Orthopaedic Surgery - Puncture Wounds of the Foot

Basics

Puncture wounds of the foot are penetrating injuries that most commonly involve the:

Plantar forefoot

or

Heel.

The penetrating object is often a:

Nail

Needle

Pin

but other materials may include:

Thorns

Glass

Wood splinters

or any sharp object capable of penetrating the plantar soft tissues.

Classification

Puncture wounds may be considered according to the timing of presentation.

Early Presentation

An early presentation occurs:

On or shortly after the day of injury.

At this stage, the major concerns are:

Wound contamination

Retained foreign body

Depth of penetration

Involvement of bone, tendon, or joint

Late Presentation

A late presentation generally occurs:

Several days after injury, often at least 3–5 days later.

At this stage, symptoms may reflect a developing:

Deep soft-tissue infection

Abscess

Septic arthritis

Tenosynovitis

or

Osteomyelitis.

Prevention

Preventive measures include:

Avoiding barefoot walking in areas containing nails, wood fragments, glass, or construction debris

and using appropriate:

Protective footwear.

Epidemiology

Puncture wounds are particularly common in:

Children and active adults.

Historical reports suggest a greater frequency in:

Males.

Incidence

Puncture wounds of the foot have historically accounted for approximately:

0.5–1% of pediatric emergency-department visits.

Most heal without deep infection.

Historical series reported deep infection in approximately:

0.6% of affected children.

Risk Factors

Important risk factors include:

Walking barefoot

Construction work

Outdoor activity

Exposure to contaminated debris

Penetration through footwear

Etiology

The penetrating object may inoculate organisms from:

Skin

Soil

Sock material

Shoe lining or sole

into deeper tissues.

Microbiology

The organisms involved depend on:

Depth

Environment

Footwear

Host factors

and

Anatomic structures penetrated.

Superficial soft-tissue infections are commonly caused by:

Staphylococcus species

and

Streptococcus species.

Pseudomonas

Pseudomonas aeruginosa is particularly associated with certain plantar puncture wounds, especially those occurring:

Through footwear, classically through the sole of an athletic shoe.

It is an important pathogen in:

Post-puncture osteomyelitis.

Polymicrobial Infection

Some puncture-related infections may be:

Polymicrobial, particularly in highly contaminated wounds or immunocompromised patients.

Deep Infection

When infection spreads deeply, it may involve structures lined by synovial tissue, including:

Tendon sheath

Joint

Bursa

and eventually

Bone.

Diagnosis

Diagnosis is based on:

Mechanism

Timing

Physical examination

and selective use of:

Laboratory tests and imaging.

Signs and Symptoms

Acute Phase

Early symptoms may include:

Pain

Swelling

Bleeding

Localized tenderness

Late Presentation

Delayed infection may produce:

Erythema

Increasing pain

Tenderness

Cellulitis

Fluctuance

Purulent or serous drainage

Altered Gait

Patients may:

Limp

Refuse to bear weight

or

Walk on the heel

to avoid loading a painful forefoot puncture site.

History

Important questions include:

When did the injury occur?

What object caused it?

Where did the puncture occur?

Was the patient barefoot or wearing a shoe?

Did the object penetrate through a sock or shoe sole?

How contaminated was the environment?

Could part of the object remain in the foot?

Early Physical Examination

Inspect the puncture site carefully for:

Depth

Wound size

Contamination

Foreign material

Associated laceration

Retained Foreign Body

Palpate for:

Focal deep tenderness

or a palpable foreign body.

Persistent focal pain after a puncture should raise suspicion for:

Retained glass, wood, thorn, or other material.

Joint Involvement

Consider whether the tract passes near a:

Metatarsophalangeal joint

Interphalangeal joint

Midfoot joint

Evaluate adjacent joint motion.

Pain with passive motion may suggest:

Septic arthritis

or another deep process.

Footwear Examination

If available, inspect the shoe for:

Location of penetration

Depth of damage

Possible retained material

This can help reconstruct the wound tract.

Late Physical Examination

Assess for local and systemic infection.

Look for:

Erythema

Swelling

Warmth

Cellulitis

Fluctuance

Drainage

Lymphatic Examination

Regional lymph nodes may become enlarged, including:

Popliteal

and

Inguinal lymph nodes.

Deep Swelling

Circumferential or dorsal swelling following a plantar puncture wound should raise concern for:

Deep infection.

Laboratory Tests

Early Presentation

Laboratory studies are usually:

Not necessary

for a fresh uncomplicated puncture wound.

Late Presentation

When infection is suspected, useful tests may include:

CBC with differential

ESR

CRP

These tests are supportive but:

Not specific.

Aspiration

If infection appears to involve a:

Joint

Bursa

or

Tendon sheath

aspiration may be performed.

Fluid should be sent for:

Gram stain

Cell count

Culture and susceptibility testing

Imaging

Plain Radiographs

Radiographs may be obtained to evaluate for:

Fracture

Bone involvement

Radiopaque foreign body

Soft-tissue gas

Late Radiographic Findings

In delayed presentations, radiographs may also show features suggesting:

Osteomyelitis

although early bone infection can still have normal radiographs.

Foreign Bodies

Plain radiographs are particularly useful for:

Metal

Glass

and other radiopaque materials.

They are less sensitive for:

Wood

Thorns

and some plastics.

Ultrasound

Ultrasound can help identify:

Soft-tissue abscess

and

Radiolucent retained foreign bodies, particularly wood.

It can also assist with:

Image-guided removal or aspiration.

MRI

MRI is useful when there is concern for:

Deep abscess

Osteomyelitis

Septic arthritis

Tendon sheath infection

It may also identify some retained foreign bodies and define the extent of deep soft-tissue involvement.

Diagnostic Wound Exploration

Local exploration may be appropriate to:

Assess wound depth

Remove contamination

Identify retained foreign material

Aggressive blind probing should be avoided because it can:

Damage deeper structures

or enlarge contamination.

Differential Diagnosis

Important complications or alternative diagnoses include:

Cellulitis

Soft-tissue abscess

Septic bursitis

Tenosynovitis

Septic arthritis

Osteomyelitis

Retained foreign body reaction

Treatment

General Principles

Management depends on:

Timing of presentation

Contamination

Depth

Presence of a retained foreign body

Evidence of infection

Patient comorbidities

Acute Presentation

Fresh wounds should undergo:

Careful cleansing

Irrigation

and, when necessary,

Limited debridement.

Any clearly visible foreign material should be removed.

Tetanus Prophylaxis

Tetanus prophylaxis should be updated according to:

Wound type

and

The patient’s immunization history.

This may include:

Tetanus-containing vaccine booster

and, in selected incompletely immunized patients with high-risk wounds,

Tetanus immune globulin.

Antibiotic Prophylaxis

Routine prophylactic antibiotics are:

Not required for every uncomplicated acute puncture wound.

They may be considered when there is:

Gross contamination

Delayed presentation

Deep penetration

High-risk host factors

or concern that follow-up will be unreliable.

Follow-Up Instructions

Patients and caregivers should be advised to return promptly for:

Increasing pain

Redness

Swelling

Drainage

Fever

Difficulty bearing weight

Late Presentation

Delayed wounds with established deep infection require more aggressive treatment.

Management may include:

Surgical irrigation and debridement

Deep tissue cultures

Targeted antibiotic therapy

Cellulitis

Cellulitis without abscess may initially be treated with antibiotics directed primarily against:

Staphylococcal

and

Streptococcal organisms.

The patient should be reassessed closely.

Failure to Improve

Failure to improve should prompt evaluation for:

Abscess

Retained foreign body

Deep-space infection

Pseudomonas infection

Osteomyelitis

Abscess

Any area of:

Fluctuance

should generally be treated with:

Incision and drainage.

Cultures should be obtained when clinically appropriate.

Pseudomonas Coverage

Empiric antipseudomonal therapy is not necessary for every puncture wound.

It should be considered particularly when:

Deep infection follows penetration through footwear

Pseudomonas is isolated from culture

or

Clinical features strongly suggest this organism.

Antibiotic selection should account for:

Patient age

Allergies

Local resistance patterns

and infection severity.

Weight Bearing

Weight bearing can be resumed gradually as:

Pain and tenderness resolve.

Deep infections or surgically treated wounds may require temporary:

Protected weight bearing.

Medication

Acute Injury

Analgesics may be used for:

Pain control.

Antibiotic use is individualized rather than automatic.

Established Infection

Antibiotics should initially cover the most likely organisms and then be changed according to:

Culture results.

Surgery

Surgical treatment is indicated for:

Deep abscess

Septic arthritis

Osteomyelitis requiring debridement

Retained foreign body not removable safely at bedside

Failure of medical treatment

Localization

Before surgery, the infection or foreign body should be localized using:

Physical examination

Radiographs

Ultrasound

or

MRI, depending on the suspected pathology.

Surgical Approach

The surgical approach should:

Reach the abnormality directly

and, when useful, follow the:

Original puncture tract.

Plantar Incisions

Plantar incisions may be used when necessary.

Whenever possible, they should avoid major:

Weight-bearing pressure points

such as the:

Central heel

or

Metatarsal heads.

Debridement

Surgical treatment should include:

Removal of devitalized tissue

Removal of foreign material

Drainage of purulence

Copious irrigation

Cultures

Deep cultures should be obtained before or during antibiotic treatment when feasible.

Special cultures for organisms such as:

Mycobacteria

or fungi may be considered when the history or chronic course suggests atypical infection.

Follow-Up

Patients should be reassessed if symptoms:

Persist

Worsen

or recur.

Follow-up may be provided by:

Primary care

Emergency medicine

Orthopaedics

Podiatry

or

Infectious disease specialists, depending on severity.

Prognosis

The prognosis is generally:

Good.

Most uncomplicated puncture wounds heal without major sequelae.

Deep Infection Risk

Historical pediatric series reported subsequent osteomyelitis in approximately:

0.6–1.8% of puncture wounds.

Complications

Potential complications include:

Cellulitis

Abscess

Retained foreign body

Septic arthritis

Tenosynovitis

Osteomyelitis

Osteomyelitis

Bone infection is uncommon but important.

It should be suspected when there is:

Persistent deep pain

Failure to improve

Recurrent drainage

Difficulty bearing weight

or persistent inflammatory findings after a puncture wound.

Septic Arthritis

A puncture tract entering or passing close to a joint may result in:

Septic arthritis.

This requires prompt:

Joint drainage

and

Antibiotic therapy.

Overall Complication Rate

One historical study reported an overall complication rate of approximately:

3.2%.

Patient Monitoring

Monitoring should focus on:

Pain

Swelling

Erythema

Drainage

Weight-bearing ability

Range of motion of nearby joints

Evidence of deep infection

Patients should continue follow-up until:

The wound has healed

and

Normal function has returned.

Key Principle

A plantar puncture wound is usually a minor injury, but a penetrating object can inoculate bacteria and leave behind a retained foreign body, resulting in delayed deep infection.

The most important early priorities are:

Thorough examination, wound cleansing, assessment for a retained foreign body, and appropriate tetanus prophylaxis.

Persistent or delayed symptoms should raise concern for:

Abscess, septic arthritis, or osteomyelitis, with Pseudomonas being particularly important in deep infections following puncture through footwear.

Orthopaedic Surgery - Pronator Syndrome

Basics

Pronator syndrome is a compressive neuropathy of the:

Median nerve in the proximal forearm.

It typically presents with:

Vague aching pain in the proximal volar forearm

Paresthesia in the median nerve distribution

and sometimes:

Mild weakness of median nerve–innervated muscles.

The disorder is considerably less common than:

Carpal tunnel syndrome.

Anatomy

The median nerve enters the proximal forearm and passes through or beneath several structures that may potentially compress it.

Important sites include:

Ligament of Struthers

Lacertus fibrosus

Between the humeral and ulnar heads of pronator teres

Fibrous arch of flexor digitorum superficialis

The anterior interosseous nerve branches from the median nerve distal to the proximal forearm region.

