Orthopaedic Surgery - Osteochondral Defect of the Talus

Basics

An osteochondral defect of the talus is an injury involving the articular cartilage and underlying subchondral bone of the talar dome within the ankle joint.

The term osteochondral lesion of the talus (OLT) is also commonly used.

The talus is one of the more frequent sites of osteochondral injury, after the:

Knee

and

Elbow.

Lesions most often involve the:

Posteromedial talar dome

or

Anterolateral talar dome.

Historically, approximately 53% have been reported medially and 46% laterally.

Classification

The classic classification is based on the Berndt and Harty system, with later modifications.

Stage I

There is:

Compression or contusion of the subchondral bone

without a clearly separated osteochondral fragment.

Stage II

There is a:

Partially detached osteochondral fragment.

The fragment remains incompletely separated from the talus.

Stage III

The osteochondral fragment is:

Completely detached but remains nondisplaced and stable within the defect.

Stage IV

The fragment is:

Completely detached and displaced.

This may create a loose body within the ankle.

Stage V

A later modification added:

Subchondral cyst formation.

This stage is particularly relevant in chronic lesions.

Prevention

There is no proven method that prevents all talar osteochondral lesions.

Because many lesions are related to ankle trauma, preventive strategies include:

Reducing recurrent ankle sprains

Rehabilitating ligament injuries appropriately

Treating significant chronic ankle instability

Correction of persistent ankle instability may reduce repetitive shear injury to the talar dome.

Epidemiology

Most patients are diagnosed in the:

Second through fourth decades of life.

Historical studies report a mean age of approximately:

27 years.

Men have traditionally represented approximately 65% of affected patients in some series.

Incidence

Osteochondral lesions of the talus are relatively uncommon compared with routine ankle sprains and fractures.

Older reports estimate that they account for approximately:

0.09% of all fractures

and a small proportion of all osteochondral lesions.

Their true frequency is probably underestimated because some lesions are occult on initial radiographs.

Risk Factors

Because most lesions are traumatic, important risk factors include:

Previous ankle fracture

Ankle sprain

Recurrent ankle sprains

Chronic ankle instability

Genetics

There is limited evidence suggesting that genetic factors may influence susceptibility in selected patients, but trauma remains the dominant recognized cause.

Pathophysiology

Osteochondral lesions are produced by combinations of:

Shear forces

Compression

Impact loading

These forces damage the articular cartilage and subchondral bone.

Etiology

The most common cause is trauma.

Acute Trauma

An acute lesion may follow:

Ankle sprain

or

Ankle fracture.

Chronic Trauma

Repeated instability may cause recurrent:

Shear and impact injury to the talar dome, eventually producing cartilage and subchondral bone damage.

Lateral Lesions

Lateral talar lesions are particularly strongly associated with trauma.

Historically, a recognizable traumatic episode has been identified in approximately:

93% of lateral lesions.

They are often more:

Shallow

Wafer-shaped

and

Displaced

than medial lesions.

Medial Lesions

Medial lesions have also been associated with trauma, but less consistently.

Historical data identify a recognized traumatic event in approximately:

61% of medial lesions.

These lesions are often:

Deeper

Cup-shaped

and more likely to become chronic or cystic.

Other Causes

Possible nontraumatic contributors include:

Ischemic injury

Avascular necrosis

Abnormal local bone biology

Associated Conditions

Common associated conditions include:

Ankle fracture

Ankle sprain

Chronic lateral ankle instability

Diagnosis

Diagnosis requires a combination of:

Clinical suspicion

Physical examination

and

Imaging.

History

Important questions include:

Was there a previous ankle injury?

Has the patient had repeated ankle sprains?

Is there a history of ankle instability?

Are there mechanical symptoms such as catching or locking?

Signs and Symptoms

Patients commonly report:

Deep ankle pain

Pain with weight bearing

Swelling

Intermittent stiffness

Catching or locking

Persistent symptoms after an ankle sprain

The pain may be poorly localized.

Mechanical Symptoms

Catching, clicking, or locking suggests:

An unstable fragment, loose body, or irregular articular surface.

Physical Examination

A complete foot and ankle examination should be performed.

Swelling and Effusion

Assess for:

Ankle swelling

Joint effusion

Talar Dome Tenderness

Localized tenderness over the talar dome may be present, although deep lesions can be difficult to palpate directly.

Ankle Instability

Evaluate for ligamentous instability using:

Anterior drawer test

and

Talar tilt test.

Generalized ligamentous laxity should also be assessed.

Range of Motion

Evaluate ankle:

Dorsiflexion

Plantarflexion

and rotational movement.

Look for:

Pain

Crepitus

Catching

Mechanical restriction

Exclusion of Other Causes of Ankle Pain

Other abnormalities that may explain chronic ankle pain should be excluded, including:

Peroneal tendon subluxation

Lateral process fracture of the talus

Fifth metatarsal fracture

Syndesmotic injury

Tarsal coalition

Imaging

Imaging is central to diagnosis.

Weight-Bearing Radiographs

Initial imaging should generally include:

Weight-bearing ankle radiographs.

Plain films are inexpensive and can identify:

Osteochondral fragments

Subchondral cysts

Sclerosis

Arthritis

Other fractures or structural abnormalities

However, talar osteochondral lesions may be difficult to visualize on routine radiographs.

Historical sensitivity has been approximately 70%, with high specificity.

CT

CT provides excellent evaluation of:

Subchondral bone

Lesion dimensions

Cyst formation

Fragment displacement

Osseous architecture

Historically reported sensitivity is approximately 81%, with specificity near 99%.

Role of CT

When a lesion is visible on radiographs, CT is particularly useful for confirming and defining:

Its size, depth, and bony extent.

It is often the best study for accurate characterization of the subchondral component.

MRI

MRI is highly sensitive for detecting osteochondral lesions.

Historical studies report:

Sensitivity around 96%

and

Specificity around 99%.

Role of MRI

MRI is especially useful for identifying:

Bone marrow edema

Cartilage injury

Subchondral cysts

Associated ligament injury

Tendon abnormalities

Synovitis

It is generally the best modality for evaluating associated soft-tissue pathology.

MRI Limitations

MRI may overestimate lesion size because surrounding:

Bone marrow edema

can make the abnormal area appear larger.

Metallic implants can also produce artifact that limits interpretation.

CT Versus MRI

Both CT and MRI are highly useful.

CT is superior for:

Detailed bony architecture

whereas MRI is superior for:

Cartilage, marrow, and soft tissues.

The preferred modality depends on the clinical question.

Bone Scintigraphy

Bone scanning was historically used to identify metabolically active occult lesions.

It is less commonly required now because MRI provides more detailed information.

Arthroscopy

Ankle arthroscopy provides the most direct assessment of the:

Articular cartilage surface.

It also permits simultaneous treatment.

Limitations of Arthroscopy

Arthroscopy is:

Invasive

Operator dependent

and does not fully demonstrate:

Deep subchondral bone pathology.

Pathological Findings

In chronic nondisplaced lesions, an osteochondral fragment may remain attached to the defect by:

Fibrous tissue.

Subchondral Bone Violation

If the subchondral bone is penetrated, healing occurs primarily through formation of:

Fibrous tissue or fibrocartilage.

Intact Subchondral Bone

When the subchondral plate remains intact, intrinsic healing is limited because articular cartilage has poor regenerative capacity.

Displaced Fragments

The cartilage cap of a fragment may remain viable, but the underlying bone can become:

Avascular

with reduced healing potential, particularly in chronic lesions.

Differential Diagnosis

The differential diagnosis includes most causes of chronic ankle pain.

Important alternatives include:

Occult fracture

Fifth metatarsal fracture

Lateral process fracture of the talus

Medial or lateral malleolar fracture

Ankle sprain

Syndesmotic injury

Chronic ankle instability

Peroneal tendon subluxation

Anterior ankle impingement

Tarsal coalition

Ankle or subtalar synovitis

Posterior tibial tendon pathology

Treatment

General Principles

Treatment depends on:

Lesion stage

Size

Location

Stability

Presence of cysts

Duration of symptoms

Patient activity level

Previous treatment

Nonoperative Treatment

Nonoperative management can be attempted for:

Stage I

Stage II

and some

Stable Stage III lesions.

Immobilization

Treatment may include:

Activity modification

Walking boot

Short-leg cast

Temporary non-weight bearing

The exact protocol varies according to symptoms and lesion characteristics.

Success Rate

Historical studies report successful nonoperative treatment in approximately:

50% of patients.

Failure of conservative treatment does not necessarily worsen the results of later surgery.

Pediatric Considerations

Children are believed to have greater healing potential than adults because of:

Greater biological activity and remaining skeletal growth.

Therefore, nonoperative treatment is often favored initially.

However, favorable results are not guaranteed.

One older pediatric series reported good or excellent outcomes in only about:

38% of children treated without surgery.

Activity Modification

Nonoperative recommendations range from:

Avoidance of impact activity

to

Strict non-weight bearing in a cast.

Return to sport should be based on:

Pain resolution

Restoration of motion and strength

Healing or stability of the lesion

Physical Therapy

Rehabilitation may include:

Ankle range-of-motion exercises

Peroneal strengthening

Progressive weight bearing

Proprioceptive training

Balance exercises

Treatment of chronic ankle instability

Surgery

Surgery is considered for:

Unstable lesions

Displaced fragments

Persistent symptoms despite conservative treatment

Large lesions

Cystic lesions

Recurrent lesions after previous surgery

A variety of techniques are available.

Fragment Reduction and Fixation

Large viable osteochondral fragments may be:

Reduced and internally fixed.

This is most appropriate when the fragment:

Is large enough to accept fixation

Has viable bone

Can be anatomically restored

Acute lesions generally have a better healing potential than chronic displaced lesions.

Bone Marrow Stimulation

The most common initial surgical treatment for small lesions includes:

Débridement

Curettage

Microfracture

or

Subchondral drilling.

These procedures are often performed arthroscopically.

Surgical Technique

The surgeon removes:

Loose bodies

Fibrous tissue

Unstable cartilage

The underlying subchondral bone is then penetrated to allow:

Bleeding and clot formation.

Mechanism of Healing

The resulting fibrin clot contains marrow-derived cells, including:

Mesenchymal progenitor cells.

These cells form repair tissue that is primarily:

Fibrocartilage.

Fibrocartilage

Fibrocartilage is mechanically inferior to normal:

Hyaline articular cartilage

but can provide satisfactory symptom relief in appropriately selected small lesions.

Lesion Size

Bone marrow stimulation tends to perform best for relatively small defects.

Historically, lesions with a surface area under approximately:

1 cm²

have had more favorable outcomes than larger lesions.

Postoperative Management After Microfracture

Following microfracture or drilling, patients are commonly kept:

Non-weight bearing for approximately 4–6 weeks.

Early ankle range of motion is often encouraged.

Osteochondral Autograft Transfer

Osteochondral autograft transfer, also called:

OATS or mosaicplasty, transfers plugs containing viable hyaline cartilage and subchondral bone into the talar defect.

Donor Site

Grafts are usually harvested from a:

Low-load region of the ipsilateral knee.

Advantages and Limitations of OATS

Advantages include restoration of:

Hyaline cartilage and subchondral bone.

Limitations include:

Donor-site morbidity

Limited graft availability

Need for more extensive surgical exposure

Osteotomy for Access

Large medial or posterior lesions may require:

Medial malleolar osteotomy

or another osteotomy to expose the talar dome.

Patients remain non-weight bearing until the osteotomy heals.

This commonly requires approximately:

4–8 weeks.

Range of Motion After Osteotomy

Ankle motion is generally started within:

2–6 weeks, depending on fixation stability and healing.

Osteochondral Allograft Transfer

Fresh osteochondral allograft can be used to reconstruct:

Large or deep defects.

The graft is harvested from donor talar tissue and transplanted into the lesion.

Indications for Allograft

This technique is particularly useful for:

Large defects

Cystic lesions

Failed previous surgery

Lesions too large for practical autograft harvest

Historically, allograft transplantation has been considered for defects larger than approximately:

3 cm².

Autologous Chondrocyte Implantation

Autologous chondrocyte implantation is a cartilage restoration technique in which:

Cartilage cells are harvested, expanded in culture, and implanted into the defect.

Earlier Generations

First- and second-generation techniques used:

Cell suspension placed beneath a periosteal flap or collagen membrane.

Newer Generations

Later techniques use:

Three-dimensional scaffolds or matrices

to deliver and retain chondrocytes.

Limitations of Chondrocyte Techniques

Although clinical outcomes may be favorable, repair tissue may not consistently reproduce normal:

Hyaline cartilage architecture.

Some biopsy studies demonstrate mixed cartilage or fibrocartilage.

Future Directions

Emerging approaches include:

Improved biologic scaffolds

Growth factors

Mesenchymal stem-cell strategies

Tissue-engineered cartilage

The goal is to reproduce the structure and mechanical properties of native articular cartilage more closely.

Chronic Ankle Instability

When an osteochondral lesion coexists with chronic ligamentous instability, the instability should also be addressed.

This may require:

Ligament repair or reconstruction.

Failure to correct instability may expose the repaired cartilage to continued abnormal loading.

Follow-Up

Patients should be reassessed regularly after treatment.

Monitoring focuses on:

Pain

Swelling

Range of motion

Mechanical symptoms

Return of strength

Weight-bearing tolerance

Osteotomy Follow-Up

When an osteotomy has been performed, serial radiographs are used to confirm:

Progressive union before unrestricted weight bearing.

Prognosis

With appropriate treatment, the overall prognosis is generally good.

Outcomes are influenced by:

Lesion size

Chronicity

Location

Cystic change

Cartilage stability

Associated ankle instability

Previous surgery

Complications

Potential complications include:

Persistent pain

Ankle stiffness

Failure of cartilage repair

Malunion of an osteotomy

Nonunion of an osteotomy

Progressive ankle arthritis

Post-Traumatic Arthritis

Large, chronic, or inadequately treated lesions can cause progressive cartilage loss and eventually lead to:

Degenerative ankle arthritis.

Patient Monitoring

Follow-up should continue until the patient demonstrates:

Clinical improvement

Restored ankle motion

Adequate strength

Healing of any osteotomy

Resolution or acceptable control of symptoms

Return to running and sport should be gradual.

Key Principle

An osteochondral lesion of the talus is a combined injury of the talar articular cartilage and subchondral bone, most commonly related to ankle trauma.

Management is determined primarily by:

Lesion size, stability, chronicity, cyst formation, and patient symptoms.

