Orthopaedic Surgery - Growth-Plate Injury

Basics

A growth-plate injury involves the physis, the cartilaginous region responsible for longitudinal growth of a child’s bone.

Not every physeal injury produces a growth abnormality. Most heal without long-term consequences, but injuries that significantly crush, displace, or destroy part of the growth plate may result in growth arrest, angular deformity, or limb-length discrepancy.

Common Sites

Physeal fractures occur most frequently in the long bones of growing children.

The growth plates most commonly injured include the:

Distal radius, distal tibia, phalanges, and proximal humerus.

Sites at Greatest Risk of Growth Disturbance

Although some physes are injured more frequently, the distal femoral and distal tibial physes are particularly important because injuries in these locations have a relatively high risk of subsequent growth disturbance.

Synonyms

Growth-plate injuries are also called physeal injuries or physeal fractures.

The term Salter-Harris fracture refers to the widely used classification system for traumatic injuries involving the physis.

Epidemiology

Physeal injuries account for approximately 15–30% of pediatric fractures.

They can occur throughout childhood but are particularly common during periods of rapid growth.

Age

Peak incidence generally occurs around 11–12 years in girls and 12–14 years in boys, corresponding approximately to the adolescent growth spurt.

Sex

Boys are affected more frequently overall, with some series reporting approximately twice as many injuries in boys as in girls.

Remaining Growth

Younger children have more growth remaining and therefore have a greater amount of potential deformity if a physeal arrest develops.

Conversely, a similar growth arrest occurring near skeletal maturity may have relatively little effect on final limb length or alignment.

Risk Factors

Adolescent boys are at increased risk because of their higher frequency of traumatic injuries during periods when the growth plate remains open.

Prevention of Sequelae

Early recognition of physeal damage may allow intervention before severe deformity develops.

Physeal Bar

A physeal bar is a bridge of bone that forms across part of an injured growth plate and can tether further growth.

If the bar is relatively small and the child has substantial growth remaining, surgical excision may allow more symmetric growth to resume.

Historically, bar resection has been considered when less than approximately 50% of the physis is involved, although candidacy also depends on bar location and remaining growth.

Other Corrective Options

When growth arrest has already produced substantial deformity, treatment may include:

Physeal bar resection, contralateral epiphysiodesis, ipsilateral hemiepiphysiodesis, corrective osteotomy, or limb-lengthening procedures.

Contralateral Epiphysiodesis

When a predictable limb-length discrepancy is expected, growth of the opposite limb may be intentionally slowed or stopped to improve final symmetry.

Etiology

Trauma is the most common cause of growth-plate injury.

Other processes may also damage the physis.

Nontraumatic Causes

Potential causes include:

Infection, tumor, medications or hormonal exposure, and severe thermal injury from excessive heat or cold.

Classification

The Salter-Harris classification is the standard system used to describe traumatic physeal fractures.

It is based on the relationship of the fracture line to the physis, metaphysis, and epiphysis.

Salter-Harris Type I

The fracture passes entirely through the physis, separating the epiphysis from the metaphysis without extending into either adjacent bone.

Because the germinal portion of the growth plate may remain intact, the prognosis is usually good after appropriate reduction.

Salter-Harris Type II

Type II is the most common physeal fracture pattern.

The fracture passes through the physis and then exits through the metaphysis, leaving a metaphyseal fragment attached to the epiphysis.

Salter-Harris Type III

The fracture passes from the physis through the epiphysis and into the joint surface.

Because it is intra-articular and crosses the growth plate, accurate reduction is important to restore both joint congruity and physeal alignment.

Salter-Harris Type IV

The fracture extends through the metaphysis, physis, and epiphysis, crossing the entire growth plate and entering the joint.

This pattern carries an increased risk of growth arrest and post-traumatic joint incongruity if reduction is inadequate.

Salter-Harris Type V

Type V represents a compression or crush injury of the physis.

It may be difficult to recognize on initial radiographs and is associated with a relatively high risk of premature growth arrest.

Rang Type VI

A so-called Type VI or Rang VI injury involves damage to the peripheral perichondral ring.

It is not part of the original Salter-Harris classification but may produce asymmetric growth and angular deformity.

Risk by Classification

In general, the risk of growth disturbance increases with increasing complexity of physeal injury.

Types III, IV, and V are particularly concerning because they either cross the articular surface, disrupt the germinal layer more extensively, or crush the physis.

Associated Injuries

Physeal trauma may occur with other injuries, including:

Ligament injury, neurovascular injury, and additional chest, abdominal, or head trauma in high-energy mechanisms.

Diagnosis

Accurate diagnosis requires knowledge of the normal appearance and timing of secondary ossification centers and physeal closure at each skeletal location.

A fracture may be difficult to identify if much of the epiphysis remains cartilaginous.

Signs and Symptoms

The most common findings are pain, swelling, and tenderness over the involved growth plate.

Visible deformity may be present if the fracture is displaced.

Lower-Extremity Injuries

Children with a lower-extremity physeal fracture may be unable or unwilling to bear weight.

Upper-Extremity Injuries

Upper-extremity fractures commonly produce pain, swelling, and reduced active range of motion.

Crepitus

Crepitus may occasionally be present but should not be deliberately elicited because repeated manipulation can worsen pain or displacement.

Physical Examination

The entire injured limb should be examined carefully.

Skin

The examiner should look for open wounds, abrasions, bruising, swelling, and skin compromise.

Any wound near a fracture should raise concern for an open injury.

Neurovascular Status

Distal pulses, capillary refill, sensation, and motor function should be documented before and after splinting or reduction.

Pathological Findings

The physis is organized into several histologic zones:

Resting zone, proliferative zone, hypertrophic zone, zone of provisional calcification, and adjacent metaphysis.

Site of Fracture Propagation

Many physeal fractures propagate through the relatively weak hypertrophic and provisional calcification regions.

Permanent Physeal Injury

Permanent growth disturbance may occur when the injury destroys growth-plate cells, causes marked displacement or malalignment of the physis, or produces a bony bridge across the plate.

Infection can similarly damage the growth plate and result in arrest.

Imaging

Plain Radiographs

Initial imaging should include AP and lateral radiographs of the involved region.

An oblique view may be useful when the fracture pattern remains unclear.

Comparison Views

Comparison with the opposite side may occasionally help in very young children, although this is not routinely required.

CT

CT is useful for complex fractures, particularly those with intra-articular extension, when precise definition of the fracture geometry is required for treatment planning.

It is especially valuable for Salter-Harris III and IV injuries around complex joints.

MRI

MRI is the most sensitive modality for evaluating established physeal damage, occult physeal injury, and physeal bars.

It clearly demonstrates cartilage and can distinguish the growth plate from surrounding bone.

Acute MRI Findings

Possible findings include:

Physeal widening, increased fluid-sensitive signal within the injured physis, and adjacent bone marrow edema.

Physeal Bar Mapping

MRI can define the size, position, and percentage of physeal involvement by a bony bridge.

Three-dimensional or semiautomated mapping may assist prognosis and surgical planning.

Ultrasound

Ultrasound can be useful in infants and very young children because substantial portions of the epiphysis remain cartilaginous and may not be visible on conventional radiographs.

Differential Diagnosis

In acute trauma, the primary concern is identifying whether the injury truly involves the physis.

In chronic cases, other causes of growth-plate damage must be considered.

Infection

Physeal or metaphyseal infection may be insidious and can produce growth disturbance long after the initial illness.

Other Causes

Tumor, metabolic disease, previous surgery, radiation, thermal injury, and prior trauma may also cause physeal arrest.

Treatment

Initial Measures

Immediate management includes immobilization, elevation, ice when appropriate, pain control, and assessment of neurovascular status.

Nondisplaced Fractures

Nondisplaced physeal fractures should be immobilized promptly in an appropriate splint.

Displaced Fractures

Displaced injuries generally require reduction under suitable analgesia or anesthesia.

Options may include procedural sedation, regional or hematoma block in appropriate fractures, or general anesthesia.

After reduction, the limb is splinted and repeat imaging is obtained to confirm alignment.

Early Follow-Up

Patients with physeal fractures should usually be reviewed within approximately 3–5 days, particularly when substantial swelling is present.

Splint to Cast Conversion

A splint is often used initially because it accommodates swelling.

After edema has decreased, commonly after approximately 1–2 weeks, a circumferential cast may be applied if continued immobilization is required.

Weight Bearing

Lower-extremity physeal fractures are often treated with restricted or non-weight bearing until adequate stability and healing are demonstrated.

Upper-extremity injuries are generally protected with a sling or other supportive device.

Duration of Immobilization

Many uncomplicated physeal fractures heal relatively quickly because of the vascularity and remodeling potential of children.

Immobilization frequently lasts approximately 3–4 weeks, although duration varies substantially by age, fracture location, stability, and treatment method.

Medication

Analgesia should be provided according to pain severity.

Persistent or escalating pain should prompt reassessment for complications such as compartment syndrome rather than simply increasing medication.

Surgery

Goal of Reduction

Restoring appropriate alignment is one of the most important methods of reducing the risk of later deformity.

For intra-articular physeal injuries, restoration of the joint surface is also essential.

Repeated Reduction Attempts

Repeated forceful reduction attempts should be avoided because additional manipulation may further injure the growth plate.

Delayed Reduction

Forceful closed reduction performed more than approximately 5–7 days after injury is generally avoided in many physeal fractures because healing has already begun and manipulation may damage the physis.

Management should instead be individualized according to deformity, fracture type, and remaining growth.

Open Reduction

Salter-Harris III and IV fractures may require open reduction when acceptable anatomic alignment cannot be achieved by closed techniques.

Internal Fixation

Fractures that remain unstable after reduction may require percutaneous pinning, screws, or other internal fixation.

Crossing the Physis

When fixation must cross an open physis, smooth pins placed as centrally and perpendicularly as practical are generally preferred because they minimize physeal injury.

Eccentric or threaded implants crossing the physis may increase the risk of growth disturbance.

Open Fractures

Open physeal fractures require urgent antibiotics, tetanus assessment, surgical irrigation and debridement, stabilization, and orthopaedic management.

Follow-Up

Prognosis

Most growth-plate fractures heal without major difficulty.

The likelihood of growth disturbance depends on fracture type, anatomic location, degree of displacement, quality of reduction, patient age, and extent of physeal injury.

Effect of Salter-Harris Type

Higher-grade Salter-Harris injuries generally have a greater risk of subsequent growth abnormality.

Effect of Skeletal Maturity

The closer the patient is to skeletal maturity, the less remaining growth exists and therefore the smaller the potential effect of a growth arrest on final limb length.

High-Risk Anatomic Sites

The distal femoral and distal tibial physes have relatively high rates of growth disturbance and warrant particularly careful follow-up.

Lower-Risk Sites

The distal radius and proximal humerus often tolerate physeal injury better because of their substantial remodeling potential and the pattern of growth at those sites, although growth arrest can still occur.

Complications

Growth Arrest

A portion or all of the physis may stop growing prematurely.

Complete arrest can produce limb shortening, whereas partial arrest may create progressive angular deformity.

Growth Disturbance

Asymmetric growth across an injured physis may result in varus, valgus, flexion, extension, or rotational deformity, depending on the location of the arrest.

Limb-Length Discrepancy

Loss of growth from a major physis may produce clinically significant shortening of the affected limb.

Malunion

A fracture that heals in poor alignment may produce deformity even without a true growth arrest.

Growth Acceleration

Children younger than approximately 10 years may occasionally demonstrate temporary overgrowth after fracture because of increased local blood flow and stimulation of growth.

The resulting length increase is usually modest, often approximately 5–10 mm.

Patient Monitoring

Children at increased risk of growth disturbance require prolonged surveillance.

This includes Salter-Harris III–V fractures and all significant distal femoral or distal tibial physeal injuries.

Duration

Follow-up should generally continue for at least 6–12 months, and longer when substantial growth remains or there is concern for partial arrest.

Clinical Assessment

The physician should compare limb lengths, angular alignment, gait, and joint motion.

Radiographic Assessment

Follow-up radiographs should assess whether the growth plate remains open and symmetric.

A growth-arrest line, sometimes called a Harris line, may form after the injury.

If subsequent growth is normal, this line should progressively move away from the physis in a parallel and symmetric fashion.

Failure of the line to migrate normally, or asymmetric tethering toward one side of the physis, may suggest developing growth arrest.

Orthopaedic Surgery - Growing Pains

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Basics

Growing pains are a common, benign, noninflammatory pain syndrome of childhood characterized by recurrent episodes of lower-extremity discomfort without objective musculoskeletal abnormalities.

Despite the name, the condition has not been shown to result directly from periods of rapid skeletal growth.

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Typical Pattern

The pain usually occurs after active days and is most prominent during the late afternoon, evening, or nighttime.

Children may occasionally awaken from sleep because of the discomfort.

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Resolution of Episodes

Each episode resolves completely.

The child is generally normal and pain free between episodes.

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Location

Symptoms occur predominantly in the lower extremities and may involve one or both legs.

Pain is usually vague rather than sharply localized.

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Frequency

Episodes occur unpredictably.

Pain-free intervals may last days, weeks, or even months.

Some severely affected children may experience symptoms almost daily.

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Physical Findings

Growing pains produce no persistent objective abnormalities.

There should be no focal tenderness, swelling, joint restriction, weakness, or limp.

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Synonyms

Other terms include benign nocturnal limb pains of childhood, leg aches, and night pains.

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Epidemiology

Growing pains are very common.

Approximately 15–36% of children are reported to experience symptoms consistent with this syndrome at some point.

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Age

The condition most commonly affects children between approximately 4 and 14 years of age.

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Sex

Girls may be affected slightly more often than boys.

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Risk Factors

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High Activity Level

Symptoms are frequently reported in otherwise healthy, highly active children.

Episodes may be more noticeable after days involving substantial running, jumping, or sports participation.

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Family History

A positive family history is common.

A parent or sibling has been reported to have experienced similar childhood pains in nearly 70% of cases in some series.

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Etiology

The precise mechanism remains uncertain.

The disorder has been proposed to represent a form of relative musculoskeletal overuse or stress-related pain in otherwise normal children.

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Possible Contributing Factors

Proposed contributors include increased physical activity, relatively reduced bone strength, altered pain perception, and a lower pain threshold.

None of these explanations completely accounts for the syndrome.

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Diagnosis

Growing pains are a clinical diagnosis of exclusion.

The history and examination must be typical, and findings suggesting infection, inflammatory disease, malignancy, neurologic disease, or structural orthopaedic pathology should be absent.

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Signs and Symptoms

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Relationship to Activity

Pain frequently occurs after periods of increased activity.

Symptoms most often develop in the evening or at night.

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Nocturnal Pain

Children may awaken because of discomfort, although they should return to normal function afterward.

Persistent morning pain is not typical.

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Duration

Individual attacks may last from several minutes to several hours.

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Laterality

Pain is commonly bilateral, although episodes may occasionally affect only one leg at a particular time.

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Character

The pain is generally diffuse, vague, and poorly localized, often involving the calves, thighs, shins, or region behind the knees.

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Severity

Pain intensity varies considerably.

Some children describe only mild aching, whereas others experience episodes severe enough to cry or awaken from sleep.

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Episodic Course

A characteristic feature is the presence of completely pain-free intervals.

