A Limping 6-Year Old
Radiology Cases in Pediatric Emergency Medicine
Volume 4, Case 16
Martin I. Herman, MD
LeBonheur Children's Medical Center
University of Tennessee School of Medicine
This is a 6-year old male who presents with a chief
complaint of a limp which began 6 months ago. There
is no history of trauma, fever, swelling or pain.
Recently, he began complaining of right hip pain and
the limping became more noticeable. He was seen by
his physician on two occasions in the last six months for
this complaint. Mother was advised to administer
ibuprofen on both visits. He was diagnosed as having
toxic synovitis of the hip joint on the first encounter and
a non-specific soft tissue injury at the second visit.
His past history is not contributory. His family
history is negative for arthritis or skeletal disorders. His
growth and development are normal.
Exam: VS T36.9 C, P 108, R 24, BP 110/68. Wt.
24.3 kg. Alert, active, well developed, in no acute
distress. He is not toxic. HEENT exam negative. Neck
without lymphadenopathy or thyromegaly. Heart
regular without murmurs. Lungs clear bilaterally.
Abdomen soft, no organomegaly, no masses. Normal
male genitalia. Extremities: There is a 2 cm leg length
discrepancy. His right thigh is smaller than his left.
There is pain with hip extension and external rotation.
Trendelenburg test: no hip abductor weakness. Gait:
shortened stance phase on the right. The right knee is
flexed indicative of a leg length discrepancy.
Lab studies: CBC WBC 7,000, Hgb 12.0, Hct 36%,
ESR 13 mm/hr. UA normal. Radiographs of his hips
are obtained.
View hip radiographs.
The right hip (left on the image) shows widening of
the joint space. The femoral epiphysis is fragmented
and flattened. The physis appears narrow. The
femoral neck is short and wide (Coxa magna). There is
flattening of the femoral capitellum (Coxa plana). Not
seen here but common in patients with this disease is
lateral displacement of the femur relative to the
acetabulum (Coxa varus).
Discussion
Avascular necrosis (AVN) of the femoral head may
be idiopathic (Legg-Calve-Perthe's Disease) or due to
some insult to the vascular supply of the femur. For
example, septic arthritis of the hip, trauma to the hip,
especially with dislocation, or steroid use may result in
avascular necrosis. In our patient, there is no recall of
trauma, steroid use or known congenital hip disease to
explain his AVN, leaving Legg-Calve-Perthe's Disease
to be the best explanation of his radiographic findings
and limp.
Pathophysiology. The blood supply of the femoral
head changes with time and growth. Initially the main
source of nutrition is supplied directly by nutrient
vessels within the femoral head. A small amount of
blood passes to the head via the ligamentum teres. By
the time the child reaches 1.5 years of age the blood
supply has changed. Now most of the blood is being
supplied by the femoral circumflex arteries, which enter
the femoral epiphysis after traversing the hip capsule.
Any injury to the hip can result in avascular necrosis
since the blood supply is so tenuous.
Limping is a dysfunction in gait which can be divided
into two phases, the stance and the swing phase. The
stance phase begins with the heel strike and ends with
the toe off. The swing phase begins with the push off
and ends with the heel strike. Both feet are on the
ground for about 20% of the cycle. Any aberration of
the cycle will be noticed as a limp. The gait may
appear choppy or labored and may be due to pain,
weakness or deformity. Determining the cause of the
limp may be easier if one can determine what type of
limp is present. Historically, limps have been divided
into three types: antalgic, Trendelenburg, and short
leg.
Antalgic gait is caused by pain and is also called
the quick step gait. Patients with this will have a shorter
stance phase on the affected leg. This quick step
minimizes the time stress is placed on the painful
extremity. A compensatory acceleration is seen in the
contralateral swing phase.
Trendelenburg gait, also called the abductor lurch
gait, is seen in children with chronic hip disease. In this
type of gait the hip drops down (pelvic tilt) during the
swing phase due to weakness of the contralateral
gluteus medius muscle. With bilateral involvement, the
trunk will sway from side to side with walking.
Trendelenburg gaits do not affect the amount of time
standing on either foot. You can detect gluteus medius
paresis by performing the Trendelenburg test. In this
test, the patient is asked to stand with one foot off the
ground and is observed for dropping or tilting of the
pelvis on that side. A slight rise in the pelvis is to be
expected. In the case of our patient, the Trendelenburg
test was negative for pelvic tilt on either side, indicating
that the cause of his limp was not due to muscle
weakness, nor was the condition present long enough
to result in atrophic weakness of the gluteus medius
muscles.
