Orthopaedic Surgery - Turf Toe

Basics

Turf toe is a:

Hyperextension sprain of the first metatarsophalangeal joint.

It involves injury to the:

Plantar capsuloligamentous complex

of the great toe MTP joint.

Historical Background

The term:

Turf toe

was introduced in 1976 after the injury was recognized frequently in collegiate football players competing on:

Artificial turf

while wearing relatively:

Flexible footwear.

Anatomy

The first MTP joint is stabilized by several plantar structures, including the:

Plantar plate

Joint capsule

Sesamoid complex

Flexor hallucis brevis

and surrounding:

Collateral ligaments.

Functional Importance

The first MTP joint is essential for:

Push-off

during walking, running, jumping, and:

Cutting maneuvers.

Injury can therefore significantly impair:

Athletic performance.

Classification

Turf toe is commonly divided into:

Grade I

Grade II

and

Grade III injuries

according to the severity of capsuloligamentous disruption and clinical instability.

Grade I

Grade I represents a:

Mild sprain or stretching injury

of the plantar capsuloligamentous complex.

Typical findings include:

Localized plantar or medial tenderness

Minimal swelling

and

No significant ecchymosis.

Joint stability is generally:

Preserved.

Grade II

Grade II represents a:

Partial tear

of the plantar capsuloligamentous complex.

Typical findings include:

More diffuse tenderness

Mild to moderate swelling

and

Mild to moderate ecchymosis.

There is usually greater pain with:

Great-toe motion

and temporary loss of:

Athletic participation.

Grade III

Grade III represents a:

Complete or severe capsuloligamentous disruption.

Typical findings include:

Severe diffuse tenderness

Marked swelling

Moderate to severe ecchymosis

and

Painful or restricted motion.

There may be:

Gross MTP instability

and significant loss of:

Push-off strength.

Epidemiology

Turf toe is particularly associated with:

Football

and other sports requiring repeated:

Acceleration

Cutting

and

Forefoot loading.

Incidence

Historical studies have reported a high prevalence among:

Professional football players.

One older series reported that approximately:

45% of professional football players

had experienced turf toe at some point.

Playing Surface

Historical series have reported that a large proportion of cases occurred on:

Artificial turf.

One report found approximately:

83%

of cases associated with synthetic playing surfaces.

Collegiate Football

An incidence of approximately:

0.062 injuries per 1,000 athlete exposures

has been reported in NCAA football players in one study.

Rates vary according to:

Sport

Surface

Position

and

Study methodology.

Risk Factors

Important risk factors include:

Artificial turf

Flexible footwear

Repeated cutting maneuvers

Previous turf toe injury

and high-intensity:

Game participation.

Competition Versus Practice

The injury is more commonly reported during:

Live competition

than during:

Practice

or preseason and postseason activities.

Athlete Characteristics

Risk may increase with:

Older age

and

More years of participation in the sport.

Football Positions

In football, positions requiring frequent acceleration and cutting may be particularly affected, including:

Running backs

Quarterbacks

and

Receivers.

Pathophysiology

The classic mechanism is forced:

Hyperextension of the first MTP joint.

Plantar Injury

As the great toe is forcibly dorsiflexed, the:

Plantar capsule

and

Plantar plate

are placed under excessive tension.

Tear Pattern

MRI studies commonly demonstrate tearing of the plantar structures:

Distal to the sesamoids.

Severity

The injury may range from:

Microscopic stretching

to

Partial tearing

or

Complete disruption.

Etiology

Turf toe was historically uncommon before widespread use of:

Artificial playing surfaces

and very:

Flexible athletic shoes.

Mechanism in Sports

A common mechanism occurs when an athlete’s:

Forefoot is fixed against the playing surface

while the heel is forced upward, producing:

Excessive dorsiflexion of the great toe.

Associated Conditions

Turf toe may occur with:

Sesamoid fracture

Diastasis of a bipartite sesamoid

Articular injury of the metatarsal head

or

Acute traumatic hallux valgus.

Sesamoid Injury

Because the sesamoids are incorporated into the plantar complex, severe hyperextension may produce:

Fracture

or

Separation of a bipartite sesamoid.

Chondral Injury

The metatarsal head may sustain:

Articular cartilage injury

or

Impaction damage.

Diagnosis

Diagnosis is based on:

Mechanism

Physical examination

and

Imaging.

Signs and Symptoms

Patients typically report:

Pain beneath the first MTP joint

after a hyperextension injury.

Swelling

There may be:

Localized or diffuse swelling

around the:

First MTP joint.

Ecchymosis

Bruising on the plantar or medial side of the joint suggests a more significant:

Capsuloligamentous injury.

Push-Off Weakness

Patients may complain of difficulty with:

Push-off

during:

Walking

Running

or

Jumping.

Physical Examination

Inspect the first MTP joint for:

Swelling

Ecchymosis

Deformity

and evidence of:

Instability.

Range of Motion

Assess:

Dorsiflexion

and

Plantarflexion

of the first MTP joint.

Compare the injured side with the:

Contralateral foot.

Hyperextension Pain

Pain with passive:

MTP dorsiflexion

is a common finding.

Plantar Tenderness

Palpate the:

Plantar plate

Sesamoids

and surrounding:

Capsule.

Great-Toe Lachman Test

A:

Great-toe Lachman test

or sagittal-plane drawer test can assess:

MTP instability.

Technique

The proximal phalanx is translated relative to the:

First metatarsal head.

Increased translation or loss of a firm endpoint suggests:

Plantar plate insufficiency.

Imaging

Weight-Bearing Radiographs

Initial imaging should include:

Weight-bearing foot radiographs

when tolerated.

Radiographic Findings

Radiographs may demonstrate:

Capsular avulsion fracture

Sesamoid fracture

Metatarsal head impaction

Proximal sesamoid migration

or

Diastasis of a bipartite sesamoid.

Sesamoid Position

Proximal migration of the sesamoid complex may indicate substantial disruption of the:

Plantar plate.

Dorsiflexion Stress View

A:

Dorsiflexion lateral stress radiograph

may help evaluate plantar complex integrity.

Sesamoid-to-Phalanx Relationship

The distance between the:

Distal sesamoid

and

Base of the proximal phalanx

should remain relatively constant as the MTP joint moves from:

Plantarflexion to dorsiflexion.

Abnormal change may suggest:

Plantar plate disruption.

MRI

MRI is particularly useful in:

Grade II

and

Grade III injuries

or when plain radiographs show:

Abnormal findings.

MRI Assessment

MRI can evaluate:

Plantar plate injury

Capsular disruption

Sesamoid injury

and

Chondral damage.

Differential Diagnosis

Important alternatives include:

Sesamoiditis

Bipartite sesamoid diastasis

Sesamoid fracture

Sesamoid stress fracture

Sesamoid osteonecrosis

Traumatic hallux valgus

First MTP osteochondral injury

Hallux fracture

and

MTP dislocation.

Treatment

Treatment depends on:

Injury grade

Instability

Associated injuries

and the patient’s:

Athletic demands.

Initial Measures

Acute treatment includes:

Rest

Ice

Compression

and

Elevation.

Grade I Treatment

Grade I injuries can usually be managed with:

Symptomatic treatment

and protection against:

Excessive dorsiflexion.

Footwear

A:

Stiff-soled shoe

or

Rigid insert

can reduce painful first-MTP motion.

Taping

The hallux may be taped to limit:

Hyperdorsiflexion.

Athletic Participation

Some athletes with mild Grade I injuries may continue participation as symptoms permit with:

Protective taping and stiff footwear.

Grade II Treatment

Grade II injuries usually require a period of:

Reduced activity

and often:

Walking-boot immobilization.

Crutches

Crutches may be used when:

Weight bearing is painful.

Immobilization

A:

Walking boot

helps protect the plantar complex while reducing stress across the:

First MTP joint.

Return to Play

Historical return-to-play estimates for Grade II injury are approximately:

3–14 days

although more significant injuries may require:

Longer recovery.

Grade III Treatment

Grade III injuries generally require more prolonged:

Immobilization

and careful evaluation for:

Surgical indications.

Nonoperative Grade III Treatment

Selected stable injuries may be treated with:

Boot or cast immobilization

followed by carefully controlled:

Range of motion.

Surgical Grade III Injury

Surgery may be considered when there is:

Gross instability

Complete plantar plate disruption

Persistent pain

or marked loss of:

Push-off strength.

Early Motion

Once the injury is sufficiently stable, gentle motion is encouraged to reduce the risk of:

MTP stiffness.

Physical Therapy

Therapy may include:

Active range of motion

Passive range of motion

Strengthening

and gradual:

Gait retraining.

Return to Sport

Return should be based on resolution of:

Pain

Swelling

Instability

and restoration of:

Push-off strength.

Surgery

Operative treatment is uncommon but appropriate for selected:

Severe injuries.

Indications

Potential indications include:

Grade III injury with gross instability

Persistent pain after appropriate conservative treatment

Persistent loss of push-off strength

and significant associated:

Sesamoid or chondral injury.

Plantar Plate Repair

Complete disruption of the plantar structures may be treated with:

Direct plantar plate repair.

Sesamoid Fracture

A displaced or symptomatic sesamoid fracture may require:

Internal fixation

or selected:

Sesamoidectomy.

Sesamoid Preservation

When possible, preservation of the sesamoid is desirable because the sesamoid complex contributes to:

Flexor hallucis brevis function

and

Great-toe biomechanics.

Abductor Hallucis Transfer

Selected severe medial plantar complex injuries may require:

Abductor hallucis transfer

as part of reconstruction.

Postoperative Care

Postoperative rehabilitation is:

Gradual

because excessive early dorsiflexion may stress the:

Repair.

Non-Weight-Bearing

After major repair, patients may remain:

Non-weight-bearing

in a boot for approximately:

4 weeks.

Early Motion

Gentle passive range of motion may begin at approximately:

1 week

depending on the:

Repair.

Protective Footwear

A:

Stiff-soled shoe

may be introduced around:

6–8 weeks

when healing is satisfactory.

Return to Sport

Protected return to sport with limitation of excessive MTP dorsiflexion may begin around:

4 months

in selected patients.

Full Recovery

Complete recovery after severe operative injuries may require approximately:

6–12 months.

Follow-Up

Follow-up should monitor:

Pain

MTP motion

Joint stability

Sesamoid position

and

Push-off strength.

Prognosis

Most Grade I and Grade II injuries have a:

Good prognosis

with nonoperative treatment.

Historical Athletic Outcomes

In one historical series of 19 collegiate and professional athletes, 9 required surgery and:

7 returned to full athletic activity.

Nonoperative Series

Another historical series of 56 collegiate athletes, mostly football players on synthetic turf, found that:

53 returned to sport within approximately 3 weeks

after treatment with:

Stiff footwear

Orthotics

and

Taping.

Only one patient required:

Surgery.

Larger Collegiate Series

A study of 147 turf toe injuries in collegiate football players reported an average loss of approximately:

10 days of athletic participation.

Fewer than:

2%

required surgery.

These figures reflect specific athletic populations and should not be assumed for every:

Patient.

Complications

Complications may be:

Early

or

Delayed.

Medial Plantar Nerve Injury

An uncommon short-term complication is injury to the:

Medial plantar nerve.

Persistent Pain

Long-term symptoms may include:

Persistent pain during athletic activity.