This episodic pattern helps distinguish growing pains from many inflammatory, infectious, neoplastic, or structural disorders.

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Physical Examination

A careful examination is essential because growing pains should not produce abnormal findings.

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Observation of Gait

The child should be observed walking naturally, preferably before becoming aware that gait is being assessed.

There should be no limp, stiffness, guarding, or reluctance to bear weight.

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Palpation

The lower extremities should be palpated systematically.

Growing pains should not produce focal bony, muscular, or joint-line tenderness.

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Range of Motion

Range of motion of the hips, knees, and ankles should be full and symmetric.

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Hip Examination

Particular attention should be given to the hips because hip disease may initially present as vague thigh or knee pain.

Gentle internal and external rotation of the hip, sometimes called the roll test or log-roll test, should not produce guarding or restriction.

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General Findings

There should be no swelling, erythema, warmth, muscle wasting, weakness, neurologic deficit, or systemic illness.

Any such finding should prompt investigation for another diagnosis.

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Laboratory Tests

Routine laboratory testing is not necessary when the history and physical examination are entirely typical.

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Atypical Presentation

If the history is unusual or concerning, investigations may include a complete blood count and inflammatory markers such as ESR and/or C-reactive protein.

Further testing should be directed toward the suspected alternative diagnosis.

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Imaging

Routine imaging is unnecessary for classic growing pains.

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Plain Radiographs

Radiographs may be obtained when pain is persistently localized, unilateral, associated with trauma, or accompanied by an abnormal examination.

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Advanced Imaging

Bone scintigraphy or other advanced imaging may occasionally help localize an occult source of pain when the clinical picture is atypical.

MRI is often preferred when an occult infection, stress injury, tumor, or inflammatory condition is suspected.

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Differential Diagnosis

Because growing pains are a diagnosis of exclusion, important alternative causes of childhood limb pain include:

Legg-Calvé-Perthes disease, chronic or subacute osteomyelitis, leukemia, sickle cell disease, juvenile idiopathic arthritis, Lyme disease, Osgood-Schlatter disease in older children, restless legs syndrome, and muscle cramps.

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Other Concerning Diagnoses

Depending on the clinical setting, stress fracture, bone tumor, inflammatory arthropathy, infection, trauma, neurologic disease, and referred hip pain should also be considered.

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Red Flags

Findings that are inconsistent with typical growing pains include persistent unilateral pain, focal tenderness, swelling, warmth, morning stiffness, joint restriction, limp, weakness, fever, weight loss, fatigue, night sweats, or progressively worsening symptoms.

These findings require further evaluation.

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Treatment

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Reassurance

Once the diagnosis is reasonably established, the most important treatment is reassurance of the child and family.

The condition is benign and does not damage bones, joints, or muscles.

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Stretching

A regular stretching program may decrease the frequency of symptoms.

Useful stretches target the hamstrings, quadriceps, and calf muscles, particularly before bedtime.

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Home Program

The stretching program can usually be performed with parental supervision and does not require formal physical therapy.

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Activity Modification

Most children can remain active.

If symptoms become frequent or severe, temporary reduction of particularly strenuous activities may help bring discomfort into a tolerable range.

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Orthoses

In selected children with substantial foot pronation or other biomechanical abnormalities, shoe inserts or orthotic devices may be considered.

However, orthoses are not routinely required for children with otherwise typical growing pains.

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Physical Therapy

Formal physical therapy is generally unnecessary.

It may be helpful when flexibility is poor, symptoms persist despite a home stretching program, or another biomechanical problem is present.

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Medication

Simple analgesics may be used occasionally for troublesome episodes.

Examples include acetaminophen or NSAIDs when appropriate.

Continuous routine medication is usually unnecessary.

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Follow-Up

Children with a completely typical presentation generally require only limited follow-up.

Repeated visits may sometimes be useful when the diagnosis remains uncertain or when the evolving pattern of symptoms needs to be observed.

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Prognosis

The prognosis is excellent.

Growing pains almost always resolve spontaneously as the child matures, without permanent musculoskeletal consequences.

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Patient Monitoring

Parents should monitor the character, frequency, location, and timing of pain.

A simple symptom diary may be useful when episodes are frequent.

The stretching program can be continued, and activity may be adjusted according to symptom severity.

Reevaluation is appropriate if the pattern changes or if the child develops persistent focal pain, swelling, limp, fever, morning symptoms, weakness, or other objective abnormalities.

Orthopaedic Surgery - Giant Cell Tumor

Basics

Giant cell tumor of bone is a benign but frequently locally aggressive primary bone neoplasm characterized histologically by numerous evenly distributed osteoclast-like multinucleated giant cells within a background of proliferating mononuclear stromal cells.

Although histologically benign in most cases, the tumor can behave aggressively, destroy surrounding bone, extend into soft tissues, recur after treatment, and rarely metastasize.

Typical Location

Giant cell tumors usually occur near the articular end of a long bone in skeletally mature patients.

Approximately half arise around the knee, particularly in the distal femur and proximal tibia.

Other common sites include the:

Distal radius, proximal femur, proximal humerus, distal tibia, and sacrum.

Flat Bones

When flat bones are affected, the sacrum and pelvis are the most common locations.

Giant cell tumors associated with Paget disease may involve flat bones, including the craniofacial skeleton.

Multifocal Disease

Multifocal giant cell tumor is rare.

Most patients have a single lesion.

Classification

The Musculoskeletal Tumor Society, or Enneking staging system, can be used to describe the biologic behavior of giant cell tumors.

The stages are based on symptoms, radiographic appearance, biologic activity, and local extent.

Stage I: Latent

Stage I tumors account for fewer than approximately 5% of cases.

They are usually minimally symptomatic or completely asymptomatic and may be discovered incidentally.

Radiographs or CT typically show a lesion with a well-defined sclerotic rim.

The tumor may demonstrate relatively little activity on bone scintigraphy.

Histologically, it remains benign.

Pathologic fracture can occasionally occur.

Stage II: Active

Stage II tumors account for approximately 70–85% of cases.

Patients are usually symptomatic.

The lesion expands the cortex but does not yet clearly break through it.

Bone scintigraphy is generally active.

Pathologic fracture may occur.

Histologically, the tumor remains benign.

Stage III: Aggressive

Stage III tumors represent approximately 10–15% of cases.

They typically present with increasing pain, swelling, and a rapidly enlarging mass.

Imaging demonstrates cortical destruction with extension into surrounding soft tissues.

Bone-scan activity may extend beyond the margins visible on plain radiographs.

The tumor may appear markedly hypervascular on angiographic studies.

Although the lesion remains histologically benign, it demonstrates aggressive local behavior with cortical violation and soft-tissue invasion.

Epidemiology

Age

Peak incidence occurs during the third decade of life, with frequency gradually decreasing thereafter.

The tumor is uncommon after approximately 55 years of age.

Skeletal Maturity

Giant cell tumor almost always develops after closure of the growth plates.

Approximately 10–15% of patients are younger than 20 years, but most of these individuals are already skeletally mature.

Fewer than approximately 2% of giant cell tumors occur adjacent to an open physis.

Therefore, the diagnosis should be reconsidered carefully when a similar lesion occurs in a skeletally immature child.

Frequency

Giant cell tumor accounts for approximately 5% of biopsied primary bone tumors and approximately 20% of benign bone tumors.

It is among the more common primary osseous neoplasms.

Sex

Females are affected slightly more often than males, with reported female-to-male ratios of approximately 1.3–1.5:1.

Risk Factors

Paget disease of bone is a rare predisposing condition.

Etiology

The precise cause of most giant cell tumors is not fully explained by conventional clinical risk factors.

Rare tumors may arise in association with pre-existing Paget disease of bone.

Associated Conditions

Paget Disease

Giant cell tumor can rarely complicate Paget disease.

Such tumors may involve different anatomic sites from conventional giant cell tumor, including the craniofacial skeleton.

Secondary Aneurysmal Bone Cyst

Secondary aneurysmal bone cyst formation is a relatively common associated histologic finding.

These cystic changes can alter the imaging appearance and complicate interpretation.

Diagnosis

Signs and Symptoms

Clinical presentation is often nonspecific.

Because the tumors frequently occur close to joints, patients may initially present with symptoms that resemble primary joint disease.

Pain

Approximately 90% of patients complain of pain.

Pain may be accompanied by localized swelling or a palpable mass.

Pathologic Fracture

Approximately 5–10% of patients present with a pathologic fracture through the weakened bone.

Joint Symptoms

Patients may complain of reduced motion, joint stiffness, or discomfort with weight bearing if the lesion is close to an articular surface.

Physical Examination

There is no pathognomonic physical examination finding.

Localized tenderness is commonly present over the involved epiphyseal region adjacent to a joint.

Swelling

A palpable mass or swelling may develop as the lesion expands.

Joint Effusion and Motion

Joint effusion or restriction of motion may occur when the lesion has substantially weakened or approached the subchondral cortex.

Laboratory Tests

Routine serum chemistry studies are generally normal.

Calcium and Phosphate

Serum calcium and phosphate should be assessed when the differential diagnosis includes hyperparathyroidism.

Evaluation may also include parathyroid hormone testing when clinically appropriate.

This is particularly important because a brown tumor of hyperparathyroidism can histologically and radiographically resemble a giant cell tumor.

Imaging

Plain Radiographs

Radiographs typically show an eccentric, expansile, radiolucent lesion near the end of a long bone.

The lesion is usually sharply defined but often lacks a prominent surrounding rim of reactive sclerosis.

Epiphyseal Involvement

A classic feature is involvement of the epiphysis in a skeletally mature patient.

The tumor commonly extends from the metaphysis toward the subchondral bone and articular surface.

Cortical Expansion

The cortex may become progressively thinned and expanded.

Aggressive lesions may break through the cortex and extend into adjacent soft tissues.

Reactive Sclerosis

Unlike many other benign bone lesions, giant cell tumor typically has little or no reactive sclerosis around its margin.

Spinal Involvement

When the spine is affected, the lesion usually involves the anterior vertebral body.

Multicentric Disease

Multicentric giant cell tumor is rare, occurring in approximately 1% of cases.

Chest Imaging

Chest imaging is appropriate during staging because a small proportion of patients develop pulmonary metastases despite histologically benign primary disease.

Historically, approximately 2% of patients have been reported to develop lung metastases.

Bone Scintigraphy

Bone scans are frequently positive because of increased metabolic activity around the lesion.

However, some lesions may demonstrate relatively little uptake, particularly less active tumors.

Pathological Findings

Microscopically, the tumor consists of a proliferating population of relatively uniform mononuclear stromal cells with numerous multinucleated giant cells distributed evenly throughout the lesion.

Mononuclear Cells

The stromal cells are generally round, oval, epithelioid, or spindle shaped.

They have relatively large nuclei and inconspicuous nucleoli.

These stromal cells represent the neoplastic component of the tumor.

Giant Cells

Multinucleated osteoclast-like giant cells are dispersed relatively uniformly among the mononuclear cells.

Their nuclei often resemble those of the surrounding stromal cells.

Mitotic Activity

Mitotic figures may be frequent, even in histologically benign tumors.

The presence of mitoses alone does not necessarily imply malignant transformation.

Aneurysmal Bone Cyst Component

A secondary aneurysmal bone cyst may be present within the tumor.

Vascular Invasion

Tumor cells may occasionally extend into blood vessels.

Involutional Changes

Some lesions contain lipid-laden histiocytes or other degenerative changes.

Differential Diagnosis

Brown Tumor of Hyperparathyroidism

A brown tumor may closely resemble giant cell tumor histologically and radiographically.

Serum calcium, phosphate, and parathyroid hormone levels help distinguish the two conditions.

Giant Cell Reparative Granuloma

Giant cell reparative granuloma may also contain numerous giant cells but generally has a different clinical setting and histologic organization.

Nonossifying Fibroma

NOF can produce an eccentric lucent lesion but usually occurs in younger patients, is metaphyseal rather than epiphyseal, and typically has a sclerotic border.

Benign Fibrous Histiocytoma

Benign fibrous histiocytoma may share fibrohistiocytic features but usually has a different histologic pattern and distribution.

Aneurysmal Bone Cyst

A primary aneurysmal bone cyst may resemble a giant cell tumor, particularly when secondary aneurysmal cystic change is prominent.

Telangiectatic Osteosarcoma

Telangiectatic osteosarcoma is an important malignant differential diagnosis because it can appear expansile and cystic.

Biopsy and careful histopathologic interpretation are essential.

Treatment

General Principles

Treatment aims to eradicate local disease while preserving the adjacent joint and maintaining limb function whenever possible.

Patients with large lesions at risk for pathologic fracture may be advised to use crutches or protected weight bearing until definitive treatment.

Radiotherapy

Radiotherapy is generally avoided whenever complete surgical treatment is feasible.

Historically, irradiation was associated with an increased risk of secondary malignant transformation.

It is now reserved for uncommon situations in which surgery is not feasible or would carry unacceptable morbidity.

Physical Therapy

Physical therapy is used after treatment to restore joint range of motion, strength, gait, and function.

Surgery

The standard surgical approach for many accessible giant cell tumors consists of extended intralesional curettage.

Curettage

The tumor is removed from the cavity while preserving as much normal bone and articular surface as possible.

High-Speed Burr

A high-speed burr is commonly used to remove microscopic residual tumor from the walls of the cavity and extend the margin of curettage.

Local Adjuvant Treatment

Local adjuvants may be used to reduce residual tumor cells.

Historically, agents such as phenol have been applied to the cavity.

Other modern local adjuvant techniques may also be used depending on surgeon preference and anatomic location.

Polymethylmethacrylate Cement

The resulting cavity may be filled with polymethylmethacrylate (PMMA) bone cement.

Cement provides immediate structural support and facilitates radiographic recognition of recurrent lytic disease at the cement-bone interface.

Bone Grafting

Cancellous or structural bone graft may be used, particularly near the subchondral surface when preservation of the joint is important.

Subchondral Reconstruction

Bone graft can help restore the subchondral region and reduce direct loading of articular cartilage overlying a large defect.

Internal Fixation

Internal fixation may be required when the remaining bone is structurally weak or when there is a pathologic fracture.

Wide Resection

Wide resection may be appropriate when the tumor involves an expendable bone such as the fibula, when there is extensive soft-tissue extension, or when recurrent disease has destroyed the adjacent joint.

Reconstruction

Large periarticular resections may require complex reconstruction.

Around the knee, options may include prosthetic replacement, osteoarticular allograft reconstruction, or arthrodesis, depending on patient factors and extent of disease.

Amputation

Amputation is rarely necessary.

It may be considered for extremely advanced neglected tumors with extensive soft-tissue involvement or for selected uncontrollable recurrent lesions.

Follow-Up

Prognosis

Giant cell tumors have a substantial tendency to recur locally.

Simple Curettage

Historically, recurrence rates after simple curettage alone have been reported as high as 40–60%.

Modern Extended Curettage

With extended curettage using high-speed burring and local adjuvant techniques, recurrence rates are substantially lower, commonly around 10–15%.

Timing of Recurrence

Most recurrences occur within the first 2 years following treatment.

Nearly all are detected within approximately 5 years, although longer surveillance may still be appropriate.

Complications

Local Recurrence

Local recurrence is the most important complication after limb-preserving treatment.

Pathologic Fracture

Structural weakening of bone can produce fracture before treatment or occasionally during follow-up.

