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Orthopaedic Surgery - Ankle Sprain
Basics
An acute lateral ankle sprain is one of the most common injuries in sport and is also frequently encountered in the general population.
The injury usually involves the lateral ligament complex of the ankle. The anterior talofibular ligament (ATFL) is affected most often, either as a partial tear or complete rupture. More severe injuries may additionally involve the calcaneofibular ligament (CFL).
Most lateral ankle sprains occur through an inversion mechanism, often while the ankle is plantarflexed.
Classification
Lateral ankle sprains are commonly classified according to the degree of ligament injury.
Grade I injuries involve a partial tear or stretching of the lateral ligaments without major mechanical instability.
Grade II injuries involve a partial or complete tear of the ATFL together with partial injury of the CFL.
Grade III injuries represent complete rupture of both the ATFL and CFL and are generally associated with greater swelling, bruising, pain, and instability.
Sequence of Ligament Injury
As the severity of an inversion injury increases, the lateral stabilizing structures tend to fail in sequence.
The anterolateral joint capsule is generally injured first, followed by the ATFL.
With greater force, the injury may progress to involve the CFL.
This sequence explains why isolated ATFL injuries are more common than combined ATFL and CFL tears.
Anterior Talofibular Ligament
The ATFL is the most frequently injured ligament of the ankle.
It is the principal restraint to inversion when the ankle is in a plantarflexed position.
The ligament is particularly vulnerable when the foot is subjected to a combination of inversion, plantarflexion, and internal rotation.
Because many ankle sprains occur in this position, ATFL injury is extremely common.
Calcaneofibular Ligament
The CFL contributes to stability of both the ankle and subtalar joints.
It becomes particularly important in resisting inversion when the ankle is in a neutral or dorsiflexed position.
CFL injury therefore tends to occur when inversion forces are applied while the ankle is less plantarflexed.
Involvement of the CFL usually indicates a more severe sprain.
Dynamic Stabilizers
The peroneal muscles and tendons are the primary dynamic stabilizers resisting ankle inversion.
Rapid contraction of the peroneal muscles can help prevent excessive inversion and protect the lateral ligament complex.
Weakness, fatigue, or delayed neuromuscular response of the peroneals may increase the risk of recurrent sprains.
Epidemiology
Ankle sprains are among the most common musculoskeletal injuries.
In the United States, approximately 27,000 ankle sprains occur each day.
They are considered the most frequent athletic injury and occur particularly often in activities involving running, jumping, landing, and rapid changes in direction.
Risk Factors
Athletes are at increased risk because of repetitive loading and frequent changes in direction.
Dancers are also vulnerable because of repeated extreme ankle positions and balance demands.
Structural abnormalities such as congenital tarsal coalition may alter hindfoot mechanics and predispose to recurrent sprains.
A varus hindfoot alignment also increases the tendency for the ankle to invert and may contribute to repeated injury.
Etiology
The usual mechanism is inversion of the foot while body weight is transmitted through the ankle.
The degree of plantarflexion at the time of injury influences which ligament is most likely to be damaged.
Inversion in plantarflexion primarily stresses the ATFL, whereas inversion with the ankle closer to neutral or dorsiflexion places greater stress on the CFL.
Diagnosis
Signs and Symptoms
Patients commonly present with pain, tenderness, and swelling over the lateral aspect of the ankle.
Bruising may develop over the lateral malleolus and surrounding soft tissues.
Weight-bearing may be painful, and patients with more severe sprains may initially have considerable difficulty walking.
History
The mechanism of injury should be carefully established.
An inversion injury occurring with the ankle in plantarflexion is more suggestive of ATFL injury.
Inversion occurring with the ankle in dorsiflexion or near-neutral position places greater stress on the CFL.
The history should also determine whether the patient heard or felt a pop, was able to continue activity, and has sustained previous ankle sprains.
Physical Examination
Tenderness and swelling are usually localized to the lateral aspect of the ankle, particularly anterior and inferior to the tip of the lateral malleolus.
The degree of swelling and bruising should be documented.
The entire ankle and foot should be examined to ensure that an associated fracture or other injury is not overlooked.
Muscle Strength
Manual strength testing should include the major muscle groups acting across the ankle.
Particular attention should be given to the peroneal muscles and tendons, because they provide important dynamic resistance to inversion.
Pain, weakness, or loss of function may indicate associated tendon injury.
Neurovascular Examination
A complete neurovascular examination should be performed.
The superficial peroneal nerve can occasionally sustain a traction or stretching injury during an inversion sprain.
Sensation over the dorsum of the foot, motor function, pulses, and capillary refill should therefore be assessed.
Assessment of Ligament Stability
Mechanical stability should be evaluated once pain and swelling permit.
The injured ankle should always be compared with the contralateral side because a certain degree of physiologic laxity may be normal.
The main clinical tests are the anterior drawer test and inversion or talar tilt test.
Anterior Drawer Test
The anterior drawer test primarily assesses the ATFL.
The distal tibia is stabilized firmly with one hand while the other hand grasps the heel.
With the ankle in a neutral or slightly plantarflexed position, the heel and hindfoot are drawn anteriorly relative to the tibia.
Excessive anterior translation compared with the opposite side suggests ATFL insufficiency.
Inversion Tilt Test
The inversion tilt test primarily evaluates the CFL.
The ankle is positioned in neutral dorsiflexion.
The examiner stabilizes the distal tibia with one hand and applies an inversion force to the hindfoot with the other.
Excessive talar tilt or inversion compared with the uninjured ankle suggests CFL disruption.
Imaging
Plain Radiographs
When imaging is clinically indicated, standard ankle radiographs include anteroposterior, lateral, and mortise views.
Radiographs are primarily used to exclude associated fractures.
They may also demonstrate an osteochondral lesion of the talus, pre-existing arthritis, or another bony abnormality.
CT
Computed tomography is not routinely required for a straightforward ankle sprain.
CT may be useful when an occult fracture is suspected despite normal plain radiographs.
It may also assist in the assessment of a suspected tarsal coalition or other complex bony abnormality.
MRI
MRI is rarely necessary for an uncomplicated acute ankle sprain.
It may be appropriate when symptoms are unusually severe or persistent, or when an associated tendon tear, osteochondral injury, or other soft-tissue abnormality is suspected.
MRI provides detailed visualization of the ligaments, tendons, cartilage, and bone marrow.
Differential Diagnosis
Important differential diagnoses include a distal fibular fracture, osteochondral fracture of the talar dome, peroneal tendon subluxation, congenital tarsal coalition, talar fracture, and calcaneal fracture.
Persistent or atypical pain after an apparent ankle sprain should prompt reconsideration of these alternative diagnoses.
Treatment
General Measures
Most acute ankle sprains are treated nonoperatively.
Initial treatment commonly follows the RICE protocol: rest, ice, compression, and elevation.
These measures help reduce pain and swelling during the acute phase.
Prolonged complete immobilization is generally avoided when the injury is stable because early protected movement helps restore function.
Weight-Bearing
Weight-bearing can usually be advanced gradually as pain permits.
An ankle brace may provide support and allow earlier ambulation while limiting excessive inversion.
Patients with mild injuries can often progress rapidly, whereas more severe sprains may require a longer period of protected weight-bearing.
Ankle Bracing
A functional ankle brace can reduce painful motion while allowing controlled mobility.
Bracing is particularly useful during the early return to walking and athletic activity.
Continued brace use during high-risk sports may also reduce the likelihood of recurrent injury.
Range of Motion
Gentle active ankle movement should begin as tolerated.
Early range-of-motion exercises help reduce stiffness and improve circulation.
Patients may perform simple exercises such as drawing the alphabet with the great toe to encourage controlled multidirectional ankle movement.
Proprioceptive Training
For mild sprains, a home-based proprioceptive program may be sufficient.
Exercises may include single-leg balance activities, controlled ankle movements, and progressive balance challenges.
Proprioceptive retraining is important because ankle sprains can impair joint-position awareness and neuromuscular control.
Severe Sprains
More severe injuries may benefit from a formal physical therapy program.
Treatment should address swelling, mobility, muscle strength, endurance, balance, and proprioception.
The rehabilitation program should progress gradually toward running, jumping, cutting, and other sport-specific activities.
Activity Modification
Sporting activity should be restricted until pain and swelling have improved and ankle function has recovered.
Return to sport should not be based solely on the passage of time.
The patient should regain adequate strength, range of motion, balance, and confidence before resuming unrestricted activity.
Physical Therapy
Physical therapy should emphasize range of motion, strengthening, and proprioceptive retraining.
Both concentric and eccentric strengthening may be used, with particular attention to the peroneal muscles.
Balance-board exercises and single-leg activities can improve neuromuscular control and reduce the risk of recurrent sprains.
Medication
NSAIDs and simple analgesics may be used when pain is significant.
However, medication is often unnecessary for mild sprains.
Pain control should complement, rather than replace, functional rehabilitation.
Surgical Management
Surgical repair of an acute lateral ankle ligament tear is rarely necessary.
Most even high-grade sprains heal satisfactorily with appropriate nonoperative treatment and rehabilitation.
Primary repair of the ATFL and CFL may be considered only in selected acute situations.
Surgery for Recurrent Instability
Surgery may become appropriate when repeated sprains lead to chronic mechanical instability despite adequate rehabilitation and bracing.
Operative treatment may involve direct repair of the lateral ankle ligaments.
Reconstruction using tendon tissue, including part of the peroneus brevis tendon, has historically been used when direct repair is not feasible.
Follow-Up
Patients should be reviewed according to the severity of the injury and their functional demands.
Recovery should be assessed by evaluating pain, swelling, range of motion, strength, balance, and stability.
Persistent symptoms should prompt reassessment for an associated osteochondral, tendon, or bony injury.
Prognosis
The prognosis is excellent for most patients.
Recovery time varies according to the severity of the ligament injury.
Grade I sprains generally improve relatively quickly, whereas grade II and III injuries may require a longer period of rehabilitation before full athletic function returns.
Complications
Possible complications include an osteochondral lesion of the talus, recurrent ankle sprains, chronic instability, and ankle impingement.
Inadequate rehabilitation is an important contributor to recurrent symptoms.
Repeated sprains may eventually produce chronic ligamentous laxity, cartilage injury, and degenerative change.
Recurrent Sprains
A previous ankle sprain substantially increases the risk of another injury.
Residual weakness, impaired proprioception, ligamentous laxity, and premature return to sports all contribute to recurrence.
Structured rehabilitation and preventive bracing are therefore important after the initial injury.
Ankle Impingement
Repetitive injury may lead to scar formation, synovitis, osteophytes, or other tissue changes around the ankle.
These abnormalities can produce painful mechanical impingement during ankle movement.
Persistent pain or restricted motion after apparently successful treatment should therefore be investigated further.
Patient Monitoring
Patients should regain full or near-full strength and range of motion before returning to unrestricted sports.
They should also be able to perform functional activities such as running, jumping, cutting, and single-leg balance without pain or instability.
Functional bracing or taping during the return to athletics may help reduce the risk of recurrence, particularly in patients with a history of previous ankle sprains.
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Orthopaedic Surgery - Ankle Pain
Basics
Ankle pain is an extremely common clinical complaint with a broad range of possible causes. It may result from traumatic injury, degenerative or inflammatory arthritis, sports-related conditions, overuse, infection, systemic disease, or neoplastic processes.
Successful treatment depends on accurately identifying the underlying pathology. A detailed knowledge of ankle anatomy, careful history-taking, and a systematic physical examination are therefore essential for developing an appropriate differential diagnosis.
Ankle Anatomy
The ankle joint is formed by the talus, distal tibia, and distal fibula.
The lateral ligament complex consists of the anterior talofibular ligament (ATFL), calcaneofibular ligament (CFL), and posterior talofibular ligament (PTFL).
The distal tibiofibular syndesmosis is supported primarily by the anterior inferior tibiofibular ligament and posterior inferior tibiofibular ligament.
Medial ankle stability is provided by the superficial and deep components of the deltoid ligament complex.
Epidemiology
Ankle pain is extremely common and may affect individuals of all ages.
Its prevalence generally increases with age because degenerative joint disease, chronic tendinopathy, and systemic inflammatory conditions become more frequent in older individuals.
Etiology
Potential causes include acute trauma, degenerative arthritis, inflammatory arthritis, stress fractures, repetitive overuse, osteochondral lesions of the talus, tendinitis, tendon tears, acute ligament sprains, and chronic ankle instability.
Infectious conditions such as septic arthritis and osteomyelitis can also produce ankle pain.
Less commonly, pain may result from a bone or soft-tissue neoplasm.
Traumatic Causes
Pain developing immediately after a traumatic episode may result from an ankle sprain, fracture, tendon strain or rupture, osteochondral injury, or dislocation.
The mechanism of injury, location of tenderness, ability to bear weight, swelling, and presence of deformity help determine the likely diagnosis.
Arthritis
Ankle arthritis may be either degenerative or inflammatory.
Degenerative arthritis commonly produces activity-related pain, progressive stiffness, swelling, and reduced range of motion.
Inflammatory arthritis may produce prolonged morning stiffness, warmth, swelling, and involvement of multiple joints.
Stress and Overuse Injuries
Repetitive loading can result in stress fractures, tendinitis, chronic tendinosis, and osteochondral lesions.
Symptoms commonly develop gradually and worsen with activity.
Pain may initially resolve with rest but can become persistent if repetitive loading continues.
Infection
Acutely severe ankle pain associated with warmth, erythema, swelling, and marked pain during passive movement should raise concern for septic arthritis.
Osteomyelitis should be considered when pain is associated with chronic wounds, previous surgery, systemic infection, or persistent unexplained symptoms.
Prompt recognition is essential because untreated infection may rapidly damage bone and articular cartilage.
Geriatric Considerations
In older individuals, common causes of ankle pain include degenerative arthritis, inflammatory arthritis, posterior tibial tendon dysfunction, chronic tendinosis, and gout.
Reduced bone quality, muscle weakness, altered balance, and age-related changes in tendons and cartilage may also contribute.
Pediatric Considerations
In children and adolescents, ankle pain frequently follows trauma.
Other important causes include an occult tarsal coalition and bone or soft-tissue tumors.
Persistent unexplained pain, particularly when accompanied by night symptoms, swelling, or a mass, requires further investigation.
Pregnancy Considerations
During pregnancy, transient ankle pain may occur because of lower-extremity edema and altered biomechanics.
Increased body weight, changes in posture, ligamentous laxity, and altered gait can increase mechanical loading around the ankle.
However, other common adult causes should still be considered when symptoms are significant or persistent.
Associated Conditions
Systemic disorders associated with ankle pain include rheumatoid arthritis, other inflammatory arthropathies, gout, and Lyme disease.
Structural disorders such as tarsal coalition may also cause chronic pain, stiffness, and recurrent ankle symptoms.
Diagnosis
Signs and Symptoms
Well-localized pain after an acute traumatic event may represent an ankle sprain, fracture, or tendon injury.
Severe pain without trauma, together with substantial swelling, warmth, erythema, and marked pain during passive range of motion, should raise suspicion for septic arthritis or an acute gout attack.
Chronic activity-related ankle pain in adults commonly suggests degenerative arthritis, whereas prolonged morning stiffness may suggest an inflammatory disorder.
Ankle pain and swelling accompanied by a skin rash following a tick bite may indicate Lyme disease.
History
A detailed history should identify the onset, duration, location, and character of the pain.
The clinician should ask about previous trauma, activities that reproduce symptoms, sporting participation, occupational demands, and previous ankle disorders.
The relationship of symptoms to activity and rest can provide important diagnostic information.
Important Historical Features
The presence of morning pain or stiffness may indicate inflammatory disease.
A history of gout, particularly previous involvement of the great toe, should be documented.
Constitutional symptoms such as fever, night sweats, unexplained weight loss, night pain, or rest pain may suggest infection, inflammatory disease, or neoplasm.
A history of tick exposure should also be obtained when clinically relevant.
Physical Examination
Physical examination should begin by identifying the exact site of pain and tenderness.
The medial and lateral malleoli, hindfoot, and proximal fifth metatarsal should be palpated, particularly after trauma.
The tendons, ligaments, and joint line should then be examined systematically.
Tendon Examination
The posterior tibial tendon, peroneal tendons, Achilles tendon, and extensor tendons should be palpated.
Pain, swelling, crepitus, weakness, or tenderness may indicate tendinitis, tendinosis, or tearing.
Resisted muscle testing can help determine whether a particular tendon is contributing to symptoms.
Ligament Examination
The medial deltoid ligament, lateral ligament complex, and distal tibiofibular syndesmotic ligaments should be examined for tenderness and instability.
Provocative testing may help identify acute or chronic ligamentous injury.
Findings should be compared with the opposite ankle whenever possible.
Joint-Line Examination
The anterior ankle joint line and capsule should be palpated for tenderness or swelling.
Joint-line pain and effusion may occur with arthritis, synovitis, osteochondral injury, or infection.
Range of Motion
Both active and passive ankle motion should be assessed and compared with the unaffected side.
Restricted motion may occur with arthritis, post-traumatic stiffness, joint effusion, tarsal coalition, or infection.