Small stable lesions may be treated nonoperatively or with arthroscopic marrow stimulation, whereas larger, displaced, cystic, or recurrent lesions may require:

Fragment fixation, osteochondral grafting, cartilage restoration, and correction of associated ankle instability.

Orthopaedic Surgery - Osteoarthritis

Basics

Osteoarthritis is the most common form of arthritis and may affect nearly any synovial joint.

It is a chronic degenerative joint disorder characterized by progressive loss of articular cartilage, accompanied by secondary changes in the subchondral bone.

Typical structural changes include:

Joint-space narrowing

Osteophyte formation

Subchondral sclerosis

Subchondral cyst formation

The disease may involve a single joint or multiple joints.

There is currently no definitive cure, and advanced disease can result in substantial:

Pain

Stiffness

Deformity

Loss of function

Synonyms

Osteoarthritis is also called:

Degenerative joint disease

Degenerative arthritis

Wear-and-tear arthritis

The term “wear-and-tear” is commonly used but is an oversimplification because osteoarthritis results from complex mechanical, biologic, genetic, and inflammatory processes.

Classification

Osteoarthritis can be classified according to:

Number of joints involved

and

Underlying cause.

Primary Osteoarthritis

Primary osteoarthritis develops without a single identifiable precipitating disorder.

It commonly affects joints such as:

Knees

Hips

Hands

Spine

Secondary Osteoarthritis

Secondary osteoarthritis occurs after a known process has damaged the joint.

Examples include:

Trauma

Septic arthritis

Avascular necrosis

Congenital or developmental deformity

Inflammatory disease

Epidemiology

Osteoarthritis becomes increasingly common with age.

It is especially prevalent in adults older than approximately 60 years.

Commonly Affected Joints

The knee is among the most commonly affected major weight-bearing joints.

Other frequently affected sites include:

Hands

Hips

Spine

First metatarsophalangeal joint

Historical Prevalence Data

In one older study of women older than 65 years:

Knee osteoarthritis was identified in approximately 30%

Hand osteoarthritis in approximately 15%

Hip osteoarthritis in approximately 8%

Another study found hand osteoarthritis in approximately 23% of women older than 65 years.

Hand Osteoarthritis

The hand joints most commonly involved include:

Distal interphalangeal joints

and

First carpometacarpal joint of the thumb.

Sex Distribution

Osteoarthritis occurs more frequently in women than men, particularly after middle age.

Risk Factors

Important risk factors include:

Advancing age

Obesity

Female sex

Previous joint injury

Avascular necrosis

Previous septic arthritis

Malalignment

Repetitive joint loading

Obesity

Obesity substantially increases loading across weight-bearing joints, especially the:

Knees

and may accelerate symptom development and structural progression.

Metabolic factors may also contribute.

Previous Joint Injury

Prior trauma may damage:

Articular cartilage

Menisci

Ligaments

Subchondral bone

and increase the risk of later post-traumatic osteoarthritis.

Genetics

Osteoarthritis has a significant genetic component.

Susceptibility is polygenic, meaning that multiple genes interact with:

Age

Mechanical loading

Body weight

Joint anatomy

Environmental factors

to influence disease development.

Etiology

The exact cause of primary osteoarthritis is multifactorial.

The final common pathway involves:

Progressive cartilage degeneration

with increasing mechanical stress on the remaining joint surfaces.

Cartilage Degeneration

As cartilage deteriorates:

Proteoglycan content decreases

Collagen architecture becomes disrupted

Cartilage softens and fibrillates

Cartilage thickness progressively decreases

Eventually, areas of subchondral bone may become exposed.

Secondary Bone Changes

Abnormal load transmission produces characteristic osseous responses, including:

Subchondral sclerosis

Osteophytes

Subchondral cysts

Remodeling and deformity

Secondary Osteoarthritis

Any process that significantly damages the articular surface can produce secondary osteoarthritis.

Post-Traumatic Arthritis

Fractures involving the joint surface, ligament instability, or meniscal injury may result in:

Abnormal contact forces and progressive cartilage deterioration.

Postinfectious Arthritis

Septic arthritis may rapidly destroy articular cartilage and later produce severe degenerative changes.

Osteoarthritis Associated With Avascular Necrosis

Collapse of necrotic subchondral bone can distort the articular surface and cause secondary joint degeneration.

Associated Conditions

Osteoarthritis is primarily a joint disorder rather than a systemic disease.

However, it may occur secondary to many disorders that alter:

Cartilage integrity

Joint alignment

Bone structure

Joint stability

Diagnosis

Diagnosis is based on:

Symptoms

Physical examination

and

Characteristic imaging findings.

Signs and Symptoms

Typical symptoms include:

Pain with weight bearing

Pain with joint movement

Stiffness

Reduced range of motion

Functional limitation

Pain Pattern

Pain commonly worsens with:

Activity

Prolonged standing or walking

Repetitive joint use

Some patients also experience stiffness after:

Prolonged inactivity or rest.

Functional Limitation

Progressive osteoarthritis may interfere with:

Heavy physical work

Walking long distances

Climbing stairs

Putting on shoes

Tying shoelaces

Getting into or out of a chair

Daily self-care activities

History

Important historical features include:

Duration of pain

Activity-related symptoms

Morning or post-rest stiffness

Swelling

Previous trauma

Prior infection

Previous surgery

Functional limitations

Pain and swelling often worsen with increased use.

Physical Examination

The principal findings include:

Joint stiffness

Loss of range of motion

Pain with movement

Joint effusion

Crepitus

Angular deformity

Gait abnormality

Range of Motion

Range of motion may become progressively restricted because of:

Osteophytes

Capsular contracture

Pain

Joint deformity

Joint Effusion

A small or moderate joint effusion may occur, particularly in the knee.

This reflects a degree of secondary synovial inflammation.

Deformity

Advanced disease may produce:

Varus or valgus alignment

Fixed flexion deformity

Joint enlargement

Loss of normal contour

Gait

Lower-extremity osteoarthritis may produce:

Antalgic gait

Reduced walking speed

Shortened stance phase on the painful limb

Laboratory Tests

There is no specific laboratory test for osteoarthritis.

Routine inflammatory markers are typically normal unless another disorder is present.

Laboratory testing is useful primarily when excluding conditions such as:

Inflammatory arthritis

Infection

Crystal arthropathy

Imaging

Plain Radiographs

Plain radiographs remain the main imaging modality.

Standard studies usually include:

AP

and

Lateral views

with additional views depending on the joint.

Weight-Bearing Radiographs

Weight-bearing radiographs are particularly important for:

Knee

Foot

Ankle

because they demonstrate joint-space narrowing and alignment under physiologic load.

Typical Radiographic Findings

Classic features include:

Joint-space narrowing

Marginal osteophytes

Subchondral sclerosis

Subchondral cysts

Bone remodeling

MRI

MRI is not routinely required for typical established osteoarthritis.

It may be useful to evaluate alternative or associated diagnoses such as:

Avascular necrosis

Occult or stress fracture

Neoplasm

Meniscal or ligament injury

Early cartilage or subchondral disease

Pathological Findings

The principal abnormality is loss of normal articular cartilage structure.

Pathologic changes include:

Loss of cartilage thickness

Disorganization of the collagen matrix

Reduction in proteoglycan content

Surface fibrillation

Full-thickness cartilage loss in advanced disease

Subchondral Bone

As the cartilage deteriorates, subchondral bone becomes exposed to increased load.

This results in:

Sclerosis

Cyst formation

Microfracture

Remodeling

Differential Diagnosis

Moderate or advanced osteoarthritis is usually straightforward to diagnose.

Early disease may resemble other conditions.

Tendinitis and Bursitis

Periarticular disorders may produce pain around a joint without true cartilage degeneration.

Stress Fracture

Stress fractures can cause activity-related pain similar to osteoarthritis.

MRI or other imaging may be required when radiographs are normal but suspicion remains high.

Synovial Proliferative Disorders

Conditions involving abnormal synovial proliferation may produce:

Pain

Swelling

Effusion

and can occasionally mimic osteoarthritis.

Other Differential Diagnoses

Additional considerations include:

Inflammatory arthritis

Crystal arthropathy

Avascular necrosis

Infection

Occult malignancy

Treatment

General Principles

Treatment is initially nonoperative and aims to:

Reduce pain

Maintain mobility

Improve strength

Preserve independence

Delay functional deterioration

Activity Modification

Activities that consistently provoke severe pain should be modified.

High-impact activities such as:

Running

Contact sports

Heavy repetitive loading

may worsen symptoms in advanced disease.

Low-impact alternatives include:

Cycling

Swimming

Walking

Elliptical exercise

Rest

Short periods of rest may help during symptom flares.

Prolonged inactivity should be avoided because it contributes to:

Muscle weakness

Joint stiffness

Loss of conditioning

Weight Loss

Weight reduction is particularly important in overweight patients with lower-extremity osteoarthritis.

Even modest weight loss may reduce:

Joint loading

Pain

Functional limitation

Assistive Devices

A cane can decrease forces across the painful lower-extremity joint.

For hip or knee arthritis, the cane is generally held in the:

Contralateral hand.

This may improve:

Balance

Gait

Pain

Physical Therapy

Exercise therapy is an important component of treatment.

Goals include:

Maintaining range of motion

Preserving muscle strength

Preventing contractures

Improving balance

Maintaining aerobic conditioning

Strengthening

For knee osteoarthritis, strengthening of the:

Quadriceps

Hip abductors

Hamstrings

may improve function and reduce symptoms.

Range-of-Motion Exercises

Regular motion helps minimize:

Capsular stiffness

Contracture

Loss of function

Complementary Therapies

Acupuncture may provide short-term pain relief for some patients, particularly with knee osteoarthritis.

The clinical benefit varies among individuals.

Herbal and Nutritional Products

Numerous herbal preparations are marketed for osteoarthritis.

Evidence supporting many of these treatments remains limited or inconsistent.

Medication

NSAIDs

NSAIDs are among the most commonly used medications for symptomatic osteoarthritis.

They can reduce:

Pain

and

Inflammatory symptoms

but do not reverse cartilage damage.

NSAID Adverse Effects

Potential complications include:

Gastritis

Gastrointestinal ulceration or bleeding

Renal dysfunction

Fluid retention

Cardiovascular adverse effects

Risk increases with:

Older age

Higher doses

Long-term use

Relevant comorbidities

COX-2 Inhibitors

Selective COX-2 inhibitors may provide similar analgesic effects with a different gastrointestinal risk profile.

They still require consideration of:

Cardiovascular and renal risks.

Acetaminophen

Acetaminophen may provide modest pain relief and is an alternative for patients unable to tolerate NSAIDs.

Its benefit is generally less pronounced than that of NSAIDs for many patients.

Glucosamine and Chondroitin

The effectiveness of:

Glucosamine

and

Chondroitin sulfate

remains controversial.

Large studies have generally not demonstrated consistent clinically important benefit.

Intra-Articular Corticosteroid Injection

Corticosteroid injections can provide:

Short-term reduction in joint pain

and may be useful during symptomatic flares.

Relief is usually temporary and may last:

Several weeks.

Hyaluronic Acid Injection

Viscosupplementation with hyaluronic acid has been used for knee osteoarthritis.

Some patients report modest symptom improvement, but overall benefit is variable and remains debated.

Opioids

Opioids are generally avoided for routine long-term osteoarthritis treatment because of:

Tolerance

Dependence

Sedation

Falls

Other adverse effects

They may occasionally be considered in carefully selected patients with severe pain who are not surgical candidates and have exhausted safer options.

Surgery

Two major reconstructive strategies are:

Realignment osteotomy

and

Joint replacement.

Realignment Osteotomy

An osteotomy changes the mechanical axis of the limb by cutting and repositioning bone.

The objective is to:

Transfer load away from the diseased portion of the joint toward healthier cartilage.

Indications for Osteotomy

Osteotomy is most useful in selected patients with:

Unicompartmental disease

Correctable malalignment

Preserved motion

Relatively healthy opposing joint surfaces

It may occasionally be combined with:

Ligament reconstruction

Meniscal procedures

Arthroplasty

Joint replacement removes or resurfaces the damaged articular surfaces and replaces them with prosthetic components.

Common procedures include:

Total hip arthroplasty

Total knee arthroplasty

Total shoulder arthroplasty

Bearing Surfaces

Common arthroplasty bearing combinations include:

Metal or ceramic components articulating with highly cross-linked polyethylene, depending on the joint and implant design.

Indications for Joint Replacement

Arthroplasty is generally considered when the patient has:

Severe pain

Major functional limitation

Advanced radiographic arthritis

Failure of appropriate nonoperative treatment

Referral

Patients with:

Severe pain

Progressive deformity

Marked loss of function

Advanced arthritis

should be referred to an orthopaedic surgeon before severe fixed contractures or profound deconditioning develop.

Follow-Up

The interval between visits depends on:

Severity of symptoms

Rate of progression

Type of treatment

Patients may be reviewed every:

3–12 months

when symptoms are stable.

Imaging frequency should be based on clinical need rather than a fixed schedule.

Prognosis

Osteoarthritis is generally a progressive disorder, although the rate of progression varies substantially.

Symptoms may fluctuate over time.

There is no treatment that reliably restores normal cartilage once advanced degeneration has occurred.

Joint Replacement Prognosis

Modern joint replacement can provide substantial:

Pain relief

Improvement in mobility

Restoration of function

for appropriately selected patients.

Long-term implant survival is generally very good, although no prosthetic joint lasts indefinitely.

Complications of Osteoarthritis

Progressive disease can produce:

Increasing stiffness

Joint deformity

Loss of mobility

Muscle weakness

Reduced independence

Lower-Extremity Disease

Severe hip or knee osteoarthritis may eventually result in:

Marked walking limitation

Dependence on walking aids

and, in advanced cases,

Wheelchair dependence.

Upper-Extremity Disease

Severe arthritis of the shoulder, elbow, wrist, or hand may interfere with:

Dressing

Personal hygiene

Eating

Work

Other activities of daily living

Treatment Complications

Treatment itself may cause complications.

NSAIDs

Potential complications include:

Gastritis

Peptic ulceration

Gastrointestinal bleeding

Renal impairment

Cardiovascular events

Surgical Complications

Potential complications after arthroplasty include:

Infection

Deep-vein thrombosis

Pulmonary embolism

Dislocation

Periprosthetic fracture

Implant loosening or wear

Need for revision surgery

Patient Monitoring

Patients should be monitored for:

Pain progression

Loss of function

Joint deformity

Range-of-motion loss

Medication adverse effects

Need for assistive devices

Failure of conservative therapy

Key Principle

Osteoarthritis is a progressive degenerative joint disorder characterized by cartilage loss and secondary subchondral bone changes.