Pulmonary Metastasis

A small proportion of histologically benign giant cell tumors metastasize to the lungs.

These metastases may behave relatively indolently but require specialist assessment.

Secondary Malignant Giant Cell Tumor

A secondary malignant giant cell tumor occurs when a sarcoma develops at the site of a previously treated giant cell tumor.

Postirradiation Sarcoma

Historically, approximately 10–15% of irradiated giant cell tumors were reported to develop postirradiation sarcoma in older series.

This risk is one reason radiotherapy is now used very selectively.

Sarcomatous Transformation Without Radiation

Malignant transformation can also occur without previous radiation, particularly in recurrent tumors, but it is uncommon.

Patient Monitoring

Close postoperative surveillance is required because of the risk of recurrence.

Patients may initially be reviewed approximately every 3 months during the first 2 years, with clinical examination and local imaging.

Chest Surveillance

Periodic chest imaging is appropriate because of the small risk of pulmonary metastasis.

Historically, annual chest radiography has been used.

Long-Term Monitoring

Follow-up should assess pain, swelling, joint motion, structural integrity, radiographic evidence of recurrence, pulmonary disease, and complications of reconstruction.

Orthopaedic Surgery - Genu Valgum (Knock-Knee)

Basics

Genu valgum, commonly called knock-knee, describes a lower-extremity alignment in which the knees angle toward one another while the ankles remain separated.

A degree of genu valgum is a normal developmental finding in young children, particularly between approximately 2 and 4 years of age.

Normal Development

Girls normally demonstrate slightly more physiologic valgus than boys.

As growth continues, the valgus gradually decreases, and the lower extremities usually approach the typical adult alignment by approximately 6–7 years of age.

Pathologic Genu Valgum

Persistent or excessive valgus may result from disorders such as rickets, previous trauma, skeletal dysplasia, or genetic abnormalities.

Some children have persistent idiopathic genu valgum without an identifiable underlying disorder.

When substantial valgus persists beyond approximately 7 years of age, it is less likely to represent normal physiologic development.

Anatomic Location

The deformity most commonly arises from altered growth around the knee, particularly involving the distal femoral and proximal tibial physes.

The deformity may originate from the femur, tibia, or both.

Epidemiology

Pathologic genu valgum is uncommon.

The reported incidence is less than approximately 1 per 1,000 children.

Age

Patients requiring evaluation commonly present between approximately 3 and 11 years of age.

Physiologic valgus is most apparent in early childhood.

Sex

Physiologic genu valgum is somewhat more pronounced and more commonly noticed in females than males.

Risk Factors

A family history of genu valgum may increase the likelihood of persistent idiopathic deformity.

Proximal Tibial Metaphyseal Fracture

A proximal tibial metaphyseal fracture in a child, sometimes referred to as a Cozen fracture, can be followed by asymmetric overgrowth and progressive valgus deformity.

Parents should be informed of this possibility, even when the initial fracture heals uneventfully.

Genetics

Several metabolic and skeletal disorders associated with genu valgum have an inherited basis.

Certain forms of rickets are genetic, and idiopathic valgus alignment may also cluster within families.

Etiology

Potential causes include physiologic development, metabolic disease, steroid-related skeletal effects, post-traumatic growth disturbance, skeletal dysplasia, and chromosomal disorders.

Physiologic Genu Valgum

Physiologic genu valgum represents a normal stage of lower-extremity development and generally corrects spontaneously with growth.

Metabolic Disease

Rickets and renal osteodystrophy may weaken the metaphyseal bone and disturb physeal growth, resulting in progressive angular deformity.

Post-Traumatic Deformity

A proximal tibial fracture may lead to asymmetric growth and delayed valgus deformity.

The deformity can appear months after the original injury.

Skeletal Dysplasia

Conditions such as pseudoachondroplasia and metaphyseal dysplasia may produce substantial valgus because of abnormal growth around the knee.

Chromosomal Disorders

Genu valgum may also occur in association with chromosomal conditions such as Klinefelter syndrome or Down syndrome.

Associated Conditions

Important associated disorders include proximal tibial fracture, pseudoachondroplasia, renal osteodystrophy, metaphyseal dysplasia, rickets, Down syndrome, and multiple osteochondromas.

Diagnosis

Signs and Symptoms

The most common reason for presentation is parental concern regarding the appearance of the child’s legs.

Most children with physiologic genu valgum have no pain or functional limitation.

Pain

Childhood genu valgum is usually painless.

Occasionally, excessive valgus may be associated with patellofemoral discomfort or altered patellar tracking.

Adult Symptoms

Persistent severe valgus in adulthood can increase loading across the lateral compartment of the knee and may contribute to lateral compartment osteoarthritis and patellofemoral symptoms.

Physical Examination

Range of Motion

Knee range of motion should be assessed and compared bilaterally.

Associated flexion contracture, hyperextension, or rotational abnormality should be documented.

Growth Assessment

Height and weight should be measured and plotted against age-appropriate growth charts.

Short stature or abnormal growth patterns may suggest skeletal dysplasia, endocrine disease, or another systemic disorder.

Femorotibial Angle

The angle between the femoral and tibial axes can be measured clinically using a goniometer.

This provides an estimate of the degree of valgus.

Intermalleolar Distance

With the patient standing and the knees touching, the distance between the medial malleoli is measured.

An increased intermalleolar distance reflects greater valgus deformity.

Adjacent Joints

The hips and ankles should also be examined because deformity or contracture at these levels may alter apparent knee alignment.

Rotational Profile

Femoral and tibial rotation should be assessed.

Rotational abnormalities may exaggerate or mask the appearance of genu valgum.

Gait

The patient’s gait should be observed for abnormal alignment, circumduction, instability, or patellar maltracking.

Ligament Examination

The medial and lateral collateral ligaments should be tested for laxity.

Ligamentous instability may contribute to apparent or progressive valgus alignment.

Laboratory Tests

Laboratory testing is unnecessary for typical physiologic genu valgum.

It is indicated when a metabolic or endocrine disorder is suspected.

Evaluation for Rickets or Metabolic Bone Disease

Potential studies include serum calcium, phosphate, alkaline phosphatase, blood urea nitrogen, creatinine, and vitamin D levels.

Vitamin D Assessment

When evaluating rickets, measurement of 25-hydroxyvitamin D is particularly useful.

Additional studies, including 1,25-dihydroxyvitamin D and renal or endocrine investigations, may be obtained depending on the suspected cause.

Hypophosphatemic Rickets

Familial hypophosphatemic rickets is an important inherited cause of progressive lower-extremity deformity.

Serum phosphate and related metabolic studies are therefore important when this condition is suspected.

Imaging

When Imaging Is Unnecessary

Routine radiographs are generally unnecessary in children younger than approximately 6 years when the genu valgum is symmetric, painless, and clearly physiologic.

Indications for Imaging

Imaging should be obtained when the deformity is asymmetric, severe, progressive, painful, persistent beyond the expected age, associated with short stature, or accompanied by suspicion of metabolic or skeletal disease.

Standing Long-Leg Radiograph

The preferred initial study is a standing AP radiograph of the entire lower extremity from hip to ankle.

The patella should face directly forward to minimize rotational error.

Femorotibial Angle

The radiograph allows measurement of the femorotibial angle and helps determine whether the deformity arises primarily from the distal femur, proximal tibia, or both.

Mechanical Axis

The mechanical axis of the lower extremity should be assessed.

In normal alignment, a line from the center of the femoral head toward the center of the ankle passes near the central portion of the knee.

Increasing lateral displacement indicates worsening genu valgum.

Differential Diagnosis

The principal diagnostic task is distinguishing physiologic valgus from pathologic valgus.

It is also important to determine whether the deformity is developmental or acquired.

Physiologic Genu Valgum

Physiologic genu valgum occurs without evidence of rickets, skeletal dysplasia, trauma, tumor, or other disease and improves spontaneously with growth.

Skeletal Dysplasia

Important skeletal dysplasias associated with valgus include metaphyseal dysplasia, pseudoachondroplasia, and multiple osteochondromas.

Developmental Causes

Developmental causes include physiologic valgus, idiopathic persistent genu valgum, and skeletal dysplasia.

Acquired Causes

Acquired causes include metabolic disease, post-traumatic growth disturbance, and neoplastic or other physeal disorders.

Treatment

Physiologic Genu Valgum

No treatment is required for physiologic genu valgum in children younger than approximately 7 years of age when the deformity is symmetric and within normal developmental limits.

Reassurance and observation are usually sufficient.

Persistent Idiopathic Genu Valgum

If substantial deformity persists beyond approximately 7 years of age, continued observation may be appropriate until the child approaches an age at which guided growth could be considered.

Surgical treatment is generally reserved for persistent, progressive, or symptomatic deformity.

Pathologic Valgus

The underlying disorder should be addressed before or together with correction of the angular deformity.

Metabolic Disease

In patients with renal osteodystrophy, rickets, or another metabolic condition, medical control of the underlying disease is essential.

Management often requires coordination with an endocrinologist or nephrologist.

Bracing

Bracing has not been shown to reliably correct or prevent progression of structural genu valgum.

Osteotomy

Severe deformity associated with skeletal dysplasia or metabolic disease may require one or more corrective osteotomies once the underlying disease has been adequately controlled.

Post-Traumatic Valgus

Children with proximal tibial metaphyseal fractures should be followed for several years because valgus deformity can develop after apparent fracture healing.

Early Osteotomy

Early corrective tibial osteotomy is generally avoided because post-traumatic valgus may spontaneously improve and early osteotomy has historically been associated with recurrence.

Persistent Deformity

If unacceptable valgus remains after approximately 1–2 years of observation, guided growth or corrective osteotomy may be considered depending on remaining growth and severity.

Skeletal Dysplasia

Children with pseudoachondroplasia or metaphyseal dysplasia may develop progressive valgus.

Corrective osteotomy or guided growth may be required when the deformity becomes substantial or symptomatic.

Activity

No routine activity restrictions are required for physiologic genu valgum.

Children may participate in normal play and sports unless another underlying disorder requires limitation.

Physical Therapy

Physical therapy does not alter physeal growth or correct structural genu valgum.

Exercises therefore do not change the natural history of the deformity.

Therapy may still be useful for associated weakness or postoperative rehabilitation.

Surgery

The two principal surgical strategies are hemiepiphysiodesis and corrective varus osteotomy.

Hemiepiphysiodesis

Hemiepiphysiodesis is a guided-growth procedure used in skeletally immature children with sufficient growth remaining.

Principle

Growth on the medial side of the distal femoral or proximal tibial physis is temporarily slowed, allowing continued growth on the lateral side to gradually correct the valgus.

Techniques

Guided growth may be achieved using staples, transphyseal screws, or plate-and-screw tension-band devices.

Indications

Hemiepiphysiodesis may be considered when the mechanical axis passes markedly lateral to the knee, particularly into the lateral-most zones of the tibial plateau.

Pain combined with significant mechanical-axis deviation may also support intervention.

Advantages

The procedure is relatively minimally invasive, does not substantially weaken the bone, and usually allows early weight bearing.

Goal

The objective is to achieve satisfactory mechanical alignment by the time skeletal growth is completed.

Careful timing and follow-up are necessary to avoid overcorrection.

Corrective Osteotomy

Osteotomy is preferred when immediate correction is required or insufficient growth remains for guided growth to work effectively.

Procedure

The involved bone is divided, realigned into a more neutral or varus position, and stabilized with internal fixation.

The osteotomy may be performed at the distal femur, proximal tibia, or both depending on the site of deformity.

Recovery

Recovery is more demanding than after hemiepiphysiodesis because the bone is completely divided and must heal before unrestricted activity.

Surgical Success

Appropriately selected surgical correction has an overall success rate greater than approximately 90%.

Follow-Up

Prognosis

Physiologic genu valgum has an excellent prognosis and usually resolves as growth continues.

Mild deformity, particularly valgus less than approximately 15°, often improves by approximately 7–10 years of age when no metabolic or skeletal disorder is present.

Complications of Untreated Genu Valgum

Severe persistent valgus may cause patellofemoral pain, abnormal patellar tracking, gait disturbance, and increased loading of the lateral compartment of the knee.

Over many years, this can contribute to degenerative arthritis.

Surgical Complications

Potential complications include infection, compartment syndrome, neurovascular injury, recurrent deformity, and overcorrection into genu varum.

Guided-growth procedures additionally require careful monitoring to prevent excessive correction.

Patient Monitoring

Children with idiopathic genu valgum can generally be followed at approximately 12–24-month intervals while spontaneous improvement is expected.

Follow-up should document intermalleolar distance, femorotibial angle, gait, mechanical-axis alignment, symmetry, pain, growth, and progression or improvement of the deformity.

Orthopaedic Surgery - Friedreich Ataxia

Basics

Friedreich ataxia is an uncommon inherited neurodegenerative disorder characterized by progressive degeneration of the spinal cord and peripheral nervous system, with prominent involvement of coordination and gait.

The musculoskeletal manifestations most frequently encountered are scoliosis and cavovarus foot deformity, while progressive ataxia represents the major neurologic feature.

Systems Involved

Friedreich ataxia primarily affects the central and peripheral nervous systems, cardiovascular system, and musculoskeletal system.

Endocrine abnormalities, particularly diabetes mellitus, may also occur.

Classification

There are no major orthopaedic subclassifications of Friedreich ataxia.

It belongs to the broader group of hereditary ataxic or spinocerebellar degenerative disorders.

Epidemiology

Friedreich ataxia is rare.

Older estimates placed its prevalence at approximately 1 in 50,000 individuals, while more recent molecularly based estimates have suggested a prevalence closer to 1 in 29,000 in some populations.

Age at Presentation

Symptoms most commonly become apparent between approximately 5 and 25 years of age.

Earlier onset is generally associated with more severe and rapidly progressive disease.

Sex

Males and females are affected approximately equally.

Population Distribution

The condition is more common in populations of European ancestry and has historically been reported with increased frequency in some French-Canadian populations.

Genetics

Friedreich ataxia is inherited in an autosomal recessive pattern.

Affected individuals generally inherit a pathogenic allele from each parent.

Frataxin Gene

The disorder is caused by pathogenic changes involving the FXN gene on chromosome 9, which encodes the mitochondrial protein frataxin.

GAA Trinucleotide Repeat

The most common genetic abnormality is expansion of a GAA trinucleotide repeat within the FXN gene.

This reduces expression of frataxin.

Relationship to Disease Severity

In general, larger GAA repeat expansions are associated with earlier onset and more severe disease, although clinical variability is considerable.

Frataxin Function

Frataxin is a mitochondrial protein involved in cellular iron handling and normal mitochondrial energy metabolism.

Loss of adequate frataxin function contributes to oxidative injury and progressive neurologic and cardiac dysfunction.

Associated Conditions

Important associated conditions include hypertrophic cardiomyopathy, diabetes mellitus, scoliosis, and cavovarus deformity of the feet.

Diagnosis

The diagnosis is established primarily through molecular genetic testing identifying pathogenic variants in the FXN gene.

Historically, diagnosis relied more heavily on clinical manifestations and neurophysiologic findings.

Clinical Features

Classic Neurologic Findings

A characteristic clinical combination includes:

Progressive ataxia, loss or reduction of deep tendon reflexes, and an extensor plantar response or Babinski sign.