Severe pain during passive movement should increase concern for significant intra-articular pathology.
Stability and Strength
Ligamentous stability should be assessed with appropriate stress testing.
Manual muscle strength should also be evaluated.
Weakness may result from tendon injury, neurologic dysfunction, chronic instability, or inhibition caused by pain.
Skin Examination
The skin around the ankle should be assessed for bruising, erythema, wounds, scars, rash, swelling, and increased warmth.
The presence of a joint effusion should also be noted.
Skin findings may provide useful clues to traumatic, infectious, inflammatory, or systemic causes.
Neurovascular Examination
A complete neurovascular assessment of the foot and ankle should be performed.
Motor function, sensation, pulses, and capillary refill should be documented.
Neurologic abnormalities may indicate peripheral nerve injury or another neurologic condition contributing to the pain.
Gait Assessment
The patient’s gait should be observed whenever possible.
An antalgic gait may indicate pain with weight-bearing.
Other abnormalities, such as altered foot progression, inability to perform heel rise, or reduced ankle motion, may suggest tendon dysfunction, arthritis, instability, or structural deformity.
Laboratory Tests
Laboratory investigations are selected according to the suspected diagnosis rather than ordered routinely.
When septic arthritis is suspected, investigations commonly include a complete blood count with differential, erythrocyte sedimentation rate, and C-reactive protein.
Inflammatory Arthritis Investigations
Patients suspected of having rheumatoid or another inflammatory arthritis may undergo appropriate rheumatologic testing.
Investigations may include rheumatoid factor, inflammatory markers, antinuclear antibodies, and other disease-specific serologic tests.
Laboratory findings should be interpreted in conjunction with the patient’s clinical presentation.
Gout Investigations
A serum uric acid level may support the assessment of suspected gout.
However, uric acid may be normal during an acute attack, and a normal result does not exclude the diagnosis.
Joint aspiration and crystal analysis provide greater diagnostic certainty.
Lyme Disease Investigations
When the clinical presentation and exposure history suggest Lyme disease, Lyme antibody testing may be appropriate.
Testing should be guided by geographical exposure, tick history, rash, and associated systemic manifestations.
Imaging
Plain Radiographs
Initial imaging commonly consists of standing anteroposterior, lateral, and mortise radiographs of the ankle.
These views help identify fractures, alignment abnormalities, arthritis, osteophytes, joint-space narrowing, and other bony abnormalities.
Foot Radiographs
An oblique radiograph of the foot may be obtained when calcaneonavicular coalition is suspected.
Additional specialized views may be selected according to the location and suspected cause of symptoms.
MRI
MRI is valuable for detecting occult conditions that may not be visible on plain radiographs.
It may identify stress fractures, osteochondral lesions, occult fractures, tendon abnormalities, tendon tears, ligamentous injuries, bone marrow abnormalities, and neoplasms.
MRI also provides detailed information regarding cartilage and other soft-tissue structures.
CT
CT provides detailed assessment of bony anatomy.
It can define fracture fragments, articular involvement, and complex fracture patterns.
CT may also help identify tarsal coalition, bone cysts, osteoid osteoma, and other osseous lesions.
Arthrocentesis
Joint aspiration is particularly useful when septic arthritis, gout, or pseudogout is suspected.
Synovial fluid can be analyzed for cell count, Gram stain, bacterial culture, and crystals.
Septic Arthritis Findings
Synovial fluid from a septic joint may demonstrate a positive Gram stain or bacterial culture.
Staphylococcus aureus is among the most common organisms responsible for septic arthritis.
Because infection can rapidly destroy the joint surface, investigation and treatment should proceed urgently when suspicion is high.
Crystal Arthropathy
In gout, synovial fluid contains monosodium urate crystals.
Pseudogout is characterized by calcium pyrophosphate crystals.
Crystal analysis helps distinguish these conditions from septic arthritis and other inflammatory disorders.
Differential Diagnosis
The differential diagnosis includes ankle sprain, ankle fracture, tendon strain or rupture, stress fracture, tendinitis, chronic tendinosis, and degenerative osteoarthritis.
Other possibilities include rheumatoid or inflammatory arthritis, septic arthritis, Lyme disease, acute gout, and osteochondral lesions of the talar dome.
Additional Differential Diagnoses
Less common but important causes include bone tumors, soft-tissue neoplasms, and tarsal coalition.
The patient’s age, history of trauma, duration of symptoms, examination findings, and imaging results help narrow the diagnosis.
Treatment
General Measures
Treatment should be directed at the underlying cause.
Minor ankle sprains and low-grade traumatic injuries may initially be treated with rest, ice, compression, and elevation (RICE).
Weight-bearing can then be gradually increased as pain and swelling improve.
Management of Ankle Fractures
Patients with ankle fractures should be appropriately splinted.
They should generally remain non-weight-bearing until the fracture has been fully evaluated for stability.
Displaced or unstable fractures require prompt orthopedic assessment and may require surgical fixation.
Hot and Swollen Ankle
A hot, erythematous, swollen ankle requires careful evaluation.
Arthrocentesis may be necessary to distinguish septic arthritis from gout or another inflammatory process.
This distinction is particularly important because septic arthritis requires urgent treatment.
Activity
Patients with minor sprains or low-grade trauma may begin progressive weight-bearing as tolerated.
Activity should be increased according to pain, swelling, stability, and recovery of function.
Non-Weight-Bearing
Patients with unstable ankle fractures should remain non-weight-bearing while awaiting definitive orthopedic management.
Crutches, a walker, or another assistive device may be required.
Protected Weight-Bearing
Protected weight-bearing in a cast, boot, or brace can be useful for tendon strains, tendinitis, chronic tendinosis, stress fractures, osteochondral lesions of the talus, and symptomatic tarsal coalition.
The duration of protection depends on the specific diagnosis and severity.
Physical Therapy
Physical therapy is useful in many cases after the diagnosis has been established and appropriate initial treatment completed.
Rehabilitation may include range-of-motion exercises, strengthening, proprioceptive training, balance exercises, gait retraining, and gradual return to sport or work.
The treatment program should be tailored to the underlying disorder.
Medication
First-Line Therapy
Nonsteroidal anti-inflammatory drugs may be used for ankle sprains, tendon injuries, stress-related disorders, and arthritis.
Analgesic treatment should be individualized according to symptom severity and patient comorbidities.
Fracture Pain
Severe fracture pain may occasionally require stronger analgesic medication.
Medication should be used as part of a broader treatment strategy that includes immobilization and definitive management of the fracture.
Gout Treatment
Acute gout may be treated with NSAIDs, colchicine, or other anti-inflammatory medications.
Patients with recurrent attacks may require long-term urate-lowering therapy such as allopurinol after appropriate assessment.
Septic Arthritis Treatment
Septic arthritis requires prompt antibiotic treatment and drainage of the infected joint.
Drainage may be achieved by aspiration or surgical irrigation and debridement depending on the clinical circumstances.
Corticosteroid Injection
Corticosteroid injection may provide symptomatic relief for selected forms of ankle arthritis.
Infection must be excluded before any intra-articular corticosteroid injection is performed.
Surgical Management
Surgery may be required for several underlying causes of ankle pain.
Unstable fractures commonly require reduction and internal fixation.
Chronic ligament instability, significant tendon tears, or symptomatic osteochondral lesions may also eventually require operative treatment.
Surgery for Septic Arthritis
Surgical irrigation and debridement may be preferred for chronic infections, infections caused by difficult organisms, or cases that fail to respond to aspiration and antibiotics.
Operative treatment may also be favored in immunocompromised patients or when substantial purulent material is present.
Surgery for Ankle Arthritis
Severe arthritis that remains painful despite appropriate nonsurgical treatment may require ankle arthrodesis or total ankle arthroplasty.
The choice depends on patient age, activity level, alignment, bone quality, severity of degeneration, and condition of adjacent joints.
Management of Neoplasms
A suspected bone or soft-tissue tumor requires appropriate staging and biopsy before definitive treatment.
Benign lesions may require procedures such as curettage and bone grafting.
Malignant lesions may require wide surgical excision, limb-sparing reconstruction, systemic treatment, or, in selected advanced cases, amputation.
Referral
Acute fractures requiring definitive stabilization should be referred to an orthopaedic surgeon.
Chronic ankle pain that does not improve despite rest, activity modification, medication, rehabilitation, or immobilization should also prompt specialist referral.
Musculoskeletal Oncology Referral
A suspected bone or soft-tissue neoplasm should be referred to a musculoskeletal oncologist for proper staging and biopsy planning.
Biopsy should ideally be coordinated with the specialist responsible for definitive tumor treatment because poorly planned biopsy placement may complicate later surgery.
Prognosis
The prognosis depends on the underlying cause.
Minor sprains, tendon irritation, and many overuse conditions usually respond well to appropriate treatment.
More serious disorders, including advanced arthritis, infection, unstable fractures, and neoplasms, may require prolonged treatment and can produce significant long-term disability.
Complications
Many causes of ankle pain can lead to progressive pain, stiffness, weakness, instability, and loss of range of motion.
Untreated traumatic or degenerative disease may progress to chronic arthritis.
Infection can cause rapid destruction of cartilage and bone, while tumors may progressively damage surrounding structures.
Patient Monitoring
Careful short-term follow-up is important to monitor pain, swelling, gait, and recovery of ankle motion.
Range of motion should be maintained whenever clinically safe to reduce the risk of stiffness and contracture.
Patients should be reassessed promptly if there is increasing pain, swelling, fever, inability to bear weight, progressive deformity, neurologic symptoms, or other concerning clinical changes.
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Orthopaedic Surgery - Ankle Instability
Basics
Chronic ankle instability usually develops after recurrent ankle sprains, most commonly caused by inversion of a plantarflexed ankle. Repeated injury can lead to persistent pain, recurrent episodes of giving way, and loss of confidence in the ankle during walking or athletic activity.
Ankle instability is broadly divided into functional instability and true mechanical instability.
Functional instability occurs when the patient experiences a subjective sensation that the ankle is unstable despite the absence of major ligamentous laxity. Pain, impaired proprioception, delayed neuromuscular responses, and weakness may contribute to the feeling that the ankle is “giving way.”
Mechanical instability is caused by structural insufficiency of the stabilizing ligaments. Physiologic joint motion is exceeded, and examination may demonstrate abnormal laxity with a positive anterior drawer test or talar tilt test.
General Prevention
Appropriate treatment of the initial ankle sprain is important in reducing the likelihood of developing chronic instability.
Early management should include activity modification, appropriate bracing, and a structured functional rehabilitation program.
Rehabilitation should continue until range of motion, strength, balance, proprioception, and functional performance have returned to satisfactory levels.
Epidemiology
Ankle sprains are extremely common athletic injuries and may account for as much as 40% of all sports-related injuries.
Approximately 27,000 ankle sprains occur each day in the United States.
Following an inversion injury of the lateral ankle ligaments, symptomatic chronic ankle instability may develop in up to approximately 20% of patients.
Prevalence
Chronic ankle instability is particularly common in athletes participating in sports that require repeated cutting, jumping, landing, and rapid changes in direction.
It is frequently encountered among soccer and basketball players.
Risk Factors
The most important risk factor is a previous ankle sprain.
Once an ankle has been injured, impaired proprioception, residual ligamentous laxity, weakness, and inadequate rehabilitation increase the likelihood of further sprains.
Other risk factors include connective-tissue disorders and a cavovarus foot alignment, which places the ankle in a mechanically vulnerable position for recurrent inversion injury.
Etiology of Functional Instability
Functional instability is multifactorial.
Neurologic factors include impaired proprioception, protective reflexes, and muscle reaction time.
Muscular contributors include deficits in strength, power, and endurance, especially involving the peroneal muscles.
Mechanical factors may coexist, particularly residual laxity of the lateral ligament complex.
These abnormalities can combine to produce recurrent instability even when gross mechanical laxity is not prominent.
Sequence of Lateral Ligament Injury
An inversion ankle sprain may produce sequential disruption of the lateral stabilizing structures.
The anterolateral joint capsule is injured first, followed commonly by the anterior talofibular ligament (ATFL).
With increasing injury severity, the calcaneofibular ligament (CFL) may also tear.
The posterior talofibular ligament is considerably stronger and is rarely disrupted except in severe injuries such as ankle dislocation.
Anterior Talofibular Ligament
The ATFL is the most frequently injured ligament of the ankle.
It is the primary restraint to inversion when the ankle is in plantarflexion.
The ligament is particularly vulnerable when inversion is combined with plantarflexion and internal rotation.
Anatomically, the ATFL arises approximately 1 cm proximal to the tip of the lateral malleolus and travels anteriorly toward its insertion on the talus.
It inserts approximately 18 mm superior to the subtalar joint, runs roughly perpendicular to the fibula, and is closely associated with the ankle joint capsule.
The ligament measures approximately 7 mm in width and 10 mm in length.
Calcaneofibular Ligament
The CFL contributes to stability of both the ankle and subtalar joints.
It is particularly important in resisting inversion when the ankle is dorsiflexed.
The ligament may tear when a dorsiflexed ankle is subjected to excessive inversion.
It originates near the ATFL, approximately 8 mm proximal to the tip of the fibula, and passes posteriorly and distally toward the calcaneus.
The CFL courses at approximately 130° relative to the fibula and inserts on the calcaneus approximately 13 mm distal to the subtalar joint.
It is extracapsular and contributes to the floor of the peroneal tendon sheath.
Posterior Talofibular Ligament
The posterior talofibular ligament is the strongest component of the lateral ankle ligament complex.
It is rarely injured during routine inversion sprains.
Disruption usually occurs only with severe trauma, particularly ankle dislocation.
Dynamic Stabilizers
The peroneal tendons and muscles are the major dynamic restraints against excessive ankle inversion.
Rapid activation of the peroneal muscles helps resist inversion forces and protects the lateral ankle ligaments.
Weakness, poor endurance, or delayed peroneal muscle response therefore contributes significantly to recurrent functional instability.
Associated Conditions
Chronic ankle instability may be associated with systemic connective-tissue disorders such as Ehlers-Danlos syndrome.
Generalized ligamentous laxity can make both conservative and surgical stabilization more difficult.
Diagnosis
The central diagnostic task is to differentiate functional instability from mechanical ligamentous instability.
Approximately 15–30% of patients following a simple ankle sprain may continue to experience residual symptoms, including peroneal weakness and functional instability.
Evaluation should therefore assess ligament integrity as well as neuromuscular and functional deficits.
Signs and Symptoms
Common symptoms include recurrent lateral ankle pain, intermittent swelling, and episodes of instability.
Patients frequently describe the ankle as suddenly “giving way,” particularly while walking on uneven ground, descending stairs, running, or participating in sports.
Symptoms may disappear completely between episodes.
History
A typical history includes repeated ankle sprains occurring with relatively minor trauma.
Patients may report repeated episodes of rolling the ankle during activities that previously would not have caused injury.
The subjective sensation of giving way is particularly characteristic.
Important historical factors include the number and severity of previous sprains, previous rehabilitation, use of braces, and the patient’s sporting and occupational demands.
Hindfoot Alignment
The hindfoot should be inspected while the patient is standing.
A cavovarus alignment predisposes the ankle to recurrent inversion and may contribute to failure of ligament reconstruction if left untreated.
Alignment should therefore be incorporated into both diagnosis and surgical planning.
Gait Assessment
The patient’s gait should be observed for protective patterns, abnormal loading, or recurrent inversion.
Walking, heel rise, and other functional maneuvers may reveal instability that is less obvious during a seated examination.
Neurovascular Examination
A complete neurovascular examination should be performed.
Patients with recurrent ankle sprains have an increased incidence of injury involving the superficial peroneal nerve.
Sensation, motor function, pulses, and capillary refill should therefore be assessed and documented.
Peroneal Tendons
The peroneal tendons should be palpated for tenderness, swelling, subluxation, or tearing.
Peroneal tendon pathology frequently accompanies chronic lateral ankle instability and can itself contribute to persistent lateral ankle pain.
Dynamic examination during active ankle movement may help identify tendon subluxation.
Range of Motion
Ankle range of motion should be measured, with particular attention to dorsiflexion.
Pain or crepitus during motion may suggest associated intra-articular cartilage injury or degenerative changes.
Restricted motion may also alter ankle mechanics and contribute to recurrent sprains.
Subtalar Joint Examination
Subtalar motion should be assessed carefully.
A rigid subtalar joint may raise suspicion for tarsal coalition or another structural abnormality.
Subtalar stability should also be examined because the CFL contributes to both ankle and subtalar stability.
Assessment of CFL Integrity
The CFL can be assessed with the ankle dorsiflexed while an inversion force is applied to the calcaneus.
Excessive medial translation or inversion of the calcaneus may indicate subtalar instability and CFL insufficiency.
Comparison with the opposite side is useful.
Anterior Drawer Test
The anterior drawer test primarily evaluates the integrity of the ATFL.
The ankle is placed near neutral, and an anterior or anterolateral force is applied to the heel while the distal tibia is stabilized.
Excessive forward translation of the talus relative to the tibia suggests ATFL insufficiency.