The so called short leg gait is the result of true or
pseudo leg length discrepancies. In this gait, the longer
leg will have persistent knee flexion on standing. The
child might also walk on the toes of the shorter leg to
compensate. An up and down motion of the pelvis may
be seen in this gait, but the Trendelenburg test will be
normal. True leg length abnormality can be
determined by measuring the anterior iliac spine to
medial malleolus distance. Apparent or pseudo-leg
length mismatches may be due to joint contractures of
either hip or knee flexors. In this case, measuring the
umbilical to medial malleolus distance will quantify the
differences more accurately.
Our patient had a 2 cm discrepancy and, when
standing, it appeared that the right leg was longer as he
kept the right knee flexed. His gait was consistent with
both an antalgic gait and a short leg gait.
The differential diagnosis of limping may be divided
into categories by disease class and also sub-divided
by age at presentation. For the purposes of this
discussion, I have divided the etiologies of limp into
pathophysiologic groups as follows: vascular (vasculitic
and inflammatory), infectious, congenital, trauma,
toxic/metabolic, neoplastic, degenerative,
neuromuscular, and other.
Vascular causes include juvenile rheumatoid arthritis,
ankylosing spondylitis, systemic lupus erythematosis,
scleroderma, Henoch Schonlein purpura, psoriasis,
insect venoms, Stevens-Johnson syndrome, and deep
venous thrombosis. Rheumatologic conditions such as
juvenile rheumatoid arthritis (JRA) can present in a
single joint and are easily mistaken for a septic joint.
An associated rash or iridocyclitis may help in making
the diagnosis. Limping may also be a presenting
problem in Henoch Schonlein purpura (HSP) as arthritis
may occur in association with HSP.
Rheumatic Fever, Lyme Disease and Kawasaki's
Disease should be kept in mind (see infectious causes).
Other inflammatory conditions associated with limping
include serum sickness, Stevens-Johnson syndrome,
reactions to insect venom and overuse syndromes.
Deep Vein Thrombosis (DVT) is rare in children but
may present in patients with hypercoagulable states,
poor blood flow, or after trauma to the lower extremities.
The diagnosis of DVT may be made via Doppler flow
studies, impedance plethysmography or venograms.
Treatment will vary depending on the age of the
thrombus, location and co-existing disease. Psoriasis
may have an arthritis associated with its dermatologic
manifestations and, ironically, the arthritis can precede
the skin changes. The collagen vascular disorders and
rheumatoid diseases constitute a wide assortment of
diseases that may present with limping. Often,
radiographic findings will be absent until degenerative
changes occur.
Infectious causes include osteomyelitis, septic
arthritis, toxic synovitis, diskitis, Lyme arthritis,
tuberculous arthritis, etc. Bone and joint infections can
be easily missed and can result in permanent sequelae
if the diagnosis is delayed. Usually there is fever with
swelling, erythema and tenderness near the area of
infection, but often the only help in detecting
osteomyelitis or pyogenic arthritis is the limp. Major
etiologic agents include Staphylococcus aureus and
Streptococcus pyogenes (group A beta-hemolytic
strep). In neonates, group B streptococcus may be
causative. Adolescents need to be screened for
Neisseria gonorrhea and, in patients with sickle cell
anemia, Salmonella species may be the cause.
Evaluation should include the spine and pelvis in
addition to the extremity to avoid missing diskitis or
sacroiliac disease.
Not to be confused with infectious arthritis, toxic
synovitis presents as joint pain with low grade fever
usually associated with or shortly after a viral illness. It
is self-limited and can be treated with analgesics and
observation. Rubella vaccine can also cause an
arthritis.
Lyme arthritis is a sequelae to Lyme disease, a
tick-borne infection due to Borrelia burgdorferi.
Characteristically the disease starts with erythema
migrans. It may involve all major body systems,
including the brain, peripheral nerves (Bell's Palsy is
seen, often bilaterally) and joints. Five types of arthritis
can occur: 1) episodic, involving 1-4 joints for < 1 week
recurring at least 2 weeks later, 2) acute pauciarticular,
1-4 joints for < 4 weeks, 3) chronic pauciarticular, 1-4
joints > 4 weeks, 4) > 3 joints in sequence, and 5) > 5
joints. Treatment may include amoxicillin, doxycycline
(if older than 9) or ceftriaxone.
Tuberculous disease of the bones was once a major
concern and may be showing a resurgence in today's
medical environment because of multiple drug
resistance, AIDS and other immune suppressed
patients in our communities. There are some infectious
diseases that will have an arthritic component to them.