Management is directed toward:

Pain control, preservation of motion and strength, weight management, activity modification, and maintenance of function, with osteotomy or joint replacement reserved for appropriately selected patients with advanced symptomatic disease.

Orthopaedic Surgery - Open Fractures

Basics

An open fracture is a fracture in which the fracture site communicates with the external environment through a full-thickness wound.

The fractured bone does not need to protrude through the skin.

Any full-thickness laceration located within the zone of injury should be assumed to communicate with the fracture until proven otherwise.

Open fractures are important because disruption of the skin and soft-tissue envelope exposes the fracture to:

Bacterial contamination

Soft-tissue devitalization

Bone devascularization

and an increased risk of:

Infection, delayed union, and nonunion.

Gustilo–Anderson Classification

Open fractures are commonly classified using the Gustilo–Anderson system.

The classification is based on:

Energy of injury

Wound size

Degree of contamination

Soft-tissue damage

Adequacy of coverage

Presence of vascular injury

Final classification is often most accurate after operative débridement.

Type I

A Type I injury is generally:

Low energy

with a:

Clean wound less than 1 cm in length.

Soft-tissue damage is limited.

Type II

A Type II open fracture typically involves:

Low- to moderate-energy trauma

with a:

Wound greater than 1 cm

but without extensive:

Soft-tissue stripping, crushing, or devitalization.

Type III

Type III injuries are more severe and generally result from:

High-energy trauma

or involve:

Extensive soft-tissue destruction

Marked contamination

Segmental fractures

High-energy penetrating injuries

They are subdivided according to soft-tissue coverage and vascular injury.

Type IIIA

There is substantial soft-tissue injury, but:

Adequate viable tissue remains to cover the bone.

Type IIIB

There is:

Extensive soft-tissue loss, periosteal stripping, and exposed bone

such that satisfactory coverage cannot be achieved without:

Rotational flap

or

Free-tissue transfer.

Type IIIC

A Type IIIC injury is an open fracture associated with an:

Arterial injury requiring repair, regardless of wound size.

Risk Factors

Bones with a thin soft-tissue envelope are more likely to become exposed after fracture.

The classic example is the:

Tibia.

By contrast, the femur is surrounded by a much thicker soft-tissue envelope and is less likely to present as an open fracture after an equivalent degree of injury.

Pathophysiology

The major principles of treatment are to:

Prevent infection

Remove devitalized tissue

Provide skeletal stability

Restore viable soft-tissue coverage

Infection is promoted by:

Bacterial contamination

Necrotic muscle

Devitalized bone

Dead space

Retained foreign material

Poor vascular supply

Associated Conditions

Open fractures frequently occur in the setting of:

High-energy trauma and multiple injuries.

Initial management should therefore follow ATLS principles, with attention to immediately life-threatening injuries before definitive limb reconstruction.

Associated Injury Assessment

The entire patient should be examined.

Particular attention should be given to:

The spine

Adjacent joints

Other extremities

Chest

Abdomen

Pelvis

An obvious open fracture should not distract from other major injuries.

Diagnosis

Signs and Symptoms

Open fractures may follow either:

High-energy

or

Low-energy mechanisms.

The defining feature is communication between the fracture and an external wound.

History

Important questions include:

When did the injury occur?

What was the mechanism?

Was it high or low energy?

Was the wound exposed to soil or barnyard contamination?

Was there freshwater or marine contamination?

Was the wound exposed to oil, grease, or industrial material?

These details influence contamination risk and antibiotic selection.

Physical Examination

The examination has two major objectives:

Recognize the injury as an open fracture

and

Assess the overall fracture, limb, and patient.

Findings Suggesting an Open Fracture

Potential signs include:

Bone protruding from the skin

Fat, marrow, or blood emerging from a wound

A laceration directly over or near the fracture

Large soft-tissue wounds in the zone of injury

Visible bone is not required.

General Fracture Examination

Examine:

The joint above

The joint below

and other potentially injured regions.

Vascular Assessment

Evaluate limb perfusion by assessing:

Palpable pulses

Capillary refill

Skin color

Temperature

Doppler signals when necessary

Ankle-brachial or arterial pressure indices when appropriate

A pulseless or poorly perfused limb requires urgent vascular assessment.

Soft-Tissue Assessment

Assess:

Skin viability

Muscle viability

Contusion

Crush injury

Periosteal stripping

Foreign material

Gross contamination

Soft-tissue loss

Repeated manipulation of the wound should be minimized.

Neurologic Examination

Document motor and sensory function distal to the injury before and after:

Reduction, splinting, and surgery.

Compartment Syndrome

Open fractures do not protect against compartment syndrome.

Suspicion should remain high when there is:

Increasing pain

Pain with passive stretch

Tense compartments

Progressive neurologic deficit

Unexplained swelling

Laboratory Tests

Because most open fractures require operative treatment, appropriate preoperative laboratory studies are usually obtained.

These may include:

CBC

Electrolytes

Renal function

Coagulation studies

Blood type and screen

according to injury severity and anticipated surgery.

Imaging

Radiographs should be tailored to the fracture location.

Standard imaging generally includes:

AP and lateral views of the injured bone

with adequate visualization of:

The joint above and the joint below.

CT

CT may be useful for:

Articular fractures

Complex fracture patterns

Pelvic or periarticular injury

However, CT should not unnecessarily delay:

Urgent antibiotics, débridement, vascular treatment, or stabilization.

Compartment Pressure Monitoring

If the patient cannot be examined reliably or if there is substantial swelling and concern for compartment syndrome, compartment pressures may be measured.

Clinical examination remains central whenever it is reliable.

Differential Diagnosis

Occasionally, a laceration may coexist with a fracture without communicating with it.

However, the safest approach is:

Assume that any full-thickness wound within the fracture zone represents an open fracture until proven otherwise.

Treatment

Initial Stabilization

After life-threatening injuries have been addressed according to trauma principles:

Cover the wound with a sterile dressing

Splint the extremity

Administer intravenous antibiotics promptly

Provide tetanus prophylaxis when indicated

Perform and document neurovascular examination

Unnecessary repeated removal of the dressing should be avoided.

General Treatment Goals

The primary objectives are to:

Prevent infection

Remove devitalized tissue and contamination

Restore alignment and stability

Achieve durable soft-tissue coverage

Preserve limb function

Antibiotics

Early intravenous antibiotic administration is one of the most important interventions.

Antibiotics should be given:

As soon as possible after presentation, rather than waiting for the operating room.

Antibiotic Selection

Historically, treatment included:

A first-generation cephalosporin for lower-grade open fractures

with additional gram-negative coverage for severe Type III injuries.

Current antibiotic protocols vary by institution and local resistance patterns.

Typical regimens provide:

Gram-positive coverage for all open fractures

with broader coverage considered for:

Type III injuries

Gross contamination

Water exposure

Farm injuries

Heavy soil contamination

Penicillin or Anaerobic Coverage

Additional anaerobic coverage may be considered in wounds contaminated by:

Farm soil

Fecal material

Extensive devitalized tissue

or other situations with high risk of clostridial contamination.

Special Contamination

Antibiotic selection may need modification for:

Freshwater exposure

Marine exposure

Industrial contamination

Known resistant organisms

Duration of Antibiotic Therapy

Prophylactic antibiotics are generally continued for a limited period after definitive débridement and closure.

The exact duration depends on:

Fracture severity

Wound closure timing

Institutional protocol

Prolonged prophylaxis without infection is generally avoided.

If established infection develops, treatment becomes:

Culture-directed therapeutic antibiotic management.

Pain Control

Pain may be treated with:

Acetaminophen

Opioids when necessary

and other appropriate analgesics.

Pain control should not interfere with repeated assessment for:

Compartment syndrome or neurologic deterioration.

Tetanus Prophylaxis

Tetanus immunization status should be reviewed.

Patients may require:

Tetanus booster

and, in selected inadequately immunized patients,

Tetanus immune globulin.

Surgery

Most open fractures require operative treatment.

The central surgical principle is:

Meticulous irrigation and débridement.

Débridement

The goal is to leave:

Viable tissue, minimal contamination, adequate perfusion, and a clean wound suitable for reconstruction.

Skin and Subcutaneous Tissue

Nonviable skin and subcutaneous tissue should be excised back to:

Healthy, bleeding tissue.

Muscle Viability

Muscle viability is traditionally assessed according to:

Color

Consistency

Contractility

Capacity to bleed

Nonviable muscle should be removed.

Bone Débridement

Loose cortical fragments that have:

No soft-tissue attachment and no viable blood supply

may require removal.

However, viable bone should be preserved whenever possible.

Irrigation

Copious irrigation is used to:

Reduce bacterial contamination

Remove debris

Clear foreign material

Normal saline is commonly used.

Older teaching recommended fixed volumes such as 6–10 L, but current practice generally tailors irrigation volume to:

Wound size, contamination, and tissue damage.

Timing of Débridement

The historical rigid “6-hour rule” is no longer considered mandatory for every open fracture.

Urgency depends on:

Gross contamination

Vascular injury

Compartment syndrome

Severe soft-tissue compromise

Overall patient condition

Débridement should nevertheless occur promptly and should not be unnecessarily delayed.

Repeat Débridement

Severely contaminated or questionable wounds may require:

Repeat operative débridement within approximately 24–48 hours.

This allows reassessment of tissue viability before definitive closure.

Wound Closure

The timing of closure depends on:

Cleanliness of the wound

Tissue viability

Contamination

Ability to achieve tension-free coverage

Primary Closure

Many Type I and selected Type II wounds can be:

Closed primarily after adequate débridement

when the tissue is viable and contamination is controlled.

Delayed Closure

More severe wounds may require:

Delayed primary closure

after repeat evaluation or débridement.

Soft-Tissue Reconstruction

Large wounds with exposed bone or implants may require plastic surgical reconstruction using:

Local rotational flaps

Muscle flaps

Free-tissue transfer

Early durable coverage is important for both:

Infection control and fracture healing.

Fracture Stabilization

Stable fixation reduces:

Pain

Soft-tissue injury

Dead space

Continued contamination

and facilitates:

Wound care and rehabilitation.

Implant Selection

The fixation method depends on:

Fracture location

Soft-tissue condition

Contamination

Fracture severity

Options include:

External fixation

Intramedullary nailing

Plate-and-screw fixation

External Fixation

Temporary external fixation is useful when there is:

Severe soft-tissue injury

Major contamination

Polytrauma

Vascular repair

Need for staged reconstruction

Definitive Fixation

After the soft tissues and overall condition permit, definitive stabilization may involve:

Intramedullary nailing

Plate fixation

Definitive external fixation

depending on the fracture.

Activity

Weight-bearing and activity restrictions depend on:

Fracture stability

Fixation method

Soft-tissue healing

Associated injuries

Nursing Care

The injured extremity is commonly elevated when appropriate to help control:

Swelling and discomfort.

Care must be taken not to compromise:

Perfusion or wound monitoring.

Physical Therapy

Rehabilitation is individualized.

Goals include:

Maintaining joint range of motion

Restoring strength

Preventing stiffness

Progressing weight bearing safely

Early motion is encouraged when fracture and soft-tissue stability allow.

Follow-Up

Follow-up depends on:

Gustilo type

Fracture location

Soft-tissue reconstruction

Presence of infection

Method of fixation

Wound Monitoring

The wound should be assessed for:

Increasing erythema

Drainage

Persistent swelling

Necrosis

Wound dehiscence

Fever or systemic symptoms

Referral

All open fractures require:

Prompt orthopaedic evaluation.

In complex injuries, additional consultation may be required from:

Plastic surgery

Vascular surgery

Trauma surgery

Infectious disease

Prognosis

Outcome depends heavily on:

Severity of soft-tissue injury

Degree of contamination

Vascular status

Fracture pattern

Presence of infection

Patient comorbidities

Infection Risk

Historical infection rates increase markedly with injury severity.

Approximate older ranges include:

Type I: around 2%

Type II: approximately 2–10%

Type III: approximately 10–50%, depending on subtype, contamination, and location.

Modern treatment may produce lower rates in many settings, but Type III injuries remain at substantially greater risk.

Osteomyelitis

Deep infection may progress to:

Chronic osteomyelitis

with:

Persistent drainage

Bone destruction

Hardware failure

Nonunion

Treatment may require repeated débridement and prolonged culture-directed antibiotics.

Nonunion

The risk of nonunion rises with:

Periosteal stripping

Bone loss

Infection

Mechanical instability

Poor vascularity

Malunion

If alignment is not restored and maintained, the fracture may heal with:

Angular

Rotational

or

Length deformity.

Post-Traumatic Arthritis

Open fractures involving a joint may later produce:

Post-traumatic arthritis, particularly when the articular surface is severely damaged.

Other Complications

Additional complications include:

Compartment syndrome

Vascular compromise

Nerve injury

Hardware failure

Soft-tissue necrosis

Chronic pain

Limb-length discrepancy

Amputation in severe cases

Key Principle

An open fracture should be regarded as both:

A fracture

and

A contaminated soft-tissue injury.

Successful treatment depends on:

Early antibiotics, tetanus prophylaxis, careful sterile wound management, thorough débridement, stable skeletal fixation, restoration of viable soft-tissue coverage, and close surveillance for infection and nonunion.

Orthopaedic Surgery - Nursemaid’s Elbow

Basics

Nursemaid’s elbow is a common injury of early childhood involving the annular ligament around the radial head.

It occurs when longitudinal traction on the arm causes the annular ligament to become displaced or entrapped between the radial head and capitellum.

The child typically responds by:

Guarding the arm

Refusing to use the elbow

Holding the affected upper extremity close to the body

The injury is commonly referred to as a radial head subluxation, although the underlying abnormality primarily involves displacement of the annular ligament rather than a true complete dislocation of the radial head.

Synonyms

Nursemaid’s elbow is also called:

Pulled elbow

Radial head subluxation

Annular ligament entrapment

Prevention

The principal preventive measure is to avoid sudden traction on a young child’s arm.

Parents and caregivers should avoid:

Pulling or lifting a child by one hand or forearm

Swinging a child by the arms

Jerking the arm when the child pulls away

The child should instead be lifted by supporting the trunk or under the arms.

Epidemiology

Nursemaid’s elbow most commonly affects children between:

1 and 5 years of age.

It is one of the most frequent elbow injuries encountered in young children.

Historically, boys and girls have been considered to be affected with similar frequency, although some series report a slight female predominance.

Risk Factors

Important risk factors include:

Age between 1 and 5 years

Previous nursemaid’s elbow

Sudden pulling or traction on the arm

A young child pulling away from an adult who is holding the hand can create the classic mechanism.

