PODIATRIC RADIOLOGY Ward’s triangle – area of low trabecular density in the
anterior inferior portion of the calcaneus.
INTERPRETATION OF PEDAL RADIOGRAPHS
X-ray interpretation is a written notation of pathological
findings made in objective terminology. Correlation of
radiographic findings along with clinical and lab findings
allows a physician to arrive at differential diagnoses. X-ray
interpretation follows the 5-step approach:
1. Quality of Film
• Too light or too dark (background/film density)
• Proper projection
• Proper positioning
• Adequate contrast
2. Soft Tissue Assessment
• Increased ST density (edema, obesity)
• ST calcification (vascular, traumatic, chronic)
• ST contour – thicker medially and proximally
• Foreign bodies (r/o artifact w/ multiple views)
3. Bone Assessment
• Number of osseous structures – start distally and
work proximally
• Integrity and morphology of osseous structures – are
cortices intact? Are there structural changes?
• Density of osseous structures – evaluate 2nd MT
o Rule of 1/3s – in individuals <40 y/o,
middle 1/3 should be medullary, outer 2/3 should
be cortical
o Rule of 1/2s – in individuals >40 y/o, half
bone should be cortical, half medullary
o 1/3 of bone is lost before apparent on X-ray
o Cortical bone lost at a rate of 2%/year (>35
y/o)
o Medullary bone lost at a rate or 1% per year
4. Joints and Joint Spaces
• Is there narrowing? Is it symmetrical/asymmetrical?
• Absence of joint = coalition/joint fusion
• Increased space is due to joint effusion
5. Biomechanical Assessment
• Measure of angular relationships for treatment goals
• Determines surgical procedure and post-op correction
• Performed in angle and base of gait
• Serial radiographs to check progression of healing
Conclusion – use systematic approach to avoid missing
details. Review the entire film. Do not let your eyes be drawn
to the obvious. Cite only differentials which make sense and
are defensible to you.
RADIOGRAPHIC VARIANTS
Identification of variants requires knowledge of normal
anatomy. Often normal variants are mistaken for pathology.
The simplest error in this regard is structural overlap due to
wrong projections ordered.
Benign fibrocortical defect – small area of discontinuity
usually in long bones. Eventually fades away over time.
Nutrient foramen – may look like a fx, but discontinuity
“stops” halfway through the cortex.
Epiphyseal plates can look similar to fractures, if the X-ray
passes through the plane of the plate. Closed epiphyseal plates
also leave epiphyseal scars which may look like stress fxs.
These occur in predictable anatomical areas. Epiphyseal
plates tend to close from medial to lateral in teenagers.
Talar beaking is a finding on lateral of the distal neck of the
talus that occurs secondary to capsular pressure.
Trabeculae in some circumstances may be accentuated, and
look possibly like a fx.
The calcaneal apophysis is located at the posterior aspect of
the calcaneus, and has irregular margins. It is often mistaken
for a fracture. It also may be normally bifid.
Compact bony islands are normal and benign variants.
A simulated fracture may occur in any bone w/ more than
one ossification center.
The silver dollar navicular is a normal (small) variant of
navicular development – be sure to r/o Kohler’s dz.
A pronated foot may cause the spaces between bones in the
midfoot to be accentuated, causing a simulated lisfranc’s fx.
A pseudo-epiphysis is a secondary ossification center.
The gun-barrel effect is seen when a bone (usually phalanx)
is perpendicular to the film plane. It may look like a cyst.
Distal phalangeal condyles are normal variants.
Cone-shaped epiphyses may be normal but are frequently
syndromic as well.
ACCESSORY OSSICLES AND SESAMOIDS
Accessory ossicles and sesamoids are normal variants in
anatomy that occur in predictable locations. Accessory
ossicles usually arise earlier, are larger, and irregular
compared to sesamoids (which are usually present in tendons.)
Os Trigonum (2-8%) – occurs posterior to the lateral tubercle
of the talus. When fused (~18 y/o) is called steida’s process.
Os Tibiale Externum (3-12%) – secondary ossification center
of the navicular tuberosity. The pre-hallux type is pyramidal
in shape, while the accessory navicular is in the PT tendon.
Os Intermetatarsium (1-10%) – occurs btw the 1st cuneiform
and 1st and 2nd MT bases. May fuse.
Os Supranaviculare (1%) – located on the dorsal aspect of
the TN joint (may look like fx/osteophyte).
Os Calcaneus Secundarius (1%) – located at the anterior
process of the calcaneus – may be confused w/ rowe fx.
Os Sustentaculi (<1%) – is located posterior to the
sustentaculum tali, often fused. Is assoc w/ STJ coalition.
Os Supratalare is located on the dorsum of the talar head.
Os Vesalinum (<1%) – occurs at the proximal 5th MT base.
Usually confused w/ apophysitis, or a stewart/jones fracture.
Accessory ossicle of the Hallux occurs usually at the base of
the distal phalanx at the medial or lateral aspect.
Os Subtibiale/Subfibulare (4%) - occur distal to the medial
and lateral malleoli. R/o trauma
Hallux IPJ Sesamoids (50%) – located at the IPJ of the
hallux, may remain cartilaginous. Assoc w/ plantar HPKs.
Lesser IPJ Sesamoids occur in the joint capsule and short
flexor tendons of the lesser digits. Does not occur in the 3rd.
Os Peroneum (20%) - a sesamoid in the PL tendon near the
cuboid. Often is not ossified.
Constant Sesamoids occur in the MPJ of the hallux and
ossify around 10-12 y/o. The tibial sesamoid is larger and is
commonly bipartite. Partitions occur in cardinal body planes,
and their combined size is greater than a single sesamoid. You
must r/o fx when dxing a bipartite sesamoid.
THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS
STEP 2: SOFT TISSUE ANALYSIS
The soft tissue analysis of plain film incorporates two main
features:
1. Tissue Density
2. Tissue Contour
First you want to determine what kind of view you
are looking at. The most common is of course the DP view of
the foot, which may be taken WB or NWB. To tell the
difference, look at the joint spaces and see if they are clearly
visible. If the MPJs are clearly visible the view is probably
WB, which is taken at 15 degrees as opposed to NWB, which
is shot at 0. You may also look to see the ankle position (90 in
WB.) The view is important because WB views will show the
soft tissue somewhat distorted due to pressure. On the DP this
presents as extra thickness of the S.T. on the lateral column,
and on the lateral it presents as flatness on the plantar surface.
The first point, density evaluation, requires
knowledge of different tissue densities to be of any use. The
least dense material is of course gas or air, which is
pathologic. The next higher density is fat, typically seen in
kager’s/bohler’s/toygar’s triangle, as well as on the plantar
surface. Next dense from fat is water, which is the primary
composition of the soft tissues including muscle and tendon.
Muscular compartments of the foot as well as the tendo
Achilles will be of this density. Next dense is atrophied or
devitalized tissue, which is somewhat dehydrated. Like gas,
tissues of this density are pathologic and should be explained
fully. Next dense is calcific density, which is the density of
calcium deposits in the tissues. This is most often pathologic.
Next dense is ossific density, which is the density of bone.
Bones are only slightly denser than calcified structures – they
are normally differentiated by their internal architecture.
Finally, the densest structures radiologically are metallic or
glass structures, which are almost completely radioopaque.
Objects of this density are almost always foreign bodies,
although in many cases they simply represent fixation or
implants from prior surgery.
Pathologic changes in soft tissue density may be
either an increase or decrease in character. Edema causes
generally an increased radiodensity which matches that of
muscle or tendon, usually in areas where fat density is normal.
This is important in the posterior triangle as well as on the
plantar surface of the foot as extravasation of blood or fluid
will show up as an obliteration of normal fat anatomy on film.
Edema also causes an increase in soft tissue contour, which is
the second point to evaluate in soft tissue analysis. Edema is
normally classified by its cause. Obstructive edema is
caused by obstruction of the lymphatic channels draining the
affected area. This may be normal for the individual with
congenital lymph blockage, as in lymphedema praecox, but
with insidious onset of obstructive edema a previously
undiagnosed pathology may be at work. D/Dx include tumor,
trauma, radiation (repeated exposure to radiation damages
lymphatic channels), inflammation, surgery, burns, infection,
or helminthic infestation. Inflammatory edema is associated
with systemic disorders, particularly arthridites and metabolic
disorders. D/Dx include A vitaminosis, RCPS, melorheotosis,
collagen vascular diseases, dilantin use, reynaud’s disease, and
thyroid dysfunction (thyroid acropachy – nodular myxedema.)
Traumatic edema will be localized to the site of trauma and
should be consistent with the history. Besides direct trauma,
this type of edema is seen in stress fractures, infection, and in
surgical sites post-op. Of particular clinical significance is
edema in the posterior triangle (bordered by the posterior
flexor hellucis longus, the anterior tendo Achilles, and the
posterior-superior calcaneus.) Edema or hematoma from
injury to the tendo Achilles will cause this triangle to
disappear, which is a pathologic finding. Another pathologic
finding is the teardrop sign of the ankle, which is visible as
increased tissue density surrounding the ankle joint. This is
caused by extravasation of fluid to the ankle joint subsequent
to trauma. Ligamentous sprain is visible as diffuse edema
surrounding the area of the affected ligament.
Burns and frostbite cause areas of devitalized tissue
to show up on radiographs as areas of increased density.
Small localized areas of increased density are visible in the
case of focal gigantism associated with acromegaly. Bony
growth is also affected in this disorder and diagnosis should be
easy to make if it has not been made already.
Heel pad thickening is a finding associated with a
number of pathologies, and as such measuring the heel pad is
recommended in routine analysis of NWB views. Possible
D/Dx include acromegaly, dilantin use, plantar edema, plantar
infection, obesity, trauma, myxedema, and thyroid acropachy.
The accepted limit for normal heel pad thickness is 25mm.
Soft tissue emphysema is a decrease in radiodensity
due to the presence of air or gas in the tissues. Always
pathological and often the sign of an emergent situation, S.T.
emphysema is a worthy finding. Gas is almost always
produced by bacteria, especially clostridium perfringens,
which may produce superficial emphysema (radiographic
emphysema) or deep emphysema (deep intramuscular
emphysema). The only non-emergent emphysema finding is
of a gas abscess which is a localized ulceration containing gas
which does not spread to other areas. Gas abscesses are
typically found only in the distal part of the digits. It is
important to distinguish emphysema from the decreased
radiographic density caused by a sinus tract leading to an
ulcer. A sinus tract will always track back to the surface of the
skin, whereas emphysema is contained within the soft tissues.
Some disorders which affect only soft tissue contour
are worthy of note as well. Ainhum’s disease is a thickening
of fascial bands about the base of the proximal phalanges of
the digits, causing a constriction of the underlying tissues that
is visible on x-ray. This constriction eventually leads to
autoamputation, and although it is easy to diagnose from X-
ray, there is no known treatment for this disorder. The
sullivan’s sign sometimes seen on radiograph is a splaying of
digits which are abducted away from each other at the level of
the MPJ. This is caused usually by a space-occupying lesion
like a neuroma or interstitial fibrosis following surgery.
Sometimes, however, the etiology is biomechanical, due to the
unequal pull of flexor tendons that can result from DM motor
neuropathy, or simply from closely positioned metatarsal
heads.
Vascular calcification is seen in varicose veins,
monckeberg’s sclerosis, ASO, thrombophlebitits, and DVT.
They appear on X-ray as thin parallel or curvilinear lines.
Phleboliths are small round or oval calcifications that appear
within superficial veins.
Dracunculosis is a rare finding that is seen in
patients who have had a history of filiaria medinasis infection.
These helminthes, which burrow into the dermis of the foot,
remain after death as bits of foreign tissue that sometimes
calcify. The dracunculosis is the radiographic finding of these
calcified helminthes, which present as curvilinear lines of
radiodensity that do not follow any vascular anatomy.
Hemosiderin deposits may calcify in tissues
following the trauma or disease state that caused them. This
type of increased radiodensity is typically seen in periarticular
tissue, arthritic joints, or the subcutaneous area of the ankle.
General calcification of the soft tissues can be
distinguished from ossification by the degree of organization
seen in the radiodense area. Calcification is non-homogenous
and disorganized, giving a “salt and pepper” appearance.
Ossification, in contrast, is highly organized, often exhibiting
a trabecular pattern, and may have a cortex. In general, soft
tissue calcification is much more common that ossification.
Calcification etiologies are organized into three broad
categories: metastatic, dystrophic, and calcinosis.
Metastatic calcification is systemic calcification of a
metabolic derivative, such as hyperparathyroidism,
hypervitaminosis D, renal osteodystrophy, sarcoidosis, or
cancer. The calcifications are caused by an imbalance in
calcium or phosphorus metabolism. The calcifications may
appear vascular, but are typically more numerous and less
organized than vascular calcifications. Advanced
hyperparathyroidism causes chunky calcification, in which
separate calcifications conglomerate into calcified patches that
are prone to ulceration.
Dystrophic calcification is calcification of
devitalized tissues without metabolic imbalance.
Theoretically calcium precipitates in devitalized tissue, giving
rise to this type of presentation. Examples of possible
etiologies include ehlers-danlos syndrome, pseudoxanthoma
elasticum, fibromatosis, tumor, cyst, hematoma, focal
necrosis, trauma of any kind, and vascular disease. One
peculiar finding is that of hemarthrosis, which is calcification
of blood exudate in a joint space. These calcifications may
aggregate as “pebbles” within the capsule, visible on x-ray,
that can limit ROM of the affected joint (common in the
ankle.)
Calcinosis is the term applied to califications that are
idiopathic in nature. There are four syndromes associated
mainly with calcinosis. Calcinosis interstitialis universalis
presents as a calcification of subcutaneous structures,
progressing deeper with time. It may affect any soft tissue,
but calcifications are generally laid down in linear
aggregations parallel to the long axis of the limb. This
condition is very rare and is diagnosed in youth. Calcinosis
circumscripta is a distal subcutaneous calcification that is
normally associated with collagen-vascular diseases,
particularly CREST syndrome. Calcinosis circumscripta
associated with frank scleroderma is termed thiberge-
weissenback syndrome. These distal calcifications
predispose the digit to ulceration. Tumoral calcinosis is not
associated with cancer as the name implies, but rather is a
descriptive term referring to the presentation of the
calcification. Seen in renally compromised patients (usually
DM type II), these calcifications begin near joints as small
nodules that eventually grow in size to possibly impinge
neurovascular structures, limit ROM, and cause ulceration.
The typical presentation is near the 5th MPJ. This type of
growth is benign.
The last form of calcinosis is calcified bursa
secondary to irritation (usually posterior heel, medial 1st MPJ,
lateral 5th MPJ.)
Soft tissue ossification is distinguished from soft
tissue calcification by the degree of organization within the
ossified segment, typically with trabecular patterns.
Additionally, ossifications that occur near bone
characteristically do not cause periosteal reaction.
Progressive myositis ossificans (aka fibrodysplasia ossificans
progressive) is a rare childhood disorder in which there is
extensive and unexplained muscular ossification which causes
extraarticular ankylosis and disuse osteoporosis.
Neurological myositis ossificans has a similar presentation
but occurs in conjunction with a neurogenic lesion (stroke,
spina bifida, encephalitis, syphilis, brain trauma,
myelomeningocoele, spinal cord hemisection, tuberculosis,
and poliomyelitis). The calcifications occur at levels below
the neurogenic lesion. Finally, myositis post-traumatica
(circumscripta) is an area of localized ossification secondary
to acute trauma. Ossification begins soon after the traumatic
incident, but cortical formation is only seen 6-8 weeks after
the incident. Ectopic bone within the muscle may also be seen
parallel to the muscle fibers. On X-ray the mass appears
similar to an egg, with well-defined borders. Histologically it
contains the same sections as an epiphyseal plate.
Foreign body analysis in soft tissue is vital to
localizing the foreign body for surgical removal. Analysis of
the film typically calls for the ”tunnel technique” in which a
piece of paper is rolled up into a tube, which is used to analyze
small segments of the film at a time. Often needles are placed
in three planes near the affected area so that when films are
taken the exact location of the object can be triangulated. For
some foreign bodies, particularly wood, advanced imaging
modalities (ultrasound, CT, MRI, xerogram) should be
employed.

THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS
STEP 3: BONE EVALUATION
OSTEOLYTIC DISORDERS
Osteoporosis is an absolute reduction in bone mass
and density. Osteopenia is a generalized term to denote a
relative loss in bone density regardless of any etiology.
Osteoporosis is the most common skeletal pathology, common
in smaller older individuals who are less active. Females are
affected more commonly then males overall. (Age-related, or
“senile” osteoporosis affects men and women equally.)
Environmental factors that contribute to osteoporosis include
smoking, alcohol intake, estrogen deficiency, and the use of
certain medications. The most common presentation of
osteoporosis is vertebral fracture, followed by hip fracture.
Bone loss in osteoporosis is mostly cortical (80%),
but 33-50% of bone must be lost before the disease is evident
on x-ray. Peak bone mass is realized at age 35, with
involutional bone loss due to age beginning at age 35-40.
Cortical bone is lost at a rate of about 1% per year after this
point. Bone has a gray appearance on x-ray w/ the primary
trabeculae accentuated and the secondary trabeculae reduced.
Primary osteoporosis is that which has no underlying
disorder. Secondary osteoporosis is caused secondary to a
pathology like steroid tx, myeloma, metastasis, gastric sx,
anticonvulsants, hyperparathyroidism, heparin, DM,
alcoholism, disuse, hypogonadism, amenorrhea, and anorexia.
Generalized osteoporosis affects all bones, particularly of the
axial skeleton, and may be post-menopausal or senile. Post-
menopausal osteoporosis affects females aged 51-75, and is
caused by the increased osteoclastic action present in states of
estrogen deficiency. Mainly only medullary bone is lost, with
coarsened trabeculae. It is particularly associated with
vertebral, hip, and colle’s fx (wrist.) Lab values for this type
of osteoporosis are normal except for a decrease in PTH.
Senile osteoporosis has about an equal distribution btw males
and females over 70 y/o. There is a proportionate loss of
cortical and trabecular bone due to generalized loss of
osteoblast activity. Lab values show increased PTH. The
most common presenting symptom is extra-capsular hip fx.
Regional osteoporosis occurs only in a particular segment,
usually due to disuse atrophy. Localized osteoporosis affects
one part of a bone, and is due to tumor, arthritis, or infection.
Diagnosis of osteoporosis is preferred with a device
called a DEXA scanner, or dual-energy x-ray absorbiometry.
This measures the absolute density of bone via penetrance of
x-rays. CT can also be used to diagnose this disease.
Osteoporosis is graded using the calcaneal index:
Grade V (normal) – all trabeculae are uniformly present
Grade IV (normal) – posterior compressive trabeculae are
divided into two separate columns
Grade III (borderline) – posterior tensile trabeculae are lost
Grade II (osteoporotic) – anterior tensile trabeculae lost
Grade I (severe) – all tensile, most compression trabeculae
are lost
Regional Complex Pain Syndrome (RCPS) also
known as the “great mimicker,” manifests on x-ray as an acute
painful regional osteopenia following minor trauma. Males
and females are equally affected, and patients are typically
over age 50 and of type A personality. Presenting s/sx are
progressive onset of pain, stiffness, swelling, and atrophy
distal to the site of injury over a 3-6 month period. The cause
is hyperactivity of the sympathetic nervous system. In type I
RCPS no specific nerve damage can be identified. In type II
RCPS direct nerve injury has occurred. In 70% of pts, the
disease can spread up the extremity, sometimes even to the
opposite limb. RCPS can also be staged.
Stage I describes localized edema, muscle pain, joint stiffness,
and vasospasm with duration of about 3mos. Additionally,
trigger points form where touch causes pain out of character to
the stimulus (causalgia.) Osteopenia is noted on x-ray distal to
the lesion.
Stage 2 includes increased pain and area of involvement,
brawny edema, hair loss, brittle nails, and spotty osteopenia.
(Osteopenia w/ areas of normal bone.)
Stage 3 trophic damage becomes irreversible at this stage, w/
intractable pain, muscle atrophy, joint weakness, flexor tendon
contracture (producing deformity) and deossification.
Tx for RCPS includes pain tx (NSAIDs, opiates), nerve
blocks, physical therapy, and sx sympathectomy.
Osteomalacia is a lack of calcium in osteoid matrix
laid down by osteoblasts, resulting in improper bone
mineralization. Symptoms include muscle weakness, bone
pain on palpation, and bone deformity. X-ray shows osteoid
seams, lines of unmineralized bone that appear as pseudofxs
(aka increment fx, looser line, umbua zonen, milkman
syndrome). The cortex is thin and blurs into the medullary
bone (endosteal blurring.)
Rickets is osteomalacia seen in children, usually due
to vitamin D deficiency (but also due to renal dz.) It typically
affects children 6-12 months old, and will be accompanied by
muscle tetany, irritability, and weakness. Physical
development is impaired, bone growth is impaired and
deforms. Cartilage in the epiphyseal plates hypertrophies and
is surrounded by edema. CXR shows a rachitic rosary about
the costo-chondral junctions. Proximal calcification of the
metaphyses is absent, and margins are frayed and cupped.
Pseudofractures are also seen in rickets as well as
tibial/femoral bowing.
Scurvy is a disease caused by long-term deficiency
of vit. C. It takes 4 months to be apparent on X-ray, and
typically affects infants aged 4-8months. Scurvy is
characterized by improper collagen formation, leading to
spontaneous capillary hemorrhage, osteopenia, and poor
cartilage. Radiographically, there is a dense zone of
provisional calcification (line of frankel), ring epiphyses
(wimberger’s sign), irregular metaphyseal margins (corner
sign), metaphyseal protuberance (pelken’s spurs), scorbutic
zones (trummerfield zones), and sub-periosteal hemorrhage.
Hyperparathyroidism is ostepenia due to
overactivity of the parathyroid gland. Primary
hyperparathyroidism is caused by parathyroid
adenoma/carcinoma/hyperplasia, or an ectopic PTH-secreting
tumor. Secondary hyperparathyroidism is caused by renal
disease. Typical presentation is female, 30-50 y/o, weakness,
lethargy, polydipsia/uria, hypercalcemia and kidney stones.
Serum calcium and phosphate are elevated. The radiographic
hallmark is sub-periosteal bone resorbtion (1), followed by
accentuated trabeculae and reduced medullary bone (2), and
formation of brown tumors. (3) Bone resorbtion typically
occurs first in the phalanges, and soft tissue ossifications may
also be seen. Brown tumors are “holes” in the bone that are
filled with osteoclast-laden fibrous tissue, seen in both primary
and secondary forms.
OSTEOBLASTIC DISORDERS
Melorheostosis of Leri – “flowing hyperostosis” that looks
like candlewax dripping down the bone. Etiology unknown.
No gender predilection. Joint effusion w/ decreased ROM and
contracture, one limb (monomelic) affected, muscle wasting,
lymphedema all are symptoms. X-ray shows wavy cortical
thickening, narrowing of endosteal space.
Osteopathia Striata – “Voorhoeve’s Disease” most
commonly seen in the hip metaphysic. Seen as a linear band
of bone density of unknown etiology, typically coexisting with
sclerosing dysplasias.
Osteopetrosis – “Albers-Schoenberg Disease” also known as
“brittle bone disease.” Medulla is completely destroyed – all
bone is cortical. Existing bone thus has no shock absorbing
ability and is very brittle. It is a hereditary disorder in which
the osteochondroid tissue of developing bone fails to mature
into medullary and lamellar bone. There are 2 types:
osteopetrosis tarda (benign, a dominant trait) and osteopetrosis
congenital (malignant, recessive trait w/ neck LAD and HSM.)
Lack of bone remodeling results in long bones having an
Erlenmeyer flask deformity (flared metaphysis.) Variably,
some persons present with a spotty osteopetrosis which
appears like a “bone within a bone” or as striations of normal
bone with osteopetrotic bone.
Osteopoikilosis – “Osteopathia condensans disseminata” or
“spotty bone disease” is a hereditary disorder that presents as
multiple compact bone islands existing within normal bone.
The disease is asymptomatic and is usually an incidental
finding. Turnover is also very high, such that two radiographs
taken in the same year may show completely different
presentations. 25% of patients have a coexisting
dermatological problem (dermatofibrosis, scleroderma,
syndactyly), 20% have arthralgia. X-ray shows multiple
compact bony islands in long bones with uniform density.
Rarely, bone islands may have a radiolucent center.
Compact Bone Islands are normal variants seen in regular
radiographs. They appear as small areas of radiodensity,
usually in flat or tubular bones. What may appear normally as
a compact bone island can rarely be a osteoid osteoma.
Osteoid Osteoma is a painful benign tumor that is typically
<1cm, appearing as a compact bone island with a radiolucent
center. They are usually located near the cortex. Symptoms
include pain at night, relieved by ASA. Dx w/ bone scan.
Heavy Metal Poisoning can be by lead (plumbism),
phosphorus, or bismuth. Lead lines at the metaphyses are
visible on radiographs one month after exposure. Lead
deposition may also be seen at the distal ends of the digits.
Lead line density is determined by the amount of lead
ingested, the width is the single-time duration of exposure, and
the number equals the number of exposures. What may
appear as lead lines in a 4 y/o or younger is actually a normal
finding. Lead foreign bodies do not cause plumbism (unless
located within a joint space.)
Hypervitaminiosis A presents with dermatitis, pruritis,
alopecia and skin yellowing. X-rays show solid periosteal
bone at the ulna and metacarpals.
Hypervitaminosis D presents with nausea, anorexia, polyuria
and polydipsia. X-rays show extensive calcification of blood
vessels, soft-tissue, kidney, and peri-articular spaces.
BONE AND FRACTURE HEALING
Bone Characteristics: Bones support our frame as well as
protect the vital organs, provide a source of calcium, a site of
insertion for tendons and ligaments, and provide the rigidity
needed for movement against gravity. Bones comprise 1/10th
of our body weight. They resist axial stresses very well but
are weak against rotational forces. Tubular bones are built for
axial support and locomotion. Flat bones are built for
protection of vital organs.
Bone Healing: Consists mainly of spontaneous regeneration.
Tubular bone forms by endochondral ossification, flat bones
by intramembranous ossification. The periosteum surrounds
and protects the bone, and is made up of an outer fibrous layer
and an inner “cambium” layer which contains osteocytes. It is
this inner layer of the periosteum as well as the endosteum that
are most closely associated with bone healing.
FRACTURE TERMINOLOGY
Avulsion Fx – pulloff fx consisting of a fragment of bone
pulled off by a muscle, tendon, or ligament.
Butterfly Fx – triangular shaped cortical fragment that is part
of a communuted fracture.
Chip/Corner Fx – small fragment of bone from a joint
margin. Distinguish from a joint mouse, which is a piece of
osteophytic bone that breaks off into a joint space.
Closed Fx – does not penetrate the skin.
Comminuted Fx – consists of more than 2 pieces.
Fleck Sign – avulsion fx by the lisfranc’s ligament of the base
of the 2nd metatarsal.
Impaction Fx – telescoping of bone segments (also called
“bayoneting”) that results in shortening of a segment.
Greenstick Fx – incomplete fx in which one cortex is affected
and the fracture line follows down the axial line of the bone.
Torus Fx – trabeculae are buckled inwards with a cortical
bulge around the fracture site
Insufficiency Fx – aka pathological fx, caused by normal
physiological stresses through diseased bone.
Oblique Fx – fx is 45 degrees from the long axis of the bone
Occult Fx – see also stress fx; subtle and difficult to identify
Open/Compound Fx – skin is penetrated
Simple Fx – two bone fragments are involved
Spiral Fx – fx is circumferential and longitudinal in bone
Stress Fx – due to repetitive stresses, no fx line is apparent but
bony callus forms 10-14d on X-ray. Must rely on clinical Sx.
Transverse Fx – fx at 90 degrees to the long axis of bone.
FRACTURE REPAIR
Displacement/Distraction – requires reduction
Closed Reduction – realign fragments through manipulation
of ST, stabilize w/ cast
Open Reduction – realign fragments surgically, using ORIF
Inflammatory Phase – Periosteum, haversian system
damaged, bleeds to form hematoma. Osteocytes die from
ischemia, creating necrotic tissue that induces the
inflammatory response of vasodilation, edema, and
macrophage attraction.
Reparative Phase – governed by vascularity, the reparative
phase involves the formation of a callus which is mainly fibrin
from inflammation invaded w/ pluripotent cells for healing. A
collar callus forms around the bone to stabilize, dictated by
the periosteum, while the internal callus is dictated by the
endosteum and dictates bridging and union between the two
segments. Compression encourages bone rather than fibrous
tissue formation. Necrotic tissue is simultaneously removed.
Clinical Union – the goal of reduction, clinical union is the
resolution of symptoms w/ palpable rigidity to the affected
bone. Clinical union precedes radiographic union.
Remodeling Phase – begins while the reparative phase is
winding down, in the remodeling phase the callus is resorbed
and the trabecular bone remodeled along lines of stress,
resulting in a bone that is stronger than when it broke.
Cancellous bone heals faster than cortical bone, and has a
smaller callus. Cortical healing is limited by vascularity and
the amount of movement permitted during the healing phase.
COMPLICATIONS OF FRACTURE REPAIR
Delayed Union – union is not achieved w/in the expected time
(6 wks.) This is due to inadequate reduction, soft-tissue
imposition in the fx, excess ST destruction, vascular
disruption, inadequate immobilization, fragment distraction, or
inadequate fixation. AO principles dictate that bone healing
fails in tension and heals in compression.
Non-Union – complete arrest of bony repair, replaced instead
by fibrous, cartilaginous, or synovial compensation for the fx
site. It is variably classified as being diagnosable 6-8 months
post-fx. Others say non-union is dx if no radiographic healing
changes are seen for 3 months. Classification of non-union is
by Weber and Cech, and are divided into two major
categories, hypertrophic and avascular (or hypotrophic.)
Hypertrophic Non-Union may be of the elephant’s foot type,
the horse’s hoof type, or the oligotrophic type. Elephant’s foot
type is usually due to early WB and inadequate stabilization.
Horse’s hoof is caused by inadequate internal fixation that has
allowed a small amount of movement. Oliogotrophic non-
union has poor callus, and is usually due to inadequate
alignment of fx ends.
Avascular Non-Union – consists of four types; torsion
wedge, comminuted, defect, and atrophic. Torsion wedge is
incomplete healing of a fx in which there are three or more
pieces, in which some pieces fuse together but others do not
because of inadequate vascularity. It is sometimes seen with
plate fixation, usually in the tibia. Comminuted non-union is
the presence of one or more fragments that become necrotic,
the callus fails, and any involved fixation may break from
stress. Defect non-union is the loss of a devitalized fragment
of cortical bone that leaves a dead space within the bone
which cannot be bridged. Atrophic non-union is a long-term
result of insufficient vascularity that causes fx ends to become
osteopenic and atrophic.
Radiographic Findings of Nonunion
Sclerosis of the fracture ends, failure of changes of healing,
progressive bowing, increased bone atrophy above and below
fx site, excessive callus formation, and absence of remodeling.
Bone scans show up “hot” in non-union; increased uptake at
the fracture ends may be indicative of pseudoarthrosis
formation.
Pseudoarthrosis
This is a variant of non-union characterized by scar tissue and
false joint formation. Congenital pseudoarthrosis is present
at birth and is assoc w/ neurofibromatosis. It typically occurs
in the distal tibia/fibula. Acquired pseudoarthrosis causes
pain, instability, and bowing, with sclerotic bone ends and
lucency between fragments. It is most common in the distal
tibia.
Malunion
Bone healing that occurs in non-reduced fx, in which bones
are in improper position. It can spontaneously correct in peds.
THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS
STEP 4: EVALUATION OF JOINT SPACE
PEDAL COALITIONS
A coalition is a union of separate things into a single body or
group; true coalitions are intra-articular fusions of bones,
and bar/bridge coalitions are extra-articular fusions of bone.
A complete coalition is osseous and limits all motion. An
incomplete coalition is a union by fibrous or cartilaginous
tissue. A rudimentary coalition is an osseous projection
which limits motion but does not produce a union of parts.
