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Orthopaedic Surgery - Clubfoot
Basics
Clubfoot, also known as talipes equinovarus, is a complex congenital deformity of the foot that is present at birth.
The deformity consists of three major components: equinus of the heel, varus with internal rotation of the hindfoot, and adduction of the forefoot.
Components of the Deformity
Equinus describes a plantarflexed position of the ankle and heel.
Varus refers to inward turning of the hindfoot, while forefoot adduction causes the front of the foot to deviate medially.
Together, these abnormalities cause the foot to point downward and inward.
Weight-Bearing Pattern
If the deformity remains untreated, the child may bear weight along the lateral border or even the dorsolateral aspect of the foot rather than on the plantar surface.
This abnormal loading can eventually lead to callus formation, pain, and gait difficulty.
Classification
Clubfoot can be divided broadly into two categories.
The first is isolated or idiopathic clubfoot, in which no other congenital abnormality is identified.
The second is syndromic or secondary clubfoot, occurring in association with other congenital or neuromuscular disorders.
Syndromic Clubfoot
Associated conditions include amniotic band syndrome, arthrogryposis, myelodysplasia, diastrophic dysplasia, Larsen syndrome, Freeman–Sheldon syndrome, Möbius syndrome, and Loeys–Dietz syndrome.
Clubfeet associated with these conditions are usually more rigid, more severe, and more resistant to nonoperative treatment than idiopathic clubfeet.
They therefore have a greater likelihood of requiring surgical correction.
Bony Anatomy
The talar neck is characteristically directed medially and plantarward.
The talonavicular relationship is also abnormal, contributing substantially to the medial and plantar displacement of the foot.
Foot Size
The involved foot is usually smaller than normal.
In unilateral cases, the affected foot may be slightly shorter than the contralateral side, generally by less than approximately 1 cm.
The calf may also remain smaller because of associated muscle hypoplasia.
Epidemiology
Clubfoot occurs in approximately 1 in every 1,000 live births.
Males are affected about twice as often as females, producing a male-to-female ratio of roughly 2:1.
Risk Factors
A positive family history substantially increases the likelihood of clubfoot.
Important risk factors include having an affected parent or sibling and the presence of congenital disorders known to be associated with clubfoot.
Associated Congenital Disorders
Conditions linked with clubfoot include amniotic band syndrome, arthrogryposis, myelodysplasia, Möbius syndrome, Freeman–Sheldon syndrome, Larsen syndrome, diastrophic dysplasia, and Loeys–Dietz syndrome.
Certain teratogenic drug exposures during pregnancy, historically including aminopterin, have also been associated with congenital foot deformities.
Genetics
Idiopathic clubfoot is believed to have a multifactorial or polygenic inheritance pattern with variable penetrance.
No single genetic abnormality explains most idiopathic cases.
Familial Risk
When one child has clubfoot, the risk to a subsequent sibling has historically been estimated at approximately 2–6%.
If a parent has clubfoot, the risk to each child has been estimated at approximately 10%.
Etiology
The exact cause of idiopathic clubfoot remains uncertain.
A genetic contribution is strongly suspected, although environmental and developmental factors may also participate.
Associated Conditions
Clubfoot may occur together with other congenital musculoskeletal or neurologic abnormalities.
The presence of other deformities should prompt evaluation for an underlying syndrome or neurologic disorder.
Diagnosis
Signs and Symptoms
The diagnosis is usually evident from the appearance of the newborn foot.
The foot is excessively turned downward and inward, often with a deep medial crease.
Older Children
Untreated clubfoot in an older child can cause difficulty walking, poor shoe fit, painful callosities, and abnormal weight-bearing.
Severe untreated cases may result in walking on the lateral or dorsal aspect of the foot.
Pain
Pain is uncommon in infancy but may develop in older children or adults if the deformity remains uncorrected or becomes rigid.
Physical Examination
The typical examination demonstrates heel equinus, hindfoot varus or supination, and adduction of the midfoot and forefoot.
Together, these findings produce the characteristic appearance of a curved or “kidney-shaped” foot.
Medial Crease
A prominent medial or plantar crease is commonly present.
The foot projects medially from the leg and may resemble the shape of a club.
Flexibility
The examiner should determine how much of the deformity can be passively corrected.
Flexibility is important for assessing severity and planning treatment.
Muscle Function
Ankle and toe muscle activity should be evaluated.
The absence of active toe dorsiflexion may indicate more severe neuromuscular involvement and is associated with a less favorable prognosis.
Calf Hypoplasia
A smaller calf is a characteristic feature.
Even after successful correction of the foot position, some degree of calf hypoplasia usually persists.
Imaging
General Role of Radiographs
Radiographs are not routinely necessary for the diagnosis or early treatment of typical idiopathic clubfoot.
They may be useful when there is concern for underlying bony fusion, atypical anatomy, or when operative treatment is being planned.
Simulated Weight-Bearing Views
When imaging is obtained in a young child who cannot stand, simulated standing AP and lateral radiographs may be used.
Obtaining adequate images can be difficult because of the rigid deformity.
Positioning
The foot should be corrected as close to neutral as possible during imaging.
A Plexiglas plate or similar device may be used to hold the foot in position.
AP Radiograph
On the AP view, the forefoot is typically markedly adducted.
In a normal foot, the talus roughly aligns with the first metatarsal and the calcaneus with the fifth metatarsal.
Kite Angle
The angle between the longitudinal axes of the talus and calcaneus is known as the talocalcaneal or Kite angle.
On an AP radiograph, the normal angle is approximately 20–40°.
Kite Angle in Clubfoot
In clubfoot, the talus and calcaneus are nearly parallel.
As a result, the AP talocalcaneal angle is substantially reduced.
Lateral Radiograph
The lateral view demonstrates the equinus position of the foot.
In a normal foot, the lateral talocalcaneal angle is approximately 35–50°.
Lateral Talocalcaneal Angle in Clubfoot
In clubfoot, the talus and calcaneus remain relatively parallel in the sagittal plane, producing a markedly decreased talocalcaneal angle.
These angular relationships can help assess the adequacy of correction.
Pathological Findings
The principal bony abnormality is medial deviation of the talar neck with subluxation of the talonavicular joint.
Soft-tissue abnormalities are also prominent.
Muscle Abnormalities
Histologic studies have demonstrated that muscle fibers on the affected side may be smaller than normal.
This contributes to the characteristic calf hypoplasia.
Soft-Tissue Contracture
The fascia, tendons, and joint capsules on the medial and posterior aspects of the foot are thickened and contracted.
These soft-tissue abnormalities contribute to the rigidity of the deformity.
Differential Diagnosis
Metatarsus Adductus
Severe metatarsus adductus can resemble clubfoot because the forefoot is turned inward.
The key difference is that metatarsus adductus does not have the fixed hindfoot equinus component characteristic of true clubfoot.
Treatment
General Principles
Treatment should begin as soon as practical after birth.
The current standard for most idiopathic clubfeet is serial manipulation and casting using the Ponseti method.
Ponseti Method
The Ponseti technique gradually corrects the deformity through a specific sequence of gentle manipulations followed by long-leg casting.
Correction proceeds progressively rather than attempting to force the foot immediately into a normal position.
Correction Sequence
The forefoot is gradually abducted while the heel and talus are stabilized.
This corrects the cavus, adduction, and hindfoot varus components.
Equinus is corrected last, after the foot has been brought into appropriate alignment.
Long-Leg Casting
A cast is applied from the toes to above the knee to maintain each stage of correction.
The cast is typically changed at approximately weekly intervals until adequate correction is achieved.
Duration of Casting
Correction often requires approximately 6–8 weeks, although the number of casts varies with the severity and rigidity of the deformity.
Achilles Tenotomy
Persistent equinus is very common after correction of the other components.
A percutaneous Achilles tenotomy is therefore frequently performed to obtain adequate ankle dorsiflexion.
Post-Correction Bracing
After successful correction, maintenance bracing is essential to reduce recurrence.
A foot-abduction brace, commonly consisting of shoes attached to a Denis Browne-type bar, is used.
Brace Schedule
The brace is generally worn essentially full-time during the initial post-correction period and subsequently during sleep and naps for several years.
Adherence to bracing is one of the most important factors in preventing recurrence.
Physical Therapy
Stretching
Stretching of the heel cord and medial soft tissues may be helpful.
However, stretching alone is usually insufficient to correct a true clubfoot.
Maintenance of Correction
Exercises are most useful after casting as an adjunct to preserve ankle and foot flexibility.
They should not substitute for appropriate casting and bracing.
Medication
Medication has little role in the routine correction of clubfoot.
Botulinum toxin has been investigated as an adjunct to casting and splinting in selected cases, but it is not a standard substitute for established Ponseti treatment.
Surgery
Indications
Surgery is reserved primarily for persistent or recurrent deformity that cannot be adequately corrected with repeat casting and less invasive measures.
Modern Ponseti treatment has substantially reduced the need for extensive surgical release.
Treatment of Relapse
Recurrent deformity can frequently be managed with repeat casting, repeat Achilles tenotomy, or anterior tibialis tendon transfer.
The specific treatment depends on the pattern and flexibility of the recurrence.
Anterior Tibialis Tendon Transfer
An anterior tibialis tendon transfer may be useful in a child with recurrent dynamic supination after initial successful correction.
The tendon is repositioned to rebalance the foot during gait.
Extensive Surgical Release
If casting fails completely, more extensive surgery may be necessary.
The goal is to release contracted structures while avoiding excessive dissection that could lead to stiffness and scarring.
Medial Release
Medial procedures may include lengthening or release of the posterior tibial tendon and flexor tendons, together with release of contracted medial structures.
Posterior Release
Posterior correction may require Achilles tendon lengthening and release of contracted posterior joint capsules.
Minimize Capsular Dissection
Extensive capsular release should be minimized whenever possible because over-dissection increases the risk of postoperative stiffness, scarring, weakness, and later pain.
Temporary Fixation
Pins may occasionally be used to maintain correction after surgical release.
When used, they may remain in place for several weeks while the soft tissues heal.
Repeat Surgery
A minority of children treated surgically may require additional procedures later because of recurrent deformity or residual imbalance.
Historically, repeat surgery has been required in approximately 10–20% of surgically treated patients.
Follow-Up
Referral
Children with suspected clubfoot should be referred to an orthopaedic surgeon experienced in pediatric foot deformity and Ponseti treatment.
Early specialist management improves the likelihood of successful nonoperative correction.
Prognosis
With appropriate treatment, most children achieve a plantigrade, functional foot that allows normal or near-normal walking and activity.
Residual Differences
Certain features cannot be fully corrected.
The affected foot often remains somewhat smaller, the calf may remain thinner, and slight limb or foot shortening may persist.
These differences usually have little effect on overall function.
Complications
Residual Deformity
Incomplete correction may leave persistent equinus, varus, adduction, or cavus.
Residual deformity may interfere with shoe wear or gait.
Rocker-Bottom Foot
Overly forceful correction, particularly dorsiflexion before adequate correction of hindfoot and forefoot alignment, can produce a rocker-bottom deformity.
This should be avoided through proper sequential correction.
Overcorrection
Excessive correction can result in hindfoot valgus or other alignment abnormalities.
Stiffness
Extensive surgical treatment may result in a stiff foot.
This is one reason modern management emphasizes serial casting and limited procedures whenever possible.
Pain
Pain can develop later in childhood or adulthood, particularly if residual deformity, overcorrection, stiffness, or degenerative changes are present.
Patient Monitoring
Long-Term Follow-Up
Children require regular follow-up for several years because recurrence may occur even after an initially successful correction.
Timing of Recurrence
Idiopathic clubfoot may recur through approximately 6–7 years of age, although most relapses occur during the first several years of life.
Monitoring for Relapse
Follow-up should assess ankle dorsiflexion, hindfoot alignment, forefoot adduction, dynamic supination, brace adherence, gait, and shoe fit.
Management of Recurrence
Early recurrence can often be successfully treated with repeat Ponseti casting, Achilles tenotomy, or anterior tibialis tendon transfer, avoiding the need for extensive surgery.
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Orthopaedic Surgery - Clinodactyly
Basics
Clinodactyly is a congenital deformity in which a finger is angulated in the radioulnar plane.
The little finger is affected most often and typically deviates toward the radial side.
The deformity usually results from an abnormally short, delta-shaped or trapezoidal middle phalanx.
Clinodactyly may occur as an isolated finding or as part of a congenital syndrome such as Down syndrome.
Synonym
Clinodactyly is sometimes referred to simply as a bent finger.
General Prevention
There is no known method for preventing clinodactyly.
There is also no evidence that early nonsurgical intervention alters its natural history when the deformity is caused by abnormal bony growth.
Epidemiology
Clinodactyly is usually apparent at birth or during early childhood.
It is more common in males, and when present in boys it is frequently bilateral.
Incidence
The reported frequency in otherwise healthy children varies widely, from approximately 1–19.5%.
It appears to be least common among Caucasian populations.
Risk Factors
Clinodactyly is strongly associated with several chromosomal and congenital syndromes.
In children with Down syndrome, the reported incidence is approximately 35–70%.
It may also be seen in Klinefelter syndrome, trisomy 18, and other congenital disorders.
Genetics
Clinodactyly may follow an autosomal dominant inheritance pattern with variable expressivity.
Some cases occur sporadically without a known family history.
Etiology
The deformity develops because of asymmetric longitudinal growth of the involved phalanx.
This is commonly related to formation of a physeal bracket, in which the growth plate extends abnormally around part of the phalanx.
Unequal growth on opposite sides of the bone causes progressive angulation.
Associated Conditions
Clinodactyly may be associated with symphalangism, brachydactyly, chromosomal trisomies, Treacher Collins syndrome, Silver syndrome, Holt–Oram syndrome, and Prader–Willi syndrome.
When other skeletal or systemic abnormalities are present, evaluation for an underlying syndrome may be appropriate.
Diagnosis
Signs and Symptoms
The affected finger, usually the fifth digit, is visibly deviated in either the radial or ulnar direction.