Pathophysiology

Compression of the median nerve proximal to its major motor and sensory branches may affect:

Motor fibers

and

Sensory fibers.

This explains why pronator syndrome can produce sensory symptoms involving both:

The radial digits

and

The palm.

Palmar Cutaneous Branch

The palmar cutaneous branch of the median nerve arises proximal to the carpal tunnel.

Therefore, proximal median nerve compression can produce sensory symptoms in the:

Thenar eminence or central palm.

This helps distinguish pronator syndrome from:

Carpal tunnel syndrome, in which palmar cutaneous sensation is usually preserved.

Prevention

There is no specific established preventive strategy.

Reducing excessive repetitive forearm loading may be helpful in individuals whose symptoms are clearly activity related.

Epidemiology

Pronator syndrome is:

Rare.

It most commonly presents in:

Middle-aged adults, often around the fifth decade of life.

Sex

Historical series have reported a female predominance, with women affected approximately:

Four times more often than men.

Because the disorder is uncommon, precise incidence and prevalence remain poorly defined.

Risk Factors

Potential anatomic or mechanical risk factors include:

Supracondylar process of the humerus

Repetitive pronation and supination

Repetitive elbow or wrist flexion

Hypertrophied forearm musculature

Supracondylar Process

A supracondylar process is an uncommon bony projection from the distal humerus.

It may be connected to the medial epicondyle by the:

Ligament of Struthers.

The median nerve can occasionally be compressed beneath this structure.

Genetics

There is no known Mendelian inheritance pattern.

Etiology

The exact cause is often:

Poorly defined.

The syndrome is believed to result from mechanical compression of the:

Median nerve in the proximal forearm.

In many patients, no single compressive structure can be definitively identified clinically.

Diagnosis

Diagnosis is based mainly on:

History

Physical examination

and exclusion of other median nerve disorders.

Electrodiagnostic studies are often more useful for excluding alternative diagnoses than for confirming pronator syndrome itself.

Signs and Symptoms

The characteristic clinical picture includes:

Proximal forearm pain

Median-distribution paresthesia

and sometimes

Mild motor weakness.

Sensory Symptoms

Paresthesias may involve the median nerve distribution, including:

Thumb

Index finger

Middle finger

Radial half of the ring finger

Unlike carpal tunnel syndrome, symptoms may also involve:

The palm or thenar eminence.

Pain

Pain is usually located in the:

Proximal volar forearm.

It may become worse with:

Forearm pronation and supination

or repetitive upper-extremity activity.

Night Symptoms

Pronator syndrome generally produces:

Few or minimal nocturnal symptoms.

Prominent nighttime numbness or awakening is more characteristic of:

Carpal tunnel syndrome.

Motor Weakness

Weakness may involve median nerve–innervated muscles such as:

Pronator teres

Flexor carpi radialis

Palmaris longus

Flexor pollicis longus

Flexor digitorum superficialis

Flexor digitorum profundus to the index and middle fingers

Thenar muscles

Radial two lumbricals

However, objective weakness is often:

Mild or absent.

Physical Examination

A complete neurologic and vascular examination of the upper extremity should be performed.

Sensory Examination

Assess sensation in:

Thumb

Index finger

Middle finger

Radial half of the ring finger

and

Palm over the thenar eminence.

Sensory change in the palm supports a lesion proximal to the:

Carpal tunnel.

Motor Examination

Assess strength of:

Forearm pronation

Wrist flexion

Thumb flexion

Index and middle finger flexion

Thumb opposition and abduction

Provocative Testing

Different provocative maneuvers may help localize the suspected level of compression.

A test is considered suggestive when it reproduces the patient’s:

Typical pain or paresthesia.

Lacertus Fibrosus Compression

Compression beneath the lacertus fibrosus may be provoked by:

Resisted elbow flexion with the forearm supinated.

This tensions the bicipital aponeurosis over the median nerve.

Pronator Teres Compression

Compression between the heads of pronator teres may be provoked by:

Resisted forearm pronation with the elbow extended.

Reproduction of the patient’s symptoms supports this site.

Flexor Digitorum Superficialis Arch

Compression at the FDS arch may be suggested when symptoms are reproduced by:

Resisted PIP joint flexion, particularly of the middle finger.

Tinel Sign

Percussion over the proximal course of the median nerve may produce:

Tingling or radiating paresthesia.

A positive Tinel sign can support the diagnosis but is not specific.

Scratch-Collapse Test

The scratch-collapse test has been described for proximal median nerve compression.

Its diagnostic accuracy is variable, so it should be interpreted only as part of the:

Overall clinical examination.

Laboratory Tests

No routine laboratory tests are useful for diagnosing isolated pronator syndrome.

Laboratory studies may be obtained only when there is concern for:

Inflammatory disease

Metabolic neuropathy

or another systemic disorder.

Imaging

Plain Radiographs

Radiographs are not routinely required.

They may be useful when there is concern for:

Supracondylar process

Bony deformity

Previous fracture

or another structural abnormality.

Supracondylar Process and Ligament of Struthers

When a supracondylar process is present, the median nerve may be compressed beneath a fibrous band extending to the medial epicondyle known as the:

Ligament of Struthers.

MRI or Ultrasound

Advanced imaging may be useful when a:

Mass

Ganglion

Tumor

or other space-occupying lesion is suspected.

Ultrasound may also demonstrate:

Dynamic nerve compression

or local nerve enlargement in selected cases.

Electrodiagnostic Studies

Electromyography and nerve-conduction studies may be obtained to:

Exclude carpal tunnel syndrome

Exclude cervical radiculopathy

Exclude anterior interosseous neuropathy

Identify more proximal median nerve injury

Limitations of Electrodiagnostic Testing

Electrodiagnostic studies are often:

Normal or nondiagnostic

in pronator syndrome.

Only a minority of patients demonstrate clear evidence of proximal median nerve compression.

Therefore, a normal study does not completely exclude the diagnosis.

Differential Diagnosis

Important alternatives include:

Carpal tunnel syndrome

Anterior interosseous nerve syndrome

Cervical radiculopathy

Median nerve lesion at another level

Flexor-pronator muscle strain

Anterior Interosseous Nerve Syndrome

Anterior interosseous nerve syndrome is primarily a:

Motor neuropathy.

It causes weakness of muscles such as:

Flexor pollicis longus

Index flexor digitorum profundus

Pronator quadratus

but does:

Not produce sensory loss.

This distinguishes it from pronator syndrome.

Carpal Tunnel Syndrome

Carpal tunnel syndrome usually causes:

Median-distribution paresthesia

with prominent:

Night symptoms.

The:

Palmar cutaneous branch is spared

because it passes superficial to the carpal tunnel.

Thus, numbness over the thenar eminence or palm favors a more proximal median nerve lesion.

Treatment

General Principles

Initial treatment is nearly always:

Nonoperative.

Management focuses on reducing mechanical irritation and allowing the nerve to recover.

Rest

Temporary rest from aggravating activity is often recommended.

Activity Modification

Patients should reduce activities involving:

Repeated pronation-supination

Forceful gripping

Repeated elbow flexion

Heavy wrist-flexor strengthening

if these reproduce symptoms.

Splinting

Temporary rotational or forearm immobilization may be used in selected patients to reduce repetitive nerve irritation.

Prolonged immobilization should be avoided because of the risk of:

Stiffness

and

Weakness.

Physical and Occupational Therapy

Therapy may include:

Stretching of the flexor-pronator musculature

Median nerve-gliding exercises

Range-of-motion exercises

Soft-tissue mobilization

Activity and ergonomic modification

Nerve Gliding

Median nerve–gliding exercises aim to improve:

Neural mobility

and reduce mechanical irritation during forearm motion.

Exercises should not provoke persistent:

Pain or paresthesia.

Medication

NSAIDs may be used for:

Short-term pain relief

when appropriate.

Medication does not correct fixed mechanical compression.

Surgery

Surgical decompression may be considered when there is:

Failure of prolonged conservative treatment

Progressive motor weakness

Significant functional loss

or a clear structural compressive lesion.

Timing of Surgery

A trial of approximately:

3–6 months of conservative management

is often appropriate before surgery when weakness is not progressive.

Earlier intervention may be considered for:

Progressive motor deficit

or definite structural compression.

Surgical Decompression

Surgery involves exploration of the median nerve through the proximal forearm and release of all potential compression sites.

Structures Released

Potential sites include:

Ligament of Struthers

Lacertus fibrosus

Pronator teres

Fibrous arch of flexor digitorum superficialis

Ligament of Struthers

If present and compressive, the ligament is:

Released or excised.

Lacertus Fibrosus

The bicipital aponeurosis may be released when it is contributing to:

Median nerve compression.

Pronator Teres

The median nerve may be decompressed between the:

Humeral

and

Ulnar heads

of pronator teres.

FDS Arch

A distinct fibrous arch at the origin of:

Flexor digitorum superficialis

may form an important distal site of compression.

When encountered during surgery, it should be:

Adequately released.

Referral

Referral to a hand or peripheral nerve specialist is appropriate for:

Progressive weakness

Significant motor deficit

Failure of conservative treatment

Diagnostic uncertainty

Follow-Up

Patients undergoing nonoperative treatment should be reviewed periodically to monitor:

Pain

Paresthesia

Motor strength

Response to activity modification

Prognosis

The overall prognosis is generally:

Good.

Historical series suggest that approximately:

90% of patients

may improve with either conservative or operative management, although persistent symptoms can occur.

Surgical Outcomes

No single operative technique has been conclusively shown to be superior.

Successful surgery depends primarily on:

Correct diagnosis

and

Complete release of the relevant compression sites.

Complications

The main complication is:

Persistent or recurrent symptoms.

Potential surgical complications include:

Scar sensitivity

Incomplete decompression

Iatrogenic nerve injury

although major nerve injury is uncommon.

Patient Monitoring

Patients should be followed regularly during conservative treatment to evaluate:

Median nerve sensation

Forearm pain

Motor function

Thenar strength

Progression or resolution of symptoms.

Key Principle

Pronator syndrome is a proximal median nerve entrapment syndrome characterized by proximal forearm pain, median-distribution paresthesia including the palm, and usually little or no motor weakness.

It differs from carpal tunnel syndrome because:

The palmar cutaneous branch may be involved and nocturnal symptoms are less prominent.

Initial treatment consists of:

Activity modification, therapy, nerve-gliding exercises, and temporary splinting, while persistent symptoms or progressive motor weakness may require:

Surgical decompression of the median nerve at all potential proximal forearm compression sites.

Orthopaedic Surgery - Prepatellar Bursitis

Basics

Prepatellar bursitis is inflammation or distention of the:

Prepatellar bursa

located directly anterior to the patella.

Bursae are small, fluid-containing sacs positioned between tissues that move against one another. Their purpose is to:

Reduce friction

and facilitate smooth movement.

The bursal lining consists of synovial tissue that both:

Produces

and

Resorbs fluid.

Classification

Prepatellar bursitis may be classified as:

Traumatic

Septic

Inflammatory

Traumatic Bursitis

Traumatic bursitis may result from:

A direct blow

or

Repeated low-grade pressure and microtrauma.

Septic Bursitis

Septic bursitis results from:

Infection of the prepatellar bursa.

This may follow:

Skin abrasion

Puncture wound

Direct inoculation

or occasionally spread from surrounding tissue.

Inflammatory Bursitis

The bursa may become inflamed in association with systemic or crystal-related disease such as:

Gout

Rheumatoid arthritis

and, much less commonly,

Tuberculosis

or other chronic inflammatory/infectious disorders.

Synonyms

Common historical names include:

Housemaid’s knee

Carpenter’s knee

Carpet-layer’s knee

These terms reflect the association with repeated:

Kneeling.

Epidemiology

Prepatellar bursitis is:

Common.

It is especially frequent in:

Middle-aged and older adults

and in individuals whose work or activities require prolonged kneeling.

Both sexes may be affected.

Risk Factors

The principal risk factor is:

Repeated pressure or trauma over the anterior knee.