Ataxia

Progressive impairment of coordination affects standing, walking, and fine motor tasks.

Gait becomes broad-based and unstable as disease advances.

Areflexia

Deep tendon reflexes, particularly in the lower extremities, are commonly reduced or absent because of peripheral nerve involvement.

Babinski Sign

Despite reduced peripheral reflexes, corticospinal tract disease may produce an extensor plantar response.

Additional Signs

Other findings may include pes cavus or cavovarus feet, optic atrophy, nystagmus, abnormal electrocardiographic findings, scoliosis, and kyphosis.

Symptoms

Patients may experience progressive loss of coordination, weakness, painful muscle spasms, hearing impairment, fatigue, and depression.

Symptoms related to diabetes mellitus may also occur when endocrine involvement is present.

Physical Examination

Gait and Coordination

Gait should be observed carefully.

Tandem, or heel-to-toe, walking is useful for demonstrating impaired balance and coordination.

The finger-to-nose test can assess upper-extremity dysmetria and cerebellar dysfunction.

Spine Examination

Standing alignment should be assessed for excessive kyphosis and scoliosis.

The forward-bend test is useful for detecting rotational prominence associated with scoliosis.

Reflexes

Upper- and lower-extremity deep tendon reflexes should be documented.

Plantar responses should also be assessed.

Foot Examination

The feet should be evaluated for cavus, hindfoot varus, equinus, clawing of the toes, calluses, and skin pressure areas.

The examiner should determine whether the deformity remains flexible or has become rigid.

Muscle Strength

Muscle strength should be documented throughout the upper and lower extremities.

Weakness progresses with disease and ultimately contributes substantially to loss of ambulation.

Laboratory Tests

Creatine Kinase

Creatine phosphokinase or creatine kinase levels are generally normal, helping distinguish Friedreich ataxia from some primary muscular dystrophies.

Glucose Testing

Fasting serum glucose or other appropriate diabetic screening should be obtained because of the increased prevalence of diabetes mellitus.

Cardiac Assessment

Because cardiomyopathy is common, cardiac evaluation is important.

An electrocardiogram should be obtained before major surgery, and echocardiography should be performed when clinically indicated.

Cardiomyopathy

Hypertrophic cardiomyopathy is an important cause of morbidity and mortality and substantially influences perioperative planning.

Electrodiagnostic Testing

Electromyography may demonstrate polyphasic potentials.

Nerve conduction studies can show mild slowing or other evidence of peripheral neuropathy.

Imaging

Spine Radiographs

Standing posteroanterior and lateral radiographs of the spine should be obtained when scoliosis or kyphosis is identified.

Long-Term Spinal Surveillance

Spinal deformity can continue to progress even after skeletal maturity.

Periodic radiographic monitoring is therefore appropriate in patients with established scoliosis.

Foot Radiographs

Weight-bearing radiographs of the feet may be useful when cavovarus deformity is substantial, progressive, painful, or being considered for surgery.

Differential Diagnosis

Cerebellar Tumor

Intracranial lesions affecting the cerebellum may produce ataxia and should be considered when the presentation is atypical or asymmetric.

Chiari Malformation

Chiari malformation can produce neurologic abnormalities, gait disturbance, and scoliosis.

Muscular Dystrophy

Muscular dystrophies may produce progressive weakness and spinal deformity but have a different neurologic and laboratory profile.

Spinal Dysraphism

Spinal dysraphism can produce scoliosis, cavus foot deformity, weakness, and abnormal reflexes and should be considered in the differential diagnosis.

Treatment

General Principles

Management is multidisciplinary because the disorder affects neurologic, cardiac, endocrine, and musculoskeletal systems.

Orthopaedic care focuses primarily on preserving ambulation, maintaining plantigrade feet, treating painful deformity, and monitoring scoliosis.

Orthopaedic Surveillance

Foot and spinal deformities should be monitored by an orthopaedic surgeon even when surgery is not currently planned.

Progression may occur relatively rapidly, particularly in patients with early-onset disease.

Ambulation

Walking should be maintained safely for as long as possible.

Bracing, assistive devices, therapy, and correction of severe deformity can help preserve mobility.

Foot Deformity

Stretching and nighttime positioning or bracing may help delay progression of flexible cavovarus and equinus deformities.

The aim is to maintain a painless, braceable, plantigrade foot.

Scoliosis Bracing

For scoliosis measuring approximately 25–45°, bracing may be attempted in selected patients.

Bracing may slow progression but is less reliable at permanently controlling the curve than in idiopathic scoliosis.

Physical Therapy

Physical therapy is important for maintaining strength, balance, mobility, joint range of motion, transfers, and functional independence.

It is also essential after orthopaedic surgery.

Stretching

Regular stretching of the plantar fascia, Achilles tendon, and ankle musculature may help delay fixed cavovarus and equinus deformity.

Medication

Medical treatment is primarily directed by neurology and other relevant specialists.

Symptomatic medications may be required for associated problems.

Muscle Spasms

Painful spasticity or muscle spasms may be treated with medications such as baclofen or diazepam in selected patients.

Scoliosis Surgery

Preoperative Evaluation

Because of the high prevalence of cardiomyopathy and potential respiratory impairment, a detailed cardiopulmonary assessment is required before major spinal surgery.

Risk of Progression

Rapid scoliosis progression is particularly associated with onset of Friedreich ataxia before approximately 10 years of age and development of scoliosis before approximately 15 years.

Surgical Indications

Severe progressive curves, particularly those exceeding approximately 60°, often require posterior spinal fusion and instrumentation to prevent further deformity and loss of trunk balance.

Curves of 40–60°

Curves between approximately 40° and 60° require individualized treatment.

Factors include rate of progression, skeletal maturity, neurologic status, sitting or standing balance, pulmonary function, and overall medical condition.

Bracing or surgery may be appropriate depending on these factors.

Fusion Levels

Fusion frequently extends across a long segment of the thoracic and lumbar spine because deformity may be extensive and progressive.

Modern segmental instrumentation is used to obtain correction and stability.

Severe Rigid Curves

Large, rigid, or markedly unbalanced deformities may require additional techniques to improve flexibility and correction.

Historically, anterior release procedures were sometimes used, although contemporary approaches depend on individual anatomy and modern posterior techniques.

Spinal Cord Monitoring

Intraoperative neuromonitoring may be technically challenging because baseline neurologic abnormalities are common.

Both sensory and motor modalities should be used when feasible.

Postoperative Immobilization

Routine external postoperative immobilization is generally unnecessary after stable modern internal fixation.

Cavovarus Foot Surgery

Surgery is considered when the deformity becomes painful, progressive, rigid, poorly braceable, or interferes with standing and walking.

Soft-Tissue Procedures

Flexible deformities may require procedures such as Achilles tendon lengthening and tendon balancing or transfer.

Posterior tibial tendon procedures may be incorporated when its deforming force contributes to cavovarus.

Arthrodesis

Rigid severe deformities may require fusion procedures, including triple arthrodesis, to obtain a stable plantigrade foot.

Follow-Up

Specialist Coordination

A neurologist is generally best positioned to coordinate overall disease management, with input from orthopaedics, cardiology, endocrinology, rehabilitation medicine, physical therapy, and other specialists.

Prognosis

Friedreich ataxia is a progressive disorder.

The clinical course varies according to age of onset, genetic findings, cardiac involvement, and severity of neurologic disease.

Scoliosis Prognosis

Scoliosis developing before approximately 15 years of age is more likely to become severe and may ultimately require operative correction.

Ambulation

Progressive neurologic deterioration commonly leads to loss of independent walking.

Historically, many affected individuals became wheelchair dependent during the second or third decade of life, although progression varies substantially among patients.

Survival

Cardiomyopathy and respiratory complications are major determinants of long-term survival.

Historically, severe disease was associated with reduced life expectancy, although contemporary multidisciplinary management continues to improve supportive care.

Complications

Cardiomyopathy

Cardiac involvement is one of the most important systemic complications and can lead to arrhythmia or heart failure.

Foot Skin Problems

Cavovarus deformity may create abnormal pressure points, producing calluses, painful keratoses, or skin breakdown.

Respiratory Complications

Progressive neuromuscular weakness, scoliosis, and impaired swallowing may increase the risk of pneumonia and aspiration.

Progressive Loss of Mobility

Weakness, ataxia, contracture, and deformity progressively reduce walking endurance and may ultimately result in wheelchair dependence.

Patient Monitoring

Because Friedreich ataxia is progressive, patients require regular multidisciplinary follow-up.

Walking distance, muscle strength, coordination, foot alignment, skin condition, and overall functional status may be reassessed approximately every 3–6 months, depending on severity.

Scoliosis Monitoring

Once scoliosis is identified, clinical and radiographic assessment approximately every 6 months is appropriate during periods of growth or documented progression.

Long-term surveillance may remain necessary after skeletal maturity because curves can continue to worsen.

Orthopaedic Surgery - Freiberg Disease (Freiberg Infraction)

Basics

Freiberg disease, also called Freiberg infraction, is an osteochondrosis or osteonecrotic disorder involving the metatarsal head, most commonly the second metatarsal head.

It typically presents in an adolescent, young adult, or occasionally middle-aged adult with well-localized pain at the second metatarsophalangeal (MTP) joint that worsens with activity and improves with rest.

Anatomic Distribution

The second metatarsal head is affected most frequently.

The third or other lesser metatarsal heads may occasionally be involved.

Disease may be unilateral or bilateral.

Disease Progression

The disorder progresses through a spectrum of subchondral injury, necrosis, collapse, and eventually degenerative arthritis.

Early radiographs may demonstrate subtle mottling, sclerosis, or central subchondral collapse.

Moderate disease produces flattening or collapse of the metatarsal head, often accompanied by osteophytes or loose osteochondral fragments.

Advanced disease is characterized by joint-space loss, articular destruction, and secondary MTP arthritis.

Epidemiology

Freiberg disease occurs more commonly in females than males.

The true incidence is uncertain because some cases remain asymptomatic and are discovered incidentally on radiographs.

Age

The condition is classically diagnosed during adolescence, especially between approximately 13 and 18 years of age, although symptoms may persist into adulthood or first become clinically apparent later.

Risk Factors

Important associations include running, dancing, repetitive forefoot loading, and a relatively long second metatarsal.

These factors increase mechanical stress across the affected metatarsal head.

Etiology

The exact cause is likely multifactorial.

Freiberg disease is characterized by compromise of the subchondral bone and blood supply of the metatarsal head, resulting in osteonecrosis and structural collapse.

Vascular Factors

Impaired local microcirculation has been proposed as an important contributor to the development of osteonecrosis.

Acute Trauma

A single traumatic event may damage the subchondral bone or vascular supply and initiate the disease process in some patients.

Repetitive Microtrauma

Repeated forefoot loading from running, jumping, dancing, or other high-impact activity may produce cumulative microtrauma.

Second Metatarsal Anatomy

The second metatarsal is often the longest metatarsal and is relatively rigidly fixed at its base.

These characteristics can subject the second metatarsal head to increased repetitive loading and may explain why it is affected most frequently.

Diagnosis

Signs and Symptoms

The characteristic complaint is pain localized to the second MTP joint.

Pain is aggravated by walking, running, sports, and other weight-bearing activity and generally improves with rest.

Swelling

Localized swelling or soft-tissue thickening may develop around the involved MTP joint.

Swelling may become more noticeable after prolonged activity.

Stiffness

As disease progresses, the affected MTP joint may lose motion because of synovitis, articular collapse, osteophytes, or secondary arthritis.

Physical Examination

Range of Motion

The involved MTP joint may demonstrate reduced active and passive range of motion.

Motion can become progressively restricted in later stages.

Tenderness

Direct palpation over the metatarsal head and MTP joint typically reproduces the patient’s pain.

Swelling

Soft-tissue swelling around the joint may be present, particularly after activity.

Toe-Rise Test

Standing on the toes or performing a heel rise increases loading across the metatarsal heads and may reproduce pain.

Imaging

Plain Radiographs

Initial evaluation should include weight-bearing AP, oblique, and lateral radiographs of the foot.

Radiographic appearance varies according to the stage of disease.

Early Radiographic Findings

Early findings may include localized osteopenia, subtle subchondral lucency, sclerosis, or irregularity of the metatarsal head.

Radiographs can occasionally appear normal in very early disease.

Progressive Disease

With progression, the metatarsal head may become enlarged, flattened, sclerotic, and irregular.

Subchondral cystic changes and osteophytes may also develop.

End-Stage Disease

Advanced disease produces joint-space narrowing, fragmentation, deformity, and degenerative destruction of the MTP joint.

MRI

MRI is particularly useful when early disease is suspected but radiographs are normal or equivocal.

Typical findings include bone marrow edema and abnormalities of the subchondral bone consistent with osteonecrosis or osteochondral injury.

Bone Scintigraphy

Technetium bone scanning can demonstrate focal increased tracer uptake at the involved metatarsal head.

It may help identify occult disease, although MRI is generally more useful for defining early structural abnormalities.

Pathological Findings

Characteristic pathologic changes include synovitis, loose bodies, osteophytes, and osteonecrosis of the metatarsal head.

Metatarsal Head Necrosis

The marrow space may undergo fibrosis with areas of dead trabecular bone.

Subsequent resorption and structural weakening can lead to collapse of the articular surface.

Cartilage Damage

Progressive disease eventually results in articular cartilage loss and secondary degenerative arthritis.

Classification

Several classification systems have been proposed.

The best known is the Smillie classification, which describes progressive stages based largely on the structural and macroscopic appearance of the metatarsal head.

Although useful for describing severity, the classification does not always determine treatment reliably by itself.

Natural History

Freiberg disease may progress through stages of subchondral necrosis, collapse, remodeling, and secondary arthritis.

In some patients, remodeling ultimately produces a reasonably congruent articular surface and substantial improvement in pain.

Others develop persistent deformity or degenerative arthritis.

Differential Diagnosis

Idiopathic Synovitis

MTP synovitis can produce localized pain and swelling without the characteristic osseous abnormalities of Freiberg disease.

Inflammatory Arthritis

Inflammatory arthropathies may cause forefoot pain, swelling, stiffness, and multiple-joint involvement.

Acute Fracture

An acute metatarsal or osteochondral fracture should be considered when symptoms follow trauma.

MTP Sprain

Ligamentous injury around the MTP joint can produce pain and swelling without metatarsal head osteonecrosis.

Metatarsal Stress Fracture

A stress fracture may cause activity-related forefoot pain and focal tenderness and can resemble early Freiberg disease.

Morton Neuroma

Morton neuroma produces forefoot pain, often with burning or paresthesias radiating into the toes, typically from an intermetatarsal space rather than directly from the metatarsal head.

Treatment

General Principles

Treatment depends on the stage of disease, severity of pain, degree of articular collapse, and functional limitation.

Early disease is generally treated nonoperatively.

Activity Modification

Activities that reproduce pain should be reduced or temporarily avoided.

This commonly includes running, jumping, dancing, and other high-impact loading of the forefoot.

Immobilization and Footwear

Early-stage disease may be treated with a stiff-soled shoe, walking boot, or short walking cast to decrease motion and loading across the involved MTP joint.

Metatarsal Pad

A metatarsal pad placed just proximal to the affected metatarsal head can redistribute plantar pressure away from the painful joint.

