard Luque
rods with spinous-process wiring
A B
Jeffrey M. Spivak, MD, et al
and distraction rods with supple-
mental segmental fixation.
Ferguson-Allen type III compres-
sive flexion injuries with significant
canal compromise and an incom-
plete neural deficit are treated by
one-stage anterior decompressive
vertebrectomy and autologous iliac-
crest strut grafting followed by pos-
terior compression instrumentation
and fusion. The posterior instru-
mentation incorporates only the
motion segments involving the strut
graft, provided the hooks are placed
out of the zone of spinal cord injury.
Anterior instrumentation is an ac-
ceptable fixation alternative.
Translational and rotational in-
juries are highly unstable and require
posterior segmental instrumentation.
In most cases, patients have complete
neurologic injuries but will benefit
from early stabilization and mobiliza-
tion. Following postural reduction,
fixation is achieved with hook and/or
sublaminar wire constructs, as de-
scribed for the severe compressive
flexion injuries.
Thoracolumbar Junction (T11-L2)
Ferguson-Allen type II compres-
sive flexion injuries of the thora-
Fig. 1 Anteroposterior (A)
and lateral (B) radiographs
show successful fusion fol-
lowing operative treatment
of an unstable T6 fracture in
a patient with a complete
spinal cord injury. A Luque
rectangle was used, with
sublaminar wire fixation of
three intact levels above and
three intact levels below the
injury site. Additional non-
instrumented levels within
the construct had posterior
element fractures.
357
Thoracolumbar Spine Trauma: II. Principles of Management
columbar junction are treated by pos-
terior compression instrumentation,
with the intact middle column being
used as a hinge to restore lordosis.
Type III injuries without significant
canal compromise are treated with
the use of distraction-lordosis instru-
mentation to maintain the middle-
column height and restore the
anterior-column height. Care must
be taken to avoid overdistraction in
patients with concomitant posterior-
column tension injuries. Caution
must be exercised if one chooses to
use short-segment pedicle-screw sta-
bilization in cases of anterior- and
middle-column compromise. High
fixation failure rates have been re-
ported in these clinical situations.11
We have utilized this form of treat-
ment with postoperative immobiliza-
tion in a hyperextension plaster body
cast for a minimum of 3 months and
have found fewer instrumentation
failures than reported. A custom-
molded thoracolumbosacral orthosis
may also be acceptable for postoper-
ative immobilization, but we have
no experience with it in this clinical
setting.
In cases of significant canal com-
promise and incomplete or complete
neurologic injury, we prefer anterior
decompression by means of vertebral
corpectomy and autologous iliac-crest
strut grafting, followed by posterior
compression instrumentation with the
use of hooks or transpedicular screws.
Acceptable alternative treatment op-
tions include (1) anterior decompres-
sion with reconstruction and anterior
internal fixation and (2) posterior fixa-
tion and indirect reduction followed
by postoperative examination of the
spinal canal with myelography or
computed tomography and second-
stage anterior decompression and ver-
tebral reconstruction if significant
canal compromise and neurologic
deficit persist. One objection we have
to the latter approach is that an ante-
rior structural bone graft is supported
by posterior distraction instrumenta-
358
tion, which is a less stable construct
than posterior compression instru-
mentation.
In vertical compression injuries
with compromise of the anterior and
middle columns, the decision for sur-
gical stabilization rests on the integrity
of the posterior ligament-bone com-
plex. If the posterior elements are in-
tact without significant kyphosis (less
than 20 degrees) or anterior loss of ver-
tebral body height (less than 50%), am-
bulatory nonoperative treatment with
an extension body cast or custom-
molded extension thoracolumbo-
sacral orthosis can be used (usually
including a single thigh cuff). We gen-
erally stabilize vertical compression
injuries with three-column involve-
ment posteriorly. Patients with ante-
rior thecal sac compression and an
incomplete neurologic deficit, regard-
less of the integrity of the posterior el-
ements, are treated operatively by
one-stage anterior vertebrectomy and
strut grafting followed by posterior
compression instrumentation (Fig. 2).
Anterior decompression followed by
anterior instrumentation is certainly
an acceptable option.