Genetics

There is no known genetic predisposition.

Etiology

The injury usually occurs when the forearm is subjected to longitudinal traction while the elbow is extended, often with the forearm pronated.

This can happen when:

A parent pulls the child upward by the hand

A sibling pulls the child’s arm

The child suddenly pulls away while being held

Annular Ligament Injury

With traction, part of the annular ligament may slip over the radial head and become trapped within the radiocapitellar joint.

The ligament may be:

Stretched

Partially torn

or

Displaced into the joint

This produces pain, particularly with forearm rotation.

Typical Mechanism

The classic mechanism is traction rather than a fall.

A fall onto an outstretched hand is more likely to cause another injury, such as:

Distal radius buckle fracture

Supracondylar humeral fracture

Other elbow fracture

Therefore, a history of substantial trauma should prompt consideration of an alternative diagnosis.

Diagnosis

The diagnosis is usually clinical.

Signs and Symptoms

Typical findings include:

Sudden elbow or forearm pain after a traction injury

Refusal to use the affected arm

Minimal tenderness

Little or no swelling

Absence of obvious deformity

Arm Position

The child commonly holds the affected arm:

Close to the side

with the elbow slightly flexed or extended and the forearm often pronated.

The child avoids spontaneous use of the limb.

Palpation

There is usually:

Minimal focal tenderness

and

No substantial swelling or bruising.

Marked tenderness, swelling, ecchymosis, or deformity should raise concern for fracture or another diagnosis.

Diagnostic Response to Reduction

The most characteristic diagnostic feature is rapid return of function after successful reduction.

Within several minutes, the child often begins to:

Reach for objects

Flex the elbow

Rotate the forearm

Use the arm normally

Residual tenderness should be minimal or absent.

Physical Examination

Examine the entire upper extremity before attempting reduction.

Assess for:

Swelling

Ecchymosis

Deformity

Focal bony tenderness

Skin injury

Neurovascular abnormalities

If these features are absent and the history is classic, nursemaid’s elbow is highly likely.

Laboratory Tests

No laboratory test is useful for diagnosing nursemaid’s elbow.

Laboratory studies should only be considered when another condition such as:

Infection or inflammatory disease

is suspected.

Imaging

Radiographs are not routinely required when:

The history is classic

There is no swelling or deformity

The examination is otherwise reassuring

Indications for Radiographs

AP and lateral elbow radiographs should be considered when:

The mechanism is atypical

A fall or direct trauma occurred

There is focal bony tenderness

Significant swelling or bruising is present

Reduction fails

The child continues to refuse use of the arm after reduction

Radiographic Findings

In a true nursemaid’s elbow, radiographs are generally:

Normal.

The purpose of imaging is primarily to exclude:

Fracture or other structural injury.

Pathological Findings

The annular ligament may be:

Stretched, partially torn, or displaced into the radiocapitellar joint.

Complete rupture is not usually present.

Because the condition resolves readily and surgery is almost never required, pathologic specimens are rarely available.

Differential Diagnosis

Important alternative diagnoses include:

Supracondylar humeral fracture

Distal humeral buckle or greenstick fracture

Radial neck fracture

Distal radius fracture

Physeal injury

Elbow infection

Juvenile idiopathic arthritis

Lyme arthritis

These disorders are considerably less common than nursemaid’s elbow in a child with a classic traction mechanism and minimal examination findings.

Fracture Versus Nursemaid’s Elbow

Features favoring a fracture include:

Fall or direct trauma

Substantial swelling

Bruising

Focal bony tenderness

Persistent pain after attempted reduction

Treatment

General Principles

Treatment consists of closed reduction of the displaced annular ligament.

Sedation is usually unnecessary.

Two commonly used techniques are:

Hyperpronation

and

Supination-flexion.

Hyperpronation Technique

The examiner supports the elbow and rapidly but gently pronates the forearm.

A subtle:

Click or pop

may be felt near the radial head.

This technique is commonly effective and may have a high first-attempt success rate.

Supination-Flexion Technique

The traditional maneuver involves:

Supinating the forearm

followed by

Full flexion of the elbow, bringing the child’s hand toward the shoulder.

A small click may be felt during reduction.

Response After Reduction

The child may initially remain upset because of fear or discomfort.

Successful reduction is usually followed within several minutes by spontaneous use of the arm.

The child should be observed until normal use returns.

Analgesia and Sedation

Sedation is generally not required.

Medication is often unnecessary after successful reduction.

If needed, a simple analgesic such as:

Acetaminophen

may be used.

If severe or persistent pain requires stronger analgesia, another diagnosis should be reconsidered.

Immobilization

A sling or splint is usually unnecessary after a first uncomplicated episode.

Immobilization may occasionally be considered after:

Repeated recurrence

or when discomfort persists despite successful reduction.

Activity

After successful reduction, the child may return to:

Normal age-appropriate activity as tolerated.

Parents should be advised to avoid pulling or swinging the child by the arms.

Physical Therapy

Physical therapy is not required.

Children regain normal motion and function spontaneously after reduction.

Surgery

Surgery is not indicated for uncomplicated nursemaid’s elbow.

Persistent inability to reduce the injury should prompt:

Reassessment of the diagnosis and appropriate imaging, rather than repeated forceful manipulation.

Follow-Up

Routine follow-up is usually unnecessary once the child resumes normal use of the arm.

Prognosis

The prognosis is excellent.

Most children recover completely without:

Pain

Loss of motion

Growth disturbance

Long-term elbow dysfunction

Recurrence

Some children experience recurrent nursemaid’s elbow.

Repeated episodes can generally be treated with the same reduction technique.

Recurrence becomes less common with age as the radial head enlarges and the annular ligament becomes more firmly attached.

Children usually outgrow the predisposition by approximately 5–6 years of age.

Recurrent Cases

In selected children with repeated episodes, brief immobilization for approximately:

1–2 weeks

may occasionally be used, although most recurrent episodes still require only reduction and parental education.

Complications

Nursemaid’s elbow itself generally has no significant long-term complications.

The most important potential problem is:

Misdiagnosis.

Missed Fracture

A fracture may be overlooked if an atypical presentation is assumed to be nursemaid’s elbow.

Warning signs include:

Significant swelling

Bruising

Focal tenderness

Deformity

A history of a fall or major trauma

Failure to regain arm use after reduction

Patient Monitoring

No ongoing monitoring is required after successful reduction and return of normal function.

Further evaluation is required when:

Pain persists

The child continues to avoid using the arm

Swelling develops

Reduction is unsuccessful

Key Principle

Nursemaid’s elbow is a traction-related annular ligament injury in young children that typically presents with refusal to use the arm despite minimal swelling or tenderness.

The classic features are:

A traction mechanism, a reassuring examination, successful closed reduction, and rapid return of normal arm use.

Orthopaedic Surgery - Nursemaid’s Elbow

Basics

Nursemaid’s elbow is a common injury of early childhood involving the annular ligament around the radial head.

It occurs when longitudinal traction on the arm causes the annular ligament to become displaced or entrapped between the radial head and capitellum.

The child typically responds by:

Guarding the arm

Refusing to use the elbow

Holding the affected upper extremity close to the body

The injury is commonly referred to as a radial head subluxation, although the underlying abnormality primarily involves displacement of the annular ligament rather than a true complete dislocation of the radial head.

Synonyms

Nursemaid’s elbow is also called:

Pulled elbow

Radial head subluxation

Annular ligament entrapment

Prevention

The principal preventive measure is to avoid sudden traction on a young child’s arm.

Parents and caregivers should avoid:

Pulling or lifting a child by one hand or forearm

Swinging a child by the arms

Jerking the arm when the child pulls away

The child should instead be lifted by supporting the trunk or under the arms.

Epidemiology

Nursemaid’s elbow most commonly affects children between:

1 and 5 years of age.

It is one of the most frequent elbow injuries encountered in young children.

Historically, boys and girls have been considered to be affected with similar frequency, although some series report a slight female predominance.

Risk Factors

Important risk factors include:

Age between 1 and 5 years

Previous nursemaid’s elbow

Sudden pulling or traction on the arm

A young child pulling away from an adult who is holding the hand can create the classic mechanism.

Genetics

There is no known genetic predisposition.

Etiology

The injury usually occurs when the forearm is subjected to longitudinal traction while the elbow is extended, often with the forearm pronated.

This can happen when:

A parent pulls the child upward by the hand

A sibling pulls the child’s arm

The child suddenly pulls away while being held

Annular Ligament Injury

With traction, part of the annular ligament may slip over the radial head and become trapped within the radiocapitellar joint.

The ligament may be:

Stretched

Partially torn

or

Displaced into the joint

This produces pain, particularly with forearm rotation.

Typical Mechanism

The classic mechanism is traction rather than a fall.

A fall onto an outstretched hand is more likely to cause another injury, such as:

Distal radius buckle fracture

Supracondylar humeral fracture

Other elbow fracture

Therefore, a history of substantial trauma should prompt consideration of an alternative diagnosis.

Diagnosis

The diagnosis is usually clinical.

Signs and Symptoms

Typical findings include:

Sudden elbow or forearm pain after a traction injury

Refusal to use the affected arm

Minimal tenderness

Little or no swelling

Absence of obvious deformity

Arm Position

The child commonly holds the affected arm:

Close to the side

with the elbow slightly flexed or extended and the forearm often pronated.

The child avoids spontaneous use of the limb.

Palpation

There is usually:

Minimal focal tenderness

and

No substantial swelling or bruising.

Marked tenderness, swelling, ecchymosis, or deformity should raise concern for fracture or another diagnosis.

Diagnostic Response to Reduction

The most characteristic diagnostic feature is rapid return of function after successful reduction.

Within several minutes, the child often begins to:

Reach for objects

Flex the elbow

Rotate the forearm

Use the arm normally

Residual tenderness should be minimal or absent.

Physical Examination

Examine the entire upper extremity before attempting reduction.

Assess for:

Swelling

Ecchymosis

Deformity

Focal bony tenderness

Skin injury

Neurovascular abnormalities

If these features are absent and the history is classic, nursemaid’s elbow is highly likely.

Laboratory Tests

No laboratory test is useful for diagnosing nursemaid’s elbow.

Laboratory studies should only be considered when another condition such as:

Infection or inflammatory disease

is suspected.

Imaging

Radiographs are not routinely required when:

The history is classic

There is no swelling or deformity

The examination is otherwise reassuring

Indications for Radiographs

AP and lateral elbow radiographs should be considered when:

The mechanism is atypical

A fall or direct trauma occurred

There is focal bony tenderness

Significant swelling or bruising is present

Reduction fails

The child continues to refuse use of the arm after reduction

Radiographic Findings

In a true nursemaid’s elbow, radiographs are generally:

Normal.

The purpose of imaging is primarily to exclude:

Fracture or other structural injury.

Pathological Findings

The annular ligament may be:

Stretched, partially torn, or displaced into the radiocapitellar joint.

Complete rupture is not usually present.

Because the condition resolves readily and surgery is almost never required, pathologic specimens are rarely available.

Differential Diagnosis

Important alternative diagnoses include:

Supracondylar humeral fracture

Distal humeral buckle or greenstick fracture

Radial neck fracture

Distal radius fracture

Physeal injury

Elbow infection

Juvenile idiopathic arthritis

Lyme arthritis

These disorders are considerably less common than nursemaid’s elbow in a child with a classic traction mechanism and minimal examination findings.

Fracture Versus Nursemaid’s Elbow

Features favoring a fracture include:

Fall or direct trauma

Substantial swelling

Bruising

Focal bony tenderness

Persistent pain after attempted reduction

Treatment

General Principles

Treatment consists of closed reduction of the displaced annular ligament.

Sedation is usually unnecessary.

Two commonly used techniques are:

Hyperpronation

and

Supination-flexion.

Hyperpronation Technique

The examiner supports the elbow and rapidly but gently pronates the forearm.

A subtle:

Click or pop

may be felt near the radial head.

This technique is commonly effective and may have a high first-attempt success rate.

Supination-Flexion Technique

The traditional maneuver involves:

Supinating the forearm

followed by

Full flexion of the elbow, bringing the child’s hand toward the shoulder.

A small click may be felt during reduction.

Response After Reduction

The child may initially remain upset because of fear or discomfort.

Successful reduction is usually followed within several minutes by spontaneous use of the arm.

The child should be observed until normal use returns.

Analgesia and Sedation

Sedation is generally not required.

Medication is often unnecessary after successful reduction.

If needed, a simple analgesic such as:

Acetaminophen

may be used.

If severe or persistent pain requires stronger analgesia, another diagnosis should be reconsidered.

Immobilization

A sling or splint is usually unnecessary after a first uncomplicated episode.

Immobilization may occasionally be considered after:

Repeated recurrence

or when discomfort persists despite successful reduction.

Activity

After successful reduction, the child may return to:

Normal age-appropriate activity as tolerated.

Parents should be advised to avoid pulling or swinging the child by the arms.

Physical Therapy

Physical therapy is not required.

Children regain normal motion and function spontaneously after reduction.

Surgery

Surgery is not indicated for uncomplicated nursemaid’s elbow.

Persistent inability to reduce the injury should prompt:

Reassessment of the diagnosis and appropriate imaging, rather than repeated forceful manipulation.

Follow-Up

Routine follow-up is usually unnecessary once the child resumes normal use of the arm.

Prognosis

The prognosis is excellent.

Most children recover completely without:

Pain

Loss of motion

Growth disturbance

Long-term elbow dysfunction

Recurrence

Some children experience recurrent nursemaid’s elbow.

Repeated episodes can generally be treated with the same reduction technique.

Recurrence becomes less common with age as the radial head enlarges and the annular ligament becomes more firmly attached.

Children usually outgrow the predisposition by approximately 5–6 years of age.

Recurrent Cases

In selected children with repeated episodes, brief immobilization for approximately:

1–2 weeks

may occasionally be used, although most recurrent episodes still require only reduction and parental education.

Complications

Nursemaid’s elbow itself generally has no significant long-term complications.

The most important potential problem is:

Misdiagnosis.

Missed Fracture

A fracture may be overlooked if an atypical presentation is assumed to be nursemaid’s elbow.

Warning signs include:

Significant swelling

Bruising

Focal tenderness

Deformity

A history of a fall or major trauma

Failure to regain arm use after reduction

Patient Monitoring

No ongoing monitoring is required after successful reduction and return of normal function.

Further evaluation is required when:

Pain persists

The child continues to avoid using the arm

Swelling develops

Reduction is unsuccessful

Key Principle

Nursemaid’s elbow is a traction-related annular ligament injury in young children that typically presents with refusal to use the arm despite minimal swelling or tenderness.