A synchondrosis is a cartilaginous union, a synostosis is a
bony union, and a syndesmosis is a fibous union of two parts.
Coalitions are caused by accessory ossicles (os trigonum, os
sustentaculi proprium), failure of mesenchyme to segment in
development, trauma, DJD (causing a fibrocartilaginous
fusion), inflammatory rheumatoid conditions, and fxs.
Tarsal coalitions occur in 1-2% of the population and consist
of the talo-calcaneal coalition (most common), calcaneo-
navicular, and talonavicular (least common.)
Ossification of coalitions in the tarsus occur at different times.
The age of ossificiation determines when symptoms occur.
Talonavicular coalitions 3-5 y/o
Calcaneonavicular coalitions 8-12 y/o
Talocalcaneal coalitions 12-16 y/o
S/Sx of coalitions include stiffness, decreased ROM, pain,
peroneal spasm, anterior/posterior tibial spasm, local POP,
pronation, cavus deformity, and fixed RF valgus.
Peroneal spastic flatfoot is characterized by restricted STJ
motion, RF valgus (in OKC), FF abduction, bowstrung
peroneal tendon, and extensor digitorum longus spasm.
D/Dx of coalitions include RA, JRA, trauma, neoplasm,
acromegaly, CCPV, casting (causing peroneal contracture),
extra-articular arthrodesis, overcorrected flatfoot,
osteochondral dystrophy, infection, and N/M disease.
Plain film analysis of coalitions is cheap and able to identify
most symptomatic coalitions.
IPJ coalition can be viewed on AP projection.
Synphalangism is a congenital fusion of the IPJs.
Intermetatarsal coalition may be viewed on AP and oblique
views. Diaphyseal fusions are typically the result of trauma.
Metatarsal cuneiform coalition may be viewed with AP,
med oblique (medial column), or lat oblique (lateral column.)
Navicular cuneiform coalition may be viewed with the AP
and medial oblique projections.
Navicular cuboid coalition may be viwed w/ AP or oblique.
Calcaneocuboid coalition may be viewed on lateral or lateral
oblique views (typically it is osseous and easy to pick up.)
Talonavicular coalition can be viewed on AP and medial
oblique. AP shows a “putter sign” of the fusion.
Calcaneonavicular coalition can be viewed on lateral and
lateral obliqe, and shows an “anteater sign” on lateral. These
fusions are more commonly cartilaginous or fibrous in nature.
STJ coalition is the most common tarsal fusion, and usually is
the middle facet (the posterior facet is least common.) Fusions
of the sustentaculum tali or posterior process are also possible
(though not common.) Anterior facet coalitions can be seen
on lateral oblique isherwood projections but are most
commonly dx though lateral CT. Middle and posterior
facets are viewed on harris and beath axial projections (30, 35,
40, and 45°) or broden views. The posterior and middle facets
should be parallel to one another, and the posterior facet
should be about 2/3 the width of the calcaneus. Posterior
fusion may be secondary to trauma involving the os trigonum.
(Achilles pain, end ROM plantarflexion, deep ankle pain.)
Radiographic Features of STJ coalition (lateral projection)
Talar beaking
Posteior TC joint space narrowing
Rounding of lateral process of the talus
Obscured middle facet
“Halo” effect
Do not confuse talar beaking w/ dorsal hyperostosis, which is
caused by pathomechanics. Talar beaking occurs at the
distalmost aspect of the talar neck, near the TN joint. It is
caused by stress on the talonavicular ligament and
impingement of the navicular on DF. The halo sign is a subtle
finding, which is a ring of trabeculae that form around the
coalition secondary to altered compressive forces.
Computerized Tomography is the modality of choice for
evaluation of coalitions (b/c of cortical definition.) It allows
planar analysis which may be used to determine the extent of
coalition and change to surrounding osseous structures.
Nuclear Imaging is not very useful for the diagnosis of
coalition. Increased uptake is seen adjacent to areas fusing,
and decreased uptake in already fused areas.
MRI allows planar and oblique analysis to more fully explore
the nature of a coalition. T2 weighted images are particularly
useful to note presence or absence of synovial fluid in an area.
Syndromes associated with coalitions may aid in the
diagnosis of a bony union, and vice versa. Common coalitions
typically are axial, i.e. distal to proximal fusions, whereas
syndromic coalitions tend to be medial to lateral in position.
Apert’s Syndrome results in massive tarsal synostoses, as
well as cranial synostoses and midfacial hypoplasia (“mouse”
facies). The distal phalanx of the hallux and pollux are broad.
Feet tend to have valgus attitude. Footwear is a problem
Nievergelt-Perlman Syndrome typically has synphalangism
and carpal fusion, moreso in the hands than feet. This
syndrome may also present with an atypical clubfoot and
tarsal fusions, which causes a ball-and-socket type of ankle
joint. Other findings include congenital dislocation of the
radial head and conduction deafness due to ear ossicle fusion.
Phocomelia is defective development of the arms or legs,
resulting in “flipper” extremities. Hemimelia is
underdevelopment of a specific extremity, usually a below-
knee deformity. These conditions cause unusual fusions.
Tx of coalition includes immobilization and supportive
therapy, orthotics, NSAIDs for pain, and possible surgical
intervention (resection or arthrodesis.)
Conclusion – correlate coalitions w/ pts age. Be suspicious of
changes in plain films. Consider advanced imaging to
investigate further. (Special views, CT, MRI.)
ARTHRIDITIES
Inflammatory arthridities are RA, erosive arthritis, psoriatic
arthritis, reiter’s disease, ankylosing spondylitis, and
enteropathic arthritis.
Non-Inflammatory arthritis is degenerative joint disease.
(Wait a minute – doesn’t arthritis mean joint inflammation?)
Metabolic arthritis is gout and CPPD disease.
Neuropathic arthritis is neuropathic joint disease.
Miscellaneous arthridities are DISH, PHO, and pigmented
nodular synovitis.
PSORIATIC ARTHRITIS
Seen in 7-15% of pts w/ psoriasis (80% if pt has nail changes.)
Typically affects 20-50 y/o, M:F equal. HLA-B27 frequently
positive, particularly w/ SI involvement. Distribution is
asymmetrical and is most common in the DIPJs. Often
confused w/ RA (for some reason.)
Classic radiographic features
Joint margin erosions working in to the center (similar to RA)
– eventually leads to “pencil in cup” appearance
Increased synovial fluid w/ increased intracapsular pressure
Apparent wide joint space (due to erosions)
Acroosteolysis – resorbtion of the distal phalangeal tuft
Sausage digits
Abundant periosteal activity (resulting in “whiskering”)
Ivory Phalanx – due to abundant endosteal activity
Osteopenia secondary to reduced activity
Main-en-lorngette (telescoping) – long standing disease
process resulting in collapse of diaphyses on themselves.
Posterior/Inferior calcaneus hyperostosis (not heel spurs.)
REITER’S DISEASE
Classic clinical triad – conjunctivitis, urethritis, arthritis.
Also 4th – derm lesions (keratoderma blenorrhagicum)
Usually preceded by diarrhea.
Typically males, 18-40 y/o. HLA-B27 positive almost always.
Asymmetric distribution, primarily lower extremity.
Attributed to chlamydial infection (endemic) or dysentery
(epidemic) which are the two main types of Reiter’s.
Epidemic form may affect women and children as well.
Arthritis long-term symptom; conjunctivitis/urethritis resolves
in weeks. Arthritic changes may also become chronic.
Acute Stage - weight-bearing joints are more commonly
affected. In the acute stage there is peri-articular ST edema,
deossification of opposing articular structures, Achilles
inflammation/widening, and periosteal reaction (metatarsal
metaphyses, phalangeal diaphyses, inferior surface of the
calcaneus.) Retrocalcaneal bursitis is also common.
Infracalcaneal exostoses (poorly defined or “fluffy”) form
bilaterally and cause heel pain.
Chronic stage – periarticular deossification, small marginal
erosions, symmetrical loss of joint space, ankylosis.
Specific findings – heel spurs in young men, Achilles edema,
small joint space periosteal reactions, primarily foot s/sx.
ANKYLOSING SPONDYLITIS
Affects pelvic and spinal joints, ligaments, and tendons.
Affects 15-25 y/o, usually males. Almost always HLA-B27
positive. Characterized by lower back pain due to arthritis at
the sacroiliac joint, bony proliferation at enthesiopathies,
spinal osteophyte formation, and lateral syndesmophytes.
ENTEROPATHIC ARTHROPATHY
Joint changes secondary to GI disease. Seen in young adults,
w/ malaise, anorexia, wt. loss and arthritis. Typically
sacroiliac, bilateral periostitis. X-ray findings are nonspecific.
GOUTY ARTHRITIS
Gout is the result of an inborn error of purine metabolism. It
typically affects men age 40-50 y/o, and is characterized by
elevated serum uric acid and negatively birefringent crystals in
the synovial fluid. The most commonly affected joint is the 1st
MPJ due to relative avascularity and lower temperature.
Women only get gout after menopause. Characteristic of gout
is extreme paroxysmal pain in the middle of the night.
Primary gout is hyperuricemia due to over-production of uric
acid or under-excretion of it by the kidneys. Secondary gout
is due to medications (particularly HCTZ) and
hyperparathyroidism. Urate deposits in relatively avascular
tissues like cartilage, synovial tissue, ligaments, bursae, and
subQ tissue. Hyperuricemia may never become symptomatic,
and in fact may be reduced during an acute phase attack. A 24
hour urine collection is needed to diagnose accurately.
X-ray findings of gouty arthritis only occur after several
attacks. Thus radiographs in an early attack function mainly
to r/o other pathologies (septic arthritis.) There is peri-
articular swelling of the joint margins, erosions of the joint
margins, punched-out lesions resembling RA, and complete
lysis of bone in the acute stages. Large tophi may form at
joint margins and produce “rat bite” erosions peri-articularly
that leave overhanging shelves of bone called martel’s sign.
This is not seen for 5-10 years after the attack and merely
signifies that a pt has had gout in the past. Tophus formation
can occur in the absence of an acute gout attack, and
subsequent erosions can cause subQ calcification and
pathological fxs. The joint space is preserved in gouty
arthritis. DJD may accompany the process, and the joint may
be somewhat narrowed due to subchondral cyst formation, but
is otherwise unaffected. Metastatic tumors of bone are an
important d/dx to r/o when considering asymptomatic gout.
CHONDROCALCINOSIS
Pseudogout, or calcium pyrophosphate dihydranate disease, is
a symptom similar in presentation to gout that causes the
radiographic finding known as chondrocalcinosis. CPPD
crystals are weakly positive birefringent and simulate gout
attacks when precipitated in joint spaces. The typical pt is
over 30 y/o (usually ~60) and there is no gender predilection.
The problem is associated with hyperparathyroidism,
pseudogout, acromegaly, DJD, and DM. The typically
affected joint is the knee, where the menisci as well as the
articular cartilage may calcify as a result. It also can be seen
in the wrist, hand, ankle, symphysis pubis, and elbow.
True chondrocalcification is sometimes seen after trauma or
with hyperparathyroidism.
DEGENERATIVE JOINT DISEASE
Also called osteoarthritis, DJD is a local, mechanically
caused degeneration of joint function that occurs in
conjunction with age and trauma, resulting in degradation of
the articular cartilage. Primary DJD is the most common form
and is due to aging. Secondary DJD is early onset due to
trauma or injury to the joint. Joint space narrowing is
asymmetric in DJD, the subchondral bone exhibits eburnation
(pathologic sclerosis), the articular surface becomes broad and
flat, and osteophytes form at joint margins, often breaking off
to become joint mice within the articular space. Osteophytes
typically bend towards the joint space, which causes locking
of the joint in areas where there are osteophytes on either side
of the articulation. Pseudocysts may also form in the
subchondral bone in areas where the cartilage is completely
worn away. It is important to note that the disgnosis of hallux
rigidus and limitus, which are seen in patients with DJD of
the 1st MPJ, cannot be diagnosed radiographically and are
purely clinical diagnoses. Additionally, the hands of patients
with DJD clinically may present with enlarged IPJs which are
called bouchard’s nodes (PIPJ) or heberden’s nodes (DIPJ)
that are simply the result of extensive osteophytosis in long-
standing disease.
Erosive osteoarthritis is a variant of DJD which
affects primarily females aged 40-50 y/o. Clinically an
increased ESR may be seen because there is an inflammatory
component to the erosive component. The presentation is
symmetrical and bilateral, and most commonly affects the IPJs
of the hands. Radiographically erosive osteoarthritis appears
like DJD except that the erosions are symmetric and take on
the characteristic gull wing appearance that is specific to EO.
RHEUMATOID ARTHRITIS
RA is an inflammatory seropositive joint disease affecting
primarily females between the ages of 20-40 y/o, but affect
men and women equally beyond the age of 40. 70% of pts w/
RA are seropositive for rheumatoid factor. The small joints of
the hands and feet, and articulations of the spine are typically
affected. Early presentation in the foot can easily be mistaken
for gout – most commonly small, C-shaped erosions appear at
the base of the proximal phalanges. Radiographic changes are
seen in 65% of pts who have had some disease process for at
least 3 months (85% for >6 mos.) However, no clinical s/sx
may appear until the disease has been present for 3 years.
Early radiographic findings in RA include peri-
articular edema that is fusiform in shape around the joint,
typically in IPJs and MPJs. Inflammation of the synovium
creates pannus which results in bone deossification peri-
articularly, which progressively extends proximally over time.
Secondary trabeculae are resorbed while primary trabeculae
are enhanced. Fibular deviation of the digits occurs
secondary to bony deossification that destroys the medial
collateral ligaments of the MPJs (except on the 5th MPJ.)
Early on the joint space becomes noticeably widened as
effusion and pannus formation characterize the disease
process, and often this is the only presenting sign in
undiagnosed RA. Joint space changes are most easily seen in
the ankle joint radiographically. Near the joint periosteum
may become irritated and periosteal elevation in the
epiphyseal/metaphyseal region is seen. This creates
lamellations which enlarge the bone near the articulation.
Entheses and bursae near the joint may also become inflamed
and enlarge. Localized bony erosions occur near the joint due
to herniation of the pannus through capsule, producing an area
of radiolucency with poorly defined borders. Erosions seen en
face may appear completely within the bone, while laterally
they may have a dot-dash appearance. Medial-plantar
erosions of metatarsal heads 1-4 are most common. Later
symmetrical joint narrowing is seen, particularly in the IP and
TN joints (but never the CC joint.)
RA-induced subluxations of MPJs and IPJs following
ligamentous involvement cause the characteristic swan-neck
(like mallet-toe) and boutonneire (like HDS) deformities.
These deformities are also seen in SLE and post-rheumatic
fever (jacoud’s) arthritis. Other deformities seen in RA
include main-en lorgnette deformity (“opera-glass hand”)
that is also seen in psoriatic arthritis.
Late radiographic findings in RA have obviously
no diagnostic value, but are used to track the progression of
the disease. Characteristic features include subluxation and
dislocation of the joints, ulnar deviation of the digits,
destruction of joint space, and finally bony fusion and
ankylosis of the joints altogether. Pathological fxs secondary
to osteopenia may be seen. Overall, the MPJs are most
severely affected in RA, with the IPJs of the 1st and 5th digits a
close second in frequency.
NEUROPATHIC JOINT DISEASE
More commonly known as charcot foot, neuropathic joint
disease is a destructive disease that occurs secondary to loss of
proprioception, seen in DM (5%) and syphilitics (20%.)
Clinically there is no protective sensation; instability and
crepitation are present in the joint, and neurologically the pt
suffers from ataxia and loss of DTRs. Besides the more
common pathology, neuropathic joint disease can occur
iatrogenically secondary to administration of indocin or
steroids over long periods of time (notable because of the tx
protocols for RA and gout recommend this.) The hypertrophic
form of the disease affects large, WB joints, while the
hypotrophic (atrophic) form affects NWB joints. Clinically
both undergo 3 stages; fragmentation, coalescence, and
reconstruction. Radiographically the hypotrophic form is
characterized by bone resorption, diabetic osteolysis, and a
“licked candy stick” appearance. The hypertrophic form is
characterized by the six D’s: joint distension, density
increase, debris production, dislocation, disorganization, and
destruction.
DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS (DISH)
DISH is a disorder of ligamentous ossification and
calcification that affects the spinal and extra-spinal
articulations. Typically it affects males over 50 y/o. It is
associatied (20%) w/ DM. 40% are HLA-B8 positive. All
parts of the spine, particularly the SI joint, are affected.
Radiographically flowing hyperostosis is seen over 4
consecutive vertebral bodies, usually in the area of the anterior
longitudinal ligament. In any case, the disc is preserved,
differentiating this process from syndesmoses seen in
ankylosing spondylitis. Extra-spinal presentations may be at
any enthesis, producing whiskering at the bony attachment and
ossification of the tendon or ligament while preserving the
joint space.
PULMONARY HYPERTROPHIC OSTEOARTHROPATHY (PHO)
PHO is a disease caused by bronchogenic carcinoma that is
described by the triad of digital clubbing, symmetric
arthritis, and linear periostitis. It typically affects males 40-
60 y/o. The arthritis in this process, like many seronegative
diseases, is nondescript in its clinical and lab findings. The
arthritis is specific to the extremities only. Periostitis in long
bones occurs in the metaphseal/diaphyseal region, appearing
as a “double strip sign” on bone scans (dual cortices.)
PIGMENTED VILLONODULAR SYNOVITIS
This disorder is a proliferative pathology of joints that does
not produce arthritis, but rather a mass within a joint or tendon
sheath which may affect the joints secondarily. Typically it
affects young males. Joint involvement is asymmetric.
Radiographically there is a soft-tissue mass evident with
localized bony erosions that have well-defined sclerotic
borders. Calcification is unusual.
SYSTEMIC LUPUS ERYTHEMATOSUS
SLE is a connective tissue disorder involving nearly every
organ system in the body. It is most common in females 20-
40 y/o, and is characterized by elevated ESR and ANA titer
levels. Radiographic features are most readily assessed in the
hands, and are characterized by reversible subluxation,
dislocation, and varied deformity. Calcification and atrophy
can occur secondary to deformity. Most radiographic findings
are non-specific and there is no articular degeneration.
SCLERODERMA
Scleroderma is a connective tissue disease that also involves
many organ systems and affects females predominantly (30-60
y/o.) Radiographic changes in scleroderma are most readily
appreciated in the CREST syndrome, in which soft tissue
calcification and acro-osteolysis may be seen. (r/o psoriasis)
THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS
STEP 5: BIOMECHANICAL EVALUATION
The biomechanical evaluation of radiographs is used for pre-
op planning and post-op assessment of correction as well as
for the evaluation of orthopedic pathology. Biomechanical
readings are most sensitive to positioning errors, and so great
care must be taken to ensure proper positioning in patients
needing a biomechanical evaluation.
AXES
Greater Tarsal Axis (GTA)
Line drawn parallel to the distolateral border of the calcaneus,
most easily identifiable on AP radiograph.
Lesser Tarsal Axis (LTA)
Point A is placed on the distomedial aspect of the medial
cuneiform. Point B is placed at the medial proximal aspect of
the navicular articular surface. Point C is placed at the
proximal lateral aspect of the cuboid and point D at the distal
lateral aspect of the cuboid. The midline between points A &
B and C & D are found and a line drawn between them. The
line perpendicular to this is the lesser tarsal axis.
Metatarsal Axis (MTA)
Line drawn through the midpoint of the shaft of the 2nd
metatarsal. (Or another metatarsal if specified.)
Digital Axis (DA)
Line drawn down the midpoint of the shaft of the digit in
question.
Collum Tali Axis
Line drawn down the bisection of the talar neck.
Collum Calcanei Axis
Line drawn down the bisection of the distal 1/3 of the
calcaneus.
Hallux Axis
Line drawn down bisection of the shaft of the proximal
phalanx of the hallux.
Calcaneal Pitch Axis
line drawn from distal inferior aspect of calcaneus to
anteriormost weight-bearing point of calcaneus
AP ANGLES
Lesser Tarsal Angle = GTA + LTA
Metatarsus Angle = LTA + MTA
Used to evaluate for metatarsus adductus
Digitus Angle = DA + MTA of measured digit
Forefoot Angle = GTA + MTA
Used to evaluate metatarsus adductus in peds
Talo-Calcaneal Angle = collum tali + collum calcanei axes
Used to evaluate pronation/supination
Cuneo-Metatarsal Angle = MTA(1-3) + long axis of
proximal cuneiform
Used to evaluate hypermobility, lisfranc’s injury
Calcaneocuboid Angle = Collum calcanei axis + line CD of
LTA
Used to evaluate lateral column integrity
Talometatarsal Angle = column tali axis + 1st MTA
Called Simmons Angle on AP
Used to evaluate pronation/supination
Intermetatarsal (IM) Angle = 1st MTA + 2nd MTA
Used to evaluate bunion deformity
Hallux Abductus (HA) Angle = hallux axis + 1st MTA
Used to evaluate bunion deformity
Hallux Interphalangeus Angle = hallux axis + bisection of
distal phalanx of the hallux
Metatarsal Break Angle = line between center of 1st and 2nd
metatarsal heads + line between center of 2nd and 5th metatarsal
heads.
Tibial Sesamoid Position
1 = Tibial sesamoid medially clear of 1st MTA
2 = Tibial sesamoid laterally abuts 1st MTA
3 = Tibial sesamoid laterally overlaps 1st MTA
4 = Tibial sesamoid bisected by 1st MTA
5 = Tibial sesamoid medially overlaps 1st MTA
6 = Tibial sesamoid medially abuts 1st MTA
7 = Tibial sesamoid medially clear of 1st MTA
Proximal Articular Set Angle (PASA) = line btw medial and
lateral borders of metatarsal head articulation + line
perpendicular to MTA.
Distal Articular Set Angle (DASA) = line btw medial and
lateral borders of proximal phalanx MPJ articulation + line
perpendicular to digital axis.
LATERAL ANGLES
Talar Declination Angle = collum tali axis + ground
Calcaneal Inclination Angle = calcaneal pitch axis + ground
Talocalcaneal Angle = collum tali + calcaneal pitch axes
Talonavicular Angle = collum tali + bisection of navicular
Used to evaluate for metatarsal breaks
1st Metatarsal Declination Angle = 1st MTA + ground
Talometatarsal Angle = column tali axis + 1st MTA
Called Meary’s Angle on lateral projection
Hallux Dorsiflexion Angle = 1st MTA + hallux axis
Cyma Line = position of the talonavicular joint with respect
to the calcaneo-cuboid joint on lateral projection.
Radiographic Evaluation of Supination
Talar declination angle decreases
Calcaneal inclination angle increases
Talocalcaneal angle decreases
Cyma line posteriorly displaced
Subtalar joint/sinus tarsi accentuated (bullet hole sinus tarsi)
Radiographic Evaluation of Pronation
Talar declination angle increases
Calcaneal inclination angle decreases
Talocalcaneal angle increases
Cyma line anteriorly deviated
Pseudo-sinus tarsi seen (posterior facet of STJ; real sinus
tarsi is obscured.)
Metatarsus Primus Elevatus (MPE)
Defined radiographically as an elevation of the 1st metatarsal
with respect to the 2nd metatarsal. Implied in the development
of 1st MPJ OA, sub 2nd metatarsalgia.
Total Adductory Angle (TAA)
Sum of the IM angle + the metatarsus adductus angle, used in
the evaluation of bunion deformities and in surgical planning.
A TAA >30° should warrant consideration of a proximal
osteotomy in surgical bunion correction.
Pre-Op Biomechanical Assessment
IM angle HA TAA
PASA DASA Hallux Interphalangeus
Metatarsus angle MPE Sesamoid position
Joint status Bone density 1st MT protrusion
RADIOGRAPHIC INTERPRETATION OF INFECTION
OSTEOMYELITIS
Osteomyelitis is the infection of bone, most commonly by
bacteria but also possibly by fungus, virus, or parasites. The
anatomy of vascular structures is most important when
considering osteo, and the vascular anatomy of bone changes
with age. In infants (0-1 y/o), blood vessels pass through the
epiphyseal plate in tubular bones. Because of this, it is more
common to see infection in the epiphysis because vascular
channels here are more prominent than at a later age. In
children (1-16 y/o), metaphyseal vessels end at the epiphyseal
plate, creating loops and blind-ended sacs in the metaphyseal
vasculature. The tortuosity of these vessels means that
metaphyseal infection is much more common in children. The
adult pattern begins around age 16. As the physis closes, the
metaphyseal vessels can begin to cross back into the epiphysis
again and so infection may be located anywhere in the bone.
Sequestrum is an infected area that is dead due to
cortical and medullary infarcts. Small sequestra can be
eventually resorbed by osteoclasts, while large sequestra are
walled off by the body and then expelled gradually through a
sinus tract. Involucrum is periosteal new bone formation that
occurs in response to bone infection, and represents the body’s
attempt to prevent the spread of bacteria. Both sequestrum
and involucrum are most commonly seen in hematogenous
osteomyelitis. Cloaca is a defect in the involucrum that
allows for drainage products of the infection to be expelled
from the infected area. The cloaca commonly receives small
bits of sequestrum that may have been broken down in the
disease process. Exudate from the cloaca with involucrum
will feel like sand between the fingers when handled. The
extent of the cloaca and its sinus tract to the outside of the
body can be appreciated through the use of a sonogram,
which is simply radiographic contrast media injected into the
sinus tract that can then be visualized radiographically.
Marjolin’s ulcer is a malignant degeneration of soft tissue
within the cloaca to a squamous cell carcinoma. This occurs
secondary to acidic pus and exudate from the cloaca irritating
the tissues of the sinus tract. The infection must be very
chronic (up to 20-30 years) for a marjolin’s ulcer to form, and
it is only seen in long-standing osteomyelitis. Nevertheless, it
should be kept in mind when treating a patient with history of
bone infection.
Brodie’s abscess is a localized suppurative infection of bone
which is successfully walled off and is sterile. A brodie’s
abscess is usually an incidental finding and typically is seen in
children after osteomyelitis has resolved. A similar finding is
an abscess that still contains bacteria, which can serve as a
reservoir for reinfection in the future (however, brodie’s
abscesses are sterile only.)
Routes of infection in osteomyelitis include hematogenous
spread (most common in children), direct
implantation/inoculation, direct extension, and post-op
infection. The most common infecting organism in children is
H. Influenzae, although it is now much less common than it
once was. In adults staph aureus is by far the most common
infecting organism for all types of osteo (except plantar
puncture wounds.)
Hematogenous osteomyelitis, being primarily a disorder of
children, is most commonly seen in the metaphysis of long
bones. Bone destruction begins internally, then weakens the
cortex, causes periosteal reaction, and finally breaks through
to soft tissue. Being confined within bone initially, the route
of pus evacuation can be appreciated on X-ray. Initially pus
fills the medullary space for some distance before pushing
through the periosteum. The codman’s triangle is a
triangular space of pus bounded on one side by infected cortex
and on another by elevated periosteum which attempts to lie
down new bone. Notation of this on X-ray is usually
diagnostic for hematogenous osteomyleitis.
Direct implantation osteomyelitis typically occurs as a result
of puncture wounds, human or animal bites, or open fracture.
Staph aureus is the most common infecting organism in all
cases except those of plantar puncture wounds that pass
through a shoe, in which case the infecting organism is
pseudomonas. E.Coli is sometimes implicated in direct osteo
as well. In direct implantation there is no particular order to
the infectious process, as the traumatic injury has already
disrupted the cortex.
Direct extension osteomyelitis is spread of infection to bone
from a nearby soft tissue infection or ulcer. Nail infections
and infected ulcers are the most common causative factor in
this type. The order of infection tends to follow the opposite
order as hematogenous osteomyelitis.
Post-op infections may be due to staph aureus (again most
common) or pseudomonas. This type of osteo is most
commonly seen in the hip or knee following arthroplasty,
especially when hardware is installed. Loosening of fixation
with obvious radiolucency about the device indicates infection
of this type and surgical removal is indicated.
X-RAY FEATURES OF OSTEOMYELITIS
Initially, there are no osseous findings present on X-ray –
plain film findings lag clinical findings 7-10d. In vertebral
bones there may be up to a 21d lag. 30% of bone must be lost
before the changes can be appreciated on plain films. Initially
the only evidence of infection will be soft tissue changes,
including deep ST swelling in hematogenous osteo adjacent to
the infected area. Fat planes will be elevated, displaced, or
obliterated altogether. Lines of lucency between muscles will
be obliterated. Infection tracks usually distal to proximal and
only rarely travels from medial to lateral (and vice versa.)
Breakthrough to a joint space will produce swelling of the
capsule, which in the ankle produces the classic teardrop sign
which is also seen in hemarthrosis. Periosteal response to
infection occurs usually 7-10d after the initial process has
begun. The pattern of reaction is lamellar and progresses to
formation of an involucrum. Involucrum tends to be less
dense than the established cortical bone, even infected. The
most distal the infection is in the body, the most subtle the
periosteal response will be. Resolution of the infection will
leave the involucrum to be remodeled and resorbed, however
it may sometimes persist after the healing process is finished.
Bony destruction appears “moth eaten” as there is a focal loss
of bone density in the medullary bone, with sequestrum seen
3-6 wks after the infectious process has begun. Kissing
lesions are opposed lesions seen across articular surfaces when
the joint has been involved. Often these changes are subtle
and may not be noticed unless serial radiographs are taken and
analyzed. In slow-growing, rarer cases like fungal infections,
the bone may be able to mount a more effective response
against the causative agent, and sclerosis due to endosteal
proliferation may be seen. This type of infection-caused
sclerosis is called sclerosing osteitis of Garre.
Radiographic Signs Overview
Early Signs
Latent Period (10d extremities, 21d spine)
Soft Tissue – fat plane elevation/displacement/obliteration,
increased ST density
Bone – motheaten cortical/medullary destruction, periosteal
new bone formation (involucrum, codman’s triangle)
Late Signs
Soft Tissue – draining sinus/cloaca, debris, marjolin’s ulcer
Bone – cortical destruction, involucrum, sequestrum, sclerosis
Joint – loss of joint space, ankylosis, kissing lesions.
Salmonella Osteomyelitis is a peculiar type of osteo that is
sometimes seen in patients with sickle cell anemia. If a sickle
cell crisis occurs in the intestinal vasculature, small infarcts
can allow salmonella bacteria to travel from the gut to the
bloodstream where they can seed in bones across the body.
The osteomyelitis associated with this bacterial seeding is
unique in that it predilects the diaphysis of long bones.
BONE SCANS FOR INFECTION
Technetium-99m Phosphate is the prototypical bone scan,
and is the most commonly used in clinical practice. It reacts
with calcium hydroxyapatite to form insoluble salts which
precipitate in areas of bony turnover. This makes the Tc-99
scan ideal for infectious and/or traumatic processes of bone.
Although classically infection and inflammation about a bone
cause a bone scan to read positive in that area, an increase in
vasculature to an area may increase uptake of the isotope, as
well as the articular surfaces of an inflamed joint. Thus,
findings which would otherwise be normal clinically may
show up as positive on bone scan and must be separated from
pathology. Distal bones seem to be more sensitive to Tc-99
uptake, and can more easily show up hot even if only
sustaining minor trauma. Overall, Tc-99 exposes the patient
to only a small radiation dose, and is renally excreted. For this
reason, it is generally recommended that the patient be well-
hydrated (this also aids in contrast), and care must be taken in
individuals with renal disease, especially if they have DM.
The half-life of Tc-99 is 6 hours. Normal areas of increased
uptake are the lacrimal glands, breasts, SI joint, kidneys,
bladder, and the injection site of the isotope.
Gallium-67 Citrate is another isotope that resembles the
ferric ion. It binds to iron-related plasma proteins as well as
organelles of leukocytes. This makes Ga-67 useful for
visualizing the peripheral tissues because it marks the areas
where leukocytes have localized. Ga-67 is also excreted
renally, and has a long (78 hour) half-life.