Reduced Athletic Performance

Some athletes are unable to return fully to their previous level of:

Performance.

Restricted Motion

Chronic injury may result in:

Reduced first-MTP motion.

Hallux Valgus

Instability of the medial or plantar structures may contribute to:

Hallux valgus deformity.

Hallux Rigidus

Articular injury and chronic degeneration may eventually lead to:

Hallux rigidus.

Cock-Up Deformity

Severe plantar plate insufficiency may permit excessive:

MTP dorsiflexion

and contribute to a:

Cock-up deformity of the hallux.

Patient Monitoring

Management depends on:

Injury grade

and clinical response.

Grade I Monitoring

Grade I injuries are treated symptomatically with:

Taping

Stiff-soled footwear

or a:

Rigid insert.

Grade II Monitoring

Grade II injuries may require:

Walking-boot protection

RICE

and progressive:

Range-of-motion exercises.

Return to play may occur in approximately:

3–14 days

for uncomplicated injuries.

Grade III Monitoring

Grade III injuries generally require:

Walking-boot or cast immobilization

with carefully controlled:

MTP motion.

Dorsiflexion exercises may begin after approximately:

2–3 weeks

when appropriate, while avoiding:

Hyperdorsiflexion.

Grade III Return to Sport

Historical return-to-play estimates are approximately:

2–6 weeks

for selected nonoperative Grade III injuries, although complete severe tears often require considerably:

Longer rehabilitation.

Clinical Summary

Typical mechanism: Forced hyperextension of the first MTP joint, often when the forefoot is fixed and the heel rises.

Key pathology: Injury to the plantar plate and plantar capsuloligamentous complex, sometimes with sesamoid or chondral injury.

Key examination: Plantar tenderness, pain with MTP dorsiflexion, assessment of push-off strength, and the great-toe Lachman test for instability.

Imaging: Obtain weight-bearing radiographs; MRI is particularly useful for Grade II–III injuries or suspected plantar plate disruption.

Grade I: Mild sprain; treat with taping, stiff-soled footwear, and symptomatic care.

Grade II: Partial tear; commonly requires a walking boot, temporary activity restriction, and gradual rehabilitation.

Grade III: Complete or severe tear with instability; prolonged immobilization or surgical repair may be required.

Surgical indications: Gross instability, complete plantar plate disruption, persistent pain, loss of push-off strength, or significant associated sesamoid injury.

Major long-term concerns: Persistent pain, reduced athletic performance, stiffness, hallux valgus, hallux rigidus, and cock-up deformity.

Key Principle

Turf toe is a hyperextension injury of the first MTP joint that damages the plantar capsuloligamentous complex.

The severity ranges from a mild:

Grade I sprain

to a complete:

Grade III plantar plate disruption with instability.

Diagnosis depends on:

Mechanism, examination of MTP stability, weight-bearing radiographs, and MRI when indicated.

Most mild and moderate injuries respond to:

Protection from excessive dorsiflexion, stiff-soled footwear, taping, immobilization, and rehabilitation.

Severe unstable injuries may require:

Plantar plate repair or treatment of associated sesamoid injury.

Successful recovery depends on restoring:

Joint stability, motion, and effective great-toe push-off.

Orthopaedic Surgery - Tumors

⸻

Basics

A neoplasm is an abnormal proliferation of cells characterized by:

Unregulated growth.

Neoplasms are broadly classified as:

Benign

or

Malignant.

⸻

Benign Neoplasms

A benign neoplasm generally demonstrates:

Localized growth

without the ability to:

Metastasize to distant organs.

Although benign tumors do not metastasize, some may still become locally aggressive and can:

Compress

Replace

or

Damage adjacent tissues.

⸻

Malignant Neoplasms

Malignant tumors have the capacity for:

Local invasion

and

Metastatic spread.

Tumor cells may enter:

Blood vessels

or

Lymphatic channels

and disseminate to distant:

Organs and tissues.

⸻

Important Pathologic Distinction

The distinction between benign and malignant neoplasms is based on features such as:

Local invasiveness

Cellular atypia

Growth behavior

and

Metastatic potential.

The concept of crossing a basement membrane is particularly relevant to:

Epithelial malignancies

but is not a universal defining feature of all musculoskeletal tumors.

⸻

Epidemiology

Both benign and malignant neoplasms arise through accumulation of:

Genetic and epigenetic abnormalities.

Tumor development usually requires multiple alterations affecting cellular:

Growth

Survival

and

Genome regulation.

⸻

Genetic Instability

Neoplastic cells frequently demonstrate increasing:

Genetic instability

as the tumor evolves.

Historically, approximately:

4–6 important genetic alterations

have been described as sufficient to contribute to malignant transformation in some tumor models.

⸻

Hallmarks of Malignancy

Classic biologic characteristics of cancer include:

Sustained proliferative signaling

Resistance to growth-suppressive signals

Avoidance of programmed cell death

Replicative immortality

Angiogenesis

and

Tissue invasion with metastatic potential.

⸻

Incidence

Primary malignant tumors of bone are:

Rare.

Historical estimates in the United States have been approximately:

3,000 new malignant primary bone tumors per year.

⸻

Soft-Tissue Sarcoma

Primary malignant soft-tissue tumors are more common than primary bone malignancies but remain:

Uncommon.

Historical estimates have been approximately:

9,000 new cases annually in the United States.

Incidence estimates vary by:

Year

Tumor definition

and

Data source.

⸻

Risk Factors

For most neoplasms, particularly benign musculoskeletal tumors, the exact cause is:

Unknown.

Some malignant tumors have identifiable:

Genetic

Environmental

or

Infectious risk factors.

⸻

Genetic Risk Factors

Important tumor suppressor abnormalities include:

TP53

and

RB1.

⸻

TP53

Germline TP53 mutation is associated with:

Li-Fraumeni syndrome

and an increased risk of multiple malignancies, including some:

Sarcomas.

⸻

RB1

Germline mutation of:

RB1

causes hereditary:

Retinoblastoma

and also increases the later risk of certain:

Bone and soft-tissue sarcomas.

⸻

Environmental Risk Factors

Environmental exposures associated with malignancy include:

Tobacco use

Excessive alcohol consumption

Obesity

and

Ultraviolet radiation.

⸻

Tobacco

Tobacco exposure is strongly associated with malignancies such as:

Lung cancer.

⸻

Alcohol

Heavy alcohol consumption increases the risk of several cancers, including:

Esophageal malignancy.

⸻

Obesity

Obesity is associated with increased risk of several malignancies, including:

Colorectal cancer.

⸻

Ultraviolet Exposure

Excessive ultraviolet light exposure increases the risk of:

Skin malignancy.

⸻

Infectious Risk Factors

Some malignancies are associated with specific:

Infectious agents.

⸻

Human Papillomavirus

High-risk HPV strains are strongly associated with:

Cervical cancer

and several other:

Anogenital and oropharyngeal malignancies.

⸻

Epstein-Barr Virus

EBV is associated with several malignancies, including certain:

B-cell lymphomas.

⸻

Hepatitis Viruses

Chronic:

Hepatitis B

and

Hepatitis C

infection increase the risk of:

Hepatocellular carcinoma.

⸻

Helicobacter pylori

Chronic infection with:

Helicobacter pylori

is associated with:

Gastric adenocarcinoma

and

Gastric MALT lymphoma.

⸻

Pathophysiology

Both benign and malignant tumors demonstrate:

Abnormal cellular proliferation.

Their biologic behavior differs primarily in:

Local invasiveness

Growth rate

Histologic aggressiveness

and

Ability to metastasize.

⸻

Benign Tumor Behavior

Benign tumors generally remain:

Localized.

However, some may become locally destructive because of:

Expansion

or

Pressure on surrounding structures.

⸻

Malignant Tumor Behavior

Malignant tumors can invade surrounding tissues and may disseminate through:

Bloodstream

Lymphatics

or other anatomic pathways.

⸻

Hematogenous Metastasis

Many primary bone sarcomas spread predominantly through the:

Bloodstream.

A common metastatic destination is the:

Lung.

⸻

Associated Conditions

Certain inherited disorders predispose patients to specific tumor types.

⸻

Gardner Syndrome

Gardner syndrome is associated with:

Familial adenomatous polyposis

and may include:

Osteomas

Desmoid tumors

and other:

Soft-tissue lesions.

⸻

Neurofibromatosis

Neurofibromatosis may be associated with:

Neurofibromas

and an increased risk of:

Malignant peripheral nerve sheath tumors.

⸻

Diagnosis

Evaluation begins with:

History

Physical examination

and appropriate:

Imaging.

Definitive diagnosis often requires:

Tissue biopsy.

⸻

Signs and Symptoms

Possible systemic or local symptoms include:

Fever

Night sweats

Unintentional weight loss

Bone pain

Soft-tissue mass

Abdominal pain

Visual symptoms

Abnormal bleeding

and

Persistent cough.

⸻

Bone Pain

Persistent unexplained bone pain, particularly when:

Progressive

Nocturnal

or unrelated to activity, warrants further:

Evaluation.

⸻

Soft-Tissue Mass

A newly enlarging or persistent soft-tissue mass should be assessed carefully, particularly when it is:

Deep

Firm

Painful

or

Progressively enlarging.

⸻

Physical Examination

Examination should be directed by the patient’s:

Symptoms

and

Tumor risk profile.

⸻

General Examination

The examination may include assessment of:

Skin

Lymph nodes

and other organ systems where clinically appropriate.

⸻

Musculoskeletal Examination

For suspected orthopaedic tumors, assess:

Mass size

Location

Depth

Mobility

Tenderness

Neurovascular status

and relationship to surrounding:

Bone and soft tissue.

⸻

Laboratory Tests

There is no single blood test that reliably diagnoses most:

Bone or soft-tissue tumors.

⸻

Selected Laboratory Studies

Depending on the suspected diagnosis, testing may include:

CBC

ESR

CRP

Serum calcium

Alkaline phosphatase

SPEP/UPEP

or other disease-specific:

Studies.

⸻

Imaging

Imaging plays a central role in:

Detection

Characterization

Local staging

and

Metastatic assessment.

⸻

Plain Radiographs

Plain radiographs should be obtained for areas of:

Persistent focal bone pain

or suspected:

Bone lesions.

⸻

Radiographic Assessment

Important features include:

Lesion location

Margins

Pattern of bone destruction

Matrix mineralization

Periosteal reaction

and presence of:

Soft-tissue extension.

⸻

Chest Imaging

Chest radiography or, more commonly for sarcoma staging:

CT of the chest

may be used to assess for pulmonary:

Metastases.

⸻

CT

CT is useful for:

Cortical detail

Mineralized matrix

and staging of:

Chest, abdomen, and pelvis

when clinically indicated.

⸻

MRI

MRI with and without contrast is the preferred local imaging study for many:

Soft-tissue masses

and complex:

Bone tumors.

⸻

Role of MRI

MRI helps define:

Tumor extent

Relationship to neurovascular structures

Marrow involvement

and

Soft-tissue extension.

⸻

Staging

Staging systems vary according to:

Tumor type.

⸻

Staging Methods

Staging may incorporate:

Clinical findings

Imaging

and

Histopathology.

⸻

Primary Tumor Assessment

Local tumor extent is commonly evaluated using:

MRI

or

CT.