Taping

Taping or strapping the involved toe can limit MTP motion and reduce mechanical irritation.

Medication

NSAIDs may be used to reduce pain and inflammatory swelling when appropriate.

Corticosteroid Injection

A carefully selected intra-articular corticosteroid injection may temporarily reduce symptomatic synovitis.

Such injections should be used judiciously and do not correct the underlying structural abnormality.

Surgery

Surgery is considered when substantial symptoms persist despite appropriate nonoperative treatment, particularly in patients with progressive collapse or mechanical joint symptoms.

Synovectomy

Synovectomy can be performed when persistent inflammatory synovitis contributes significantly to pain.

Joint Debridement

Debridement may include removal of fibrotic tissue, loose osteochondral bodies, and osteophytes.

This can improve motion and reduce mechanical symptoms.

Bone Grafting

Bone grafting of the metatarsal head may be considered in selected earlier-stage lesions when the subchondral bone is compromised but the articular surface has not yet undergone major collapse.

Dorsiflexion Osteotomy

A dorsiflexion osteotomy of the affected metatarsal can rotate relatively healthy plantar articular cartilage dorsally so that it articulates with the proximal phalanx.

This simultaneously unloads the damaged dorsal portion of the metatarsal head.

Resection Arthroplasty

Metatarsal head resection arthroplasty may be considered for severe end-stage disease in selected patients.

However, shortening and loss of the metatarsal head can alter forefoot load distribution.

Prosthetic Joint Replacement

Routine prosthetic replacement of the lesser MTP joint is generally not favored.

Potential problems include transfer metatarsalgia, bone resorption, loosening, and implant failure.

Follow-Up

Prognosis

The prognosis is generally favorable.

In many patients, the acute painful phase gradually resolves and is replaced by only an intermittent ache or mild activity-related discomfort.

Long-Term Outcome

Outcome depends on the degree of articular collapse and secondary arthritis.

Patients treated before extensive joint destruction generally have better preservation of motion and function.

Complications

Articular Collapse

Progressive subchondral failure can lead to flattening and collapse of the metatarsal head.

MTP Arthritis

Loss of joint congruity and cartilage can result in secondary degenerative arthritis of the second MTP joint.

Transfer Metatarsalgia

As the painful joint becomes mechanically unloaded, pressure may shift to adjacent metatarsal heads.

This can produce transfer metatarsalgia and plantar callus formation elsewhere in the forefoot.

Patient Monitoring

Patients should be monitored for pain, swelling, MTP range of motion, progression of metatarsal head collapse, development of arthritis, and ability to return to activity.

Repeat weight-bearing radiographs are useful when symptoms persist or worsen, particularly to assess structural progression and guide the need for operative treatment.

Orthopaedic Surgery - Fracture Treatment

Basics

Fractures are common injuries caused by trauma or, less commonly, by pathologic weakening of bone.

Management may be operative or nonoperative and depends on the location, displacement, stability, soft-tissue injury, patient age, bone quality, and functional requirements.

Nondisplaced Fractures

A nondisplaced fracture may involve one or both cortices, but the fragments remain essentially in their normal anatomic relationship.

These fractures can be difficult to identify on initial imaging, particularly when the fracture line is subtle.

Persistent unexplained pain after trauma should therefore raise suspicion for an occult nondisplaced fracture.

Displaced Fractures

Displacement can be described according to several features, including angulation, translation, rotation, and shortening.

Precise description is important for communication and treatment planning.

Angulation

One method of describing angular deformity is to state the direction of the fracture apex, such as “apex anterior.”

Another method is to describe the resulting alignment, such as varus or valgus angulation.

Translation

Translation refers to sideways displacement of one main fracture fragment relative to the other.

Rotation

Rotational deformity occurs when one fragment is twisted relative to the other.

Rotational malalignment may be clinically important even when plain radiographs appear relatively well aligned.

Shortening

Shortening results from fracture overlap or loss of bone length.

The amount that can be accepted varies greatly according to the bone involved, patient age, and functional demands.

Open Versus Closed Fracture

Determining whether a fracture is open or closed is one of the most important early decisions in fracture management.

Any wound anywhere near a limb containing a fracture must be treated with suspicion.

If there is a possibility that the wound communicates with the fracture or fracture hematoma, the injury should be considered an open fracture until proven otherwise.

Initial Management of an Open Fracture

Open fractures require prompt intravenous antibiotics, tetanus assessment, sterile wound coverage, fracture stabilization, and urgent surgical evaluation.

The wound should be covered with a sterile dressing after gross contamination is addressed, and repeated unnecessary manipulation should be avoided before operative debridement.

Gustilo-Anderson Classification

The Gustilo-Anderson system classifies open fractures according to wound size, injury energy, contamination, soft-tissue destruction, and vascular involvement.

Definitive grading is best assigned after operative debridement.

Type I

Type I injuries are low-energy open fractures with a relatively clean wound typically less than 1 cm in length and minimal soft-tissue damage.

Type II

Type II injuries have a wound generally greater than 1 cm but less than 10 cm, with moderate soft-tissue injury but without extensive stripping or loss of coverage.

Type III

Type III injuries are high-energy open fractures with severe soft-tissue damage, contamination, or complex injury.

Historically, a wound greater than 10 cm has been included in this category, although wound size alone does not determine severity.

Type IIIA

Type IIIA fractures have substantial soft-tissue injury but retain enough tissue for adequate coverage of the bone without requiring a major flap.

Type IIIB

Type IIIB injuries involve extensive soft-tissue destruction, periosteal stripping, exposed bone, and inadequate local coverage, often requiring flap reconstruction.

Type IIIC

Type IIIC fractures are associated with a vascular injury requiring repair, regardless of wound size.

Fracture Location

Diaphyseal Fractures

Diaphyseal fractures involve the shaft of a long bone and are commonly described according to level, such as proximal third, middle third, or distal third.

Metaphyseal Fractures

Metaphyseal fractures occur near the ends of long bones.

Some extend into the adjacent joint surface.

Intra-Articular Fractures

Intra-articular fractures disrupt the joint surface.

These injuries tolerate relatively little residual incongruity because persistent step-off or malalignment can contribute to joint stiffness and post-traumatic osteoarthritis.

Fracture Patterns

Transverse Fracture

A transverse fracture line runs approximately perpendicular to the long axis of the bone.

Oblique Fracture

An oblique fracture crosses the bone at an angle.

Spiral Fracture

A spiral fracture wraps around the bone and typically results from a rotational mechanism.

Comminuted Fracture

A comminuted fracture consists of three or more fragments at the fracture site.

Increasing comminution usually reflects greater injury energy or poor bone quality.

Segmental Fracture

A segmental fracture occurs when the same bone is broken at two separate levels, creating an isolated or “floating” intermediate segment.

Impacted Fracture

In an impacted fracture, one fragment is driven into another.

Avulsion Fracture

An avulsion fracture occurs when a tendon or ligament pulls off a fragment of bone from its attachment site.

Compression Fracture

Compression fractures occur when bone is crushed under axial load.

They are particularly common in osteoporotic vertebral bodies.

Pediatric Considerations

Children sustain several fracture patterns that are uncommon in adults because pediatric bone is more flexible and the periosteum is thicker.

Greenstick Fracture

In a greenstick fracture, the cortex and periosteum on the concave side remain intact, while the cortex on the convex side fails.

This produces an incomplete fracture with angular deformity.

Buckle or Torus Fracture

A buckle fracture is a stable metaphyseal compression injury characterized by cortical buckling rather than complete disruption.

It is often treated with removable splinting primarily for comfort and protection.

Physeal Injuries

Growth-plate fractures are commonly described using the Salter-Harris classification.

Salter-Harris Type I

Type I extends transversely through the physis alone.

Salter-Harris Type II

Type II passes through the physis and exits through the metaphysis, creating a metaphyseal fragment.

Salter-Harris Type III

Type III extends through the physis and epiphysis into the joint.

It is therefore an intra-articular fracture.

Salter-Harris Type IV

Type IV passes through the metaphysis, physis, and epiphysis, crossing the articular surface.

Precise reduction is important because both the joint and growth plate are involved.

Salter-Harris Type V

Type V is a crush injury of the physis.

It can be difficult to recognize initially and carries a significant risk of growth disturbance.

Perichondral Ring Injury

Injury to the peripheral physeal ring has sometimes been referred to as a Type VI injury, although this was not part of the original Salter-Harris classification.

Prevention

General fracture prevention includes trauma avoidance, fall prevention, appropriate safety equipment, and prevention or treatment of osteoporosis.

Pathophysiology

A fracture occurs when an applied force exceeds the mechanical strength of bone.

Healthy bone generally requires greater force to fracture than bone weakened by osteoporosis, tumor, infection, or metabolic disease.

Diagnosis

History

Most fractures follow trauma such as a motor vehicle collision, fall, sports injury, or direct blow.

Older patients may sustain fractures after relatively minor trauma because of osteoporosis.

Suspected Pathologic Fracture

When the reported mechanism seems too minor to explain the injury, an underlying pathologic process should be considered.

Examples include a humeral fracture while performing a trivial household activity or a femoral fracture after a minimal step or twist.

Possible causes include metastatic disease, primary bone tumor, osteoporosis, metabolic bone disease, or other structural abnormalities.

Nonaccidental Injury

Child abuse should be considered when fractures or bruises of different ages are present, the mechanism is inconsistent with the child’s developmental abilities, or the reported history does not adequately explain the injury.

Any concern should trigger a formal multidisciplinary safeguarding evaluation.

Physical Examination

The involved area should be inspected for deformity, swelling, bruising, warmth, skin wounds, fracture blisters, and focal tenderness.

Movement of the injured region may cause substantial pain and should be performed cautiously.

Neurovascular Examination

Motor function, sensation, pulses, capillary refill, and distal perfusion should be documented before and after reduction or splinting.

Soft-Tissue Examination

Any wound near the fracture must be examined carefully because even a small wound may communicate with the fracture.

Imaging

Plain Radiographs

Plain radiographs in at least two orthogonal planes are the basic imaging study for most fractures.

The images should generally include the joint above and below the fracture when practical, especially for long-bone injuries.

CT

CT is superior to plain radiography for defining many complex fractures, particularly those involving the spine, pelvis, hindfoot, and articular surfaces.

It is especially useful when operative planning requires detailed assessment of joint involvement and fragment morphology.

MRI

MRI can detect radiographically occult fractures and associated soft-tissue injury.

It is especially useful for stress fractures, occult hip fractures, and injuries involving ligaments or cartilage.

Bone Scintigraphy

Bone scintigraphy can identify occult or multifocal fractures when other imaging is unavailable or nondiagnostic, although MRI is now preferred for many indications.

Initial Treatment

Ice and Elevation

Ice and elevation may help limit pain and swelling in appropriate extremity injuries.

Immobilization

Early immobilization reduces pain, limits further soft-tissue injury, and helps maintain alignment.

Reduction

Displaced fractures should be reduced when necessary under appropriate analgesia, sedation, regional anesthesia, or general anesthesia.

Principles of Definitive Fracture Treatment

Regardless of whether management is operative or nonoperative, two fundamental goals apply:

Restoration of acceptable alignment and provision of sufficient stability to permit healing and function.

Splinting

During the acute swollen phase, a splint is often preferred over a circumferential cast.

Splints accommodate swelling and therefore reduce the risk of excessive pressure, skin injury, and compartment syndrome.

Casting

Casts are commonly used for stable or nondisplaced fractures and for fractures that remain acceptably aligned after closed reduction.

Cast Valving

A cast may be univalved or bivalved when significant swelling is anticipated.

This reduces circumferential pressure.

Three-Point Mold

A well-applied cast uses three-point molding to resist the deforming forces acting across the fracture and maintain reduction.

Functional Bracing

Functional braces permit controlled motion while maintaining fracture alignment.

They have been used successfully for selected humeral shaft and tibial shaft fractures.

Activity

Weight-bearing and joint-motion recommendations depend on fracture location, stability, fixation, and healing.

Operative fixation often permits earlier motion and, in some cases, earlier weight bearing than prolonged cast treatment.

Nursing Care

Careful monitoring is required for complications such as compartment syndrome, cast pressure, skin breakdown, swelling, neurovascular compromise, and uncontrolled pain.

Medication

Open Fracture Antibiotics

Open fractures require prompt intravenous antibiotic prophylaxis, ideally as soon as possible after injury.

Antibiotic selection depends on the Gustilo grade, contamination, local resistance patterns, and institutional protocol.

First-generation cephalosporins such as cefazolin are commonly used for gram-positive coverage in lower-grade injuries.

Broader gram-negative coverage is generally added for selected severe Type III injuries rather than simply for all Type II fractures.

Farm or Grossly Contaminated Injuries

Fractures contaminated with soil, farm material, fecal material, or other high-risk substances may require additional anaerobic coverage according to local trauma and infectious-disease protocols.

Tetanus Prophylaxis

Tetanus immunization status should be assessed in all open wounds, with booster vaccination or immune globulin provided when indicated.

Analgesia

Pain control should be tailored to injury severity.

Options include acetaminophen, NSAIDs when appropriate, regional anesthesia, and opioids for severe pain.

Surgery

The decision for operative treatment depends on fracture severity, instability, soft-tissue condition, patient factors, need for early mobilization, and ability to obtain or maintain acceptable alignment nonoperatively.

Intra-Articular Fractures

Displaced intra-articular fractures often require anatomic or near-anatomic reduction and stable fixation to restore the joint surface and allow early motion.

Failure to restore congruity increases the risk of stiffness and post-traumatic arthritis.

Diaphyseal Fractures

Shaft fractures may require fixation to restore length, rotation, and alignment and to permit earlier mobilization.

Plates and Screws

Plate-and-screw constructs are frequently used for intra-articular, metaphyseal, periarticular, and selected diaphyseal fractures.

They allow direct or indirect restoration of alignment and stable fixation.

Intramedullary Nails

Intramedullary nails are commonly used for long-bone diaphyseal fractures, particularly of the femur and tibia.

They function as load-sharing implants and often permit relatively early weight bearing.

External Fixation

External fixation is useful when there is severe soft-tissue injury, gross contamination, vascular compromise, marked swelling, or a need for temporary damage-control stabilization.

It may also be used definitively in selected injuries.

Damage-Control Orthopaedics

Severely injured polytrauma patients may not tolerate lengthy definitive fracture surgery immediately.

In these cases, temporary external fixation can provide rapid skeletal stabilization while minimizing the additional physiologic stress sometimes described as a “second hit.”

Definitive fixation is performed later after resuscitation and physiologic stabilization.

Referral and Safeguarding

When nonaccidental injury is suspected in a child, a pediatrician, child-protection team, and social worker or equivalent safeguarding professional should be involved promptly.

Prognosis

Prognosis depends on fracture location, displacement, soft-tissue injury, vascular status, infection, and patient factors.

In general, intra-articular fractures and fractures with major soft-tissue damage have a worse prognosis than uncomplicated shaft fractures.

Complications

Delayed Union

Delayed union refers to fracture healing that is progressing more slowly than expected.

Older definitions often used approximately 3–4 months, but the diagnosis should be interpreted according to the bone, fracture pattern, and biologic environment.

Nonunion

Nonunion is failure of a fracture to unite despite sufficient time and biologic opportunity.