Podiatric indications for bone scan
Osteomyelitis
Trauma
Inflammatory Arthritis
Stress Fracture (if >7 hours)
Tumors
Non-specific pain (to check for occult causes)
Combined use of bone scan isotopes can be used to
differentiate the infectious process. Soft tissue infection can
be distinguished from osteomyelitis by decreased uptake in
the third phase of the Tc-99 scan, and will be strongly positive
in Ga-67, whereas osteomyelitis shows up hot in all three Tc-
99 phases and is cold in Ga-67 scanning. When performed
together, the Tc-99 test is done first because of the shorter
half-life. Gallium is typically used to clarify the issue of
infection site, but is not as effective at determining the course
of an infection. The practice of using a gallium scan to
determine when the infectious process (and thus the treatment
regimen) is finished has been thoroughly disproved.
Indium-111 isotope is a rarer, more specialized bone scan that
tags WBCs in drawn blood with the isotope and re-injects
them into the bloodstream. I-111 is useful in distinguishing
osteomyelitis from neurotrophic joint changes in the diabetic
individual, which is normally a very difficult clinical
diagnosis. A negative I-111 scan would tend to r/o osteo and
provide for a positive diagnosis of charcot, while the reverse is
also true.
COMPUTERIZED TOMOGRAPHY FOR INFECTION
CT allows planar analysis of anatomy to determine the extent
of infection. Although sensitive for soft tissue infections, CT
tends to overestimate their involvement, and is much more
reliable at determining bony involvement. Very subtle cortical
or periosteal changes may be appreciated on a CT scan.
MAGNETIC RESONANCE IMAGING FOR INFECTION
In contrast to CT, MRI is much better at evaluating soft tissue
infection versus bone infection. MRI cannot distinguish
between infection in a joint space and effusion in a joint,
however, and this is a major limitation if joint involvement is
suspected. The infected area appears dull on a T1WI, and
more typically has greater intensity on a T2WI.
THOUGHT PROCESS BEHIND THE RADIOLOGY OF INFECTION
From plain films the distinction must be made as to the
location of an infection. If soft tissue is suspected, MRI is the
best modality. If bone is suspected, CT is the best modality. If
the symptomatology is diffuse, the Tc-99 and Ga-67 bone
scans should be considered to determine involvement.
BONE TUMORS AND TUMOR-LIKE LESIONS
Evaluation of plain films – plain film analysis offers the most
diagnostic information for the analysis of bone lesions.
Biopsies of bone alone do not give the pathologist enough
information to make a definitive diagnosis; clinical and
radiographic evidence is needed to support what is seen under
the microscope. Some lesions also may become activated or
react against an invasive biopsy technique.
Basic approach to solitary bone lesions
1) History – age, sex, and symptoms. Age of the patient is
important because many tumors predilect younger or older
patients. Ewing’s sarcoma, chondrosarcoma, and unicameral
bone cysts are almost exclusively tumors of children, while
metastatic tumors and multiple myeloma are only seen in older
individuals. Osteosarcoma tends to affect younger patients,
chondrosarcoma the middle aged, and fibrosarcoma the
elderly. The tumors paraosteal osteosarcoma, giant cell tumor,
and aneurismal bone cyst are the only tumors seen more
commonly in women than men. Pain is the most common
symptom in sarcomas. The character, onset, frequency, and
aggravating factors should be assessed.
2) Location should be described in relation to the position in
long bones, cortical or medullary, and eccentric or centrally
located. Epiphyseal lesions include chondroblastoma, intra-
osseous ganglion, and clear cell chondrosarcoma. Physeal
lesions are only seen in giant cell tumors. Metaphyseal
lesions include metastatic tumors, osteomyelitis,
osteo/chondro/fibrosarcoma, malignant fibrous histiocytoma,
non-ossifying fibroma, and unicameral bone cysts.
Diaphyseal lesions include lymphoma, eosinophilic
granuloma, metastasis, multiple myeloma, and ewing’s
sarcoma. Peripheral/cortical lesions include
osteochondroma and para or periosteal osteosarcoma.
3) Rate of growth is characterized by the borders of the
lesion. Permeative lesions have a wide zone of transition and
are typical of fast-growing lesions, typically malignant tumors
and osteomyelitis. Moth-eaten lesions have intermediate
zones of transition with irregular borders. They may be
malignant or benign tumors. Geographic lesions have well-
defined sclerotic borders with a short zone of transition. This
finding is typical of benign tumors and cysts (although low-
grade malignancies may also sometimes look like this.)
4) Periosteal reaction appearance may give clues to the type
of tumor. Single-layer periosteal reaction is typical of
osteomyelitis, benign tumors, and lower-grade malignant
tumors. Onion-skinning is typical of repetitive insults to the
periosteum, seen in osteosarcoma and ewing’s.
Perpendicular periosteal reaction has a spiulcated, sunburst
appearance that is almost always malignant. Codman’s
triangle is similarly a sign of malignancy in tumors.
5) Tumor matrix description can help determine the tissue
type involved. Osseous lesions appear cloud-like and
amorphous with usually a “fluffy” appearance. Cartilaginous
lesions appear punctuate w/ C-shaped lesions and numerous
small calcifications in the center are typical. Fibroosseous
lesions have a ground-glass character with no discernible
trabeculae. No visible matrix is a pertinent negative and may
be a giant cell tumor or cyst.
CT imaging of tumors is used to evaluate tumor matrix more
effectively and determine cortical vs medullary lesions.
MRI of tumors in used to asses soft tissue and marrow
involvement, but does not provide much for osseous tumors.
Osteoid Osteoma (OO) is a fairly common tumor seen in 10-
30 y/o. It is characterized by a visible central nidus of less
then 1cm that is seen in the tibia/fibula or spine (causing
painful scoliosis.) The nidus may or may not have a central
area of calcification. Pain is felt at night and is described as a
dull pain which responds to ASA. It may take 6-24 months to
make a Dx. If near a joint the OO can cause joint effusion and
pain that can look clinically like JRA. The main D/dx is stress
fx. MRI is frequently misleading in dx. Tx is sx or
radiofrequency ablation (90° C.)
Osteoblastoma (OB) is a very large osteoid osteoma that is
also very rare. It is seen in the same populations and in the
same locations but with milder symptoms (despite greater
size.) The nidus may be greater than 1.5cm and can have
multiple internal calcifications. It causes less reactive
sclerosis than OO.
Osteosarcoma (OS) has several variants. Paraosteal and
medullary (low grade) have good prognoses. Pagetoid and
radiation-induced OS has a poor prognosis. Telangectatic OS
causes many complications, but often responds to chemotx.
Classically, OS is a medullary tumor seen in the metaphysis of
10-25 y/o. Most are seen in the femur near the knee.
Diagnosis is by pain, X-ray, and elevated levels of alk phos.
Radiographically it appears cloud-like with sunburst periosteal
reaction and codman’s triangle. Skip lesions or lung
metastasis indicates a poor prognosis. Paraosteal
osteosarcoma (PaOS) is seen 5-10 years later then medullary
OS and is more common in females. It causes dull aching
pain and carries a better prognosis than OS, unless it extends
into the medulla. Periosteal osteosarcoma (PeOS) is a rarer
lesion that has similar age, location, and s/sx as medullary, but
is located in the diaphysis and carries a better prognosis.
Paget’s Disease (P) is thought to have a viral cause, and is
seen primarily in English-speaking countries. Affected bones
have a thick cortex and accentuated trabeculae. Paget’s
predisposes an individual to OS, CS, FS, GCT, and MFH.
Enchondroma (E) is a benign, intramedullary, cartilaginous
lesion. It occurs in any age and is characteristically painless.
It is normally seen in hands and feet and may cause
pathological fx. The lesions appear geographic with central
calcifications, possibly with endosteal scalloping or expansion.
Ollier’s disease is the condition of multiple enchondromatosis
that may predispose to malignancy. It is more common in
children and causes growth disturbances. Maffucci’s disease
is hereditary multiple enchondromatosis with soft tissue
telangiectasias as well. Prognosis for Maffucci’s is very poor,
with almost 100% malignancy.
Juxtacotical Chondroma (JC) is a solitary cartilaginous
tumor that causes erosion of surrounding bone. The average
age is 22 y/o and is seen most commonly in long bones of the
hands and feet. The tumor is symptomatic, causing pain and
swelling in the area. In 50% of cases ST calcification may
also be seen, with erosion and “saucerization” of the bone.
Chondroblastoma (CB) is a benign cartilaginous tumor of the
epiphysis. It is seen in individuals with open growth plates
(teenaged) and is geographic in nature. Calcifications are seen
in 50% of cases. Pain and joint effusion may cause CB to be
mistaken for arthritis, much like OO.
Chondromyxoid Fibroma (CF) is a very rare tumor that is
metaphyseal, geographic, and multiloculated. It occurs in all
ages and is seen in the LE. Pain is “vague.” It may extend all
the way to the physis.
Osteochondroma (OC) is a cartilage-capped exostosis of
bone. It is common in the general population, and is usually
discovered in adolescence as a painless, hard “lump.” The
location is usually metaphyseal, and the exostoses
characteristically point away from the joint. Malignant
transformation may have occurred if painful, greater then 2cm,
or growing after skeletal maturity. Multiple hereditary
osteochondromatosis (MHO) is a multiple variant that is
autosomal dominant. It frequently causes growth disturbances
in children and carries a 20% chance of malignancy.
Benign Perosteal Osteochondromatous Proliferation
(BPOP) is a very rare finding seen in adults aged 20-30 y/o.
Sometimes also called “nora’s lesion,” BPOP is benign, but
has a very high rate of recurrence if removed.
Chondrosarcoma (CS) occurs de novo or secondarily from
conversion of a benign lesion. The average age is 40 y/o.
Pain is the primary s/sx. Lesions are typically geographic and
metaphyseal, with lucent centers filled with small
calcifications. Tx is w/ sx. Variants of CS include clear cell
chondrosarcoma (CCC) which is an epiphyseal lesion (looks
like CB but in older patients) and dedifferentiated
chondrosarcoma in which part of the lesion is low-grade and
another part is high grade.
Non-Ossifying Fibroma (NOF) and its relative the Benign
Fibrocortical Defect (BFOD) differ only in their location; the
NOF is medullary and the BFOD is cortical. It is most
common in children, and is usually asymptomatic unless there
is a pathological fx. X-ray shows a sclerotic border in the
growth plate to the diaphysis. DO NOT BIOPSY NOFs.
With age the lesion usually regresses. Jaffe-Campanacii
syndrome is multiple NOFs with café au-lait spots.
Fibrous Dysplasia (FD) is a benign fibroosseous lesion of
bone that is usually unilateral (75%) and has a geographic
appearance. The hallmark radiographic feature of FD is a
ground glass matrix. Dense areas of calcification may also
be seen. FD presents typically with deformity and sometimes
pain, secondary to fx. Albright’s syndrome is polyostotic FD
with café au-lait spots and endocrine abnormalities. As
opposed to Jaffe-Campanacci syndrome, where the lesions
have a smooth border, albright’s syndrome lesions have a
rough border. Mazabraud’s syndrome is polyostotic FD
with intramuscular myxomas. The shepherd’s crook
deformity is also a hallmark of this type of lesion.
Osteofibrous Dysplasia is an intracortical FD of the tibia
(usually) seen in childhood. It is very uncommon. It is
usually painless and has the characteristic ground glass
appearance. It is associated with adamantinomas.
Fibrosarcoma (FS) occurs in the 3rd to 6th decades of life and
present as an aggressive lytic lesion with no matrix and no
periosteal reaction. Its location is generally metaphyseal. It
may also arise secondary to other lesions as well (including
infarcts.)
Giant Cell Tumor (GCT) is a locally aggressive lesion that is
usually benign but not always. It presents as a lytic lesion in
the metaphysis extending into the epiphysis (and is the only
one to occur in this area.) There is no matrix associated with
GCT. The lesion may destroy the cortex and invade the ST as
well. It most commonly occurs in the femur, radius, humerus,
and sacrum. It is slightly more common in females. S/sx
include pain. The Giant cell reparative granuloma is a
cousin of GCT presenting with lucent lesions of the hands and
feet seen in children. It typically does not break through the
periosteum. It may mimic and be hard to distinguish from
brown’s tumors, even on histology. It is also called a solid
aneurismal bone cyst.
Unicameral Bone Cyst (UBC) is a very common benign
lesion often seen in the distal calcaneus. It is medullary and
fluid-filled, and may be an incidental finding (although it can
cause pathological fx.) It is geographic, with sclerotic borders.
It typically arises at a growth plate, migrating later into the
diaphysis with age. 90% are seen in the humerus and femur.
The hallmark of the UBC is the fallen fragment sign (piece of
cortex within the center of the lesion.) Tx is observation,
steroid injection, of sx bone graft packing.
Aneurysmal Bone Cyst (ABC) is a lytic expansile lesion
noted for the blood-filled cavities it forms. It may arise de
novo or post trauma, or may be associated with CB, GCT,
NOF, OB, CMF, or FD. It presents with pain in the long
bones and axial skeleton. It is usually seen in teenagers. Its
hallmark are fluid-fluid levels of two layers seen on MRI
representing old coagulated blood and new, unsettled blood.
Fluid-fluid levels are also seen in telangectatic OS, MFH, and
FD.
Interosseous Lipoma (IL) is a benign asymptomatic lesion
that is typically an incidental finding. It is usually seen in the
calcaneus. It can have a central area of calcification, but is
noted for its central area of fat on CT and MRI. It is seen in
the same locations as UBCs.
Intraosseous Ganglion (IG) is a benign lesion of the
subcortical bone typically seen in the middle-aged. It can
present with pain. It may resemble a subchondral cyst on x-
ray (but in the absence of DJD). It is most commonly seen in
the medial malleolus. It may also look like GCT but with a
lobulated matrix.
Ewing’s Sarcoma (ES) is a common primary bone tumor
seen in children, presenting with pain, low-grade fever, wt
loss, and an elevated sed rate. It is rare in AAs. It has the
appearance of a small blue-cell tumor which it shares with
primary lymphoma and multiple myeloma. It is most common
in the lower extremities. The lesion is permeative and has no
matrix. It produces an onion-skin type periosteal reaction.
The location can be metaphyseal or metadiaphyseal, and
produces a soft tissue mass surrounding the lesion. A variant
of Ewing’s is primitive neuroendothelial tumor (PNET)
which has the same appearance, prognosis, and treatment, but
is associated with a chromosome translocation.
Primary lymphoma of Bone appears similar to ES but in a
much older patient. Pain is usually the presenting symptom,
but there are no systemic signs.
Multiple Myeloma (MM) is the most common primary
malignancy of bone, seen in older individuals. It presents with
pain, weakness, or neurological symptoms. It sometimes
presents with a solitary bone lesion called a plasmacytoma.
On x-ray there are cookie-cutter lesions that appear osteopenic
and without sclerosis. Bone scans and MRI are unreliable in
dx. MM commonly has the POEMS syndrome –
polyneuropathy, oganomegaly, endocrine abnormalities, M
proteins, and skin lesions.
Hemangioma is a common benign or congenital lesion most
commonly seen in the skull and spine. It appears to have
vertical striations in the spine and radial spokes in the skull.
CT shows a polka-dot pattern. It is usually asymptomatic.
Hemangioendothelioma is a rare lesion seen in the lower
extremities. It presents as a cortical defect similar to
hemangioma. It is typically seen in the middle-aged.
Eosinophilic Granuloma (EG) is a non-infectious granuloma
with histiocytes and eosinophils proliferating. Most are seen
in the skull and vertebrae, but it may also occur in the lower
extremity. Langerhans Histiocytosis is unifocal EG in one
organ system. Hand-Schuller-Christian Disease is
multifocal in one organ system. Letterer-Siwe Disease is
multifocal and multisystem. The average age of EG is 15 y/o.
There is little periosteal reaction, and there may be a
sequestrum (especially in the skull.) The lesions may appear
punched-out. The typical presentation is with a spontaneous
compression fx. They are typically diaphyseal. Bone scans
are unreliable in dx.
Adamantinoma is a rare, locally aggressive lesion seen
almost exclusively in the tibia. It appears in the 3rd to 5th
decades as an eccentric, lobulated lesion. Periostitis is rare.
Local pain and swelling are apparent on examination.