⸻

Metastatic Evaluation

Metastatic staging may include:

CT chest

Bone scintigraphy

PET/CT

or other imaging tailored to the:

Specific malignancy.

⸻

Biopsy

When malignancy is suspected, biopsy should generally be performed:

After complete imaging

and ideally planned by the team that will perform definitive:

Tumor resection.

⸻

Biopsy Principles

The biopsy tract should be positioned so that it can be:

Removed during definitive surgery.

Poorly planned biopsy can contaminate:

Uninvolved tissue planes

and complicate future:

Limb-sparing surgery.

⸻

Differential Diagnosis

A bone or soft-tissue lesion may represent:

Benign neoplasm

Primary malignancy

Metastatic disease

Hematologic malignancy

Infection

or a:

Tumor-like condition.

⸻

Benign Bone Lesions

Common benign or incidental bone lesions include:

Bone islands

Enchondromas

and

Bone infarcts.

⸻

Treatment

The primary goals of cancer treatment are:

Local tumor control

and prevention or treatment of:

Metastatic disease.

⸻

Multidisciplinary Care

Treatment often requires collaboration among:

Orthopaedic oncology

Medical oncology

Radiation oncology

Pathology

and

Radiology.

⸻

Chemotherapy

Chemotherapy is important for selected malignancies such as:

Osteosarcoma

Ewing sarcoma

and many:

Hematologic cancers.

⸻

Immunotherapy

Immunotherapy may be effective for selected tumors with appropriate:

Biologic or molecular targets.

⸻

Radiation Therapy

Radiation may be used for:

Definitive local control

Adjuvant treatment

or

Palliation

depending on tumor type.

⸻

Surgical Resection

Surgery remains central to treatment of many:

Primary bone and soft-tissue sarcomas.

The goal is usually complete removal with an appropriate:

Oncologic margin.

⸻

Limb Salvage

When possible, malignant musculoskeletal tumors may be treated with:

Limb-sparing resection

followed by reconstruction.

⸻

Amputation

Amputation remains appropriate in selected cases involving:

Extensive neurovascular invasion

Uncontrollable infection

or when limb salvage would not provide acceptable:

Function or oncologic control.

⸻

Follow-Up

Patients require ongoing:

Clinical surveillance

and

Restaging imaging.

⸻

Purpose of Surveillance

Follow-up aims to detect:

Local recurrence

and

Metastatic disease

at an early stage.

⸻

Duration of Follow-Up

The frequency and duration of surveillance depend on:

Tumor type

Grade

Stage

and time since:

Treatment.

⸻

Prognosis

Prognosis varies widely according to:

Histologic diagnosis

Tumor grade

Tumor size

Location

Resectability

and presence or absence of:

Metastatic disease.

⸻

Patient Monitoring

Surveillance may include:

Physical examination

Local imaging

and imaging of common metastatic sites such as the:

Lungs.

⸻

Patient Teaching

Patients should be educated to recognize possible signs of:

Local recurrence.

⸻

Warning Symptoms

They should seek medical evaluation for:

New pain

New swelling

or development of a:

New mass

near the site of a previous tumor.

⸻

Frequently Asked Questions

Are all bone lesions cancerous?

No. Most incidentally discovered bone lesions are:

Benign.

Examples include:

Bone islands

Enchondromas

and

Bone infarcts.

Their appearance and behavior are assessed primarily with:

Imaging characteristics.

⸻

Can an orthopaedic oncologist determine whether a bone lesion is aggressive?

Often, yes. Features such as:

Margins

Bone destruction

Periosteal reaction

Cortical involvement

and

Soft-tissue extension

help determine whether a lesion appears:

Nonaggressive or aggressive.

Musculoskeletal radiologists can provide important additional:

Imaging interpretation.

⸻

Is a bone scan always needed to determine whether a lesion is active?

No. Bone scintigraphy may be useful in selected situations, but activity is often assessed with:

Plain radiographs

MRI

CT

or other imaging depending on the:

Lesion.

⸻

Can staging studies determine whether a malignant tumor has metastasized?

Staging studies are useful for identifying:

Macroscopic metastatic disease.

However, they cannot reliably detect:

Microscopic metastases.

Therefore, apparently localized disease on imaging does not prove that no microscopic tumor cells are:

Present elsewhere.

⸻

Clinical Summary

Definition: A neoplasm is an abnormal proliferation of cells classified as benign or malignant according to its biologic behavior.

Benign tumors: Usually remain localized and do not metastasize, although some may be locally aggressive.

Malignant tumors: Invade surrounding tissues and may metastasize, often hematogenously in primary bone sarcomas.

Key warning features: Progressive bone pain, enlarging soft-tissue mass, constitutional symptoms, or an aggressive lesion on imaging.

Initial imaging: Plain radiographs for bone lesions and MRI with contrast for suspicious soft-tissue masses or local tumor staging.

Staging: Often includes local MRI or CT plus metastatic evaluation such as CT chest, PET/CT, or bone scintigraphy, depending on tumor type.

Biopsy principle: Biopsy should be planned after imaging and ideally by the team performing definitive tumor surgery.

Treatment: May include surgical resection, chemotherapy, radiation therapy, and immunotherapy, depending on the specific malignancy.

Follow-up: Requires surveillance for both local recurrence and metastatic disease.

⸻

Key Principle

Musculoskeletal tumors range from common benign incidental lesions to rare but potentially lethal:

Primary bone and soft-tissue malignancies.

The most important early steps are:

Recognizing aggressive clinical or imaging features

Obtaining appropriate local imaging

and

Planning biopsy correctly before definitive treatment.

Most bone lesions are:

Benign, but suspected malignant tumors should be evaluated using a coordinated:

Multidisciplinary oncologic approach.

For malignant disease, treatment aims to achieve:

Local control

while preventing or treating:

Metastatic spread.

Orthopaedic Surgery - Trigger Finger

Basics

Trigger finger is a form of:

Stenosing flexor tenosynovitis

that causes painful:

Catching

Clicking

or

Locking

of a digit during flexion and extension.

The condition develops when normal gliding between the:

Flexor tendon

and its surrounding:

Tendon sheath

becomes impaired.

Pathophysiology

The most common site of mechanical obstruction is the:

A1 pulley.

A thickened flexor tendon or tendon nodule passes with difficulty through this relatively narrowed pulley, producing:

Triggering.

Self-Perpetuating Mechanism

Repeated catching produces additional:

Mechanical irritation

and

Tendon swelling.

This may further worsen the mismatch between the tendon and:

A1 pulley.

Tendinopathy Rather Than Tendinitis

Histologic studies generally demonstrate:

Degenerative tendon and pulley changes

rather than prominent inflammatory-cell infiltration.

Therefore, adult trigger finger is more accurately considered a:

Stenosing tendinopathy

than a true inflammatory:

Tendinitis.

Quinnell Classification

Trigger finger severity may be graded using the:

Quinnell classification.

Grade 0

Pain with movement

without mechanical:

Catching or triggering.

Grade 1

There is:

Uneven movement

or

Clicking during flexion

but no true locking.

Grade 2

The digit:

Triggers

but the patient can actively:

Correct or extend it.

Grade 3

The digit triggers or locks and requires:

Passive correction

using the opposite hand.

Grade 4

The digit is:

Locked

or has developed a fixed:

Flexion contracture.

Pediatric Triggering

Pediatric trigger thumb and trigger fingers are now regarded as predominantly:

Acquired

rather than truly:

Congenital.

Their underlying mechanism differs from typical adult trigger finger.

Epidemiology

Triggering can involve:

Any digit.

Adults

In adults, the most commonly affected digits are:

Thumb

Ring finger

and

Middle finger.

Children

In children, the:

Thumb

is affected most frequently.

The:

Middle finger

is among the more frequently involved non-thumb digits.

Age

Trigger finger is particularly common in:

Middle-aged adults.

Pediatric cases usually present during:

Early childhood.

Sex

Adult trigger finger is more common in:

Women

than in men.

Incidence

The lifetime incidence in adults is approximately:

2.6%.

Diabetes

Among patients with diabetes, the incidence is substantially higher, historically reported around:

4–10%.

Multiple-digit involvement is also more common in:

Diabetes.

Pediatric Incidence

Pediatric trigger thumb occurs in approximately:

1–3 per 1,000 children.

Pediatric trigger fingers are much less common and have been reported to occur roughly:

10 times less frequently

than pediatric trigger thumb.

Pregnancy

Triggering may occur more frequently during:

Pregnancy

because of soft-tissue and fluid-related changes.

Symptoms may improve after:

Pregnancy.

Risk Factors

Important risk factors include:

Increasing age

Diabetes mellitus

and

Rheumatoid arthritis.

Other Associated Disorders

Trigger finger may also be associated with:

Gout

and other systemic conditions affecting:

Connective tissue or tendon sheaths.

Etiology

In adults, a thickened area or nodule may develop in the:

Flexor tendon.

Mechanical Impingement

The thickened tendon catches as it passes beneath the:

A1 pulley

at the level of the:

MCP joint.

Triggering

As the patient flexes and extends the digit, the tendon may suddenly pass through the narrowed pulley, producing:

Snapping

or

Locking.

Pediatric Trigger Thumb

In children approximately:

1–4 years of age

a nodular thickening of the flexor pollicis longus may be present.

This is commonly called a:

Notta node.

Notta Node

A Notta node may be palpable near the:

MCP flexion crease

and can prevent smooth passage of the tendon through the:

A1 pulley.

Pediatric Trigger Finger

Non-thumb trigger digits in children have a more complex and less well-understood:

Etiology.

Possible abnormalities include:

Anomalous lumbrical insertion into the flexor digitorum superficialis

or an abnormal relationship between the:

FDS

and

FDP tendons.

Associated Conditions in Children

Pediatric trigger fingers may be associated with:

Mucopolysaccharidoses

Juvenile idiopathic arthritis

Ehlers-Danlos syndrome

and

Down syndrome.

Associated Conditions in Adults

Adults may have associated conditions such as:

Carpal tunnel syndrome

or

de Quervain tenosynovitis.

Diagnosis

Trigger finger is primarily a:

Clinical diagnosis.

Signs and Symptoms

Typical findings include:

Pain

Tenderness

Clicking

and

Locking.

Palmar Nodule

A palpable nodule may be present along the:

Flexor tendon

near the:

Distal palmar crease.

A1 Pulley Tenderness

Tenderness is usually maximal over the:

A1 pulley.

Painful Locking

The digit may become locked in:

Flexion

and then release suddenly during:

Extension.

Snapping

Patients may describe a painful:

Snap

or

Pop

during movement.

Radiation of Pain

Pain may occasionally radiate proximally into the:

Palm

or

Forearm.

Physical Examination

Palpate the flexor tendon sheath at the level of the:

A1 pulley

while asking the patient to repeatedly:

Flex and extend the digit.

Palpable Triggering

The examiner may feel:

Tendon thickening

A nodule

or the actual:

Triggering event.

Examine All Digits

All digits should be examined because:

Multiple trigger digits

may occur, particularly in patients with systemic:

Disease.

Bilateral Pediatric Disease

Approximately:

25% of pediatric trigger-thumb cases

may have bilateral involvement.

Fixed Contracture

Chronic disease may produce a fixed:

PIP or IP flexion contracture.

Laboratory Tests

No serum laboratory study is specific for:

Trigger finger.