High-risk activities include occupations involving:

Frequent kneeling

Crawling

Direct pressure on the kneecap

Examples include:

Flooring work

Carpentry

Carpet laying

Household cleaning

Genetics

There is no known Mendelian inheritance pattern.

Etiology

Common causes include:

Acute direct trauma

and

Repetitive minor trauma.

Acute Trauma

A direct injury such as:

A fall onto the knee

or

Motor vehicle trauma

may produce hemorrhage and inflammation within the bursa.

Repetitive Microtrauma

Repeated kneeling may irritate the synovial lining and lead to:

Chronic fluid accumulation

Synovial thickening

and sometimes

Fibrosis.

Diagnosis

Diagnosis is primarily based on:

History

Physical examination

and, when infection is suspected,

Bursal aspiration.

Signs and Symptoms

Typical findings include:

Anterior knee swelling

Pain

Tenderness

and sometimes

Erythema.

Pain

Pain is often worsened by:

Kneeling

Direct pressure over the patella

and

Knee movement when the enlarged bursa is compressed.

Swelling

The characteristic finding is a:

Visible, localized swelling directly over the patella.

The swelling is typically:

Extra-articular

rather than representing a true knee-joint effusion.

Erythema and Warmth

Redness and increased warmth may occur in both inflammatory and septic bursitis.

Marked:

Erythema

Tenderness

Warmth

or systemic symptoms should increase concern for:

Infection.

Physical Examination

The affected knee should be compared with the:

Contralateral side.

Bursa Examination

Assess:

Size of swelling

Tenderness

Fluctuance

Skin integrity

Warmth

Erythema

Joint Effusion

Determine whether there is an associated:

Intra-articular effusion.

In isolated prepatellar bursitis, the swelling remains primarily:

Anterior to the patella.

Extensor Mechanism

Palpate the:

Quadriceps tendon

Patella

Patellar tendon

and confirm active:

Knee extension.

This helps exclude associated:

Patellar fracture

Quadriceps tendon rupture

Patellar tendon rupture.

Patellar Tenderness

Direct bony tenderness over the patella should raise concern for:

Fracture

or another osseous abnormality.

Range of Motion

Knee motion may be mildly limited because of:

Pain or mechanical pressure from the enlarged bursa.

Marked pain with passive range of motion is less typical and should raise concern for:

Septic arthritis or another intra-articular process.

Laboratory Tests

Routine laboratory studies are not required in every uncomplicated traumatic case.

If infection is suspected, useful tests may include:

Complete blood count

ESR

CRP

Bursal Aspiration

When septic bursitis is suspected, aspirated fluid should be sent for:

Cell count with differential

Gram stain

Culture and sensitivity

Crystal analysis

Crystal Analysis

Crystal examination may identify:

Monosodium urate crystals

or

Calcium pyrophosphate crystals

suggesting:

Gout

or

CPPD.

Imaging

Plain Radiographs

AP and lateral knee radiographs may be obtained when there is concern for:

Fracture

Foreign body

Calcification

Underlying bony abnormality

or another intra-articular disorder.

Radiographs are often normal in isolated bursitis.

Ultrasound

Ultrasound may help demonstrate:

Fluid within the prepatellar bursa

and can assist with:

Needle aspiration

when the anatomy is difficult or the collection is small.

Pathological Findings

In septic prepatellar bursitis, the most common causative organism is:

Staphylococcus aureus.

Other gram-positive organisms, particularly:

Streptococcal species

may also be responsible.

Differential Diagnosis

Important alternatives include:

Septic arthritis

Cellulitis

Patellar fracture

Intra-articular effusion

Inflammatory arthritis

Crystal arthropathy

Traumatic hematoma

Septic Arthritis

Septic arthritis usually produces:

Severe pain with passive joint motion

Marked restriction of motion

and often a:

True intra-articular effusion.

This distinction is clinically important because septic arthritis requires urgent treatment.

Cellulitis

Cellulitis may produce:

Diffuse erythema

Warmth

Tenderness

without a clearly defined fluctuant bursal collection.

Treatment

General Principles

Treatment depends on whether the bursitis is:

Traumatic

Inflammatory

or

Septic.

Traumatic or Aseptic Bursitis

Initial management generally includes:

Activity modification

Avoidance of kneeling

Compression

Ice or heat for comfort

NSAIDs when appropriate

Immobilization

A knee immobilizer may be used temporarily when pain is substantial.

Prolonged immobilization should generally be avoided because it can lead to:

Knee stiffness

and

Quadriceps weakness.

Spontaneous Resolution

Many traumatic cases improve with:

Conservative treatment alone.

Aspiration in Aseptic Bursitis

Aspiration may be considered for a very large or symptomatic bursa, but repeated aspiration should be avoided when possible because it increases the risk of:

Infection

and

Chronic drainage.

Septic Bursitis

When infection is suspected:

Aspirate the bursa before antibiotics when clinically feasible

and obtain appropriate cultures.

Antibiotic Therapy

Empiric treatment should cover common gram-positive organisms, particularly:

Staphylococcus aureus

while awaiting culture results.

The antibiotic route and setting depend on:

Severity

Systemic illness

Comorbidities

Local infection extent.

Not every septic bursitis case requires parenteral therapy; clinically stable patients may sometimes be managed with appropriate oral antibiotics and close follow-up.

Hospital Admission

Hospitalization and intravenous antibiotics are appropriate when there is:

Systemic toxicity

Rapidly progressive infection

Ascending lymphangitis

Immunocompromise

or inability to manage safely as an outpatient.

Incision and Drainage

Operative drainage may be required when there is:

Persistent purulent collection

Failure to improve with aspiration and antibiotics

Loculated infection

or

Chronic draining infection.

Physical Therapy

Formal therapy is not routinely required in uncomplicated cases.

It may be useful after prolonged symptoms or immobilization to restore:

Knee range of motion

Quadriceps strength

Normal gait.

Medication

NSAIDs

NSAIDs may be used for:

Pain

and

Inflammation

in traumatic or noninfectious bursitis.

Analgesics

Acetaminophen or other analgesics may be used when NSAIDs are inappropriate.

Antibiotics

Antibiotics are indicated for:

Septic bursitis.

Definitive therapy should be adjusted according to:

Culture and susceptibility results.

Surgery

Surgical excision or bursectomy is uncommon.

It may be considered for:

Chronic recurrent bursitis

Persistent fibrotic or thickened bursa

Painful nodular synovial thickening

Refractory septic bursitis

Chronic Bursectomy

Patients with longstanding occupational bursitis may occasionally develop:

Fibrosis

Thickened synovium

or

Painful nodules

that fail to respond to conservative treatment.

These may require:

Surgical bursectomy.

Follow-Up

Follow-up should be individualized according to:

Cause

Symptoms

and

Response to treatment.

Septic cases require closer reassessment to ensure:

Clinical improvement

Resolution of erythema

Decreasing swelling

No progression of infection.

Referral

Urgent orthopaedic or hospital evaluation is appropriate for:

Suspected septic arthritis

Progressive septic bursitis

Ascending lymphangitis

Systemic illness

Failure of outpatient treatment.

Prognosis

The prognosis is generally:

Good.

Most traumatic or inflammatory cases improve with:

Activity modification

NSAIDs

Protection from pressure

and time.

Septic Prognosis

Septic bursitis usually responds well when treated promptly with:

Appropriate drainage

and

Antibiotic therapy.

Complications

Infection

A previously sterile bursa may become infected, particularly after:

Repeated aspiration

Skin breakdown

or

Direct contamination.

Chronic Drainage

Repeated procedures or persistent infection may lead to:

A draining sinus

or chronic wound problems.

Recurrence

Continued kneeling or failure to modify the provoking activity may result in:

Recurrent bursitis.

Stiffness

Prolonged immobilization can cause:

Loss of knee motion

and

Quadriceps weakness.

Patient Monitoring

Patients should be monitored for:

Swelling

Pain

Erythema

Warmth

Range of motion

and, in infectious cases,

Signs of systemic spread.

Key Principle

Prepatellar bursitis is inflammation or distention of the bursa directly anterior to the patella, most commonly caused by repetitive kneeling, direct trauma, or infection.

The key clinical distinction is between:

Aseptic traumatic/inflammatory bursitis

and

Septic bursitis.

Most aseptic cases respond to:

Pressure avoidance, symptomatic treatment, and short-term activity modification, whereas suspected septic bursitis requires:

Aspiration, culture-directed antibiotic therapy, and drainage when necessary.

Orthopaedic Surgery - Posteromedial Bow of the Tibia

Basics

Posteromedial bowing of the tibia is a congenital deformity characterized by:

Posterior and medial angulation of the distal tibia

that is apparent at birth.

The affected foot is typically positioned in:

Calcaneovalgus, with excessive dorsiflexion and eversion.

The deformity arises primarily from abnormal curvature of the:

Tibia

rather than from an isolated foot abnormality.

Natural History

In most children, the tibial bow gradually:

Corrects spontaneously during growth.

However, the associated shortening of the affected tibia generally:

Persists

and may increase proportionally as the child grows.

Therefore, while the angular deformity often improves dramatically, the major long-term issue is usually:

Limb-length discrepancy.

Epidemiology

Posteromedial tibial bowing is:

Rare.

It is recognized:

At birth.

Boys and girls appear to be affected:

Approximately equally.

Laterality

The disorder is almost always:

Unilateral.

Risk Factors

No established environmental, maternal, or mechanical risk factors are known.

Genetics

There is no recognized Mendelian inheritance pattern.

Etiology

The exact cause is:

Unknown.

It may represent a congenital disturbance of:

Tibial growth

or asymmetric physeal development.

Growth Disturbance

One proposed mechanism is an intrinsic abnormality of:

Physeal growth

that produces both:

Angular deformity

and

Relative tibial shortening.

Birth Trauma

The disorder is unlikely to be the result of an unrecognized fracture because the limb demonstrates:

Persistent proportional shortening during growth

rather than the typical healing pattern of a traumatic fracture.

Associated Conditions

Posteromedial tibial bowing generally occurs as:

An isolated congenital deformity.

No consistent systemic or syndromic association is recognized.

Diagnosis

Diagnosis is usually straightforward based on:

Appearance at birth

Physical examination

and

Plain radiographs.

Signs and Symptoms

The typical newborn has:

Visible posteromedial bowing of the distal tibia

combined with a:

Calcaneovalgus foot position.

Foot Position

The ankle is usually held in:

Marked dorsiflexion

and the foot in:

Valgus or eversion.

The dorsum of the foot may approach the:

Anterior surface of the leg

in more pronounced cases.

Tibial Bow

The most obvious deformity is usually located in the:

Distal third of the tibia

just proximal to the ankle.

Pain

The condition is:

Painless.

Pain is not expected in an uncomplicated case.

Limb Shortening

The involved leg may already appear:

Shorter below the knee

at birth.

This discrepancy may become progressively more apparent during:

Childhood growth.

History

There is usually no history of:

Birth trauma

Difficult delivery

or

Gestational complication

that explains the deformity.

Physical Examination

A complete examination of both lower extremities should be performed.

Limb Length

Measure and compare:

Femoral length

Tibial length

Overall limb length

The shortening is typically concentrated in the:

Affected tibia.

Foot and Ankle Motion

Assess:

Dorsiflexion

Plantarflexion

Inversion

Eversion

The calcaneovalgus posture is often flexible.

Muscle Function

Confirm active function of:

Dorsiflexors

Plantarflexors

Invertors

Evertors

The surrounding muscles and tendons are generally intact.

Neurologic Examination

A routine neurologic assessment should confirm normal:

Motor function

Sensation

and

Reflexes, when age appropriate.

Laboratory Tests

No laboratory investigations are routinely required.

Imaging

Plain Radiographs

Plain radiographs demonstrate the:

Posteromedial tibial bow

and help exclude other congenital tibial disorders.

Degree of Angulation

The deformity may initially be substantial, with angulation reported up to approximately:

60°.

Bone Appearance

The tibia may appear:

Normally mineralized

or

Thickened.