Yersenia enterocolitica, hepatitis A & B, infectious
mononucleosis, rubella, rubeola, coxsackie virus and
human parvovirus B-19 all cause arthritis/arthralgias
and should be considered as possible etiologies in the
evaluation of the limping patient.
One particularly common infectious source of
limping is Hallux incarnatus or ingrown toenail. This
usually affects teenagers, especially those active in
sports. The mechanism in this disorder involves the
way the nail is clipped or manually pared. Treatment
consists of soaking and local treatment. If infection
recurs, surgical removal of the nail or part of the nail is
effective.
Congenital causes of limp include coxa vara,
congenital hip dysplasia, congenital short femur, spinal
dysraphism, and other congenital limb deficiencies.
Congenital hip dislocation (CHD) usually presents in the
nursery but may not be detected until the child is older.
This topic was presented in Pediatrics in Review, vol.
16, no. 8, 1995. Please refer to that issue for more
details. Another radiographic case of congenital hip
dislocation and a discussion are presented in Case 13
of Volume 2, Vomiting Following Reduction of
Intussusception.
As some children may not have dislocated hips at
birth, the term congenital hip dislocation is a misnomer.
For those whose dislocation occurs later in the first year
of life, the term "acquired hip dislocation" is more
appropriate. Meyers dysplasia, which can look similar
to Legg-Calve-Perthes disease, involves the growth
plates of both femoral capital epiphyses only. Also,
multiple epiphyseal dysplasia and hypothyroidism can
mimic LCP. Multiple epiphyseal dysplasia is inherited
as an autosomal-dominant trait. It presents in two
ways: hip abnormalities and short stature. Hip pain
occurs by age 5 and certainly by age 10. The epiphysis
will appear flattened but otherwise normal.
Examples of trauma include toddler's fracture, stress
fracture, patellofemoral pain, spondylolisthesis, ruptured
plantaris tendon, knee strain, meniscal injuries,
herniated nucleous pulposis. When trauma is the
cause of the limp, the older child or adolescent will
provide an accurate description of the forces invoked.
Toddlers (age 1-3 years), however, can present without
a history for injury, or the witness may have felt the
trauma was too insignificant to cause a fracture. Such
a scenario is often found in children who have a
non-displaced fracture of the tibia, known as the
toddler's fracture.
The toddler's fracture usually is a spiral fracture of
the distal tibia without displacement. Refer to Case 17
in Volume 4, The Toddler's Fracture: Accident or Child
Abuse. Sometimes the fracture is only picked up on
follow-up radiographs or by bone scan. In addition to
the toddler's fracture, two other injuries noted in the
limping toddler include fibula fractures caused by
recurrent infant walker trauma and occult cuboid
fractures. Always consider the possibility of inflicted
injuries when assessing infants and children with
limping, and look for bucket handle fractures or corner
fractures that are suggestive of child abuse.
Also remember that contusions, muscle injuries,
splinters, foreign bodies and shoe abnormalities can
result in limping. Teenagers and school age children
may have sprains of the ankle, knee or hip resulting in
limping. Other traumatic causes of limping would
include an avulsion fracture of the base of the fifth
metatarsal, ankle sprains, and stress fractures of the
metatarsals. Salter Harris Type 1 fractures of the distal
fibula may appear as simple ankle sprains. Refer to
Case 3 of Volume 3, Ankle Injuries: A Sprained
Ankle?
Also the limping patient may have torn his plantaris
tendon. This structure is an aponeurosis found in the
lower leg posterior compartment and may rupture
during exercise. Patients report a snapping noise, then
onset of pain. Pain is increased with dorsiflexion.
Treatment involves resting the lower leg (splinting and
non-weight bearing) and analgesics.
Patellofemoral disorders include patellar subluxation,
recurrent patellar dislocation and chondromalacia
patella. This is more commonly seen in females and is
easily aggravated by repetitive bending. Permanent
injury to the cartilage is rare. Typically pain is elicited
by squeezing the patella or is exacerbated by stair
climbing. Treatment includes anti-inflammatory
medications, rest and ice applications. Rarely, a
surgeon may need to debride the underside of the
patella.
Ruptured vertebral disc is more a disease of adults
but has been seen in teenagers, especially those
involved in heavy weight training or arduous labor.
Symptoms are similar to those found in adults with
paresthesias, foot drop, or intractable pain. Treatment
depends on the extent of nerve impingement and may
involve physical therapy, exercises, chemonucleolysis
or surgery.
Toxic/metabolic causes include drugs, rickets,
scurvy, hyperparathyroidism. Surprisingly, some drugs
can cause limb pains and present as limping. Vitamin A
intoxication and carbamazepine have been implicated.