The classic features are:

A traction mechanism, a reassuring examination, successful closed reduction, and rapid return of normal arm use.

Orthopaedic Surgery - Nonunion of Fractures

⸻

Basics

A fracture nonunion is a failure of normal bone healing in which the fracture shows little or no further progression toward union over an appropriate period of time.

The diagnosis is based on a combination of:

Clinical symptoms

Serial radiographs

Fracture biology

Mechanical stability

There is no single time threshold that applies to every fracture because expected healing varies according to the bone, fracture location, injury severity, fixation method, and patient factors.

⸻

Epidemiology

The likelihood of nonunion varies substantially among different bones and fracture patterns.

Historical approximate rates include:

Tibial shaft fractures: about 10%

Clavicular shaft fractures: about 5%

Femoral shaft fractures: about 1%

Metaphyseal and epiphyseal fractures generally have a strong healing potential, although they may heal in an abnormal position and result in malunion if the original displacement is not adequately corrected.

⸻

Risk Factors

The most important modifiable risk factor is:

Tobacco smoking.

Nicotine and other tobacco-related effects impair vascularity and bone healing.

⸻

Nutritional Factors

Poor nutritional status can interfere with fracture healing.

Potential contributors include:

Vitamin D deficiency

Protein-calorie malnutrition

Other vitamin or mineral deficiencies

⸻

Systemic Disease

Patients with systemic illness may have impaired fracture healing.

Examples include conditions that compromise:

Metabolism

Vascular supply

Immune function

Bone quality

⸻

Open Fractures

Severe open fractures are at particularly high risk.

This is especially true for Gustilo-Anderson Type III open fractures, which may be associated with:

Extensive soft-tissue injury

Contamination

Bone loss

Compromised blood supply

Infection

⸻

Etiology

Nonunion usually results from one or more problems involving:

Biology

Mechanical stability

Infection

or

Bone loss.

⸻

Open Fractures

Open fractures may impair healing because of:

Soft-tissue destruction, periosteal stripping, contamination, and vascular injury.

⸻

Bone Loss

A fracture gap or loss of a segment of bone can prevent the fragments from making sufficient biological or mechanical contact for union.

⸻

Osteomyelitis

Bone infection is an important cause of nonunion.

An infected nonunion must be recognized because its treatment differs fundamentally from that of an aseptic nonunion.

⸻

Diagnosis

⸻

Signs and Symptoms

Persistent pain is a common presentation.

Typical symptoms include:

Pain with weight bearing

Pain with limb use

Failure of symptoms to improve over time

⸻

History

Important historical features include:

Original fracture mechanism

Whether the injury was open

Previous operations

Smoking history

Nutritional status

Systemic disease

Prolonged wound drainage after the initial operation

Persistent or recurrent wound drainage raises particular concern for infection.

⸻

Physical Examination

⸻

Motion at the Fracture Site

Abnormal motion at a fracture that should have healed suggests nonunion.

⸻

Pain With Stress

Applying stress across the involved bone may reproduce pain at the fracture site.

This may indicate persistent mechanical instability.

⸻

Wound Examination

Inspect carefully for:

Persistent drainage

Sinus formation

Soft-tissue loss

Erythema

Swelling

These findings may indicate infection or inadequate soft-tissue coverage.

⸻

Limb Function

Assess:

Alignment

Length

Rotation

Joint motion

Muscle strength

Neurovascular status

A healed bone alone is not the only objective; the limb must also have useful function.

⸻

Imaging

⸻

Plain Radiographs

Serial radiographs are the first-line imaging study.

Typical findings may include:

Persistent fracture line

Failure of the proximal and distal fragments to unite

Lack of bridging callus

Broken fixation hardware

Lucency around screws

Progressive deformity

⸻

Hardware Failure

Broken plates, screws, nails, or other implants often indicate persistent mechanical loading across a fracture that has not united.

Lucency around screws may reflect:

Loosening, infection, or both.

⸻

CT

CT is often the most useful advanced imaging study when plain radiographs are inconclusive.

It can demonstrate:

Absence of bridging bone across the fracture

Persistent fracture gaps

Partial union

Hardware failure

Complex deformity

⸻

Laboratory Evaluation for Infection

When infection is suspected, evaluation may include:

CBC

ESR

CRP

These tests are supportive but cannot definitively rule infection in or out.

Definitive diagnosis often requires:

Deep tissue or bone cultures obtained at surgery.

⸻

Pathological Findings

The fracture gap is commonly filled with:

Fibrous tissue rather than bridging bone.

⸻

Pseudoarthrosis

With longstanding instability, a false joint may develop between the bone ends.

This can form a synovial pseudoarthrosis, in which the opposing surfaces behave like an abnormal joint.

⸻

Classification by Biology

Although not specified in the original entry, nonunion is commonly described biologically as:

Hypertrophic

Oligotrophic

Atrophic

This distinction can help guide treatment.

⸻

Hypertrophic Nonunion

A hypertrophic nonunion demonstrates abundant callus but failure of bridging because of excessive motion.

The principal problem is usually:

Insufficient mechanical stability.

⸻

Atrophic Nonunion

An atrophic nonunion has little callus and poor biological activity.

Contributing factors may include:

Poor vascularity

Bone loss

Soft-tissue compromise

Infection

⸻

Differential Diagnosis

The most important distinction is between:

Septic nonunion

and

Aseptic nonunion.

⸻

Septic Nonunion

An infected nonunion may be suggested by:

Persistent drainage

Sinus tract

Elevated inflammatory markers

Implant loosening

Previous deep infection

However, infection may occasionally be clinically subtle.

⸻

Aseptic Nonunion

Aseptic nonunion occurs without active infection and is more commonly related to:

Mechanical instability

Poor biological environment

Bone loss

or a combination of these factors.

⸻

Synovial Pseudoarthrosis

The presence of a mature false joint may alter surgical planning because fibrous and synovial tissue must usually be removed before definitive healing can occur.

⸻

Treatment

⸻

General Principles

Treatment begins by identifying why the fracture failed to unite.

Successful management requires correction of every important problem rather than simply adding more fixation.

⸻

Smoking Cessation

All tobacco and nicotine products should be stopped.

Continued smoking substantially reduces the likelihood of successful union.

⸻

Nutritional Optimization

Correct identifiable deficiencies, including:

Vitamin D deficiency

Poor protein intake

Other nutritional abnormalities

⸻

Medical Optimization

Systemic conditions that impair healing should be treated or optimized whenever possible.

⸻

Surgical Planning

Before surgery, determine:

Is the nonunion infected?

Is there adequate blood supply?

Is there significant bone loss?

Is the fixation mechanically inadequate?

Is deformity present?

Is the soft-tissue envelope adequate?

⸻

Septic Nonunion

If infection is present, identifying the causative organism is critical.

Failure to obtain appropriate microbiologic diagnosis can lead to:

Persistent infection and repeated treatment failure.

⸻

Microbiologic Diagnosis

Multiple deep tissue cultures are generally preferred.

Superficial swabs are less reliable.

Management may include:

Débridement

Culture-directed antibiotics

Removal or revision of infected hardware

Staged reconstruction

⸻

Débridement

All nonviable tissue may need to be removed, including:

Necrotic bone

Fibrous tissue

Infected soft tissue

Loose implants

The goal is to leave a viable biological environment capable of healing.

⸻

Soft-Tissue Coverage

Adequate vascularized soft-tissue coverage is essential.

If local tissue is inadequate, reconstruction may require:

Rotational muscle flap

or

Free tissue transfer.

⸻

Mechanical Stability

When excessive movement is the primary cause, treatment must reduce motion at the fracture site.

Stable fixation may be achieved using:

Revision intramedullary nailing

Plate fixation

Compression plating

Dual plating

External fixation

depending on the bone and fracture pattern.

⸻

Rigid Fixation

Some nonunions require very rigid stabilization, such as:

Double-plate fixation, particularly when substantial mechanical instability is present.

⸻

Bone Grafting

When biology is insufficient, bone grafting may be used to stimulate healing.

Options may include:

Autologous cancellous bone graft

Structural graft

Vascularized bone graft

Bone graft substitutes in selected situations

⸻

Bone Defects

Large segmental defects may require:

Bone transport

Masquelet-type induced membrane techniques

Vascularized grafting

or other reconstructive strategies.

⸻

Follow-Up

⸻

Prognosis

Union can be achieved in most patients when:

Infection, biology, alignment, and mechanical stability are all addressed appropriately.

⸻

Limb Salvage

Even when union is eventually achieved, the functional result depends on:

Joint condition

Muscle function

Nerve function

Soft-tissue quality

Limb alignment

⸻

Amputation

In rare situations, amputation may be appropriate when:

Repeated reconstruction fails

Infection cannot be controlled

The limb remains severely painful

Useful function cannot be restored

⸻

Complications

⸻

Infection

Infection is one of the most important complications.

The risk of infection increases with repeated operative procedures.

Historical teaching suggests that infection risk may approximately double with each additional surgery, although the actual risk varies substantially according to injury and patient factors.

⸻

Persistent Nonunion

Despite appropriate treatment, some fractures may fail to heal again.

Persistent nonunion may require:

Repeat fixation

Further grafting

Soft-tissue reconstruction

Bone transport

or, occasionally,

Amputation.

⸻

Other Complications

Potential complications include:

Hardware failure

Malalignment

Joint stiffness

Limb-length discrepancy

Chronic pain

Refracture

Donor-site morbidity from bone grafting

⸻

Patient Monitoring

Serial radiographs are used to assess progression toward union.

Historically, imaging may be obtained approximately every 4 weeks, although the interval should be individualized according to:

Fracture location

Treatment method

Symptoms

Expected rate of healing

⸻

CT Monitoring

CT may occasionally be required when:

Plain radiographs do not clearly demonstrate whether bridging bone is present.

⸻

Clinical Healing

Progress should be assessed using both imaging and clinical findings.

Important indicators include:

Reduced pain

Improved weight-bearing tolerance

Loss of abnormal motion

Improved limb function

Progressive radiographic bridging

⸻

Key Principle

Successful treatment of fracture nonunion depends on identifying and correcting the underlying cause.

The central questions are:

Is infection present?

Is the biology adequate?

Is the soft-tissue envelope viable?

Is fixation sufficiently stable?

Is bone grafting or vascularized tissue needed?

When these factors are addressed systematically, most nonunions can ultimately be brought to union.

Orthopaedic Surgery - Neurofibromatosis

Basics

Neurofibromatosis is an inherited multisystem disorder that primarily affects tissues derived from the neural crest.

The skeletal and nervous systems account for many of its most important clinical manifestations.

The most common form is neurofibromatosis type 1 (NF1), which is the form discussed here.

NF1 has historically been called von Recklinghausen disease.

NF1 and NF2

NF1 should be distinguished from neurofibromatosis type 2, now more specifically associated with NF2-related schwannomatosis.

NF2 classically presents with:

Bilateral vestibular schwannomas, historically called bilateral acoustic neuromas.

The skeletal manifestations described here are primarily those of NF1.

Age at Presentation

NF1 is present genetically from birth, but many manifestations emerge gradually.

Some findings, such as:

Café-au-lait macules

may be visible during infancy.

Other features, including:

Neurofibromas, scoliosis, and other skeletal abnormalities

may not become apparent until later childhood or adolescence.

For this reason, the diagnosis may not be established immediately after birth.

Epidemiology

NF1 occurs in approximately:

1 in 3,000 newborns.

Males and females are affected with approximately equal frequency.

Risk Factors

The strongest risk factor is:

An affected parent or first-degree relative.

Advanced paternal age has historically been associated with an increased rate of new NF1 mutations.

Genetics

NF1 is inherited in an autosomal-dominant pattern.

Approximately half of affected individuals inherit the condition from an affected parent, while the remainder develop it from a de novo pathogenic variant.

Penetrance is nearly complete, although the severity and pattern of clinical manifestations vary widely.

Etiology

NF1 results from pathogenic variants in the NF1 gene, which encodes the protein neurofibromin.

Neurofibromin functions as an important regulator of cellular growth signaling.

Loss of normal neurofibromin activity contributes to:

Tumor formation, abnormal tissue growth, skeletal dysplasia, and other manifestations of NF1.

Associated Conditions

NF1 may affect multiple organ systems.

Important associated findings include:

Learning difficulties

Developmental delay

Attention or cognitive problems

Hypertension

Renal artery stenosis

Pheochromocytoma

Optic pathway glioma

Peripheral nerve tumors

Cognitive and Developmental Findings

A substantial proportion of children with NF1 have some degree of:

Learning disability, developmental delay, attention difficulty, or impaired school performance.

Severe intellectual disability is less common.

Hypertension

Hypertension may result from:

Renal artery stenosis

Pheochromocytoma

or ordinary essential hypertension.

Blood pressure should therefore be checked regularly.

Diagnosis

Diagnosis is based primarily on characteristic clinical findings.

Historically, the NIH criteria required two or more characteristic features.

Modern diagnostic criteria remain centered on similar manifestations, together with molecular testing when appropriate.

Café-au-Lait Macules

One classic diagnostic feature is:

Six or more café-au-lait macules.

Traditionally, size thresholds are:

At least 5 mm in prepubertal children

and

At least 15 mm after puberty.

These lesions are typically:

Flat, hyperpigmented, and well demarcated.

Axillary or Inguinal Freckling

Freckling in the:

Axillae or groin

is another characteristic finding.

It usually develops later than café-au-lait macules.

Neurofibromas

Diagnostic findings include:

Multiple cutaneous neurofibromas

or

A plexiform neurofibroma.

Cutaneous Neurofibromas

Cutaneous neurofibromas arise from peripheral nerves within or beneath the skin.

They usually cause few symptoms but may become numerous with age.

Plexiform Neurofibromas

Plexiform neurofibromas involve multiple branches of a nerve and may produce:

Pain

Neurologic deficit

Disfigurement

Functional impairment

They also carry a risk of malignant transformation.

Lisch Nodules

Lisch nodules are benign iris hamartomas.

Two or more Lisch nodules support the diagnosis.

They are best detected using a:

Slit-lamp ophthalmologic examination.

Optic Pathway Glioma

Optic pathway glioma is an important manifestation of NF1.

It may cause:

Visual impairment, proptosis, strabismus, or precocious puberty, depending on tumor location.

Skeletal Lesions

Characteristic osseous abnormalities include:

Dystrophic scoliosis

Vertebral scalloping

Rib penciling

Congenital tibial dysplasia and pseudarthrosis

Long-bone bowing

Other skeletal dysplasias may also occur.