Systemic Disease Evaluation

Laboratory investigation is not routinely required but may be appropriate when an underlying systemic disorder such as:

Rheumatoid arthritis

Gout

or another metabolic disease is suspected.

Imaging

Imaging is usually:

Unnecessary.

Radiographs

Plain radiographs may be helpful when a fixed deformity raises concern for:

Arthritis

Joint contracture

Loose body

or other:

Bony pathology.

Ultrasound

Ultrasound can demonstrate thickening of the:

Flexor tendon

or

A1 pulley

but is not routinely required for diagnosis.

Differential Diagnosis

Important alternatives include:

Flexor tendon rupture

Joint contracture or ankylosis

Congenital clasped thumb

Extensor tendon deficiency

Tumor of the tendon sheath

and

Loose body within the MCP joint.

Treatment

Management depends on:

Age

Severity

Number of involved digits

and whether symptoms are:

Adult or pediatric in origin.

General Measures

Mild symptoms may temporarily improve with:

Rest

and

Activity modification.

Multiple Trigger Digits

Multiple symptomatic trigger digits may suggest:

Systemic disease

and may increase the likelihood that:

Surgical treatment

will eventually be required.

Pediatric Trigger Thumb

Many pediatric trigger thumbs may resolve:

Spontaneously.

Resolution may take as long as:

Several years.

Observation in Children

Observation is appropriate in selected young children without:

Fixed deformity

or progressive:

Contracture.

Timing of Pediatric Surgery

Persistent pediatric trigger thumb may require surgery, particularly when there is:

Fixed IP flexion contracture

or failure to improve with:

Growth.

Historically, release has often been considered before approximately:

4 years of age

when contracture is persistent.

Pediatric Trigger Finger

Non-thumb pediatric trigger fingers may be treated initially with:

Observation

or

Splinting

but are more likely than trigger thumb to involve:

Complex tendon abnormalities.

Adult Trigger Finger

In adults, first-line treatment commonly includes:

Corticosteroid injection.

Splinting

Splinting may be useful for:

Mild cases

particularly when the patient can comply consistently with:

Orthotic use.

Activity After Injection

Routine activity restrictions are usually unnecessary after:

Corticosteroid injection

although temporary avoidance of painful repetitive use may improve:

Comfort.

Physical Therapy

Formal physical therapy is generally:

Not required.

Hand Therapy

Selected patients may benefit from instruction regarding:

Splinting

Tendon gliding

and

Activity modification.

Medication

The principal medication treatment in adults is:

Corticosteroid injection.

Injection Technique

Corticosteroid, often combined with:

Local anesthetic

is injected into or adjacent to the:

Flexor tendon sheath

at the level of the:

A1 pulley.

Avoid Intratendinous Injection

Medication should not be injected directly into the:

Flexor tendon

because this may increase the risk of:

Tendon injury or rupture.

Injection Success

A single corticosteroid injection has historically produced improvement in approximately:

45–92% of patients.

Factors Associated With Injection Failure

Injection is less likely to succeed in patients with:

Diabetes

Multiple trigger digits

and sometimes younger patients with:

Long-standing symptoms.

Injection Complications

Potential complications include:

Skin depigmentation

Subcutaneous fat atrophy

Transient hyperglycemia

and, rarely,

Tendon attrition or rupture.

Surgery

Surgical release is indicated when symptoms persist despite appropriate:

Nonoperative treatment

or when the digit is:

Fixed or severely locked.

A1 Pulley Release

The standard procedure is:

Release of the A1 pulley.

Open Release

Open surgical release remains the most established and reliable:

Procedure.

Surgical Incision

A small:

Longitudinal

Transverse

or

Oblique incision

is made over the affected:

A1 pulley.

Pulley Division

The A1 pulley is carefully divided while protecting the adjacent:

Digital nerves

and

Digital vessels.

Persistent Triggering

If triggering persists after complete A1 pulley release, selected patients may require excision of the:

Ulnar slip of the FDS tendon.

Percutaneous Release

Some surgeons use:

Percutaneous A1 pulley release

in appropriately selected:

Adult patients.

Pediatric Trigger Finger Surgery

Pediatric non-thumb trigger fingers may require more extensive procedures, including:

Partial A2 pulley release

A3 pulley release

or

FDS slip excision.

Pediatric Trigger Thumb Surgery

Trigger-thumb release requires particular care because the:

Radial digital nerve

crosses near the operative:

Field.

Postoperative Care

The hand is usually covered with a:

Light dressing

for several days.

Motion

Early:

Finger motion

is generally encouraged after surgery to prevent:

Stiffness.

Activity

Normal activity is resumed:

Gradually

as wound healing and comfort permit.

Follow-Up

Follow-up after injection is based on:

Persistence or recurrence of symptoms.

After Surgery

After uncomplicated release, prolonged monitoring is usually:

Not necessary.

Prognosis

Overall prognosis is:

Good to excellent.

Corticosteroid Injection

Injection is less successful in patients with:

Diabetes mellitus

and may also be less effective when several digits are involved.

Surgical Success

Open A1 pulley release has a reported success rate exceeding:

97%.

Pediatric Prognosis

Open release provides highly reliable outcomes in:

Pediatric trigger thumb

and

Pediatric trigger finger.

Pediatric Recurrence

Recurrence after surgery is more common in pediatric:

Trigger fingers

than in pediatric:

Trigger thumbs.

Complications

Potential injection complications include:

Digital nerve injury

Vascular injury

Tendon injury

and

Skin changes.

These are generally:

Uncommon.

Surgical Complications

Potential surgical complications include:

Digital nerve laceration

Flexor tendon injury

Infection

Stiffness

Persistent triggering

and

Complex regional pain syndrome.

Recurrence

Incomplete release of the:

A1 pulley

or unrecognized additional pathology may lead to:

Persistent or recurrent triggering.

Patient Monitoring

Following successful surgical release, extensive long-term monitoring is usually:

Unnecessary.

Patients should return if they develop:

Recurrent triggering

Wound problems

Neurologic symptoms

or persistent:

Stiffness.

Clinical Summary

Typical presentation: Painful clicking, catching, or locking of a finger during flexion and extension, with tenderness over the A1 pulley.

Key pathology: Thickening of the flexor tendon and/or A1 pulley causes impaired tendon gliding.

Most commonly affected adult digits: Thumb, ring finger, and middle finger.

Diagnosis: Primarily clinical; imaging and laboratory tests are usually unnecessary.

First-line adult treatment: Corticosteroid injection into or around the flexor tendon sheath, with splinting as an option in mild cases.

Surgery: A1 pulley release is indicated for persistent, recurrent, fixed, or severe triggering and has a very high success rate.

Pediatric trigger thumb: Often observed initially because spontaneous resolution can occur, but persistent fixed contracture may require surgical release.

Important association: Trigger finger is more common and often more resistant to injection in patients with diabetes mellitus.

Key Principle

Trigger finger is a stenosing flexor tenosynovial disorder caused by impaired passage of the flexor tendon through the A1 pulley.

The characteristic findings are:

Tenderness over the A1 pulley, a palpable tendon nodule, and painful clicking, catching, or locking.

Diagnosis is almost always:

Clinical.

In adults, treatment usually begins with:

Corticosteroid injection, while persistent or severe disease is treated with:

A1 pulley release.

Children, particularly those with:

Trigger thumb, have a different natural history and may initially be observed, but persistent fixed contracture warrants:

Surgical evaluation.

Orthopaedic Surgery - Triangular Fibrocartilage Complex Tear

Basics

The:

Triangular fibrocartilage complex

or

TFCC

is a group of ligamentous and fibrocartilaginous structures located on the:

Ulnar side of the wrist.

It is an important stabilizer of the:

Distal radioulnar joint

during:

Pronation

and

Supination.

Load Transmission

The TFCC also contributes to transmission of axial load across the:

Ulnocarpal wrist.

Approximately:

20% of load across the wrist

may normally be transmitted through the:

Ulnar-sided structures.

Anatomy

The TFCC extends broadly between the:

Distal radius

and

Ulna

with attachments extending from the region of the:

Ulnar styloid and fovea

toward the:

Sigmoid notch of the distal radius.

Components

The TFCC includes the:

Triangular fibrocartilage disc proper

Dorsal distal radioulnar ligament

Volar distal radioulnar ligament

Meniscus homolog

Ulnar collateral ligament

Ulnotriquetral ligament

Ulnolunate ligament

and

Extensor carpi ulnaris tendon subsheath.

Deep Component

The deep portion of the radioulnar ligament complex inserting into the:

Ulnar fovea

has historically been termed the:

Ligamentum subcruentum.

This component is especially important for:

Distal radioulnar joint stability.

Meniscal Variant

Some wrists contain a true:

Meniscal-like structure

with a free edge that may be visible during:

Arthroscopy.

Clinical Importance

TFCC injury may produce:

Acute

or

Chronic ulnar-sided wrist pain.

Symptoms are often aggravated by:

Forearm rotation

Grip

and

Axial loading.

Classification

The:

Palmer classification

divides TFCC lesions into:

Traumatic Class 1

and

Degenerative Class 2 injuries.

Palmer Class 1

Class 1 lesions are:

Traumatic.

Type 1A

Type 1A is a:

Central perforation.

Because the central TFCC is relatively:

Avascular

these tears have limited spontaneous healing capacity.

Type 1B

Type 1B is a tear of the:

Ulnar attachment.

These peripheral injuries may involve the:

Foveal or styloid attachment

and can produce:

Distal radioulnar joint instability.

Type 1C

Type 1C represents detachment of the TFCC from its:

Carpal attachment

including injury to the:

Volar ulnocarpal ligaments.

Type 1D

Type 1D is a tear involving the:

Radial attachment

of the TFCC.

Palmer Class 2

Class 2 lesions are:

Degenerative.

They often result from chronic:

Ulnocarpal loading

and may be associated with:

Positive ulnar variance.

Ulnar Positive Variance

When the ulna projects farther distally than expected relative to the radius, increased loading across the:

TFCC

and

Ulnocarpal joint

may contribute to:

Degenerative tearing.

Epidemiology

TFCC tears are increasingly recognized because of improvements in:

Clinical examination

MRI

and

Wrist arthroscopy.

Age

Symptomatic tears are commonly encountered between approximately:

30 and 60 years of age.

Risk Factors

Activities that repeatedly load the wrist during:

Pronation-supination

Radial-ulnar deviation

or

Heavy lifting

increase stress on the:

TFCC.

Sports and Occupational Exposure

Examples include activities involving:

Racquet sports

Gymnastics

Weight lifting

Manual labor

or repetitive:

Forearm rotation.

Etiology

Traumatic tears may result from forceful:

Hyperpronation

or

Wrist dorsiflexion.

Mechanism

A fall onto the hand or twisting injury can produce excessive stress across the:

TFCC

and

Distal radioulnar joint.

Associated Fractures

TFCC injury may occur with fractures of the:

Distal radius

Distal ulna

or both bones.

Distal Radioulnar Joint

A major TFCC tear may function biomechanically like disruption of the:

Distal radioulnar stabilizers

and produce:

DRUJ instability.

Diagnosis

Diagnosis is based on:

History

Focused physical examination

and

Imaging.

Arthroscopy

Wrist arthroscopy remains the:

Gold standard

for directly identifying and characterizing a:

TFCC tear.