The deformity can arise at the PIP joint, middle phalanx, or DIP joint.
Distal involvement is particularly common.
Pain
Clinodactyly is typically painless.
Most patients present because of cosmetic appearance rather than discomfort.
Functional Limitation
Mild deformities usually do not interfere with hand function.
More severe angulation can occasionally cause difficulty with grasp, finger overlap, or interaction with adjacent digits.
Physical Examination
The degree of angulation should be measured carefully.
The examiner should document whether the deformity occurs primarily at the PIP joint, middle phalanx, or DIP joint.
Range of Motion
Both active and passive movement of each finger joint should be recorded.
This helps determine whether the deformity is purely bony or whether associated joint stiffness is present.
Examination for Associated Abnormalities
The remainder of the hand and skeleton should also be examined.
Additional congenital abnormalities may suggest an underlying syndromic diagnosis.
Laboratory Testing
Routine laboratory studies are not required for isolated clinodactyly.
If a chromosomal or congenital syndrome is suspected, chromosome analysis or appropriate genetic testing may be indicated.
Imaging
Plain Radiographs
Conventional radiographs of the affected finger are useful for defining the underlying bony anatomy.
Imaging is particularly important when surgical correction is being considered.
Normal Angulation
Angulation of less than approximately 10° may fall within normal anatomical variation.
Greater deformity should be interpreted in relation to symptoms, function, and progression.
Radiographic Findings
Radiographs may show a shortened, wedge-shaped, delta-shaped, or trapezoidal phalanx.
The joint surface may be oblique because of asymmetric development.
Pathological Findings
The underlying abnormality is maldevelopment of one of the phalanges.
Unequal growth causes angulation of the bone and its associated joint surface.
Differential Diagnosis
Delta Phalanx
A delta phalanx is a wedge-shaped phalanx with an oblique articular surface.
It is closely related to the underlying developmental mechanism of many cases of clinodactyly.
Fracture Malunion
A previously fractured finger that heals in an angulated position may resemble clinodactyly.
History of trauma and radiographic evidence of prior fracture help distinguish malunion from congenital deformity.
Treatment
General Measures
Most cases of clinodactyly are primarily cosmetic and do not require treatment.
Mild deformity without functional impairment should generally be observed.
Manipulation and Casting
Manipulation or casting is usually ineffective because the deformity arises from abnormal bone growth rather than a flexible soft-tissue contracture.
These methods can also be difficult for children to tolerate.
Indications for Surgery
Surgical correction may be considered when there is substantial persistent deformity, functional impairment, overlap with adjacent fingers, or unacceptable appearance, particularly after approximately 6 years of age.
Expectations From Surgery
Surgery can improve finger alignment and appearance.
However, correction may come at the cost of scarring, stiffness, and possible loss of motion.
These trade-offs should be considered carefully in a condition that is often asymptomatic.
Activity
No activity restrictions are necessary for uncomplicated clinodactyly.
Children may participate normally in play, sports, and daily activities.
Physical Therapy
Physical or hand therapy is not usually required before surgery.
After operative correction, therapy may help restore range of motion, strength, and hand function.
Surgery
General Principles
Surgical treatment depends on the child’s age, skeletal maturity, severity of deformity, and underlying physeal abnormality.
Procedures include osteotomy and reconstruction of the abnormal growth plate region.
Young Children
In children younger than approximately 6 years, correction may involve excision of the abnormal central portion of the continuous epiphysis and underlying physis.
A free-fat graft is then inserted to prevent reformation of the physeal bracket and allow more symmetric growth.
Free-Fat Graft Procedure
The aim of fat-graft interposition is to remove the tethering growth abnormality while preserving the remaining growth potential of the phalanx.
Gradual improvement in alignment can then occur as the finger continues to grow.
Older Children
After approximately 6 years of age, a corrective closing-wedge osteotomy can usually be performed more predictably.
The bone is surgically realigned to improve the axis of the digit.
Osteotomy
Corrective osteotomy provides relatively immediate correction of the deformity.
It is generally technically straightforward but still carries risks of stiffness, scar formation, recurrence, or incomplete correction.
Follow-Up
Prognosis
The overall prognosis is excellent.
Clinodactyly does not usually cause pain, progressive disability, or degenerative joint disease.
Observation
Many patients require only periodic observation.
Progression of angulation can be followed clinically as the child grows.
Patient Monitoring
Patients or families can monitor the degree of finger angulation and functional effect over time.
Reassessment is appropriate if the deformity becomes more pronounced, interferes with function, causes finger overlap, or becomes cosmetically unacceptable enough to consider surgical correction.
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Orthopaedic Surgery - Claw Toes
Basics
Claw toes are deformities of the lesser toes characterized by hyperextension at the metatarsophalangeal (MTP) joint together with flexion of the proximal interphalangeal (PIP) joint.
The distal interphalangeal joint may be either flexed or extended, depending on the specific deformity and underlying muscle imbalance.
Epidemiology
The frequency of claw-toe deformity increases with advancing age.
It occurs more commonly in women than men.
Genetics
When claw toes result from a hereditary motor and sensory neuropathy, the underlying disorder may follow an autosomal dominant inheritance pattern.
This is particularly relevant in patients with disorders such as Charcot–Marie–Tooth disease.
Pathophysiology
The most common mechanism is an imbalance between the intrinsic and extrinsic muscles of the foot.
Weakness or loss of the intrinsic muscles allows the long flexor and extensor tendons to act without their normal balancing forces.
Development of the Deformity
The process may begin with synovitis and attenuation of the plantar plate at the MTP joint.
As the plantar plate weakens, the proximal phalanx progressively hyperextends at the MTP joint.
Role of MTP Hyperextension
Hyperextension at the MTP joint displaces the intrinsic tendons dorsally relative to the axis of the joint.
This changes their mechanical action and contributes further to flexion of the interphalangeal joints, producing the characteristic claw configuration.
Extrinsic Muscle Contracture
Concurrent tightness or contracture of the long toe flexors and extensors can worsen the deformity.
Without effective intrinsic muscle opposition, the toe becomes progressively hyperextended at the MTP joint and flexed distally.
Underlying Disorders
Claw toes frequently develop secondary to neurologic or inflammatory conditions that disrupt normal muscle balance or weaken passive ligamentous restraints.
They may also occur without an identifiable underlying disease.
Causative Factors
Associated or contributing factors include tight footwear, hallux valgus, inflammatory arthropathy, peripheral neuropathy, diabetes mellitus, hereditary sensorimotor neuropathy, neuromuscular disease, spasticity, and delayed or missed compartment syndrome.
Diagnosis
Signs and Symptoms
A prominent feature is a dorsal prominence of the PIP joint of the affected lesser toe.
This prominence may rub against footwear and produce pain, callus formation, or skin irritation.
Callosities
Repeated pressure from shoes can produce painful callosities over the dorsal PIP joint.
Plantar calluses may also form beneath the metatarsal heads because of abnormal forefoot loading.
Pain
Pain may occur over the dorsum of the toe or beneath the ball of the foot.
Pain beneath the metatarsal heads is commonly described as metatarsalgia.
Difficulty With Footwear
Patients often have difficulty finding comfortable shoes because the elevated toe rubs against the upper portion of the shoe.
This problem tends to become more severe as the deformity becomes rigid.
History
Patients may seek treatment because of pain, difficulty wearing shoes, or dissatisfaction with the appearance of the toes.
A painful bursa may develop over the dorsal PIP prominence.
Plantar Fat Pad Migration
As the MTP joint hyperextends, the plantar fat pad may shift distally away from the metatarsal head.
Loss of normal cushioning beneath the metatarsal head can contribute to painful plantar calluses.
Ulceration
In patients with loss of protective sensation, particularly those with diabetic or hereditary neuropathy, pressure points can progress to skin breakdown and ulceration.
This is an important reason for close monitoring.
Physical Examination
Claw toes often involve several adjacent digits and may be bilateral.
They are frequently associated with cavus foot deformity or Achilles tendon contracture.
Neuromuscular Examination
A complete neuromuscular examination should be performed to identify an underlying cause.
Muscle strength, reflexes, gait, and associated deformities should be assessed.
Sensory Examination
Sensation in the foot should be tested carefully.
Loss of protective sensation substantially changes treatment decisions because it increases the risk of pressure injury and ulceration.
Diabetic Neuropathy Assessment
In patients with diabetes, a Semmes–Weinstein monofilament examination can be used to assess protective sensation and identify peripheral neuropathy.
Vascular Examination
The vascular status of the foot should be assessed, particularly when surgery is being considered.
Poor circulation increases the risk of wound-healing complications and may limit operative options.
Flexible Versus Rigid Deformity
The toes should be manipulated to determine whether the deformity is flexible or fixed.
This distinction is central to treatment planning.
MTP Joint Assessment
The MTP joint should be assessed for alignment, stability, subluxation, dislocation, and pain with manipulation.
Instability at this joint may indicate advanced plantar plate insufficiency.
Imaging
Plain Radiographs
Plain radiographs may show MTP joint subluxation or dislocation and flexion deformity at the PIP joint.
Weight-bearing images can help demonstrate the severity of alignment abnormalities.
Differential Diagnosis
Hammer Toe
Hammer toe can resemble claw toe but typically involves PIP flexion without the characteristic MTP hyperextension pattern seen in a true claw toe.
Mallet Toe
Mallet toe primarily involves a flexion deformity of the distal interphalangeal joint.
The MTP joint is not characteristically hyperextended.
Treatment
General Measures
Initial treatment is usually nonoperative and directed toward relieving pressure, reducing pain, and accommodating the deformity.
Options include bracing, taping, padding, cushions, and shoe modification.
Budin Splint
A Budin splint may help maintain improved toe alignment in patients with a flexible deformity.
It is less effective once the deformity becomes rigid.
Silicone Padding
Silicone or other soft padding can protect prominent areas of the toes from friction and pressure.
This may reduce callus formation and discomfort.
Cushioned Insoles
Cushioned insoles can decrease plantar pressure and help relieve metatarsalgia.
They are particularly useful when plantar calluses are present.
Footwear Modification
Shoes with a wide forefoot and high toe box can reduce rubbing over the elevated toes.
Footwear modification is one of the most useful conservative treatments.
Geriatric Considerations
Claw toes are particularly common in older women.
When significant comorbidities such as diabetes mellitus or peripheral vascular disease are present, conservative treatment is preferred whenever possible.
Surgery should be approached cautiously because wound and infection risks may be increased.
Pediatric Considerations
Congenital curly toes may be present from birth and can resemble lesser-toe deformities.
They are usually asymptomatic and commonly managed with observation.
Surgery
General Principles
Surgical treatment depends primarily on whether the deformity is flexible or rigid.
Associated hindfoot or midfoot pathology should also be addressed because persistent proximal deformity can contribute to recurrence.
Flexible Deformity
Flexible claw toes often correct when the ankle is plantarflexed or when the toe is manually manipulated.
These deformities are primarily caused by muscle imbalance rather than fixed joint contracture.
Flexor-to-Extensor Tendon Transfer
A flexor-to-extensor tendon transfer may be used to correct a flexible claw toe.
The transferred tendon helps rebalance the toe and reduce PIP flexion and MTP hyperextension.
Rigid Deformity
Rigid claw toes require correction of contracted soft tissues and, in some cases, bone procedures.
The MTP capsule and collateral ligaments may need to be released.
Extensor Tendon Release or Lengthening
A tight extensor tendon can maintain MTP hyperextension.
Release or lengthening may therefore be necessary as part of correction.
MTP Joint Dislocation
Claw toes associated with MTP dislocation may require an oblique distal metatarsal shortening osteotomy, such as a Weil-type osteotomy.
Shortening the metatarsal reduces tension and facilitates reduction of the MTP joint.
Rigid PIP Contracture
A fixed PIP joint deformity may require partial phalangectomy or PIP joint arthrodesis.
Fusion provides stable correction when the joint can no longer be passively straightened.
Associated Hindfoot and Midfoot Deformity
Underlying cavus, hindfoot varus, Achilles contracture, or other deformities should be treated when they contribute to the forefoot abnormality.
Failure to correct these problems can increase the likelihood of recurrence.
Follow-Up
Indications for Referral
Specialist referral is appropriate when pain persists despite conservative treatment or when the deformity causes significant functional limitation.
Difficulty Wearing Shoes
Inability to wear appropriate footwear despite shoe modification is a common reason to consider operative correction.
Skin Ulceration
Ulceration or impending ulceration over a pressure point warrants prompt assessment.
This is particularly important in patients with neuropathy or diabetes.
Prognosis
Claw-toe deformity is usually progressive.
Without treatment, both the structural deformity and associated pain may gradually worsen.
Flexible deformities may eventually become fixed as capsular and tendon contractures develop.
Complications
Stiffness
Postoperative stiffness can occur, particularly after joint release or fusion procedures.
Wound Infection
Surgical treatment carries a risk of wound infection.
This risk is greater in patients with diabetes, neuropathy, or peripheral vascular disease.
Persistent Pain
Pain may continue despite technically successful correction, especially when associated metatarsalgia or neuropathy is present.
Incomplete Correction
The deformity may not be fully corrected if significant contracture or unrecognized contributing pathology remains.
Recurrence
Claw toes can recur, particularly when the underlying muscle imbalance or proximal foot deformity persists.
Floating Toe
A floating toe deformity may develop after a distal metatarsal shortening procedure such as a Weil osteotomy.
The affected toe may fail to contact the ground normally during standing or gait.
Patient Monitoring
Follow-up should assess toe alignment, flexibility, skin integrity, shoe tolerance, plantar pressure symptoms, sensation, and vascular status.
Patients with diabetes or neuropathy require especially careful surveillance for calluses, pressure injury, and ulceration.
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Orthopaedic Surgery - Chronic Exertional Compartment Syndrome
Basics
Chronic exertional compartment syndrome (CECS) is an important cause of exercise-related leg pain, particularly in athletes and physically active individuals.