Unlike congenital pseudarthrosis, there is typically no:

Cystic lesion

Dysplastic segment

or

Pseudarthrosis.

Fibula

The fibula should also be evaluated for:

Length

Shape

and associated deformity.

Pathological Findings

The principal abnormality is:

Bony bowing and thickening of the tibia.

The surrounding:

Muscles

Tendons

Ligaments

and other soft tissues are generally normal.

Muscle Development

The anterolateral musculature may appear:

Relatively underdeveloped

but remains functionally intact.

Differential Diagnosis

Important alternatives include:

Healed or congenital tibial fracture

Fibular hemimelia

Isolated calcaneovalgus foot

Congenital pseudarthrosis of the tibia

Neurofibromatosis-associated tibial dysplasia

Calcaneovalgus Foot

An isolated calcaneovalgus foot may resemble the associated foot position seen with posteromedial tibial bowing.

However, in isolated calcaneovalgus:

The tibial shaft itself is not substantially bowed.

Congenital Pseudarthrosis

Congenital pseudarthrosis of the tibia is an important distinction because it is typically associated with:

Anterolateral bowing

rather than posteromedial bowing.

It may also show:

Tibial dysplasia

Cortical narrowing

Cystic change

and may be associated with:

Neurofibromatosis type 1.

Fibular Hemimelia

Fibular hemimelia may produce:

Limb shortening

Foot deformity

and

Abnormal tibial alignment

but is distinguished by deficiency or absence of the:

Fibula

and frequently by additional foot-ray abnormalities.

Treatment

General Principles

Initial treatment is usually:

Observation.

The angular deformity improves spontaneously in the majority of children as the tibia grows.

Spontaneous Correction

Most of the bowing remodels during early childhood.

A small amount of residual deformity may persist, often approximately:

6–8° or less.

Limb-Length Discrepancy

Unlike the angular deformity, limb shortening generally:

Does not completely correct.

At skeletal maturity, some patients may have a discrepancy of up to approximately:

5 cm, although many have considerably less.

Casting and Bracing

Routine:

Casting

Bracing

and

Stretching

do not substantially accelerate correction of the tibial bow and are therefore usually unnecessary.

Foot Splinting

In unusually severe cases, temporary splinting may help position the foot:

Plantigrade

so that walking and shoe wear are easier.

This is aimed at function rather than changing the natural history of the tibial bow.

Activity

No routine activity restriction is required.

Children can generally participate in:

Normal age-appropriate activities.

Shoe Lift

A:

Heel lift or shoe lift

may improve gait and comfort in children with a clinically important limb-length discrepancy.

Physical Therapy

Routine physical therapy is:

Not usually indicated.

Therapy may be useful only if there is an unusual secondary problem involving:

Motion

Strength

or

Gait.

Surgery

Surgery is directed primarily at:

Limb-length discrepancy

or, less commonly,

Persistent angular deformity.

Contralateral Epiphysiodesis

The most common operative strategy for a predicted moderate limb-length discrepancy is:

Epiphysiodesis of the longer contralateral limb.

This is usually performed:

Near adolescence

after most of the tibial bow has already corrected.

Indications for Limb-Length Equalization

If the predicted discrepancy at skeletal maturity is greater than approximately:

2 cm

surgical equalization may be considered.

The choice depends on:

Magnitude of predicted discrepancy

Remaining growth

Patient preference

and whether the family favors:

Shortening the longer limb

or

Lengthening the shorter limb.

Tibial Lengthening

Patients with a larger discrepancy or those wishing to avoid shortening the opposite leg may undergo:

Tibial lengthening.

This is a substantially more involved treatment than epiphysiodesis.

Corrective Osteotomy

Persistent clinically important angulation is uncommon but may require:

Tibial osteotomy.

This is generally reserved for patients with residual deformity that affects:

Mechanical alignment

Gait

or

Function.

Residual Angulation

Approximately:

5–10% of patients

have been reported to retain enough angular deformity to raise concern for corrective surgery.

Follow-Up

Long-term follow-up is important because:

The bow improves

while

The limb-length discrepancy may progressively increase.

Early Limb-Length Assessment

Formal radiographic assessment of limb length may be obtained by approximately:

5 years of age.

Options include:

Standing long-leg radiographs

or

Scanogram-type measurements.

Growth Prediction

Serial measurements can be plotted over time to estimate:

Expected discrepancy at skeletal maturity.

Posteromedial tibial bowing commonly produces:

Proportionate growth inhibition, so the relative discrepancy may remain fairly predictable.

Prognosis

The overall prognosis is:

Good.

Most children experience substantial spontaneous correction of the:

Angular deformity.

Long-Term Outcome

When clinically significant limb-length discrepancy is appropriately addressed, patients generally have:

Good function

Normal activity

and few long-term sequelae.

Complications

Limb-Length Discrepancy

The principal long-term complication is:

Persistent shortening of the affected tibia.

The discrepancy may increase as the child grows.

Growth Disturbance

The shortening is thought to result from:

Reduced growth of the involved tibial physis

possibly related to the developmental process responsible for the original bowing.

Residual Bowing

A small amount of posteromedial bowing may persist after growth.

In most patients this is:

Mild and asymptomatic.

Gait Asymmetry

A larger untreated limb-length discrepancy may produce:

Pelvic obliquity

Compensatory gait

or functional asymmetry.

Patient Monitoring

Children should be followed periodically during growth with attention to:

Tibial alignment

Limb-length discrepancy

Foot position

Gait

Lower-extremity function

Radiographic measurements are useful for predicting:

Final limb-length inequality

and deciding whether future:

Epiphysiodesis

Lengthening

or, rarely,

Corrective osteotomy

will be necessary.

Key Principle

Posteromedial bowing of the tibia is a rare congenital deformity recognized at birth, usually accompanied by a calcaneovalgus foot.

The tibial bow generally:

Remodels spontaneously with growth, while the associated:

Tibial shortening persists and may progressively increase.

For most children, management consists of:

Observation and serial monitoring of limb length.

Surgery is reserved primarily for:

Clinically important predicted limb-length discrepancy or persistent symptomatic angular deformity.

Orthopaedic Surgery - Posterior Tibial Tendon Rupture

⸻

Basics

Posterior tibial tendon dysfunction (PTTD) is a common cause of adult acquired flatfoot deformity.

Modern terminology increasingly describes the broader deformity as:

Progressive collapsing foot deformity (PCFD)

because the disorder involves not only the posterior tibial tendon but also progressive failure of the:

Medial ligamentous structures

Spring ligament complex

Hindfoot alignment

and eventually, in advanced cases,

Ankle alignment.

Posterior tibial tendon rupture may represent the advanced end of this degenerative process or, less commonly, may occur acutely after trauma.

⸻

Posterior Tibial Tendon Anatomy

The posterior tibialis muscle originates from the:

Posterior tibia

Posterior fibula

and

Interosseous membrane.

The tendon courses:

Posterior and inferior to the medial malleolus

before entering the medial foot.

It passes:

Posterior to the ankle axis

and

Medial to the subtalar joint axis.

⸻

Insertion

The principal insertion is on the:

Navicular tuberosity.

Additional expansions attach to the:

Cuneiforms

and bases of the:

Second

Third

and

Fourth metatarsals.

⸻

Function

The posterior tibial tendon contributes to:

Ankle plantarflexion

Subtalar inversion

Hindfoot stabilization

Support of the medial longitudinal arch

During gait, it helps invert the hindfoot and lock the:

Transverse tarsal joints

during push-off, creating a rigid lever for efficient propulsion.

⸻

Consequences of Dysfunction

When posterior tibial tendon function deteriorates, the medial arch loses an important dynamic stabilizer.

This places increased stress on structures such as the:

Spring ligament

Talonavicular capsule

Medial midfoot ligaments

Over time, these structures may stretch and attenuate, producing:

Progressive arch collapse

Hindfoot valgus

Forefoot abduction

and later

Fixed deformity and arthritis.

⸻

Gait Effect

Posterior tibial tendon insufficiency also reduces the ability of the foot to become a rigid lever during push-off.

This may make the:

Gastrocnemius-soleus complex

less mechanically efficient and contribute to:

Weak or altered gait.

⸻

Acute Rupture

A true acute posterior tibial tendon rupture is uncommon.

When traumatic rupture occurs, patients may develop:

Sudden medial ankle or arch pain

followed by:

Weakness

and progressive flattening of the foot.

⸻

Classification

The traditional Johnson-Strom classification, later modified by Myerson, describes progression from tendon disease to fixed deformity and ankle involvement.

⸻

Stage I

Stage I consists primarily of:

Posterior tibial tendinitis, tenosynovitis, or early tendinosis

without structural flatfoot deformity.

The foot remains:

Normally aligned and flexible.

Typical findings include:

Pain and swelling along the tendon

with possible mild weakness.

⸻

Stage II

Stage II is characterized by:

Flexible acquired flatfoot deformity.

Typical findings include:

Hindfoot valgus

Forefoot abduction

Loss of medial arch height

Posterior tibial weakness

The deformity remains:

Passively correctable.

⸻

Stage II Forefoot Position

As the hindfoot collapses into valgus, the forefoot may appear:

Abducted relative to the hindfoot.

Once the hindfoot is manually corrected, a compensatory:

Forefoot varus or supination

may become apparent.

⸻

Stage III

Stage III represents:

Rigid flatfoot deformity.

There is fixed:

Hindfoot valgus

and/or fixed:

Midfoot abduction and forefoot supination.

The subtalar deformity is:

No longer passively correctable.

Degenerative arthritis may be present in the:

Subtalar

Talonavicular

or

Calcaneocuboid joints.

⸻

Stage IV

Stage IV represents advanced disease with:

Flatfoot deformity plus ankle involvement.

There may be:

Deltoid ligament insufficiency

Valgus tilt of the talus within the ankle mortise

and, in advanced cases,

Ankle arthritis.

⸻

Synonyms

Traditional terms include:

Posterior tibial tendon dysfunction

Posterior tibial tendon insufficiency

Adult acquired flatfoot deformity

Modern terminology increasingly uses:

Progressive collapsing foot deformity.

⸻

Epidemiology

Posterior tibial tendon dysfunction is one of the most common causes of:

Acquired flatfoot in adults.

⸻

Age

It most often affects adults between approximately:

40 and 60 years of age.

Prevalence generally increases with:

Age.

⸻

Sex

The disorder is more commonly reported in:

Middle-aged women.

⸻

Risk Factors

Important risk factors include:

Obesity

Pre-existing pes planus

Diabetes mellitus

Inflammatory arthropathy

Seronegative spondyloarthropathy

Previous ankle trauma

Accessory navicular

⸻

Corticosteroid Injection

Injection of corticosteroid directly around or into the posterior tibial tendon has historically been associated with:

Tendon weakening or rupture.

For this reason, intratendinous corticosteroid injection should generally be avoided.

⸻

Genetics

There is no recognized Mendelian inheritance pattern.

Foot shape and ligamentous characteristics may have hereditary influences, but these do not explain most cases.

⸻

Etiology

Most cases result from:

Chronic degenerative tendinopathy

rather than an acute inflammatory process.

Repeated mechanical overload may produce:

Microtearing

Collagen degeneration

Fibrosis

Tendon elongation

and eventually:

Partial or complete rupture.

⸻

Hypovascular Zone

The segment of the tendon just posterior and distal to the:

Medial malleolus

has relatively limited vascularity.

This may contribute to:

Degeneration

and

Poor healing capacity.

⸻

Mechanical Predisposition

Pre-existing:

Flatfoot

or an:

Accessory navicular

may alter the mechanical demands placed on the tendon and increase susceptibility to degeneration.

⸻

Trauma

Less commonly, rupture may occur after:

Ankle fracture

Ankle sprain

Direct blow

or other traumatic injury.

⸻

Associated Conditions

Progressive hindfoot valgus may lead to secondary shortening or contracture of the:

Gastrocnemius

Soleus

or

Achilles tendon.

This can further worsen deformity by increasing:

Forefoot and midfoot loading.

