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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.

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.

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.

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.

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.

Orthopaedic Surgery - Achilles Tendon Rupture

Basics

The Achilles tendon is the strongest tendon in the human body and is capable of withstanding forces of approximately 5–7 times body weight during activity. Achilles tendon rupture refers to disruption of the tendon, most commonly occurring within its relatively poorly vascularized watershed region.

The Achilles tendon represents the terminal confluence of the medial and lateral heads of the gastrocnemius together with the soleus muscle. It measures approximately 15 cm in length and inserts onto the posterior calcaneal tuberosity.

The tendon is surrounded by a paratenon, which allows smooth gliding movement relative to the surrounding tissues. Histologically, it is composed predominantly of type I collagen.

The poorest blood supply is found approximately 2–6 cm proximal to the calcaneal insertion, creating a watershed region that is particularly susceptible to degeneration and rupture. As the tendon travels distally, it undergoes approximately 90° of rotation, which further concentrates mechanical stress within this vulnerable region.

Achilles tendon ruptures may be classified as acute or chronic, open or closed, and complete or incomplete.

General Prevention

Regular conditioning, progressive training, and appropriate stretching may promote adaptation of the Achilles tendon. Repeated loading produces structural adaptation, including an increase in tendon cross-sectional area.

Gradual increases in physical activity are preferable to sudden changes in exercise intensity, particularly in individuals who participate in vigorous sport intermittently.

Epidemiology

Achilles tendon rupture demonstrates a bimodal age distribution.

The first major group consists of young to middle-aged athletes, commonly between 30 and 40 years of age. Approximately 60–75% of ruptures in this group occur during sporting activity.

The particular sport responsible varies between countries and regions depending on local patterns of participation.

A second group consists of older, relatively inactive individuals. A smaller proportion of ruptures, approximately 13%, occur in older nonathletic patients.

Incidence

The precise incidence varies considerably among published studies, with estimates ranging from approximately 2 to 37.3 cases per 100,000 population.

The incidence of Achilles tendon rupture has increased over recent decades, possibly reflecting greater participation in recreational sport and physical activity among middle-aged adults.

Prevalence

Achilles tendon rupture predominantly affects males.

The left Achilles tendon has been reported to rupture more frequently than the right. One proposed explanation is that many right-hand-dominant athletes preferentially use the left leg as the push-off limb during sporting activity.

The condition is more frequently reported in industrialized countries and is especially associated with so-called weekend warriors, who participate in vigorous sporting activity intermittently without consistent conditioning.

Risk Factors

A previous Achilles tendon rupture increases the risk of rupture of the opposite tendon. In some studies, subsequent contralateral rupture has occurred in up to approximately 6% of patients.

Several medications are associated with an increased risk of tendon degeneration and rupture. These include systemic corticosteroids, local corticosteroid injections around the Achilles tendon, anabolic steroids, and fluoroquinolone antibiotics.

A number of systemic diseases have also been associated with spontaneous Achilles tendon rupture, although these account for a relatively small proportion of cases. Important examples include diabetes mellitus, rheumatoid arthritis, other inflammatory arthritides, and gout.

Pathophysiology

Histological examination of ruptured Achilles tendons commonly demonstrates underlying chronic degenerative abnormalities.

Features of tendinosis, including collagen disorganization, mucoid degeneration, and deterioration of the normal tendon architecture, are frequently present even when the patient did not have significant symptoms before rupture.

This suggests that an apparently sudden rupture often represents an acute mechanical failure of a tendon that has already undergone chronic structural degeneration.

Etiology

The most common mechanism is an indirect injury rather than direct trauma.

A typical rupture occurs when the patient forcefully pushes off from a weight-bearing foot while simultaneously extending the knee. This produces a sudden and substantial load across the Achilles tendon.

Another common mechanism involves forceful eccentric contraction of the gastrocnemius–soleus complex, in which the muscle contracts while the tendon is being lengthened.

Direct trauma is much less common. Penetrating injuries such as a laceration or gunshot wound may directly divide the Achilles tendon.

Associated Conditions

Achilles tendon rupture may occur in association with pre-existing Achilles tendinopathy.

Insertional disorders may include retrocalcaneal bursitis and insertional Achilles tendinopathy, whereas noninsertional pathology may include tendinosis and peritendinitis.