Metastatic bone tumors are the most common type of bone
malignancy, primarily from the breast, prostate, lung, and
kidney. Periosteal reaction is rare. Location is based on the
tissue type. Blow-out lesions are renal and thyroid based.
Peripheral and cortical lesions are lung metastases.
RADIOLOGY OF SYSTEMIC DISORDERS
Changes in the trabecular pattern in bone are indicative of
reconstructive mechanisms and may suggest systemic disease.
Osteoporosis, osteomalacia, and hyperparathyroidism all cause
a generalized loss and coarsening of the trabeculae. In many
cases, this can also happen with anemias, storage diseases, and
neoplastic disorders as well. Etiologies of abnormal bone
texture include generalized overactivity of cancellous bone
resorption, infarction due to disruption of blood supply, and
growth retardation due to localized hypoxia (in children.)
ANEMIAS
Anemias that affect bone density include sickle cell
anemia, thalassemias, and iron deficiency anemia. Sickle Cell
Anemia puts pts at risk for salmonella infections seeded
hematogenously, with osteomyelitis occurring in the
diaphyseal region. Marked edema of the hands and feet may
be seen secondary to this infection. Bone density is lost in the
spine, flat bones, and long bones with a coarse trabecular
pattern. The hallmark is fish vertebrae that appears as a
biconcavity of the vertebral bodies on lateral x-ray (with disc
space preserved.) Periostitis is also seen in the hands and feet.
Bones of the hands and feet can also be infracted in children
with sickle cell – the hand and foot syndrome causes
localized infarction leading to early closure of growth plates in
the affected bones. This causes periosteal new bone
formation (appearing 1-2wks post injury) and may lead to
AVN. Cortical infarcts are more common, and the femoral
head is most affected. Infarcts within long bones may present
on x-ray as calcified fat necrosis, which may look like a tumor
(fibrous dysplasia.) The bone infarcts can also make the bone
prone to infection and pathological fx. Infarct of the distal
tibia can lead to premature closure of the epiphysis laterally,
causing a characteristic tibiotalar slant with a valgus attitude.
Thalassemias are gene deletions of primary hemoglobin
subunits, causing a microcytic hypochromic anemia.
Radiographically they present similarly to sickle-cell anemia,
with the notable exception that infarcts are generally not seen.
Trabeculae may take on a “honeycomb” pattern and long
bones typically take on an Erlenmeyer flask morphology.
Secondary centers of ossification may be delayed. Iron
Deficiency Anemia characteristically causes osteoporosis of
the hands (in severe cases) and transverse striping of the
metaphyses. Radiographic changes are more readily apparent
in the pediatric population.
LIPID STORAGE DISEASES
Gaucher’s Disease is a disorder characterized by the
accumulation of cerebrosides in reticuloendothelial cells. The
lower extremities are more commonly affected. The classic
presentation is ischemic necrosis of the proximal femur with
Erlenmeyer flask deformity.
Niemann-Pick Disease is an inherited abnormality of
sphingomyelin metabolism seen most commonly in persons of
jewish descent. Radiographically a widening of the medullary
cavity, coarse trabecular pattern, thinned cortex, failure of
tabulation, and loss of bone density are seen. The Erlenmeyer
flask deformity is also seen.
Sarcoidosis is a systemic granulomatous disease involving the
skin, lungs, lymph nodes, and viscera. 10% of patients have
bone involvement. Children are rarely affected.
Radiographically dx is made with CXR; in the extremities the
middle and distal phalanges can show cyst-like punched out
lesions in the cortex.
Pancreatitis causes fat necrosis of the bone marrow (which is
also seen in cancer of the head of the pancreas.)
Radiographically bone infarction follows the fat necrosis
stage, with calcification and ossification of the affected
marrow. The long bones of the hands and feet are most
affected.
Dysbaric Osteonecrosis (Caisson disease) is a pressure-
induced osteoarthopathy seen in deep-sea divers. It presents
as small localized infarctions of bone due to the formation of
nitrogen bubbles within the body.
Hemophilia is a disorder of blood coagulation due to plasma
clotting factor deficiency. Classic hemophilia (A) is due to
factor VIII, Christmas disease (B) is due to factor IX. Both
are X-linked diseases. Radiographically bleeding is apparent
sub-periostally, intraosseously, and intra-articularly. The
chronic hemarthrosis due to joint bleeding causes destruction
of the hyaline cartilage secondary to lysosomal enzyme release
in the breakdown of blood products. Hemophilia can also
cause premature closure of the epiphyseal plates, causing
tibiotalar slant seen also in sickle cell anemia.
Metaphyseal and Diaphyseal Infarcts are usually due to
occlusive vascular disease, sickle-cell anemia, caisson disease,
infiltrative/collagen diseases, infection and/or idiopathic. The
increase in bone density seen in an infarct is due to crushing of
the avascular debris, calcification of fat necrosis, hyperemic
removal of viable bone surrounding, bony apposition, and
periosteal involucrum formation.
ENDOCRINE DISORDERS
Acromegaly/Gigantism are both disorders characterized by
excess in growth hormone. The result is joint space
narrowing, bony sclerosis, cyst formation, and osteophytes
similar to DJD. It usually affects the acral skeleton most. In
the foot there is seen sausage digits, enlarged sesamoids/MPJs,
prominent metatarsal heads, prominent tufts and bases of
phalanges, enthesis development, and constriction of proximal
phalangeal shafts. Fat pad thickening is a radiographic
hallmark of acromegaly. Hypertrophy of the bases and tufts of
the distal phalanges causes secondary bony fusion resulting in
pseudoforamina formation unique to this disease.
Hyperparathyroidism causes generalized bone resorption
subperiosteally, intracortically, endosteally, and sub-
ligamentous. Bone sclerosis and chondrocalcinosis are also
seen. Brown’s tumors are unique to hyperparathyroidism.
Renal Osteodystrophy is a disease of chronic renal failure
that causes hyperparathyroidism, rickets/osteomalacia,
osteoporosis, soft tissue calcification, and vascular
calcification. Osteomalacia and Rickets primarily are caused
by Vitamin D disorders, and cause bowing of the tibia and
periarticular calcification.
Hypoparathyroidism may be primary (deficiency or
destruction of the gland) or secondary (gland unresponsive.) It
causes spinal calcifications that appear like osteophytes (of
DISH). Pseudohypoparathyroidism is the most common
secondary disease, causing a short stature, round face,
brachydactyly, exostoses, cone epiphyses, and wide bones.
Women are more affected than men.
Hyperthyroidism is characterized by a general catabolic state
of the body, resulting in loss of connective tissue as well as
increased bone turnover. Osteoporosis is a common initial
finding. Other findings include accelerated skeletal
maturation and myopathy. Thyroid acropachy is a
complication of hyperthyroidism that includes progressive
exopthalmos, hand and foot swelling, digital clubbing,
pretibial myxedema, and periosteal new bone formation (mid-
diaphyseal), particularly of the 1st metatarsal. The edema has a
nodular appearance.
Hypothyroidism (Myxedema) is caused by a deficiency of
TSH, thyroid hormone, or iodine. In infants the disorder is
called cretinism. In adults the disorder causes edema, dry
skin, coarse hair, lethargy, fatigue, paresthesia, and
bradycardia. Tarsal tunnel syndrome is also a common
finding.
Paget’s Disease (Osteitis Deformans) is a disease of unknown
etiology. It, as well as fibrous dysplasia, are known as the
great masqueraders of bone disease. (Outside of bone, gout
and syphilis are also known as great masqueraders.) Paget’s is
normally seen in the axial skeleton, but can affect any bone.
The pelvis, femur, skull, and tibia are most common. Its
incidence is 4-6% in individuals over 40 y/o. Deformities
associated with Paget’s include femoral bowing (shepherd’s
crook), tibial bowing (sabre shin), liontiasis (lion facies), and
pathological fracture (banana fxs.) Pseudofractures, seen
also in osteomalacia/rickets, are also known as umbua zonen
and looser’s lines – they represent demineralized areas of bone
that are not actually fxs, although they appear that way on x-
ray. The stages of Paget’s disease are
1) Destructive phase – increased osteoclastic activity and
osteoporosis circumscripta, both difficult to dx early.
2) Combined phase – bone destruction/turnover and fibrous
bone replacement.
3) Sclerotic stage – uniformly thickened trabeculae, ivory
appearance of bone (see also psoriasis), and bone expansion.
4) Malignant degeneration – metaplasia to osteosarcoma (rare)
Lab findings for Paget’s show elevated alk phos (x20) and
hypercalcemia. UA may show urinary hydroxyproline. Bone
scan shows multiple hot spots (sometimes solitary). Course is
slow and treatement is with calcitonin and supportive therapy.
Massive Osteolysis (Disappearing bone disease) is a disorder
causing sudden resorption of large areas of bone without
malignancy. It is associated with lymphangioma or
hemangioma and clinically presents with pain. X-ray findings
show apparent disappearance of bone, (tapering off in long
bones), with no periosteal reaction noted.
Diabetic Osteolysis is a disorder characterized by marked
resorption with neuropathic changes. It is seen in the absence
of an infectious process, although that is usually a d/dx. It
may be the result of a viral infection. Radiographically a
decrease in ST density, local osteoporosis, distal resorption,
licked candy stick appearance, and apparent bone
“regeneration” are apparent on x-ray.
Poliomyelitis radiographically presents with severe cavus
deformity, severe osteoporosis, short metatarsals and
phalanges, and a ground glass appearance of medullary bone.
Neurofibromatosis is a hereditary disease of mesodermal
origin causing café-au-lait spots, skin neurofibromas, bone
deformity, and local gigantism. Bone deformities include
kyphosis, bony erosion, local overgrowth, overtubulation of
long bones, pseudoarthroses, and lytic areas of bone.
AVASCULAR NECROSIS AND
OSTEOCHONDRITIS DESSICANS
Avascular Necrosis (AVN, epiphyseal ischemic necrosis,
osteonecrosis, osteochondrosis, epiphysitis, and aseptic
necrosis) is a disruption of the vascular supply of bone leading
to the death of an osseous structure. Primary causes are
unknown. Secondary causes can be fracture, sickle cell
anemia, long-term corticosteroid use, and alcoholism.
Clinically, AVN is variable and relatively minor in
symptomatology. Pain and disability progresses as it is
untreated. AVN normally lasts about 9 mos, but in some cases
(legg-calve-perthes) it can last up to 8 years. Spontaneous
AVN occurs in the distal femur, femoral head, and metatarsal
heads. Trauma-induced AVN occurs in the talus.
Alcoholism-induced AVN occurs in the femoral head.
Surgery can also be a cause of AVN.
The Avascular Phase of AVN is the actual loss of blood
supply, leading to bone death, failure of epiphyseal growth,
minimal bony deformity, reactive hyperemia, synovial
thickening, and edema. On x-ray you see a small epiphysis,
normal bone density, increased joint space, capsular swelling,
metaphyseal osteopenia, and a widened growth plate.
The Revascularization Phase sees infiltration of new blood
vessels and fragmentation of the dead parts. On x-ray you see
a sclerotic rim, new bone deposited on old bone (snow cap
sign), fracture inferior to the articular cortex (crescent sign),
clefts and fragmentation, flattening of articular surfaces, a
widened metaphysis, and “head within a head” appearance.
The Repair and Remodeling Phase includes new bone
deposition replacing bone resorption. On x-ray you see
reconstitution of the epiphysis and the disappearance of clefts.
The Residual Deformity (stage 4) includes restitution of the
epiphysis, with the amount of deformity dependent on
compressive forces on the affected bone. On x-ray you see a
deformed articular surface, usually flattened.
Legg-Calve-Perthes Disease is a true AVN of the capital
fragment of the femoral epiphysis in children. Males are more
commonly affected than females. 3-12 y/o is the average age.
Prognosis worsens with later ages. 1 in 10 are bilateral.
Clincally the pt has limp and a vague pain in the groin that
may extend to the knee. Pain is exacerbated with activity.
There is often muscle atrophy in the thigh and a history of
trauma in the affected individual. The etiology is unknown.
Blount’s Disease is not a true AVN, seen in infants affecting
the medial tibial epiphysis. The failure of the growth plate in
this area contributes to the formation of a tibia/genu varum.
Osgood-Schlatter Disease is not a true AVN either, affecting
the tibial tuberosity. It is caused by a partial disruption of the
tibial patellar ligament (w/ or w/o avulsion). Commonly
ossific nodules are seen with this disease, forming a large,
prominent tibial tuberosity. The course is self-limiting and
affects mainly males 11-15 y/o.
Sindig-Larsen-Johannson Disease is not an AVN, but is
looks similar to Osgood-schlatter disease. It is a traction
induced avulsion fragment of the lower patella.
Diaz Disease is a true AVN of the talus. It is usually caused
by trauma, graded by the Hawkin’s classification system. A
positive Hawkin’s sign indicates revascularization.
Sever’s Disease is a non-AVN of the calcaneus. It is
calcaneal apophysitis caused by traction of the calcaneus. It
presents with heel pain and irregular ossification on x-ray. All
radiographic findings, however, may also be seen in normal
children. Examples include a sawtooth metaphysis, decreased
metaphyseal density, increased density of the apophysis, and
fragmentation of the apophysis. Males and females are
affected equally. The primary D/dx for sever’s disease is
spring heel (hematogenous osteomyelitis of the calcaneus.) In
spring heel, the plantar tubercles typically show signs of
deossification, not seen in sever’s disease.
Kohler’s Disease is a true AVN of the navicular seen in males
around 5 y/o. It presents with localized pain, edema,
tenderness, and decreased ROM. Some pts have a
congenitally small navicular – an incidental finding of a very
small navicular on x-ray may not be kohler’s. The appearance
should be patchy or uniform sclerosis, collapse (silver dollar
sign), and fragmentation of the bone. The joint space is
usually preserved.
Iselen’s Disease is a non-AVN of the fifth metatarsal base. It
is actually a tractional apophysitis and is self-limiting.
Freiberg’s Disease is a true AVN of the metatarsal heads.
The second metatarsal is most commonly affected, particularly
in pts w/ a long 2nd metatarsal. There is tenderness and pain
over the affected MPJ, and the pain is exacerbated with
activity. Infarction of the epiphysis leaves necrotic bone that
causes degenerative changes and cortical thickening.
Adaptive changes occur on the juxta-articular surface
(flattening and broadening of the joint space.) Theimann’s
Disease is a non-AVN of the fingers and toes that is extremely
rare. It occurs secondary to trauma and is attributed to
multiple ossification centers in the phalanx.
Sesamoid AVN is called Trevor’s (fibular) or Renandier’s
(tibial) and occur secondary to trauma and fracture.
Osteochondritis Dessicans (OCD) is a disease of unknown
etiology affecting children and adolescents, typically male. A
small segment of necrotic bone forms subchondrally, which
may heal spontaneously or become a joint mouse. Joint mice
in these cases are typically symptomatic because the major
component is cartilage, which is not visible on x-ray.
Symptoms are joint effusion, pain on ROM, crepitation and
locking and localized tenderness (vague to the ankle). The
disease may be hereditary. There are two types of OCD – In-
situ and displaced according to the fragment.
Radiographically they look similar to talar dome fractures.
ADULT FOOT DISORDERS
Heel Pain – Plantar: R/O soft tissue involvement, fissuring,
tumor, and nerve entrapment. Plantar fasciitis presents
radiographically as increased ST density of the plantar fascia,
and deossification of the calcaneus with accentuation of the
tensile trabecular patterns (do not confuse w/ stress fx.) Heel
spurs are sometimes seen in plantar fasciitis but also can be
caused by the pull of the FDB, Abd hallucis, Abd digiti
minimi, and the long plantar ligament. Heel spurs account for
15% of all adult foot complaints. They are typically directed
forward from the medial tubercle. They are assoc w/ obesity,
pes cavus & pes planus, and osteophytosis. It is important to
note that the size of the spur has no effect on the symptoms,
and oftentimes the contralateral (asymptomatic foot) will have
a spur of equal or greater size. 90% do not require any type of
sx intervention to tx. Fluffy heel spurs are associated with
certain arthropathies, particularly Reiter’s, ankylosing
spondylitis, psoriatic arthritis, RA, and Paget’s disease. Other
causes of plantar heel pain include calcified bursae,
atrophied fat pad (measuring 15-23mm), steroid-induced
calcification, and nerve entrapment. Nerve entrapment can
be differentiated from plantar fasciitis by its response to
steroids (relief in plantar fasciitis, no change in nerve
entrapment), and with nuclear scanning (+ in plantar fasciitis).