⸻

Diagnosis

Diagnosis is based on:

History

Standing examination

Functional testing

and

Weight-bearing radiographs.

MRI is useful when the diagnosis or tendon integrity is uncertain.

⸻

Signs and Symptoms

Typical findings include:

Progressive flattening of one foot

Medial ankle pain

Medial arch pain

Swelling around the medial malleolus

Weakness with walking

⸻

Lateral Hindfoot Pain

As deformity progresses, pain may migrate from the medial side to the:

Lateral hindfoot.

This may result from:

Subfibular impingement

or lateral compression between the calcaneus and fibula.

⸻

History

Many patients describe an:

Insidious onset.

Symptoms may begin with:

Medial ankle swelling and pain

followed gradually by:

Flattening of the arch

and increasing deformity.

⸻

Traumatic History

A minority of patients recall a specific:

Ankle injury

or direct traumatic event.

Most cases, however, represent:

Chronic degenerative failure.

⸻

Physical Examination

⸻

Neurovascular Examination

Assess:

Distal pulses

Sensation

Motor function

before focusing on the tendon and deformity.

⸻

Standing Examination

The foot should be examined while the patient is:

Weight bearing.

Assess:

Medial arch height

Hindfoot alignment

Forefoot abduction

Overall symmetry

⸻

Gait

Observe for:

External rotation of the affected foot

Excessive pronation

Hindfoot valgus

Reduced push-off strength

⸻

Posterior Tibial Tendon Strength

The tendon can be tested by asking the patient to:

Plantarflex and invert the foot against resistance

from a position of relative:

Plantarflexion and eversion.

Pain, weakness, or inability to invert suggests:

Posterior tibial tendon dysfunction.

⸻

Tenderness

Tenderness may occur:

Along the tendon posterior to the medial malleolus

or at its insertion on the:

Navicular tuberosity.

⸻

Swelling

Early disease may produce visible swelling along the:

Medial ankle

because of:

Tenosynovitis.

⸻

Too-Many-Toes Sign

When viewed from behind, more toes are visible lateral to the heel on the affected side.

This is the:

Too-many-toes sign.

It reflects:

Forefoot abduction

and progressive collapse through the midfoot.

⸻

Single-Leg Heel-Rise Test

A normal posterior tibial tendon should allow the patient to perform a:

Single-leg heel rise

while the heel moves from valgus into:

Varus.

⸻

Abnormal Heel Rise

Patients with significant PTT dysfunction may demonstrate:

Inability to perform a single-leg heel rise

or

Failure of the heel to invert during heel rise.

Repeated heel rises may reveal weakness before a single attempt becomes impossible.

⸻

Flexibility of Deformity

The examiner should determine whether:

Hindfoot valgus

and

Forefoot abduction

remain manually correctable.

This helps distinguish:

Flexible stage II disease

from

Rigid stage III disease.

⸻

Gastrocnemius Tightness

Assess ankle dorsiflexion with the knee:

Extended

and

Flexed.

A positive:

Silfverskiöld test

may indicate isolated gastrocnemius contracture.

⸻

Laboratory Tests

No laboratory test is required for uncomplicated PTT dysfunction.

Laboratory investigations may be appropriate if there is concern for:

Inflammatory arthritis

Neuropathy

or another systemic disease.

⸻

Imaging

⸻

Weight-Bearing Foot Radiographs

Weight-bearing radiographs are essential for evaluating:

Arch collapse

Forefoot abduction

Talonavicular uncoverage

Hindfoot or midfoot arthritis.

⸻

AP Foot View

The AP view may demonstrate:

Lateral subluxation of the navicular

and

Uncovering of the talar head.

These findings reflect:

Forefoot abduction and talonavicular malalignment.

⸻

Lateral Foot View

The lateral view may show:

Loss of medial longitudinal arch height

Reduced calcaneal pitch

Plantarflexion of the talus

and other signs of collapse.

⸻

Weight-Bearing Ankle Radiographs

Ankle radiographs should be obtained when advanced disease is suspected.

They assess:

Ankle alignment

Degenerative change

and

Valgus talar tilt.

⸻

Stage IV Imaging

A mortise view may demonstrate:

Valgus tilt of the talus

resulting from:

Deltoid ligament insufficiency.

⸻

MRI

MRI is helpful when:

The diagnosis is uncertain

Tendon rupture is suspected

or

Surgical planning requires assessment of tendon quality.

⸻

MRI Findings

The posterior tibial tendon may show:

Thickening

Hypertrophy

Longitudinal splitting

Increased signal

Attenuation

or

Complete rupture.

MRI may also identify associated injury to the:

Spring ligament

and other medial stabilizers.

⸻

Ultrasound

Diagnostic ultrasound can also evaluate:

Tenosynovitis

Tendon degeneration

Partial tearing

Dynamic tendon continuity

although accuracy depends on operator experience.

⸻

Pathological Findings

Early disease may demonstrate:

Tenosynovitis.

With progression, the tendon develops:

Tendinosis

Collagen degeneration

Fibrosis

Elongation

Partial tearing

Continued mechanical loading may ultimately produce:

Complete rupture.

⸻

Differential Diagnosis

Important alternatives include:

Flexible congenital or benign flatfoot

Tarsal tunnel syndrome

Inflammatory hindfoot arthritis

Charcot neuroarthropathy

Accessory navicular syndrome

Deltoid ligament insufficiency

⸻

Benign Flatfoot

A longstanding flexible flatfoot without:

Pain

Progressive deformity

Tendon weakness

is different from acquired PTT dysfunction.

⸻

Tarsal Tunnel Syndrome

Tarsal tunnel syndrome typically produces:

Burning

Paresthesia

Numbness

rather than progressive arch collapse.

⸻

Charcot Arthropathy

Charcot neuroarthropathy should be considered in patients with:

Peripheral neuropathy

Marked swelling

Warmth

Bony fragmentation

or rapidly progressive deformity.

⸻

Treatment

⸻

General Principles

Treatment depends on:

Stage

Flexibility of the deformity

Pain

Functional demands

Presence of arthritis

⸻

Initial Nonoperative Treatment

Early symptomatic disease is initially treated with:

Activity modification

Immobilization

Orthotic support

Physical therapy

NSAIDs when appropriate

⸻

Immobilization

A:

Walking boot

Cast

or

Ankle brace

may be used temporarily until acute pain and swelling improve.

⸻

Assistive Devices

A:

Cane

or other walking aid may reduce loading during painful periods.

⸻

Orthoses

Once acute pain subsides, patients may transition to:

Semirigid arch-supporting orthoses.

These aim to support the:

Medial longitudinal arch

and reduce strain on the posterior tibial tendon.

⸻

Ankle-Foot Orthosis

More advanced flexible deformity may require an:

Ankle-foot orthosis (AFO)

to control:

Hindfoot valgus

and

Midfoot collapse.

⸻

Physical Therapy

Physical therapy may include:

Posterior tibial and invertor strengthening

Calf stretching

Ankle and foot mobility exercises

Proprioceptive training

Gait retraining

⸻

Gastrocnemius Stretching

Because calf tightness may worsen deformity, stretching of the:

Gastrocnemius-soleus complex

is often emphasized.

⸻

Ultrasound Therapy

Therapeutic ultrasound has historically been used, but the core evidence-based components of rehabilitation are:

Strengthening

Stretching

Load modification

Mechanical support.

⸻

Medication

NSAIDs may be used for:

Short-term pain relief

particularly when tenosynovitis is present.

They do not reverse:

Tendon degeneration or structural deformity.

⸻

Surgery

Surgery is considered for:

Persistent pain

Progressive deformity

Functional limitation

or

Failure of appropriate nonoperative care.

The procedure is selected according to:

Stage and deformity pattern.

⸻

Stage I Surgery

Persistent stage I disease may be treated with:

Tenosynovectomy

or debridement of diseased tendon.

Selected cases may require:

Tendon reconstruction or transfer

if significant tendon degeneration is present.

A calcaneal osteotomy is not routinely required when foot alignment remains normal.

⸻

Flexor Digitorum Longus Transfer

The:

Flexor digitorum longus (FDL)

may be transferred to augment deficient posterior tibial tendon function.

It is commonly attached near the:

Navicular.

Because tendon transfer alone does not correct the underlying deformity, it is usually combined with:

Bony realignment procedures.

⸻

Stage II Surgery

Flexible stage II deformity frequently requires a combination of procedures.

Common components include:

FDL tendon transfer

Medializing calcaneal osteotomy

and correction of additional deformity as needed.

⸻

Medializing Calcaneal Osteotomy

A medial displacement calcaneal osteotomy shifts the heel:

Medially beneath the leg.

This reduces:

Hindfoot valgus

and decreases the mechanical load on the medial reconstruction.

⸻

Lateral Column Lengthening

Marked forefoot abduction may require:

Lateral column lengthening

to improve coverage of the talar head and restore:

Midfoot alignment.

Modern reconstruction generally favors osteotomy rather than routine lateral column arthrodesis in flexible disease.

⸻

Medial Column Correction

Residual forefoot supination may require:

Plantarflexion osteotomy of the medial cuneiform

often termed a:

Cotton osteotomy.

⸻

First Tarsometatarsal Arthrodesis

When there is instability or arthritis at the:

First tarsometatarsal joint

fusion may be used to stabilize the medial column.

⸻

Gastrocnemius Recession or Achilles Lengthening

An associated equinus contracture may require:

Gastrocnemius recession

or

Achilles tendon lengthening.

The choice depends on whether tightness is isolated to the gastrocnemius or involves the entire:

Gastrocnemius-soleus complex.

⸻

Stage III Surgery

Rigid deformity with established hindfoot arthritis generally requires:

Arthrodesis.

Traditional treatment has included:

Triple arthrodesis

involving the:

Subtalar

Talonavicular

and

Calcaneocuboid joints.

Modern surgery may selectively fuse only the symptomatic arthritic joints when appropriate.

⸻

Stage IV Surgery

Stage IV treatment depends on:

Ankle arthritis

Flexibility

Deltoid ligament competence

and

Overall deformity.

Options may include:

Deltoid reconstruction

Hindfoot reconstruction

Ankle fusion

Total ankle arthroplasty in selected patients

or

Pantalar fusion in severe end-stage disease.

Pantalar arthrodesis is therefore not required for every stage IV deformity.

⸻

Referral

Patients with progressive deformity or suspected tendon rupture may be managed by an orthopaedic surgeon experienced in:

Foot and ankle reconstruction.

Complex stage II-IV disease is often referred to an:

Orthopaedic foot and ankle specialist.

⸻

Follow-Up

Patients undergoing nonoperative treatment should be reassessed for:

Pain

Swelling

Arch collapse

Hindfoot alignment

Heel-rise ability

Progression of deformity.

⸻

Prognosis

Early disease can often be controlled with:

Bracing

Orthoses

Activity modification

and

Rehabilitation.

This may be especially effective in:

Older or lower-demand patients.

⸻

Progression

If the deformity remains unsupported and continues to progress, patients may develop:

Rigid hindfoot collapse

Subfibular impingement

Hindfoot arthritis

and eventually

Ankle valgus and arthritis.

⸻

Surgical Prognosis

Appropriately selected reconstructive procedures generally provide:

Substantial pain relief

Improved alignment

Better walking function

and high patient satisfaction.

Outcome depends on:

Disease stage

Deformity severity

Presence of arthritis

Patient comorbidities.

⸻

Complications

⸻

Persistent Weakness

Even after treatment, some patients may have residual:

Inversion weakness

or reduced push-off strength.

⸻

Recurrent Deformity

Progressive ligamentous failure or inadequate correction may result in:

Recurrent hindfoot valgus

Recurrent arch collapse

⸻

Arthritis

Longstanding deformity may lead to progressive:

Subtalar

Talonavicular

Midfoot

and eventually

Ankle arthritis.

⸻

Surgical Complications

Depending on the procedure, complications may include:

Nonunion

Malunion

Wound problems

Nerve injury

Hardware irritation

Overcorrection or undercorrection

⸻

Patient Monitoring

Patients are typically reassessed every:

Several months during active treatment

until symptoms and function stabilize.