Family History

A first-degree relative with confirmed NF1 strongly supports the diagnosis in an individual with compatible clinical findings.

Signs and Symptoms

Symptoms vary according to the involved organ system.

Plexiform Neurofibromas

These may cause:

Pain

Weakness

Sensory change

Compression of adjacent structures

Symptoms follow the distribution and location of the involved nerve.

Cutaneous Neurofibromas

These generally produce few neurologic symptoms but may cause:

Cosmetic concern, irritation, or local discomfort.

Physical Examination

A complete examination should include:

Skin inspection

Spinal assessment

Limb alignment

Neurologic evaluation

Blood pressure measurement

Developmental assessment

Skin Examination

Inspect the entire skin surface, including the:

Axillae and groin.

Look for:

Café-au-lait macules

Axillary or inguinal freckling

Cutaneous neurofibromas

Plexiform neurofibromas

Spine Examination

Assess the neck and entire spine for:

Scoliosis

Kyphosis

Asymmetry

Rapidly progressive deformity

NF-related spinal deformity can progress rapidly, especially when dystrophic features are present.

Limb Assessment

Measure:

Limb lengths

and assess for:

Bowing, angular deformity, pseudarthrosis, or asymmetric overgrowth.

A classic lower-extremity manifestation is anterolateral bowing of the tibia.

Ophthalmologic Examination

Children with suspected or confirmed NF1 should undergo appropriate ophthalmologic evaluation.

Assessment may include:

Visual acuity

Slit-lamp examination for Lisch nodules

Evaluation for optic pathway abnormalities

Laboratory Tests

Routine laboratory tests do not show a specific abnormality diagnostic of NF1.

Genetic testing can identify an NF1 pathogenic variant in many patients and is particularly useful when:

Clinical findings are incomplete, the diagnosis is uncertain, or genetic counseling is required.

Imaging

Plain Radiographs

Radiographs are useful for identifying many skeletal manifestations.

Spinal Findings

Radiographic abnormalities may include:

Posterior vertebral body scalloping

Rib penciling

Short, sharply angulated scoliosis

Severe vertebral rotation

Malformed or wedged vertebrae

Enlarged neural foramina

Dystrophic Scoliosis

Dystrophic scoliosis in NF1 is characteristically:

Short-segmented

Sharp

Highly rotated

and often associated with:

Kyphosis and penciled ribs.

It behaves more aggressively than ordinary idiopathic scoliosis.

Nondystrophic Scoliosis

Some patients initially have a longer, more typical scoliosis without obvious dystrophic features.

Because nondystrophic curves may later develop dystrophic changes, continued surveillance is important.

Dural Ectasia

NF1 may be associated with:

Dural ectasia, in which the dural sac becomes enlarged and may erode or remodel surrounding bone.

This can contribute to:

Vertebral scalloping, widening of neural foramina, and spinal instability.

Pseudomeningocele

Pseudomeningoceles may also develop and can alter the anatomy of the spinal canal and posterior elements.

MRI of the Spine

MRI should be obtained when significant spinal deformity is present, especially before surgery.

It helps assess:

Spinal cord position

Dural ectasia

Pseudomeningoceles

Neurofibromas

Intraspinal tumors

Neural compression

CT of the Spine

CT is useful for defining:

Pedicle morphology

Laminae

Vertebral dysplasia

Bone available for instrumentation

This information is particularly important when spinal fixation is planned.

Long-Bone Lesions

NF1 may produce a wide spectrum of long-bone abnormalities.

These range from:

Mild cortical scalloping

to

Marked dysplasia, bowing, fracture, and pseudarthrosis.

Some lesions can appear aggressive radiographically and mimic malignancy.

Tibial Dysplasia and Pseudarthrosis

A classic lesion is anterolateral bowing of the tibia, which may progress to fracture and pseudarthrosis.

Radiographic findings may include:

Cystic changes

Narrowing of the bone

Sclerosis

Tapering or pointed bone ends

Established nonunion

Some fractures occur very early in life.

Advanced MRI Techniques

Specialized MRI or metabolic imaging may be used when there is concern for:

Malignant transformation of a plexiform neurofibroma or other tumor complication.

Pathological Findings

NF1 affects tissues derived from the embryonic neural crest, helping explain its involvement of numerous organ systems.

Lisch Nodules

Lisch nodules are:

Hamartomatous deposits of the iris.

Pseudarthrosis

Bone at a pseudarthrosis site often shows:

Fibrosis, poor osteogenic activity, and limited osteoblast function.

This contributes to difficult fracture healing.

Neurofibromas

Cutaneous neurofibromas contain:

Schwann cells, fibroblasts, and connective-tissue elements.

Differential Diagnosis

Legius Syndrome

Legius syndrome can resemble NF1 because patients may develop:

Multiple café-au-lait macules and axillary freckling

but typically do not develop the neurofibromas, Lisch nodules, or characteristic tumors seen in NF1.

Proteus Syndrome

Proteus syndrome may resemble NF1 because of:

Segmental overgrowth, tumors, and skeletal abnormalities.

Its pattern of asymmetric overgrowth and other characteristic findings help distinguish it.

Congenital Tibial Pseudarthrosis

A child with apparently isolated congenital tibial dysplasia or pseudarthrosis should be followed carefully because other NF1 findings, especially café-au-lait macules, may become apparent later.

NF2-Related Schwannomatosis

NF2-related disease is distinct from NF1.

Its classic manifestation is:

Bilateral vestibular schwannomas, together with other nervous-system tumors.

Treatment

General Principles

NF1 requires lifelong multidisciplinary surveillance.

Patients should be followed by clinicians familiar with the disorder to detect:

Developmental problems

Growth abnormalities

Spinal deformity

Neurologic deterioration

Hypertension

Tumor complications

Activity

Activity should generally be encouraged and should not be restricted unnecessarily.

Restrictions are appropriate when a skeletal lesion creates a significant risk of:

Fracture or neurologic injury.

Tibial Bracing

Children with tibial dysplasia or pre-pseudarthrosis should generally receive protective bracing, especially during weight-bearing activity.

Protection may need to continue until:

Skeletal maturity.

Plexiform Neurofibroma Treatment

Management depends on:

Symptoms, location, growth, neurologic effects, and risk of malignant transformation.

Surgery may be difficult because plexiform lesions can be:

Diffuse and highly vascular.

Targeted Medical Therapy

Modern treatment for selected symptomatic, inoperable plexiform neurofibromas may include targeted inhibition of the RAS/MAPK pathway, such as MEK-inhibitor therapy.

This may reduce tumor volume and improve symptoms in selected patients.

Scoliosis Treatment

Nondystrophic Curves

Nondystrophic scoliosis may initially be treated similarly to idiopathic scoliosis, depending on:

Curve magnitude, progression, and skeletal maturity.

However, close follow-up is required because dystrophic features can develop.

Dystrophic Scoliosis

Dystrophic curves have a greater tendency to:

Progress rapidly, develop severe kyphosis, and fail nonoperative treatment.

Evidence of progression warrants early specialist evaluation.

Spinal Surgery

Surgery is frequently considered when there is:

Progressive dystrophic scoliosis

Severe kyphosis

Neurologic compromise

Marked deformity

Older treatment approaches frequently recommended combined anterior and posterior fusion for:

Focal kyphosis or curves greater than approximately 50–60° in skeletally immature patients.

Modern techniques may use posterior-only segmental instrumentation in selected cases, depending on anatomy and deformity severity.

Neurologic Risk During Correction

Severe dystrophic kyphosis may be associated with:

Malformed vertebrae, dural ectasia, and compromised spinal anatomy.

Aggressive correction can cause neurologic injury, so deformity correction must be planned carefully.

Tibial Pseudarthrosis

When tibial dysplasia is identified before fracture, prevention of fracture is a major priority.

If fracture and pseudarthrosis occur, treatment may include:

Intramedullary fixation

Bone grafting

Vascularized fibular grafting

Compression-distraction treatment using circular external fixation

Protection After Union

Even after apparent union, the affected tibia remains at risk for refracture.

Continued protection, often with bracing, may be required through the end of growth.

Limb-Length Discrepancy

Limb-length inequality should be monitored serially.

If discrepancy becomes significant, options may include:

Contralateral epiphysiodesis

or

Limb lengthening

depending on predicted discrepancy and remaining growth.

Follow-Up

Prognosis

Many patients with NF1 remain functionally independent.

Prognosis varies according to the severity of:

Neurologic disease

Skeletal deformity

Tumor burden

Malignant transformation

Life expectancy may be reduced in patients with severe complications.

Malignancy

NF1 is associated with an increased risk of several tumors.

One of the most important is:

Malignant peripheral nerve sheath tumor, which can arise from a preexisting plexiform neurofibroma.

Warning signs include:

Rapid tumor growth

New persistent pain

Hardening of a previously soft lesion

New neurologic deficit

These findings require prompt evaluation.

Central Nervous System Tumors

Patients also have an increased risk of:

Optic pathway glioma and other nervous-system tumors.

Severe Pseudarthrosis

Persistent tibial pseudarthrosis can be extremely difficult to treat.

In rare severe cases with repeated failed reconstruction and major functional impairment, amputation may become a salvage option.

Spinal Complications

Dystrophic scoliosis and kyphosis may cause:

Progressive deformity

Pain

Pulmonary compromise

Neurologic injury

Patient Monitoring

Children with NF1 require regular surveillance throughout growth.

Spine Monitoring

Physical examination for scoliosis should be performed at least:

Yearly during growth, with more frequent follow-up when deformity is present.

Limb-Length Monitoring

Children with limb-length inequality may require serial measurements or standing limb-length imaging.

Historically, annual scanograms have been used.

Blood Pressure

Blood pressure should be checked regularly because of the increased risk of:

Renal artery stenosis, pheochromocytoma, and other causes of hypertension.

Neurologic Monitoring During Surgery

Spinal cord monitoring should be used during major spinal reconstruction whenever feasible because patients with severe dystrophic deformity have increased neurologic risk.

Key Principle

NF1 is a multisystem genetic disorder with important orthopaedic manifestations, especially:

Dystrophic scoliosis, tibial dysplasia and pseudarthrosis, limb-length inequality, and tumor-related neurologic compromise.

Successful management depends on:

Early recognition, lifelong surveillance, protection of dysplastic bone, careful monitoring of spinal deformity, evaluation for malignant transformation, and multidisciplinary care.

Orthopaedic Surgery - Neck Pain

Basics

Neck pain is a common musculoskeletal complaint in adults.

In adults, it is most often related to:

Degenerative disc disease

Cervical spondylosis

Facet arthritis

In children and adolescents, persistent neck pain is less common and should prompt consideration of more serious causes such as:

Infection

Neoplasm

Inflammatory disease

Congenital or structural abnormalities

Neck pain is also common after trauma, particularly following motor vehicle collisions.

Prevention

No specific method reliably prevents all causes of neck pain.

General preventive measures include:

Seat-belt use

Appropriate head restraints

Protective equipment during sports

Avoidance of high-risk trauma when possible

Attention to posture, ergonomics, and conditioning may reduce some episodes of mechanical neck pain.

Epidemiology

Neck pain is common in the general population.

Older epidemiologic studies suggested that approximately 10% of people may experience neck pain at any given time.

One survey reported that nearly 35% of adults experienced neck pain during the preceding year.

Chronic neck pain has historically been reported in approximately:

9.5% of men

and

13.5% of women

in some populations.

Risk Factors

Potential risk factors include:

Congenital cervical fusion, such as Klippel–Feil syndrome

Positive family history

Degenerative cervical disease

Previous trauma

Occupational or postural stress

Etiology

The causes of neck pain can broadly be divided into:

Atraumatic

and

Traumatic causes.

Atraumatic Neck Pain

Common causes include:

Degenerative disc disease

Facet arthritis

Inflammatory arthritis

Disc herniation

Infection

Neoplasm

Muscle strain and nonspecific mechanical pain are also frequent causes.

Traumatic Neck Pain

Traumatic causes include:

Ligament sprain

Muscle strain

Fracture

Subluxation

Dislocation

Disc herniation

Some of these abnormalities, particularly degenerative changes and disc disease, may also occur without trauma in older adults.

Diagnosis

Signs and Symptoms

Common symptoms include:

Localized neck pain

Stiffness

Loss of cervical motion

Paraspinal muscle spasm

Cervical radicular pain

Cervical Radiculopathy

Cervical nerve-root compression may produce:

Pain radiating into the shoulder or arm

Numbness or paresthesia

Weakness

Diminished reflexes

The specific pattern depends on the involved nerve root.

History

Important historical features include:

Onset and duration of pain

Traumatic versus atraumatic mechanism

Radiation into the arm

Weakness or numbness

Difficulty walking

Bowel or bladder symptoms

Fever

Weight loss

History of malignancy

Immunosuppression

Previous cervical surgery

In trauma, the mechanism and energy of injury should be clearly established.

Physical Examination

The examination differs between routine neck pain and acute cervical trauma.

Routine Cervical Examination

Evaluation should focus on:

Range of motion

Areas of tenderness

Muscle spasm

Neurologic function

Range of Motion

Assess:

Flexion

Extension

Rotation

Lateral bending

Painful restriction or asymmetry should be documented.

Palpation

Palpate the:

Midline posterior cervical structures

Paraspinal muscles

Trapezius

Assess for:

Midline tenderness

Muscle spasm

Focal bony tenderness

Neurologic Examination

A complete neurologic examination should include:

Motor strength

Sensation

Deep tendon reflexes

Gait

Upper motor neuron signs

Upper Motor Neuron Findings

Findings suggesting cervical spinal cord involvement include:

Hyperreflexia

Clonus

Hoffmann sign

Babinski sign

Hand clumsiness

Gait disturbance

These findings warrant evaluation for cervical myelopathy or spinal cord compression.

Trauma Examination

In a patient with suspected cervical spine trauma, the neck should be protected until clinically significant instability has been excluded.

Evaluation should include:

Immobilization when indicated

Complete neurologic examination

Appropriate cervical spine imaging

Movement of the neck should not be forced when fracture or instability is suspected.

Spurling Test

The Spurling maneuver is used to evaluate for cervical radiculopathy.

The test generally involves:

Cervical extension and rotation toward the symptomatic side with gentle axial loading.

Reproduction of the patient’s characteristic arm pain or paresthesia supports nerve-root irritation.

The maneuver should be avoided in patients with suspected cervical instability or acute major trauma.

Laboratory Tests

Laboratory studies are not routinely required for uncomplicated mechanical neck pain.

When infection is suspected, useful tests include:

Complete blood count

ESR

CRP

Further testing is guided by the suspected cause.