Corticosteroids, ergotamine, phenothiazines and
thiazides may cause muscle cramps. Also, recall that
some drugs can cause a lupus-like syndrome.
Hypercalcemia can cause bone pains. Rickets may be
associated with fractures and pain. The most common
form of rickets seen in the U.S. is vitamin D-resistant. It
is inherited in an X-linked dominant manner. The defect
is in the proximal absorption of phosphate which leads
to hyperphosphaturia. Skeletal changes occur as the
child ages. Other metabolic diseases that affect the
skeletal system include the mucopolysaccharidoses.
All of these disorders usually involve some type of
spinal deformity, with kyphosis being the most common.
Neoplastic causes include benign bone tumors
(unicameral and aneurysmal bone cysts), malignant
bone tumors, metastatic bone disease, and leukemia.
Sarcoma may involve the hip, femur or proximal tibia.
Growing children are affected most often, with the peak
incidence occurring in the teen years. The two most
often seen are Ewing's sarcoma and osteogenic
sarcoma.
Leukemia may present with limb pain or a limp.
Metastatic disease from other primary sites such as
neuroblastoma and lymphoma may also cause bone
pain and limping. Another cause of lower extremity
weakness, and hence limping, is a sacrococcygeal
teratoma. Benign bone lesions such as
osteochondromas and osteoid osteoma may be found
in the limping child.
Degenerative causes include avascular necrosis of
the femoral head (Legg-Calve-Perthe's Disease). Legg
described a non-tuberculous degeneration of the hip
among American children in 1909 at the same time
Perthes of Germany and Calve of France did.
Originally thought to be due to some infectious process,
Legg-Calve-Perthes (LCP) is currently believed to be
caused by avascular necrosis of the femoral head
ossification center. It is seen in about 1 out of 750
children who usually present between ages 4 and 10.
Most likely LCP is due to repeated trauma to the hip in
active boys which may impair the blood supply to this
area. Typical patients will complain of pain with hip
motion and limp. The pain may radiate down the thigh
towards the knee. Swelling and tenderness on exam
are rare. Other findings might include limited internal
rotation, decreased hip abduction, and mild hip flexion
contractures. Occasionally, the thigh is atrophic.
Laboratory examinations are all normal, and the
diagnosis is made by plain radiographs of the hips once
significant necrosis has occurred. Radiographs may be
negative early on. Management of patients with LCP
depends on when they present. Young children who
still have substantial femoral head cartilage have a
good prognosis. Goals of therapy include resolving the
hip joint inflammation and positioning the femoral head
in such a way as to promote healing. If 50% or more of
the femoral head can be seen, therapy is aimed at
maintaining the range of motion until healing occurs.
When more than 50% of the head is involved,
orthopedists will place the hip in an abduction brace, or
hip spica cast, or perform an osteotomy of the proximal
femur to position the femoral head well into the
acetabulum. Usually the brace is used for children
under 7, and osteotomy reserved for the older patient.
Ultimately, the outcome for those who present with less
than 50% of their femoral head involved is good.
Children under 6 do very well, but those over 10 or
those with flattening of the femoral head do not.
Avascular necrosis of the tarsal navicular (Kohler's
disease) can be difficult to diagnose. Irregular
ossification of tarsal bones is common and, when they
occur in the absence of pain or swelling, the diagnosis
should be that of a normal variant. However when
there is pain or swelling, Kohler's disease is present.
This disorder typically is seen in boys between 4 and 7
years. Pain is aggravated by running. Radiographs
show a flattened navicular, which is radiodense and
may appear fragmented. Bilateral changes occur
commonly. For severe symptoms, a short walking cast
(3-6 weeks) may be helpful. If asymptomatic, no
treatment is needed.
Sever's disease results in a painful heel and limping.
It is most common in active children between 9 and 12
years. The calcaneal apophysis joins with the
secondary ossification center to form the posterior
portion of the calcaneus. The Achilles tendon inserts
onto the secondary ossification center. Stress on this
insertion results in microfractures, which lead to
inflammation and pain. Although it was previously held
that the fragmentation and sclerotic changes seen on
lateral radiographs of the calcaneal apophysis were
diagnostic of this condition, it is now thought these
changes represent one of several normal patterns for
ossification. The diagnosis is now made on clinical
grounds with a typical history and tenderness at the
insertion of the Achilles tendon. Treatment may include
heel pads or Achilles stretching prior to participation in
sports. Ice may also be of benefit following exercise.
Refer to Case 20 in Volume 1, Sever's Disease.
Osgood Schlatter's disease is characterized by pain
just below the knee in the vicinity of the tibial tuberosity.