Heel Pain – Posterior: Tendo-Achilles (partial tear or
complete tear/AODM), retro-achillean bursa (caused by
shoe irritation), or retro-calcaneal bursae/Haglund’s
deformity (most common.)
Heel Pain – Medial: Tarsal Tunnel Syndrome is caused by
chronic irritation of the posterior tibial nerve in the flexor
retinaculum and inferior to the medial malleolus (seen w/ RA,
AODM, trauma, fx, and dislocation.) Medial calcaneal nerve
entrapment and posterior tibial tendon dysfunction are
other causes of medial heel pain. (Radiographically
represented by increased TC angle, anterior Cyma line, and
sagging of the metatarsocuneiform joint.
Heel Pain – Lateral: Lateral heel pain is the most rare
presentation. It can be caused by sural nerve entrapment,
calcaneo-fibular irregularities, peroneal tendon problems,
tarsal coalition, and ankle/RF varus deformities.
Midfoot to Rearfoot Relationship: Calcaneal pitch is
normally between 10-20 degrees – greater than this is pes
cavus and less is pes planus. A supinated foot will have an
accentuated or bullet hole sinus tarsi, while the pronated foot
will have a pseudo sinus tarsi which is in fact the posterior
subtalar joint facet being brought into the plane of the film.
Cavus Foot Structure: Typically caused by neurological or
muscular imbalance. Forefoot cavus has an apex at the
lisfranc’s joint. Midfoot cavus has its apex at the chopart’s
joint. Rearfoot cavus is calcaneal in nature and has a
calcaneal inclination angle of >30 degrees (and claw toes.)
Foot Faults are sections of the foot where adjacent segments
are improperly aligned. Hindfoot/Subtalar/Midtarsal Fault
Syndrome is characterized by an anterior Cyma line, pseudo
sinus tarsi, increased talar declination angle, decreased
calcaneal inclination angle, everted cuboid, and less than 85%
coverage of the talar head. The cuneiform-navicular fault
occurs at the CN joint. The medial cuneiform is plantarly
displaced, and the CC joint has decreased joint space dorsally
(with increased space plantarly.) The foot appears longer.
Pes Valgo-Planus: The acquired form has a calcaneal
inclincation angle >10 degrees (normal) but the inferior
surface of the calcaneus is concave. The congenital form
(CCPV) has a low calcaneal inclincation angle with a convex
inferior surface of the calcaneus.
Diabetic Neuropathy occurs an average of 16 years after the
diagnosis of Type 2 DM (AODM). 74% present with a foot
ulcer, particularly if loss of proprioception is involved. The
forefoot ulcerates twice as commonly as the rearfoot. Charcot
neuroarthropathy has three stages of destruction, coalescence,
and remodeling.
Stress Fractures (aka march/fatigue fx) occurs most
commonly in the metatarsals, esp the 2nd (38%), then the
calcaneus (28%), and tibia (24%). Early X-rays appear
normal, however it may appear radiographically over time and
as symptoms persist.
Hallux Abducto-Valgus (HAV): Is evaluated
biomechanically by radiograph.
Normals: IM 10-20 PASA 0-8
HA 0-15 DASA 0-5
MA 12-15
Other factors evaluated are tibial sesamoid position, total
adductory angle, metatarsal break angle, and bone density.
The joint status is described as congruous, deviated, or
subluxed. Positional HAV is one where PASA+DASA<HA.
Structural HAV is one where PASA+DASA>HA.
Combined HAV is if the PASA+DASA >>>HA.
Hallucial Sesamoids are located in the tendon of FHB and
ossify between the ages of 8-12 (earlier in females than
males.) Up to 1/3 are multipartite, esp the tibial.
Osteonecrosis of the tibial is termed renandier’s, while that of
the fibular sesamoid is trevor’s. An interphalangeal sesamoid
is present in 43% of individuals (esp males), and is usually
bilateral. It may contribute to IPJ HPK formation.
PEDIATRIC RADIOLOGY
Ossification of bones in the foot occurs sequentially from birth
to adolescence, and knowledge of this order is necessary for a
physician to determine the correct skeletal age of a patient.
The talus, calcaneus, metatarsals, and sometimes cuboid are
ossified at birth. Then the order of ossification is medial
cuneiform at 6 months, intermediate cuneiform at 1 year,
medial cuneiform at 1.5 years, and finally the navicular at 2.5-
5 years. The sesamoids ossify around 7-8 years of age.
Common variations include an independent ossification center
of the medial malleolus (20%) or of the distal phalanx of the
hallux, irregular epiphyseal plates, absent epiphyseal
ossification in the middle phalanges, 5th digit synphalangism,
bilateral/symmetric cone-shaped epiphyses (which fuse earlier
than normal epiphyses), and pseudoepiphyses, fissues, and
exostoses that may appear similar to fracture.
An accessory navicular is seen in 10% of children, posterior
to the navicular tuberosity, which can cause pes planovalgus
deformity that requires sx excision. The navicular itself
ossifies by multiple ossification centers which are
asymmetrical and may look like kohler’s disease.
Similarly, the calcaneal apophysis has multiple ossification
centers which may look like sever’s disease. The calcaneus
may also have a pseudocyst called the ward’s or neutral
triangle which appears as a radiolucent circle/triangle in the
anterior calcaneus (10%). The calcaneus often has compact
bone islands as well. The apophysis of the 5th metatarsal base
runs parallel to the shaft, and should be distinguished from a
fracture.
RADIOGRAPHIC EVALUATION OF THE PEDIATRIC PATIENT
The standard AP in infants must use a simulated WB position
which is accomplished with the knees flexed and held together
and an additional 15 degree angulation of the tube. Lateral
views are positioned similarly, with the beam aimed at the
ankle. CT scanning is used in peds to determine tarsal
coalitions as well as growth plate abnormalities. MRI can be
used to evaluate unossified structures.
GROWTH VARIATIONS
Macrodactyly is a localized gigantism of the digits caused by
fat infiltration, long-standing hyperemia (leading to
hypertrophy), or neurofibromatosis.
Kippel-Trenaunay Syndrome is a localized gigantism of the
hands or feet, usually in only one extremity. Varicose veins
and port-wine hemangiomas are also present.
Larsen’s Syndrome is characterized by a double ossification
center of the calcaneus with a cleft palate, joint dislocation,
equinovarus/valgus foot, broad thumbs, and vertebral
abnormalities.
Gorham’s Disease (vanishing bone disease) is massive
osteolysis following episodes of trauma that can to opposing
bones across joint spaces. Radiographically the bones will
appear tapered with an absence of periosteal reaction. The
primary d/dx is charcot foot.
Neurofibromatosis is characterized by multiple
neurofibromas with café-au lait spots, lipomas,
kyphoscoliosis, enlargement of the foot bones, multiple ST
densities, congenital pseudoarthroses (mainly in fibula/tibia),
marked cortical thickening, and a hypoplastic pelvis.
Dwarfism is a plastic condition of localized bony
undergrowth. It occurs when tumor, radiation, or primary
developmental defects cause the epiphyseal plates to
prematurely close. The tibia is typically shorter than the
fibula, the distal femoral metaphysis is hypoplastic, and the
tibial and fibular metaphyses are cupped. Kyphosis is the
most common skeletal abnormality. Equinus is a common
foot deformity. There are 3 types of short-limb dwarfism:
Rhizomelic Dwarfism is a shortening of the proximal
segment (humerus or femur)
Mesomelic Dwarfism is a shortening of the intermediate
segment (tibia/fibula or radius/ulna)
Acromelic Dwarfism is a shortening of the distal
segment (hand, foot)
Hurler’s Syndrome is a syndrome characterized by dwarfism,
mental retardation, kyphosis, hepatosplenomegaly, and coarse
facial features. Radiographically you see shortened shafts of
the long bones with tapered ends, particularly in the upper
extremities. There is also a coax valga and genu varum.
Aplasia/Hypoplasia (dysmelia) describes any reduction
malformation. The cause is unknown. They are classified by
extent and orientation. Phocomelia is loss of the intermediate
segment of a limb. Meromelia is partial absence of a limb.
Hemimelia is absence of a half (longitudinally) of a limb.
They are a part of Fanconi’s anemia and thrombocytopenia-
absent radius synd. Proximal femoral focal deficiency (PFFD)
is assoc w/ absence of the ipsilateral fibula as well.
Polydactyly is the most common excess malformation. It can
be isolated or occur w/ syndromes. There is no sex
predilection and it is most common in the AA population.
50% of cases are bilateral. The tetamy & McKusick
classification is preaxial (tibial side of 2nd digit) or postaxial
(fibular side of 2nd digit – 80%). The venn-watson
classification is that preaxial polydactyly has a short
metatarsal w/ wide metatarsal head. Postaxial has a Y or T
shaped metatarsal, or complete metatarsal duplication.
Brachydactyly is shortening of the digits due to hypoplasia or
syndactyly. It is seen in pseudo(pseudo)hypoparathryroidism,
turner’s synd, sickle-cell, Down’s, and fetal dilantin synd.
Fusion deformities are errors of segmentation. Syndactyly
can be simple (only soft tissues fused) or complex (varying
degrees of bony involvement).
Apert’s syndrome (discussed earlier) is manifested
radiographically by multiple bony coalitions all over the body,
leading to limitation of motion that is progressive.
Nievergelt-Perlman syndrome is characterized by clubfoot,
synphalangism, conduction deafness, ball&socket ankle joint,
flexion deformities, and phocomelia or hemimelia.
Carpenter’s syndrome is polysyndactyly w/ premature
synostosis of the skull.
Poland’s syndrome is syndactyly and digital hypoplasia.
Amniotic band syndrome (streeter’s bands) is the formation
of constriction rings around the limbs, present at birth, which
leads to distal loss of the limb. The cause is unknown.
BIOMECHANICAL ABNORMALITIES
Kite’s (TC) angle is normally 25-50° in peds; however, this
angle requires the use of estimated axes for involved bones.
Another method is to compare the long axis of the talus and 1st
MT – they should line up.
Rearfoot Valgus is characterized by a high Kite’s and talar
declination angles, and is seen in flatfoot deformities,
congenital vertical talus, and neuromuscular disease.
Rearfoot Equinus is a calcaneal inclincation angle >90°. It is
seen in congenital equinovarus and congenital vertical talus.
Rearfoot Varus is characterized by a low Kite’s angle and
nearly parallel talar and calcaneal axes. It is seen in
equinovarus and some neuromuscular diseases.
Pes Planovalgus is the most common cause of RF valgus.
The etiology is uncertain but thought to be related to
ligamentous laxity. On X-ray there is abduction of the
forefoot, laterally displaced navicular, PF calcaneus, DF
metatarsals, and PF talus. If seen w/ equinus or a short
Achilles, it is termed hypermobile flatfoot. HAV is also a
common finding. Peroneal spasm may be seen if there is
tarsal coalition. Most are asymptomatic and require no sx.
Pes Cavus is most commonly seen w/ neuromuscular disease,
particularly CMT. Typically there is high calcaneal
inclination, PF metatarsals, and clawed digits.
Talipes Equinovarus (Clubfoot) is most common in males,
Caucasians & Polynesians, and is hereditary. There are 3
etiologies – intrauterine pressure (most flexible), abnormal
tendon/ligament attachment (difficult to treat), and teratologic
(assoc w/ arthrogryphosis and myeolodysplasia. Clincally you
see FF adduction, RF varus, equinus, and TN subluxation. On
X-ray there is low Kite’s angle, FF adduction, PF calcaneus,
and stair-stepping of the metatarsals. The talonavicular
relationship is estimated – Simon’s angle should be btw 0-20°,
TC angle should be >15 and talometatarsal <15° for normal.
Tx is initially casting, then sx w/ FF correction first (then RF.)
Congenital Vertical Talus is assoc w/ arthrogryphosis,
myelomeningocoele, and chromosomal abnormalities. It is
more common in males and it 50% bilateral. On X-ray it is
similar to pes planovalgus, but talus is markedly PF, and
calcaneus may be in equinus. With DF metatarsals this makes
for a rockerbottom foot.
BASIC CXR INTERPRETATION
CXR positioning: Standard positioning is with the patient
facing the cassette for PA, or with their back to the cassette for
AP projections. The patient is instructed to inhale fully to
standardize the view. AP projections make the heart appear
magnified b/c it is farther from the cassette – the PA
projection shows clear lung fields and a normal-sized heart.
Lateral films are taken with the pathological side closer to the
film. Normally the position of the patient is standing, w/ arms
raised and chin up. However, depending on the condition of
the patient, sitting or decubitus positioning may be necessary.
The standard position decreases enlargement and distortion of
the heart and vessels, allows the diaphragm to move down,
and shows air-fluid levels better in the chest. When
positioning the film on a viewbox, it should be placed as
though the patient is facing you (i.e. heart facing their left.)
Osseous Structures to be evaluated in the chest include the
sternum, clavicles, scapulae, ribs, and thoracic vertebrae. On
lateral view there are two areas of radiolucency called the
retrosternal airspace and the retrocardial airspace – this is
normal. You should be able to visualize 10 ribs in a normal
individual. Intercostal spaces are named by the rib superior.
The Diaphragm is divided into two on the AP view by the
vertebrae, making a left and right hemidiaphragm. The right
side is normally higher due to the liver (and moreso in HSM.)
The Pleura can only be appreciated with pathology (pleurisy.)
The Lungs should be evaluated in more depth than the rest of
the chest X-ray because of subtleties that can be easily missed.
It is recommended to first do a “quick glance” of the lungs to
determine if they are the normal shape and density. Then,
divide each lung into thirds in both the transverse and sagittal
planes. Then examine each third separately from each other
with respect to the anatomy of each and densities seen therein.
If pathology is suspected, determine if it is confined within
lobar divisions – almost all lung pathology except tumors are
lobar in nature. The costophrenic angles are also important to
note, as blunting of these angles may be a sign of infection or
left ventricular hypertrophy. Bronchi are not normally seen
on X-ray unless they are thickened, which is the case in cystic
fibrosis, CHF, or lymphatic obstruction secondary to tumor.
Supporting structures of the lungs are similarly not seen
normally on X-ray, but in pathological processes these lung
septa, as well as lymphatic channels, can be seen and are
referred to as Kerley lines. Kerley A lines are apically
located, extending out from the hilum or upper margins.
Kerley B lines are basilar in location, found in the lower lung
periphery, about the diaphragm. Kerley C lines appear
anywhere in the lung, but have a crosshatch appearance.
Kerley lines are seen in interstitial edema/fibrosis, sarcoidosis,
pneumonia, lymphatic obstruction, connective tissue disease,
RA, and scleroderma.
The Mediastinum is the last part of the CXR to examine.
Primarily noted in the mediastinum are the heart and great
blood vessels. An area of increased density is seen usually on
the left side of the trachea and is called the aortic knob – this
is where the aorta turns back on itself. The size of the heart is
estimated using the cardiothoracic ratio which is normally
2:1 (the heart should be half the width of the lungs in total.)
Cardiomegaly, also known as a “boot-shaped heart,” can be
caused by sports conditioning (normal), CHF, mitral valve
stenosis, chronic HTN, pericardial effusion, and left
ventricular hypertrophy. Masses in the medastinum usually
represent aortic aneurysms. The trachea, located superiorly in
the mediastinum, is used to determine the midline of the body
in the CXR. When compared with the aortic knob (which
should be slightly to the left) and the right atrium (which
should be slightly to the right), it can be determined if the
patient was standing in the correct position for the AP/PA
view. In peds it is sometimes necessary to visualize the
thymus, however it is normally obscured by other mediastinal
contents. Therefore, it is the only case in which you take
expiratory CXR views, so that the thymus may be allowed to
deviate away from the midline and be visualized before the
lung fields. Lastly, the hilar lymph nodes are located on
either side of the medistinum and are readily appreciable on
X-ray when adenopathy is present.