A difference of more than approximately 3 mm compared with the opposite side, or absolute anterior translation greater than approximately 10 mm, supports mechanical instability.
Stress radiography may be used to confirm abnormal translation.
Talar Tilt Test
The talar tilt test primarily evaluates the CFL.
The patient is usually seated with the ankle near neutral.
The examiner applies an inversion force to the hindfoot and midfoot as a single unit while preventing the forefoot from simply rotating medially.
A total talar tilt exceeding approximately 9–10°, or a difference of more than approximately 3° compared with the opposite side, suggests mechanical instability.
Stress mortise radiographs may be used for objective confirmation.
Imaging
Standard Radiographs
Initial imaging generally includes lateral and mortise radiographs of the ankle.
Radiographs are useful not only for assessing instability but also for identifying chronic post-traumatic abnormalities.
Possible findings include tibial marginal osteophytes, talar exostoses near the ATFL insertion, osteochondral lesions of the talus, and an os subfibulare.
Stress Radiographs
Stress radiographs can provide objective evidence of lateral ligament insufficiency.
Anterior talar translation is assessed on a lateral stress view.
The perpendicular distance between the posterior articular margin of the tibia and the talus is measured.
Anterior translation that is approximately 3–5 mm greater than the opposite side, or an absolute value around 10 mm or greater, supports mechanical instability.
Talar Tilt on Stress Imaging
Talar tilt is measured on a stress mortise radiograph.
The angle formed between the distal tibial articular surface and the talar dome is assessed during inversion stress.
A talar tilt approximately 3–5° greater than the opposite ankle, or an absolute tilt of about 10° or more, is consistent with mechanical lateral instability.
Differential Diagnosis
Chronic ankle pain may coexist with instability but may also arise from other disorders.
Important differential diagnoses include intra-articular fibrosis or synovitis, osteochondral lesions of the talus, peroneal tendon tears, and peroneal tendon subluxation.
A fracture of the lateral process of the talus should also be considered, particularly following a significant inversion injury.
Persistent symptoms after a supposedly uncomplicated ankle sprain should therefore prompt evaluation for associated pathology.
Treatment
General Measures
Initial treatment of chronic ankle instability is generally nonoperative.
Early symptomatic management may include the RICE protocol: rest, ice, compression, and elevation.
More importantly, treatment should address the functional deficits that contributed to recurrence.
A structured rehabilitation program is therefore the central component of conservative management.
Bracing
An ankle brace can provide external support while injured ligaments and neuromuscular control recover.
Patients with moderate or severe sprains may continue using a functional brace for up to approximately 6 months, particularly during athletic activity.
Bracing can reduce recurrent inversion episodes while allowing continued participation in rehabilitation.
Importance of Rehabilitation
Persistent lateral ankle pain and functional instability are frequently related to incomplete or inadequate rehabilitation after the original injury.
Simply allowing pain and swelling to settle without restoring strength, endurance, proprioception, and balance can leave the ankle vulnerable to repeated sprains.
A comprehensive rehabilitation program is therefore essential before surgery is considered.
Activity
Sports participation should be restricted until rehabilitation has been completed adequately.
The patient should regain near-normal strength, range of motion, balance, and confidence before returning to unrestricted athletic activity.
Sport-specific tasks such as running, cutting, pivoting, and jumping should be performed without pain or instability before full return.
Bracing During Return to Sport
Functional bracing or taping during return to athletics may reduce the risk of recurrent sprains.
Appropriately fitted braces generally do not cause a significant reduction in athletic performance.
Athletes with previous ankle sprains may therefore benefit from continued preventive bracing during high-risk activities.
Physical Therapy
Physical therapy should focus on several key areas.
Range-of-motion exercises help restore normal ankle mechanics.
Both concentric and eccentric strengthening should be performed, particularly for the peroneal muscles.
Endurance training is important because fatigue can delay protective muscle responses and increase the risk of recurrent inversion.
Proprioceptive Training
Proprioceptive retraining is a major component of rehabilitation.
Exercises may include single-leg balance, unstable-surface training, and tilt-board exercises.
Progressive balance challenges improve joint-position awareness and neuromuscular reaction time.
This is particularly important in patients with functional instability.
Indications for Surgery
Surgery may be considered when significant instability persists despite an adequate functional rehabilitation program.
Other indications include marked mechanical laxity, recurrent sprains during routine daily activity, and persistent instability during sports despite appropriate bracing or taping.
The procedure selected depends on ligament quality, hindfoot alignment, previous surgery, patient demands, and the presence of generalized ligamentous laxity.
Anatomic Repair
Anatomic ligament repair generally produces the best results when the native ligament tissue remains of good quality.
The objective is to restore the normal anatomy of the ATFL and, when necessary, the CFL.
Advantages include preservation of subtalar motion and preservation of the peroneal tendons, which remain available as important dynamic stabilizers.
Limitations of Primary Repair
Direct anatomic repair may be unsuitable when the local ligament tissue is severely attenuated or deficient.
Examples include patients with connective-tissue disorders such as Ehlers-Danlos syndrome, failed previous stabilization surgery, or very longstanding instability with poor-quality tissue.
Patients with more than approximately 10 years of instability may have substantial ligament attenuation that makes direct repair less reliable.
Broström Repair
The Broström procedure is an anatomic repair of the lateral ankle ligaments.
The attenuated or torn ATFL is shortened and directly repaired.
The CFL may also be imbricated or repaired when instability involves both ligaments.
The operation aims to restore native anatomy without sacrificing the peroneal tendons or restricting normal subtalar motion.
Gould Modification
The Gould modification reinforces the repaired lateral ligament complex.
After the ATFL and CFL are repaired or imbricated, the inferior extensor retinaculum is advanced and attached to the fibula.
This provides additional reinforcement and improves stability.
The combined Broström-Gould repair is widely regarded as the standard operative technique for chronic lateral ankle instability and has reported success rates of approximately 90%.
Ligament Reconstruction
Ligament reconstruction is considered when direct repair is unlikely to provide adequate stability.
Indications include poor-quality or severely attenuated ligaments, failed previous Broström repair, generalized connective-tissue laxity, and selected obese or high-demand patients.
Modern anatomic reconstruction uses tendon graft tissue to reproduce the normal orientation and function of the native ATFL and CFL.
Graft Reconstruction
Autograft or allograft tendon may be used to reconstruct deficient lateral ankle ligaments.
The objective is to reproduce the native ligament anatomy and provide sufficient strength while preserving ankle and subtalar motion.
This approach is particularly useful in revision surgery or when local ligament tissue is unsuitable for primary repair.
Nonanatomic Reconstructions
Older procedures such as the Chrisman-Snook and Evans reconstructions use tendon tissue in a nonanatomic fashion to stabilize the lateral ankle.
Although these procedures can provide stability, they may alter normal ankle and subtalar mechanics.
Potential disadvantages include loss of talocrural or subtalar motion and risk of injury or dysfunction involving the peroneal tendons or nearby nerves.
For this reason, modern anatomic repairs and reconstructions are generally preferred when feasible.
Hindfoot Realignment
Persistent hindfoot varus can place excessive stress on a repaired lateral ligament complex.
In selected patients with significant cavovarus or hindfoot varus alignment, a calcaneal osteotomy may be performed together with ligament repair or reconstruction.
Correcting the underlying alignment reduces recurrent inversion forces and may improve the durability of the stabilization procedure.
Postoperative Care
Following surgery, the ankle is commonly immobilized in a cast or splint with the hindfoot positioned in slight eversion.
Immobilization generally lasts approximately 2–6 weeks, depending on the procedure and surgeon preference.
The patient is then transitioned to a removable brace.
Postoperative Rehabilitation
Physical therapy is usually continued for approximately 3 months or longer.
Rehabilitation progresses from protected range of motion to strengthening, proprioceptive training, balance exercises, and functional activity.
A protective ankle brace is commonly recommended for at least 6 months, especially during athletic activity.
Prognosis
The overall success rate of surgery for chronic lateral ankle instability is high.
Both appropriately selected anatomic repairs and reconstructive procedures can provide substantial improvement in stability, pain, and function.
Anatomic repair is generally favored when adequate native ligament tissue is available because it preserves more normal joint mechanics.
Predictors of Poor Outcome
Several factors are associated with less favorable results after surgery.
These include symptoms lasting 10 years or longer, established ankle osteoarthritis, and generalized joint hypermobility.
Uncorrected hindfoot malalignment and associated intra-articular pathology may also contribute to persistent symptoms.
Complications
Complications tend to be more common after nonanatomic reconstruction procedures than after modern anatomic repair.
Potential complications include loss of subtalar or ankle motion, stiffness, recurrent instability, and persistent pain.
Nerve Injury
Injury to the superficial peroneal or sural nerve may occur during surgical exposure or reconstruction.
This may result in numbness, dysesthesia, or painful neuroma formation.
Careful surgical technique and knowledge of the regional anatomy help minimize this risk.
Tendon-Related Complications
Procedures that use tendon tissue for nonanatomic reconstruction may alter normal tendon function.
Tendons are biomechanically different from native ligaments and are generally stiffer with less strain before failure.
Using the peroneal tendons for reconstruction can also reduce their role as dynamic stabilizers of the ankle.
Modern anatomic techniques therefore attempt to preserve the peroneal tendons whenever possible.
Patient Monitoring
Patients should be followed to assess pain, recurrent giving-way episodes, ligament stability, ankle and subtalar motion, strength, proprioception, and return to activity.
After surgery, monitoring should also include wound healing, neurologic function, brace tolerance, and progression through rehabilitation.
Long-term assessment is particularly important in patients with hindfoot deformity, generalized ligamentous laxity, or associated ankle osteoarthritis.
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Orthopaedic Surgery - Ankle Arthritis
Basics
Ankle arthritis is a degenerative condition affecting the tibiotalar joint. Although osteoarthritis can involve the ankle, it occurs less frequently than osteoarthritis of major weight-bearing joints such as the hip and knee.
Unlike hip and knee osteoarthritis, which is commonly primary or age-related, ankle arthritis is most often associated with previous trauma or abnormal ankle mechanics.
Post-traumatic ankle arthritis therefore tends to occur in a younger population than primary osteoarthritis of other major joints.
Causes of Degeneration
Previous ankle injury is the most common cause of degenerative ankle arthritis.
Fractures involving the malleoli, distal tibial plafond, or talus can alter joint congruity and produce abnormal loading of the articular cartilage.
Chronic ankle instability may similarly produce repetitive abnormal motion and uneven distribution of forces, gradually leading to cartilage deterioration.
Other Causes
Other disorders that may eventually produce ankle arthritis include osteochondral lesions of the talus, osteonecrosis, chronic infection, and inflammatory arthropathies.
Patients with rheumatoid arthritis and other systemic inflammatory conditions frequently develop involvement of both the ankle and adjacent joints of the foot.
Ankle Cartilage
The articular cartilage of the ankle differs structurally from that of the hip and knee.
Ankle cartilage is relatively thin and has a more uniform extracellular matrix.
These biological and mechanical characteristics may partly explain why primary osteoarthritis of the ankle is less common despite the high loads transmitted through the joint during walking and other activities.
General Prevention
Appropriate treatment of ankle fractures is important because restoration of joint alignment and congruity may reduce the future risk of post-traumatic arthritis.
Accurate fracture reduction and correction of persistent malalignment help minimize abnormal mechanical loading of the articular surface.
Weight control is also important. Reducing excess body weight decreases repetitive loading across the ankle and may reduce symptoms or slow progression of degenerative changes.
Epidemiology
Symptomatic ankle arthritis is considerably less common than symptomatic arthritis of the hip or knee.
It has been reported to occur approximately nine times less frequently than symptomatic hip and knee arthritis.
Despite this lower incidence, ankle arthritis may cause substantial disability because of the joint’s essential role in normal gait and weight-bearing.
Risk Factors
The major risk factors include previous ankle trauma, chronic ankle instability, and inflammatory arthritis.
Recurrent ankle sprains, ligamentous insufficiency, malalignment after fracture healing, and articular surface damage can all increase the likelihood of degenerative change.
Systemic inflammatory conditions can damage the ankle through chronic synovitis and progressive cartilage destruction.
Etiology
Trauma
Post-traumatic arthritis may develop following fractures involving the ankle joint.
Common injuries include malleolar fractures, tibial plafond or pilon fractures, and talar fractures.
Even appropriately treated fractures may later lead to arthritis if the articular cartilage was damaged at the time of injury.
Ankle Instability
Chronic ligamentous instability causes abnormal translation and rotation of the talus within the ankle mortise.
Repeated episodes of instability may concentrate load on limited areas of cartilage and accelerate joint degeneration.
Untreated or recurrent instability is therefore an important mechanical cause of ankle osteoarthritis.
Inflammatory Disease
Inflammatory conditions such as rheumatoid arthritis may cause chronic synovial inflammation and progressive destruction of the articular cartilage.
Multiple joints of the foot and ankle may be involved simultaneously.
The resulting deformity and instability can further accelerate degeneration.
Osteonecrosis
Osteonecrosis, particularly involving the talus, may lead to collapse of the subchondral bone.
Loss of the normal talar contour produces joint incongruity and abnormal load transmission, which may result in secondary ankle arthritis.
Osteochondral Lesions
An osteochondral defect or osteochondritis dissecans lesion of the talus may damage both the articular cartilage and underlying subchondral bone.
Large or chronic lesions may eventually contribute to degenerative arthritis of the ankle.
Infection
Previous septic arthritis can cause substantial destruction of the joint cartilage.
Even after successful eradication of infection, residual joint incongruity, stiffness, and cartilage loss may lead to severe postinfectious arthritis.
Diagnosis
Signs and Symptoms
Pain is the most common symptom of ankle arthritis.
Patients may also report swelling, stiffness, instability, giving way, locking, or deformity.
Symptoms usually worsen during prolonged standing, walking, running, or other weight-bearing activities.
As the disease progresses, pain may also occur during routine daily activities or at rest.
History
A detailed history should identify any previous ankle injury, fracture, dislocation, recurrent sprains, or surgical treatment.
The clinician should determine how the original injury was managed and whether residual deformity or instability remained.
Medical history should also include conditions associated with inflammatory arthritis, infection, osteonecrosis, or systemic disease.
Physical Examination
The ankle should be examined both while the patient is seated and while standing.
Standing examination is important for evaluating overall alignment, deformity, and weight-bearing mechanics.
The joint should be inspected for swelling, deformity, erythema, muscle wasting, and surgical scars.
Palpation
The examiner should palpate the ankle joint for tenderness, warmth, and effusion.
Tenderness should be localized carefully to determine whether pain originates from the tibiotalar joint or from neighboring structures such as the subtalar joint.
This distinction is important because ankle and subtalar arthritis may coexist but require different treatment strategies.
Range of Motion
Ankle dorsiflexion and plantarflexion should be measured and compared with the opposite side.
Arthritis commonly causes progressive loss of motion, particularly dorsiflexion.
Restricted motion may contribute to compensatory gait patterns and increased stress on adjacent joints.
Ligament Stability
The ankle ligaments should be assessed for mechanical instability.
Anterior drawer and talar tilt testing may help identify chronic ligamentous insufficiency.
Persistent instability may be both a cause of arthritis and an important consideration when planning reconstructive surgery.
Neurologic Examination
Motor and sensory function should be examined to identify associated neurologic abnormalities.
Weakness or sensory loss may indicate peripheral neuropathy, nerve injury, radiculopathy, or another neurologic disorder that may affect treatment and rehabilitation.
Vascular Examination
The vascular status of the extremity should be assessed carefully.
The dorsalis pedis and posterior tibial pulses should be palpated, and capillary refill should be checked.
Adequate circulation is particularly important when surgical treatment is being considered because vascular compromise increases the risk of wound-healing complications.
Gait Assessment
The patient’s gait should be observed.
An antalgic gait is common because the patient reduces the amount of time spent weight-bearing on the painful ankle.
Patients with limited dorsiflexion may compensate by externally rotating the foot or circumducting the limb during swing phase.
Other compensatory gait patterns may develop depending on the degree of stiffness and deformity.
Imaging
Plain Radiographs
Initial imaging should include standard weight-bearing radiographs of the ankle.
Routine views include anteroposterior, lateral, and mortise radiographs.
Weight-bearing images are particularly useful because they demonstrate joint-space loss and alignment under physiologic loading conditions.
Radiographic Findings
Typical features of ankle arthritis include joint-space narrowing, subchondral sclerosis, subchondral cyst formation, and osteophytes.
Joint-space loss may be uniform or asymmetric depending on the underlying cause.
Post-traumatic malalignment may produce focal narrowing on one side of the joint.
Radiographs may also demonstrate previous fractures, deformity, hardware, or talar collapse.
CT
Computed tomography provides more detailed evaluation of the bony architecture.
CT may help determine the severity and distribution of arthritis and is useful for evaluating complex deformity or previous fractures.
It can also assess associated subtalar joint degeneration, which may influence the choice of surgical procedure.
MRI
MRI is not routinely required for straightforward end-stage ankle arthritis.
It may be helpful when plain radiographs suggest an osteochondral lesion, osteonecrosis, or tumor.
MRI can also evaluate surrounding tendons, ligaments, cartilage, and other soft-tissue structures when these are suspected as additional sources of pain.