However, many patients can initially be evaluated using:

Clinical examination and MRI.

Signs and Symptoms

The most common complaint is:

Ulnar-sided wrist pain.

Provocative Activities

Pain is often worsened by:

Pronation

Supination

Gripping

and

Axial loading of the wrist.

Trauma History

Many patients recall a specific:

Traumatic event.

Others, particularly those with degenerative tears, may describe more gradual:

Symptom onset.

Clicking

Patients may experience:

Clicking

Snapping

or

Catching

particularly during:

Forearm rotation.

Physical Examination

The examination should carefully localize the source of:

Ulnar-sided wrist pain.

Range of Motion

Assess wrist and forearm:

Flexion

Extension

Radial deviation

Ulnar deviation

Pronation

and

Supination.

Crepitus and Snapping

Examine for:

Crepitus

Clicking

Painful snapping

and

Instability.

TFCC Compression Test

The TFCC compression test is a provocative maneuver.

The examiner applies:

Axial load

while rotating the:

Ulnar-deviated wrist.

Positive Compression Test

Reproduction of:

Ulnar-sided pain

or a painful:

Click

supports TFCC or ulnocarpal pathology.

Foveal Tenderness

Tenderness in the soft spot between the:

Ulnar styloid

and

Flexor carpi ulnaris tendon

near the ulnar fovea may support a:

Peripheral TFCC injury.

DRUJ Examination

Assess the distal radioulnar joint for:

Translation

Pain

and

Instability

in:

Neutral

Pronation

and

Supination.

ECU Examination

The:

Extensor carpi ulnaris tendon

should be palpated during wrist flexion-extension and:

Pronation-supination.

This helps identify:

ECU tendinitis

or

ECU tendon subluxation

as alternative causes of:

Ulnar-sided pain.

Imaging

Plain Radiographs

Standard:

AP

and

Lateral wrist radiographs

are obtained initially.

Purpose of Radiographs

Radiographs help identify:

Fracture

Arthritis

Malalignment

and abnormalities of:

Ulnar variance.

DRUJ Instability

Radiographs obtained in different forearm positions may occasionally help assess:

Distal radioulnar joint alignment.

Ulnar Variance

Ulnar variance should be measured on appropriately positioned:

Neutral-rotation radiographs.

A standardized:

90-90 view

may also be used, with the shoulder abducted approximately 90° and the elbow flexed:

90°.

CT

CT of both wrists may help assess:

DRUJ congruity

and

Rotational instability

particularly when comparison with the contralateral side is useful.

MRI

MRI is commonly used for detailed evaluation of:

TFCC morphology

and associated:

Wrist pathology.

3-Tesla MRI

High-resolution:

3-Tesla MRI

may improve visualization of:

TFCC tears.

MR Arthrography

MR arthrography may be useful when conventional MRI is:

Equivocal.

Arthrography

A full-thickness TFCC tear may permit contrast to pass between the:

Radiocarpal joint

and

Distal radioulnar joint.

Normally, these spaces do not freely:

Communicate.

Differential Diagnosis

The differential diagnosis for ulnar-sided wrist pain includes:

Distal radius fracture

Distal ulna fracture

Carpal fracture

ECU tendinitis

ECU subluxation

FCU tendinitis

Lunotriquetral ligament injury

Ulnocarpal arthritis

Pisotriquetral arthritis

DRUJ arthritis

Ulnar impaction syndrome

and

Ulnar artery thrombosis.

Treatment

Treatment depends on:

Traumatic versus degenerative origin

Fracture association

DRUJ stability

Tear location

and

Ulnar variance.

Associated Fracture

If a TFCC injury occurs with a distal forearm fracture, the fracture should first be:

Reduced and stabilized.

DRUJ Assessment

After reduction of a distal radius or ulna fracture, the:

Distal radioulnar joint

should be checked for:

Congruity and stability.

Acute Repair With Fracture Surgery

When operative fracture fixation is required and significant TFCC instability remains, acute:

TFCC repair

may be performed.

Injury Without Fracture

Initial treatment for an isolated stable TFCC injury is usually:

Nonoperative.

Immobilization

A:

Below-elbow cast or brace

may be used with the forearm near:

Neutral rotation.

Duration

Immobilization may continue for approximately:

4–6 weeks

depending on symptoms and:

Stability.

Long-Arm Immobilization

When control of:

Pronation and supination

is particularly important, some clinicians use:

Long-arm immobilization

or a brace that limits:

Forearm rotation.

Analgesia

Short-term:

Analgesic medication

may be used during the acute phase.

Range of Motion

After immobilization, gentle:

Wrist

and

Forearm range of motion

is gradually reintroduced.

Corticosteroid Injection

In chronic stable TFCC pain, a:

Corticosteroid injection

may provide temporary:

Symptom relief.

Persistent Symptoms

Continued:

Pain

or

Instability

despite adequate conservative treatment should prompt further:

Assessment

and consideration of:

Surgery.

Physical Therapy

Hand therapy is useful when injury or immobilization has caused:

Wrist stiffness

or reduced:

Forearm rotation.

Rehabilitation Goals

Therapy focuses on restoring:

Wrist ROM

Pronation-supination

Grip strength

and controlled return to:

Activity.

Medication

Oral analgesics are generally required only during the:

Acute symptomatic period.

Surgery

Surgical treatment depends heavily on:

Tear location

and whether the DRUJ is:

Stable or unstable.

Peripheral TFCC Tear

A repairable peripheral tear may be treated with:

Arthroscopic

or

Open repair.

Healing Potential

Peripheral TFCC tissue has a better:

Blood supply

than the central disc.

Therefore, peripheral tears are more suitable for:

Repair.

Central Tear

Central TFCC tears without instability are generally treated with:

Arthroscopic debridement

rather than:

Repair.

Reason for Debridement

The central TFCC is relatively:

Avascular

and has limited capacity for:

Biologic healing.

Ulnar Positive Variance

When degenerative tearing is associated with substantial:

Positive ulnar variance

treatment may need to reduce:

Ulnocarpal loading.

Ulnar Shortening Osteotomy

An:

Ulnar shortening osteotomy

may be performed to decrease:

Ulnocarpal contact pressure

and unload the:

TFCC.

Wafer Procedure

When only a small amount of shortening is required, typically less than approximately:

2–3 mm

a:

Wafer procedure

may be considered.

DRUJ Reconstruction

Chronic instability with irreparable TFCC tissue may require reconstruction of the:

Distal radioulnar joint stabilizers

using:

Tendon graft

or

Fascial tissue.

Advanced DRUJ Arthritis

In severe cases with advanced:

Distal radioulnar arthritis

a salvage procedure may be required.

Sauvé-Kapandji Procedure

One option is the:

Sauvé-Kapandji procedure

which combines:

DRUJ arthrodesis

with creation of a proximal ulnar:

Pseudoarthrosis

to preserve:

Forearm rotation.

Follow-Up

Postoperative immobilization varies according to:

Repair type

and

Stability.

Immobilization Duration

Patients may be immobilized for approximately:

2–8 weeks

after surgery.

Rehabilitation

After sufficient healing, therapy progresses through:

Range of motion

Strengthening

and

Functional loading.

Return to Sports

Return to unrestricted sports is often expected at approximately:

5–6 months

after major repair, although timing depends on:

Healing

Strength

and

Procedure performed.

Prognosis

The overall prognosis is generally:

Fair to good.

Persistent Pain

Some patients continue to experience:

Ulnar-sided wrist pain

despite adequate:

Treatment.

Long-Term Degeneration

Posttraumatic degenerative change may develop:

Years or decades

after the initial injury.

Complications

Potential complications of surgery include:

Infection

Nerve injury

Iatrogenic cartilage damage

Tendon injury

Persistent pain

and

Complex regional pain syndrome.

Persistent Instability

Failure of repair or unrecognized deep foveal injury may lead to persistent:

DRUJ instability.

Stiffness

Prolonged immobilization may result in:

Wrist stiffness

or loss of:

Pronation-supination.

Clinical Summary

Typical presentation: Ulnar-sided wrist pain after trauma or repetitive loading, often worsened by pronation-supination, gripping, or axial loading.

Key anatomy: The TFCC stabilizes the distal radioulnar joint and transfers part of the load across the ulnar wrist.

Key examination: Localize ulnar-sided tenderness, perform the TFCC compression test, assess DRUJ stability, and examine the ECU tendon.

Imaging: Start with AP and lateral wrist radiographs and assess ulnar variance; MRI is useful for soft-tissue evaluation, while arthroscopy remains the diagnostic gold standard.

Treatment: Stable injuries are initially treated with immobilization, analgesia, and gradual rehabilitation.

Surgery: Peripheral tears may be repaired, whereas central avascular tears are usually arthroscopically debrided.

Positive ulnar variance: Degenerative tears associated with ulnar impaction may require ulnar shortening or a wafer procedure.

Main complications: Persistent pain, DRUJ instability, stiffness, posttraumatic arthritis, and CRPS.

Key Principle

The TFCC is a complex ulnar-sided stabilizing structure of the wrist and distal radioulnar joint.

TFCC tears typically present with:

Ulnar-sided wrist pain, clicking, and pain during forearm rotation or axial loading.

Diagnosis combines:

Focused clinical examination, radiographs, and MRI, while:

Wrist arthroscopy

remains the most definitive diagnostic method.

Stable acute injuries are usually treated with:

Immobilization and rehabilitation.

When surgery is necessary:

Peripheral vascular tears are repaired, whereas:

Central avascular tears are usually debrided.

Associated:

Positive ulnar variance, ulnar impaction, or DRUJ instability

must be recognized and addressed to optimize long-term outcome.

Orthopaedic Surgery - Torticollis

Basics

Torticollis is a condition in which the:

Head and neck are held in an abnormal tilted and rotated position.

The deformity may result from:

Muscular

Skeletal

Neurologic

or other systemic abnormalities.

Typical Posture

The characteristic posture consists of:

Lateral flexion of the head toward one side

with rotation of the:

Chin toward the opposite side.

Classification

Torticollis can broadly be divided into:

Congenital

and

Acquired forms.

Congenital Torticollis

Congenital causes include:

Congenital muscular torticollis

and

Congenital cervical skeletal abnormalities.

Acquired Torticollis

Acquired torticollis may result from:

Trauma

Inflammation

Atlantoaxial rotatory subluxation

Neurologic disease

Ocular disorders

or other:

Systemic conditions.

Synonyms

Historical terms include:

Wry neck

Congenital wry neck

Skeletal wry neck

and

Cock-robin deformity.

Sandifer Syndrome

Sandifer syndrome refers to episodic torticollis or abnormal head positioning associated with:

Gastroesophageal reflux

and sometimes:

Hiatal hernia.

Prevention

Prompt recognition and treatment of the underlying cause may prevent:

Fixed deformity

and reduce the need for:

Surgery.

Epidemiology

Torticollis can occur at:

Any age

depending on the underlying cause.

Congenital Muscular Torticollis

Congenital muscular torticollis usually becomes apparent during the first:

6–8 weeks of life.

Atlantoaxial Rotatory Subluxation

In children, one important acquired cause is:

Atlantoaxial rotatory subluxation.

This may follow:

Upper respiratory infection

Pharyngitis

or

Trauma.

Sex

Males and females are affected approximately:

Equally.