LUNG PATHOLOGY
Alveolar processes appear as triangular-shaped areas of
increased readiodensity, depending on the extent of
involvement. This presentation is seen in pneumonia,
advanced CHF, ARDS, and PE. Occasionally there may be
the addition of fluffy margins in the case of longer standing
pathology, due to extension of fluid through adjacent acini
through the pore of Kohn. The silhouette sign is the name
given to alveolar pathology that exists in close proximity to
the heart or great vessels – the water-density of the pathology
makes the outline of the heart and vessels (also water dense) to
be indistinct.
CHF and pulmonary edema cause the hilar lymph nodes and
vessels to become more distinct on X-ray. The fanning out of
the lymphatic vessels bilaterally produces a “batwing” or
“butterfly” appearance and is described so radiographically.
Interstitial processes are those that cause an increase in
radiodensity of the interstitium, meaning bronchi, septa, and
lymphatics. This type of pathologic process is seen in
interstitial pulmonary edema, fibrosis, TB, viral pneumonia,
metastatic tumor, connective tissue disease, and interstitial
pneumonitis. Miliary TB is seen as multiple tiny focal areas
of increased radiodensity. Asbestosis appears as an interstitial
process in the basilar lung fields. Emphysema is a loss of
interstitial density due to loss of tissue in the interstitium.
Besides a change in density, the diaphragm is pulled low
(making the lung fields appear “tall”), and the heart is deviated
medially. On a lateral view, the sternal angle may be
increased.
Primary lung lesions may be seen virtually anywhere in the
lung fields. A general rule of thumb when assessing primary
lung tumor is that dense masses tend to be benign, while fluffy
and ill-defined masses are more likely malignant. Also, if a
lesion is particularly dense (meaning possibly a calcified
center), it is increasingly likely that the lesion is a granuloma.
Another way to differentiate tumor from granuloma is by
looking at blood flow to the area – tumors tend to be
associated with blood vessels anatomically, whereas
granulomas are not. Also important to keep in mind is that
(for some reason) nipples are visible radiographically, and it is
important to note where these are initially, so that they are not
mistaken for a tumor later.
If a lesion is metastatic, it may take on a localized metastasis
pattern (one large tumor surrounded by many small ones), or if
from another source may be scattered throughout the lung
fields. Central cavitation in large tumors is indicative of rapid
growth and carries a poor prognosis.
NUCLEAR IMAGING
Nuclear imaging (scintigraphy) is used to analyze a number of
organ systems in the body, most commonly bone. This is due
to the fact that bone loss must reach 33-50% to be detected
radiographically, whereas with nuclear imaging changes can
be detected within hours. Nuclear imaging can also pick up
pathology that is not clinically visible. Most common
pathologies indicated are bone tumors, osteomyelitis, stress
fracture, non-specific bone pain, and AVN. The primary
disadvantage to nuclear imaging is poor resolution, which
makes this imaging modality non-specific (despite high
sensitivity.)
Uptake of the nuclear tracer in a bone scan occurs in an
area where the normal process of bony turnover is upset in any
way. Areas where turnover is increased (typical in injury)
show up “hot” or darker on the image, whereas areas where
infarction or compromised blood supply have occurred show
up “cold” or blank.
There are a variety of imaging agents available for use in
bone scanning, each with advantages and disadvantages. In
addition to availability and half-life, imaging agents also vary
according to the carrier molecule that they bind. Technetium
is the most common, and may be bound to phosphate (Tc-99,
for bone), pernechate (for brain/blood flow, joint imaging), or
albumin (for lung perfusion/VQ scans). Also available are
gallium (Ga-67, for inflammation) and indium (I-111, also for
inflammation). A new agent, ceretec, uses Tc-labeled
leukocytes and has a shorter t½ as well as increased specificity
over I-111. For most agents, renal dysfunction is a
contraindication for use.
The most basic bone scan uses Tc-99, which incorporates
as phosphate in areas of new bone formation. The t½ is 6h,
and requires adequate blood supply. Post-injection, uptake
will be greatest in the bladder, SI joint, ASIS, kidneys,
nasopharynx, lacrimal glands, and epiphyseal plates.
Scanning for Tc-99 occurs in 4 phases. First is the
dynamic/blood flow phase which is taken immediately after
injection. Little is seen in this phase normally. The second
phase, blood pool, occurs 1-6 minutes post-injection, and
shows vascularity to a particular region. The third phase,
bone imaging, is taken 2-4h post injection and shows bony
turnover (usually the most important.) The last phase,
delayed, is taken 24h post injection, and measures clearance
of the Tc-99 agent from the tissue. For osteomyeltits, Tc-99
can pick up changes w/in 24h (compared to 10d for X-ray.)
Gallium 67-citrate is a different agent which is not
sensitive to osteoblastic activity, and has a long (72h) t½. It is
used to image ST inflammation through binding to iron
binding proteins in WBCs. Normal uptake is seen in the liver,
spleen, stomach, lacrimal glands, intestine, salivary glands,
and breast. Ga-67 is taken up in tumors and abscesses w/in
2h, but is ideally scanned at 36-72h. It is less dependent on
vascular supply than Tc-99, but is only sensitive to infection.
Post-surgical sites can stay hot to Ga-67 for up to 2wks.
Chronic osteomyelitis is negative in Ga-67, + in acute. Tc-99
remains positive in both.
Indium is an agent that is tagged to leukocytes in the
patient’s blood and reintroduced via I.V. It is more specific
than Ga-67 but more dependent on leukocyte chemotaxis. T½
is 28d. I-111 is used to evaluate osteomyelitis (acute), DM
neuropathy, joint infections, bone marrow, and ST infection.
It may show false positives in inflammatory arthritis.
COMPUTERIZED TOMOGRAPHY (CT)
CT is an imaging modality that uses highly focused X-rays to
create detailed images with subtle changes in tissue density
and accurate descriptions of lesion location and size.
Computerization also allows 3D reconstruction. The primary
disadvantages of CT are cost and increased radiation exposure.
It is indicated for trauma, coaltions, ST masses, and infection.
The X-ray tube rotates around the patient in a CT scan, while
opposite the tube are detectors that are used to create an
image. The image produced is divided into a grid, of which
each 2D segment is a pixel, which when coupled with the 3D
depth is called a voxel. The depth of the voxel is determined
by slice thickness. Each voxel is then assigned a number
based on the amount of radiation that passed through that
segment. If the density of tissue is greater than water, the
number is positive, whereas if the tissue is less dense than
water it gets a negative number. (Bone is 1000-3000, air is
-1000.) In an image, the lowest density is represented by
black, while the highest is white, and everything inbetween is
a gray scale, as in X-ray. However, in CT particular densities
can be windowed, that is, anything below the density window
is black and anything above is white. This means that great
levels of contrast can be achieved if only the desired
pathological tissue is windowed (others are ignored.) Larger
windows, then, have lower contrast values.
When ordering CT scans, the specific area of interest
should be stated (possibly w/ bone scan), along w/ plain films.
Any lesions should have a measurement request, and
reconstructions and magnification are avalible if appropriate.
CT scans include a scout film, which shows the location of
specific slices as well as slice thickness. The scout film looks
similar to a plain film x-ray. Image reconstruction in CT is
used to view sagittal plane slices, which are out of phase with
the CT scanner and thus must be calculated by the computer.
These reconstructed images are also called secondary slices.
Finally, there is a specialized CT you can order called a
scanogram, which is an image of the entire lower extremity
from the pelvis, used to measure LLD. A scanogram is
basically a scout film with measurements to determine
absolute length of bony segments.
Overall, CT terminology and analysis is very similar to
plain films. It is most effective at analyzing osseous
pathology, and is often used in conjunction with bone scans.
It is less expensive than MRI but inferior to MRI for analysis
of soft tissues.
MAGNETIC RESONANCE IMAGING (MRI)
MRI is an imaging modality that allows for the visualization
of hydrogen protons in the human body. Hydrogen protons
are present in nearly all materials and are electrically charged,
within a magnetic field, and spins on its own axis. This makes
it ideal for differentiating between different tissue types and
analysis of hydrogen proton concentration gives clues to the
chemical makeup of the tissues analyzed.
The most important component of an MRI scanner is the
magnet, which can be permanent (exerting 0.4T) or super-
conducting (1.5-2.5T) and initiates the process by which the
hydrogen protons may be visualized. In the first step of the
process, magnetic field, the magnet is activated around the
patients body in the area to be visualized. The second step,
radiofrequency pulse, is a pulsing of electromagnetic energy
in accordance with the precession (spin) of the hydrogen
atoms, which is a frequency called the larmor frequency.
This pulsing at the larmor frequency causes all the hydrogen
protons to spin in the direction of the magnetic field. Then, in
the last step, relaxation, the magnetic field is turned off, and
the hydrogen atoms slowly return to their normal spin axes.
The time which it takes for this to happen is termed relaxation
also, and each tissue type has different relaxation rates.
Measurement of spin relaxation is the basic principle
behind how the MRI produces an image, and the intensity with
which tissues show up on the image relate to time values
associated with relaxation. One of these values is T1, which is
the time it takes for a particular tissue to regain 63% of its
longitudinal spin. Another value, T2, is the time it takes for a
proton to lose 63% of its transverse spin. (Note: T2 is always
a longer value than T2.) Other values include TR (time to
repeat – the duration of one imaging cycle), and TE (time to
echo – time in which magnetization is converted to RF signal.)
Weighted images are those that emphasize a particular time
value, to focus on a particular tissue type. A type of image
called proton density is a balance of a long TR and short TE
interval, which does not emphasize any particular time value.
A STIR image is a special form of inversion recovery in
which the T1 time is very short – this is also called “fat
suppression” because fat tends to show up black. In addition
to weighting images, contrast can be added (gadolinium,
gadolinium DTPA) to visualize vascular lesions.
NORMAL ANATOMY ON MRI
Bone Marrow is mostly composed of fat, which has a short
relaxation time and thus shows up at high intensity for T1
images or low intensity on T2 images. It should be
homogenous in appearance.
Cortical Bone lacks free hydrogen, so it appears to have low
signal intensity on all images.
Tendons and Ligaments have low hydrogen content also,
(though higher than bone) and has low intensity in all images.
Tendons are contrasted best in T1 weighted images, however.
Subcutaneous Fat and all other fatty areas have a high T1
signal intensity and low T2 signal intensity.
Vascular Supply to an area shows up with low intensity in
MRI due to movement, called a flow void. This is why
contrast media are required to visualize blood vessels on MRI.
Muscle is intermediate in hydrogen density, and thus shows
up intermediate intensity in all images.
SAFETY CONSIDERATIONS
MRI cannot be used with electrically or magnetically activated
implants like pacemakers, defibrillators, or cochlear implants.
Metallic objects located within the body will not cause harm,
but cause artifact on the MRI readout which may render it
useless. If it is suspected that a patient may have a metallic
foreign body in the vicinity of the eyes, an orbital X-ray is
indicated. Lastly, it has not yet been proven that MRI is safe
to use on gravid females; for women in their first trimester, it
is advised that a risk/benefit analysis be done before making
the decision to go ahead with MRI.
PATHOLOGY ON MRI
Osseous trauma, including stress fractures, will typically
show up as a decrease in signal intensity on T1WI in the area
of trauma, with diffuse increase in intensity on T2WI due to
localized inflammation to the area. STIR images can be
utilized to see marrow edema.
Avascular necrosis will show a well-defined line of
demarcation between viable bone and devascularized bone on
T1WI.
Osteochondritis dessicans will show up as a decreased area
of signal intensity on a T1WI in the acute stage, but as the
condition becomes chronic intensity increases.
ST infection is best visualized as increased intensity on T2 or
STIR images due to inflammation in the area. The degree of
contrast seen can differentiate abscess from cellulitis.
Osteomyelitis shows high intensity on T2WI for cortical bone
as well as low signal intensity on T1WI for medullary bone.
Charcot neuroarthropathy shows up as a decrease in signal
intensity on T1 and T2WI for affected joints.
Bone tumors typically have a low to intermediate signal on
T1WI and higher intensity on T2WI, although they may be
high on T1WI if fat or blood-filled. Calcification within a
tumor will also show up as lower intensity on all images.
Soft tissue tumors also show up with low T1WI signal
intensity and high T2WI signal intensity, however, the
composition of the tumor will affect this. Benign lesions tend
to be well demarcated, homogenous, and have a less
pronounced change in signal intensity.
Ganglion cysts are easy to pick out on MRI because of their
very low T1WI intensity and very high T2WI intensity.
Enchondroma shows up as homogenous and loculated with a
high T2WI and STIR intensity due to cartilage. Calcifications
may show up as a heterogenous intensity.
Lipomas tend to be superficial homogenous lesions with the
same signal intensity as surrounding fat, unless calcifications
are present.
MISCELLANEOUS IMAGING MODALITIES
Xeroradiography is a dry process that uses electrostatic
forces to produce an image. Positive xeroradiographs are used
to visualize bone and non-metallic foreign-bodies. Negative
xeroradiographs visualize soft tissue and metallic foreign
bodies.
Digital Radiography is an X-ray method by which plain films
are replaced with phosphor plates that transfer the image to a
digital signal. This process may produce very detailed images
and can zoom in or out to the tastes of the interpreter.
Liquid Crystal Thermography produces an image dependent
on skin surface temperature. This is useful in diabetic
neuropathy to predict the location of future ulcers, as well as
vascular and dermatologic pathologies. Digital
thermography is a similar process that involves recording an
image with a thermal camera.
Ultrasonography produces an image converted from high-
energy sound waves. Contrast is produced by variations in the
way that different tissues reflect sound. It is most useful for
distinguishing solid from fluid-filled masses, and in most
pathologies tissue alteration is significant enough for
ultrasound to detect.
Sinography is an X-ray taken after injecting a sinus with
radioopaque fluid. It is used to determine the size and extent
of a sinus tract and the location of potential abscesses.
Sinography cannot be used if the patient is allergic to iodine.
Local tissue necrosis and infection are other side effects.
Arthrography is radiographic imaging of a joint space using
injected contrast media. A single contrast arthrogram uses a
single contrast agent, and is used to determine the extent of
acute injury or ligamentous damage. Double-contrast
arthrograms utilize both positive and negative (air) contrast
media, and is used for chronic processes (such as OCD.)
Arthrograms may not be taken if the patient has cellulitis in
the area, and joint sepsis is a potential side effect.
A normal arthrogram of the ankle should show smooth
synovial lining with redundant ankle capsule, medial and
lateral recesses, smooth and uniform articular cartilage, and a
syndesmotic recess ~2.0cm to the interosseous membrane. In
15% of pts, there is a communication btw the ankle and
posterior STJ facet. In 15-20% there is a communication btw
the ankle and FHL/FDL sheaths.
Pathology seen in an arthrogram is typically due to lateral
ankle injury, and must be imaged w/in 48h of the incident.
Contrast leakage is usually indicative of ligamentous injury.
Injury of the ATF ligament shows extravasation anterior and
lateral to the fibula. The CF ligament is close to the peroneal
tendons and thus with CFL injury extravasation into these
tendon sheaths is seen. Chronic injury to the CFL will have a
persistent communication between these two structures. The
PTF ligament is rarely injured and is always seen with either
an ATFL or CFL rupture as well. Medial ankle injuries are
extremely uncommon. Syndesmotic tears are associated with
medial ankle ligament injury, and shows extravasation
superior to the syndesmotic recess.
Other uses for arthrography besides ligament injury may be to
visualize joint mice, synovial hypertrophy, joint infection
(which shows uptake of contrast to lymphatics), and capsulitis.
Tenography is the use of contrast media injected into a
tendon sheath to visualize the course of the tendon it encloses.
It is useful for visualizing post-traumatic tendon injury.
Venography is the use of contrast media to visualize the
course of a vein. It is the gold-standard for visualizing DVTs
but cannot be used in pts w/ an iodine allergy. Side effects
include allergic rxn, induced DVT, and localized skin
necrosis.
Arteriography is the use of contrast media to evaluate
vascular supply. Its use is contraindicated in trauma,
athrosclerosis, AV malformations, emboli, or tumors.
Angiography is visualization of the arterial supply using
computerized digial subtraction to remove non-vascular
structures from the picture. It is indicated in evaluation of
atherosclerosis and AV malformation.