Differential Diagnosis
Important differential diagnoses include osteochondritis dissecans or osteochondral lesions of the talus, osteonecrosis or avascular necrosis, posterior tibial tendinitis, and subtalar joint arthritis.
A bone or soft-tissue tumor should also be considered when imaging or clinical findings are atypical.
Accurate localization of the pain is essential because conditions involving adjacent joints and tendons may mimic ankle arthritis.
Treatment
General Measures
Initial treatment is generally nonoperative.
The aim is to reduce pain, decrease mechanical stress across the joint, maintain function, and postpone or avoid surgery when possible.
Treatment should be individualized according to symptom severity, degree of arthritis, alignment, age, activity level, and patient expectations.
Medication
Nonsteroidal anti-inflammatory drugs are commonly used to reduce pain and inflammation.
Simple analgesics may also be used as needed.
Medication provides symptomatic relief but does not reverse the underlying cartilage degeneration.
Orthotic Devices
Bracing may reduce painful ankle motion and improve stability.
An ankle-foot orthosis (AFO) can limit excessive movement, support deformity, and redistribute load across the lower extremity.
More rigid braces may be useful in patients with advanced disease or significant instability.
Footwear Modification
Appropriate footwear can substantially reduce symptoms in some patients.
A rocker-bottom sole allows the body to progress over the foot while reducing the amount of motion required through the ankle joint.
A solid ankle cushion heel or other shoe modifications may also decrease painful loading and improve gait efficiency.
Corticosteroid Injection
An intra-articular corticosteroid injection may provide temporary pain relief and reduce synovial inflammation.
Injection can also help confirm that the ankle joint itself is the primary source of pain.
The duration and degree of benefit vary among patients.
Weight Loss
Weight reduction should be encouraged in overweight patients.
Lower body weight decreases repetitive forces across the ankle during standing and walking.
Weight management may improve symptoms and reduce stress on both the diseased ankle and adjacent joints.
Duration of Nonoperative Treatment
A reasonable trial of nonsurgical treatment is generally recommended before considering major reconstructive surgery.
If symptoms remain disabling despite approximately 3–6 months of appropriate conservative treatment, surgical options may be discussed.
The timing of surgery should also take into account the patient’s age, functional demands, deformity, and radiographic severity.
Activity Modification
Patients should limit activities that produce repetitive high loads across the ankle.
Excessive walking may need to be reduced during symptomatic periods.
High-impact activities such as running, jumping, and cutting or pivoting sports should generally be avoided when they produce significant pain.
Low-Impact Exercise
Low-impact exercise should be encouraged to maintain cardiovascular fitness and muscle conditioning.
Suitable activities include stationary cycling, swimming, and aquatic exercise.
These activities reduce impact loading while allowing continued physical activity.
Assistive Devices
A cane, crutches, or other walking aids can reduce weight transmitted through the painful ankle.
A cane is usually held in the hand opposite the affected ankle.
Assistive devices are particularly useful during severe exacerbations or while awaiting definitive treatment.
Physical Therapy
Physical therapy is not always central to the initial management of isolated ankle arthritis.
However, therapy may help maintain strength, optimize gait, and address compensatory abnormalities.
Physical therapy is particularly important after surgical treatment to restore motion, strength, balance, and functional mobility.
Complementary Therapies
The effectiveness of supplements such as glucosamine for ankle arthritis remains uncertain.
Evidence from other arthritic conditions cannot necessarily be directly applied to the ankle.
Patients should understand that these products have not been clearly demonstrated to alter the progression of ankle osteoarthritis.
Surgical Management
Surgery is considered when pain and functional impairment remain substantial despite appropriate nonsurgical treatment.
The procedure selected depends on the severity and distribution of arthritis, alignment, age, activity level, bone quality, and condition of neighboring joints.
Options range from joint-preserving procedures to fusion or total ankle replacement.
Ankle Arthroscopy
Arthroscopy may be useful in selected patients with relatively early or focal disease.
The procedure allows removal of impinging osteophytes, loose bodies, and unstable chondral fragments.
Debridement can improve symptoms when mechanical impingement is a major source of pain.
Arthroscopy is generally less useful in diffuse end-stage arthritis with complete joint-space loss.
Distraction Arthroplasty
Ankle distraction arthroplasty is a joint-preserving option for selected patients with mild to moderate arthritis.
An external fixator is used to distract the joint surfaces temporarily, reducing mechanical loading across the articular cartilage.
The aim is to decrease pain and potentially improve the biological environment of the joint while preserving ankle motion.
This procedure is generally reserved for carefully selected patients.
Supramalleolar Osteotomy
A supramalleolar tibial osteotomy may be considered when ankle arthritis is associated with malalignment.
Indications may include fracture malunion, tibial deformity, or arthritis predominantly involving one part of the ankle joint.
By realigning the distal tibia, the procedure shifts load away from the damaged portion of the joint toward healthier cartilage.
This can relieve pain while preserving the ankle joint.
Ankle Arthrodesis
Ankle arthrodesis, or ankle fusion, remains an established salvage procedure for severe ankle arthritis.
Fusion eliminates painful movement at the tibiotalar joint by permanently joining the tibia and talus.
Internal fixation is commonly achieved with screws, although other fixation techniques may be used.
Indications for Fusion
Ankle fusion has broad indications and may be used for post-traumatic or degenerative arthritis, postinfectious arthritis, large osteochondral defects, rheumatoid or other inflammatory arthritis, and talar osteonecrosis.
It is particularly useful when the joint is severely destroyed, unstable, deformed, or unsuitable for replacement.
Outcomes After Fusion
Most appropriately selected patients experience substantial pain relief after successful fusion.
Although ankle range of motion is permanently lost, many patients remain satisfied because painful movement is eliminated.
Motion from the subtalar, midfoot, and forefoot joints partially compensates during walking.
However, these adjacent joints may experience increased mechanical stress over time.
Total Ankle Arthroplasty
Total ankle arthroplasty, or ankle replacement, has become increasingly accepted with improvements in implant design and surgical technique.
The damaged tibial and talar joint surfaces are replaced with prosthetic components while preserving movement at the ankle.
Modern implant designs have improved outcomes compared with earlier generations.
Advantages of Total Ankle Replacement
A major advantage compared with fusion is preservation of ankle range of motion.
Maintaining motion may allow a more physiologic gait and may reduce compensatory loading of neighboring joints.
There is also the potential for a lower risk of secondary hindfoot and midfoot arthritis caused by altered mechanics, although long-term outcomes depend on multiple factors.
Disadvantages of Total Ankle Replacement
Ankle replacement has several limitations compared with fusion.
It may be associated with a greater number of perioperative complications and requires appropriate bone quality, alignment, ligament stability, and soft-tissue condition.
Prosthetic components also have a finite lifespan.
Wear, loosening, subsidence, or mechanical failure may eventually require revision surgery.
Revision Considerations
Failure of a total ankle replacement can lead to loss of bone stock.
Substantial bone loss may make subsequent revision arthroplasty or conversion to fusion technically difficult.
For this reason, patient selection is critical, especially in younger or highly active individuals.
Follow-Up
Patients with ankle arthritis should be reviewed periodically to assess progression of symptoms and functional limitation.
Follow-up allows modification of conservative treatment and provides an opportunity to discuss surgical options if pain becomes increasingly disabling.
Changes in alignment, instability, adjacent-joint symptoms, and walking ability should also be monitored.
Prognosis
The overall prognosis is fair and depends heavily on the underlying cause and severity of the disease.
Mild or moderate symptoms may remain manageable for prolonged periods with activity modification, bracing, medication, and other conservative measures.
However, many patients with severe end-stage arthritis ultimately require surgery to achieve satisfactory pain control and restore function.
Complications of Nonoperative Treatment
Nonoperative management is generally associated with few major complications.
Potential concerns include medication-related adverse effects, temporary discomfort from braces, skin irritation, and progressive functional limitation if the arthritis continues to worsen.
The underlying degenerative process may continue despite symptomatic treatment.
Surgical Complications
Potential surgical complications include wound-healing problems, infection, malalignment, nerve injury, and vascular injury.
Following fusion, nonunion or malunion may occur, and increased mechanical stress may eventually contribute to secondary arthritis of the subtalar or midfoot joints.
Following total ankle arthroplasty, complications may include implant loosening, subsidence, wear, fracture, infection, and eventual prosthetic failure.
Adjacent-Joint Arthritis
Loss of ankle motion after fusion alters the mechanics of the hindfoot and midfoot.
Over time, this may increase stress across adjacent joints and contribute to progressive degenerative change.
This potential complication should be considered when counseling younger patients who may live for many decades after fusion.
Patient Monitoring
Patients should be followed according to their symptoms and the severity of arthritis.
Clinical monitoring should include pain, swelling, range of motion, alignment, instability, gait, neurovascular function, and activity tolerance.
Repeat radiographs may be obtained when symptoms progress or when surgical treatment is being considered.
The overall goal is to maintain function and pain control while determining the most appropriate timing and type of intervention.
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Orthopaedic Surgery - Aneurysmal Bone Cyst
Basics
An aneurysmal bone cyst (ABC) is a benign, expansile, reactive cystic lesion of bone that occurs predominantly in children and adolescents. The lesion can enlarge rapidly and cause marked expansion of the affected bone.
An aneurysmal bone cyst may arise as a primary lesion, without another underlying bone abnormality, or it may develop as a secondary lesion associated with another tumor or bone disorder.
Secondary aneurysmal bone cyst formation may occur in association with lesions such as giant cell tumor, chondromyxoid fibroma, fibrous dysplasia, osteoblastoma, and osteosarcoma.
Although benign, ABCs can behave aggressively at the local level because progressive expansion may destroy surrounding cortical bone and adjacent structures.
Incidence
Aneurysmal bone cyst is a relatively common benign bone lesion.
It occurs most frequently in children and adolescents with open growth plates, reflecting its predominance in the skeletally immature population.
The lesion may involve a variety of bones but is commonly encountered in the metaphyseal regions of long bones.
Risk Factors
There are no clearly established specific risk factors for development of a primary aneurysmal bone cyst.
Secondary lesions occur in association with certain benign and malignant bone tumors, but the presence of these conditions does not necessarily predict development of an ABC.
Pathophysiology
Aneurysmal bone cyst is characterized by abnormal vascular spaces within a reactive bone lesion.
These vascular channels contribute to progressive expansion of the lesion and enlargement of the affected bone.
As the cyst enlarges, the inner or endosteal surface of the bone is progressively resorbed.
At the same time, the periosteum may produce a thin shell or rim of new bone around the expanding lesion, giving the characteristic appearance of an expansile lesion surrounded by a delicate bony margin.
Local Destructive Effects
Despite being histologically benign, an aneurysmal bone cyst may become locally destructive.
Progressive expansion can erode the cortex and weaken the structural integrity of the bone.
When the lesion is located near a joint or growth plate, it may damage the physis, articular cartilage, and surrounding ligamentous structures.
Large lesions can therefore produce significant deformity, functional impairment, or pathologic fracture.
Etiology
An aneurysmal bone cyst is considered a benign reactive vascular lesion.
The precise initiating cause is not completely understood.
Primary ABCs develop without another identifiable bone lesion, whereas secondary ABCs represent cystic and vascular changes occurring within another underlying bone tumor or disorder.
Associated Conditions
Primary aneurysmal bone cysts are not typically associated with systemic disease.
However, secondary aneurysmal bone cyst changes may occur within other bone lesions, including giant cell tumor, osteoblastoma, chondromyxoid fibroma, fibrous dysplasia, and osteosarcoma.
Identifying an underlying lesion is important because treatment and prognosis may differ substantially.
Diagnosis
Signs and Symptoms
The most common presenting symptom is localized pain over the affected bone.
As the lesion expands, a visible or palpable soft-tissue mass may develop.
Pain may gradually increase over a relatively short period because these lesions can enlarge rapidly.
When the lower extremity is involved, the patient may develop a limp or antalgic gait because weight-bearing produces discomfort.
Physical Examination
Examination commonly demonstrates localized tenderness over the affected area.
An expansile lesion may produce a palpable mass or visible swelling.
The overlying skin is usually normal unless the lesion has become very large.
Range of motion of a nearby joint should be assessed, particularly when the lesion is close to the articular surface.
The affected extremity should also be examined for deformity, weakness, and signs of impending or established pathologic fracture.
Imaging
Plain Radiographs
Radiographs frequently demonstrate an eccentric, expansile lesion, often involving the metaphysis of a long bone.
The lesion may progressively thin or destroy the cortex.
A thin shell of periosteal new bone may surround the lesion as the bone expands.
The overall appearance may be described as expansile or ballooned, with varying degrees of cortical thinning and destruction.
CT
Computed tomography provides detailed assessment of the cortical bone and internal architecture of the lesion.
An aneurysmal bone cyst typically appears as an expansile lesion without mineralized tumor matrix.
CT is particularly helpful for evaluating cortical destruction, defining the extent of the lesion, and planning surgery in anatomically complex areas.
MRI
MRI is useful for assessing both the internal characteristics and the full extent of an aneurysmal bone cyst.
A characteristic finding is the presence of multiple fluid-fluid levels, caused by layering of blood products of different densities within the cystic spaces.
MRI may also demonstrate edema in the surrounding cancellous bone, reactive changes in adjacent soft tissues, and periosteal reaction.
It is especially useful when determining involvement of the growth plate, joint surface, neurovascular structures, or surrounding soft tissues.
Differential Diagnosis
The major differential diagnoses include giant cell tumor and telangiectatic osteosarcoma.
Telangiectatic osteosarcoma is particularly important because it can resemble an aneurysmal bone cyst clinically and radiologically, including the presence of fluid-fluid levels on MRI.
Careful imaging assessment and histological evaluation are therefore required when the diagnosis is uncertain.
Treatment
General Measures
Prompt evaluation and treatment are important because aneurysmal bone cysts can enlarge very rapidly.
Some lesions may increase markedly in size over only a few weeks.
Rapid enlargement can cause progressive cortical destruction, weakening of the bone, involvement of the growth plate, and damage to nearby articular or ligamentous structures.
Management should therefore focus both on controlling the lesion and preventing pathologic fracture.
Activity Modification
The affected extremity should be protected while definitive treatment is being planned.
For lesions involving the lower extremity, patients may be advised to use two crutches and reduce or avoid weight-bearing when there is significant structural weakening.
For upper-extremity lesions, activities that place excessive force through the involved bone should be avoided.
These precautions are intended to decrease the risk of a pathologic fracture through the weakened area.
Physical Therapy
Physical therapy is mainly used to educate the patient regarding safe mobilization and protection of the affected extremity.
Before surgery, the therapist may teach appropriate use of crutches or other assistive devices.
After treatment, rehabilitation can help restore joint motion, muscle strength, gait, and normal function while protecting the healing bone.
The rehabilitation program depends on the location and size of the lesion and the type of surgical reconstruction performed.
Surgical Management
Surgery is commonly required for aneurysmal bone cysts.
The traditional surgical approach involves intralesional curettage, in which the cystic and abnormal tissue is removed from within the affected bone.
Because the lesion is benign, a wide oncologic resection is not routinely required in most cases.
However, thorough removal is important because residual lesion tissue may contribute to local recurrence.
Curettage
During curettage, the cyst is opened and the abnormal tissue is carefully removed from the cavity.
The walls of the lesion may be further treated according to surgeon preference in an attempt to reduce recurrence.
The resulting bone defect can be substantial, particularly in large lesions.
The defect therefore often requires reconstruction to provide structural support and facilitate bone healing.
Bone Grafting and Bone Graft Substitutes
After curettage, the remaining cavity may be filled with bone graft or a bone graft substitute.
Various synthetic or processed materials are available.
The selected material should be biologically compatible and should not create an unnecessary immunologic response.
When graft substitutes are used, materials without risk of disease or viral transmission are preferred.
The choice of graft material depends on lesion size, location, patient age, and the amount of structural support required.
Follow-Up
Patients should be monitored closely after treatment because aneurysmal bone cysts can recur locally.
Follow-up usually includes periodic clinical assessment and radiographs.
When the patient remains asymptomatic and radiographs show satisfactory healing, plain radiographs alone are often sufficient for surveillance.
Evaluation of Recurrent Pain
The development of new or recurrent pain during follow-up should raise concern for local recurrence.
In this situation, repeat radiographs should be obtained.
MRI is also useful when symptoms recur because it can identify recurrent cystic changes before they become obvious on plain radiographs and can assess the surrounding bone and soft tissues.
Prognosis
The overall prognosis is excellent because an aneurysmal bone cyst is a benign lesion.
Most patients achieve good long-term function after successful treatment.
Outcome depends on adequate control of the lesion, restoration of bone strength, and preservation of nearby growth plates, joints, and neurovascular structures.
Local recurrence may occur, particularly in younger patients or after incomplete treatment, but recurrence can usually be managed with further therapy.
Complications
Despite its benign nature, an aneurysmal bone cyst can become very large and produce significant local destruction.
Potential complications include cortical destruction, pathologic fracture, deformity, and loss of mechanical strength of the affected bone.