Incidence

Because torticollis has many causes, the exact incidence is difficult to define.

Historical estimates range from approximately:

1 in 100

to

1 in 1,000 individuals.

Risk Factors

Risk factors depend on the specific:

Etiology.

Congenital Muscular Torticollis Risk Factors

Potential associations include:

Difficult delivery

Birth trauma

and localized injury or ischemia involving the:

Sternocleidomastoid muscle.

Atlantoaxial Rotatory Subluxation Risk Factors

Potential triggers include:

Upper respiratory infection

Pharyngitis

and

Neck trauma.

Genetics

Several congenital disorders associated with torticollis have:

Genetic components.

Down Syndrome

Down syndrome is an important genetic condition associated with:

Cervical instability

including abnormalities involving the:

Atlantoaxial joint.

Etiology

The cause depends on whether the disorder is:

Muscular

Skeletal

Neurologic

Inflammatory

or

Traumatic.

Congenital Muscular Torticollis

Congenital muscular torticollis results from shortening and fibrosis of the:

Sternocleidomastoid muscle.

Sternocleidomastoid Effect

Contracture of one sternocleidomastoid causes the head to:

Tilt toward the affected side

while the chin rotates:

Away from the affected side.

Congenital Bony Torticollis

Congenital skeletal causes include abnormalities of the:

Occipitocervical junction

and

Cervical vertebrae.

Bony Abnormalities

Examples include:

Cervical hemivertebrae

Congenital vertebral fusion

and

Asymmetry of the occipital condyles.

Atlantoaxial Rotatory Subluxation

This condition involves abnormal rotation of:

C1 relative to C2.

It may occur after:

Trauma

Inflammation

or occasionally as part of a:

Congenital abnormality.

Diagnosis

Diagnosis begins with careful assessment of:

Head position

Neck motion

Neurologic status

and possible:

Underlying systemic disease.

Signs and Symptoms

The hallmark feature is:

Head tilt with restricted cervical range of motion.

Direction of Motion

The patient may be able to rotate the head farther:

Away from the neutral position

but may have difficulty rotating toward:

Correction.

Neck Mass

Infants with congenital muscular torticollis may have a palpable:

Sternocleidomastoid mass.

This represents localized:

Fibrosis or thickening.

Pain

Pain is less prominent in infants but is more common in:

Older children and adults.

Occipital Symptoms

Some patients report:

Occipital pain

Vertigo

or

Dizziness

that worsens with certain:

Head movements.

Plagiocephaly

Persistent torticollis in infancy may cause secondary:

Plagiocephaly

or facial:

Asymmetry.

Physical Examination

Observe the patient’s:

Head

Face

Neck

and

Shoulder alignment.

Characteristic Position

The ear is typically tilted toward the:

Affected side

while the chin points toward the:

Opposite side.

Range of Motion

Assess:

Active

and

Passive cervical rotation

and

Lateral flexion.

Sternocleidomastoid Examination

Palpate the sternocleidomastoid for:

Tightness

Fibrosis

or a localized:

Mass.

Craniofacial Asymmetry

Longstanding torticollis may produce:

Flattening of the skull

Facial asymmetry

or altered:

Ear position.

Cervical Skeletal Abnormality

A patient with congenital cervical fusion may have a:

Short neck

Low posterior hairline

and reduced:

Cervical motion.

These findings may suggest:

Klippel-Feil syndrome.

Neurologic Examination

A complete neurologic examination should assess:

Strength

Sensation

Reflexes

and

Coordination.

Laboratory Tests

There are no laboratory tests specific for:

Torticollis.

Inflammatory or Neoplastic Evaluation

If infection, inflammatory disease, or malignancy is suspected, laboratory studies may include:

CBC

ESR

and

C-reactive protein.

Additional Specialist Evaluation

When no obvious musculoskeletal cause is present, additional assessment may be needed by:

Ophthalmology

Audiology

or

Gastroenterology.

Imaging

Plain Radiographs

AP and lateral cervical spine radiographs may be used to identify:

Congenital bony abnormalities

Fracture

Dislocation

or abnormal:

Alignment.

CT

CT is particularly useful for evaluating:

Atlantoaxial rotatory subluxation

Occipitocervical injury

Fracture

or

Dislocation.

Rotatory Subluxation

CT may demonstrate persistent abnormal rotational alignment between:

C1

and

C2.

MRI

MRI is indicated when there is concern for:

Spinal cord

Brainstem

Soft-tissue

or other:

Neurologic lesions.

Pathological Findings

In congenital muscular torticollis, the:

Sternocleidomastoid muscle

typically demonstrates:

Fibrosis

and

Shortening.

Differential Diagnosis

The differential diagnosis is broad.

Neurogenic Causes

Potential neurologic causes include:

Brainstem tumor

Cervical spinal cord tumor

Cerebellar tumor

and

Syringomyelia.

Ocular Causes

An ocular disorder may cause compensatory:

Head tilt

to optimize:

Vision.

Traumatic Causes

Traumatic causes include:

Atlantoaxial subluxation

Cervical fracture

and

Occipitocervical dislocation.

Inflammatory Causes

Potential causes include:

Cervical lymphadenitis

and

Rheumatoid arthritis.

Congenital Skeletal Causes

Examples include:

Hemivertebra

Congenital fusion

and

Occipital condyle asymmetry.

Gastrointestinal Cause

In infants, episodic abnormal head positioning may result from:

Sandifer syndrome

associated with:

Gastroesophageal reflux.

Treatment

Treatment depends on the:

Underlying cause

and duration of the:

Deformity.

Congenital Muscular Torticollis

Early treatment consists primarily of:

Stretching exercises.

Early Prognosis

When treatment begins before approximately:

1 year of age

stretching is successful in the vast majority of:

Infants.

Positioning

Parents can position:

Toys

Lights

or other points of interest so the child is encouraged to rotate the head toward the:

Restricted side.

Home Program

A structured home stretching program should focus on:

Gentle cervical rotation

and

Lateral flexion.

Atlantoaxial Rotatory Subluxation

Recent-onset atlantoaxial rotatory subluxation may respond to:

Rest

Analgesics

Physical therapy

and a:

Soft cervical collar.

Early Treatment

Patients treated within approximately the:

First week

often recover without:

Surgery.

Muscle Relaxants

Selected patients may require:

Muscle relaxants

when painful spasm prevents:

Reduction.

Rigid Immobilization

Persistent symptoms may require a:

Hard collar

or another form of:

Cervical bracing.

Traction

If treatment is delayed or the deformity becomes fixed, reduction may require:

Cervical traction.

Activity

Contact sports and strenuous activity should be restricted until the:

Cause is identified

and cervical stability is:

Confirmed.

Physical Therapy

Physical therapy can be curative for many cases of:

Congenital muscular torticollis

and

Recent-onset atlantoaxial rotatory subluxation.

Stretch Direction

The therapist should receive clear instructions regarding:

Direction of stretching

and whether:

Traction

is appropriate.

Medication

Pain may be treated with:

Acetaminophen

or

Ibuprofen

when medically appropriate.

Surgery

Surgery is reserved for selected cases that fail appropriate:

Nonoperative treatment.

Muscular Torticollis Surgery

Persistent congenital muscular torticollis may require:

Sternocleidomastoid release

or

Lengthening.

Timing

Surgery is generally considered when:

Persistent contracture

Restricted motion

or progressive:

Craniofacial asymmetry

remains despite adequate:

Stretching.

Atlantoaxial Rotatory Subluxation Surgery

Severe or chronic atlantoaxial rotatory subluxation that cannot be reduced with:

Traction

may require:

Reduction and C1–C2 fusion.

Congenital Bony Abnormality

Selected congenital cervical abnormalities causing severe persistent deformity or instability may also require:

Spinal fusion.

Follow-Up

Follow-up should assess:

Head position

Range of motion

Neurologic findings

and development of:

Craniofacial asymmetry.

Prognosis

Most cases of torticollis improve:

Spontaneously

or with appropriate:

Treatment.

Early Muscular Torticollis

Congenital muscular torticollis treated early generally has an:

Excellent prognosis.

Delayed Treatment

Delayed treatment increases the risk of:

Persistent contracture

and

Plagiocephaly.

Complications

Potential complications include:

Fixed atlantoaxial subluxation

Persistent neck deformity

and

Plagiocephaly.

Fixed Subluxation

Untreated atlantoaxial rotatory subluxation may become:

Fixed

and increasingly difficult to:

Reduce.

Plagiocephaly

Persistent head positioning in infancy may cause permanent:

Cranial or facial asymmetry

if treatment is delayed beyond the period of active:

Remodeling.

Patient Monitoring

Neurologic status should be followed:

Closely.

Imaging Follow-Up

Bony abnormalities such as persistent:

Atlantoaxial rotatory subluxation

may require repeat:

Imaging.

CT use should be balanced against cumulative:

Radiation exposure, particularly in children.

Clinical Summary

Typical presentation: Head tilted toward one side with the chin rotated to the opposite side and restricted neck motion.

Most common infant cause: Congenital muscular torticollis from sternocleidomastoid fibrosis or contracture.

Important acquired cause in children: Atlantoaxial rotatory subluxation, often after trauma or an upper respiratory infection.

Key examination: Assess cervical ROM, palpate the sternocleidomastoid, look for plagiocephaly, and perform a complete neurologic examination.

Imaging: Plain cervical radiographs for bony abnormalities; CT for suspected C1–C2 rotatory subluxation or fracture; MRI for suspected spinal cord, brainstem, or other neurologic disease.

Initial treatment: Early muscular torticollis responds to stretching and positioning; recent atlantoaxial rotatory subluxation may respond to analgesics, therapy, and cervical immobilization.

Surgery: Reserved for persistent muscular contracture or irreducible/fixed atlantoaxial abnormalities.

Red flags: New neurologic deficits, severe pain, trauma, fever, progressive deformity, or acquired torticollis without an obvious benign explanation.

Key Principle

Torticollis is a clinical posture characterized by lateral head tilt with rotation of the chin in the opposite direction.

It may arise from:

Muscular, skeletal, neurologic, inflammatory, traumatic, ocular, or gastrointestinal causes.

In infants, the most common form is:

Congenital muscular torticollis, which usually responds well to early:

Stretching and positioning.

In older children with acute painful torticollis, especially after:

Trauma or upper respiratory infection, consider:

Atlantoaxial rotatory subluxation.

Persistent, painful, neurologically abnormal, or atypical torticollis requires evaluation for an underlying:

Structural or neurologic cause.

Orthopaedic Surgery - Toe Walking

Basics

Toe walking describes a gait pattern in which a child walks predominantly on the:

Forefoot

with limited or absent:

Heel strike.

Idiopathic toe walking is relatively common in:

Toddlers and young children.

Idiopathic Toe Walking

Many children who toe walk have no identifiable:

Neurologic

Orthopaedic

or

Neuromuscular disorder.

When other causes have been excluded, the condition is termed:

Idiopathic toe walking.

Achilles Tendon Tightness

Some children develop or have an associated shortened:

Achilles tendon

or tight:

Gastrocnemius-soleus complex.

This may restrict:

Ankle dorsiflexion

and reinforce the toe-walking pattern.

Natural History

Some children spontaneously develop a normal:

Heel-toe gait

as they:

Grow.