Because many disorders can produce similar symptoms, exertional leg pain requires a careful diagnostic evaluation.
Important alternative diagnoses include stress fracture, medial tibial stress syndrome, deep vein thrombosis, popliteal artery entrapment syndrome, and peripheral nerve entrapment.
Typical Compartment Involvement
The anterior and lateral compartments are affected most frequently and account for approximately 95% of symptomatic cases.
Symptoms are often bilateral, occurring in both legs in approximately 60–80% of patients.
Deep Posterior Compartment
The deep posterior compartment may also be involved.
Some series have reported deep posterior symptoms in as many as 40% of patients.
This form can be more difficult to diagnose and may respond less predictably to surgery.
Characteristic Symptom Pattern
The classic presentation is transient leg pain triggered by exercise and relieved by rest.
Symptoms typically recur at a predictable level of activity, such as after a certain running distance, duration, or intensity.
Epidemiology
Patients with CECS are generally young, with an average age of approximately 20–24 years.
The condition is particularly associated with running and other repetitive endurance activities.
Civilian Risk Factors
Within civilian populations, women and endurance runners have been reported to have a higher risk of developing CECS.
Military Risk Factors
Among military personnel, increased risk has been associated with older age within the military population, female sex, Caucasian race, and junior enlisted rank.
Repetitive high-volume physical training likely contributes to the development of symptoms.
Associated Conditions
No specific disease has been shown to have a direct causal relationship with CECS.
However, because many affected patients are young female endurance athletes, associated conditions such as stress fracture or components of the female athlete triad/relative energy deficiency spectrum may coexist and should be considered when clinically appropriate.
Diagnosis
Signs and Symptoms
The principal complaint is exercise-induced leg pain.
Pain usually develops predictably after a reproducible amount of physical activity and gradually resolves once exercise stops.
Predictable Exertional Pain
Patients often describe pain that begins at approximately the same distance, running speed, duration, or training intensity during each episode.
The reproducibility of symptoms is an important clinical clue.
Progression of Symptoms
In more advanced or longstanding cases, the threshold required to provoke symptoms may decrease.
Pain may eventually occur with ordinary walking and, in severe cases, may occasionally persist even at rest.
Muscle Weakness
Neuromuscular symptoms may accompany pain.
Progressive compression can result in weakness of muscles within the affected compartment.
Foot Drop
When the anterior compartment is involved, weakness of the ankle dorsiflexors may develop.
This can cause transient or, in chronic severe cases, more persistent foot drop.
Physical Examination
The physical examination may be completely normal when the patient is evaluated at rest.
For this reason, examination immediately after exercise may be more informative.
Swelling
Postexercise swelling or increased firmness of the involved compartment may be present.
This finding is more dramatic in acute compartment syndrome but may also be observed in CECS.
Neurovascular Examination
A thorough neurovascular examination should evaluate the muscles, sensory territories, and pulses related to each compartment of the leg.
Findings should be compared before and after symptom-provoking exercise whenever possible.
Compartment Tenderness
The involved compartments may become tender after activity.
The muscles may also feel tense or firm.
Pain With Passive Stretch
Passive stretching of muscles within the affected compartment may reproduce discomfort.
For example, stretching the ankle or toes opposite the action of the involved muscles may provoke pain.
Sensory Changes
Paresthesias may occur because of transient nerve compression.
In anterior compartment involvement, sensory disturbance may be noted in the first dorsal web space, corresponding to the deep peroneal nerve distribution.
Muscle Herniation
Occasionally, a focal fascial defect allows muscle to bulge through the fascia.
A palpable muscle herniation may therefore be present, particularly after exercise.
Laboratory Tests
Routine laboratory testing does not diagnose CECS.
If surgery is planned, standard preoperative blood tests may be obtained according to the patient’s age, comorbidities, and general health.
Imaging
Plain Radiographs
AP and lateral radiographs may be obtained when there is focal bony tenderness or concern for a fracture.
Their main role is to exclude other causes of exertional leg pain rather than to confirm CECS.
MRI
MRI is particularly useful for excluding stress fractures and other structural abnormalities.
It is one of the most sensitive imaging studies for stress injury of the tibia and other lower-extremity bones.
Postexercise MRI
Postexercise T2-weighted MRI may demonstrate increased muscular edema in the symptomatic compartment.
These signal changes may correlate with increased intracompartmental pressures.
Near-Infrared Spectroscopy
Near-infrared spectroscopy can assess tissue oxygenation by measuring relative amounts of oxygenated and deoxygenated blood.
Persistent elevation of the deoxygenated-to-oxygenated blood ratio after exercise may support the diagnosis.
Compartment Pressure Testing
Gold Standard
Direct intramuscular compartment pressure measurement has traditionally been considered the diagnostic gold standard for CECS.
Pressures are measured at rest and after a symptom-provoking exercise protocol.
Four-Compartment Testing
When clinically indicated, pressures may be measured in each of the four major compartments of the leg.
Testing should target the compartments suggested by the patient’s symptoms and examination.
Pedowitz Criteria
The commonly cited Pedowitz criteria use pressure measurements obtained at rest and at specific times following exercise.
A test is considered positive when one or more of the following thresholds are reached:
Resting pressure greater than 15 mm Hg
Pressure greater than 30 mm Hg at 1 minute after exercise
Pressure greater than 20 mm Hg at 5 minutes after exercise
These findings should be interpreted together with the patient’s clinical presentation.
Differential Diagnosis
Medial Tibial Stress Syndrome
Medial tibial stress syndrome commonly produces exercise-related pain along the posteromedial tibial border.
Unlike CECS, symptoms are usually associated with diffuse bony tenderness rather than a tense muscular compartment.
Tibial Stress Fracture
Stress fracture may cause focal exertional pain that eventually persists at rest.
MRI is particularly useful when radiographs are normal but clinical suspicion remains high.
Popliteal Artery Entrapment Syndrome
Popliteal artery entrapment can cause exercise-related calf pain and vascular symptoms.
Diminished pulses or abnormal vascular testing during provocative maneuvers may help distinguish it from CECS.
Deep Vein Thrombosis
Deep vein thrombosis should be considered when leg pain is associated with persistent swelling, risk factors for thrombosis, or symptoms not directly linked to exercise.
Nerve Entrapment
Peripheral nerve entrapment may produce pain, paresthesias, or weakness.
The neurologic distribution and lack of a characteristic pressure-dependent exercise pattern may help differentiate it from CECS.
Achilles Tendon Tightness
A tight gastrocnemius-soleus complex or Achilles tendon can alter lower-extremity mechanics and produce exertional discomfort.
It should be evaluated during the physical examination.
Treatment
General Measures
The most effective conservative strategy is to reduce or stop the activity that predictably produces symptoms.
Complete symptom relief is often possible if the patient permanently avoids the provoking activity.
Activity Modification
Patients may benefit from changing running distance, intensity, training surface, frequency, or type of exercise.
Transition to lower-impact activities may allow continued fitness while reducing symptoms.
Ice and Anti-Inflammatory Measures
Ice and NSAIDs may provide temporary symptomatic relief.
However, because CECS is primarily a pressure-related mechanical problem, medication alone rarely provides durable resolution when provoking activities continue.
Massage
Massage and soft-tissue techniques are sometimes used as adjunctive treatment.
Evidence for lasting benefit is limited, but some patients report temporary improvement in discomfort.
Footwear Modification
Changing shoes may alter lower-extremity mechanics and reduce symptoms in selected patients.
Footwear should be appropriate for the athlete’s foot type, running surface, and training demands.
Gait Modification
Modification of running technique may reduce compartment loading.
Changes in cadence, foot-strike pattern, and running mechanics have been explored as nonoperative strategies in selected athletes.
Limitations of Nonoperative Treatment
Conservative management has a relatively high failure rate.
This is partly because diagnosis is often delayed and many athletes are unwilling or unable to permanently reduce the activity that causes their symptoms.
Surgery
Indications
Surgical treatment is considered when symptoms remain significant despite an adequate trial of nonoperative management and the diagnosis has been supported clinically and, when appropriate, by pressure testing.
Fasciotomy
The standard surgical procedure is fasciotomy of the involved compartment or compartments.
The fascia is opened to increase the available volume and prevent pathologic rises in pressure during exercise.
Selective Compartment Release
Only compartments demonstrated to be symptomatic should generally be released.
The decision is based on the patient’s history, physical examination, and compartment pressure findings.
Surgical Approaches
Both single-incision and limited two-incision techniques have been described.
Endoscopic assistance may also be used.
No approach has clearly demonstrated universal superiority.
Superficial Peroneal Nerve
During anterior and lateral compartment release, particular care is required to protect the superficial peroneal nerve.
The nerve can be injured during surgical exposure or fasciotomy.
Fascial Bands and Nerve Compression
The superficial peroneal nerve should be identified when necessary, and constricting fascial bands or adhesions should be released.
Failure to recognize persistent nerve compression may result in incomplete symptom relief after surgery.
Follow-Up
Prognosis
Outcomes are generally better after release of the anterior and lateral compartments than after surgery involving the deep posterior compartment.
Anterior and Lateral Compartment Outcomes
Symptom resolution after isolated anterior and/or lateral compartment release has been reported in approximately 80% of patients.
Deep Posterior Compartment Outcomes
Release of the deep posterior compartment has a less predictable result, with symptom resolution reported in approximately 60% of cases.
The deeper anatomy and diagnostic difficulty may contribute to the lower success rate.
Return to Sport
In studies of elite athletes, approximately 84% returned to their previous level of sport after surgical fasciotomy.
One reported average return-to-sport time was approximately 10.6 weeks.
Actual recovery time depends on the compartments released, wound healing, rehabilitation, and sport demands.
Complications
Nerve Injury
Peripheral nerve injury is one of the most important surgical complications.
The superficial peroneal nerve is particularly vulnerable during anterior or lateral compartment release.
Deep Vein Thrombosis
Deep vein thrombosis can occur following surgery, although it is uncommon.
Persistent calf swelling or pain after surgery should therefore be evaluated appropriately.
Infection
Surgical-site infection may complicate fasciotomy.
Appropriate wound care and postoperative monitoring are required.
Wound Dehiscence
The operative wound may separate or heal slowly, particularly when swelling is significant.
Activity progression should therefore be coordinated with wound healing.
Complex Regional Pain Syndrome
A small number of patients may develop complex regional pain syndrome, characterized by disproportionate pain, sensory disturbance, autonomic changes, and functional limitation.
Patient Monitoring
Patients managed nonoperatively should be reassessed for progression of pain, weakness, sensory disturbance, or decreasing exercise tolerance.
Following surgery, monitoring should focus on wound healing, nerve function, recurrent symptoms, ankle strength, and gradual return to activity.
Persistent or recurrent exertional pain should prompt reassessment for incomplete release, involvement of another compartment, or an alternative diagnosis.
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Orthopaedic Surgery - Clavicle Fractures
Basics
Clavicle fractures are among the most common upper-extremity fractures encountered in the emergency department.
They occur most frequently in males younger than 20 years, while among older adults, particularly those over 65 years, women account for a greater proportion of cases.
Clavicle fractures are classified according to their location, displacement, comminution, and possible intra-articular extension.
Classification
Several classification systems are available, including the Neer, Edinburgh, and Müller AO systems.
From an anatomic perspective, fractures are divided into middle-third, lateral-third, and medial-third injuries.
Middle-third fractures are by far the most common, followed by lateral and then medial clavicle fractures.
Open Fractures
Open clavicle fractures are uncommon.
When they occur, they are often associated with substantial trauma involving the head, thorax, or major vessels.
Clavicle fractures are also frequently encountered in patients with multiple traumatic injuries.
Fracture Displacement
The characteristic displacement of a midshaft clavicle fracture is produced by opposing muscular and gravitational forces.
The sternocleidomastoid muscle pulls the medial fragment superiorly, while the pectoralis major and the weight of the arm tend to pull the lateral fragment inferiorly and medially.
These forces may create visible shortening or deformity.
Neurovascular Anatomy
The clavicle lies directly over the subclavian vein and is close to the subclavian artery and brachial plexus.
Although injury to these structures is uncommon, neurovascular damage may occur at the time of trauma or during operative fixation.
A careful neurovascular examination is therefore essential.
Lateral Clavicle Fractures
The displacement pattern of lateral clavicle fractures depends strongly on the integrity of the coracoclavicular ligaments, acromioclavicular joint, and surrounding ligamentous structures.
Disruption of these stabilizers may make the fracture unstable and increase the risk of nonunion.
General Prevention
Fall prevention is particularly important in patients with impaired balance or a history of recurrent falls.
Assistive devices, home-safety assessment, and nursing or rehabilitation evaluation may help reduce future injury.
In older adults sustaining a clavicle fracture after a low-energy fall, evaluation and treatment of possible osteoporosis may reduce the risk of subsequent fragility fractures.
Epidemiology
Clavicle fractures occur more often in men than women among patients younger than 65 years, with a reported male-to-female ratio of approximately 2.2:1.
The mean age at the time of fracture has been reported to be approximately 48 years.
Fractures occur more frequently during weekends and summer months, probably reflecting increased recreational and sporting activity.
Incidence
Reported incidence varies between populations.
One epidemiologic study found approximately 5.8 clavicle fractures per 10,000 people, while a recent U.S. study reported approximately 24.4 fractures per 100,000 person-years.
The highest incidence occurs between approximately 10 and 19 years of age.
Risk Factors
Risk factors include male sex, young age, recurrent falls, osteoporosis, participation in sports, bicycle accidents, motor vehicle collisions, and other forms of trauma.
Sports account for a substantial proportion of emergency-department presentations involving clavicle fractures.
Genetics
Genetic disorders that weaken bone may increase susceptibility to clavicle fracture.
Examples include Ehlers-Danlos syndrome and fibrous dysplasia, although most clavicle fractures occur without an underlying hereditary disorder.
Etiology
The most common mechanism is a fall, frequently directly onto the shoulder.