Monitoring should focus on:

Pain

Alignment

Foot flexibility

Single-leg heel-rise ability

Response to orthoses or bracing

Radiographic progression when indicated.

⸻

Key Principle

Posterior tibial tendon dysfunction is a major cause of progressive acquired flatfoot in adults, but the deformity reflects failure of the entire medial stabilizing complex rather than the tendon alone.

The characteristic progression is from:

Medial tendon pain and tenosynovitis

to

Flexible hindfoot valgus and forefoot abduction

and ultimately to

Rigid deformity, arthritis, and possible ankle valgus.

Early disease is usually treated with:

Immobilization, orthoses, strengthening, and calf stretching, whereas progressive symptomatic deformity may require:

Stage-specific tendon reconstruction, osteotomy, or arthrodesis.

Orthopaedic Surgery - Posterior Interosseous Nerve Entrapment

Basics

Posterior interosseous nerve syndrome (PINS) is a compressive neuropathy involving the:

Posterior interosseous nerve (PIN)

which is the predominantly motor branch of the radial nerve supplying many of the finger and thumb extensor muscles.

The syndrome produces:

Motor weakness without sensory loss.

The related condition known as:

Radial tunnel syndrome (RTS)

is considered separately.

RTS is characterized primarily by:

Pain over the proximal lateral forearm

without the motor weakness typical of PINS.

The diagnosis of radial tunnel syndrome remains somewhat controversial because objective electrodiagnostic abnormalities are often absent.

Anatomy

The posterior interosseous nerve arises from the:

Deep branch of the radial nerve.

It passes through the proximal forearm and enters the:

Supinator muscle.

During this course, it may be compressed at several potential anatomical sites.

Arcade of Frohse

The most common site of compression is the:

Fibrous proximal edge of the superficial head of the supinator

known as the:

Arcade of Frohse.

Other Potential Compression Sites

Additional sites include:

Fibrous bands near the radiocapitellar joint

Fibrous tissue over the radial head

Radial recurrent vessels, known as the leash of Henry

Medial or fibrous edge of the extensor carpi radialis brevis

Distal margin of the supinator

Compression may also result from:

Ganglion cyst

Lipoma

Tumor

or another space-occupying lesion.

Posterior Interosseous Nerve Syndrome Versus Radial Tunnel Syndrome

The distinction is important.

Posterior interosseous nerve syndrome primarily produces:

Motor weakness.

Radial tunnel syndrome primarily produces:

Pain without objective motor weakness.

Neither usually produces cutaneous sensory loss because the superficial sensory branch of the radial nerve travels separately.

Epidemiology

PINS is uncommon.

It most frequently occurs in individuals between approximately:

20 and 50 years of age.

The true incidence is uncertain and may be underestimated because mild cases can be missed or attributed to other causes.

Risk Factors

Risk may increase with repetitive activities involving:

Forearm supination

Powerful gripping

Repetitive wrist or finger extension

Occupational and athletic repetitive-loading activities may therefore contribute.

Genetics

There is no known Mendelian inheritance pattern.

Etiology

The most common mechanism is:

Mechanical compression of the posterior interosseous nerve.

Compression may occur spontaneously or secondary to:

Repetitive mechanical stress

Inflammatory tissue

Fibrous bands

Vascular structures

Mass lesions

Associated Conditions

PINS or radial tunnel symptoms may coexist with:

Lateral epicondylitis

Radial tunnel syndrome

Rheumatoid arthritis

Systemic lupus erythematosus

Inflammatory synovitis around the proximal radioulnar region may increase local nerve compression.

Diagnosis

Diagnosis is based primarily on:

History

Motor examination

Anatomic localization

and, when needed,

Electrodiagnostic testing or imaging.

Signs and Symptoms

The hallmark of PINS is:

Weakness of finger and thumb extension without sensory loss.

Onset

Weakness may develop:

Spontaneously

without an obvious traumatic event.

Finger Extension Weakness

Patients may have difficulty extending the:

MCP joints of the fingers.

Because the interphalangeal joints can still extend through intrinsic muscle function, the deficit may be most apparent at the:

MCP joints.

Thumb Extension Weakness

Weakness may affect:

Thumb extension

and sometimes:

Thumb abduction through the extensor mechanism.

Wrist Extension

Wrist extension is usually preserved because:

Extensor carpi radialis longus

is innervated proximal to the PIN.

However, the wrist may extend with:

Radial deviation

because the ulnar-sided wrist extensor, extensor carpi ulnaris, is PIN-innervated and may be weak.

Pain

Prominent aching or radiating pain is more suggestive of:

Radial tunnel syndrome

than pure PINS.

Sensory Symptoms

Numbness and cutaneous sensory loss are usually:

Absent

in both PINS and radial tunnel syndrome.

The superficial radial sensory nerve does not travel through the same deep motor tunnel.

Physical Examination

A complete neurovascular examination of the upper limb should be performed.

Motor Examination

Assess PIN-innervated muscle function, particularly:

Finger MCP extension

Thumb extension

Thumb retropulsion

Wrist extension pattern

Weakness in these functions supports:

Posterior interosseous neuropathy.

Wrist Extension Pattern

Preserved wrist extension with:

Radial deviation

is characteristic because extensor carpi radialis longus remains functional while more distal PIN-innervated extensors are impaired.

Sensory Examination

Sensation over the:

Forearm

Dorsal radial hand

and

Digits

should remain normal in isolated PINS.

Sensory loss suggests another diagnosis or a more proximal radial nerve lesion.

Tenodesis Effect

Passive wrist flexion normally causes finger extension through the:

Tenodesis effect.

Preservation of passive tenodesis despite inability to actively extend the fingers supports a:

Neurologic deficit

rather than rupture of the extensor tendons.

Radial Tunnel Tenderness

In radial tunnel syndrome, maximal tenderness is usually located approximately:

3–5 cm distal to the lateral epicondyle.

This is more distal than the tenderness typically seen with:

Lateral epicondylitis.

Resisted Supination

Pain reproduced by:

Resisted forearm supination

may support radial tunnel syndrome.

Resisted Middle-Finger Extension

Pain produced by resisting extension of the:

Middle finger

has historically been described as a provocative maneuver for radial tunnel syndrome.

However, this test is not highly specific and should not be interpreted in isolation.

Lateral Epicondylitis Comparison

Lateral epicondylitis typically produces maximal tenderness:

Directly over or just distal to the lateral epicondyle

rather than farther down the radial tunnel.

Diagnostic Injection

A local anesthetic injection into the radial tunnel may occasionally help distinguish:

Radial tunnel pain

from other sources such as:

Lateral epicondylitis.

Interpretation should be cautious because local anesthetic can spread to adjacent structures.

Laboratory Tests

Routine laboratory studies are not helpful for isolated PINS.

Tests may be obtained only when an associated inflammatory or systemic disorder is suspected.

Imaging

Plain Radiographs

Radiographs are not routinely required.

They may be useful when there is concern for:

Fracture

Arthritis

Bony deformity

or another osseous source of compression.

MRI

MRI may be useful when there is suspicion of:

Ganglion cyst

Tumor

Lipoma

Synovitis

or another space-occupying lesion.

It may also demonstrate denervation changes in affected muscles.

Ultrasound

High-resolution ultrasound may also identify:

Nerve enlargement

Compression

Ganglion cyst

or other superficial masses.

Dynamic examination can occasionally assist with localization.

Electrodiagnostic Studies

Electromyography and nerve-conduction studies are useful for:

Confirming PINS

Localizing the lesion

Estimating severity

Assessing denervation

They can also help exclude:

Cervical radiculopathy

Brachial plexopathy

More proximal radial neuropathy

Radial Tunnel Syndrome and EMG

Electrodiagnostic studies are often:

Normal or nonspecific

in radial tunnel syndrome because the condition is primarily a pain syndrome without major axonal injury.

Pathological Findings

At surgical exploration, the PIN may show compression most commonly at:

The arcade of Frohse.

Nerve Appearance

Chronic compression may produce:

Flattening

Focal constriction

Swelling proximal to the compression

or a:

Pseudoneuroma.

Differential Diagnosis

Important alternatives include:

Lateral epicondylitis

Cervical radiculopathy

Neuralgic amyotrophy

Extensor tendon rupture

Superficial radial sensory nerve entrapment

More proximal radial nerve palsy

Lateral Epicondylitis

Lateral epicondylitis typically causes:

Pain directly over the lateral epicondyle

with pain during resisted:

Wrist extension

but does not cause PIN-pattern motor weakness.

Cervical Radiculopathy

Cervical radiculopathy may cause:

Neck pain

Radiating arm pain

Sensory abnormalities

Weakness involving several muscle groups

The distribution depends on the involved cervical nerve root.

Neuralgic Amyotrophy

Neuralgic amyotrophy, or:

Parsonage–Turner syndrome

may mimic a focal motor neuropathy.

It often begins with:

Severe acute shoulder or arm pain

followed days or weeks later by:

Weakness and muscle wasting.

Superficial Radial Nerve Entrapment

Entrapment of the superficial radial sensory nerve is known as:

Wartenberg syndrome

or

Cheiralgia paresthetica.

It produces:

Pain

Burning

Numbness

over the dorsoradial aspect of the hand without motor weakness.

Treatment

General Principles

Initial management is usually:

Nonoperative

unless there is:

Progressive motor weakness

A compressive mass

or another structural lesion requiring treatment.

Activity Modification

Repetitive activities involving:

Supination

Forceful gripping

Repetitive forearm rotation

should be reduced when they reproduce symptoms.

Rest

Temporary avoidance of the suspected causative activity may permit recovery in mild compressive neuropathy.

Splinting

If no clear cause is identified or symptoms are aggravated by motion, temporary immobilization using an:

Elbow or forearm splint

may be considered.

Prolonged immobilization should be avoided because it can lead to stiffness.

Physical and Occupational Therapy

Therapy should begin as soon as it is safe after the acute symptoms settle.

An experienced:

Hand therapist

can assist with:

Range of motion

Nerve protection

Gradual strengthening

Activity modification

Ergonomic changes

Strengthening

Progressive strengthening should begin only after:

Pain is controlled

and

Nerve recovery is evident.

Medication

NSAIDs may be used for:

Short-term pain and inflammation control, particularly when radial tunnel pain or surrounding inflammation is present.

They do not reverse established motor denervation.

Surgical Indications

Surgical decompression should be considered when there is:

Progressive motor weakness

A definite structural compressive lesion

Failure of appropriate conservative treatment

or

No evidence of spontaneous neurologic recovery.

Timing of Surgery

Older protocols suggested considering surgery when there was no spontaneous recovery by approximately:

3 months

after symptom onset despite at least:

6 weeks of conservative management.

Modern timing is individualized according to:

Severity

Electrodiagnostic findings

Rate of progression

Presence of a mass lesion

Surgical Decompression

Surgery consists of exploration and decompression of the:

Posterior interosseous nerve

along its course through the proximal forearm.

Structures Released

Potential constricting structures include:

Arcade of Frohse

Fibrous bands around the radial head

Leash of Henry

Extensor carpi radialis brevis edge

Supinator muscle

Arcade of Frohse Release

The most important component is often release of the:

Fibrous proximal supinator edge.

Vascular Compression

Radial recurrent vessels of the:

Leash of Henry

may be ligated or mobilized if they are clearly compressing the nerve.

Severe Nerve Injury

Rarely, severe focal nerve damage may require:

Excision of a nonviable segment

followed by:

Direct repair

or

Nerve grafting.

Tendon Transfer

If nerve recovery fails and useful motor function cannot be restored, late reconstruction may require:

Tendon transfer procedures

to restore:

Finger extension

Thumb extension

and other lost functions.

Radial Tunnel Syndrome Surgery

Surgical decompression for radial tunnel syndrome remains more controversial than surgery for objective PINS.

Published success rates have varied widely, historically from approximately:

40–95%.

Patient selection is therefore important.