Persistent Toe Walking

Persistent, nearly exclusive toe walking beyond approximately:

5 years of age

should prompt careful assessment for an underlying:

Neurologic or neuromuscular disorder.

Epidemiology

Toe walking is usually first noticed when the child begins:

Independent walking.

Incidence

Transient toe walking is:

Common

during early childhood.

Sex

Boys and girls are affected approximately:

Equally.

Risk Factors

Potential associations include:

Positive family history

Premature birth

Low Apgar score

and other:

Neuromotor abnormalities.

Genetics

A familial tendency is relatively common.

Historical studies have reported a positive family history in up to approximately:

50% of patients.

Etiology

Idiopathic toe walking is thought to involve a combination of:

Neuromotor patterning

and, in some children,

Achilles tendon shortening.

Diagnosis

Idiopathic toe walking is primarily a:

Clinical diagnosis.

Importantly, it is a:

Diagnosis of exclusion.

A neurologic, neuromuscular, or structural cause should be excluded before labeling the gait:

Idiopathic.

History

The clinician should establish:

When toe walking began

Whether it has always been present

and whether the child can voluntarily walk with:

Heel strike.

Developmental History

Ask about:

Birth history

Prematurity

Developmental milestones

and any history of:

Motor delay.

Family History

Ask whether parents or siblings had:

Toe walking

Neuromuscular disease

or abnormal:

Gait development.

New-Onset Toe Walking

Toe walking that begins after a period of normal:

Heel-toe gait

is more concerning than toe walking present from the onset of:

Walking.

This pattern warrants evaluation for an acquired:

Neurologic

Spinal

or

Musculoskeletal cause.

Physical Examination

The child should ideally be examined wearing:

Shorts

with the lower extremities fully visible.

Gait Observation

Observe the feet throughout:

Standing

Walking

and, when possible,

Running.

Heel Strike

Determine whether the child demonstrates:

Heel strike

at any point during the gait cycle.

Voluntary Correction

Ask the child to attempt:

Heel-toe walking.

The ability to correct the gait voluntarily may support a diagnosis of:

Idiopathic toe walking.

Neurologic Examination

A complete neurologic examination should assess for:

Spasticity

Weakness

Hyperreflexia

Abnormal tone

and other signs of:

Neuromuscular disease.

Ankle Range of Motion

Measure ankle:

Dorsiflexion

with the knee:

Flexed

and

Extended.

Silfverskiöld Principle

Comparing ankle dorsiflexion with the knee flexed and extended helps distinguish:

Gastrocnemius tightness

from combined:

Gastrocnemius-soleus contracture.

Calf Examination

Palpate and inspect the calf for:

Atrophy

Abnormal masses

or

Pseudohypertrophy.

Pseudohypertrophy

Prominent calf enlargement can be a clue to conditions such as:

Muscular dystrophy.

Hamstrings and Adductors

Examine the:

Hamstrings

and

Hip adductors

for abnormal:

Tightness.

This may suggest an underlying:

Neurologic disorder.

Passive and Active Motion

Document both:

Passive

and

Active ankle range of motion.

Testing

Additional investigations are usually unnecessary when the history and physical examination are entirely consistent with:

Idiopathic toe walking.

Neuromuscular Testing

When muscular dystrophy or another myopathic process is suspected, testing may include:

Creatine kinase

and selected:

Genetic studies.

Muscle biopsy is now reserved for selected cases when the diagnosis remains:

Uncertain.

Imaging

MRI of the spine may be appropriate when examination suggests:

Spinal cord pathology

Tethered cord

or another cause of:

Spasticity.

Differential Diagnosis

Important conditions to exclude include:

Cerebral palsy

Muscular dystrophy

Tethered cord syndrome

Hereditary spastic paraplegia

Charcot-Marie-Tooth disease

and

Arthrogryposis.

Cerebral Palsy

Toe walking from cerebral palsy is often accompanied by:

Spasticity

Hyperreflexia

and other abnormalities of:

Motor control.

Muscular Dystrophy

Muscular dystrophy may produce:

Proximal weakness

Gower sign

and

Calf pseudohypertrophy.

Tethered Cord

Tethered cord or other spinal pathology may present with:

New gait abnormality

Weakness

Spasticity

or abnormalities of:

Bladder or bowel function.

Charcot-Marie-Tooth Disease

Charcot-Marie-Tooth disease may cause:

Distal weakness

Pes cavus

and altered:

Gait mechanics.

Treatment

Treatment depends on:

Age

Severity

Ankle range of motion

and whether the child can voluntarily achieve:

Heel-toe gait.

General Measures

Initial management usually consists of:

Observation

Stretching

and

Encouragement of normal heel-toe walking.

Mild Cases

Young children with:

Flexible ankles

and no underlying disorder may simply be:

Observed.

Stretching

Regular stretching of the:

Gastrocnemius-soleus complex

may help preserve or improve:

Ankle dorsiflexion.

Orthotics

Orthotic devices may help guide gait in selected children but, when used alone, do not reliably correct persistent:

Toe walking.

Serial Casting

Serial casting may be used when ankle dorsiflexion is:

Restricted.

Casting Technique

The ankle is gradually positioned into increasing:

Dorsiflexion.

The goal is often to achieve at least approximately:

10° of dorsiflexion

while facilitating development of a:

Heel-toe gait.

Cast Changes

Casts are typically changed approximately:

Weekly

until the desired:

Range of motion

is obtained.

Night Bracing

Night splints holding the ankle in:

Dorsiflexion

may help preserve gains achieved through:

Casting

or

Surgery.

Physical Therapy

Physical therapy may be helpful in children with:

Mild or flexible toe walking.

Range-of-Motion Exercises

Therapy may include:

Passive ankle stretching

and

Active dorsiflexion exercises.

Gait Training

Children who can dorsiflex beyond neutral may practice:

Heel walking

and

Heel-toe gait.

This can reinforce a more typical:

Motor pattern.

Strengthening

Therapy may also focus on strengthening the:

Ankle dorsiflexors

and improving:

Balance and gait control.

Surgery

Surgery is considered when conservative measures fail and persistent:

Achilles contracture

prevents normal:

Heel strike.

Achilles Lengthening

The principal operative procedure is:

Achilles tendon lengthening.

Techniques

Lengthening may be performed using:

Percutaneous

or

Open techniques.

A:

Z-lengthening

is one traditional approach.

Timing

Surgery is generally considered when a child has persistent toe walking approaching the:

School-age years

and fails to develop a functional:

Heel-toe gait.

Goal of Surgery

The objective is to restore sufficient:

Ankle dorsiflexion

to permit normal:

Heel contact during gait.

Avoiding Overlengthening

Excessive Achilles lengthening must be avoided because it may produce:

Weak plantarflexion

and a:

Calcaneal or crouched gait.

Referral

Referral to a pediatric orthopaedic specialist is appropriate when:

Toe walking begins after previously normal gait

or when the child fails to improve by:

Kindergarten or early school age.

Neurologic Referral

Neurology or other specialist evaluation may be required when examination suggests:

Spasticity

Weakness

Developmental delay

or another:

Neuromuscular disorder.

Follow-Up

Children should be reassessed for changes in:

Gait pattern

Ankle dorsiflexion

and

Achilles tendon flexibility.

Prognosis

Many children with idiopathic toe walking spontaneously develop a normal:

Heel-toe gait.

Early Resolution

A substantial number improve by approximately:

3 years of age.

Persistent Toe Walking

Persistent toe walking into adolescence or adulthood may result in:

Metatarsal calluses

Achilles contracture

and impaired:

Balance.

Complications

Important complications include:

Failure to recognize an underlying neurologic disorder

Recurrence after treatment

and complications of:

Achilles lengthening.

Missed Neurologic Diagnosis

The most important diagnostic complication is incorrectly labeling pathologic toe walking as:

Idiopathic.

Recurrence

Toe walking may recur after:

Casting

or

Surgery

particularly if the underlying gait pattern persists.

Achilles Overlengthening

Excessive surgical lengthening can produce:

Plantarflexion weakness

and abnormal:

Calcaneal or crouch gait.

Patient Monitoring

Follow-up should document:

Heel strike

Ankle dorsiflexion

Gait symmetry

Muscle strength

and any emerging:

Neurologic findings.

Clinical Summary

Typical patient: Toddler who has walked on the toes since beginning independent ambulation but otherwise has normal development and neurologic examination.

Key diagnostic principle: Idiopathic toe walking is a diagnosis of exclusion; cerebral palsy, muscular dystrophy, tethered cord, hereditary spastic disorders, and peripheral neuropathy must be considered.

Key examination: Observe gait and measure ankle dorsiflexion with the knee both flexed and extended while performing a complete neurologic examination.

Testing: Usually unnecessary unless the examination suggests a neurologic, spinal, or myopathic disorder.

Natural history: Many children improve spontaneously, particularly by about 3 years of age.

Initial treatment: Observation, Achilles stretching, gait training, and selected physical therapy.

Persistent contracture: Serial casting and night bracing may improve ankle dorsiflexion.

Surgery: Achilles lengthening is reserved for persistent toe walking with fixed equinus that fails conservative management.

Red flag: New-onset toe walking after a previously normal heel-toe gait warrants further investigation.

Key Principle

Idiopathic toe walking is a common childhood gait pattern characterized by forefoot walking without an identifiable neurologic or orthopaedic cause.

It is a:

Diagnosis of exclusion.

Persistent toe walking beyond approximately:

5 years of age, new-onset toe walking, weakness, spasticity, abnormal reflexes, or developmental abnormalities should prompt evaluation for:

Neuromuscular or spinal disease.

Children with flexible ankles often improve with:

Observation, stretching, and gait retraining.

Persistent equinus may be treated with:

Serial casting and night bracing, while:

Achilles tendon lengthening

is reserved for selected children with fixed contracture and persistent functional toe walking.

Orthopaedic Surgery - Tibial Torsion

Basics

Tibial torsion describes rotational alignment of the:

Tibia

together with the:

Ankle and foot

either internally or externally around the longitudinal axis of the leg.

Some degree of tibial rotation is part of:

Normal development.

The condition becomes clinically abnormal when rotation is markedly outside the normal range for:

Age.

Definition of Abnormality

Abnormal torsion is often defined as rotational alignment greater than approximately:

Two standard deviations from the age-adjusted mean.

Classification

Tibial torsion may be classified as:

Internal tibial torsion

External tibial torsion

or

Neuromuscular tibial torsion.

Internal Tibial Torsion

Internal tibial torsion produces:

In-toeing

with the foot directed inward relative to the:

Knee.

External Tibial Torsion

External tibial torsion produces:

Out-toeing

with the foot directed outward relative to the:

Knee.

Neuromuscular Torsion

Abnormal tibial rotation may occur with neuromuscular conditions such as:

Cerebral palsy

or

Spina bifida.

Synonyms

Internal tibial torsion may be referred to as:

In-toeing

or historically:

Pigeon-toeing.

External tibial torsion produces:

Out-toeing.

Epidemiology

Abnormal tibial rotation is a common reason for:

Pediatric orthopaedic evaluation.

Age

Internal tibial torsion is most commonly noticed after the child begins:

Walking

and is especially frequent in children younger than approximately:

3 years.

Normal Development

Younger children normally have relatively greater:

Internal tibial rotation.

With growth, the tibia progressively rotates:

Externally.

Sex

No important consistent difference has been demonstrated between:

Boys and girls.