Other mechanisms include bicycle and motorcycle accidents, motor vehicle collisions, and contact-sport injuries.
Sports-Related Injuries
Among sporting activities, bicycling is particularly commonly associated with clavicle fracture.
Football and soccer are other frequent causes.
Age and Injury Mechanism
Men are more likely to sustain clavicle fractures through higher-energy mechanisms, whereas women, particularly older women, more often sustain fractures after falls or other relatively low-energy trauma.
Associated Conditions
Associated injuries are common, particularly after high-energy trauma.
Important associated conditions include rib fractures, pneumothorax, cervical spine injury, head injury, scapular fracture, vascular injury, and nerve injury.
Polytrauma
Patients with a clavicle fracture after major trauma require a complete trauma assessment.
Concurrent fractures may involve the spinal column, scapula, cranium, forearm, proximal humerus, or other parts of the shoulder girdle.
Spinal column fractures are among the important associated skeletal injuries.
Scapulothoracic Dissociation
A widely displaced clavicle fracture in a high-energy injury should raise concern for scapulothoracic dissociation.
This severe shoulder-girdle injury may be associated with major vascular and brachial plexus injury.
Diagnosis
Signs and Symptoms
Typical findings include pain with movement of the affected upper extremity, visible or palpable deformity over the clavicle, swelling, bruising, and ecchymosis.
Patients often support the injured arm with the opposite hand.
Skin Tenting
The displaced fracture fragment may push against the overlying skin, producing skin tenting.
Marked tenting or blanching indicates threatened skin integrity and may represent an indication for urgent operative treatment.
Physical Examination
The clavicular region and the entire upper extremity should be inspected carefully.
The examiner should look for open wounds, abrasions, skin tenting, expanding hematoma, abnormal alignment, or evidence of additional injury.
Neurovascular Examination
A careful neurovascular examination is essential.
Motor function and sensation throughout the upper extremity should be evaluated and compared with the opposite side.
Vascular Examination
Although vascular injury is rare, the examiner should confirm symmetric distal pulses and brisk capillary refill.
An expanding hematoma, diminished pulse, cool extremity, or other evidence of vascular compromise requires urgent assessment.
Examination for Associated Injuries
The remainder of the injured extremity should be palpated and the major joints examined.
Additional fractures, shoulder dislocation, or other injuries may coexist and should not be overlooked.
Trauma Examination
Patients injured through high-energy mechanisms require a complete trauma examination to identify associated thoracic, spinal, abdominal, cranial, or extremity injuries.
Elderly Patients After Falls
Older adults who sustain a clavicle fracture after a fall should also be evaluated for head and cervical spine injury.
This is particularly important in patients with recurrent falls or those taking anticoagulant medication.
Imaging
Dedicated Clavicle Radiographs
Standard evaluation includes dedicated radiographs of the clavicle.
An anteroposterior view and approximately 20° cephalad view are commonly obtained.
Chest Radiograph
An AP chest radiograph can help assess fracture displacement and compare the injured clavicle with the opposite side.
It may also reveal associated injuries such as rib fractures or pneumothorax.
Shoulder Radiographs
Dedicated shoulder radiographs can help exclude associated injuries involving the scapula, acromioclavicular joint, or proximal humerus.
CT
CT is not routinely required for uncomplicated midshaft fractures.
It may be helpful for medial clavicle fractures, complex fracture patterns, or when the relationship to adjacent thoracic structures is unclear.
Vascular Imaging
If vascular injury is suspected, angiographic imaging may be required to evaluate the subclavian or other nearby vessels.
Additional Imaging
Additional radiographs or advanced imaging should be obtained according to the mechanism of injury and clinical suspicion for associated trauma.
Pathologic Fracture Evaluation
Pathologic testing is not routinely necessary.
A pathologic fracture should be considered when the injury occurs after an unusually minor mechanism, when there is a personal or strong family history of malignancy, or when radiographs demonstrate a suspicious underlying bony lesion.
Differential Diagnosis
The differential diagnosis includes acromioclavicular joint separation, rib fracture, scapular fracture, shoulder dislocation, sternoclavicular joint dislocation, and proximal humerus fracture.
Treatment
General Principles
Treatment depends on both patient factors and fracture characteristics.
Most clavicle fractures can be managed nonoperatively, although operative fixation has become more common in selected displaced fractures.
Nondisplaced Fractures
Nondisplaced or minimally displaced fractures usually heal successfully with nonoperative care.
A sling, pain control, and gradual restoration of shoulder motion are typically sufficient.
Medial and Lateral Fractures
Many medial and lateral clavicle fractures can also be managed without surgery when alignment and stability are acceptable.
However, unstable lateral fractures require closer assessment because the risk of nonunion is higher.
Children Versus Adults
Children have greater remodeling potential and a higher likelihood of healing displaced fractures than adults.
Consequently, substantial displacement that might prompt surgery in an adult may still be treated successfully without surgery in a younger child.
Monitoring Displaced Fractures
Displaced fractures treated nonoperatively should undergo repeat radiographs during the first several weeks to ensure that alignment has not worsened.
Sleeping Position
During the painful acute phase, patients may find it more comfortable to sleep in a chair or recliner rather than lying flat.
Activity
Sling Immobilization
A sling is commonly used for approximately 2–4 weeks.
During the early period, the involved upper extremity is generally kept non-weight-bearing.
Early Joint Motion
The sling should be removed several times each day for gentle elbow, wrist, and hand range-of-motion exercises.
This helps prevent stiffness in uninvolved joints.
Shoulder Motion
Gentle shoulder range of motion can usually begin after approximately 2–4 weeks, depending on pain, fracture stability, and clinical progress.
More strenuous motion and strengthening are delayed until healing has progressed.
Figure-of-Eight Brace
A figure-of-eight clavicle brace may be used, but it has not shown a clear advantage over a simple sling.
It may also produce greater discomfort during the early treatment period.
Axillary Care
When using a sling, the axillary fold should be kept clean and dry to prevent irritation, moisture accumulation, and skin breakdown.
Preoperative Activity
Patients awaiting surgery should generally remain non-weight-bearing in a sling.
After fixation, activity restrictions depend on the surgical construct, implant, and surgeon’s postoperative protocol.
Physical Therapy
Nonoperative Rehabilitation
Formal physical therapy is not necessary for every patient.
For nonoperatively treated fractures, gentle motion can begin after approximately 2–4 weeks.
Early Exercises
Rehabilitation may begin with pendulum and pulley exercises.
These are gradually advanced toward full shoulder range of motion as pain decreases and healing progresses.
Postoperative Therapy
The timing of physical therapy after surgery varies according to fixation stability, patient factors, and surgeon preference.
Stable fixation often allows earlier controlled motion.
Medication
First-Line Treatment
Pain management may include ice, acetaminophen, and NSAIDs when appropriate.
Some surgeons limit NSAID use because of theoretical concerns regarding bone healing, although practice varies.
Additional Analgesics
Tramadol may be considered for selected patients.
Short courses of opioid analgesics are sometimes required during the acute painful period.
Opioid Considerations
Before prescribing opioids, factors such as patient age, comorbidities, concurrent medications, fall risk, and overall health should be considered.
Surgery
Indications
Operative treatment may be considered for an open fracture, threatened skin, floating shoulder, severe displacement, significant shortening, or other unstable fracture patterns.
Shortening greater than approximately 2 cm may contribute to the decision for surgery in selected displaced midshaft fractures.
Floating Shoulder
A floating shoulder refers to major disruption of the shoulder suspensory complex, often involving an ipsilateral scapular neck fracture together with clavicular injury.
This pattern may warrant operative stabilization depending on displacement and overall injury severity.
Open Reduction and Internal Fixation
Surgery commonly involves open reduction and internal fixation (ORIF) with plates, screws, or other internal fixation devices.
The goals are restoration of length and alignment, stable fixation, and facilitation of earlier functional rehabilitation.
Follow-Up
Prognosis
Most clavicle fractures heal successfully.
Outcome depends on fracture location, displacement, age, soft-tissue condition, and whether the fracture is treated surgically or nonoperatively.
Operative Treatment of Displaced Midshaft Fractures
Surgical fixation of appropriately selected displaced midshaft fractures can reduce the rates of nonunion and symptomatic malunion compared with nonoperative treatment.
It may also permit a quicker early return to work and improved short-term functional recovery.
Hardware Removal
One disadvantage of operative fixation is the relatively high rate of subsequent procedures.
Many patients request hardware removal because the clavicle is subcutaneous and plates can be prominent or irritating.
Nonunion
Some displaced midshaft fractures treated nonoperatively progress to nonunion.
Not all nonunions are sufficiently symptomatic to require further treatment.
Lateral Clavicle Nonunion
Nonunion is relatively common after certain lateral clavicle fractures.
However, some radiographic nonunions remain minimally symptomatic and do not require surgery.
Complications
Infection
Surgical fixation carries a risk of wound infection and deep implant-related infection.
Hardware Failure
Internal fixation devices may loosen, break, or fail, especially if union is delayed or excessive loading occurs too early.
Nonunion
Failure of the fracture to unite is more likely with marked displacement, shortening, comminution, smoking, and certain unstable lateral fracture patterns.
Symptomatic Malunion
A clavicle fracture that heals with substantial shortening or deformity may produce pain, weakness, altered shoulder mechanics, or cosmetic dissatisfaction.
Symptomatic malunion is more commonly encountered after markedly displaced fractures treated nonoperatively.
Shoulder Stiffness
Prolonged immobilization or associated shoulder injury may result in post-traumatic stiffness.
Early controlled motion after an appropriate period of fracture protection can reduce this risk.
Supraclavicular Nerve Symptoms
Numbness over the clavicle or upper chest may occur because the cutaneous supraclavicular nerve branches can be stretched or injured during the initial trauma.
They may also be cut or stretched during surgical exposure.
Neurovascular Injury
Although rare, injury to the brachial plexus or subclavian vessels can occur because of their close relationship to the clavicle.
These complications can occur from the initial fracture or during operative treatment.
Patient Monitoring
Early Radiographic Monitoring
Radiographs should be obtained every few weeks during the early post-injury or postoperative period to confirm maintenance of alignment.
This is especially important for displaced fractures treated without surgery.
Healing Surveillance
After the acute period, imaging may be repeated approximately every 4–6 weeks until satisfactory clinical and radiographic union is demonstrated.
Clinical Monitoring
Follow-up should assess pain, skin condition, neurovascular status, shoulder range of motion, tenderness at the fracture site, and functional recovery.
Increasing pain, new neurologic symptoms, skin compromise, or progressive deformity should prompt earlier reassessment.
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Orthopaedic Surgery - Chordoma
Basics
Chordoma is a low-grade malignant bone tumor arising from remnants of the embryologic notochord.
It accounts for approximately 1–4% of primary malignant bone tumors and is one of the most important primary malignant tumors involving the axial skeleton, particularly the spine and sacrum.
Anatomic Distribution
Chordomas most commonly arise in the sacrococcygeal region, which accounts for approximately 55% of cases.
Around 30% occur in the skull base, particularly the sphenoid or clival region, while approximately 15% develop within the cervical, thoracic, or lumbar spine.
Delayed Diagnosis
Diagnosis is frequently delayed because symptoms are often nonspecific.
Sacral chordoma may present simply as chronic low back, pelvic, or sacral pain and may therefore be mistaken for much more common degenerative musculoskeletal disorders.
Dedifferentiation
Although conventional chordoma is generally considered a low-grade malignancy, a small proportion of tumors, historically reported at less than 5%, may undergo dedifferentiation into a high-grade spindle-cell sarcoma.
Dedifferentiated chordoma behaves much more aggressively than the conventional form.
General Precautions
One of the most important diagnostic pitfalls is failure to consider sacrococcygeal chordoma in a patient with persistent unexplained low back or sacral pain.
Chronic symptoms that are progressive, atypical, or associated with neurologic, bowel, or bladder dysfunction warrant further investigation.
Epidemiology
Chordoma is extremely rare.
The reported annual incidence is approximately 0.08 cases per 100,000 people.
It most commonly presents in adulthood, with a peak incidence around the fourth to fifth decades of life, although it may occur outside this age range.
Risk Factors
No established environmental or lifestyle risk factors have been identified.
Most cases occur sporadically.
Genetics
No common hereditary predisposition is recognized in the majority of patients.
The disease is generally not associated with a typical familial pattern.
Etiology
Chordoma develops from persistent notochordal remnants within the axial skeleton.
The notochord normally contributes to embryologic development of the spine and largely disappears before birth, but residual cells may persist and later undergo malignant transformation.
Tumor Growth
Chordomas often extend beyond the confines of bone.
Sacral tumors, in particular, may produce a large anterior soft-tissue mass extending into the pelvis.
Because the tumor may become very large before producing obvious symptoms, substantial local destruction can be present by the time of diagnosis.
Associated Conditions
No specific associated systemic disorders are typically present.
Diagnosis
Signs and Symptoms
Symptoms depend on tumor location but are usually slowly progressive and nonspecific.
Sacral lesions commonly produce low back pain, pelvic pain, sacral discomfort, or anal pain.
Difficulty Sitting
Patients with sacrococcygeal tumors may find prolonged sitting increasingly uncomfortable.
Pain may arise from direct pressure on the tumor or involvement of adjacent pelvic structures.
Bowel and Bladder Symptoms
Constipation, urinary disturbance, or other pelvic-organ symptoms may develop as the tumor enlarges.
These findings can result from compression or invasion of adjacent pelvic structures or sacral nerve roots.
Radiculopathy
Tumor extension around neural structures may compress or destroy adjacent nerve roots.
This can produce radicular pain, sensory loss, or motor dysfunction corresponding to the level of involvement.
In sacral chordoma, the S1, S2, and S3 roots are commonly at risk.
Physical Examination
Physical findings are often limited despite substantial tumor size.
There may be little to suggest an underlying bone malignancy on routine examination.
Rectal Examination
Large sacral chordomas frequently extend anteriorly into the pelvis.