Lesions adjacent to a growth plate may damage the physeal cartilage, potentially producing growth disturbance or angular deformity.
Joint and Ligament Damage
When an aneurysmal bone cyst extends toward a joint, it may damage the articular cartilage, potentially affecting long-term joint function.
Expansion may also disrupt nearby ligamentous structures.
These complications are particularly concerning in large or rapidly progressive lesions and provide an additional reason for timely treatment.
Patient Monitoring
Regular orthopedic follow-up is recommended after treatment.
Monitoring should include assessment of pain, swelling, limb function, joint movement, deformity, and evidence of pathologic fracture.
Serial radiographs are used to evaluate bone healing and detect local recurrence.
If new pain, swelling, or functional deterioration develops, MRI should be considered to assess for recurrent or residual disease.
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Orthopaedic Surgery - Acromioclavicular Joint Separation
Basics
Acromioclavicular joint separation is a common traumatic shoulder injury, particularly among physically active individuals who participate in contact sports. It most often results from a direct blow to the superior or superolateral aspect of the shoulder.
The injury occurs more frequently in males and may range from a mild sprain of the acromioclavicular joint capsule to complete disruption of the acromioclavicular and coracoclavicular ligaments with major displacement of the distal clavicle.
Stability of the acromioclavicular joint depends primarily on two ligamentous systems. The acromioclavicular ligaments provide mainly horizontal or anteroposterior stability, whereas the coracoclavicular ligaments provide vertical stability between the clavicle and scapula.
Rockwood Classification
The Rockwood classification is commonly used to describe acromioclavicular joint separations. It is based on the anatomical structures damaged and the degree and direction of distal clavicle displacement.
Types I and II mainly involve injury to the acromioclavicular joint capsule and ligament complex. Types III and higher involve more extensive disruption, including injury to the coracoclavicular ligaments.
Type I Injury
A type I injury consists of a sprain or partial injury of the acromioclavicular joint capsule and ligament.
There is no significant displacement of the distal clavicle, and radiographs usually appear normal.
The coracoclavicular ligaments remain intact.
Type II Injury
A type II injury involves more substantial disruption of the acromioclavicular capsule and ligament while the coracoclavicular ligaments remain intact or only mildly injured.
Radiographically, the coracoclavicular distance is increased by less than 25% compared with the opposite side.
There may be mild superior displacement of the distal clavicle, but gross deformity is uncommon.
Type III Injury
A type III injury involves complete disruption of both the acromioclavicular and coracoclavicular ligament complexes.
The distal clavicle appears displaced superiorly, with an increase in the coracoclavicular distance of approximately 25–100% compared with the contralateral side.
The apparent deformity is partly caused by the weight of the arm pulling the acromion and scapula downward relative to the clavicle.
A type III separation can usually be reduced temporarily by applying upward pressure beneath the arm.
Type IV Injury
A type IV injury is characterized by posterior displacement of the distal clavicle.
The clavicle may penetrate or become displaced through the trapezius muscle.
This injury is generally irreducible by simple upward pressure on the arm.
Posterior displacement is best appreciated clinically and on an axillary lateral radiograph.
Type V Injury
A type V injury represents a more severe version of a type III separation.
The coracoclavicular distance is increased by more than 100% compared with the opposite shoulder, sometimes reaching several times the normal distance.
There is significant disruption of the deltotrapezial fascia, and the distal clavicle may become prominent beneath the skin.
The distal clavicle may become incarcerated within the disrupted soft tissues, making the deformity irreducible.
Type VI Injury
A type VI injury is rare and involves inferior displacement of the distal clavicle.
The clavicle may become positioned beneath the acromion or coracoid.
Because of the severity and unusual direction of displacement, these injuries generally require operative treatment.
General Prevention
Complete prevention is difficult because most injuries occur suddenly during trauma.
Avoidance of high-risk contact sports or hazardous activities can reduce exposure to injury, although this is not practical for many athletes.
Appropriate protective equipment, proper tackling or falling techniques, and sports-specific conditioning may potentially reduce injury risk.
Epidemiology
Acromioclavicular joint separation occurs far more commonly in males, with a reported male-to-female ratio of approximately 8.5:1.
Around half of all injuries occur in individuals between 20 and 39 years of age.
Sporting activity is the most frequent mechanism of injury, particularly in contact and collision sports.
Among Rockwood classifications, type III injuries are among the most frequently encountered clinically significant separations.
Incidence
The overall reported incidence is approximately 1.8 injuries per 10,000 person-years.
Among athletes, the incidence is considerably higher and has been reported at approximately 9.2 per 1,000 person-years.
Rates vary depending on the type of sport and the degree of physical contact involved.
Risk Factors
The principal risk factor is participation in contact or collision sports.
Common high-risk activities include rugby, ice hockey, American football, and wrestling.
Male sex is also associated with a substantially greater incidence, likely reflecting patterns of participation in high-risk sporting activities.
Genetics
There is no recognized genetic predisposition to acromioclavicular joint separation.
The injury is traumatic and mechanical rather than inherited.
Etiology
The typical mechanism is a direct impact to the superolateral aspect of the shoulder, usually while the arm is adducted.
The force drives the acromion and scapula downward and medially while the clavicle remains relatively fixed.
Depending on the magnitude of the force, the acromioclavicular capsule, AC ligaments, coracoclavicular ligaments, and deltotrapezial fascia may fail sequentially.
Associated Conditions
ACJ separation is usually an isolated injury but may occasionally occur together with more severe injuries around the shoulder girdle.
A simultaneous sternoclavicular dislocation and ACJ injury can produce a so-called bipolar clavicle injury.
An associated scapular fracture can create a floating shoulder, particularly when disruption of the superior shoulder suspensory complex is present.
Rotator cuff contusion may also accompany the acute trauma.
Diagnosis
Signs and Symptoms
Patients usually develop immediate pain around the superior aspect of the shoulder.
Shoulder movement, particularly elevation and cross-body activity, typically increases pain.
Swelling and bruising may be present over the distal clavicle and ACJ.
Higher-grade injuries may produce an obvious deformity with prominence of the distal clavicle.
Some patients also report neck discomfort, numbness, or tingling, although major neurologic injury is uncommon.
Physical Examination
Type I and II injuries generally produce localized swelling and tenderness over the ACJ without major visible deformity.
Pain is often reproduced by cross-body adduction of the affected shoulder.
Type III and higher injuries may demonstrate obvious prominence of the distal clavicle.
The contour of the injured shoulder should always be compared with the opposite side.
Reducibility
The distinction between type III and type V injuries can be clinically important.
In a type III separation, applying upward pressure beneath the arm may temporarily reduce the deformity.
In a type V injury, reduction is usually not possible because the distal clavicle may be trapped within disrupted deltotrapezial tissue.
This distinction can influence treatment planning.
Type IV Examination Findings
A type IV injury may present with posterior prominence or protrusion of the distal clavicle.
The posterior displacement may be difficult to appreciate on a standard anteroposterior view, making clinical inspection and an axillary radiograph particularly important.
Neurovascular Examination
A complete neurovascular examination should be performed in all patients.
Although associated neurovascular injuries are uncommon, distal pulses, capillary refill, motor function, and sensation should be documented.
The remainder of the upper extremity should also be inspected and palpated to exclude additional injuries.
Stability Assessment
Anteroposterior and vertical stability of the acromioclavicular joint should be assessed gently.
The examiner should evaluate whether the distal clavicle is excessively mobile relative to the acromion.
In the acute setting, pain may make a detailed assessment of the rotator cuff, labrum, or biceps tendon difficult.
These structures may need reassessment after the acute pain subsides.
Imaging
Anteroposterior Radiographs
An anteroposterior radiograph of the affected ACJ is part of the initial evaluation.
The position of the distal clavicle relative to the acromion and the coracoclavicular distance should be assessed.
Comparison with the opposite shoulder can be particularly useful because normal anatomical measurements vary between individuals.
Zanca View
A Zanca view is commonly used for better visualization of the ACJ.
This radiograph is obtained with approximately 15° of cephalad angulation and provides a clearer assessment of the distal clavicle, acromion, and joint space.
It can help quantify superior displacement in type III and type V injuries.
Axillary Lateral View
An axillary lateral radiograph is important for identifying posterior displacement of the distal clavicle.
This view is particularly useful when a type IV injury is suspected.
Failure to obtain an axillary view can result in posterior displacement being overlooked.
Contralateral Comparison
An anteroposterior image of the opposite ACJ may be obtained to compare the coracoclavicular distance.
The coracoclavicular distance is measured from the superior surface of the coracoid to the inferior border of the clavicle.
The percentage increase compared with the uninjured side helps determine the Rockwood grade.
Additional Radiographs
Radiographs of the entire clavicle, shoulder, or scapula should be obtained when associated injury is suspected.
These images help exclude clavicle fracture, scapular fracture, coracoid fracture, shoulder dislocation, and other injuries.
A complete clavicle radiograph is particularly important when a bipolar clavicle injury is suspected.
Weighted Radiographs
Weighted stress radiographs were historically used to exaggerate displacement and distinguish lower-grade from higher-grade injuries.
However, these studies are uncomfortable and are generally not recommended routinely.
Some clinicians may still use them selectively when attempting to differentiate a type III from a type V injury.
Radiographic Appearance by Type
Type I and many type II injuries may appear normal or nearly normal on routine radiographs.
Type III injuries demonstrate approximately 25–100% increase in coracoclavicular displacement relative to the opposite side.
Type V injuries may demonstrate approximately 100–300% displacement.
Type IV injuries are defined by posterior displacement of the distal clavicle, best demonstrated on an axillary view.
CT and MRI
Computed tomography and MRI are not routinely required for an uncomplicated ACJ separation.
CT may be useful when associated fractures, complex shoulder girdle injuries, or a bipolar clavicle injury are suspected.
MRI is rarely necessary in the acute setting but may be considered when persistent symptoms suggest associated rotator cuff, labral, or other soft-tissue pathology.
Pathological Findings
Histopathological examination is not routinely required for this injury.
Diagnosis is established through clinical examination and imaging.
Differential Diagnosis
Important differential diagnoses include clavicle fracture, particularly a distal clavicle fracture, coracoid fracture, rib fracture, scapular fracture, shoulder dislocation, sternoclavicular dislocation, and proximal humeral fracture.
A coracoid fracture may mimic an ACJ separation, but the coracoclavicular relationship may remain intact.
A radiograph of the entire clavicle should be obtained when concern exists for a simultaneous sternoclavicular and acromioclavicular injury.
CT may be required when complex fracture patterns are suspected.
Treatment
General Principles
Treatment depends on the Rockwood grade, patient age, activity level, functional requirements, occupation, lifestyle, and individual goals.
Correct identification of the injury grade is important because management differs considerably between low-grade and high-grade injuries.
Type I and II Injuries
Type I and II injuries are generally treated nonoperatively.
Treatment includes short-term sling immobilization, analgesia, ice, and activity modification.
Movement is gradually restored as pain decreases.
Most patients recover good function without surgery.
Type III Injuries
Treatment of type III ACJ separation remains controversial.
Many patients can be treated successfully without surgery, especially those with lower physical demands.
Surgery may be considered in selected individuals with persistent pain, significant functional impairment, high occupational demands, cosmetic concerns, or elite athletic requirements.
The treatment decision should therefore be individualized.
Type IV to VI Injuries
Types IV, V, and VI are generally treated surgically because of marked displacement, soft-tissue disruption, instability, and difficulty obtaining or maintaining satisfactory reduction nonoperatively.
Operative stabilization aims to restore the relationship between the distal clavicle and scapula while allowing ligament healing or reconstruction.
Physical Therapy
Physical therapy is not universally required for minor injuries but may help patients regain motion, strength, and shoulder function.
For nonoperatively treated injuries, gentle range-of-motion exercises may begin approximately 2–4 weeks after injury, depending on pain and stability.
Initial exercises may include pendulum movements and pulley-assisted motion.
The program is gradually advanced toward full range of motion and strengthening over the following weeks.
Postoperative Rehabilitation
Physical therapy is routinely incorporated after surgical stabilization or reconstruction.
The exact protocol depends on the operative technique and surgeon preference.
Rehabilitation generally progresses from an initial period of protection to passive and active-assisted motion, followed by active movement, strengthening, and eventual return to sport or heavy activity.
Medication
First-line medications include nonsteroidal anti-inflammatory drugs and acetaminophen.
These medications can help control pain during the acute phase.
Short courses of stronger analgesics, including tramadol or other opioid medications, may occasionally be used for severe acute pain.
When prescribing these agents, the patient’s age, medical conditions, concurrent medications, and overall risk profile should be considered.
Sling and Local Measures
A sling is commonly used initially to support the arm and reduce traction on the injured ACJ.
Ice can help control swelling and pain during the early period.
Sleeping with the upper body elevated or in a reclined position may improve comfort during the first several days after injury.
Surgical Management
Surgery is generally recommended for type IV, V, and VI injuries, and it may be considered for selected type III injuries.
Surgery can also be performed for chronic type III or higher injuries when persistent pain, weakness, instability, or functional disability remains despite adequate nonoperative treatment.
Operative Techniques
A variety of operative methods are available.
Techniques may involve open reduction and internal fixation using plates, screws, suture-based devices, or other implants.
The objective is to restore anatomical or near-anatomical alignment and maintain stability while the damaged ligaments heal.
Some constructs permit earlier controlled shoulder motion.
Ligament Reconstruction
Modern reconstruction frequently involves restoration of the coracoclavicular ligament complex.
Autograft or allograft tendon tissue may be used to reconstruct the stabilizing ligaments.
Coracoid-based fixation devices are also commonly incorporated to restore vertical stability.
Technique selection depends on whether the injury is acute or chronic, the surgeon’s experience, and the quality of the surrounding tissues.
Chronic Injuries
Chronic ACJ separations can be more difficult to treat because the native ligaments have limited healing potential after a prolonged period.
Reconstruction may therefore require tendon graft augmentation or other biological reconstruction rather than simple fixation.
Persistent pain and instability are the most common indications for delayed surgery.
Follow-Up
Patients should be reviewed periodically to ensure that pain is improving, shoulder motion is recovering, and the alignment of the ACJ remains stable.
Although alignment usually remains unchanged after the initial injury, follow-up is important because an injury initially thought to be type I or II may occasionally prove to be of a higher grade.
Prognosis
The overall prognosis is generally good, particularly for low-grade injuries.
Athletes lose an average of approximately 18 days from sporting activity, although recovery varies significantly with injury severity.
Low-grade injuries may result in approximately 10 days of lost activity, whereas high-grade injuries may require approximately 64 days or longer before return.
Return to Sport
Return to sporting activity should be based on recovery of painless motion, strength, stability, and sport-specific function rather than on time alone.
Higher-grade injuries generally require substantially longer rehabilitation than type I or II injuries.
Some athletes with high-grade injuries elect to undergo surgical stabilization or reconstruction.
Surgical Outcomes
Good or excellent outcomes can be achieved after operative treatment when anatomical stability is restored and complications are avoided.
However, surgical treatment has a notable complication rate.
Some studies have reported overall complication rates approaching 27%, emphasizing the importance of careful patient selection and surgical technique.
Complications
Potential complications include infection, loss of reduction, clavicle fracture, graft rupture, adhesive capsulitis, implant failure, painful hardware, chronic instability, and post-traumatic ACJ arthritis.
Persistent deformity may also remain after both surgical and nonsurgical treatment, even when shoulder function is satisfactory.
Loss of Reduction
Loss of reduction is one of the more important postoperative complications.
It may result from failure of fixation, graft stretching, recurrent trauma, or inadequate biological healing.
Minor radiographic loss of alignment does not always produce symptoms, but major recurrent displacement may lead to pain or instability.
Hardware-Related Problems
Internal fixation devices may become prominent or painful, particularly in thin individuals.
Implant breakage, migration, or irritation may occasionally require additional surgery for removal.
The risk varies according to the reconstruction method used.
Chronic Instability and Arthritis
Residual horizontal or vertical instability may persist after treatment.
Abnormal joint mechanics can contribute to later development of post-traumatic acromioclavicular joint arthritis.
Some patients develop chronic pain despite satisfactory radiographic alignment.
Patient Monitoring
Patients should be followed at regular intervals during recovery.
Clinical assessment should include pain severity, shoulder range of motion, strength, joint stability, deformity, and ability to perform daily or sporting activities.
Radiographs may be repeated when there is concern about increasing displacement, loss of fixation, or an initially underestimated injury grade.
The main goals of follow-up are to ensure satisfactory pain control, progressive recovery of motion and strength, and maintenance of appropriate ACJ alignment.
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Orthopaedic Surgery - Acromioclavicular Joint Arthritis
Basics
Acromioclavicular joint arthritis is the most common disorder affecting the acromioclavicular joint (ACJ). Degenerative changes typically begin during the third or fourth decade of life and become increasingly common with advancing age.
Degeneration of the ACJ is more frequent than osteoarthritis of the glenohumeral joint. The ACJ is formed by the distal clavicle articulating with the acromion, and a small fibrocartilaginous disc is normally present between the opposing articular surfaces.