A B
Journal of the American Academy of Orthopaedic Surgeons
Distractive flexion injuries are
treated by reduction and compression
instrumentation, as described previ-
ously. Lateral flexion injuries can be
treated with combined ipsilateral dis-
traction and contralateral compres-
sion, applied with the use of hooks or
transpedicular screws above and be-
low the level of injury. The compres-
sion force is applied first, to improve
the lordosis and prevent kyphosis
from the distraction force.
Translational and torsional flex-
ion injuries are treated by segmental
instrumentation, preferably with
pedicle screws. Hook constructs
and screw-hook combination con-
structs can also be used.
Low Lumbar Injuries (L3-L5)
Compressive flexion and vertical
compression injuries of the low
lumbar spine are managed by
transpedicular screw instrumenta-
tion, fusing one level above and one
level below the injury (Fig. 3). Cau-
tion must be exercised with the use of
short-segment instrumentation
when there is loss of anterior- or mid-
dle-column support, because of the
Fig. 2 Anteroposterior (A)
and lateral (B) radiographs
obtained after surgical treat-
ment of a patient with an in-
complete neurologic deficit
and significant bony canal
compromise after a Fergu-
son-Allen type III compres-
sive flexion injury. The
procedure involved a one-
stage anterior L1 corpectomy
with autogenous iliac-crest
strut grafting and posterior
T12-L2 fusion with compres-
sion-rod instrumentation.

A B
potential for screw failure. Trans-
pedicular bone grafting of the in-
jured level may be of benefit, but we
have no experience with this tech-
nique. If decompression is needed,
we prefer the posterior direct tech-
nique via laminotomy, although an-
terior decompression can be done as
well. Decompression should be con-
sidered even for complete neurologic
lesions, to allow for possible addi-
tional lumbosacral root return. Dis-
A B
Vol 3, No 6, November/December 1995
Fig. 3 Anteroposterior (A)
and lateral (B) radiographs
obtained after operative
treatment of an L5 vertical
compression injury in a 21-
year-old man with a partial
neurologic deficit. The opera-
tive procedure included L5
laminectomy and direct poste-
rior decompression and stabi-
lization with pedicle-screw
fixation, with which mild dis-
traction and lordosis forces
were applied. Postopera-
tively, the patient was allowed
to ambulate in a body cast,
molded in extension and in-
corporating a thigh segment.
traction-rod instrumentation is less
desirable in this region because of the
associated loss of lordosis and the
need to instrument additional levels
above and below the injury site.
Translational and flexion-rotation
injuries in the low lumbar spine also
require segmental instrumentation.
This is easily accomplished by
transpedicular screw fixation one
level above and one level below the
injury (Fig. 4).
Fig. 4 Anteroposterior (A)
and lateral (B) radiographs
show segmental transpedic-
ular instrumentation of a
highly unstable translational
injury after postural reduc-
tion. (This is the same injury
seen in Figure 6, C, in the ac-
companying article.)
Jeffrey M. Spivak, MD, et al
Rehabilitation
In patients with a residual neuro-
logic deficit, passive motion exer-
cises and splinting are useful in the
early postinjury period to maintain
joint flexibility and maximize func-
tional potential. Upper-body
strength training is essential for
functional paraplegic patients to fa-
cilitate self-transfers and a return to
independence in society. The appli-
cation and use of orthotic devices
with appropriate training can allow
independent ambulation by patients
with functional motor strength at
low lumbar levels. Assistive devices
and vocational retraining help the
patient to regain maximal functional
and financial independence.
Summary
Successful management of thora-
columbar spine injuries protects
the patient from further spinal de-
formity and neurologic deficit. The
majority of patients with thora-
columbar injuries are still treated
nonoperatively with cast or brace
immobilization and early ambula-
tion. There is no clear consensus as
to the absolute indications for surgi-
cal intervention in patients with
many types of thoracolumbar frac-
tures. Opinions vary most in cases
of complete spinal cord injury or no
neurologic deficit at all. Operative
treatment, including both decom-
pression and stabilization, is more
universally accepted in cases of in-
complete spinal cord injury with
radiographic evidence of persistent
mechanical compression of the
neural structures. Controlled
prospective studies evaluating con-
temporary classification systems
and recommended treatment pro-
tocols (both nonoperative and op-
erative) are necessary to better
define the role of surgical interven-
tion in these potentially devastat-
ing injuries.
359
Thoracolumbar Spine Trauma: II. Principles of Management
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