Diagnosis

Signs and Symptoms

Patients commonly report a sudden snap or pop in the posterior ankle at the time of injury.

A characteristic description is the sensation of having been struck, kicked, or hit in the back of the lower leg despite no external contact occurring.

Pain may initially be severe. Localized swelling, tenderness, and a palpable defect along the Achilles tendon, together with weakness of active plantarflexion, strongly suggest rupture.

History

A complete foot and ankle history should be obtained, including the exact mechanism of injury and the patient’s activity level.

The clinician should specifically ask about previous episodes of Achilles pain, stiffness, swelling, or symptoms suggestive of chronic tendinopathy, because degenerative changes frequently precede rupture.

Medication history and relevant systemic disorders should also be reviewed.

Physical Examination

A general examination of the foot and ankle should be performed, with particular attention to the posterior ankle.

The Achilles tendon should be inspected and palpated for tenderness, swelling, bruising, and a palpable gap in the tendon.

Plantarflexion strength should be assessed carefully. A patient with a complete Achilles rupture may still be able to plantarflex the ankle because other muscles can assist with the movement. However, plantarflexion will usually be substantially weaker than on the unaffected side.

The patient will generally be unable to perform a single-leg heel rise on the injured side.

Knee Flexion Test

The patient is positioned prone with both knees flexed to approximately 90°.

The resting position of the affected ankle is compared with that of the normal side. An intact Achilles tendon maintains resting tension within the gastrocnemius–soleus complex and therefore holds the ankle in slight plantarflexion.

When the Achilles tendon is ruptured, this normal resting tension is lost, and the affected ankle assumes a relatively more dorsiflexed position compared with the opposite side.

Thompson Test

The Thompson test is an important clinical test for Achilles tendon rupture.

The patient is placed prone with the feet extending beyond the examination table. The examiner compresses the calf musculature.

With an intact Achilles tendon, compression of the gastrocnemius–soleus complex produces passive plantarflexion of the ankle.

If the Achilles tendon is completely disrupted, calf compression fails to produce normal passive plantarflexion, strongly indicating loss of tendon continuity.

Laboratory Tests

Routine laboratory investigations are generally unnecessary for diagnosing an acute Achilles tendon rupture.

Preoperative laboratory tests are obtained when surgical treatment is planned and should be selected according to the patient’s age, medical history, and perioperative requirements.

Imaging

Plain Radiographs

Plain radiographs may be obtained to evaluate the osseous structures of the ankle and hindfoot.

Although radiographs do not directly demonstrate most Achilles tendon ruptures, they are useful for excluding associated fractures and other bony abnormalities.

If radiographs suggest an avulsion fracture involving the calcaneal tuberosity together with the Achilles tendon insertion, computed tomography (CT) may be useful for defining the fracture pattern and assisting surgical planning.

MRI and Ultrasound

Most acute Achilles tendon ruptures can be diagnosed clinically without advanced imaging.

When the diagnosis remains uncertain, MRI can demonstrate the location and extent of the rupture, the degree of tendon retraction, and the condition of the surrounding tissues.

Ultrasound may also be used to confirm tendon discontinuity or partial tearing. It can be particularly useful as a rapid, dynamic imaging technique when appropriate expertise is available.

Differential Diagnosis

Important differential diagnoses include Achilles tendinopathy, partial Achilles tendon rupture, and calcaneal fracture.

Partial tears may be more difficult to recognize clinically because some tendon continuity and plantarflexion function are preserved.

Initial Stabilization

Once an Achilles tendon rupture has been diagnosed, the ankle should be immobilized promptly.

A well-padded below-knee splint is applied with the ankle maintained in equinus or plantarflexion. This position brings the torn tendon ends closer together and reduces tension across the rupture site.

Initially, the patient is generally kept non-weight-bearing. Ice application and elevation are useful for reducing swelling and discomfort.

General Treatment Principles

Management may be either operative or nonoperative.

The choice depends on several factors, including the patient’s age, general medical health, functional demands, sporting activity, rupture characteristics, and personal preferences.

Historically, surgical treatment has often been favored for younger, healthy, highly active patients. However, contemporary functional rehabilitation protocols have improved outcomes following nonoperative treatment.

Both surgical and nonsurgical approaches have specific advantages and complications, and the treatment decision should therefore be individualized.