Imaging

Plain Radiographs

Plain radiographs may be useful in selected patients with:

Persistent symptoms

Suspected degenerative disease

Possible deformity

Certain low-risk trauma patterns

Standard views may include:

AP and lateral cervical spine radiographs.

In modern significant cervical trauma, CT is generally preferred because of its greater sensitivity for fracture.

Oblique Views

Oblique radiographs can demonstrate:

Neural foramina

and may help identify:

Foraminal narrowing or osteophytic encroachment.

They are used selectively because CT and MRI often provide more useful information.

Open-Mouth Odontoid View

The open-mouth view is designed to visualize:

C1 lateral masses

C2 odontoid process

It can be useful in selected settings, although CT has largely replaced it in significant trauma.

Flexion–Extension Views

Dynamic flexion and extension radiographs may be used selectively to evaluate:

Segmental instability

They should not be performed acutely when an unstable fracture or significant ligament injury has not been excluded.

CT

CT is excellent for evaluating:

Cervical fractures

Facet dislocations

Bony canal narrowing

Congenital osseous abnormalities

Small cortical lesions such as osteoid osteoma

It is rapid and highly sensitive for osseous injury.

MRI

MRI is the preferred study for evaluating:

Spinal cord compression

Nerve-root compression

Disc herniation

Ligamentous injury

Bone marrow disease

Tumor

Infection

Foraminal stenosis

MRI is particularly important when neurologic abnormalities are present despite normal or equivocal radiographs or CT.

Differential Diagnosis

Adults: Atraumatic Causes

Important causes include:

Degenerative disc disease

Cervical spondylosis

Rheumatoid arthritis

Ankylosing spondylitis

Discitis

Vertebral osteomyelitis

Meningitis

Disc herniation

Neoplasm

Adults: Traumatic Causes

Consider:

Ligament sprain

Fracture

Subluxation

Dislocation

Traumatic disc herniation

Children: Atraumatic Causes

Important diagnoses include:

Atlantoaxial rotatory subluxation

Retropharyngeal or other deep-neck abscess

Osteomyelitis

Discitis

Neoplasm

Children: Traumatic Causes

Consider:

Ligamentous injury

Fracture

Dislocation

Spinal cord injury without obvious radiographic abnormality

SCIWORA

Spinal cord injury without radiographic abnormality, historically termed SCIWORA, is particularly relevant in children because their flexible spine may sustain cord injury without an obvious fracture on initial plain imaging.

Neurologic deficits after trauma may occasionally be delayed.

Therefore, transient symptoms such as:

Arm or leg weakness

Numbness

Paresthesias

following cervical trauma should be taken seriously.

MRI is important when spinal cord injury is suspected.

Treatment

General Principles

Treatment depends on the underlying cause.

Most uncomplicated mechanical neck pain is initially managed nonoperatively.

Rest and Activity

A short period of relative rest may be useful during the most painful stage.

Prolonged inactivity should be avoided because it may contribute to:

Muscle deconditioning and stiffness.

Activity should be resumed gradually as symptoms improve.

NSAIDs and Analgesia

NSAIDs may help reduce:

Pain and inflammation

when not contraindicated.

Acetaminophen may also be used for pain relief.

Cervical Collar

A soft cervical collar may provide temporary comfort in selected patients.

However, prolonged use should be avoided because it can cause:

Paraspinal muscle deconditioning and increased stiffness.

Posture and Ergonomics

Modification of:

Sitting posture

Workstation ergonomics

Pillow or sleep position

may be beneficial in mechanical neck pain.

Exercise

Appropriate exercise helps maintain:

Cervical range of motion

Postural control

Muscular endurance

Shoulder-girdle strength

Physical Therapy

Physical therapy may be useful for:

Restoring motion

Strengthening cervical and scapular stabilizers

Improving posture

Reducing muscle spasm

Managing chronic mechanical pain

Traction

Gentle cervical traction may reduce symptoms in selected patients with:

Cervical radiculopathy or nerve-root irritation.

It should not be used when instability, fracture, infection, or tumor is suspected.

Medication

NSAIDs are commonly used for a limited period, often several weeks, depending on symptom severity.

Medication should be discontinued or reduced when symptoms resolve.

Long-term medication use should be individualized according to risks and benefits.

Surgery

Surgery is rarely indicated for isolated axial neck pain alone.

Outcomes are generally less predictable when surgery is performed solely for nonspecific neck pain.

Surgical Indications

Operative treatment is more commonly considered when there is:

Progressive neurologic deficit

Spinal cord compression

Persistent nerve-root compression

Instability

Fracture or dislocation

Tumor

Infection requiring surgical management

Degenerative Disease

Surgery for degenerative disease typically aims to:

Decompress the nerve roots or spinal cord

and, when necessary,

Stabilize or fuse the affected segment.

Follow-Up

Patients with uncomplicated neck pain can generally be reviewed at approximately 4–6-week intervals until symptoms improve.

Earlier reassessment is necessary if neurologic symptoms appear or worsen.

Prognosis

The prognosis depends on the underlying cause.

Most patients with uncomplicated mechanical or inflammatory neck pain improve with:

Activity modification

Analgesia

Physical therapy

Postural correction

Persistent Axial Pain

Recovery from isolated axial neck pain can be unpredictable because many cases are:

Degenerative, multifactorial, or nonspecific.

Serious Causes

Prognosis is less favorable when neck pain results from:

Malignancy

Severe infection

Progressive myelopathy

Major trauma

Complications

The most important complication is progressive neurologic dysfunction from:

Nerve-root or spinal cord compression.

Warning Signs of Neural Compression

Concerning symptoms include:

Weakness of the arms or hands

Persistent sensory loss

Loss of hand dexterity

Difficulty walking

Balance problems

Bowel or bladder dysfunction

These findings warrant urgent evaluation.

Patient Monitoring

Follow-up should assess:

Pain severity

Range of motion

Motor strength

Sensation

Reflexes

Gait

Development of upper motor neuron signs

Patients with progressive neurologic findings, persistent constitutional symptoms, or worsening pain require further investigation.

Key Principle

Most uncomplicated adult neck pain is related to mechanical or degenerative disease and responds to nonoperative care.

The critical task is to identify patients with red flags for:

Trauma, infection, tumor, nerve-root compression, or cervical spinal cord involvement, because these conditions require more urgent imaging and specialist evaluation.

Orthopaedic Surgery - Musculoskeletal Radiography

Basics

Plain radiography is often the first imaging study obtained when evaluating a musculoskeletal complaint.

Radiographs are useful because they are:

Widely available

Relatively inexpensive

Rapid to obtain

Excellent for evaluating bone alignment, fracture, joint space, and many osseous lesions

The quality of the study and its interpretation depend heavily on the clinical information supplied with the imaging request.

Clinical Information on the Radiograph Request

When ordering musculoskeletal radiographs, the clinician should provide a clear description of:

The location of symptoms

The suspected diagnosis

Mechanism of injury

Relevant examination findings

Previous surgery or known disease

Adequate clinical information helps the radiologist select the correct views and interpret subtle abnormalities more accurately.

Diagnosis

History

For traumatic injuries, the mechanism of injury should be included.

Examples include:

Fall

Direct blow

Twisting injury

Hyperextension

Axial loading

Crush injury

Understanding the mechanism can help identify expected fracture or dislocation patterns.

Physical Examination

Any focal areas of:

Tenderness, swelling, deformity, or limited motion

should be specified.

Precise localization can guide imaging toward the most likely site of pathology.

General Radiographic Principles

Two Orthogonal Views

Most suspected fractures should be assessed with at least two projections obtained approximately 90° to one another.

The classic combination is:

Anteroposterior and lateral views.

A fracture or dislocation that is difficult to appreciate on one projection may be obvious on the perpendicular view.

Trauma Imaging

In substantial extremity trauma, imaging should include the injured segment and consideration of the:

Joint above and joint below the suspected injury.

This is particularly important with long-bone fractures or when associated dislocation may be missed.

The exact extent of imaging should be tailored to the mechanism and examination rather than applied mechanically to every minor injury.

Additional Views

Specialized projections may be required when standard AP and lateral studies do not adequately visualize the region.

Examples include:

Oblique views

Axillary views

Scapular Y views

Patellar or skyline views

Weight-bearing views

Stress views

General Indications by Anatomic Region

Neck Pain

Initial cervical spine radiographs, when clinically indicated, commonly include:

AP and lateral views.

Additional projections or CT may be more appropriate depending on trauma severity and the clinical question.

Routine chest radiography is not required solely because cervical pain is present unless there is another indication.

Neck and Arm Pain

When cervical radiculopathy or another source of referred upper-extremity pain is suspected, imaging may include:

Cervical spine radiographs

and, depending on examination findings,

Shoulder, humerus, forearm, wrist, or hand radiographs.

Imaging should be directed toward the suspected level rather than routinely obtaining every segment.

Shoulder Pain

Nontraumatic Shoulder Pain

Initial radiographs often include:

AP views in appropriate rotation

and

An axillary or scapular Y view.

These help evaluate:

Glenohumeral alignment

Arthritis

Calcification

Acromial morphology

Osseous lesions

Traumatic Shoulder Pain

When the patient cannot move the arm because of pain, useful views include:

AP

and

Scapular Y views.

The Y view is useful because it can often be obtained without substantial shoulder movement and helps assess for dislocation.

Elbow Pain

Standard elbow radiographs generally include:

AP and lateral views.

Oblique views may be added for suspected:

Radial head, coronoid, or other subtle fractures.

Forearm Pain

Forearm imaging should include:

AP and lateral views of the entire radius and ulna, with adequate visualization of both the:

Elbow

and

Wrist.

This is especially important because forearm fractures may be associated with injuries such as:

Monteggia or Galeazzi fracture-dislocations.

Wrist Pain

Standard wrist imaging generally consists of:

PA/AP

Lateral

and often

Oblique views.

Special views may be required for suspected scaphoid or carpal injury.

Hand Pain

Standard hand radiographs commonly include:

PA/AP

Oblique

and

Lateral views.

Wrist imaging should be added when symptoms extend proximally or when the mechanism suggests associated carpal injury.

Low Back Pain

When plain radiographs are clinically indicated, typical views include:

AP and lateral lumbosacral spine radiographs.

An AP pelvis may be useful when:

Hip, sacroiliac, or pelvic pathology is also suspected.

Routine radiography is not necessary for uncomplicated acute low back pain without concerning clinical features.

Thoracic or Middle Back Pain

When indicated, standard thoracic spine radiographs include:

AP and lateral views.

These may identify:

Compression fracture

Deformity

Degenerative change

Destructive lesion

Pelvic Pain

Initial pelvic imaging often begins with:

An AP pelvis radiograph.

Additional hip or lumbosacral views are obtained according to the location of symptoms and suspected diagnosis.

Hip Pain

Typical radiographic evaluation may include:

AP pelvis

and

AP and lateral views of the affected hip.

Lumbosacral imaging may be considered when symptoms could represent referred spinal pain.

Knee Pain

Standard knee imaging commonly includes:

Weight-bearing AP or PA view

Lateral view

Patellofemoral view

Depending on the suspected disorder, additional views may include:

Tunnel, Rosenberg, or long-leg alignment studies.

Weight-bearing views are particularly useful when evaluating osteoarthritis.

Ankle Pain

Typical ankle radiographs include:

AP

Lateral

Mortise views.

Foot radiographs may be added when tenderness or trauma extends into the foot.

Foot Pain

Standard foot imaging usually includes:

AP

Lateral

Oblique views.

Weight-bearing radiographs are especially useful for:

Alignment disorders, midfoot instability, hallux valgus, and flatfoot evaluation.

Ankle views should be added when symptoms extend proximally.

Interpretation Principles

Radiographs should be reviewed systematically.

Alignment

Evaluate:

Overall limb and joint alignment

Joint congruity

Dislocation or subluxation

Bone

Inspect for:

Fracture lines

Cortical disruption

Trabecular abnormalities

Lytic or sclerotic lesions

Periosteal reaction

Joint Space

Assess:

Joint-space width

Symmetry

Articular congruity

Osteophytes

Subchondral sclerosis

Erosions

Soft Tissues

Do not ignore the soft tissues.

Radiographs may reveal:

Swelling

Joint effusion

Calcification

Gas

Foreign bodies

Soft-tissue masses

Comparison Views

Comparison with the opposite extremity may occasionally help in:

Pediatric injuries

Subtle alignment abnormalities

Congenital conditions

Routine bilateral imaging is not necessary for every injury.

Follow-Up

If initial radiographs are normal but significant symptoms persist, management depends on the clinical problem.

Repeating radiographs after a period of time may reveal abnormalities that were initially occult.

Repeat Radiographs

Certain fractures become more visible after:

Callus formation or bone resorption at the fracture margins.

Repeat imaging may therefore be useful after approximately 1–2 weeks for selected occult fractures.

A routine delay of 6–8 weeks is generally not necessary when significant pathology is suspected and more sensitive imaging is available.

Persistent Unexplained Pain

When radiographs remain normal but important symptoms persist, additional imaging should be selected according to the likely diagnosis.

Options include:

MRI

CT

Bone scintigraphy

Bone Scintigraphy

Technetium bone scanning provides a whole-skeleton survey of areas with increased bone turnover.

It may be useful when:

The location of disease is uncertain

Multifocal skeletal disease is suspected

Stress injury, infection, or metastasis is under consideration

Limitations of Bone Scanning

A positive scan is nonspecific and may occur with:

Fracture

Arthritis

Infection

Tumor

Other causes of increased bone remodeling

Some disorders, such as multiple myeloma, may be occult on technetium bone scanning.

Computed Tomography

CT provides excellent visualization of:

Cortical bone

Complex fracture anatomy

Subtle osseous lesions

Joint surfaces

Spinal and pelvic anatomy

It is especially useful when plain radiographs are inconclusive but detailed bony anatomy is required.

Magnetic Resonance Imaging

MRI is often the most sensitive study for detecting occult musculoskeletal pathology.

It is particularly useful for:

Bone marrow disease

Occult fracture

Ligament and tendon injury

Meniscal or labral pathology

Tumor

Infection

Spinal cord and nerve-root disease

Limitations of MRI

MRI has practical limitations including:

Greater cost

Longer acquisition time than radiography or CT

Sensitivity to patient motion

Claustrophobia

Device- or implant-related safety considerations

Modern MRI studies often take substantially less than the historically quoted 40–60 minutes, depending on the region and protocol.

Claustrophobia

Patients with significant claustrophobia may require:

Reassurance

Wide-bore or open MRI

Anxiolytic medication

or, rarely,

Sedation or anesthesia.