ACJ arthritis may occur as an isolated degenerative condition, as part of an inflammatory arthropathy, or together with other painful shoulder disorders. Frequently associated conditions include rotator cuff tears, biceps tendinopathy, and adhesive capsulitis.
The condition is particularly common in individuals who repeatedly load the shoulder overhead, including manual laborers, weight lifters, and overhead athletes.
General Prevention
Prevention is difficult because the exact cause of ACJ osteoarthritis is multifactorial and not completely understood.
Degeneration appears to result from a combination of genetic susceptibility and environmental exposure, particularly repetitive mechanical loading.
In patients with rheumatoid arthritis, early and effective control of systemic inflammatory disease can reduce the severity and progression of ACJ involvement.
Epidemiology
Manual laborers have an increased prevalence of ACJ arthritis. The likelihood of degeneration appears to rise with the number of years spent performing manual work.
There may also be a weak association with prolonged exposure to vibration during occupational activity.
The frequency of ACJ degeneration increases substantially with age.
Incidence
The true incidence of symptomatic ACJ arthritis is uncertain because radiographic degeneration is common even in individuals without shoulder pain.
Anatomical studies have demonstrated degenerative ACJ changes in approximately 11.6% of cadaveric specimens, with increasing prevalence in older individuals and no significant difference between males and females or between the right and left sides.
Ultrasound studies have shown evidence of ACJ osteoarthritis in approximately 65% of asymptomatic men between 40 and 79 years of age.
ACJ involvement is also common in inflammatory disease, with arthritis of the joint reported in approximately 59% of patients with rheumatoid arthritis.
Risk Factors
Important risk factors include advancing age, previous ACJ separation, prior distal clavicle fracture, manual labor, and participation in sports involving repetitive shoulder loading.
Patients with spinal cord injury have been reported to have a substantially increased risk of severe ACJ degeneration, possibly up to four times that of the general population.
Certain anatomical features may also predispose to ACJ pathology, including a type III acromion and a relatively narrow supraspinatus outlet.
Genetics
Osteoarthritis has a familial tendency, suggesting a genetic contribution to susceptibility.
However, the specific genes involved in the development of ACJ osteoarthritis remain poorly defined.
Genetic predisposition likely interacts with age, mechanical loading, occupational exposure, and previous injury.
Etiology
Primary osteoarthritis of the ACJ probably develops through an interaction between genetic susceptibility and cumulative mechanical stress.
Repetitive heavy lifting, weight training, and overhead sporting activities can accelerate articular cartilage degeneration.
In rheumatoid arthritis, synovial inflammation leads to pannus formation and release of destructive inflammatory mediators that progressively damage the articular cartilage and subchondral bone.
Osteonecrosis and Post-Traumatic Arthritis
Avascular necrosis of the distal clavicle may cause subchondral bone death, structural collapse, and secondary arthritis.
Post-traumatic arthritis may occur after a distal clavicle fracture. Irregular healing or joint incongruity can alter load distribution across the ACJ and lead to abnormal wear.
Similarly, previous acromioclavicular joint separation can damage cartilage and bone while also producing ligamentous laxity or soft-tissue contracture. These changes alter joint mechanics and may eventually result in degenerative arthritis.
Associated Conditions
ACJ arthritis frequently coexists with other abnormalities of the shoulder.
Associated conditions include distal clavicle osteolysis and ACJ cyst formation.
Rotator cuff tears have been reported in a high proportion of patients with symptomatic ACJ arthritis, while labral pathology and biceps tendon abnormalities may also occur.
Reported associations include approximately 81% with rotator cuff tears, 33% with labral tears, and 22% with biceps tendon abnormalities in selected patient populations.
Diagnosis
Signs and Symptoms
Pain may be sharply localized directly over the ACJ or may present less specifically as aching involving the superior shoulder or adjacent neck region.
Symptoms are commonly aggravated by overhead activity, reaching across the body, lifting, or weight-bearing through the upper extremity.
Patients may also experience nocturnal pain, particularly when lying on the affected shoulder.
Physical Examination
Patients frequently identify the ACJ itself as the precise source of pain.
Shoulder range of motion is usually preserved, with both active and passive motion remaining relatively intact unless another shoulder disorder is present.
Both shoulders should be inspected and compared for asymmetry, deformity, swelling, or prominence of the distal clavicle.
Palpation
The ACJ is typically tender to direct palpation in symptomatic patients.
However, firm pressure over the joint may also cause discomfort in asymptomatic individuals. Tenderness should therefore be compared with the opposite shoulder and correlated with the patient’s usual symptoms.
Localized pain that reproduces the patient’s typical complaint is more clinically meaningful than tenderness alone.
Cross-Body Adduction Test
The cross-body adduction test is commonly used to provoke pain from the ACJ.
The shoulder is flexed to approximately 90° and then brought horizontally across the chest into adduction.
Reproduction of focal pain directly over the ACJ is considered a positive finding and supports the diagnosis of ACJ pathology.
Active Compression Test
The active compression test may also help identify ACJ pathology.
The arm is forward flexed to approximately 90° and adducted slightly across the body, usually by about 10°.
Resistance is applied while the forearm is pronated, and the maneuver is then repeated with the forearm supinated.
Pain localized to the ACJ during resisted pronation that improves or disappears with resisted supination is considered a positive test.
Imaging
Plain Radiographs
Standard shoulder radiographs are usually sufficient for initial evaluation of the ACJ.
Typical degenerative findings include joint-space narrowing, marginal osteophytes, subchondral sclerosis, cyst formation, and irregularity of the distal clavicle or acromial surface.
However, radiographic findings must be interpreted together with the clinical examination because degenerative changes are common in asymptomatic individuals.
Zanca View
The Zanca view provides a particularly useful radiographic assessment of the ACJ.
This projection uses approximately 15° of cephalad angulation, allowing improved visualization of the joint space and distal clavicle compared with routine shoulder radiographs.
It can help demonstrate subtle joint-space narrowing, osteophytes, distal clavicular changes, and other ACJ abnormalities.
Limitations of Radiographs
Radiographic appearance does not always correlate with symptoms.
Some patients have substantial degenerative changes on imaging but remain completely asymptomatic.
Conversely, patients may have significant ACJ pain despite apparently normal or only mildly abnormal radiographs because cartilage wear may not always be visible on routine imaging.
Clinical correlation is therefore essential.
MRI
MRI is not routinely required when isolated ACJ arthritis is clinically obvious.
It becomes useful when the diagnosis is uncertain or when additional shoulder pathology is suspected.
In symptomatic ACJ arthrosis, MRI may demonstrate edema within the distal clavicle or adjacent acromion, which can support the diagnosis.
MRI is particularly helpful for identifying associated rotator cuff tears, labral pathology, biceps tendon disease, or other soft-tissue disorders.
Ultrasonography
Ultrasound may demonstrate osteophytes, narrowing of the ACJ, capsular abnormalities, and associated soft-tissue pathology.
It can also be used to guide needle placement for joint aspiration or corticosteroid injection, improving the accuracy of intra-articular procedures.
Pathological Findings
Histopathological examination is not routinely required for the diagnosis of ACJ arthritis.
Diagnosis is usually established clinically with the assistance of imaging and, when necessary, a diagnostic injection.
Differential Diagnosis
Important conditions that may mimic ACJ arthritis include ACJ infection, osteonecrosis of the distal clavicle, distal clavicle osteolysis, and ACJ cyst formation.
Crystal arthropathies such as gout or calcium pyrophosphate deposition disease should also be considered in appropriate patients.
Other shoulder disorders that can produce similar symptoms include superior labral anterior-posterior (SLAP) tears, rotator cuff tears or tendinitis, and biceps tendinopathy.
Treatment
General Measures
Initial management is usually nonoperative.
Treatment should focus on reducing painful mechanical loading while maintaining shoulder mobility and function.
A diagnostic injection of local anesthetic, such as lidocaine, into the ACJ may be useful when the source of pain is uncertain.
Significant temporary pain relief following injection supports the ACJ as the primary pain generator.
Activity Modification
Patients should reduce or temporarily avoid activities that reproduce pain.
Examples include heavy bench pressing, repetitive overhead lifting, cross-body loading, and sleeping directly on the affected shoulder.
Modification rather than complete cessation of activity is usually appropriate.
Ice and Heat
Ice may be helpful during painful inflammatory exacerbations, particularly after activity.
Heat can sometimes reduce stiffness and improve comfort before exercise or rehabilitation.
The choice depends largely on patient preference and symptom response.
Physical Therapy
Physical therapy has a less clearly established role in isolated ACJ arthritis than in many other shoulder disorders.
Because the degenerative process is localized to a small joint, therapy cannot reverse the underlying cartilage damage.
Nevertheless, selected patients may benefit from a short course of rehabilitation aimed at optimizing shoulder mechanics, maintaining motion, and strengthening the surrounding musculature.
Physical therapy may be particularly valuable when ACJ arthritis coexists with rotator cuff weakness, scapular dysfunction, or other shoulder abnormalities.
Medication
First-line pharmacological treatment commonly includes nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen.
These medications may reduce pain and improve tolerance of daily activities.
Medication should generally be combined with activity modification rather than used as the sole treatment.
Corticosteroid Injection
Injection of corticosteroid into the ACJ can provide both diagnostic and therapeutic benefit.
A local anesthetic is commonly combined with corticosteroid.
Pain relief may be temporary, but injections can reduce inflammation and improve shoulder function in appropriately selected patients.
Repeated injections should be used cautiously, particularly if only brief benefit is obtained.
Surgery
Surgical treatment is generally reserved for patients with persistent symptoms despite an adequate trial of nonoperative management.
The standard operative treatment is distal clavicle excision, also known as distal clavicle resection.
The procedure removes a small portion of the distal clavicle to eliminate painful bone-to-bone contact while preserving overall shoulder function.
Open Distal Clavicle Excision
Distal clavicle excision may be performed using an open surgical approach.
The distal portion of the clavicle is resected while attempting to preserve the stabilizing structures of the ACJ.
Careful repair of the deltotrapezial fascia is important because inadequate closure may contribute to weakness, deformity, or postoperative pain.
Arthroscopic Distal Clavicle Excision
Arthroscopic resection can achieve the same basic goal through a minimally invasive technique.
Potential advantages include smaller incisions, reduced soft-tissue disruption, and the ability to assess and treat associated intra-articular or subacromial shoulder pathology during the same procedure.
Appropriate resection is essential because insufficient bone removal may leave persistent contact and pain, whereas excessive resection can produce instability.
Follow-Up
Patients managed conservatively should be reviewed periodically, often at intervals of approximately 3–4 months, depending on symptom severity and treatment response.
At follow-up, pain, function, range of motion, activity tolerance, and associated shoulder pathology should be reassessed.
Patients whose symptoms remain localized and disabling despite conservative treatment may be considered for surgical management.
Postoperative Care
After distal clavicle excision, a sling is commonly provided for comfort during the early postoperative period.
Active shoulder range-of-motion exercises can generally begin as pain permits.
Rehabilitation is advanced progressively according to wound healing, pain, strength, and the presence of any additional procedures performed during surgery.
Prognosis
The prognosis is generally favorable.
Intra-articular ACJ injections can provide short-term pain relief and may improve shoulder range of motion, although the duration of benefit varies considerably among patients.
Both open and arthroscopic distal clavicle excision have been associated with good clinical outcomes when the diagnosis is accurate and an adequate but not excessive amount of bone is removed.
Factors Affecting Outcome
Surgical results may be less predictable in patients involved in workers’ compensation claims, ongoing litigation, or very heavy manual occupations.
Persistent symptoms may also occur when associated shoulder disorders are not recognized before surgery.
Rotator cuff, biceps, labral, and other shoulder abnormalities should therefore be evaluated and treated when clinically appropriate.
Complications
The most common postoperative problem is persistent pain.
One important cause is inadequate distal clavicle resection, leaving residual contact between the clavicle and acromion.
Excessive resection or overly aggressive disruption of the surrounding ligaments may instead produce ACJ instability.
Other Surgical Complications
Additional complications include infection, postoperative stiffness, fracture, complex regional pain syndrome, and heterotopic ossification.
Regrowth or reossification of the distal clavicle may occasionally recreate painful contact.
Following open surgery, inadequate repair of the deltoid or deltotrapezial fascia may cause deltoid dehiscence, weakness, and persistent discomfort.
Patient Monitoring
Patients undergoing nonoperative treatment should be reassessed regularly to determine whether symptoms are improving and whether additional investigations or interventions are needed.
After surgery, monitoring should include wound healing, pain, shoulder motion, strength, ACJ stability, and return to functional activity.
The sling is used primarily for comfort, and active range of motion can generally be advanced as pain allows.
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Orthopaedic Surgery - Achondroplasia
Basics
Achondroplasia is the most common skeletal dysplasia and is characterized by disproportionate short stature caused primarily by impaired endochondral bone growth.
Adult height is usually less than approximately 4.5 ft, with the greatest shortening affecting the proximal portions of the limbs, particularly the humerus and femur. This pattern of proximal limb shortening is known as rhizomelia.
Typical craniofacial features include frontal bossing and midface hypoplasia. Although degenerative arthritis is uncommon, spinal stenosis is one of the most important and potentially serious complications.
The disorder primarily affects the skeletal and neurologic systems. Characteristic skeletal features include ligamentous laxity and impaired longitudinal growth of the long bones. Neurologic complications may result from narrowing of the foramen magnum in infancy or lumbar spinal stenosis later in life.
Most characteristic features are already apparent at birth. In heterozygous individuals, life expectancy is usually near normal.
Epidemiology
Achondroplasia affects males and females approximately equally.
The frequency of spinal stenosis and degenerative disc disease increases with age. Neurologic manifestations may begin during childhood, although they become considerably more common in later adulthood.
Approximately 10% of affected individuals may demonstrate neurologic signs by around 10 years of age, while a much larger proportion may develop findings such as neurogenic claudication, hyperreflexia, or other manifestations of spinal stenosis by the sixth decade.
Prevalence
Achondroplasia occurs in approximately 1 in 15,000 individuals.
It is found across different populations and ethnic groups and represents the most frequently encountered form of disproportionate short-limb dwarfism.
Risk Factors
Advanced paternal age has been associated with an increased risk of new mutations causing achondroplasia, with parental age greater than approximately 33 years identified as a contributing factor in some studies.
Having an affected parent also increases the likelihood that a child will inherit the disorder because achondroplasia follows an autosomal dominant inheritance pattern.
Genetics
Achondroplasia is inherited as an autosomal dominant condition.
However, approximately 80% of affected individuals are born to parents of average stature and develop the disorder as a result of a new spontaneous mutation.
When one parent has achondroplasia, each child has a 50% chance of inheriting the affected gene.
When both parents have achondroplasia, there is a possibility of inheriting two abnormal copies of the gene. The homozygous form is usually lethal in early infancy.
Pathophysiology
The primary abnormality occurs within the growth plates, where there is reduced cellular organization and diminished chondrocyte activity.
This causes defective endochondral ossification, resulting in impaired longitudinal bone growth.
The overall width of the growth plate may remain relatively normal, but microscopic examination demonstrates disruption of the usual orderly arrangement of cartilage cells into longitudinal columns.
Other tissues and bone formed by intramembranous ossification remain largely normal.
Because circumferential growth of the shafts of long bones depends primarily on membranous bone formation, the bones may maintain relatively normal thickness despite marked reduction in length.
Characteristic skeletal changes can be recognized radiographically as early as approximately 3 months of gestation.
Etiology
Achondroplasia results from an abnormality involving the fibroblast growth factor receptor 3 (FGFR3) protein.
The pathologic process begins during fetal development. Excessive FGFR3 signaling inhibits normal chondrocyte proliferation and maturation at the epiphyseal growth plates.
As a result, cartilage growth becomes slowed and disorganized, leading to reduced longitudinal growth of the long bones.
Associated Conditions
Common associated problems include spinal stenosis, possible hydrocephalus, and a tendency toward overweight or obesity.
Neurologic complications may arise from compression at the foramen magnum during infancy or narrowing of the spinal canal later in life.
Diagnosis
Signs and Symptoms
The characteristic physical appearance is usually evident at birth.
Affected individuals have disproportionately short stature, a relatively long trunk, and pronounced proximal shortening of the limbs.
The thighs and upper arms are affected more severely than the distal portions of the extremities.
A large head with a prominent forehead and parietal or frontal bossing is common, together with midfacial hypoplasia.
Lower Limb Findings
The lower extremities may appear relatively straight in infancy, but genu varum frequently develops as the child grows.
Ligamentous laxity may contribute to progressive angular deformity of the knees.
Internal tibial torsion may accompany the varus deformity.
Children may also demonstrate varus-valgus instability and knee hyperextension.
Upper Limb and Hand Findings
The upper limbs demonstrate marked rhizomelic shortening, particularly involving the humerus.
The fingers are typically short, broad, and relatively thick.
A characteristic separation between the middle and ring fingers produces the classic “trident hand”, in which the fingers appear divided into three groups.
Elbow extension may be limited, and some patients develop flexion contractures or radial head abnormalities. These findings usually cause relatively minor functional impairment.