Nonoperative Management

Traditional nonoperative treatment involves immobilization of the lower leg in a below-knee cast with the ankle initially positioned in full equinus.

Over approximately 6–10 weeks, the ankle is gradually brought toward a neutral or plantigrade position. This may be achieved by serial cast changes, commonly at intervals of approximately two weeks.

Weight-bearing is usually introduced after approximately 4–6 weeks, depending on the rehabilitation protocol and clinical progress.

After the immobilization period, a heel lift may be used for several months to decrease tension on the healing Achilles tendon.

Functional Bracing

Modern nonoperative protocols increasingly use a removable boot or functional brace rather than prolonged rigid casting.

The brace initially restricts ankle dorsiflexion while allowing a degree of plantarflexion.

As healing progresses, the dorsiflexion restriction is gradually reduced, permitting increasing ankle motion and progressive loading of the tendon.

Functional bracing allows rehabilitation to begin earlier while maintaining the tendon in a protected position.

Activity

With traditional nonoperative management, full weight-bearing is usually avoided during the first 4–6 weeks.

More modern functional rehabilitation protocols may permit earlier protected weight-bearing, depending on tendon position, patient factors, and the treating surgeon’s protocol.

Return to unrestricted activity should be gradual and guided by restoration of tendon strength, ankle motion, balance, and functional performance.

Physical Therapy

A variety of rehabilitation protocols are available after both operative and nonoperative treatment.

Early rehabilitation generally begins with controlled active ankle motion within a protected range.

As tendon healing progresses, therapy advances to progressive weight-bearing, strengthening, balance training, and restoration of calf endurance.

Later stages focus on functional exercises and gradual return to running, jumping, and sport-specific activity.

Surgical Management

Open Repair

Open surgical repair is one established treatment option for an acute Achilles tendon rupture.

Surgery may be delayed briefly, often for approximately one week, to allow acute swelling to decrease.

The patient is generally positioned prone. Both lower extremities may be included in the operative field so that the resting position and tension of the repaired ankle can be compared with those of the normal side.

A longitudinal medial incision adjacent to the Achilles tendon is commonly used because this approach helps reduce the risk of injury to the sural nerve.

Tendon Repair Technique

Strong sutures are placed into the proximal and distal tendon segments and tied with the tendon ends appropriately opposed.

Locking suture configurations with multiple strands passing through each tendon segment can provide substantial repair strength.

The paratenon should be preserved whenever possible and repaired at the conclusion of the procedure. Restoration of the paratenon may improve tendon gliding and reduce postoperative adhesions.

When present and suitable, the plantaris tendon may be opened and wrapped around the Achilles repair as an additional biological layer and to potentially reduce adhesion formation.

Percutaneous Repair

Several minimally invasive and percutaneous Achilles tendon repair techniques have been developed.

These procedures use multiple small stab incisions and specialized instruments to approximate and suture the ruptured tendon ends.

Potential advantages include smaller incisions, reduced soft-tissue disruption, and a lower risk of wound complications compared with traditional open surgery.

However, percutaneous techniques may carry a greater risk of injury to the sural nerve, depending on the technique used.

Surgical Management of Chronic Ruptures

Chronic Achilles tendon ruptures are technically more difficult to repair because the tendon ends may retract and scar, and the gastrocnemius–soleus complex may become shortened or atrophic.

Treatment depends largely on the size of the tendon defect and the quality of the remaining tissue.

When direct end-to-end repair is possible, the tendon ends may be mobilized and repaired primarily.

If a large gap prevents direct repair, reconstructive options include V–Y advancement or lengthening, turndown tendon flaps, tendon transfers, tendon augmentation, and allograft reconstruction.

Tendon Transfer and Augmentation

When substantial tissue loss or chronic degeneration is present, local tendon transfer may be required.

The flexor hallucis longus (FHL) is commonly used because of its anatomical proximity, strength, and similar direction of pull.

The flexor digitorum longus may also be used in selected cases.

Large chronic defects may occasionally require an allograft tendon or other reconstructive techniques to restore continuity between the gastrocnemius–soleus complex and calcaneus.

Follow-Up

Both operative and nonoperative treatment can provide good functional outcomes when accompanied by appropriate rehabilitation.