A mass may be palpable during rectal examination in approximately half of patients with sufficiently advanced sacral disease.
Imaging
Plain Radiographs
Plain radiographs may appear normal or show only subtle abnormalities.
Findings can include bone destruction, cortical expansion, or a lytic sacral lesion.
Limitations of Radiography
Sacral tumors are particularly easy to miss on plain radiographs because bowel gas and fecal material may obscure the lesion.
A normal radiograph therefore does not exclude chordoma when clinical suspicion remains high.
CT
CT is highly sensitive for demonstrating the bony component of chordoma.
Typical findings include midline osseous destruction and an anterior soft-tissue mass.
Calcification
Scattered internal calcifications may be visible on CT.
These mineralized areas can help characterize the lesion but are not specific to chordoma.
MRI
MRI is the preferred modality for defining the full extent of the tumor and its relationship to surrounding structures.
Chordomas are typically low signal intensity on T1-weighted images and high signal intensity on T2-weighted images.
Contrast-Enhanced MRI
Contrast-enhanced MRI helps delineate the dimensions of the mass and its relationship to the spinal canal, nerve roots, pelvic organs, vessels, and surrounding soft tissues.
This information is essential for operative planning.
Imaging the Entire Sacrum
Sacrococcygeal lesions may lie at the extreme inferior edge of lumbar or pelvic MRI studies.
The tumor can therefore be overlooked if the imaging field does not extend far enough inferiorly.
When sacral chordoma is suspected, imaging should include the entire sacrum and coccyx down to the coccygeal tip.
Nuclear Medicine
Conventional technetium bone scans and PET have historically been less useful than CT and MRI for primary characterization of chordoma.
Cross-sectional imaging remains central to diagnosis, staging, and surveillance.
Differential Diagnosis
Destructive Spinal Lesions
Important alternative diagnoses include metastatic bone disease, multiple myeloma, and lymphoma, all of which can produce destructive lesions of the spine or sacrum.
Sacral Tumors
Chondrosarcoma and giant cell tumor may also arise in the sacrum.
Both can produce bone destruction, soft-tissue extension, and in some cases mineralization, making differentiation from chordoma necessary.
Chondrosarcoma
Chondrosarcoma may resemble chordoma radiographically, particularly when it occurs in the pelvis or sacrum.
Tumor location, pattern of calcification, MRI appearance, and histology help distinguish the two lesions.
Treatment
General Principles
The primary treatment for chordoma is complete surgical removal whenever technically feasible.
Because local recurrence strongly influences survival, achieving adequate margins is critical.
Wide En Bloc Resection
The preferred operative strategy is wide en bloc resection with negative surgical margins.
The tumor is removed as a single specimen together with a surrounding margin of uninvolved tissue when anatomy permits.
Importance of Surgical Margins
Incomplete excision or tumor contamination during surgery substantially increases the risk of local recurrence.
Unfortunately, chordomas often lie immediately adjacent to major nerves, blood vessels, bowel, bladder, or spinal structures, making wide margins difficult to achieve.
Chemotherapy
Conventional chemotherapy has little established role in the routine treatment of classic chordoma.
The relatively indolent biology of the tumor and limited chemosensitivity make surgery and local control the major therapeutic priorities.
Radiotherapy
High-dose radiation, particularly proton-beam or other conformal particle-based radiotherapy, may be considered in selected patients.
It can be used when surgical margins are limited, the tumor is unresectable, or as part of a combined treatment strategy.
Follow-Up
Prognosis
Chordoma has a prolonged but potentially aggressive natural history.
Historical series report a median survival of approximately 6.3 years.
Five-year survival has been reported in the range of approximately 50–67%, while 10-year survival has ranged from roughly 28–46%.
Metastatic Risk
The risk of distant metastasis has historically been estimated at approximately 10–40%.
Common metastatic sites include the lungs, bone, liver, and lymph nodes.
Importance of Local Recurrence
Chordoma is unusual among low-grade tumors because local recurrence can itself be a major cause of mortality.
Repeated local growth can progressively involve vital neural, vascular, gastrointestinal, and genitourinary structures.
Relationship Between Recurrence and Survival
Local recurrence is associated with poorer survival.
The best chance for durable control therefore comes from achieving adequate surgical margins during the initial operation whenever possible.
Complications
Wound-Healing Problems
Wound complications are common after major sacral resections.
Historical series have reported wound-healing problems in as many as 45% of patients.
Large incisions, dead space, radiation, extensive soft-tissue dissection, and contamination risk may all contribute.
Injury to Pelvic Structures
Sacral chordoma surgery may place important anterior pelvic structures at risk.
Potential injuries include damage to the iliac vessels, rectum, bladder, ureters, and other pelvic organs.
Sacral Nerve-Root Sacrifice
The functional consequences of surgery depend heavily on which sacral nerve roots must be sacrificed to achieve tumor clearance.
Higher-level bilateral sacrifice produces more severe neurologic deficits.
Bilateral S1 Sacrifice
Sacrifice of both S1 nerve roots, as may occur with total sacrectomy, can result in major lower-extremity motor and sensory deficits together with loss of bowel and bladder function.
Bilateral S2 Sacrifice
Historical data indicate that bilateral S2 root sacrifice is associated with an extremely high likelihood of bowel and bladder dysfunction.
Some patients may require permanent diversion procedures.
Bilateral S3 Sacrifice
Bilateral S3 sacrifice carries a substantial risk of bowel and bladder dysfunction.
Historical series have reported bowel dysfunction in approximately 60% and bladder dysfunction in approximately 75% of such patients.
Bilateral S4 Sacrifice
Sacrifice limited to both S4 roots is associated with a lower risk of bowel dysfunction, although bladder disturbance may still occur.
Historical series reported minimal bowel dysfunction but bladder dysfunction in approximately 31% of patients.
Sexual Dysfunction
Loss of sacral nerve function may also produce sexual dysfunction, depending on the level and extent of nerve-root sacrifice.
Spinopelvic Instability
Major sacral resections can disrupt continuity between the spine and pelvis.
This may produce spinopelvic instability or discontinuity and can require complex reconstruction.
Sacral Insufficiency Fracture
Remaining sacral or pelvic bone may be vulnerable to insufficiency fracture following extensive resection.
Mechanical reconstruction may be required when stability is compromised.
Patient Monitoring
Long-Term Surveillance
Patients require lifelong surveillance because chordoma can recur many years after initial treatment.
Follow-up commonly includes CT or MRI of the operative region once or twice each year, with intervals individualized according to recurrence risk and prior treatment.
Surveillance for Metastases
Imaging should also assess for distant metastatic disease, particularly involving the lungs.
Long-term chest surveillance is therefore commonly incorporated into follow-up.
Clinical Monitoring
Follow-up should assess for new pain, neurologic symptoms, bowel or bladder dysfunction, changes in sitting tolerance, and evidence of wound or reconstructive complications.
Any new or progressive symptom should prompt timely imaging because recurrent disease may initially be subtle.
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Orthopaedic Surgery - Chondrosarcoma
Basics
Chondrosarcoma is a primary malignant bone tumor composed of neoplastic cartilage-forming cells within a cartilaginous matrix.
It most commonly involves the pelvis, proximal femur, region around the knee, and spine, although other skeletal sites may also be affected.
Its biologic behavior varies widely depending on histologic subtype and grade.
Tumor Grade and Metastatic Risk
Low-grade, or grade 1, chondrosarcoma has a relatively low metastatic potential, generally less than approximately 5%.
Intermediate-grade, or grade 2, disease carries a higher metastatic risk, commonly around 20–30%.
High-grade or dedifferentiated tumors have a much more aggressive course, with metastatic rates that may approach or exceed 70%.
Mesenchymal chondrosarcoma is also highly aggressive, with a metastatic risk greater than 50%.
Epidemiology
Chondrosarcoma accounts for approximately 20% of primary malignant bone tumors and occurs about half as frequently as osteosarcoma.
It is predominantly a disease of older adults, most often presenting in the sixth through eighth decades of life.
Risk Factors
Important predisposing conditions include hereditary multiple exostoses, Ollier disease, and Maffucci syndrome.
These disorders increase the likelihood of malignant transformation in pre-existing cartilaginous lesions.
Genetics
The genetic basis of chondrosarcoma is heterogeneous and incompletely understood.
Abnormalities involving several chromosomes have been described, including chromosomes 2–11, 14, 15, and 21.
EXT Mutations
Patients with hereditary multiple exostoses caused by an EXT1 mutation appear to have a greater risk of malignant transformation than patients with EXT2 or EXT3 abnormalities.
Myxoid Chondrosarcoma Genetics
Myxoid variants have been associated with a characteristic chromosomal translocation involving chromosomes 9 and 22.
Etiology
Most chondrosarcomas arise de novo, meaning they develop as primary malignant tumors without a known pre-existing lesion.
Others are secondary tumors that develop through malignant transformation of a previously benign cartilage lesion.
Secondary Chondrosarcoma
Secondary chondrosarcoma may arise from a pre-existing osteochondroma or enchondroma.
This is particularly important in patients with hereditary multiple exostoses, Ollier disease, or Maffucci syndrome.
When malignant transformation occurs in these settings, the resulting tumor is often initially low grade.
Dedifferentiated Chondrosarcoma
Dedifferentiated chondrosarcoma accounts for approximately 10% of cases.
It contains a conventional cartilaginous tumor adjacent to a highly malignant noncartilaginous component.
This is one of the most aggressive forms of chondrosarcoma and carries a poor prognosis.
Associated Conditions
Chondrosarcoma is associated particularly with disorders that produce multiple exostoses or enchondromatosis.
Recognition of these underlying conditions is important because changes in pain, lesion size, or imaging appearance may indicate malignant transformation.
Diagnosis
Signs and Symptoms
The typical presentation is deep, gradually progressive pain.
Symptoms may be present for months or even years because many chondrosarcomas grow relatively slowly.
Pain Characteristics
Pain may be worse at night and may persist despite rest.
Unlike many benign musculoskeletal conditions, the discomfort often becomes progressively more constant.
Analgesics or NSAIDs may provide partial relief but usually do not eliminate the symptoms.
Soft-Tissue Mass
With longstanding disease or cortical breakthrough, a palpable soft-tissue mass may develop.
This suggests extension of the tumor beyond the confines of the bone.
History
A high index of suspicion is appropriate when an adult with a known cartilaginous lesion develops new pain, night pain, progressive enlargement, or pain that is no longer relieved by rest.
These features are particularly concerning for malignant transformation.
Physical Examination
The examination is generally nonspecific.
Patients may have tenderness with deep palpation or, in more advanced disease, a palpable soft-tissue mass.
Joint motion may be limited if the tumor is large or located near an articulation.
Laboratory Tests
Routine serum tests are generally not diagnostic.
There are no specific blood markers that reliably establish the diagnosis of chondrosarcoma.
Imaging
Plain Radiographs
Standard AP and lateral radiographs are often highly suggestive of the diagnosis.
The tumor usually appears as an intramedullary lesion containing stippled, ring-like, or arc-shaped calcifications within a cartilaginous matrix.
Cortical Changes
More aggressive lesions may produce substantial cortical abnormalities.
These can include cortical erosion, thickening, expansion, endosteal scalloping, and frank bone destruction.
Chest Imaging
Because chondrosarcoma can metastasize, particularly to the lungs, staging commonly includes chest imaging.
Chest radiographs or, more commonly, CT of the chest may be obtained to evaluate for pulmonary metastases.
MRI
MRI of the affected region is useful for defining the intramedullary extent, cortical involvement, soft-tissue extension, neurovascular relationships, and relationship to nearby joints.
It is also valuable for planning the biopsy approach and surgical resection margins.
Biopsy Planning
The biopsy should be planned carefully because the biopsy tract must usually be removed during definitive tumor resection.
Whenever possible, biopsy planning should be coordinated with the surgeon who will perform the definitive oncologic procedure.
Pathological Findings
Histologic distinction between a benign enchondroma and a well-differentiated low-grade chondrosarcoma can be difficult.
For this reason, pathologic interpretation must be correlated closely with the clinical and radiographic findings.
Trabecular Permeation
A characteristic malignant feature is permeation of pre-existing trabecular bone by the cartilaginous tumor.
This supports an infiltrative rather than expansile benign growth pattern.
Chondroid Matrix
The tumor contains malignant cartilage-producing cells within a chondroid matrix.
Lobulated growth is common.
Cellular Features
Histologic findings may include binucleated chondrocytes, increased cellularity, nuclear atypia, and progressive anaplasia with increasing tumor grade.
Histologic Grading
Conventional chondrosarcomas are usually graded from 1 through 3 according to cellularity, nuclear atypia, mitotic activity, and degree of anaplasia.
Higher grade correlates with a greater risk of metastasis and poorer survival.
Differential Diagnosis
The principal differential diagnoses include enchondroma and bone infarction.
Distinguishing a low-grade chondrosarcoma from an enchondroma can be particularly difficult and often requires integration of symptoms, imaging, and histology.
Treatment
General Measures
Surgery is the mainstay of treatment for conventional chondrosarcoma.
The goal is complete tumor removal with an adequate oncologic margin, thereby minimizing the risk of local recurrence.
Role of Chemotherapy and Radiotherapy
Conventional chondrosarcoma is relatively resistant to both chemotherapy and radiotherapy.
These modalities therefore have a limited role in routine treatment, although selected aggressive subtypes or metastatic disease may be managed differently.
Wide Resection
A wide resection removes the entire tumor together with a surrounding cuff of normal tissue.
This is the standard surgical principle for most intermediate- and high-grade lesions.
Low-Grade Disease
Low-grade lesions may be managed with appropriately selected surgical excision and close radiographic surveillance.
Follow-up commonly includes serial imaging at approximately 6-month intervals during the early surveillance period.
Intermediate- and High-Grade Disease
Patients with grade 2 or 3 chondrosarcoma require more intensive metastatic surveillance.