Traditionally, absence of healing by about 6 months has been used in some settings, although modern definitions depend on clinical and radiographic progression rather than time alone.

Malunion

Malunion occurs when the fracture heals in an unacceptable position, producing deformity such as angulation, rotation, shortening, or translation.

Osteonecrosis

Osteonecrosis, or avascular necrosis, results from disruption of the blood supply to bone.

It is particularly associated with fractures involving the femoral head and neck, talar neck, proximal scaphoid, proximal humerus, and selected periarticular regions.

Osteomyelitis

Bone infection is a major complication, particularly after open fractures, severe contamination, or infected fixation.

Compartment Syndrome

Acute compartment syndrome occurs when pressure within a closed fascial compartment compromises tissue perfusion.

It is a surgical emergency.

Disproportionate pain, pain with passive stretch, tense swelling, neurologic changes, and progressive symptoms require immediate attention.

Pulmonary Complications

Major fractures, especially long-bone and pelvic injuries, may be associated with serious pulmonary complications.

Acute Respiratory Distress Syndrome

Severe trauma and systemic inflammation may contribute to acute respiratory distress syndrome.

Fat Embolism Syndrome

Fat embolism syndrome may follow long-bone or pelvic fractures and can produce respiratory, neurologic, and hematologic abnormalities.

Venous Thromboembolism

Deep venous thrombosis and pulmonary embolism are important risks, particularly in patients with lower-extremity fractures, major trauma, or prolonged immobility.

Complex Regional Pain Syndrome

The condition historically called reflex sympathetic dystrophy is now generally termed complex regional pain syndrome.

It may cause persistent pain, swelling, stiffness, and autonomic changes after fracture or surgery.

Post-Traumatic Arthritis

Fractures involving joint surfaces may eventually lead to degenerative arthritis, particularly when residual incongruity, cartilage injury, or instability remains.

Geriatric Considerations

Treatment decisions in older adults require careful balancing of operative risk against the consequences of immobility and deformity.

Common comorbidities include diabetes, coronary artery disease, peripheral vascular disease, osteoporosis, and frailty.

Early mobilization is often particularly important in this population.

Patient Monitoring

Patients with fractures should be followed clinically and radiographically until healing is established.

Serial assessment should evaluate alignment, stability, callus formation, pain, function, neurovascular status, implant position when applicable, and evidence of complications such as infection, nonunion, malunion, or post-traumatic arthritis.

Orthopaedic Surgery - Foot and Ankle Anatomy and Examination

Basics

For normal function, the foot should be plantigrade, meaning that it rests evenly on the ground, and it should permit painless weight bearing and propulsion.

Foot and ankle function depends on coordinated activity of both extrinsic muscles, which originate in the leg, and intrinsic muscles, which originate within the foot.

Extrinsic Muscles

The major extrinsic muscle-tendon groups can be divided functionally into dorsiflexors, evertors, plantarflexors, and invertors.

Dorsiflexors

The principal anterior extensor tendons include the tibialis anterior, extensor digitorum longus, peroneus tertius, and extensor hallucis longus.

These tendons cross superficially over the anterior ankle and are readily palpable.

Because of their superficial position, they are vulnerable to laceration from sharp objects.

Evertors

The primary evertors are the peroneus longus and peroneus brevis.

Their muscle bellies lie along the lateral leg, and their tendons pass posterior to the lateral malleolus.

Damage to the peroneal tendon sheath or superior peroneal retinaculum may allow the tendons to subluxate or dislocate over the lateral malleolus.

Plantarflexors and Invertors

Several important tendons pass posteromedial to the ankle.

The posterior tibial tendon is the major dynamic inverter and an important supporter of the medial longitudinal arch.

In adults, posterior tibial tendon degeneration, tenosynovitis, or rupture can contribute to adult-acquired flatfoot deformity.

Extrinsic Toe Flexors

The major extrinsic flexors of the toes are the flexor digitorum longus and flexor hallucis longus.

They contribute to toe flexion and assist with propulsion during gait.

Intrinsic Foot Muscles

The intrinsic muscles consist of one dorsal layer and three plantar layers.

Together, they control fine toe movements, support the arches, and contribute to balance and stabilization during stance.

Muscle Imbalance

An imbalance between intrinsic and extrinsic muscle forces may contribute to deformities such as hammer toes, claw toes, and mallet toes.

Bony Anatomy

Most bones and major bony landmarks of the foot and ankle are readily palpable, making systematic examination particularly useful.

The foot is conventionally divided into the hindfoot, midfoot, and forefoot.

Ankle Joint

The ankle, or tibiotalar joint, is formed by the articulation of the distal tibia, fibula, and talus.

It primarily permits plantarflexion and dorsiflexion.

Range of Motion

Normal ankle motion is approximately 40° of plantarflexion and 20° of dorsiflexion, although values vary among individuals.

Ankle Ligaments

Syndesmotic Ligaments

The distal tibiofibular syndesmosis is stabilized by the anterior and posterior tibiofibular ligaments, together with other components of the syndesmotic complex.

Injury to this complex produces a high ankle sprain.

Deltoid Ligament

The superficial and deep portions of the deltoid ligament extend from the medial malleolus to the talus, calcaneus, and navicular region.

They provide important medial ankle stability.

Lateral Ligament Complex

The lateral ankle is supported by the anterior talofibular ligament (ATFL), calcaneofibular ligament (CFL), and posterior talofibular ligament (PTFL).

The ATFL is the ligament most commonly injured during a typical inversion ankle sprain.

Hindfoot

The hindfoot consists principally of the talus and calcaneus.

These bones articulate at the subtalar joint.

Subtalar Motion

The subtalar joint permits inversion and eversion, with an overall motion arc of approximately 40°.

This motion allows the foot to adapt to irregular or uneven surfaces.

Talus

The talus is covered extensively by articular cartilage and has a relatively vulnerable blood supply.

Fracture or major subtalar dislocation can disrupt its vascular supply and lead to avascular necrosis.

Calcaneus

The calcaneus is the major weight-bearing bone of the heel and acts as an important shock absorber.

An axial load after a fall from height is a classic mechanism of calcaneal fracture.

Midfoot

The midfoot is organized into two principal rows.

Proximally, the navicular and cuboid articulate with the hindfoot.

Distally, the three cuneiforms and cuboid articulate with the metatarsals through the tarsometatarsal joints.

Tarsometatarsal Complex

Ligaments connect most adjacent metatarsal bases.

A notable exception exists between the first and second metatarsal bases, where there is no strong direct intermetatarsal ligament.

Lisfranc Ligament

The strong Lisfranc ligament extends from the medial cuneiform to the base of the second metatarsal.

It is a key stabilizer of the tarsometatarsal complex.

Forefoot

The forefoot consists of five metatarsals and 14 phalanges.

These structures contribute to balance, load distribution, and propulsion.

Gait Cycle

The gait cycle can be divided into stance and swing phases.

Stance Phase

The stance phase consists broadly of heel strike, foot-flat or midstance, and toe-off.

Heel Strike

At heel strike, the tibialis anterior and long toe extensors are active.

The foot undergoes pronation, which increases midfoot flexibility and allows better absorption of impact and accommodation to the ground.

Foot Flat

As weight progresses over the foot, the posterior tibialis and peroneal muscles contribute to dynamic control.

External rotation of the leg and subsequent foot supination help make the midfoot more rigid and stable for weight bearing.

Toe-Off

During push-off, the gastrocnemius-soleus complex becomes highly active.

This produces plantarflexion and propels the body forward.

Windlass Mechanism

Dorsiflexion of the toes, particularly the great toe, tightens the plantar fascia.

This windlass mechanism elevates the medial longitudinal arch and increases midfoot rigidity.

The foot is thereby converted from a flexible shock absorber into a stable lever for push-off.

Swing Phase

During swing, the tibialis anterior and long toe extensors remain active to dorsiflex the ankle and prevent the toes from dragging.

Clinical History

A thorough history should establish the nature of the patient’s symptoms and relevant systemic factors.

Acute Injury

For trauma, the mechanism should be documented carefully because it can suggest the injured bone, ligament, tendon, or joint.

Pain

Pain should be characterized according to severity, location, quality, radiation, duration, aggravating factors, and relieving factors.

Mechanical Symptoms

Locking, catching, clicking, giving way, or instability may suggest an intra-articular or ligamentous abnormality.

Neurologic Symptoms

The patient should be asked about numbness, dysesthesia, tingling, burning, or weakness.

Relevant Medical History

Important conditions include diabetes mellitus, neurologic disease, peripheral vascular disease, and inflammatory arthritis.

Surgical History

Previous surgery involving the foot, ankle, leg, or associated joints should be documented.

Functional History

Shoe wear, occupation, sports participation, and recreational activities can provide important information about repetitive loading and functional demands.

Physical Examination

The involved extremity should always be compared with the contralateral side.

The examination should be performed both standing and seated when possible.

Standing Examination

Alignment

While the patient stands, foot and ankle alignment should be observed.

Viewed from behind, the hindfoot can be categorized as varus, neutral, or valgus.

Too-Many-Toes Sign

When more lateral toes are visible from behind on the affected side than on the opposite side, the finding is called the too-many-toes sign.

This suggests forefoot abduction associated with collapse of the medial arch, as seen in flatfoot deformity.

Gait

The patient’s gait should be observed for abnormalities such as steppage gait, circumduction, scissoring, or an antalgic pattern.

Heel Rise

Double- and single-leg heel-rise testing evaluates dynamic foot function.

It helps assess posterior tibial tendon strength, arch reconstitution, hindfoot inversion, and balance.

Seated Examination

Vascular Examination

The dorsalis pedis pulse is palpated on the dorsum of the foot, typically just lateral to the extensor hallucis longus tendon.

The posterior tibial pulse is palpated posterior to the medial malleolus.

Venous Status

The foot and ankle should also be examined for pitting edema, venous stasis changes, skin discoloration, and other evidence of vascular insufficiency.

Sensory Examination

Sensation should be assessed according to peripheral nerve distribution.

Superficial Peroneal Nerve

The superficial peroneal nerve supplies most of the dorsum of the foot.

Deep Peroneal Nerve

The deep peroneal nerve is tested in the first dorsal web space.

Saphenous Nerve

The saphenous nerve supplies the medial border of the foot.

Sural Nerve

The sural nerve supplies the lateral border of the foot.

Tibial Nerve

The plantar surface of the foot is supplied primarily through branches of the tibial nerve.

Protective Sensation

The ability to perceive a 5.07 Semmes-Weinstein monofilament on the plantar surface correlates with protective sensation.

Loss of this sensation is particularly important in patients with diabetic or other peripheral neuropathy.

Neurologic Examination

Deep tendon reflexes should be assessed when appropriate.

The examination may also include evaluation for Babinski response and clonus when upper motor neuron disease is suspected.

Motor Examination

Strength testing should be combined with palpation of the corresponding tendons.

Ankle Dorsiflexion

Dorsiflexion primarily tests the tibialis anterior.

Ankle Plantarflexion

Plantarflexion is generated mainly by the gastrocnemius-soleus complex.

Eversion

Eversion evaluates the peroneal muscles.

Inversion

Inversion, especially with the foot slightly plantarflexed, assesses the posterior tibial tendon.

Great Toe Motion

Flexion of the distal phalanx of the great toe assesses the flexor hallucis longus, while extension tests the extensor hallucis longus.

Range of Motion

Both active and passive motion should be evaluated.

Ankle Motion

Ankle plantarflexion and dorsiflexion should be measured, preferably with any correctable hindfoot deformity brought into a neutral position.

Subtalar Motion

Hindfoot inversion and eversion assess the mobility of the subtalar joint.

Chopart Joint

Abduction and adduction through the transverse tarsal, or Chopart, joint can be assessed while stabilizing the hindfoot.

Lisfranc Joint

The tarsometatarsal complex should be palpated and stressed gently with plantarflexion and dorsiflexion of the metatarsals.

Pain or instability may indicate a Lisfranc injury.

Metatarsophalangeal and Toe Joints

Motion of the MTP and interphalangeal joints should be assessed for stiffness, instability, pain, and deformity.

Palpation

Systematic palpation helps localize pathology.

Malleoli

The medial and lateral malleoli should be palpated for tenderness suggestive of fracture or ligament injury.

Ankle Joint

The ankle joint should be assessed for joint-line tenderness or effusion, which may suggest synovitis or an osteochondral lesion.

Posterior Tibial Tendon

The posterior tibial tendon should be palpated from behind the medial malleolus to its insertion on the navicular.

Tenderness may indicate posterior tibial tendinitis or tendon dysfunction.

Navicular Tuberosity

The navicular tuberosity is located approximately 2 cm distal and plantar to the medial malleolus.

Tenderness in this region may reflect an accessory navicular, navicular stress fracture, posterior tibial tendon insertional pathology, or talonavicular disorder.

Achilles Tendon

The Achilles tendon and retrocalcaneal bursa should be palpated along the posterior ankle and hindfoot.

The examiner should look for defects, nodules, thickening, swelling, or tenderness suggestive of tendinopathy or rupture.

Peroneal Tendons

The peroneal tendons should be palpated posterior to the lateral malleolus.

The peroneus brevis can be followed to the base of the fifth metatarsal, while the peroneus longus passes beneath the foot through a groove near the cuboid.

Tenderness may reflect tendinitis or associated fifth-metatarsal pathology.

Peroneal Subluxation

The ankle can be circumducted while the tendons are observed and palpated for abnormal subluxation over the lateral malleolus.

Sinus Tarsi

The sinus tarsi lies approximately 1 cm distal to the lateral malleolus.

Tenderness may suggest subtalar joint inflammation or instability.

Syndesmosis

Tenderness between the distal tibia and fibula just proximal to the ankle joint raises concern for a syndesmotic, or high ankle, sprain.

Plantar Fascia

The plantar fascia should be palpated from its origin at the plantar calcaneus.

Tenderness near the medial plantar heel that becomes more pronounced with toe dorsiflexion is characteristic of plantar fasciitis.

Lisfranc Region

Tenderness at the base of the second metatarsal is concerning for a Lisfranc injury.

Plantar ecchymosis in this region is particularly significant.

Sesamoids

The plantar aspect of the great-toe MTP joint should be examined for tenderness related to sesamoiditis or sesamoid fracture.

Lesser Metatarsal Heads

Tenderness beneath the lesser MTP joints may indicate metatarsalgia.

Intermetatarsal Spaces

Tenderness in the metatarsal interspaces, sometimes accompanied by radiating paresthesias into the toes, may suggest an interdigital neuroma.

Special Tests

Anterior Drawer Test

The anterior drawer test assesses lateral ankle instability, particularly the ATFL.

The examiner stabilizes the distal tibia and translates the heel and talus anteriorly relative to the tibia.

The ATFL is stressed most effectively with the ankle in slight plantarflexion, whereas testing nearer neutral places relatively greater contribution on the broader lateral ligament complex.

Excessive anterior translation or a soft endpoint compared with the opposite ankle suggests instability.

Thompson Test

The Thompson test evaluates integrity of the Achilles tendon.

With the patient prone and the foot hanging freely, the examiner squeezes the calf.

An intact Achilles tendon produces plantarflexion of the foot.

Failure of plantarflexion strongly suggests Achilles tendon rupture.

Lesser-Toe Deformities

Mallet, hammer, and claw toe deformities should be assessed systematically.