Follow-up should assess tendon healing, ankle motion, calf strength, gait, heel-rise ability, swelling, and functional recovery.

Progression of activity should be gradual to avoid excessive loading of the healing tendon.

Prognosis

The overall prognosis after Achilles tendon rupture is generally favorable with either operative or appropriately structured nonoperative treatment.

Clinical trials have demonstrated that both approaches can result in comparable return to sports, strength, endurance, and ankle range of motion when effective rehabilitation protocols are used.

A substantial proportion of patients treated by either method regain normal or near-normal function, although residual calf weakness or reduced endurance may persist in some individuals.

Complications of Surgical Treatment

Potential complications following surgical repair include adhesions, altered sensation, sural nerve symptoms, wound infection, wound dehiscence, and rerupture.

Reported surgical complication rates vary according to surgical technique and patient characteristics.

Wound complications are particularly important because the posterior ankle has relatively limited soft-tissue coverage and can be vulnerable to delayed healing.

Complications of Nonoperative Treatment

The major concern following nonsurgical treatment is rerupture, particularly when prolonged immobilization protocols are used without early functional rehabilitation.

Other potential complications include adhesions, excessive tendon lengthening, persistent weakness, and reduced push-off strength.

Excessive healing in an elongated position can impair calf function even when the tendon remains intact.

Deep Vein Thrombosis

Deep vein thrombosis (DVT) is an important complication following Achilles tendon rupture and can occur after either operative or nonoperative treatment.

The combination of lower-limb injury, immobilization, and reduced weight-bearing contributes to venous stasis.

Patients should therefore undergo individualized assessment for venous thromboembolism risk, and thromboprophylaxis should be considered when clinically appropriate.

Open Versus Percutaneous Repair

Compared with traditional open repair, percutaneous surgery may offer a shorter operative time and a lower incidence of wound infection.

However, some studies have reported higher rates of rerupture and sural nerve injury with percutaneous techniques.

Modern minimally invasive approaches and improved instrumentation may reduce these complications, and outcomes continue to evolve with newer techniques.

Patient Monitoring

Following surgical repair, sutures are commonly removed at approximately 2 weeks, provided that wound healing is satisfactory.

Immobilization or functional bracing is continued according to the selected postoperative protocol, followed by progressive ankle motion, weight-bearing, and strengthening.

Patients should be monitored for wound problems, infection, rerupture, tendon elongation, sural nerve symptoms, calf weakness, and signs of venous thromboembolism.

Appropriate DVT prophylaxis should be considered according to the patient’s individual risk factors and treatment protocol.

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.

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.

Surgery - Advanced Trauma Life Support (ATLS)

Principles of ATLS

Advanced Trauma Life Support (ATLS) provides a systematic and reliable approach to the assessment and initial resuscitation of trauma patients.

The aim is to rapidly identify and immediately treat potentially life-threatening injuries.

Once immediate threats to life have been managed, a more detailed assessment of the entire patient is performed to identify other injuries and establish definitive care.

The ATLS assessment is therefore divided into the primary survey and secondary survey.

Primary Survey

The primary survey is the initial systematic assessment of a trauma patient designed to identify and treat immediately life-threatening injuries.

Assessment and resuscitation occur simultaneously, with problems treated as soon as they are identified.

The primary survey follows the ABCDE approach.

A – Airway with cervical spine protection: Assess and secure the airway while maintaining appropriate cervical spine protection.

B – Breathing: Assess ventilation, oxygenation, and the respiratory system, and immediately treat life-threatening thoracic injuries.

C – Circulation with haemorrhage control: Assess the cardiovascular system, identify shock, and rapidly control significant haemorrhage.

D – Disability: Perform a rapid neurological assessment, including level of consciousness, pupils, and neurological status.

E – Exposure and environmental control: Fully expose the patient to identify injuries while actively preventing hypothermia.

Life-Threatening Injuries in the Primary Survey

The mnemonic ATOMIC can be used to remember important immediately life-threatening injuries.

A – Airway compromise: Airway obstruction may result in inadequate ventilation and oxygenation.

T – Tension pneumothorax: Increasing intrapleural pressure compromises ventilation and venous return and can rapidly cause cardiovascular collapse.

O – Open pneumothorax: A large open chest wall defect allows air to enter the pleural cavity and may severely compromise ventilation.