Spine and Posture
An exaggerated lumbar lordosis is common and is frequently associated with anterior pelvic tilt.
A thoracolumbar kyphosis may develop during infancy, particularly around the time the child begins sitting.
In many children, this kyphosis improves after independent walking develops and is subsequently replaced by increased lumbar lordosis.
A waddling gait is common because of altered limb proportions, hip mechanics, and lumbar posture.
Adult Height
Adult height typically ranges from approximately 42 to 56 inches.
Despite marked short stature, most individuals are capable of independent mobility and participation in routine activities of daily living.
Neurologic Manifestations
Spinal canal narrowing can produce several neurologic complications.
Lumbar stenosis may develop from narrowing of the spinal canal, disc prolapse, osteophyte formation, and characteristic vertebral abnormalities.
Compression of the spinal cord or nerve roots may lead to neurogenic claudication, weakness, sensory changes, and, in severe cases, bladder dysfunction.
Cervical or thoracic stenosis may produce upper motor neuron findings such as hyperreflexia.
History
A detailed developmental history should be obtained.
Children with achondroplasia often reach gross motor milestones later than children of average stature because of short limbs, relative hypotonia, and altered body proportions.
However, developmental expectations should be compared with achondroplasia-specific developmental standards, rather than with conventional pediatric milestones.
Cognitive development is generally normal.
In some infants, narrowing at the foramen magnum may improve as growth progresses, although persistent or severe compression requires careful monitoring.
Physical Examination
Head and Face
Typical findings include frontal bossing, a relatively large head, and midface hypoplasia.
Spine
The spine should be assessed for exaggerated lumbar lordosis, thoracolumbar kyphosis, scoliosis, and evidence of neurologic compression.
Thoracolumbar kyphosis commonly becomes apparent at approximately sitting age.
Extremities
The limbs are shortened, particularly proximally at the humerus and femur.
Muscles may appear prominent because of the relative shortness of the underlying bones.
Elbow flexion contracture may be present, sometimes associated with radial head dislocation.
The hands often demonstrate the characteristic trident configuration.
Genu varum is common, and varus-valgus laxity or hyperextension may be observed during childhood.
Neurologic Examination
Adults should be assessed carefully for evidence of lumbar spinal stenosis, including weakness in the ankles or feet, sensory abnormalities, changes in gait, and bladder dysfunction.
Hyperreflexia may suggest cervical or thoracic spinal cord compression.
Serial neurologic examination is important throughout life because neurologic complications can develop gradually.
Laboratory Tests
There are no characteristic routine laboratory abnormalities associated with achondroplasia.
Diagnosis is generally based on characteristic clinical and radiographic findings.
Genetic testing is not routinely required when the phenotype is typical, although molecular testing may be useful in diagnostically uncertain cases.
Imaging
Skull Radiographs
Characteristic cranial findings include a shortened skull base and a relatively enlarged cranium.
Frontal and occipital prominence may be evident.
The foramen magnum is characteristically small, contributing to the risk of cervicomedullary compression during infancy.
Lumbar Spine Radiographs
Typical findings include progressive narrowing of the interpedicular distance in the lower lumbar spine, spinal canal stenosis, and posterior scalloping of the vertebral bodies.
These abnormalities contribute to the high incidence of lumbar stenosis in adulthood.
Thoracolumbar Spine
Thoracolumbar kyphosis is common in infancy.
In many children, the kyphosis resolves after independent walking begins and is subsequently replaced by exaggerated lumbar lordosis.
Persistent or progressive kyphosis requires close observation because severe deformity can increase the risk of neurologic compromise.
Pelvic Radiographs
The pelvis is characteristically broad with short, wide, and relatively square iliac wings.
The greater sciatic notches are small and deep.
The superior acetabular margins tend to be relatively horizontal.
These pelvic abnormalities contribute to the characteristic body proportions and lower-limb alignment.
MRI
MRI of the brain, craniocervical junction, and upper cervical spinal cord should be considered when an infant or child demonstrates developmental delay exceeding expected achondroplasia-specific norms or when signs suggest neurologic compression.
MRI can identify brainstem compression, upper cervical cord abnormalities, hydrocephalus, and stenosis of the foramen magnum.
MRI is also useful when symptoms of lumbar or cervical spinal stenosis develop later in life.
Diagnostic Procedures
Sleep studies may be considered in infants with developmental delay or symptoms suggestive of sleep-disordered breathing.
Sleep abnormalities may indicate compression around the foramen magnum or cervicomedullary junction.
Routine genetic testing is generally unnecessary in individuals with classic clinical and radiographic findings.
Pathological Findings
There are no specific gross pathological findings beyond the characteristic growth plate abnormalities associated with defective endochondral ossification.
Other tissues are generally structurally normal.
Differential Diagnosis
Pseudoachondroplasia
Pseudoachondroplasia can also produce disproportionate short stature but typically has a normal facial appearance.
Radiographs demonstrate irregular epiphyses, particularly around the hips and knees.
Hypochondroplasia
Hypochondroplasia generally produces a milder phenotype.
Adult height is commonly greater than approximately 54 inches, craniofacial abnormalities are less pronounced, and significant spinal stenosis is less characteristic.
The typical progressive caudal narrowing of the interpedicular distance seen in achondroplasia may also be absent or less pronounced.
Treatment
General Measures
There is no treatment that completely corrects the underlying growth plate abnormality responsible for achondroplasia.
Management therefore focuses on prevention and treatment of complications, maintenance of function, and correction of specific musculoskeletal deformities when necessary.
Osteotomy may occasionally be required for significant angular deformities of the limbs.
Management of Back Pain
Adults with low back pain are initially managed with appropriate conservative measures, including activity modification, analgesia, physical therapy, and management of contributing mechanical factors.
Persistent neurologic symptoms require evaluation for spinal stenosis.
Neurologic Complications
Neurologic problems such as hydrocephalus, spinal cord compression, nerve root compression, severe spinal stenosis, or paraplegia may require surgical treatment.
Close neurologic surveillance is therefore an important part of long-term care.
Foramen Magnum Stenosis
Severe narrowing of the foramen magnum during infancy can compress the brainstem and upper cervical spinal cord.
When clinically significant compression is present, foramen magnum decompression may be required.
The procedure should be performed by an experienced neurosurgical team, ideally following multidisciplinary evaluation.
Thoracolumbar Kyphosis
Thoracolumbar kyphosis should be monitored throughout infancy and childhood.
If significant kyphosis persists beyond approximately 2–3 years of age, bracing may be considered.
Persistent severe deformity may eventually require surgical correction.
Lumbar Spinal Stenosis
Severe lumbar spinal stenosis may require decompressive surgery.
A laminectomy may be performed when progressive neurologic symptoms, significant claudication, weakness, or functional impairment are present.
Fusion may also be required in skeletally immature patients or when severe kyphosis or instability is present.
Activity and Lifestyle
Routine restriction from sporting activity is usually unnecessary unless specific neurologic or orthopedic complications are present.
Environmental modifications can improve independence.
Custom-designed chairs, appropriately positioned household equipment, and automobile hand controls can be particularly useful.
Developmental Monitoring
Children with achondroplasia should not be assessed exclusively according to developmental milestones established for children of average stature.
Gross motor milestones are often delayed because of short limbs, joint laxity, hypotonia, and altered body proportions.
Cognitive and language development are usually normal and tend to occur at expected ages.
Physical Therapy
Physical therapy can assist children in adapting to their environment and developing functional mobility.
Therapists may also monitor motor development, posture, strength, joint motion, spinal alignment, and lower-limb deformities.
Therapy should focus on optimizing function without forcing developmental activities that may increase spinal deformity.
Surgical Management
Tibial Valgus-Derotation Osteotomy
A tibial valgus-derotation osteotomy may be indicated for persistent genu varum associated with internal tibial torsion.
The procedure corrects both angular and rotational deformity of the tibia.
Fibular shortening has not been clearly demonstrated to provide consistent benefit in achondroplasia.
Spinal Fusion
Spinal fusion may be indicated for severe thoracolumbar kyphosis exceeding approximately 40° when the deformity does not respond adequately to bracing.
Surgery is most commonly considered in persistent severe deformity by approximately 8–10 years of age.
Surgeons must recognize that pedicle anatomy and vertebral morphology in achondroplasia differ substantially from those of the average spine, making instrumentation technically challenging.
Laminectomy
When decompression is required for spinal stenosis, it often needs to be extensive.
In many cases, decompression involves most or all of the lumbar spine and may extend into the lower thoracic region.
Severe kyphosis may need to be corrected simultaneously, particularly in growing children or when deformity contributes to neural compression.
One important operative complication is dural tear, which occurs relatively frequently in decompressive surgery in the achondroplastic spine.
Limb Lengthening
Limb-lengthening procedures can produce substantial increases in overall height.
Lengthening may also improve lumbar lordosis and potentially reduce some manifestations of spinal stenosis by stretching tight hamstrings and changing lower-limb mechanics.
However, achieving proportionate stature usually requires staged bilateral lengthening of the femora, tibiae, and often the humeri, making treatment prolonged and demanding.
The overall treatment program may continue for several years.
Humeral Lengthening
Humeral lengthening using monolateral external fixation can provide significant increases in upper-limb length and may improve functional reach.
Potential complications include radial nerve palsy, infection, joint stiffness, and problems with regenerate bone formation.
Excessive Limb Lengthening
Lengthening of the lower extremity beyond approximately 50% of the original bone length is associated with a higher risk of complications.
These may include impaired subsequent bone growth, reduced range of motion in adjacent joints, delayed regenerate bone formation, prolonged treatment, and delayed return to full weight-bearing.
Careful patient selection and staged planning are therefore essential.
Foramen Magnum Decompression
Foramen magnum decompression should be considered when clinically significant neurologic compression persists or progresses.
Because of the anatomical complexity and neurologic risk, the operation should be undertaken by an experienced neurosurgeon after multidisciplinary discussion.
Follow-Up
Patients with achondroplasia require long-term orthopedic and neurologic follow-up because complications can develop at different stages of life.
Particular attention should be paid to spinal alignment, lower-limb deformities, neurologic function, gait, strength, and bladder control.
Prognosis
The overall prognosis for individuals with heterozygous achondroplasia is generally good.
Approximately two-thirds of children with thoracolumbar kyphosis experience spontaneous improvement after about one year of independent walking.
There is generally no major visceral organ involvement.
The rare homozygous form is usually lethal within the first weeks or months of life.
Heterozygous individuals usually have a near-normal life span and normal intelligence.
Most individuals are able to live independently and participate fully in daily life, although adaptations may be required because of short stature.
Mortality Considerations
Compared with the general population, individuals with achondroplasia have an increased risk of mortality from neurologic and cardiovascular complications.
Reported data suggest an approximately eight-fold higher risk of neurologic-related mortality and an approximately three-fold higher risk of mortality from cardiac causes.
Careful monitoring of neurologic symptoms, sleep-disordered breathing, obesity, and cardiovascular risk factors is therefore important.
Complications
Important complications include spinal stenosis, nerve root compression, and knee pain associated with genu varum and abnormal lower-limb mechanics.
Other possible complications include foramen magnum stenosis, hydrocephalus, thoracolumbar kyphosis, lumbar lordosis, degenerative spinal disease, obesity, and sleep-disordered breathing.
Patient Monitoring
Because individuals with achondroplasia have a high lifetime risk of musculoskeletal and neurologic complications, regular clinical assessment is recommended.
Periodic examination should include evaluation of limb strength, gait, reflexes, spinal alignment, lower-limb deformity, and functional capacity.
Bladder function should also be reviewed because changes in urinary control may be an early indicator of significant spinal cord or nerve root compression.
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Orthopaedic Surgery - Achilles Tendinitis
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Basics
Achilles tendinitis is a common overuse disorder involving the Achilles tendon and the surrounding soft tissues. It represents a spectrum of conditions that may affect the tendon itself, the paratenon surrounding it, and the retrocalcaneal bursa.
The clinical spectrum ranges from acute painful inflammation of the Achilles tendon and its surrounding sheath to chronic degenerative tendinosis, partial tearing, or eventual tendon rupture.
Several related terms are commonly used. Retrocalcaneal bursitis refers to inflammation of the retrocalcaneal bursa without primary involvement of the Achilles tendon. Paratenonitis describes inflammation of the paratenon surrounding the tendon. Achilles tendinitis refers to acute inflammatory changes within the tendon, frequently associated with inflammation of the paratenon. Tendinosis describes chronic degeneration of the tendon substance with structural deterioration rather than predominantly acute inflammation.
Achilles tendon disorders are also described according to their location. Noninsertional disease usually occurs several centimeters proximal to the attachment of the tendon to the calcaneus, whereas insertional disease occurs directly at the posterior calcaneal attachment.
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General Prevention
Prevention focuses primarily on avoiding excessive or abrupt mechanical loading of the Achilles tendon. Repetitive uphill running should be limited, particularly when an athlete is not adequately conditioned.
Training errors should also be avoided. Running distance, speed, or intensity should be increased gradually rather than suddenly, because rapid increases in mileage are an important contributor to Achilles tendon overload.
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Epidemiology
Achilles tendinopathy is particularly common among recreational and competitive athletes, especially distance runners. It is also frequently encountered in physically active middle-aged adults.
The apparent male-to-female distribution generally reflects the proportion of men and women participating in the relevant sporting activity rather than a marked biological sex difference.
Chronic degenerative Achilles tendinosis can also occur in middle-aged and elderly patients who do not regularly participate in sports. Therefore, although athletic overuse is an important cause, Achilles tendon degeneration is not restricted to athletes.
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Incidence
Achilles tendon disorders have been reported in approximately 6% of runners, emphasizing the close relationship between repetitive running activity and tendon overload.
The typical area of tenderness in noninsertional Achilles tendinitis is located above the heel, usually involving a relatively broad region of the tendon.
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Risk Factors
Several systemic and local factors increase the likelihood of developing Achilles tendon disease. A prominent posterosuperior calcaneal tuberosity, commonly referred to as a Haglund prominence or Haglund process, may increase mechanical irritation around the insertion of the tendon.
Systemic conditions associated with microvascular impairment may predispose the tendon to degeneration. These include diabetes mellitus, systemic lupus erythematosus, rheumatoid disease, and other connective-tissue disorders.
Patients with chronic renal disease who undergo hemodialysis or peritoneal dialysis may also have increased susceptibility to Achilles tendon abnormalities.
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Pathophysiology
The Achilles tendon is composed predominantly of type I collagen, which accounts for approximately 95% of its collagen content. At rest, the collagen fibers have a characteristic wavy arrangement that allows the tendon to elongate and absorb force during activity.
The tendon is surrounded throughout most of its length by a thin, gliding paratenon. This tissue functions as an elastic sleeve that allows the tendon to move freely relative to surrounding structures.
Blood supply to the Achilles tendon is provided by intrinsic vessels originating from the musculotendinous and osteotendinous junctions, together with an extrinsic vascular supply derived from the paratenon.
A relatively hypovascular region exists approximately 2–6 cm proximal to the calcaneal insertion. This region corresponds closely with the common site of noninsertional Achilles tendinopathy and rupture.
True chronic inflammatory changes involving the tendon and paratenon are relatively uncommon. By contrast, tendinosis, characterized by chronic mucoid degeneration and disruption of the normal collagen architecture, is considerably more common.
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Etiology
Training errors account for a substantial proportion of cases, with approximately 60–80% related to inappropriate changes in physical activity. A sudden increase in running distance or intensity, a change in footwear, or a change in the training surface may overload the tendon.
Running on hills, rough ground, or uneven terrain increases the mechanical demand on the Achilles tendon. Improper footwear can further alter lower-limb mechanics and increase tendon stress.
Adverse environmental conditions such as snow, ice, or cold weather may also contribute by changing running mechanics or reducing tissue flexibility.
Biomechanical abnormalities anywhere along the kinetic chain, extending from the lumbar spine to the foot, may increase Achilles loading. Examples include excessive pronation, pes cavus, and leg-length discrepancy.
Insufficient preparation before exercise is another contributing factor. Repeatedly performing vigorous activity after an inadequate, shortened, or absent warm-up and stretching period may predispose the tendon to injury.
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Associated Conditions
An important associated condition is Achilles tendon rupture. Chronic tendon degeneration may progressively weaken the tendon and increase the risk of partial or complete rupture.
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Diagnosis
Signs and Symptoms
Patients usually describe a gradually increasing area of pain, swelling, and warmth along the course of the Achilles tendon. Symptoms may occur anywhere from the musculotendinous junction to the calcaneal insertion.
The most common location of pain is approximately 3–5 cm proximal to the tendon insertion on the calcaneus.
Repetitive microtrauma, such as continued running, often worsens the symptoms. An acute increase in force, such as a single powerful jump, may also produce sudden deterioration in a previously symptomatic tendon.
Pain typically improves to some degree with rest, although chronic cases may remain symptomatic during routine daily activities.
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Physical Examination
The ankle should be assessed for pain during dorsiflexion, as stretching the Achilles tendon may reproduce symptoms.
The entire tendon should be palpated carefully to identify the precise site of tenderness. In severe inflammatory cases, the tendon sheath may feel thickened or swollen, and crepitus may be present during ankle movement.