Calluses

The location of callus formation helps identify areas of abnormal pressure.

Flexibility

The examiner should determine whether the deformity is flexible and manually correctable or rigid and fixed.

MTP Stability

A modified drawer test can assess MTP joint instability by attempting to translate and reduce the proximal phalanx relative to the metatarsal head.

Hallux Valgus Examination

Calluses and Medial Eminence

Callus formation and tenderness over the medial eminence should be documented.

MTP Motion

Range of motion of the first MTP joint should be assessed with the valgus deformity gently corrected.

This helps identify associated arthritis or stiffness.

First Tarsometatarsal Hypermobility

The lateral forefoot is stabilized while the first metatarsal is translated dorsally and plantarly.

Excessive mobility suggests first tarsometatarsal joint hypermobility.

Lesser-Toe Deformities

Associated lesser-toe deformities should be identified because they may contribute to pain and influence treatment planning.

Laboratory Tests

Laboratory testing is generally guided by the suspected diagnosis.

Suspected Infection

When infection is a concern, laboratory studies may include white blood cell count, erythrocyte sedimentation rate, and C-reactive protein.

Joint Aspiration

Synovial fluid from a suspicious joint should be sent for cell count with differential, Gram stain, culture, and crystal analysis.

Imaging

Plain Radiographs

Radiographs are the first-line imaging study for most structural foot and ankle disorders.

Acute Trauma

When acute fracture or dislocation is suspected and the patient cannot safely stand, non-weight-bearing radiographs are appropriate.

Weight-Bearing Radiographs

When the patient can stand safely, weight-bearing views are generally preferred for evaluation of alignment and deformity.

Standing radiographs demonstrate bony relationships under physiologic load and may reveal pathology that is not apparent on non-weight-bearing images.

Stress Radiographs

Stress views can indirectly assess the integrity of ligamentous structures by demonstrating abnormal joint translation or widening under applied force.

CT

CT provides excellent bony detail and is particularly useful for complex fracture patterns and disorders of the midfoot and hindfoot.

It is valuable for evaluating articular congruity and planning reconstruction.

MRI

MRI is especially useful for soft-tissue and occult osseous disorders.

It can demonstrate tendon and ligament injuries, soft-tissue masses, subtle fractures, marrow abnormalities, and infection.

Bone Scintigraphy

Technetium-99m bone scintigraphy can help localize pathology when pain is vague or multifocal.

It may detect stress fractures, tumors, and other metabolically active skeletal abnormalities, although MRI is often more specific for many modern indications.

General Examination Principles

A complete foot and ankle assessment combines history, standing alignment, gait analysis, vascular and neurologic examination, muscle testing, range of motion, palpation, provocative maneuvers, and appropriately selected imaging.

Because disorders of one region frequently alter mechanics elsewhere, the entire lower extremity should be considered rather than evaluating only the painful site.

Orthopaedic Surgery - Foot and Ankle Anatomy and Examination

Basics

For normal function, the foot should be plantigrade, meaning that it rests evenly on the ground, and it should permit painless weight bearing and propulsion.

Foot and ankle function depends on coordinated activity of both extrinsic muscles, which originate in the leg, and intrinsic muscles, which originate within the foot.

Extrinsic Muscles

The major extrinsic muscle-tendon groups can be divided functionally into dorsiflexors, evertors, plantarflexors, and invertors.

Dorsiflexors

The principal anterior extensor tendons include the tibialis anterior, extensor digitorum longus, peroneus tertius, and extensor hallucis longus.

These tendons cross superficially over the anterior ankle and are readily palpable.

Because of their superficial position, they are vulnerable to laceration from sharp objects.

Evertors

The primary evertors are the peroneus longus and peroneus brevis.

Their muscle bellies lie along the lateral leg, and their tendons pass posterior to the lateral malleolus.

Damage to the peroneal tendon sheath or superior peroneal retinaculum may allow the tendons to subluxate or dislocate over the lateral malleolus.

Plantarflexors and Invertors

Several important tendons pass posteromedial to the ankle.

The posterior tibial tendon is the major dynamic inverter and an important supporter of the medial longitudinal arch.

In adults, posterior tibial tendon degeneration, tenosynovitis, or rupture can contribute to adult-acquired flatfoot deformity.

Extrinsic Toe Flexors

The major extrinsic flexors of the toes are the flexor digitorum longus and flexor hallucis longus.

They contribute to toe flexion and assist with propulsion during gait.

Intrinsic Foot Muscles

The intrinsic muscles consist of one dorsal layer and three plantar layers.

Together, they control fine toe movements, support the arches, and contribute to balance and stabilization during stance.

Muscle Imbalance

An imbalance between intrinsic and extrinsic muscle forces may contribute to deformities such as hammer toes, claw toes, and mallet toes.

Bony Anatomy

Most bones and major bony landmarks of the foot and ankle are readily palpable, making systematic examination particularly useful.

The foot is conventionally divided into the hindfoot, midfoot, and forefoot.

Ankle Joint

The ankle, or tibiotalar joint, is formed by the articulation of the distal tibia, fibula, and talus.

It primarily permits plantarflexion and dorsiflexion.

Range of Motion

Normal ankle motion is approximately 40° of plantarflexion and 20° of dorsiflexion, although values vary among individuals.

Ankle Ligaments

Syndesmotic Ligaments

The distal tibiofibular syndesmosis is stabilized by the anterior and posterior tibiofibular ligaments, together with other components of the syndesmotic complex.

Injury to this complex produces a high ankle sprain.

Deltoid Ligament

The superficial and deep portions of the deltoid ligament extend from the medial malleolus to the talus, calcaneus, and navicular region.

They provide important medial ankle stability.

Lateral Ligament Complex

The lateral ankle is supported by the anterior talofibular ligament (ATFL), calcaneofibular ligament (CFL), and posterior talofibular ligament (PTFL).

The ATFL is the ligament most commonly injured during a typical inversion ankle sprain.

Hindfoot

The hindfoot consists principally of the talus and calcaneus.

These bones articulate at the subtalar joint.

Subtalar Motion

The subtalar joint permits inversion and eversion, with an overall motion arc of approximately 40°.

This motion allows the foot to adapt to irregular or uneven surfaces.

Talus

The talus is covered extensively by articular cartilage and has a relatively vulnerable blood supply.

Fracture or major subtalar dislocation can disrupt its vascular supply and lead to avascular necrosis.

Calcaneus

The calcaneus is the major weight-bearing bone of the heel and acts as an important shock absorber.

An axial load after a fall from height is a classic mechanism of calcaneal fracture.

Midfoot

The midfoot is organized into two principal rows.

Proximally, the navicular and cuboid articulate with the hindfoot.

Distally, the three cuneiforms and cuboid articulate with the metatarsals through the tarsometatarsal joints.

Tarsometatarsal Complex

Ligaments connect most adjacent metatarsal bases.

A notable exception exists between the first and second metatarsal bases, where there is no strong direct intermetatarsal ligament.

Lisfranc Ligament

The strong Lisfranc ligament extends from the medial cuneiform to the base of the second metatarsal.

It is a key stabilizer of the tarsometatarsal complex.

Forefoot

The forefoot consists of five metatarsals and 14 phalanges.

These structures contribute to balance, load distribution, and propulsion.

Gait Cycle

The gait cycle can be divided into stance and swing phases.

Stance Phase

The stance phase consists broadly of heel strike, foot-flat or midstance, and toe-off.

Heel Strike

At heel strike, the tibialis anterior and long toe extensors are active.

The foot undergoes pronation, which increases midfoot flexibility and allows better absorption of impact and accommodation to the ground.

Foot Flat

As weight progresses over the foot, the posterior tibialis and peroneal muscles contribute to dynamic control.

External rotation of the leg and subsequent foot supination help make the midfoot more rigid and stable for weight bearing.

Toe-Off

During push-off, the gastrocnemius-soleus complex becomes highly active.

This produces plantarflexion and propels the body forward.

Windlass Mechanism

Dorsiflexion of the toes, particularly the great toe, tightens the plantar fascia.

This windlass mechanism elevates the medial longitudinal arch and increases midfoot rigidity.

The foot is thereby converted from a flexible shock absorber into a stable lever for push-off.

Swing Phase

During swing, the tibialis anterior and long toe extensors remain active to dorsiflex the ankle and prevent the toes from dragging.

Clinical History

A thorough history should establish the nature of the patient’s symptoms and relevant systemic factors.

Acute Injury

For trauma, the mechanism should be documented carefully because it can suggest the injured bone, ligament, tendon, or joint.

Pain

Pain should be characterized according to severity, location, quality, radiation, duration, aggravating factors, and relieving factors.

Mechanical Symptoms

Locking, catching, clicking, giving way, or instability may suggest an intra-articular or ligamentous abnormality.

Neurologic Symptoms

The patient should be asked about numbness, dysesthesia, tingling, burning, or weakness.

Relevant Medical History

Important conditions include diabetes mellitus, neurologic disease, peripheral vascular disease, and inflammatory arthritis.

Surgical History

Previous surgery involving the foot, ankle, leg, or associated joints should be documented.

Functional History

Shoe wear, occupation, sports participation, and recreational activities can provide important information about repetitive loading and functional demands.

Physical Examination

The involved extremity should always be compared with the contralateral side.

The examination should be performed both standing and seated when possible.

Standing Examination

Alignment

While the patient stands, foot and ankle alignment should be observed.

Viewed from behind, the hindfoot can be categorized as varus, neutral, or valgus.

Too-Many-Toes Sign

When more lateral toes are visible from behind on the affected side than on the opposite side, the finding is called the too-many-toes sign.

This suggests forefoot abduction associated with collapse of the medial arch, as seen in flatfoot deformity.

Gait

The patient’s gait should be observed for abnormalities such as steppage gait, circumduction, scissoring, or an antalgic pattern.

Heel Rise

Double- and single-leg heel-rise testing evaluates dynamic foot function.

It helps assess posterior tibial tendon strength, arch reconstitution, hindfoot inversion, and balance.

Seated Examination

Vascular Examination

The dorsalis pedis pulse is palpated on the dorsum of the foot, typically just lateral to the extensor hallucis longus tendon.

The posterior tibial pulse is palpated posterior to the medial malleolus.

Venous Status

The foot and ankle should also be examined for pitting edema, venous stasis changes, skin discoloration, and other evidence of vascular insufficiency.

Sensory Examination

Sensation should be assessed according to peripheral nerve distribution.

Superficial Peroneal Nerve

The superficial peroneal nerve supplies most of the dorsum of the foot.

Deep Peroneal Nerve

The deep peroneal nerve is tested in the first dorsal web space.

Saphenous Nerve

The saphenous nerve supplies the medial border of the foot.

Sural Nerve

The sural nerve supplies the lateral border of the foot.

Tibial Nerve

The plantar surface of the foot is supplied primarily through branches of the tibial nerve.

Protective Sensation

The ability to perceive a 5.07 Semmes-Weinstein monofilament on the plantar surface correlates with protective sensation.

Loss of this sensation is particularly important in patients with diabetic or other peripheral neuropathy.

Neurologic Examination

Deep tendon reflexes should be assessed when appropriate.

The examination may also include evaluation for Babinski response and clonus when upper motor neuron disease is suspected.

Motor Examination

Strength testing should be combined with palpation of the corresponding tendons.

Ankle Dorsiflexion

Dorsiflexion primarily tests the tibialis anterior.

Ankle Plantarflexion

Plantarflexion is generated mainly by the gastrocnemius-soleus complex.

Eversion

Eversion evaluates the peroneal muscles.

Inversion

Inversion, especially with the foot slightly plantarflexed, assesses the posterior tibial tendon.

Great Toe Motion

Flexion of the distal phalanx of the great toe assesses the flexor hallucis longus, while extension tests the extensor hallucis longus.

Range of Motion

Both active and passive motion should be evaluated.

Ankle Motion

Ankle plantarflexion and dorsiflexion should be measured, preferably with any correctable hindfoot deformity brought into a neutral position.

Subtalar Motion

Hindfoot inversion and eversion assess the mobility of the subtalar joint.

Chopart Joint

Abduction and adduction through the transverse tarsal, or Chopart, joint can be assessed while stabilizing the hindfoot.

Lisfranc Joint

The tarsometatarsal complex should be palpated and stressed gently with plantarflexion and dorsiflexion of the metatarsals.

Pain or instability may indicate a Lisfranc injury.

Metatarsophalangeal and Toe Joints

Motion of the MTP and interphalangeal joints should be assessed for stiffness, instability, pain, and deformity.

Palpation

Systematic palpation helps localize pathology.

Malleoli

The medial and lateral malleoli should be palpated for tenderness suggestive of fracture or ligament injury.

Ankle Joint

The ankle joint should be assessed for joint-line tenderness or effusion, which may suggest synovitis or an osteochondral lesion.

Posterior Tibial Tendon

The posterior tibial tendon should be palpated from behind the medial malleolus to its insertion on the navicular.

Tenderness may indicate posterior tibial tendinitis or tendon dysfunction.

Navicular Tuberosity

The navicular tuberosity is located approximately 2 cm distal and plantar to the medial malleolus.

Tenderness in this region may reflect an accessory navicular, navicular stress fracture, posterior tibial tendon insertional pathology, or talonavicular disorder.

Achilles Tendon

The Achilles tendon and retrocalcaneal bursa should be palpated along the posterior ankle and hindfoot.

The examiner should look for defects, nodules, thickening, swelling, or tenderness suggestive of tendinopathy or rupture.

Peroneal Tendons

The peroneal tendons should be palpated posterior to the lateral malleolus.

The peroneus brevis can be followed to the base of the fifth metatarsal, while the peroneus longus passes beneath the foot through a groove near the cuboid.

Tenderness may reflect tendinitis or associated fifth-metatarsal pathology.

Peroneal Subluxation

The ankle can be circumducted while the tendons are observed and palpated for abnormal subluxation over the lateral malleolus.

Sinus Tarsi

The sinus tarsi lies approximately 1 cm distal to the lateral malleolus.

Tenderness may suggest subtalar joint inflammation or instability.

Syndesmosis

Tenderness between the distal tibia and fibula just proximal to the ankle joint raises concern for a syndesmotic, or high ankle, sprain.

Plantar Fascia

The plantar fascia should be palpated from its origin at the plantar calcaneus.

Tenderness near the medial plantar heel that becomes more pronounced with toe dorsiflexion is characteristic of plantar fasciitis.

Lisfranc Region

Tenderness at the base of the second metatarsal is concerning for a Lisfranc injury.

Plantar ecchymosis in this region is particularly significant.

Sesamoids

The plantar aspect of the great-toe MTP joint should be examined for tenderness related to sesamoiditis or sesamoid fracture.

Lesser Metatarsal Heads

Tenderness beneath the lesser MTP joints may indicate metatarsalgia.

Intermetatarsal Spaces

Tenderness in the metatarsal interspaces, sometimes accompanied by radiating paresthesias into the toes, may suggest an interdigital neuroma.

Special Tests

Anterior Drawer Test

The anterior drawer test assesses lateral ankle instability, particularly the ATFL.

The examiner stabilizes the distal tibia and translates the heel and talus anteriorly relative to the tibia.

The ATFL is stressed most effectively with the ankle in slight plantarflexion, whereas testing nearer neutral places relatively greater contribution on the broader lateral ligament complex.