M – Massive haemothorax: A large accumulation of blood within the pleural cavity causes both respiratory compromise and haemorrhagic shock.

I – Incipient flail chest: Multiple rib fractures can produce an unstable chest wall segment, often associated with significant pulmonary contusion and respiratory compromise.

C – Cardiac tamponade: Accumulation of blood within the pericardial sac restricts cardiac filling and may cause obstructive shock.

Secondary Survey

The secondary survey is a thorough head-to-toe assessment performed after the primary survey and initial resuscitation have addressed immediate life-threatening problems.

Its purpose is to identify other injuries caused by the trauma that may not have been apparent during the primary survey.

It includes a detailed history, complete physical examination, appropriate investigations, and repeated reassessment of the patient.

The findings are then used to formulate a plan for definitive treatment and ongoing care.

If the patient deteriorates at any stage during the secondary survey, assessment should immediately return to the ABCDE primary survey.

Trauma Imaging

Traditionally, the standard trauma radiographic series consisted of cervical spine, chest, and pelvic X-rays.

A chest X-ray (CXR) may rapidly identify important thoracic injuries such as pneumothorax, haemothorax, and other chest pathology.

A pelvic X-ray may identify major pelvic fractures associated with significant haemorrhage.

Dedicated cervical spine X-rays have largely been replaced in many modern major-trauma pathways by CT when cervical spine imaging is indicated.

Imaging should never delay the treatment of an immediately life-threatening injury identified during the primary survey.

Surgery - Breathing

Timing of Breathing Assessment

Breathing should be assessed only after the airway has been cleared and secured.

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Mechanisms of Injury Affecting Breathing

Blunt trauma may compromise breathing through direct impact to the chest.

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Shear forces may also cause thoracic injury, such as when a patient is run over by a motor vehicle.

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Deceleration injuries may occur following high-speed road traffic collisions or falls from height.

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Penetrating trauma may result from stab wounds.

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Gunshot wounds can also cause severe penetrating thoracic injury.

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Blast injuries may follow a nearby explosion and can cause pulmonary damage secondary to capillary haemorrhage and alveolar rupture.

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Assessment of Breathing

Breathing should be assessed systematically using inspection, auscultation, palpation, and percussion.

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Inspection

Cyanosis may indicate significant hypoxia.

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An increased respiratory rate may be an early sign of respiratory compromise.

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Asymmetrical chest expansion may indicate unilateral thoracic injury.

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Use of accessory muscles, tracheal tug, or visibly increased work of breathing suggests respiratory distress.

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Paradoxical chest wall movement occurs when a segment of the chest moves inward during inspiration and outward during expiration, usually because of multiple rib fractures.

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The chest should be inspected for superficial signs of trauma such as bruising, gunshot wounds, stab wounds, and seatbelt marks.

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Auscultation

All lung zones should be auscultated for areas of reduced or absent air entry.

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Bronchial breathing may indicate underlying pulmonary pathology.

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Wheeze may occur because of bronchospasm associated with intrathoracic injury.

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Palpation and Percussion

Air movement should be assessed to confirm that the patient is breathing spontaneously.

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The trachea should be palpated for deviation.

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The chest should be percussed for areas of dullness or hyperresonance.

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Subcutaneous emphysema may indicate an underlying pneumothorax or other air leak associated with thoracic injury.

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Immediately Life-Threatening Thoracic Injuries

Four important life-threatening thoracic injuries must be identified during the primary survey.

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These are tension pneumothorax, open pneumothorax, massive haemothorax, and flail chest.

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Tension Pneumothorax

A tension pneumothorax occurs when air accumulates under pressure within the pleural cavity.

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The rising intrathoracic pressure compresses the ipsilateral lung and may displace the mediastinum and compromise the contralateral lung and venous return.

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It usually develops through a one-way valve mechanism in which air enters the pleural cavity but cannot escape effectively.

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Clinical Features of Tension Pneumothorax

Ipsilateral chest expansion may be reduced.

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The trachea may deviate away from the affected side, although this is usually a late sign.

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Percussion over the affected side may be hyperresonant.

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Air entry may be markedly reduced or absent on the affected side.

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The patient may develop tachycardia, tachypnoea, severe respiratory distress, and hypoxia.