CT imaging of the chest is commonly performed at regular intervals because the lungs are the most frequent site of metastasis.
Long-Term Surveillance
After approximately 5 years without evidence of disease, follow-up intervals may be increased.
However, long-term surveillance remains important because some chondrosarcomas can recur late.
Physical Therapy
Physical therapy is used after surgery to restore range of motion, strength, gait, and functional independence.
The specific program depends on tumor location and the type of reconstruction performed.
Medication
There is no established medication that reliably treats localized conventional chondrosarcoma.
Patients who develop metastatic disease may receive systemic therapy, but conventional chemotherapy has historically shown limited and inconsistent benefit.
Surgery
Wide resection requires removal of all involved bone and soft tissue while maintaining an adequate margin around the tumor.
The resulting defect may require substantial reconstruction.
Reconstruction
Limb reconstruction can be performed using an allograft, custom prosthesis, modular tumor prosthesis, or other reconstructive technique depending on the site and extent of resection.
Soft-Tissue Reconstruction
Muscle flaps or other reconstructive soft-tissue procedures may be required to cover large defects and protect implants or exposed structures.
Follow-Up
Close postoperative surveillance is required to detect local recurrence, metastasis, or failure of reconstruction.
The intensity of follow-up depends on tumor grade and time since treatment.
Prognosis
Prognosis is strongly determined by histologic grade and subtype.
Low-grade conventional chondrosarcoma generally has an excellent prognosis.
Grade 1 Prognosis
Grade 1 tumors have a metastatic risk of less than approximately 5% and usually have very favorable long-term outcomes when adequately resected.
Grade 2 Prognosis
Grade 2 tumors have a higher metastatic potential, generally below approximately 30%, but overall prognosis remains substantially better than for high-grade disease.
High-Grade and Dedifferentiated Disease
Grades 3 and dedifferentiated tumors carry a poor prognosis because of their high metastatic potential.
Metastatic rates may exceed 70%.
Dedifferentiated Chondrosarcoma Prognosis
Dedifferentiated chondrosarcoma is among the most aggressive subtypes.
Historical series have reported very low long-term survival, with rapid progression once metastatic disease develops.
Mesenchymal Chondrosarcoma
Mesenchymal chondrosarcoma also carries a relatively poor prognosis because of its aggressive behavior and high metastatic potential.
Complications
Important complications include local recurrence, metastatic disease, and failure of reconstruction.
The risk of recurrence rises when surgical margins are inadequate or the tumor is high grade.
Local Recurrence
Local recurrence may result from incomplete resection or microscopic residual disease.
Recurrent tumors can be more difficult to treat and may require additional wide resection or amputation in selected cases.
Metastases
Metastatic spread occurs mainly in intermediate- and high-grade tumors.
The lungs are the most common site, although other organs and bones may also be involved.
Reconstruction Failure
Large oncologic reconstructions can fail because of infection, mechanical loosening, fracture, nonunion, implant failure, or soft-tissue complications.
These problems may require revision surgery.
Patient Monitoring
Patients should initially be reviewed frequently, often at approximately 1–3-month intervals during rehabilitation, depending on the extent of surgery and tumor grade.
Subsequent surveillance should monitor the surgical site, reconstruction, local recurrence, and pulmonary metastases, with imaging intervals adjusted according to oncologic risk.
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Orthopaedic Surgery - Chondroblastoma
Basics
Chondroblastoma is a benign bone tumor of cartilaginous origin that characteristically arises in the epiphysis of skeletally immature patients.
It most often develops in the epiphyses of long bones, particularly around major joints.
The proximal humerus is the most commonly involved site, followed by the proximal tibia and femur.
Synonyms
Chondroblastoma of the proximal humeral epiphysis has historically been referred to as a Codman tumor.
Another older term is epiphyseal chondromatous giant cell tumor.
Epidemiology
Chondroblastoma has a mild male predominance, with males affected approximately twice as often as females.
It occurs mainly in adolescents and young adults whose physes are still open or have only recently closed.
Incidence
Chondroblastoma is uncommon.
In large tumor series, it has accounted for approximately 1% of all skeletal neoplasms.
Risk Factors
No specific environmental, developmental, or lifestyle risk factors have been identified.
Genetics
No well-established hereditary predisposition has traditionally been recognized for chondroblastoma.
The tumor is generally considered sporadic.
Etiology
The precise cause remains uncertain.
The neoplastic cells are believed to arise from cartilage-producing precursor cells, or chondroblasts.
Some pathologic similarities exist between chondroblastoma and chondromyxoid fibroma, although they are distinct tumors.
Associated Conditions
Chondroblastomas may contain areas resembling an aneurysmal bone cyst (ABC).
These secondary aneurysmal changes can influence the radiographic appearance and may be associated with a greater risk of recurrence.
Diagnosis
Signs and Symptoms
The most common complaint is persistent mild to moderate pain near the involved joint.
Symptoms often develop gradually and may persist for months or even years before diagnosis.
Joint Stiffness
Because the tumor develops close to an articular surface, patients frequently experience stiffness and loss of motion in the adjacent joint.
Joint Effusion
An effusion may develop in the nearby joint.
This can make the presentation resemble an intra-articular or inflammatory disorder rather than a primary bone lesion.
Local Swelling
Visible or palpable swelling is uncommon.
The tumor usually remains contained within the bone unless it becomes unusually large or extends beyond the cortex.
Physical Examination
Examination may demonstrate a joint effusion and reduced range of motion.
A palpable soft-tissue mass is unusual.
Direct joint-line tenderness is also generally not a prominent feature.
Laboratory Tests
Routine laboratory investigations are usually normal.
Blood tests generally do not assist in establishing the diagnosis.
The erythrocyte sedimentation rate is typically normal, helping distinguish the lesion from some infectious or inflammatory conditions.
Imaging
Plain Radiographs
The classic radiographic appearance is a well-defined lytic lesion within the epiphysis.
The lesion usually has a thin surrounding rim of sclerosis.
Sclerotic Rim
The presence of a narrow sclerotic border is consistent with the relatively slow-growing and benign nature of the tumor.
The lesion may nevertheless enlarge sufficiently to expand or deform the surrounding bone.
Calcification
Small punctate calcifications may occasionally be visible within the lesion.
These reflect mineralization of the cartilaginous matrix.
Role of Radiographs
In a typical young patient with an epiphyseal lesion and characteristic symptoms, the combination of clinical history and plain radiographs may strongly suggest the diagnosis.
Definitive diagnosis, however, depends on histologic evaluation.
MRI
MRI is useful when plain radiographs are not definitive or when the full extent of the lesion must be determined.
The lesion generally has a well-demarcated margin on MRI.
Peritumoral Edema
Surrounding bone marrow and soft-tissue edema are commonly seen on MRI.
This edema can sometimes appear disproportionately extensive compared with the relatively small size of the benign tumor.
Pathological Findings
Histologic confirmation requires identification of characteristic chondroblasts.
These are small round or polygonal cells containing round or oval nuclei.
Chondroblast Appearance
Chondroblasts are often described as relatively plump cells, sometimes likened to the appearance of fried eggs on microscopy.
Chicken-Wire Calcification
One of the classic histologic features is fine calcification extending in a lattice-like pattern around individual chondroblasts.
This is referred to as “chicken-wire” calcification and is strongly associated with chondroblastoma.
Giant Cells
Multinucleated giant cells are commonly scattered throughout the tumor.
Their presence can create histologic resemblance to a giant cell tumor, particularly if the epiphyseal location is not considered.
Aneurysmal Bone Cyst Change
Secondary areas of aneurysmal bone cyst formation may also be present.
These regions contain blood-filled spaces and may contribute to expansion of the lesion.
Differential Diagnosis
Important differential diagnoses include enchondroma, giant cell tumor, osteomyelitis, and fibrous dysplasia.
Age, skeletal maturity, epiphyseal location, radiographic appearance, and histology help distinguish these conditions.
Giant Cell Tumor
Giant cell tumor is an especially important differential diagnosis because both lesions can involve the epiphysis and contain numerous giant cells.
Giant cell tumor typically occurs in skeletally mature patients, whereas chondroblastoma more commonly arises before or around skeletal maturity.
Osteomyelitis
Subacute osteomyelitis can occasionally mimic a well-defined lytic lesion.
Clinical evidence of infection, inflammatory markers, MRI findings, and tissue sampling may help differentiate infection from tumor.
Treatment
General Measures
Operative treatment is generally recommended because continued tumor growth can progressively damage the epiphysis and adjacent articular surface.
The aim is complete local removal while preserving the nearby joint whenever possible.
Surgical Challenges
Treatment may be technically difficult because chondroblastomas often lie immediately beneath the articular surface.
The surgeon must remove the tumor while minimizing damage to the joint cartilage, physis, and surrounding subchondral bone.
Bone Grafting
After removal of the lesion, the residual bone defect is commonly filled with bone graft or another suitable bone-defect substitute.
This provides structural support and promotes healing.
Activity
Pathologic fracture is not usually a major concern with typical chondroblastoma.
Therefore, strict activity restrictions are generally unnecessary unless symptoms, lesion size, postoperative status, or individual anatomy warrant protection.
Physical Therapy
Physical therapy may be useful after surgery to restore joint range of motion, strength, and function.
This is particularly important when preoperative stiffness or postoperative immobilization has limited movement.
Surgery
Because chondroblastoma is a benign tumor, local surgical treatment is usually adequate.
The standard procedure consists of thorough intralesional curettage followed by filling of the resulting defect.
Curettage
The tumor is removed by carefully curetting the lesion from the surrounding bone.
Meticulous removal is important because residual tumor increases the likelihood of recurrence.
Joint Preservation
When the lesion lies directly beneath the articular surface, surgery should preserve as much subchondral bone and cartilage as possible.
Damage to the joint surface may contribute to later stiffness or degenerative change.
Follow-Up
Long-term surveillance is important because recurrence is not uncommon.
Clinical evaluation should assess for recurrent pain, loss of motion, or new joint symptoms.
Prognosis
Overall prognosis is favorable because chondroblastoma is benign.
However, local recurrence remains an important concern.
Recurrence
The recurrence rate for conventional chondroblastoma has been reported at approximately 20% within 3 years.
Recurrence is more likely when the lesion contains substantial secondary aneurysmal bone cyst change.
Complications
The principal complications are local recurrence and joint stiffness.
Joint stiffness may result from the tumor itself, prolonged symptoms, surgical exposure, or postoperative scar formation.
Patient Monitoring
Because recurrence most often develops during the first several years after treatment, serial imaging is recommended.
Radiographs are commonly repeated approximately every 6–12 months for the first 2 years after excision.
Persistent or recurrent pain should prompt earlier reassessment and additional imaging.
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Orthopaedic Surgery - Charcot–Marie–Tooth Disease (Hereditary Sensorimotor Neuropathy)
Basics
Charcot–Marie–Tooth disease (CMT) is the most common inherited motor and sensory peripheral neuropathy.
It represents the final common clinical manifestation of numerous genetic abnormalities, involving more than 80 recognized genes, that impair normal peripheral nerve signaling.
The disorder typically progresses in a distal-to-proximal pattern. Distal lower-extremity muscle wasting and weakness develop first, often resulting in cavovarus foot deformity. In some patients, weakness later involves the upper extremities.
Classification
Several major clinical and genetic forms of CMT are recognized.
The five commonly described groups are Type I, Type II, Type III, Type IV, and X-linked CMT.
Type I CMT
Type I is the hypertrophic demyelinating form and accounts for approximately half of affected patients.
The peripheral nerves become thickened because of abnormal myelin formation and repeated demyelination.
Loss of normal myelin causes marked slowing of peripheral nerve conduction.
Type II CMT
Type II is predominantly an axonal form of the disease.
Axonal degeneration produces weakness and sensory abnormalities, while the myelin sheath is relatively preserved.
Nerve conduction velocities are therefore usually only mildly reduced compared with the marked slowing seen in demyelinating disease.
Reflexes may remain relatively preserved.
Type III CMT
Type III, traditionally called Dejerine–Sottas disease, is characterized by marked segmental demyelination.
It is generally a more severe neuropathy and may present earlier than the common forms of CMT.
Type IV CMT
Type IV consists of forms inherited in an autosomal recessive pattern.
The severity and clinical manifestations vary according to the specific genetic abnormality.
X-Linked CMT
CMT-X is inherited through the X chromosome and accounts for approximately 10% of cases.
The severity of disease may differ according to the specific mutation and sex of the affected patient.
Genetics
CMT is genetically heterogeneous.
A particularly important abnormality in common demyelinating forms involves the gene encoding peripheral myelin protein 22-kDa (PMP22).
Other CMT subtypes result from mutations affecting peripheral nerve myelin, axonal structure, intracellular transport, or other components of nerve function.
Inheritance Patterns
Autosomal dominant inheritance with variable penetrance occurs in many forms of Types I, II, and III.
Type IV follows an autosomal recessive pattern.
CMT-X is inherited through the X chromosome.
A detailed family history is therefore an important part of the diagnostic evaluation.
Pathophysiology
Muscle weakness generally progresses from the distal extremities proximally.
In the lower leg, the tibialis anterior and peroneus brevis are commonly affected early.
Selective weakness of these muscles produces characteristic imbalance around the foot and ankle and contributes to development of cavovarus deformity.
Development of Cavus
Weakness of the tibialis anterior allows the peroneus longus to act relatively unopposed.
The peroneus longus plantarflexes the first ray, producing a plantarflexed first metatarsal and contributing to elevation of the medial longitudinal arch.
Development of Hindfoot Varus
Weakness of the peroneus brevis allows the posterior tibialis to dominate.
The resulting inversion force drives the hindfoot into varus.
Toe Clawing
Weakness of the intrinsic muscles and lumbricals allows the long flexor and extensor tendons to overpower the intrinsic musculature.
This imbalance leads to the characteristic clawing of the toes.
Dynamic Hindfoot Inversion
Plantarflexion of the first metatarsal can dynamically force the hindfoot into inversion during weight-bearing.