The examiner should also assess for nodular thickening or focal swelling within the tendon, which may indicate chronic tendinosis.
A Thompson test should be performed whenever tendon rupture is a concern. Failure of plantarflexion during calf compression suggests disruption of the Achilles tendon.
Swelling, warmth, or a boggy sensation immediately anterior to the insertion of the tendon is more suggestive of retrocalcaneal bursitis.
A single-limb heel-rise test is useful for evaluating Achilles tendon function and strength.
The remainder of the lower limb should also be assessed for structural abnormalities that may contribute to tendon overload. These include pes cavus, leg-length discrepancy, scoliosis, and equinus deformity.
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Laboratory Tests
Routine laboratory investigations are generally unnecessary in uncomplicated Achilles tendinopathy.
Laboratory evaluation may be appropriate when the history or clinical examination raises suspicion of an underlying inflammatory arthritis, systemic connective-tissue disorder, or another systemic inflammatory condition.
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Imaging
Plain Radiographs
Weight-bearing radiographs of the foot are useful when insertional disease or associated bony abnormalities are suspected. Standard views include anteroposterior, lateral, and oblique radiographs.
Radiographs should be examined for a prominent posterosuperior calcaneal tuberosity consistent with a Haglund deformity.
Other findings may include calcaneal insertional spurring and calcification within the Achilles tendon, the latter being associated with chronic degenerative tendinosis.
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MRI
Magnetic resonance imaging is particularly useful when the clinical findings suggest significant tendinosis, partial tearing, or tendon rupture.
A normal Achilles tendon demonstrates homogeneous low signal intensity on all MRI sequences. Its anterior surface is normally flat or slightly concave, and the tendon typically has a crescent-shaped appearance proximally and an ovoid configuration at its insertion onto the calcaneus.
Normal Achilles tendon thickness is generally less than 8 mm.
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MRI Findings in Acute Paratenonitis
In acute paratenonitis, MRI may demonstrate loss of the normal sharp interface between the Achilles tendon and the pre-Achilles fat.
T2-weighted imaging may reveal increased signal intensity surrounding the tendon and extending into the pre-Achilles fat, representing edema and inflammation. The tendon substance itself usually remains relatively low in signal intensity.
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MRI Findings in Chronic Achilles Tendinopathy
Chronic Achilles tendinopathy is commonly associated with tendon thickening. The tendon may measure more than 8 mm in thickness and may appear enlarged or fusiform.
The normally concave anterior tendon margin may become flattened or convex.
On T1-weighted MRI sequences, chronic degeneration may produce heterogeneous areas of increased signal within the tendon substance, reflecting structural disorganization.
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MRI Findings in Achilles Tendon Rupture
Achilles tendon rupture most commonly occurs approximately 3–5 cm proximal to the calcaneal insertion.
A partial tendon rupture typically produces focal areas of increased signal intensity within the tendon on T2-weighted sequences while preserving at least some continuity of the tendon fibers.
A complete rupture demonstrates complete loss of tendon continuity, with separation of the torn ends and a fluid-filled or high-signal gap on T2-weighted imaging.
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Ultrasound
Ultrasound is another useful method for assessing the Achilles tendon, although diagnostic accuracy is strongly influenced by the skill and experience of the examiner.
Ultrasound may demonstrate fluid surrounding the tendon, adhesions involving the peritendinous tissues, abnormal tendon thickening, degenerative changes, and partial or complete tendon tears.
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Differential Diagnosis
Conditions that may mimic Achilles tendinitis include precalcaneal bursitis, retrocalcaneal bursitis, peroneal tendinitis or tendon rupture, posterior tibialis tendinitis or rupture, and inflammatory arthritis.
A partial or complete Achilles tendon rupture must always be considered, particularly in patients with sudden functional deterioration. Rupture may represent the terminal stage of a chronically degenerative Achilles tendon.
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Treatment
General Measures
Treatment is usually conservative during the early and acute stages. Initial measures include rest, ice, NSAIDs, heel lifts, footwear modification, and correction of associated biomechanical abnormalities with appropriate orthoses.
Activities that aggravate symptoms should be temporarily reduced or modified. Gentle Achilles tendon stretching can be introduced as symptoms permit.
A carefully performed injection into the retrocalcaneal bursa may sometimes be considered when bursitis is the predominant pathology.
Patients who remain symptomatic despite these measures may benefit from temporary immobilization in a walking boot or cast.
Corticosteroid injection directly into or around the Achilles tendon is generally avoided because corticosteroids may weaken tendon tissue and increase the risk of subsequent rupture.
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Physical Therapy
Physical therapy plays an important role in rehabilitation. During appropriate phases of healing, modalities such as therapeutic ultrasound, phonophoresis, and iontophoresis may be used as adjunctive treatments.
Short-term use of a heel wedge can reduce tension across the Achilles tendon and may help during the painful stage.
As symptoms improve, rehabilitation should progressively focus on restoring flexibility, strength, endurance, and lower-limb conditioning.
Eccentric loading exercises are particularly important in the rehabilitation of chronic Achilles tendinopathy and are commonly incorporated into structured strengthening programs.
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Medication
First-line pharmacological treatment generally consists of nonsteroidal anti-inflammatory drugs for symptomatic pain relief during painful or inflammatory episodes.
Other simple analgesics may also be used when required.
Medication should be regarded as an adjunct to activity modification and rehabilitation rather than as definitive treatment for chronic degenerative tendinosis.
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Surgical Management
Surgical intervention may be considered when symptoms remain significant despite approximately 3–6 months of appropriate nonoperative treatment.
The surgical approach depends on the underlying pathological process.
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Surgery for Paratenonitis
Persistent symptomatic paratenonitis may be treated by surgical release or removal of diseased paratenon tissue.
This is commonly performed through a longitudinal medial incision, allowing the surgeon to release adhesions and excise chronically inflamed or fibrotic tissue surrounding the tendon.
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Surgery for Achilles Tendinosis
Chronic Achilles tendinosis may require intratendinous debridement, in which abnormal degenerative portions of the tendon are excised while preserving healthy tendon fibers.
When insertional pathology is present, surgery may also include a retrocalcaneal bursectomy and removal of a prominent Haglund exostosis.
Extensive tendon degeneration may leave insufficient healthy Achilles tendon for reliable repair. In these situations, reconstruction may require augmentation with another tendon.
Possible options include augmentation with the plantaris tendon or tendon transfer using the flexor hallucis longus tendon.
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Follow-Up
Patients should be reviewed periodically during treatment to assess pain, tendon tenderness, strength, range of motion, and functional recovery.
Return to running or sporting activity should be gradual. Full activity is generally resumed only after symptoms have settled and appropriate flexibility, strength, and endurance have been restored.
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Prognosis
The overall prognosis for Achilles tendinopathy is generally favorable, particularly when biomechanical factors and training errors are corrected.
However, recovery may be prolonged, especially in patients with chronic tendinosis. Improvement may occur gradually rather than immediately, and rehabilitation frequently requires sustained modification of activity together with a progressive strengthening program.
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Complications
Chronic degeneration may progressively weaken the Achilles tendon and ultimately result in partial or complete rupture with loss of normal function.
Persistent pain, recurrent tendinopathy, residual weakness, and incomplete recovery may occur in severe disease.
Surgical treatment also carries the possibility of unsatisfactory healing or treatment failure, particularly in patients with extensive degenerative tendon involvement.
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Patient Monitoring
Routine follow-up is recommended until symptoms have resolved and the patient has regained adequate strength and function.
Monitoring should include assessment of pain, swelling, tendon integrity, ankle motion, calf strength, heel-rise ability, and tolerance of progressively increasing physical activity.
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Orthopaedic - Accessory Navicular
Basics
An accessory navicular is an anatomical variant in which an additional ossicle is present along the medial border of the navicular bone. Accessory ossicles arise from secondary ossification centers that fail to fuse with the main bone. In many individuals, the accessory navicular is discovered incidentally on radiographs and remains completely asymptomatic.
Symptoms may develop after repetitive activity, overuse, direct trauma, or mechanical irritation. When the accessory navicular becomes painful, the condition is referred to as accessory navicular syndrome (ANS). Both children and adults may develop symptoms, although presentation is particularly common during adolescence.
Classification
Accessory navicular bones are generally classified into three major types according to their morphology and relationship with the posteromedial navicular tuberosity.
Type I, representing approximately 30% of cases, is a small 2–3 mm sesamoid ossicle located within the posterior tibialis tendon (PTT). It has no cartilaginous connection with the navicular tuberosity and is also known as the os tibiale externum.
Type II, which accounts for approximately 50% of cases and is the type most commonly associated with symptoms, is larger than type I. It originates from a secondary ossification center of the navicular and typically appears triangular or heart-shaped. It is connected to the main navicular by a cartilaginous or fibrocartilaginous synchondrosis. Type II may be further subdivided into types IIa and IIb according to its position.
Type III consists of an enlarged navicular tuberosity and is generally considered the result of fusion of a previous type II accessory navicular. It may have a prominent or pointed configuration.
Other terms used for an accessory navicular include os tibiale, os tibiale externum, naviculare secundum, and prehallux.
Pediatric Considerations
Accessory navicular syndrome frequently presents during adolescence or early adulthood. Patients may have associated pes planus, or flatfoot, together with pain around the medial longitudinal arch. However, the severity of the flatfoot deformity does not necessarily correlate with the degree of pain or symptoms caused by the accessory navicular.
Epidemiology
The reported incidence of an accessory navicular ranges from approximately 4% to 21%, making it one of the more common accessory ossicles of the foot. It is usually located adjacent to the medial aspect of the navicular bone and is commonly identified in adolescents.
Many cases are bilateral, with some studies reporting bilateral involvement in up to 90% of affected individuals. Despite its relatively frequent radiographic appearance, fewer than 1% of individuals with an accessory navicular develop clinically significant symptoms.
Prevalence
Symptoms are most frequently encountered in teenagers and young adults. The condition tends to occur more commonly and at an earlier age in females than in males.
Accessory navicular bones may also be identified incidentally in older adults. Rarely, older individuals may develop symptoms because of degenerative changes at the synchondrosis, posterior tibial tendon degeneration, or inflammation of an adjacent bursa.
Etiology and Pathophysiology
The accessory navicular itself represents a normal anatomical variation rather than a disease. Symptoms may arise when the medial bony prominence rubs against footwear or is exposed to repetitive mechanical stress.
Patients may experience diffuse pain along the medial or plantar aspect of the arch. The accessory ossicle can alter the normal insertion of the posterior tibialis tendon, reducing its mechanical efficiency and potentially contributing to dysfunction of the medial arch.
In patients with marked flatfoot deformity, lateral-sided pain may also occur because of impingement between the calcaneus and fibula. Acute trauma can injure the fibrocartilaginous synchondrosis joining a type II accessory navicular to the main navicular bone, producing pain and inflammation.
Associated Conditions
Accessory navicular syndrome may be associated with flatfoot deformity and, in some individuals, a secondary Achilles tendon contracture.
Diagnosis
Signs and Symptoms
Pain may begin after wearing poorly fitting or narrow shoes, participating in sports, increasing weight-bearing activities, or sustaining direct trauma to the foot.
Typical findings include tenderness and pain over the medial aspect of the foot at the accessory navicular. Patients may also experience pain or weakness while attempting to rise onto the toes, run, or jump. A visible or palpable prominence may be present over the medial navicular, sometimes accompanied by local swelling and erythema.
History
Patients usually describe pain centered over the medial portion of the navicular. Symptomatic accessory navicular is particularly recognized in young athletes.
Symptoms are commonly worsened by prolonged standing, walking, running, sporting activity, or wearing narrow shoes that press against the prominence. Pain generally decreases with rest and avoidance of the aggravating activity.
Physical Examination
Examination usually demonstrates localized tenderness over the medial pole of the navicular. Discomfort may increase when the foot is actively or passively abducted and adducted.
The patient’s footwear and shoe insole should also be assessed, as direct pressure from the shoe may contribute to symptoms.
Posterior tibialis tendon function should be evaluated by testing resisted plantarflexion and inversion. The ability to perform repeated single-leg heel rises is also useful when assessing PTT strength and function.
Ankle and subtalar joint motion should be examined, and the clinician should assess for associated Achilles tendon or gastrocnemius-soleus contracture.
Imaging
Initial evaluation should include weight-bearing anteroposterior, lateral, and oblique radiographs of the foot.
A type II accessory navicular typically has well-defined, smooth cortical margins and a triangular or heart-shaped appearance. It may measure approximately 9 × 12 mm and is commonly located about 1–2 mm from the medial and posterior surfaces of the native navicular. An internal oblique view may provide particularly good visualization of the ossicle.
The presence of smooth margins and a mature cortical outline helps distinguish an accessory navicular from an acute navicular avulsion fracture.
MRI
Magnetic resonance imaging is useful when conventional radiographs do not adequately explain the patient’s symptoms and has high sensitivity for detecting associated abnormalities.
In a type II accessory navicular, MRI may demonstrate the fibrocartilaginous or hyaline cartilage layer forming the synchondrosis between the accessory ossicle and the navicular tuberosity. Increased soft-tissue signal and edema may indicate sprain or disruption of this synchondrosis.
MRI may also demonstrate altered marrow signal or bone marrow edema related to chronic mechanical stress and, occasionally, osteonecrotic change. It is particularly helpful for identifying associated degeneration or tendinopathy of the posterior tibialis tendon.
Pathological Findings
In painful type II accessory navicular lesions, histological examination may demonstrate increased osteoblastic and osteoclastic activity within the tissue between the accessory ossicle and the main navicular.
Cartilage proliferation and increased vascular mesenchymal tissue may also be present, supporting the concept that repetitive mechanical stress at the synchondrosis contributes to symptoms.
Differential Diagnosis
Important differential diagnoses include an acute avulsion fracture of the navicular tuberosity, posterior tibial tendinitis or tendinopathy, and a navicular stress fracture.
Treatment
General Measures
Initial management is usually conservative. The patient should reduce or temporarily discontinue sports and other activities that reproduce symptoms. Rest and activity modification help decrease repeated mechanical stress across the accessory navicular.
Anti-inflammatory medication can be used for symptomatic pain relief. Footwear modification is also important, particularly the use of softer and wider shoes that minimize direct pressure over the medial bony prominence.
Patients with associated flatfoot may benefit from a medial arch support or orthotic. However, some individuals cannot tolerate an orthosis if it applies direct pressure to the accessory ossicle.
Persistent symptoms can be managed with immobilization in a below-knee walking cast or removable walking boot for approximately 3–6 weeks. Physical therapy may subsequently be introduced, with emphasis on strengthening, flexibility, posterior tibialis rehabilitation, and cryotherapy when appropriate.
Medication
Nonsteroidal anti-inflammatory drugs may be used for pain and inflammation. There is no clear evidence demonstrating that one particular NSAID is consistently superior to another for this condition.
Surgical Management
Most patients with a painful accessory navicular improve with nonoperative management, particularly children and adolescents.
In skeletally immature children, conservative treatment is generally preferred, especially before complete calcaneal apophyseal fusion, because symptoms may lessen with continued skeletal maturation.
Surgery may be considered when pain is progressive, recurrent, or persistent despite an adequate trial of conservative treatment.
One surgical option is excision of the accessory navicular combined with naviculoplasty, in which part of the prominent medial navicular is reshaped to restore a more normal contour. This may be useful because patients with an accessory navicular can also have a relatively broad medial native navicular.
Kidner Procedure
The traditional Kidner procedure involves excision of the accessory navicular together with repositioning of the posterior tibialis tendon to a more plantar location on the navicular.
Modern variations commonly involve removal of the accessory ossicle followed by direct reattachment or advancement of the posterior tibialis tendon to the navicular. Fixation may be achieved using suture anchors or sutures passed through drill holes.
This approach generally provides satisfactory pain relief and functional improvement, particularly in adolescents with persistent symptomatic accessory navicular syndrome.
Percutaneous Drilling
Percutaneous drilling of the synchondrosis can be considered in selected adolescent athletes. The aim is to stimulate bone union between the accessory navicular and the native navicular rather than removing the ossicle.
This technique may be suitable in skeletally immature patients in whom successful fusion of the synchondrosis is considered achievable.
Associated Flatfoot Reconstruction
Patients with severe flatfoot deformity and associated lateral impingement may require correction of the underlying deformity in addition to treatment of the accessory navicular.
Procedures may include a calcaneal osteotomy, a medial column osteotomy, or other reconstructive techniques intended to improve foot alignment. Correcting the deformity decreases abnormal mechanical stress on the posterior tibialis tendon insertion and may improve long-term function.
Follow-Up and Complications
Patients should be followed until pain has resolved and normal activity can be resumed without significant symptoms. After surgical treatment, rehabilitation should include restoration of ankle and foot motion followed by progressive strengthening of the posterior tibialis tendon and surrounding musculature.
Potential complications include persistent or incomplete pain relief, residual weakness of the posterior tibialis tendon, recurrent symptoms, and continuation of an underlying flatfoot deformity. Patients with significant structural deformity may therefore require additional corrective procedures to achieve a satisfactory functional outcome.