This disease is felt to be due to repeated microtrauma
to the insertion of the patella tendon, similar to Sever's
disease. It occurs most often in adolescent boys during
accelerated growth. The diagnosis is made based on
the presence of tenderness to palpation over the tibial
tuberosity. The tuberosity may be more prominent. No
effusions should be found and the pain should be
exacerbated by forced extension against resistance or
jumping repetitively. Resolution occurs when the
secondary ossification center fuses to the proximal
tibia, which occurs with maturation. Treatment is limiting
activity and also may involve immobilization and
anti-inflammatory medications.
Slipped capital femoral epiphysis (SCFE) is a medial
or posterior slipping of the femoral capital epiphysis. It
often presents with a limp. This diagnosis is difficult to
make and is often delayed. SCFE patients are usually
overweight or have had a significant shear stress
applied to the femoral head. SCFE will often present
with knee pain, thigh pain, groin pain, or hip pain.
SCFE should be considered when pain in one of these
areas is present. Physical exam finds the hip externally
rotated with painful range of motion, especially to
internal rotation, abduction and flexion. Early
symptoms may be subtle. Delaying the diagnosis
results in worsening of the condition and a poorer
outcome. Refer to Case 10 in Volume 2, Thigh and
Knee Pain in an Obese 10-Year Old.
Osteochondritis dessicans is a disease in which a
small island of bone dies and is then sloughed.
Typically, the child complains of poorly localized knee
pain. Osteochondritis dessicans commonly presents in
the preteen or early adolescent. Pain with full flexion is
usually found. If there is a piece of sloughed bone, one
may find an effusion. Locking of the knee can occur
while in flexion. Typically involving the distal femur,
osteochondritis dessicans can be easily identified on
plain AP radiographs of the femur. Treatment starts
with immobilization. Isometric exercises may help
retain quadriceps tone. Arthroscopic surgery is
indicated for continued pain.
Freiberg's disease is another example of avascular
necrosis. This time the second metatarsal is involved.
Treatment for this one is use of a shoe insert to ease
weight bearing. Other osteochondroses such as
Scheurmann's (involving the spine) or Ashman's
(involving the 5th metatarsal) can present as limping.
Neuromuscular conditions include any disease
causing weakness in the hip girdle or lower spine or
extremities which can present as limping. The reader is
referred to standard neurology texts for more
discussion on the myopathic or neuropathic entities.
Miscellaneous causes include sickle cell disease,
hemophilia, tarsal coalition, Blount's disease,
conversion reactions/hysteria, and growing pains.
Blount's Disease is a major cause of angular
deformation in children. It is also called infantile tibia
vara and results from some problem with the growth of
the posteriomedial aspect of the tibial physis.
Physiologic bowing usually has resolved by age 3, but
Blount's disease advances to more severe angulation.
Bracing is needed for those children between 14 and 30
months if the metaphyseal-diaphyseal angle is 9 to 16
degrees and the knee is unstable when walking. Tarsal
coalition is a congenital disorder that results in a vertical
talus with a fixed foot deformity. Patients usually
present with foot pain and limping.
Conclusion: Limping is a common symptom found
in pediatric patients. The evaluation of these patients
requires a careful history and detailed examination.
There are many other sources which discuss limping.
References
Lee RW, Demos TC. Limp and Altered Gait. In:
Rosen P, Doris PE, Barkin RM, et al (eds). Diagnostic
Radiology in Emergency Medicine, 1992, St. Louis,
Mosby YearBook, pp. 509-540.
Dabney KW, Lipton G. Evaluation of limp in
children. Curr Opin in Pediatr 1995;7:88-94.
Tolo VT, Wood B. Hip and Thigh. In: Tolo VT,
Wood B. Pediatric Orthopedics in Primary Care.
Baltimore, Williams and Wilkins, 1993, pp. 135-168.
Sheenan KM,Gordon S, Tanz R. Bilateral fibula
fractures from infant walker use. Pediatric Emerg Care
1995;11(1):27-29.
Simonian PT, et al. Fracture of the cuboid in
children. J Bone Surg 1995;77: B104-106.
Illingworth RS. Limp, Limb and Bone Pains. In:
Illingworth RS. Common Symptoms of Disease in
Children. Oxford, Blackwell Scientific Publications,
1979, pp. 239-243.
Swischuk LE, John SD. Bones and Soft TIssue. In:
Swischuk LE, John SD. Differential Diagnosis in
Pediatric Radiology. Baltimore, Williams and Wilkins,
1995, pp. 187-263.
Causey AL, et al. Missed Slipped Capital Femoral
Epiphysis: Illustrative Cases and a Review. J Emerg
Med 1995;13(2):175-189.
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