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Distended neck veins may occur because of impaired venous return, although they may be absent if the patient is also hypovolaemic.

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Open Pneumothorax

An open pneumothorax occurs when there is a chest wall defect that communicates directly with the pleural cavity.

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If the defect is sufficiently large, air preferentially enters through the chest wall wound rather than through the trachea.

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It is traditionally called a sucking chest wound because air may be heard moving through the wound during respiration.

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Clinical Features of Open Pneumothorax

There may be an obvious chest wall defect with a sucking sound during inspiration.

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Air entry is reduced on the affected side.

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Chest expansion is reduced on the affected side.

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Tachycardia and tachypnoea are common.

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Massive Haemothorax

A massive haemothorax is traditionally defined as accumulation of more than 1500 mL of blood within the pleural cavity.

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It may result from injury to intercostal vessels, pulmonary vessels, or major intrathoracic vessels.

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Clinical Features of Massive Haemothorax

Ipsilateral chest expansion is reduced.

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Percussion over the affected side is dull.

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Air entry is reduced on the affected side.

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The patient may develop tachypnoea, tachycardia, and signs of hypovolaemic shock.

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Flail Chest

Flail chest occurs when multiple adjacent ribs are fractured in multiple places, creating a free-floating segment of chest wall.

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The unstable segment may move paradoxically inwards during inspiration and outwards during expiration.

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Clinical Features of Flail Chest

Paradoxical chest wall movement may be visible.

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Crepitus may be felt on palpation of the injured area.

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Air entry may be reduced on the affected side.

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Tachypnoea and tachycardia are common.

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Associated pulmonary contusion is often an important contributor to respiratory compromise.

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Immediate Management of Tension Pneumothorax

Tension pneumothorax is a clinical diagnosis and should be treated immediately without waiting for imaging.

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Emergency decompression should be performed promptly, followed by definitive chest drain insertion.

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Needle decompression has traditionally been used, although finger thoracostomy may be preferred in some trauma systems where expertise is available.

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Landmarks for Emergency Thoracic Decompression

A traditional site for needle decompression is the second intercostal space in the mid-clavicular line.

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Many current trauma protocols also accept or prefer the fourth or fifth intercostal space in the anterior to mid-axillary line, particularly because chest wall thickness may make the anterior approach less reliable.

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Landmarks for Chest Drain Insertion

A chest drain is usually inserted within the safe triangle, commonly around the fourth or fifth intercostal space between the anterior and mid-axillary lines.

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The tube should be inserted just above the upper border of the rib to reduce the risk of injury to the intercostal neurovascular bundle.

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Management of Open Pneumothorax

The open chest wound should be covered promptly with an appropriate occlusive or vented dressing.

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A traditional temporary technique is to secure an occlusive dressing on three sides, creating a flutter-valve effect that limits air entry while allowing air to escape.

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A chest drain should then be inserted on the affected side at a separate clean site away from the wound.

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Definitive surgical closure of the chest wall defect may subsequently be required.

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Blood Investigations

A group and cross-match should be performed if significant bleeding or transfusion is anticipated.

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An arterial blood gas may provide information about oxygenation, ventilation, acid-base status, lactate, and haemoglobin concentration.

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Co-oximetry can be used to measure carboxyhaemoglobin when smoke inhalation or carbon monoxide exposure is suspected.

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Chest X-Ray

A chest X-ray remains an important investigation in thoracic trauma, although treatment of immediately life-threatening conditions should not be delayed for imaging.

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A pneumothorax may appear as a visible pleural line with loss of peripheral lung markings beyond it.

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The size of a pneumothorax should not be estimated using the old assumption that a 1 cm rim equals 10% lung-volume loss, as this is unreliable.

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A haemothorax may produce blunting of the costophrenic angle on an erect chest X-ray.

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Several hundred millilitres of pleural blood may be required before costophrenic angle blunting becomes visible on an erect film.

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Chest X-ray may also assist in identifying pulmonary contusion, parenchymal injury, rib fractures, mediastinal abnormalities, and other thoracic pathology.

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CT Imaging

CT scanning can provide more detailed information about thoracic injuries.

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It should generally be reserved for patients who are sufficiently stable for transfer to the scanner.

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CT is usually performed after immediate life-threatening problems have been addressed and often as part of the secondary survey or definitive trauma imaging pathway.