Follow-Up

After conservative or operative treatment, activity is resumed:

Gradually.

Repetitive gripping and supination should be limited initially and increased only as symptoms permit.

Prognosis

The prognosis after decompression for true PINS is generally:

Good.

Motor recovery can be slow because axonal regeneration occurs gradually.

Time to Recovery

Recovery may continue for:

Many months

and in severe cases may take:

Several years.

Older series reported continued improvement for approximately:

2–4 years.

Nonoperative Prognosis

Patients with mild compressive neuropathy may recover with:

Activity modification

Splinting

Therapy

and observation.

Radial Tunnel Syndrome Prognosis

The outcome of radial tunnel syndrome is less predictable because:

Diagnostic criteria remain controversial

and objective nerve dysfunction is usually absent.

There are no strong comparative data establishing superiority of surgery over nonoperative treatment in all cases.

Complications

Recurrence

Symptoms may recur after either:

Conservative treatment

or

Surgical decompression.

Iatrogenic Nerve Injury

Direct injury to the PIN during decompression is:

Rare

but potentially serious.

It may worsen:

Finger and thumb extension weakness.

Persistent Weakness

Incomplete nerve recovery may result in:

Residual motor deficit

Muscle atrophy

Functional impairment

Scar and Adhesion

Postoperative scar formation may occasionally contribute to:

Recurrent compression

or tethering of the nerve.

Patient Monitoring

Patients should be followed periodically, often at approximately:

3-month intervals

until neurologic recovery stabilizes.

Monitoring should include:

Finger extension strength

Thumb extension strength

Wrist extension pattern

Muscle bulk

Pain

Electrodiagnostic recovery when indicated

Key Principle

Posterior interosseous nerve syndrome is a motor neuropathy caused by compression of the deep radial nerve, most commonly at the arcade of Frohse.

The characteristic presentation is:

Weakness of finger and thumb extension with preserved sensation and often preserved wrist extension in radial deviation.

This should be distinguished from:

Radial tunnel syndrome, which primarily causes lateral proximal forearm pain without objective motor weakness.

Most mild cases begin with:

Activity modification and rehabilitation, whereas progressive motor deficit, structural compression, or failure of recovery may require:

Surgical decompression of the posterior interosseous nerve.

Orthopaedic Surgery - Posterior Cruciate Ligament Injury

Basics

Posterior cruciate ligament (PCL) injury involves disruption of the ligament that serves as the primary restraint to:

Posterior translation of the tibia relative to the femur.

The PCL also contributes to:

Rotational stability

and overall stability of the knee, particularly at higher degrees of flexion.

Classification

PCL injuries are commonly graded according to the amount of posterior tibial translation observed during the:

Posterior drawer test.

Grade I

The tibial plateau remains:

Anterior to the femoral condyles

despite increased posterior translation.

This generally represents a:

Partial or lower-grade injury.

Grade II

The anterior surface of the tibial plateau becomes approximately:

Level with the femoral condyles.

This reflects greater posterior laxity.

Grade III

The tibial plateau translates:

Posterior to the femoral condyles.

A grade III injury suggests major PCL insufficiency and should raise concern for associated injury to structures such as the:

Posterolateral corner

or other knee ligaments.

Epidemiology

PCL injuries occur most commonly in:

Young active adults.

Historically, males have been affected more frequently than females, reflecting greater exposure to:

Collision sports

and

High-energy trauma.

Associated Ligament Injuries

PCL tears frequently occur together with other knee injuries rather than in isolation.

Associated injuries may involve the:

Anterior cruciate ligament

Medial collateral ligament

Posterolateral corner

Menisci

Articular cartilage

Common Causes

Typical settings include:

Sports-related trauma

and

Motor vehicle collisions.

Incidence

PCL injury is substantially less common than:

ACL injury

and is relatively uncommon outside athletic or high-energy traumatic settings.

Risk Factors

Important risk factors include:

Motor vehicle collision

Collision sports

Direct anterior tibial trauma

Knee hyperflexion

Hyperextension injury

Genetics

There is no recognized Mendelian inheritance pattern for traumatic PCL injury.

Etiology

The classic mechanism is a:

Direct blow to the anterior proximal tibia while the knee is flexed.

This forces the tibia:

Posteriorly relative to the femur.

Dashboard Injury

A classic example occurs during a motor vehicle collision when the flexed knee strikes the:

Dashboard.

The resulting posteriorly directed force on the tibia can rupture the PCL.

Sports Mechanism

In sports, injury may occur when an athlete falls onto a:

Flexed knee with the foot plantarflexed.

The tibial tubercle or anterior proximal tibia strikes the ground and drives the tibia posteriorly.

Hyperflexion

PCL rupture can also occur through:

Extreme knee flexion

without a direct blow.

This mechanism may tension the ligament beyond its structural capacity.

Hyperextension

Severe:

Knee hyperextension

may injure the PCL, often together with other capsuloligamentous structures.

Associated Conditions

High-energy PCL injuries may be associated with:

Knee dislocation

and potentially:

Popliteal artery injury.

Because vascular compromise can threaten the limb, neurovascular examination is essential.

Diagnosis

Diagnosis is based on:

Mechanism of injury

Physical examination

and

Imaging.

Signs and Symptoms

Acute symptoms may include:

Knee pain

Swelling

Posterior knee discomfort

Mild to moderate effusion

Absence of a Pop

Unlike many ACL injuries, patients with an isolated PCL tear may not report:

An audible or subjective pop.

Symptoms can initially be less dramatic.

Instability Symptoms

Patients may describe:

Vague unsteadiness

Difficulty with deceleration

Discomfort during loaded knee flexion

rather than obvious recurrent instability.

Chronic PCL Injury

Patients with chronic PCL insufficiency may report:

Anterior knee pain

Posterior knee discomfort

Pain when descending stairs

Pain during deceleration

Giving-way sensations

Anterior Knee Pain

Chronic posterior tibial translation changes knee mechanics and increases loading of the:

Patellofemoral joint

and

Medial compartment.

This can explain anterior or medial knee pain despite the ligament injury being posterior.

Genu Recurvatum

Longstanding combined instability may occasionally produce:

Knee recurvatum

or hyperextension deformity.

This is more suggestive of a broader multiligament injury than an isolated low-grade PCL tear.

Physical Examination

A complete knee and neurovascular examination should be performed.

Neurovascular Examination

Assess:

Distal pulses

Capillary refill

Motor function

Sensation

Particular attention is required after:

High-energy trauma

or suspected:

Knee dislocation.

Posterior Drawer Test

The posterior drawer test is the primary examination maneuver for PCL integrity.

Position the patient:

Supine

with the hip flexed and knee at approximately:

90° of flexion.

The foot is stabilized while the examiner applies:

Posterior force to the proximal tibia.

Posterior Drawer Interpretation

Assess:

Amount of posterior translation

and

Quality of the endpoint.

The injured knee should be compared with the:

Contralateral side.

Excessive posterior translation indicates:

PCL insufficiency.

Posterior Sag Sign

The posterior sag sign evaluates resting posterior displacement of the tibia.

With the patient supine and the:

Hips flexed

Knees flexed approximately 90°

the affected tibia may visibly:

Sag posteriorly relative to the femur.

Loss of the normal anterior tibial step-off supports the diagnosis of:

PCL deficiency.

Quadriceps Active Test

The maneuver in which the patient actively attempts to slide the foot forward while the knee is flexed is more accurately termed the:

Quadriceps active test.

With a PCL-deficient knee, quadriceps contraction pulls the posteriorly subluxated tibia:

Anteriorly.

Visible anterior translation supports the diagnosis.

Lachman Test

The Lachman test should be performed to assess for associated:

ACL injury.

It evaluates anterior tibial translation with the knee flexed approximately:

20–30°.

Varus and Valgus Stress Testing

Collateral ligament stability should be assessed using:

Varus stress

and

Valgus stress.

Posterolateral Corner Evaluation

Grade III PCL laxity should prompt careful assessment of the:

Posterolateral corner.

Tests may include:

Dial test

Varus stress examination

Posterolateral drawer testing

depending on the clinical setting.

Laboratory Tests

No laboratory tests are routinely required for an uncomplicated PCL injury.

Imaging

Plain Radiographs

Initial radiographs generally include:

AP

and

Lateral knee views.

They are useful for identifying:

Associated fractures

Posterior tibial avulsion fracture

Other traumatic abnormalities.

Tibial Avulsion Fracture

The PCL may avulse a fragment from its insertion on the:

Posterior proximal tibia.

This is more readily seen on:

Lateral radiographs

and may alter management.

Stress Radiography

Posterior stress radiographs can objectively quantify:

Posterior tibial translation.

They are especially useful in:

Chronic injury

Surgical planning

Grading severe laxity

MRI

MRI is highly sensitive for identifying:

PCL rupture

and associated injuries involving:

ACL

Menisci

Collateral ligaments

Posterolateral corner

Articular cartilage

Acute Versus Chronic MRI

Acute PCL tears are usually readily visible on MRI.

Chronic PCL injuries can occasionally appear:

Continuous or partially healed on MRI

despite persistent functional laxity.

Therefore, chronic diagnosis should rely on:

Clinical examination and objective laxity, not MRI alone.

Pathological Findings

The PCL may fail through:

Midsubstance rupture

Proximal avulsion

Distal avulsion

or

Bony avulsion from the tibial insertion.

Differential Diagnosis

Important alternatives or associated injuries include:

ACL injury

Tibial plateau fracture

Meniscal tear

Posterolateral corner injury

Multiligament knee injury

Treatment

General Principles

Many isolated PCL tears can initially be treated:

Nonoperatively.

Treatment decisions depend on:

Injury grade

Associated ligament injury

Symptoms

Functional demands

Chronicity

Initial Stabilization

Early treatment may include:

Crutches

Knee immobilizer or brace

Ice

Activity modification

Pain control

Weight Bearing

Patients with isolated injuries may generally progress with:

Protected or partial weight bearing as tolerated

depending on pain and associated injuries.

Early Motion

Once acute symptoms permit, treatment emphasizes:

Early controlled range of motion

and

Muscle strengthening.

Prolonged unnecessary immobilization should be avoided.

Bracing

A brace may be used to reduce posterior tibial sag during healing.

Modern PCL-specific dynamic braces may provide anteriorly directed support to the tibia.

The benefit of routine bracing varies according to:

Injury severity

and

Rehabilitation protocol.

Physical Therapy

Rehabilitation is the cornerstone of nonoperative treatment.

A PCL-specific program emphasizes:

Quadriceps strengthening

Hip and core strengthening

Controlled range of motion

Proprioception

Gradual return to functional activity

Quadriceps Strengthening

The quadriceps help translate the tibia:

Anteriorly

and therefore act as a dynamic stabilizer in a PCL-deficient knee.

Quadriceps rehabilitation is particularly important.

Hamstring Loading

Early aggressive hamstring strengthening is generally avoided because hamstring contraction can:

Pull the tibia posteriorly

and increase stress on the healing PCL.

Hamstring loading is typically introduced progressively later in rehabilitation.

Range of Motion

Early flexion may be limited or controlled according to the:

Severity of injury

Healing phase

and

Associated injuries.

The goal is to restore motion without allowing excessive posterior tibial translation.

Medication

First Line

Pain may be treated with:

NSAIDs

or

Acetaminophen, when appropriate.

Severe Acute Pain

Short-term opioid medication is rarely required but may occasionally be used for:

Severe acute traumatic pain

or

Postoperative pain.

Surgery

Surgery is not required for most isolated low-grade PCL injuries.

Relative Surgical Indications

Operative treatment may be considered for:

Symptomatic grade III PCL injury

Combined posterolateral corner injury

Multiligament knee injury

Associated repairable meniscal or articular injury

Persistent instability or giving way

Activity-related pain despite rehabilitation

Progressive symptomatic degenerative change

Avulsion Fracture

A significantly displaced PCL bony avulsion may be treated with:

Reduction and internal fixation.

Fixation restores the native ligament attachment when the fragment is repairable.