Persistence

Persistent clinically significant torsion occurs in fewer than approximately:

1–2% of children.

Genetics

Internal tibial torsion is believed to reflect a combination of:

Genetic influences

and

Intrauterine positioning.

Family History

A family history of persistent abnormal torsion may influence the likelihood of:

Spontaneous correction.

Etiology

Most idiopathic internal tibial torsion appears to result from normal developmental variation influenced by:

Genetics

and

Fetal position.

Associated Conditions

In infants, internal tibial torsion may coexist with:

Metatarsus adductus

or

Developmental genu varum.

Diagnosis

Diagnosis is primarily:

Clinical.

A careful rotational profile should assess the child from:

Hip to foot.

Signs and Symptoms

Parents commonly become concerned because the child’s walking pattern looks different from that of:

Siblings or peers.

Cosmetic Concern

The principal concern is usually:

Appearance during walking or running.

Tripping

Parents may report:

Frequent tripping

or

Falling.

In young children, however, some of this may simply reflect:

Normal motor development.

Pain

Pain is:

Unusual.

A painful gait suggests that another diagnosis should be:

Considered.

Apparent Limp

Parents may describe a limp, but uncomplicated tibial torsion usually does not produce a true:

Painful limp.

Physical Examination

Examination begins with observation of:

Standing

and

Walking.

Gait

If the child is ambulatory, observe for:

Heel-toe progression

In-toeing

Out-toeing

and

Limp.

Neurologic Warning Sign

Absence of a normal:

Heel-toe gait

may be an early clue to an underlying:

Neuromuscular disorder

such as:

Cerebral palsy.

Foot Progression Angle

The:

Foot progression angle

is the angle between the long axis of the foot and the direction in which the child is:

Walking.

Normal Foot Progression

The normal angle is usually slightly:

External

but there is a broad normal range extending approximately:

15° internally to 15° externally.

Supine Examination

Before focusing on torsion, examine the hips for:

Stability

and

Abduction.

Prone Examination

The child is then placed:

Prone

to evaluate:

Hip rotation

and

Tibial torsion.

The pelvis must remain:

Level and stationary

for accurate measurement.

Femoral Anteversion

Femoral anteversion can be estimated by determining the hip position in which the:

Greater trochanter

is most prominent laterally.

Tibial Torsion Measurement

Tibial torsion is commonly estimated using the:

Thigh-foot angle

or

Transmalleolar axis.

Thigh-Foot Angle

With the child prone and the knee flexed approximately 90°, compare the long axis of the:

Thigh

with the long axis of the:

Foot.

Internal deviation suggests:

Internal tibial torsion.

Bimalleolar Axis

The relationship between the:

Medial malleolus

Lateral malleolus

and the proximal tibia can also estimate:

Tibial rotation.

Foot Examination

The shape of the foot should be assessed carefully because:

Metatarsus adductus

may itself be responsible for:

In-toeing.

Imaging

Imaging is usually:

Not required.

The clinical rotational profile generally provides sufficient information for:

Management.

Pelvic Radiograph

An AP pelvis radiograph is appropriate when there is:

Asymmetric hip abduction

or markedly restricted:

Hip abduction.

In a toddler, abduction below approximately:

60°

raises concern for:

Developmental hip dysplasia.

Foot Radiographs

Foot radiographs may help evaluate suspected:

Metatarsus adductus

when clinical findings are unclear.

Long-Leg Radiographs

Full-length lower-extremity radiographs may be useful when there is associated:

Genu varum

or another:

Angular deformity.

CT

CT can measure tibial rotation accurately but is usually:

Unnecessary

because most childhood torsional abnormalities can be evaluated:

Clinically.

Differential Diagnosis

Important alternatives include:

Blount disease

Excessive femoral anteversion

Metatarsus adductus

Cerebral palsy

and

Developmental dysplasia of the hip.

Blount Disease

Blount disease may combine:

Pathologic genu varum

with

Internal tibial torsion.

Unlike physiologic torsion, it represents a progressive:

Growth disorder.

Femoral Anteversion

Persistent in-toeing in an older child may result from increased:

Femoral anteversion

rather than ongoing tibial torsion.

Treatment

Most cases require:

Observation and reassurance.

General Measures

Internal tibial torsion is the most common cause of in-toeing in children younger than approximately:

3 years.

Natural History

With growth, the tibia normally rotates externally so that by later childhood the:

Lateral malleolus

lies approximately:

20–30° posterior

to the:

Medial malleolus.

Spontaneous Improvement

Almost all children with idiopathic internal tibial torsion demonstrate substantial improvement by approximately:

3–5 years of age.

Parental Education

The most important intervention is often:

Explanation of the natural history.

Parents should understand that most cases improve through:

Normal growth and development.

Braces and Orthotics

Devices such as:

Night splints

Denis Browne bars

Shoe wedges

Special shoes

or

Orthotics

have not been shown to alter the natural rotational development of the:

Tibia.

External Tibial Torsion

Marked external torsion is less likely to correct spontaneously, particularly when it is:

Asymmetric.

Selected persistent cases may eventually require:

Derotational osteotomy.

Persistent In-Toeing

If in-toeing persists or becomes more obvious after approximately:

3–4 years

the cause may increasingly be:

Femoral anteversion

rather than tibial torsion.

Activity

No routine activity restriction is:

Required.

Children may participate normally in:

Play

Sports

and

Physical education.

Physical Therapy

Formal physical therapy generally does not correct:

Bony tibial rotation.

Reason Therapy Is Limited

The natural change occurs over:

Years

rather than over the shorter time frame expected from:

Therapy.

Recreational Activities

Some clinicians encourage activities requiring awareness of foot position, such as:

Ice skating

Roller skating

Track

or

Ballet.

There is little evidence that these activities directly change:

Tibial torsion.

Surgery

The only operation used to correct persistent severe tibial torsion is:

Derotational tibial osteotomy.

Timing of Surgery

Surgery is rarely considered before approximately:

8–10 years of age.

Indications

Surgery may be considered when there is:

Persistent severe rotational deformity

Functional difficulty

or major:

Cosmetic concern

after the age at which spontaneous improvement is expected.

Rotational Thresholds

Historical guidelines suggest considering osteotomy when the:

Thigh-foot angle remains internally rotated by approximately 20° or more

or when external tibial torsion measures approximately:

35° or more.

These values should be interpreted together with:

Symptoms

Function

and

Age.

Neuromuscular Patients

Children with:

Cerebral palsy

have a greater risk of recurrent torsion after:

Early surgery.

Osteotomy Level

Derotational osteotomy is often performed near the:

Distal tibial metaphysis

while avoiding injury to the:

Growth plate.

Postoperative Immobilization

The leg is commonly immobilized in a cast for approximately:

6–8 weeks.

Follow-Up

Observation may be performed:

Annually

or

Every 1–2 years

when parents desire documentation of:

Rotational improvement.

Prognosis

Tibial torsion is usually:

Self-limiting

and represents part of normal:

Childhood development.

Family Alignment

If the parents and older siblings demonstrate normal rotational alignment, spontaneous correction in the child is:

Highly likely.

Familial Persistence

A strong family history of persistent tibial torsion may slightly reduce the probability of:

Complete spontaneous correction.

Arthritis Risk

Isolated idiopathic tibial torsion in childhood has not been shown to produce a significant increased risk of:

Hip

Knee

or

Spinal arthritis.

Complications

Complications are primarily related to:

Surgical treatment.

Surgical Complications

Potential complications include:

Physeal injury

Neurovascular injury

Nonunion

Malunion

and

Implant-related problems.

Patient Monitoring

Follow-up should document:

Foot progression angle

Thigh-foot angle

Hip rotation

and overall:

Gait.

Patient Teaching

Parental education is central to management.

Most children improve naturally without:

Braces

Special shoes

or

Surgery.

Showing families how rotational alignment normally changes with age may provide useful:

Reassurance.

Frequently Asked Questions

When should my child’s tibial torsion improve?

Most children progressively improve during early childhood. Continued observation is appropriate as long as improvement is occurring. Persistent severe deformity after approximately:

8–10 years of age

may justify consideration of surgery if it is functionally or cosmetically important.

Does tibial torsion cause arthritis later in life?

Isolated developmental tibial torsion has not been convincingly shown to increase the risk of:

Hip, knee, or back arthritis.

Clinical Summary

Typical patient: Toddler with painless in-toeing noticed after beginning to walk.

Key examination: Observe gait and measure the foot progression angle and thigh-foot angle while also assessing hip rotation and foot shape.

Most important differential: Femoral anteversion, metatarsus adductus, Blount disease, hip dysplasia, and neurologic disease.

Imaging: Usually unnecessary unless the examination suggests another abnormality.

Natural history: Internal tibial torsion usually improves substantially by 3–5 years of age.

Treatment: Observation and parental reassurance; braces, special shoes, and orthotics do not alter tibial rotation.

Surgery: Rarely required and generally reserved for persistent severe deformity after about 8–10 years of age.

Key Principle

Tibial torsion is usually a developmental rotational variation of the tibia, most often presenting as:

In-toeing in toddlers.

Diagnosis is primarily:

Clinical, using gait observation and measurement of the:

Foot progression and thigh-foot angles.

Most internal tibial torsion resolves spontaneously with:

Growth, and treatment consists primarily of:

Observation and reassurance.

Bracing and special footwear have not been shown to accelerate:

Correction.

Derotational osteotomy is reserved for rare cases of:

Persistent severe symptomatic torsion in older children.

Orthopaedic Surgery - Tibial Spine Fracture

Basics

A tibial spine fracture is an avulsion fracture involving the:

Intercondylar eminence of the proximal tibia.

It is also referred to as a:

Tibial eminence fracture.

Anatomy

The:

Anterior tibial spine

provides an important attachment site for the:

Anterior cruciate ligament.

Pediatric Mechanism

In the skeletally immature knee, the ACL may be stronger than the incompletely ossified:

Tibial spine.

Therefore, traumatic force may produce:

Bony avulsion of the tibial spine

rather than a midsubstance:

ACL tear.

ACL Injury in Children

Although tibial spine avulsion is characteristic of the immature knee, children can still sustain:

Midsubstance ACL tears.

Femoral Notch Anatomy

A relatively narrow:

Femoral intercondylar notch

may predispose some children toward:

Midsubstance ACL injury

rather than:

Tibial spine avulsion.

Classification

The classic:

Meyers and McKeever classification

is based primarily on the degree of:

Fracture displacement.

Type I

Type I is:

Minimally displaced or essentially nondisplaced.

The fragment remains near its normal:

Anatomic position.

Type II

Type II is a:

Hinged fracture.

The anterior portion of the fragment is elevated while the posterior portion remains attached, creating an intact:

Posterior hinge.

Type III

Type III demonstrates:

Complete separation of the fragment

with:

Upward displacement

and often:

Rotation.

Epidemiology

Tibial spine fractures are considerably more common in:

Children

than in adults.

Incidence

Historical data suggest that these fractures occur approximately:

Four times more often in children than adults.

Etiology

The injury usually results from forces that tension the:

ACL.

Common Mechanisms

Mechanisms include:

Twisting injury

Varus-valgus stress

and

Hyperextension.

Typical Causes

Common causes include:

Bicycle falls

Athletic injuries

and

Motor vehicle collisions.

Diagnosis