Excessive anterior translation or a soft endpoint compared with the opposite ankle suggests instability.

Thompson Test

The Thompson test evaluates integrity of the Achilles tendon.

With the patient prone and the foot hanging freely, the examiner squeezes the calf.

An intact Achilles tendon produces plantarflexion of the foot.

Failure of plantarflexion strongly suggests Achilles tendon rupture.

Lesser-Toe Deformities

Mallet, hammer, and claw toe deformities should be assessed systematically.

Calluses

The location of callus formation helps identify areas of abnormal pressure.

Flexibility

The examiner should determine whether the deformity is flexible and manually correctable or rigid and fixed.

MTP Stability

A modified drawer test can assess MTP joint instability by attempting to translate and reduce the proximal phalanx relative to the metatarsal head.

Hallux Valgus Examination

Calluses and Medial Eminence

Callus formation and tenderness over the medial eminence should be documented.

MTP Motion

Range of motion of the first MTP joint should be assessed with the valgus deformity gently corrected.

This helps identify associated arthritis or stiffness.

First Tarsometatarsal Hypermobility

The lateral forefoot is stabilized while the first metatarsal is translated dorsally and plantarly.

Excessive mobility suggests first tarsometatarsal joint hypermobility.

Lesser-Toe Deformities

Associated lesser-toe deformities should be identified because they may contribute to pain and influence treatment planning.

Laboratory Tests

Laboratory testing is generally guided by the suspected diagnosis.

Suspected Infection

When infection is a concern, laboratory studies may include white blood cell count, erythrocyte sedimentation rate, and C-reactive protein.

Joint Aspiration

Synovial fluid from a suspicious joint should be sent for cell count with differential, Gram stain, culture, and crystal analysis.

Imaging

Plain Radiographs

Radiographs are the first-line imaging study for most structural foot and ankle disorders.

Acute Trauma

When acute fracture or dislocation is suspected and the patient cannot safely stand, non-weight-bearing radiographs are appropriate.

Weight-Bearing Radiographs

When the patient can stand safely, weight-bearing views are generally preferred for evaluation of alignment and deformity.

Standing radiographs demonstrate bony relationships under physiologic load and may reveal pathology that is not apparent on non-weight-bearing images.

Stress Radiographs

Stress views can indirectly assess the integrity of ligamentous structures by demonstrating abnormal joint translation or widening under applied force.

CT

CT provides excellent bony detail and is particularly useful for complex fracture patterns and disorders of the midfoot and hindfoot.

It is valuable for evaluating articular congruity and planning reconstruction.

MRI

MRI is especially useful for soft-tissue and occult osseous disorders.

It can demonstrate tendon and ligament injuries, soft-tissue masses, subtle fractures, marrow abnormalities, and infection.

Bone Scintigraphy

Technetium-99m bone scintigraphy can help localize pathology when pain is vague or multifocal.

It may detect stress fractures, tumors, and other metabolically active skeletal abnormalities, although MRI is often more specific for many modern indications.

General Examination Principles

A complete foot and ankle assessment combines history, standing alignment, gait analysis, vascular and neurologic examination, muscle testing, range of motion, palpation, provocative maneuvers, and appropriately selected imaging.

Because disorders of one region frequently alter mechanics elsewhere, the entire lower extremity should be considered rather than evaluating only the painful site.

Orthopaedic Surgery - Flexor Tendon Laceration

Basics

Flexor tendon lacerations may occur anywhere along the volar surface of the fingers, palm, wrist, or forearm.

They are commonly described according to the anatomic zone of injury because tendon anatomy, repair technique, rehabilitation, and prognosis vary substantially by location.

Flexor Tendon Zones

For the fingers, flexor tendon injuries are traditionally divided into Zones I through V.

The thumb has a corresponding three-zone classification.

Zone I

Zone I extends from the fingertip proximally to the proximal interphalangeal (PIP) flexion crease.

In this region, the flexor digitorum profundus (FDP) is the principal flexor tendon because the flexor digitorum superficialis (FDS) inserts more proximally.

Zone II

Zone II extends from the PIP flexion crease proximally to the distal palmar transverse crease near the A1 pulley.

Both the FDS and FDP tendons travel together within the flexor sheath in this region.

Zone II: “No-Man’s Land”

Zone II was historically called “no-man’s land” because repairs in this region were associated with a particularly high risk of postoperative adhesions, scarring, and poor tendon gliding.

The anatomy is complex because both the superficial and deep flexor tendons pass through a confined fibro-osseous pulley system.

Modern repair techniques and early mobilization protocols have substantially improved outcomes, but Zone II injuries remain technically demanding.

Zone III

Zone III extends from the distal palmar transverse crease proximally to the distal wrist flexion crease or transverse carpal ligament.

Zone IV

Zone IV corresponds to the carpal tunnel.

Multiple flexor tendons and the median nerve are closely packed within this confined space, so associated injuries may be substantial.

Zone V

Zone V is located proximal to the carpal tunnel, extending into the distal forearm.

Lacerations in this region may involve multiple tendons together with the median or ulnar nerves and major vessels.

Classification

Flexor tendon injuries are described according to both the specific tendon injured and the zone of injury.

They may involve the FDS, FDP, flexor pollicis longus, or combinations of these structures.

Function

Each flexor tendon contributes to finger strength, coordinated motion, and independent digital control.

The FDS primarily flexes the PIP joint, whereas the FDP flexes the DIP joint and also contributes to flexion of more proximal joints.

Epidemiology

Approximately 25% of flexor tendon lacerations occur in the workplace.

Males are affected substantially more often than females, with reported male-to-female ratios of approximately 3–6:1.

Risk Factors

The principal risk factor is occupational or recreational exposure to sharp objects or machinery.

Etiology

Most injuries result from a sharp penetrating mechanism such as a knife, broken glass, sheet metal, or other cutting object.

Crush or high-energy injuries may produce more extensive tendon and soft-tissue damage and generally have a worse prognosis.

Associated Injuries

Flexor tendon lacerations may occur with injuries to adjacent structures.

Digital Nerve Injury

Digital nerve laceration accompanies approximately one-quarter of flexor tendon injuries in some series.

Digital Artery Injury

Digital arteries may also be disrupted, potentially compromising perfusion of the involved finger.

Pulley Injury

The annular or cruciate pulley system may be damaged, particularly in deeper lacerations.

Pulley loss can impair tendon gliding and produce bowstringing.

Joint Injury

A laceration may penetrate the flexor tendon sheath or enter the interphalangeal or metacarpophalangeal joint, producing a traumatic arthrotomy.

Fracture

Associated phalangeal or metacarpal fractures may occur, particularly with high-energy mechanisms.

Diagnosis

Signs and Symptoms

The typical injury is a laceration over the palmar aspect of the finger, hand, or wrist.

Loss of tendon continuity alters the resting posture of the finger.

Change in Finger Posture

The injured finger may rest in greater extension than the adjacent digits because normal flexor tendon tension has been lost.

Comparison with the opposite hand and neighboring fingers is useful.

Loss of Active Flexion

The patient may be unable to actively flex the joint controlled by the injured tendon.

The exact deficit depends on whether the FDS, FDP, or both have been divided.

Loss of Tenodesis

Normally, passive wrist extension causes the fingers to flex because of the tenodesis effect.

Loss of this automatic finger flexion may indicate flexor tendon disruption.

Wrist Squeeze Test

In children or uncooperative patients, squeezing the forearm or flexor muscle mass can produce passive finger flexion when the tendons are intact.

Failure of the expected motion raises concern for tendon injury.

Physical Examination

A careful examination should be completed before local anesthesia whenever possible so that motor, sensory, and vascular function can be accurately documented.

Flexor Digitorum Profundus Testing

To test the FDP, the examiner stabilizes the PIP joint and other proximal joints in extension while asking the patient to actively flex the DIP joint.

Ability to flex the DIP indicates an intact FDP tendon.

Failure suggests FDP disruption or dysfunction.

Flexor Digitorum Superficialis Testing

To isolate the FDS, the examiner holds the other fingers in full extension and asks the patient to flex the finger being tested.

With the other digits immobilized, the tested finger should primarily flex at the PIP joint.

Failure to flex the PIP suggests FDS injury, although anatomic variations must be considered.

Strength Testing

Each finger should be assessed individually for flexion strength.

Weakness may indicate a partial tendon injury even when active motion remains present.

Tenodesis Examination

The wrist is passively moved through flexion and extension while the examiner observes the normal cascade of the fingers.

Abnormal movement suggests disruption of the flexor mechanism.

Vascular Examination

Perfusion must be assessed carefully.

Evaluation may include capillary refill, skin color, temperature, pulse oximetry, and Doppler assessment.

A poorly perfused or dysvascular digit is a surgical emergency.

Sensory Examination

Adjacent digital nerves should be tested before anesthetic injection.

Light touch and two-point discrimination are particularly useful for identifying digital nerve injury.

Wound Exploration

The wound should be carefully evaluated for evidence of partial or complete tendon injury, pulley disruption, foreign material, fracture, and joint penetration.

Exploration should be performed in a controlled fashion to avoid additional damage.

Imaging

Plain Radiographs

Radiographs should be obtained when there is concern for fracture, dislocation, bony avulsion, or retained radiopaque foreign body.

Ultrasound

Ultrasound can identify tendon discontinuity and may be useful when the physical examination is uncertain.

MRI

MRI can also demonstrate flexor tendon injury but is rarely necessary when the history and examination clearly establish the diagnosis.

Differential Diagnosis

Phalangeal Fracture-Dislocation

A fracture or dislocation involving the phalanx or interphalangeal joint can produce pain and loss of active flexion that resembles tendon injury.

Tendon Avulsion

A tendon may be avulsed from its insertion without an open laceration.

An important example is FDP avulsion from the distal phalanx.

Tendon Rupture

Closed tendon rupture can also result in loss of flexion.

Pulley Rupture

Pulley disruption may cause pain and abnormal tendon mechanics while preserving some active flexion.

Initial Treatment

Vascular Assessment

The first priority is to determine whether the finger and hand are adequately perfused.

A dysvascular digit or hand requires emergent operative evaluation.

Severe Associated Injury

Open fractures, major tissue loss, vascular injury, or gross contamination also require urgent surgical management.

Tetanus Prophylaxis

Tetanus immunization status should be reviewed and prophylaxis administered when indicated.

Wound Irrigation

The wound should be thoroughly irrigated with normal saline and gross contamination removed.

Antibiotics

Antibiotic administration depends on contamination, mechanism of injury, open fracture, bite exposure, and other risk factors.

A perioperative intravenous dose may be given for selected injuries according to local protocols.

Elevation and Splinting

The hand should be elevated and placed in a protective splint until definitive surgical assessment is completed.

Specialist Consultation

Early consultation with a hand surgeon or orthopaedic surgeon experienced in tendon repair is appropriate.

Factors Affecting Management

Treatment planning should consider hand dominance, occupation, time since injury, injury zone, tendon involvement, associated neurovascular injury, contamination, and patient comorbidities.

Physical Therapy and Hand Therapy

Postoperative hand therapy is an essential part of treatment.

The goal is to protect the repair while restoring tendon glide and preventing stiffness and adhesions.

Timing

Passive motion is commonly initiated within approximately 3–5 days after surgery, depending on the strength of the repair and the rehabilitation protocol.

Early Active Motion

Early active-motion protocols are increasingly used when a sufficiently strong repair has been achieved and the patient can follow restrictions reliably.

Immobilization

Children, cognitively impaired patients, or adults who cannot comply with movement restrictions may require more prolonged immobilization to protect the repair.

Surgery

Timing of Repair

Primary repair generally provides the best functional outcome.

Repair is preferably performed during the acute period, often within approximately 7–10 days of injury.

Delayed primary repair may still be possible, but direct repair becomes more difficult as tendon retraction, scarring, and muscle shortening develop.

Chronic Injuries

Injuries older than approximately 3–4 weeks often cannot be treated with straightforward primary repair and may require tendon grafting, staged reconstruction, or other reconstructive techniques.

Anesthesia

Repair may be performed under general anesthesia, regional anesthesia, or wide-awake local anesthesia without tourniquet (WALANT), depending on injury pattern and surgeon preference.

Flexor Tendon Sheath Injury

When the flexor tendon sheath is also disrupted, timely repair is desirable because excessive scarring can impair tendon gliding and worsen the functional result.

Surgical Exploration

The wound is extended as necessary to identify the full extent of injury.

The surgeon evaluates the tendon, pulley system, nerves, vessels, joints, and bone.

Minimizing Tissue Trauma

Meticulous technique is important because additional surgical trauma promotes scar formation and adhesions.

Sequence of Repair

After all injuries have been identified, flexor tendon repair is generally completed before nerve and vascular repair.

Tendon Repair Technique

A variety of core suture patterns can be used.

The repair must provide enough strength for early motion while remaining sufficiently smooth and compact to glide through the tendon sheath and pulley system.

Core Sutures

Repair strength generally increases with the number of core suture strands crossing the repair site.

Modern repairs commonly use at least four core strands, with some techniques using six or more.

Epitendinous Suture

An additional circumferential epitendinous suture is commonly placed to improve repair strength and smooth the tendon surface.

Zone II Repair

Zone II injuries require particular attention because both the FDS and FDP pass through the pulley system.

FDP

The FDP is repaired to restore DIP flexion and overall digital function.

FDS

Depending on tendon damage, available space within the sheath, and intraoperative tendon gliding, the surgeon may repair both FDS slips, one slip, or neither, balancing strength against the risk of excessive bulk and adhesions.

Postoperative Splinting

A dorsal blocking splint is typically applied after repair.

The wrist is generally maintained in neutral to slight flexion, the MCP joints are flexed to approximately 70°, and the interphalangeal joints are kept near extension.

Hand Therapy

The splint is removed or adjusted under controlled conditions during supervised hand therapy, which commonly begins within 3–5 days.

The exact rehabilitation protocol depends on the injury zone and strength of repair.

Follow-Up

Prognosis

Outcome depends strongly on the location, mechanism, severity, and associated injuries.

Clean sharp lacerations generally have a better prognosis than crush, avulsion, contaminated, or high-energy injuries.

Zone II Prognosis

Zone II injuries remain particularly prone to postoperative stiffness and adhesion formation because of the complex tendon-pulley anatomy.

Complications

Loss of Motion

Reduced range of motion may result from scar formation, tendon adhesions, joint stiffness, or inadequate rehabilitation.

Adhesions

Adhesions can tether the repaired tendon to surrounding tissue and limit active flexion despite preserved passive motion.

Loss of Strength

Persistent weakness may occur even after successful healing.

Infection

Infection may complicate contaminated wounds, open fractures, joint injuries, or tendon sheath injuries.

Tendon Rerupture

The repair may rupture if excessive force is applied before adequate healing occurs.

Rerupture may require repeat repair or reconstruction.

Delayed Reconstruction

Severe scarring, chronic tendon loss, failed primary repair, or rerupture may necessitate tendon grafting, staged tendon reconstruction, or tendon transfer.

Patient Monitoring

Follow-up should closely assess wound healing, vascular status, tendon integrity, active and passive range of motion, scar formation, adhesion development, strength, and compliance with splinting and therapy.

Early recognition of excessive stiffness or repair failure allows rehabilitation or surgical planning to be modified before permanent functional loss develops.