PCL Reconstruction

Ligament reconstruction is generally reserved for patients with:

Persistent symptomatic instability

or

Pain and functional limitation despite appropriate rehabilitation.

Graft Options

Reconstruction may use:

Autograft

or

Allograft.

Arthroscopically Assisted Reconstruction

Modern PCL reconstruction is usually performed with:

Arthroscopic assistance.

These procedures are technically demanding because of the:

Deep posterior tibial insertion

and nearby:

Neurovascular structures.

Reconstruction Techniques

Techniques include:

Transtibial single-bundle reconstruction

Tibial inlay single-bundle reconstruction

Transtibial double-bundle reconstruction

Tibial inlay double-bundle reconstruction

Single- Versus Double-Bundle Reconstruction

The PCL contains functionally important:

Anterolateral

and

Posteromedial bundles.

Single- and double-bundle techniques attempt to restore these stabilizing functions to differing degrees.

The optimal approach depends on:

Surgeon experience

Anatomy

Associated injuries

Multiligament Injury

When PCL injury occurs with:

ACL

MCL

LCL

or

Posterolateral corner injury

the reconstruction strategy must address the entire pattern of instability.

Failure to recognize associated posterolateral instability can lead to:

Persistent laxity

and

Failure of PCL reconstruction.

Follow-Up

Clinical follow-up assesses:

Range of motion

Quadriceps strength

Posterior laxity

Pain

Functional stability

Return to Activity

Return to sport should be based on restoration of:

Full or near-full motion

Adequate quadriceps strength

Functional control

Absence of symptomatic instability

rather than a fixed time point alone.

Prognosis

The prognosis for many isolated PCL injuries is:

Good to excellent.

Most low- and moderate-grade isolated injuries can be treated successfully without surgery.

Chronic Natural History

Some patients tolerate chronic PCL laxity surprisingly well.

However, altered knee biomechanics can gradually increase load in the:

Medial compartment

and

Patellofemoral joint.

Complications

Recurrent Instability

Persistent PCL deficiency may lead to:

Giving way

Difficulty with deceleration

Reduced athletic confidence

Reconstruction Failure

Potential causes include:

Graft failure

Tunnel malposition

Unrecognized associated ligament injury

Poor rehabilitation

Osteoarthritis

Chronic PCL insufficiency may contribute to progressive degeneration, particularly involving the:

Medial compartment

followed by the:

Patellofemoral compartment.

Stiffness

Postoperative or post-traumatic stiffness may occur, particularly after:

Multiligament reconstruction

or prolonged immobilization.

Neurovascular Complications

Because of the PCL’s proximity to the posterior neurovascular structures, operative reconstruction carries a small but important risk of:

Vascular or nerve injury.

Patient Monitoring

Patients may be reassessed periodically, often at:

Several-month intervals during rehabilitation, depending on injury severity.

Monitoring should include:

Range of motion

Quadriceps strength

Posterior drawer laxity

Functional stability

Return to sport or work

Key Principle

The posterior cruciate ligament is the primary restraint to posterior translation of the tibia, and injury classically occurs after a posteriorly directed force to the proximal tibia with the knee flexed, such as a dashboard injury.

Most isolated PCL tears can be managed with:

Nonoperative rehabilitation emphasizing quadriceps strengthening and controlled restoration of motion.

Surgery is primarily reserved for:

Symptomatic high-grade injuries, displaced avulsion fractures, or combined multiligament instability.

Orthopaedic Surgery - Popliteal Cyst in the Child

Basics

A popliteal cyst in a child is a benign, fluid-filled soft-tissue mass located in the:

Posteromedial popliteal fossa behind the knee.

It is usually:

Painless

and is most often an isolated condition rather than a manifestation of significant intra-articular knee disease.

Epidemiology

Popliteal cysts are among the:

Most common soft-tissue masses around the knee in children.

They are typically seen between approximately:

2 and 14 years of age.

Incidence

The frequency tends to:

Decrease after approximately 9 years of age.

Sex

Historical series suggest that childhood popliteal cysts are approximately:

Twice as common in boys as in girls.

Risk Factors

Most cases occur:

In isolation.

Less commonly, a cyst may be associated with chronic inflammatory conditions such as:

Juvenile idiopathic arthritis

or another source of persistent knee synovitis.

Genetics

There is no recognized Mendelian inheritance pattern.

Etiology

Childhood popliteal cysts are thought to arise from a weak area in the:

Posteromedial knee capsule

near the interval between the:

Semimembranosus tendon

and

Medial head of the gastrocnemius.

Unlike adult Baker cysts, pediatric cysts are:

Rarely associated with intra-articular structural abnormalities.

Anatomy

The cyst typically occupies the:

Semimembranosus-gastrocnemius interval.

It contains:

Synovial-like fluid

and may communicate variably with adjacent bursae or the knee joint.

Diagnosis

Diagnosis is usually based on:

History

Physical examination

and, when necessary,

Ultrasound.

Signs and Symptoms

The typical finding is a:

Soft swelling in the posteromedial aspect of the knee.

Location

The mass is usually found between the:

Medial gastrocnemius

and

Semimembranosus/semitendinosus region.

It may appear as a swelling on the:

Medial side of the popliteal fossa.

Symptoms

Most children are:

Asymptomatic.

However, a very large cyst may occasionally cause:

Posterior knee discomfort

Tightness

or

Restriction of knee motion.

Change in Size

The cyst often:

Waxes and wanes in size.

Parents may notice that it becomes more prominent after:

Activity

and less noticeable after rest.

Duration

Many cysts are present for:

Weeks or months

before medical assessment because they are usually painless.

Physical Examination

Inspection

Inspect the affected knee for:

Posteromedial popliteal swelling

and compare with the opposite side.

Palpation

The cyst is generally:

Soft

Compressible

and

Painless.

Tenderness should prompt consideration of another diagnosis.

Knee Examination

The remainder of the knee examination is usually:

Normal.

Assess:

Range of motion

Effusion

Joint-line tenderness

Ligament stability

Gait

Observe the child’s gait.

A typical uncomplicated popliteal cyst should not produce:

A limp.

A persistent limp suggests the need to evaluate for another musculoskeletal problem.

Transillumination

Historically, transillumination has been used to support the diagnosis.

In a darkened room, a strong point light source is placed adjacent to the swelling while the child lies:

Prone.

A fluid-filled cyst may illuminate:

More evenly and brightly

than surrounding solid tissue.

This finding supports a cystic lesion but does not replace imaging when the diagnosis is uncertain.

Laboratory Tests

Routine laboratory studies are:

Not required.

Aspiration

Aspiration is not routinely performed.

If aspirated, typical cyst fluid is:

Clear

and

Gelatinous or viscous.

Abnormal Aspirate

If the fluid is:

Cloudy

Purulent

Bloody in an atypical setting

or otherwise unexpected, further evaluation may include:

Cell count

Gram stain

Culture

to exclude:

Infection

or

Abscess.

Imaging

Plain Radiographs

Plain radiographs are usually:

Optional.

They may be obtained if there is concern for:

Underlying bony abnormality

or another source of knee symptoms.

Ultrasound

Ultrasound is the preferred imaging modality when the diagnosis is uncertain.

It can confirm that the lesion is:

Cystic

and help define its:

Size

Location

Relationship to adjacent structures.

Duplex Ultrasound

Duplex imaging may be especially useful when a vascular lesion is part of the differential diagnosis.

MRI

MRI is rarely needed.

It may be obtained when the lesion is:

Atypical

Solid-appearing

Painful

Rapidly enlarging

or when there is concern for:

Soft-tissue tumor or other deep pathology.

Pathological Findings

The lesion consists of a:

Fluid-filled synovial or bursal sac

within the:

Semimembranosus-gastrocnemius interval.

In children, it is generally not caused by major intra-articular pathology.

Differential Diagnosis

Important alternatives include:

Soft-tissue sarcoma

Vascular malformation or vascular lesion

Soft-tissue abscess

Other cystic or solid popliteal masses

Soft-Tissue Tumor

An enlarging, firm, fixed, painful, or nontransilluminating lesion should raise concern for a:

Solid soft-tissue mass

and warrants appropriate imaging.

Vascular Lesion

A pulsatile lesion or one associated with vascular findings should prompt evaluation for:

Vascular anomaly.

Abscess

An abscess is more likely to be associated with:

Pain

Erythema

Warmth

Fever

or abnormal inflammatory findings.

Treatment

General Principles

Most childhood popliteal cysts require:

No treatment.

Observation is appropriate when the child has:

No pain

Normal knee motion

Normal function

and a secure diagnosis.

Natural History

Approximately:

80% of pediatric popliteal cysts

have historically been reported to resolve spontaneously over:

Months to years.

During this period, the cyst may repeatedly:

Increase and decrease in size.

Activity

Normal activity can usually continue.

If the cyst becomes very large or uncomfortable, temporary activity reduction may be reasonable.

Aspiration

Aspiration is generally:

Not first-line treatment

because recurrence is common.

It may occasionally be considered for a superficial symptomatic cyst after:

Appropriate imaging confirmation.

Post-Aspiration Care

When aspiration is performed, temporary:

Immobilization or compression

may be used after decompression.

However, recurrence remains:

Frequent.

Surgery

Surgical treatment is:

Rarely necessary.

It may be considered when the cyst causes:

Persistent pain

Significant limitation of knee motion

Repeated functional problems

or

Diagnostic uncertainty.

Surgical Excision

Excision is performed through a:

Posterior or posteromedial approach to the popliteal region.

The procedure can often be performed as:

Outpatient surgery.

Postoperative Immobilization

The knee may be immobilized for:

Several weeks

depending on the extent of the procedure and surgeon preference.

Recurrence After Surgery

Surgical excision has a substantial recurrence rate, historically approximately:

20–40%.

This is one reason observation is preferred for uncomplicated lesions.

Follow-Up

Routine long-term follow-up is usually unnecessary when:

Pain is absent

Knee motion is normal

The diagnosis is secure.

Parent Education

Parents should be advised that the cyst may:

Change in size

and often resolves without treatment.

They should return for reassessment if the lesion develops:

Pain

Rapid growth

Firmness

Skin changes

Loss of motion

Limp

or another change in character.

Prognosis

The prognosis is:

Excellent.

Most children remain fully functional and many cysts resolve spontaneously.

Complications

The principal complication of operative treatment is:

Recurrence.

Other surgical complications are uncommon but may include:

Scar problems

Stiffness

Neurovascular injury

Patient Monitoring

No routine surveillance is required in a child who has:

Normal function

No pain

and a stable, typical cyst.

Clinical reassessment is appropriate if symptoms or the characteristics of the mass change.

Key Principle

A popliteal cyst in a child is usually a benign, painless, fluid-filled mass in the posteromedial knee that is rarely associated with significant intra-articular disease.

Most cases should be managed with:

Observation and reassurance.

Because spontaneous resolution is common and surgical recurrence is relatively high, intervention is reserved for:

Persistent symptomatic or diagnostically uncertain lesions.

Orthopaedic Surgery - Popliteal Cyst in the Adult

Basics

A popliteal cyst is a fluid-filled enlargement in the posterior aspect of the knee, usually located within the popliteal fossa.

In adults, it commonly communicates with the:

Knee joint

through a posteromedial capsular opening.

The cyst is usually secondary to an underlying intra-articular disorder that produces:

Excess synovial fluid

and increased intra-articular pressure.

Synonym

A popliteal cyst is also commonly called a:

Baker cyst.

Anatomy

Most adult Baker cysts arise from enlargement of the:

Gastrocnemius-semimembranosus bursa

located between the:

Medial head of the gastrocnemius

and

Semimembranosus tendon.

A communication may develop between this bursa and the knee joint.

One-Way Valve Mechanism

The communication between the knee joint and the bursa may function as a:

One-way valve.

This allows synovial fluid to move from the joint into the cyst but limits its return.

As intra-articular fluid production increases, the cyst may progressively:

Enlarge.

Epidemiology

Popliteal cysts demonstrate a broadly:

Bimodal age distribution.

They occur in:

Children