MRI Safety

Implanted devices should not automatically be considered absolute contraindications.

MRI safety depends on whether the device is:

MR safe

MR conditional

or

MR unsafe.

Pacemakers and Defibrillators

Many modern cardiac devices are MR conditional and can be scanned under specialized protocols.

The exact device must be identified before MRI.

Orbital Metal

Patients with a history suggesting metallic fragments near the eye require careful screening.

A ferromagnetic intraorbital foreign body can move in the magnetic field and cause serious injury.

Implanted Stimulators

Neurostimulators and other implanted electrical devices require device-specific safety evaluation.

Some can be scanned under defined conditions, whereas others cannot.

Key Principle

Musculoskeletal radiography remains the first-line imaging modality for many orthopaedic conditions, particularly fractures, alignment abnormalities, and arthritis.

The most useful study is obtained when the clinician:

Provides an accurate history and examination findings, requests appropriate orthogonal and special views, and selects advanced imaging only when the clinical question requires it.

Orthopaedic Surgery - Muscular Dystrophies

Basics

Muscular dystrophies are a heterogeneous group of inherited muscle disorders characterized by progressive degeneration and weakness of skeletal muscle without a primary abnormality of the peripheral or central nervous system.

Although skeletal muscle is the principal tissue involved, many forms also affect:

Cardiac muscle

Respiratory function

The skeleton

Mobility and posture

Other organ systems

The various muscular dystrophies have traditionally been classified according to:

Distribution of weakness

Age at onset

Rate of progression

Associated systemic findings

Pattern of genetic inheritance

Because Duchenne muscular dystrophy has particularly important orthopaedic consequences, it is emphasized here.

Classification

Muscular dystrophies can be grouped according to their genetic inheritance and phenotype.

X-Linked Muscular Dystrophies

Important X-linked disorders include:

Duchenne muscular dystrophy

Becker muscular dystrophy

Emery–Dreifuss muscular dystrophy

Autosomal-Recessive Muscular Dystrophies

This group includes several forms of:

Limb-girdle muscular dystrophy

and other congenital or early-onset dystrophies.

The modern classification is increasingly based on the specific genetic or molecular defect rather than solely on clinical distribution.

Autosomal-Dominant Muscular Dystrophies

Examples include:

Facioscapulohumeral muscular dystrophy

Some distal muscular dystrophies

Oculopharyngeal muscular dystrophy

Certain other phenotypes may also follow dominant inheritance.

Epidemiology

Duchenne Muscular Dystrophy

Duchenne muscular dystrophy primarily affects boys.

Historically, the incidence has been approximately:

1 in 3,500 live male births.

Becker Muscular Dystrophy

Becker muscular dystrophy is less common, with an older estimated incidence of approximately:

1 in 30,000 live male births.

Risk Factors

For Duchenne and Becker muscular dystrophy, the major demographic risk factor is:

Male sex, because the disorders are inherited in an X-linked pattern.

A positive maternal family history also increases suspicion.

Genetics

Duchenne and Becker muscular dystrophies result from pathogenic variants in the DMD gene located on the short arm of the X chromosome.

This gene encodes:

Dystrophin, an important structural protein associated with the muscle-cell membrane cytoskeleton.

Dystrophin

Dystrophin helps stabilize the muscle-cell membrane during contraction.

Loss or marked reduction of functional dystrophin causes repeated muscle-fiber injury and progressive degeneration.

Duchenne Muscular Dystrophy

In Duchenne muscular dystrophy, functional dystrophin is:

Essentially absent or severely deficient.

The resulting phenotype is typically severe and begins early in childhood.

Becker Muscular Dystrophy

In Becker muscular dystrophy, dystrophin is:

Present in reduced quantity or abnormal form.

The clinical course is generally milder and more slowly progressive than Duchenne muscular dystrophy.

Etiology

The underlying cause is a genetic defect affecting structural proteins required for normal muscle function.

In Duchenne and Becker muscular dystrophy, abnormal dystrophin causes instability of the muscle-fiber membrane, leading to:

Repeated injury

Fiber necrosis

Replacement by fat and connective tissue

Progressive weakness

Diagnosis

Duchenne Muscular Dystrophy

Duchenne muscular dystrophy typically becomes clinically apparent between approximately 3 and 6 years of age.

Early Presentations

Common early findings include:

Delayed walking

Frequent falls

Difficulty running

Inability to hop or jump normally

Difficulty rising from the floor

Waddling gait

Trendelenburg gait

Exaggerated lumbar lordosis

Gower Maneuver

A classic finding is the Gower maneuver.

When rising from the floor, the child uses the hands to “climb” up the thighs because of marked weakness of the:

Hip extensors and proximal pelvic-girdle muscles.

Pattern of Weakness

Weakness is predominantly proximal and usually begins in the pelvic girdle.

Commonly affected muscle groups include:

Gluteal muscles

Quadriceps

Abdominal musculature

Hip abductors and extensors

Later, weakness progresses to the:

Shoulder girdle and upper extremities.

Gait

Pelvic-girdle weakness causes compensatory posture during walking.

The child may carry the:

Head and shoulders posterior to the pelvis, creating increased anterior pelvic tilt and lumbar lordosis.

This compensates for weak hip extensors.

Trendelenburg Gait

Weak hip abductors produce:

Pelvic instability and a waddling or Trendelenburg gait.

Calf Pseudohypertrophy

The calves commonly appear enlarged.

This is termed:

Pseudohypertrophy, because the increased bulk results largely from replacement of normal muscle by fat and connective tissue rather than true increased muscle strength.

Contractures

Contractures develop progressively, commonly involving:

Achilles tendons

Knees

Hips

Iliotibial bands

Upper-extremity contractures may develop later.

Shoulder-Girdle Weakness

Shoulder-girdle weakness typically develops several years after the initial lower-extremity symptoms.

The patient may be difficult to lift by supporting the axillae because the shoulder girdle fails to stabilize normally.

This historical finding has been called the Meryon sign.

Sensation

Sensory examination is usually normal.

The absence of sensory loss helps distinguish muscular dystrophy from many peripheral neuropathies.

Motor Development

Some children also demonstrate:

Developmental delay, learning difficulties, or cognitive impairment.

The degree varies considerably.

Loss of Ambulation

Historically, many boys with untreated or older-era Duchenne muscular dystrophy lost effective independent ambulation around the early adolescent years.

With contemporary corticosteroid therapy, cardiac care, respiratory support, rehabilitation, and disease-specific treatments, loss of ambulation may occur later and varies substantially among patients.

Cardiac Involvement

Cardiac involvement is common.

Potential abnormalities include:

Cardiomyopathy

Tachycardia

Conduction abnormalities

Progressive ventricular dysfunction

Cardiac surveillance is therefore essential even before symptoms develop.

Respiratory Involvement

Progressive respiratory muscle weakness leads to:

Reduced cough strength

Restrictive pulmonary dysfunction

Nocturnal hypoventilation

Respiratory insufficiency

Respiratory disease is a major determinant of long-term outcome.

Becker Muscular Dystrophy

Becker muscular dystrophy resembles Duchenne muscular dystrophy in:

Distribution of weakness and associated cardiac disease, but it is usually less severe.

Age at Onset

Symptoms generally begin later, often after approximately 7 years of age, although presentation is variable.

Progression

Muscle weakness progresses more slowly than in Duchenne muscular dystrophy.

Ambulation is often preserved for a much longer period.

Life expectancy is also generally greater, although significant cardiomyopathy may occur.

Physical Examination

The diagnosis begins with a careful history and examination.

Muscle Bulk

Assess for:

Calf pseudohypertrophy

Muscle wasting

Asymmetry

Gait Assessment

Observe for:

Waddling gait

Trendelenburg gait

Lumbar hyperlordosis

Toe walking

Difficulty rising from the floor

Proximal Weakness

Muscle strength should be tested systematically, beginning with proximal groups such as:

Hip abductors

Hip extensors

Quadriceps

Shoulder abductors

Scapular stabilizers

Gower Sign

Ask the patient to rise from the floor without assistance.

Use of the hands to push on the knees and thighs indicates proximal weakness.

Shoulder Stability

Assess scapular and shoulder-girdle control.

Difficulty supporting the upper trunk during lifting may reflect advanced proximal weakness.

Contractures

Examine for:

Achilles tightness

Knee flexion contractures

Hip flexion or abduction contractures

Elbow and wrist contractures

Spine

Examine for:

Scoliosis

Kyphosis

Pelvic obliquity

Spinal deformity becomes particularly important after loss of ambulation.

Laboratory Tests

Creatine Kinase

Serum creatine kinase is markedly elevated early in Duchenne muscular dystrophy.

Levels may be:

Many times above normal, sometimes reaching more than 100-fold elevation.

CK may decline later as functional muscle mass is progressively lost.

Genetic Testing

Molecular testing of the DMD gene is now a central component of diagnosis.

It can identify:

Deletions

Duplications

Point mutations

and other pathogenic variants.

Genetic confirmation also helps guide:

Family counseling and mutation-specific therapy.

Dystrophin Analysis

Muscle biopsy with dystrophin immunostaining is used less often now because genetic testing can establish the diagnosis in most patients.

When performed:

Duchenne muscular dystrophy shows absent or near-absent dystrophin.

Becker muscular dystrophy shows reduced or abnormal dystrophin.

Electromyography

Electromyography demonstrates a myopathic pattern characterized by:

Low-amplitude

Short-duration

Polyphasic motor-unit potentials

EMG is less important than genetic testing in modern diagnostic pathways but can help when the diagnosis is uncertain.

Cardiac Assessment

Cardiac evaluation should be performed regularly.

Monitoring may include:

Electrocardiography

Echocardiography

Cardiac MRI

depending on age and disease stage.

Imaging

Spine Imaging

Patients should be screened clinically for scoliosis.

Once deformity is suspected or identified, radiographs are used to:

Measure curve magnitude and monitor progression.

Characteristic Scoliosis

The scoliosis associated with Duchenne muscular dystrophy is typically a:

Long, collapsing thoracolumbar curve, often accompanied by pelvic obliquity.

Unlike idiopathic scoliosis, the deformity may involve most of the spine as a single sweeping curve.

Pathological Findings

Muscle pathology demonstrates:

Progressive degeneration and necrosis of muscle fibers

Variation in muscle-fiber size

Regeneration of some fibers

Replacement by connective tissue

Fatty infiltration

These changes account for progressive weakness and pseudohypertrophy.

Differential Diagnosis

Important differential diagnoses include:

Peripheral neuropathy

Anterior horn cell disease

Spinal muscular atrophy

Poliomyelitis

Congenital myopathy

Metabolic myopathy

The absence of sensory loss, markedly elevated CK, characteristic weakness pattern, and genetic testing help distinguish Duchenne muscular dystrophy.

Treatment

General Principles

There is no simple curative therapy for most muscular dystrophies.

Management is multidisciplinary and aims to:

Preserve mobility

Prevent contractures

Maintain respiratory and cardiac function

Manage skeletal deformity

Improve quality of life and independence

Modern treatment has substantially extended survival compared with historical series.

Activity

Physical activity should be encouraged within the patient’s capabilities.

The aim is to maintain:

Mobility, joint motion, conditioning, and participation.

Excessive high-resistance or eccentric exercise that causes prolonged muscle damage should be avoided.

Physical Therapy

Physical therapy is central to management.

Strength Monitoring

Serial muscle-strength assessment helps document progression.

Stretching

Daily stretching is used to reduce development of contractures.

Particular attention is given to:

Achilles tendons

Hamstrings

Hip flexors

Iliotibial bands

Upper-extremity joints

Orthoses

Ankle-foot orthoses may help:

Maintain ankle position

Delay equinus contracture

Improve nighttime stretching

They are most useful when deformity remains flexible.

Mobility Support

As weakness progresses, patients may require:

Walking aids

Standing devices

Wheelchairs

Positioning systems

The goal is to preserve function and independence rather than simply prolong ambulation at all costs.

Fractures

Lower-extremity fractures occur relatively frequently, especially in patients with:

Reduced mobility, osteoporosis, or chronic corticosteroid exposure.

Stable fractures should be treated in a manner that minimizes prolonged immobilization whenever possible because loss of mobility can lead to permanent functional decline.

Contracture Management

Contractures should initially be managed with:

Stretching

Positioning

Orthoses

Surgical release may occasionally be considered when a contracture interferes with:

Positioning, footwear, standing, hygiene, or function.

Achilles and Fascia Lata Release

Selected procedures may include:

Achilles tendon lengthening

Release of fascia lata or other contracted structures

These procedures are performed selectively because weakening an already weak muscle group can impair function.

Scoliosis

Progressive scoliosis is common in nonambulatory Duchenne muscular dystrophy.

Older series reported progression in the great majority of untreated patients.

The risk and rate may be reduced by contemporary corticosteroid therapy.

Nonoperative Spine Management

Management includes:

Postural support

Wheelchair seating optimization

Monitoring of pelvic obliquity

Respiratory assessment

Bracing has limited ability to permanently control progressive neuromuscular scoliosis.

Spinal Surgery

Spinal fusion may be considered for significant progressive deformity that compromises:

Sitting balance

Comfort

Pelvic alignment

Pulmonary mechanics

Historically, surgery was recommended for curves progressing beyond approximately 20–30°, while older operative thresholds such as 45° were also used.

Current decisions are individualized according to curve progression, remaining function, pulmonary reserve, cardiac status, and overall goals.

Fusion Levels

Correction often involves long posterior fusion extending through most of the thoracic and lumbar spine.

Instrumentation may extend to the:

Pelvis or sacrum when substantial pelvic obliquity is present.

Timing of Spine Surgery

If surgery is required, it is preferable to intervene before:

Severe pulmonary compromise or advanced cardiomyopathy

makes anesthesia and recovery excessively hazardous.

Respiratory Therapy

Respiratory management is essential.

Treatment may include:

Assisted coughing

Airway-clearance techniques

Inspiratory or expiratory muscle support

Noninvasive positive-pressure ventilation

Nocturnal ventilatory support

These interventions can substantially improve quality of life and survival.

Cardiac Management

Patients require regular cardiology follow-up.

Treatment of cardiomyopathy may include:

ACE inhibitors

Angiotensin-receptor blockers

Beta-blockers

Mineralocorticoid receptor antagonists

according to cardiac findings.

Genetic Counseling

Families should receive genetic counseling regarding:

X-linked inheritance

Carrier testing

Risk to future children

Testing of female relatives when appropriate

Medication

Corticosteroids

Corticosteroids such as:

Prednisone or deflazacort

can prolong motor function and may delay:

Loss of ambulation