This mechanism is responsible for a forefoot-driven cavovarus deformity in many patients.
Progressive Rigidity
As the deformity persists, soft-tissue contracture and bony remodeling progressively reduce foot flexibility.
The foot becomes increasingly rigid, with impaired shock absorption and abnormal loading through the hindfoot and midfoot.
Arthritis
Longstanding malalignment and abnormal joint loading may eventually produce degenerative arthritis.
The subtalar, midfoot, and ankle joints may become painful and stiff.
Ankle Instability
Persistent hindfoot varus repeatedly stresses the lateral ankle ligaments.
Over time, ligament attenuation may lead to recurrent ankle sprains and chronic lateral ankle instability.
Associated Conditions
CMT may be associated with musculoskeletal abnormalities outside the foot.
Important associated conditions include scoliosis and developmental dysplasia of the hip.
Scoliosis
Approximately 30% of patients may develop scoliosis.
A proportion of these patients have left thoracic curves, and significant thoracic kyphosis may also be present.
Hip Dysplasia
Developmental dysplasia of the hip occurs in approximately 6–8% of patients.
Hip motion, particularly abduction, should therefore be examined routinely.
Diagnosis
Signs and Symptoms
Patients commonly become symptomatic between approximately 10 and 20 years of age.
Typical presentations include a high medial arch, reduced endurance, decreased coordination, recurrent ankle instability, or a characteristic steppage gait.
Footwear Problems
Progressive cavovarus alignment produces uneven plantar loading.
Shoes may wear out rapidly and asymmetrically, especially along the lateral border.
Muscle Weakness Pattern
Weakness generally appears first in the ankle evertors and dorsiflexors.
The plantarflexors and invertors are typically affected later.
This imbalance contributes substantially to cavus and hindfoot varus.
Sensory Changes
Sensation and proprioception may be diminished.
Reduced proprioceptive input can worsen balance, gait control, and ankle instability.
Steppage Gait
Foot-drop weakness can produce a steppage gait.
The patient excessively flexes the hip and knee during the swing phase so that the toes clear the floor.
Circumduction Gait
Some patients compensate by swinging the affected limb outward in a circumduction pattern during the swing phase.
History
A detailed family history should identify relatives with high arches, claw toes, similar gait abnormalities, distal weakness, or a known diagnosis of CMT.
The rate of progression of weakness and deformity should also be documented.
Ankle Instability History
Patients should be questioned about repeated ankle sprains, giving-way episodes, or feelings of instability.
These symptoms may indicate chronic lateral ligament insufficiency caused by cavovarus alignment.
Pain History
Pain should be localized carefully.
Common symptomatic areas include the lateral ankle, plantar forefoot, midfoot, and sites of callus formation.
Physical Examination
The examination should assess muscle bulk, strength, sensation, foot alignment, deformity flexibility, gait, hip motion, spinal alignment, and upper-extremity involvement.
Calf Atrophy
Distal lower-extremity muscle wasting commonly produces visible calf atrophy.
Muscle Strength
The strength of all major foot and ankle muscle groups should be recorded and followed over time.
Particular attention should be given to dorsiflexion, eversion, inversion, and plantarflexion.
Sensory Examination
Sensation should be assessed, including light touch, proprioception, and protective sensation.
Reduced protective sensation increases the risk of pressure injury from abnormal foot loading.
Hindfoot Varus
The patient should be examined standing and at rest for the presence of hindfoot varus.
The severity of hindfoot varus is closely related to functional impairment, ankle instability, and lateral overload.
Coleman Block Test
The Coleman block test helps distinguish flexible from fixed hindfoot varus.
The patient stands with the heel and lateral border of the foot supported while the first ray hangs freely beyond the edge of the block.
If the heel corrects toward neutral, the hindfoot remains flexible and the varus is largely driven by the plantarflexed first ray.
Passive Hindfoot Correction
Manual correction of hindfoot varus should also be assessed.
A rigid deformity is more likely to require bony correction rather than soft-tissue procedures alone.
Lateral Ankle Ligaments
The lateral ankle ligaments should be examined for laxity and mechanical instability.
Chronic varus positioning can progressively stretch these structures.
First Metatarsal Position
The relative position of the first metatarsal should be compared with the lesser metatarsals.
A plantarflexed first ray is characteristic of CMT-associated cavus.
Toe Clawing
The presence and severity of clawing should be documented.
The examiner should determine whether the toe deformities are flexible or fixed.
Gait Examination
Gait should be observed for foot drop, steppage, circumduction, ankle instability, and abnormal push-off.
Functional gait findings help determine the clinical severity of disease.
Hip Examination
Hip abduction should be measured.
Restricted abduction may suggest associated hip dysplasia and should prompt further imaging.
Spine Examination
The spine should be evaluated for scoliosis using a forward-bend test and observation of shoulder and trunk symmetry.
Upper-Extremity Examination
The hands should be inspected for wasting of the ulnar-innervated intrinsic muscles, including the interossei and abductors.
Upper-extremity weakness tends to develop later than lower-extremity involvement.
Electrodiagnostic Studies
Electromyography and nerve conduction studies are commonly used to confirm the diagnosis and characterize the neuropathy.
They help distinguish predominantly demyelinating disease from axonal forms.
Electromyography
EMG may demonstrate increased motor unit duration and reduced amplitude, reflecting chronic denervation and reinnervation.
Nerve Conduction Studies
Motor and sensory nerve conduction velocities are reduced to varying degrees.
Marked slowing is especially characteristic of demyelinating forms such as CMT Type I.
Hand Function Testing
Grip strength and manual dexterity may be monitored over time.
The 9-hole peg test can be used to quantify changes in fine motor function.
Biopsy
Muscle and nerve biopsy are rarely required when the history, examination, electrodiagnostic findings, and genetic testing are characteristic.
Muscle Biopsy Findings
Muscle biopsy may demonstrate diffuse atrophy with replacement of normal muscle fibers by fibrous and adipose tissue.
Nerve Biopsy Findings
Nerve biopsy may show loss of myelinated fibers and increased fibrous tissue within the endoneurium and perineurium.
Because genetic and electrodiagnostic testing are less invasive, biopsy is generally unnecessary.
Genetic Testing
DNA testing can be performed from peripheral blood.
It may confirm the diagnosis, identify a specific subtype, allow testing of family members, and assist with genetic counseling.
Imaging
Standing Foot and Ankle Radiographs
Weight-bearing radiographs should be obtained to evaluate cavus alignment, hindfoot varus, first-ray plantarflexion, joint congruity, and degenerative arthritis.
They are particularly important for surgical planning.
Spine Radiographs
In an index patient without a known family history, spinal radiographs may be obtained to exclude other structural causes of cavus deformity.
They are also appropriate when scoliosis is identified clinically.
Pelvic Radiographs
Pelvic radiographs should be considered when hip abduction is limited or dysplasia is suspected.
Early identification of hip dysplasia allows more effective treatment.
MRI of the Spine
Spinal MRI may be appropriate when the diagnosis is uncertain or there is concern for spinal pathology.
It can demonstrate abnormalities of the spinal cord and help exclude other neurologic causes of cavus deformity.
Differential Diagnosis
Important differential diagnoses include tethered spinal cord, myelomeningocele, lipomeningocele, peroneal nerve palsy, early Duchenne muscular dystrophy, and other hereditary motor and sensory neuropathies.
An atypical or unilateral deformity should prompt particularly careful investigation for a focal neurologic cause.
Treatment
General Principles
Treatment aims to maintain mobility, preserve flexibility, improve alignment, reduce pain, support weak muscles, and prevent progression of secondary deformity.
Orthopaedic treatment cannot reverse the underlying genetic neuropathy.
Routine Surveillance
Patients should be followed regularly for progression of muscle weakness, foot deformity, ankle instability, sensory loss, and functional limitation.
Earlier treatment may prevent a flexible deformity from becoming rigid.
Stretching
Regular stretching of the Achilles tendon and plantar fascia may help preserve foot and ankle flexibility.
Stretching is most useful before fixed contracture has developed.
Orthotic Insoles
Custom orthoses can redistribute plantar pressure and improve alignment.
A lateral heel build-up or wedge may help reduce flexible hindfoot varus.
Forefoot Padding
Accommodative padding beneath the forefoot may help relieve metatarsalgia and pressure associated with claw toes.
Ankle Bracing
An ankle brace may provide support in patients with symptomatic instability or recurrent ankle sprains.
Ankle-Foot Orthosis
A custom ankle-foot orthosis (AFO) may be necessary for substantial foot drop caused by dorsiflexor weakness.
It improves toe clearance during swing and may reduce falls.
Footwear
Comfortable footwear with a wide toe box, adequate depth, and cushioned heel is recommended.
Shoes should accommodate claw toes, high arches, and pressure-sensitive areas.
Physical Therapy
Physical therapy may include Achilles and plantar fascia stretching, strengthening exercises, gait work, proprioceptive training, and balance exercises.
These measures can improve function and reduce instability but do not reverse the neuropathy itself.
Surgery
General Surgical Principles
Surgical treatment should be individualized according to the flexibility and location of the deformity.
As a general principle, flexible deformities are managed with soft-tissue releases, rigid deformities require osteotomies, and tendon transfers are used to rebalance abnormal muscle forces.
The goal is to obtain a stable, plantigrade, pain-free, and braceable foot.
Claw-Toe Correction
Claw toes may be treated with flexor-to-extensor tendon transfer, MTP joint release, or PIP joint fusion, depending on whether the deformity remains flexible.
Jones Procedure
Severe hallux clawing may be treated with hallux interphalangeal arthrodesis combined with transfer of the extensor hallucis longus tendon to the first metatarsal.
This combination is commonly known as a Jones procedure.
Plantar Release
Soft-tissue release may involve the plantar fascia, abductor hallucis, and toe flexors.
This helps reduce the cavus deformity and increase flexibility.
Plantar-Medial Release
More extensive deformity may require a plantar-medial release involving structures such as the posterior tibialis, long toe flexors, and talonavicular capsule.
Posterior Tibialis Transfer
The posterior tibialis tendon may be transferred partially or completely toward the anterior aspect of the foot.
This can improve dorsiflexion and eversion while reducing the deforming inversion force.
Peroneus Longus to Brevis Transfer
Transfer or tenodesis of the peroneus longus to the peroneus brevis reduces plantarflexion of the first ray and increases eversion strength.
This is particularly useful in flexible forefoot-driven cavovarus deformity.
Calcaneal Osteotomy
A lateral closing-wedge calcaneal osteotomy may be required when hindfoot varus is rigid.
The procedure repositions the heel toward neutral alignment.
Midfoot and Metatarsal Osteotomies
Rigid cavus involving the forefoot or midfoot may require midfoot or metatarsal closing-wedge osteotomies.
These procedures reduce the high arch and improve plantar pressure distribution.
Triple Arthrodesis
Triple arthrodesis is generally reserved for severe rigid deformity or painful hindfoot arthritis.
Fusion sacrifices motion but can provide a stable and better-aligned foot.
Ankle Ligament Reconstruction
Chronic lateral ankle instability may require ligament reconstruction.
The underlying cavovarus deformity should also be corrected because isolated ligament repair may fail if varus alignment persists.
Follow-Up
Specialist Referral
Neurologic consultation is appropriate for electrodiagnostic evaluation, genetic testing, and counseling.
Management often benefits from collaboration among neurology, orthopaedics, physical therapy, orthotics, and genetics specialists.
Prognosis
Even after appropriate surgery, the foot generally cannot be restored completely to normal because the underlying muscle weakness continues.
Progressive neuropathy may lead to further weakness or recurrence of deformity.
Life Expectancy
Typical Charcot–Marie–Tooth disease does not shorten life expectancy.
Most morbidity relates to progressive weakness, deformity, gait difficulty, and loss of distal function.
Recurrence
Deformity can recur after surgery, especially when soft-tissue procedures alone are used in a foot that already has fixed bony malalignment.
Successful reconstruction requires correction of both structural deformity and muscle imbalance.
Adjacent-Joint Degeneration
Fusion procedures, particularly triple arthrodesis, may transfer mechanical stress to neighboring joints.
This can contribute to later degeneration of the ankle or midfoot.
Hip Dysplasia
Failure to recognize associated hip dysplasia may make later treatment more difficult and less successful.
Routine hip examination is therefore important throughout growth.
Patient Monitoring
Patients should generally be reviewed yearly for ambulatory function, muscle strength, foot alignment, ankle stability, sensory changes, hand function, and spinal deformity.
Earlier reassessment is appropriate if there is rapid deterioration, new weakness, recurrent falls, worsening pain, or progression of deformity.
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Orthopaedic Surgery - Cervical Spine Anatomy and Examination
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Basics
The cervical spine consists of seven cervical vertebrae, C1 through C7, which support the head, protect the spinal cord, permit a wide range of motion, and provide passage for important neurovascular structures.
For practical purposes, the cervical spine can be divided into the upper cervical spine, consisting of C1 and C2, and the lower cervical spine, consisting of C3 through C7.
The upper and lower regions differ substantially in both morphology and function.
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Osteology
Typical cervical vertebrae contain a vertebral body, paired pedicles, paired laminae, transverse processes, articular structures, and a spinous process.
The bony architecture surrounds and protects the cervical spinal cord while contributing to stability and motion.
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Transverse Foramina
All cervical vertebrae contain transverse foramina within their transverse processes.
The vertebral arteries usually pass through the transverse foramina from C6 to C1, rather than through C7.
Protection of these vessels is one of the important functions of intact cervical vertebral anatomy.
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Upper Cervical Spine
The atlas (C1) and axis (C2) are considered atypical cervical vertebrae because their anatomy differs considerably from that of C3–C7.
Their specialized architecture allows extensive movement between the skull and upper cervical spine.
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Atlas
The atlas has no true vertebral body and no conventional spinous process.
It consists largely of anterior and posterior arches connected by lateral masses.
C1 articulates superiorly with the occipital condyles and inferiorly with the axis.
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Atlantoaxial Joint
The articulation between C1 and C2 forms the atlantoaxial joint.
Approximately 50% of cervical rotation occurs at this level.
The unique articulation between the atlas and odontoid process permits substantial axial rotation of the head.
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Axis
The axis (C2) contains a vertebral body and the characteristic odontoid process, or dens, which projects superiorly and acts as a pivot for rotation of C1.
The dens is clinically important because odontoid fractures are common upper cervical injuries.
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Odontoid Blood Supply
The odontoid process contains a relative vascular watershed region between its apex and base.
This limited blood supply can influence healing of certain odontoid fractures and contributes to the risk of nonunion in selected fracture patterns.
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Atlanto-Occipital Joint
A substantial proportion of upper cervical flexion and extension occurs at the atlanto-occipital articulation between the occiput and C1.
This joint is particularly important for nodding movements of the head.
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Cervical Lordosis
The normal sagittal alignment of the cervical spine is lordotic.
Loss or reversal of cervical lordosis may be associated with muscle spasm, degeneration, deformity, or traumatic injury, although alignment must always be interpreted in clinical context.
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Protective Function
Normal cervical vertebral anatomy protects both the spinal cord and vertebral arteries.
Trauma, instability, stenosis, or deformity can therefore have serious neurologic or vascular consequences.
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Neuroanatomy
There are eight cervical nerve roots despite only seven cervical vertebrae.
The cervical nerve roots generally exit above their correspondingly numbered vertebrae.
For example, the C5 nerve root exits between C4 and C5.
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C8 Nerve Root
The C8 nerve root exits between C7 and T1.
Below this level, thoracic and lumbar nerve roots exit below the correspondingly numbered vertebra.
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Orientation of Cervical Nerve Roots
Cervical nerve roots travel in a relatively horizontal direction as they leave the spinal canal.
Because of this arrangement, both central/paracentral and foraminal disc pathology may affect the same exiting cervical nerve root depending on the level and location of compression.
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Cervical Spine Examination
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Inspection
The examination should begin with visual inspection.
Adequate exposure is important so that the neck, shoulders, upper thorax, and surrounding soft tissues can be assessed systematically.
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Alignment
The examiner should assess gross cervical alignment and head position.
Abnormal posture, torticollis, deformity, or asymmetry may indicate muscle spasm, structural deformity, or neurologic disease.
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Skin and Soft Tissues
The skin should be inspected for wounds, scars, bruising, swelling, masses, or other soft-tissue abnormalities.
Muscle asymmetry, atrophy, or hypertrophy should also be noted.
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Anterior Bony Palpation
Palpation of the anterior neck should identify tenderness, crepitus, masses, asymmetry, or malalignment.
Several palpable landmarks can help estimate cervical spinal levels.
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Hyoid Bone
The hyoid bone approximately corresponds to the level of the C3 vertebral body.
It can serve as a useful surface landmark during examination.
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Thyroid Cartilage
The superior portion of the thyroid cartilage approximately corresponds to the C4 vertebral body.
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Cricoid Cartilage
The cricoid cartilage is located approximately at the C6 vertebral level.
It may be easier to palpate during swallowing because movement of the laryngeal structures makes the anatomy more distinct.
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Carotid Tubercle
The anterior tubercle of the C6 transverse process is known as the carotid tubercle.
The right and left carotid tubercles should not be compressed simultaneously because doing so could reduce blood flow through both carotid arteries.
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Tracheal Examination
The trachea should be palpated to confirm that it remains in the midline.
Deviation may indicate a mass, swelling, mediastinal process, or other abnormality.
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Posterior Bony Palpation
Posterior examination begins at the occiput and proceeds inferiorly along the cervical spinous processes.
Tenderness, step-off, displacement, or asymmetry should be noted.
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Inion
The inion is the most prominent palpable point of the lower occiput.
It serves as an important posterior surface landmark.
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Spinous Processes
The spinous processes should generally form a straight midline sequence.
C7 and T1 are usually the most prominent and easiest to palpate.
Deviation from normal alignment can suggest rotational injury, including unilateral facet dislocation.
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Bifid Spinous Processes
The spinous processes of approximately C3–C5 may be bifid.
This is a normal anatomical variation and should not be mistaken for pathology.
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Facet Joints
The cervical facet joints lie approximately 2.5 cm lateral to the spinous processes.
Degenerative disease frequently affects the lower cervical facets, particularly around C5–C6.
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Anterior Soft-Tissue Palpation
Anterior soft-tissue examination should include the sternocleidomastoid muscles, parotid glands, cervical lymph nodes, thyroid gland, carotid pulses, and supraclavicular fossae.
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Thyroid Examination
The thyroid gland should normally feel relatively smooth and symmetric.
Enlargement, nodularity, or asymmetry should be documented.
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Supraclavicular Fossa
The supraclavicular area should be palpated for abnormal masses or bony prominences.
A prominent structure may represent a cervical rib.
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Posterior Soft-Tissue Palpation
Posterior soft-tissue examination includes the trapezius muscles, greater occipital nerves, and ligamentum nuchae.
The trapezius should be assessed for tenderness, muscle asymmetry, or abnormal masses.
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Lymph Nodes
Palpable lymph nodes in the posterior neck should be considered abnormal if enlarged or otherwise clinically suspicious.
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Greater Occipital Nerves
The greater occipital nerves can become tender or prominent after trauma, including whiplash-type injuries.
Irritation may contribute to occipital pain or headache.
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Ligamentum Nuchae
The ligamentum nuchae extends from the inion to the C7 spinous process.
It can be palpated in the posterior midline.
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Neurologic Examination
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General Principles
Neurologic evaluation of the cervical spine includes sensory, motor, and reflex testing.
Findings should be carefully documented to identify nerve-root compression, spinal cord dysfunction, or peripheral neuropathy.
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Sensory Examination
Patients should be asked to identify altered sensation as specifically as possible.
The most commonly assessed sensory modalities are light touch and pinprick.
Comparison between sides is useful.
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Upper Cervical Dermatomes
Sensation from C2 through C4 generally progresses from the posterior scalp and neck toward the anterior neck and shoulder region.
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C5 Dermatome
The C5 dermatome is represented mainly over the lateral shoulder and upper arm.
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C6 Dermatome
The C6 dermatome extends along the lateral forearm toward the radial side of the hand, particularly the thumb and adjacent radial digits.
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C7 Dermatome
The C7 dermatome is commonly tested at the middle finger.
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C8 Dermatome
The C8 dermatome involves the ulnar side of the hand, particularly the ring and little fingers.
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T1 Dermatome
The T1 dermatome lies primarily along the medial forearm.
Dermatomal patterns overlap, so sensory findings should always be interpreted together with motor and reflex abnormalities.
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Motor Examination
Motor testing should evaluate major muscle groups corresponding to cervical nerve roots.
Strength should be graded consistently to allow changes over time to be recognized.
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Muscle Strength Grading
Grade 0: No visible or palpable muscle contraction.
Grade I: Muscle contraction is visible or palpable, but no joint movement occurs.
Grade II: Full range of motion is possible with gravity eliminated.
Grade III: Full range of motion is possible against gravity.
Grade IV: Full range of motion is possible against gravity and some resistance.
Grade V: Normal strength against full resistance.
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C3–C5 Motor Function
The levator scapulae can be assessed with resisted scapular elevation and receives contributions predominantly from C3 and C4, with possible C5 involvement.
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C5 Motor Function
The deltoid is tested with shoulder abduction and primarily reflects C5 motor function.
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C6 Motor Function
C6 function can be evaluated with elbow flexion through the biceps and wrist extension.
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C7 Motor Function
C7 is assessed through triceps-mediated elbow extension, wrist flexion, and finger extension.
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C8 Motor Function
C8 contributes substantially to finger flexion and thumb adduction.
Testing grip and intrinsic hand function can therefore help assess lower cervical nerve-root function.
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Deep Tendon Reflexes
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Reflex Examination
Deep tendon reflex testing helps distinguish nerve-root compression from spinal cord disease.
Diminished reflexes may indicate radiculopathy, whereas hyperreflexia can suggest an upper motor neuron lesion such as cervical myelopathy.
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Biceps Reflex
The biceps reflex primarily evaluates the C5 nerve root, with some contribution from C6.
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Brachioradialis Reflex
The brachioradialis reflex primarily evaluates C6.
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Triceps Reflex
The triceps reflex primarily evaluates C7.
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Range of Motion
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General Principles
Active cervical range of motion should be assessed in flexion, extension, rotation, and lateral bending.
Pain, limitation, asymmetry, and reproduction of radicular symptoms should be noted.
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Flexion and Extension
A large proportion of flexion-extension occurs in the upper cervical spine, while the remainder is distributed across the subaxial cervical levels.
The C5–C6 segment often demonstrates particularly substantial motion.
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Muscles Used in Flexion and Extension
Cervical flexion assesses muscles including the sternocleidomastoid and deeper cervical flexors.
Extension involves the paraspinal extensors and trapezius.
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Rotation
Approximately half of cervical rotation occurs at C1–C2, with the remainder distributed through the lower cervical spine.
The patient should normally be able to rotate the chin approximately 60–80° to either side.
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Rotational Muscles
The sternocleidomastoid is an important cervical rotator, although normal rotation is produced by coordinated activity of several muscle groups.
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Lateral Bending
Lateral bending is distributed throughout the cervical spine and usually occurs in combination with some rotation.
The patient is asked to bring the ear toward the ipsilateral shoulder without elevating the shoulder.
Normal lateral bending is approximately 45°.
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Muscles Used in Lateral Bending
The scalene muscles contribute substantially to cervical lateral flexion.
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Provocative Tests
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Modified Spurling Maneuver
The modified Spurling test evaluates cervical nerve-root irritation.
The neck is extended and rotated toward the symptomatic side, followed by gentle axial loading.
A positive test reproduces radicular pain or paresthesias in the ipsilateral upper extremity.
The test is relatively specific for cervical radiculopathy but has limited sensitivity.
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Shoulder Abduction Test
The patient actively or passively raises the symptomatic arm over the head.
Relief of radicular symptoms with ipsilateral shoulder abduction constitutes a positive test and may suggest cervical nerve-root compression.
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Cervical Distraction Test
The examiner applies gentle longitudinal traction to the head, typically with the neck in slight flexion or neutral alignment.
Improvement in radicular symptoms during distraction supports the possibility of cervical nerve-root compression.
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Lhermitte Sign
The Lhermitte maneuver is performed by flexing the cervical spine anteriorly.
An electric or shooting sensation traveling down the arms, trunk, or legs suggests irritation or dysfunction of the cervical spinal cord.
It may occur with cervical cord compression as well as other disorders affecting the dorsal columns.
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Hoffmann Sign
To test the Hoffmann reflex, the patient’s hand is supported and relaxed.
The examiner grasps the middle finger and sharply flicks the distal phalanx or nail.
A positive response consists of reflex flexion or adduction of the thumb and index finger.
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Significance of Hoffmann Sign
A positive Hoffmann sign can suggest upper motor neuron or corticospinal tract dysfunction, including cervical myelopathy.
It should not be interpreted in isolation and must be correlated with the remainder of the neurologic examination.
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Romberg Test
The Romberg test evaluates balance and proprioception.
The patient stands with the arms extended and eyes initially open, then closed.
Loss of balance when the eyes are closed suggests impaired proprioceptive function.
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Dynamic Balance Assessment
Observation of abnormal arm drift, progressive elevation of the arms, or instability during static or dynamic balance testing may provide additional evidence of neurologic dysfunction.
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Gait Assessment
Gait examination is an essential part of cervical neurologic evaluation.
It can provide information regarding balance, coordination, lower-extremity function, posture, spasticity, and possible spinal cord dysfunction.
Patients with cervical myelopathy may exhibit a stiff, broad-based, unsteady, or spastic gait.
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Imaging
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Plain Radiographs
Standard cervical spine radiography commonly includes anteroposterior and lateral views.
When possible, imaging is obtained with the patient upright so that physiologic alignment can be assessed.
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Trauma Radiographs
In trauma patients, an initial cross-table lateral radiograph may be used when appropriate, but the entire cervical spine must be adequately visualized for the image to be diagnostically useful.
Modern trauma evaluation frequently relies heavily on CT when significant cervical injury is suspected.
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Oblique Views
Oblique radiographs can help assess the neural foramina, facet alignment, subluxation, and facet dislocation.
They are particularly helpful in selected cases when foraminal anatomy requires further evaluation.
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Open-Mouth Odontoid View
The open-mouth view is used to assess the odontoid process, atlantoaxial joints, and alignment of the lateral masses of C1 relative to C2.
Asymmetry may indicate fracture, displacement, or rotational injury.
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Pediatric Radiographs
In young children, normal ossification centers and developmental variants may resemble fractures.
Knowledge of age-related cervical spine anatomy is therefore essential to avoid misinterpreting normal findings as traumatic injury.
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MRI
MRI is the preferred modality for evaluating soft-tissue structures of the cervical spine.
It provides detailed visualization of the intervertebral discs, spinal cord, nerve roots, ligaments, joint capsules, and other neural and soft-tissue structures.
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Clinical Role of MRI
MRI findings should be correlated with the patient’s symptoms and physical examination because asymptomatic degenerative abnormalities are common.
It is particularly valuable when evaluating disc herniation, spinal stenosis, ligamentous injury, spinal cord compression, and myelopathy.
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CT
CT provides excellent definition of cervical osseous anatomy.
It can rapidly and accurately identify fractures, facet injuries, displacement, and complex bony abnormalities.
For suspected cervical spine trauma, CT is particularly useful for fracture characterization and surgical planning.
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Integration of Examination and Imaging
Cervical spine assessment requires correlation of history, physical examination, neurologic findings, provocative testing, and imaging.
No single examination maneuver or imaging abnormality should be interpreted in isolation.
A systematic approach is particularly important when distinguishing cervical radiculopathy, myelopathy, structural injury, and peripheral nerve disease.
