Orthopaedic Surgery - Discoid Meniscus

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Basics

A discoid meniscus is an abnormally broad, thickened, disc- or pancake-shaped meniscus rather than the normal semilunar structure.

It most commonly involves the lateral meniscus, while medial discoid menisci are much less common.

The condition may produce popping, snapping, locking, or pain during childhood or early adulthood, although many individuals remain asymptomatic.

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Laterality

Approximately 75% of cases are unilateral, while around 25% are bilateral.

Because bilateral involvement is possible, the contralateral knee may also require evaluation if symptoms develop.

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Watanabe Classification

Discoid lateral menisci are traditionally divided into three types according to the Watanabe classification.

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Type 1: Complete

A complete discoid meniscus covers essentially the entire lateral tibial plateau.

The meniscus is markedly wider than normal and forms a nearly complete disc over the lateral compartment.

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Type 2: Incomplete

An incomplete discoid meniscus is larger and broader than a normal meniscus but does not completely cover the lateral tibial plateau.

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Type 3: Wrisberg Variant

The Wrisberg-type discoid meniscus has a thickened posterior horn and lacks the normal posterior meniscotibial attachment to the tibia.

Because of this absent attachment, the meniscus is excessively mobile and unstable.

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Epidemiology

The reported incidence is approximately 3–5% in the United States, although prevalence is considerably higher in some Asian populations and has been reported at more than 20% in Japan.

The true incidence is probably higher than recognized because many affected individuals never develop symptoms.

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Etiology

A discoid meniscus is considered a developmental or anatomic abnormality of the meniscus.

Genetic or familial influences may also contribute, although the exact mechanism remains uncertain.

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Diagnosis

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Clinical Presentation

Presentation varies considerably depending on the type of discoid meniscus, its stability, and whether a tear is present.

Some patients are entirely asymptomatic and the abnormality is discovered incidentally.

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Snapping Knee Syndrome

The classic presentation is the so-called snapping knee syndrome, characterized by a palpable or audible snap or clunk near the terminal limits of knee flexion or extension.

This is particularly associated with the unstable Wrisberg variant.

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Snapping in Other Variants

Snapping may also occur in an otherwise stable discoid meniscus if it becomes torn or develops secondary instability.

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Pain and Mechanical Symptoms

Symptomatic patients may report pain, clicking, popping, swelling, locking, or intermittent inability to fully move the knee.

Mechanical symptoms are especially suggestive of an associated tear or unstable meniscal tissue.

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Onset

Symptoms commonly begin gradually without a specific injury.

When symptoms appear suddenly after trauma, an acute tear of the discoid meniscus should be suspected.

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Physical Examination

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Effusion

A knee joint effusion may be present, particularly when the discoid meniscus has torn.

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Anterolateral Bulge

With the knee in full flexion, a visible or palpable anterolateral bulge may occasionally be present because of the increased meniscal tissue.

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Joint-Line Tenderness

Tenderness may be present along the lateral joint line.

It is often mild in an intact discoid meniscus but may become more pronounced when a tear is present.

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Mechanical Click

A pop or click may be appreciated during meniscal provocative testing, particularly the McMurray maneuver.

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Loss of Extension

Some patients have a mechanical block to full knee extension.

Others may show apprehension or discomfort as the knee approaches complete extension.

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McMurray Test

The McMurray test is performed by taking the knee into maximal flexion, applying rotation, and progressively extending the knee.

A positive test consists of pain, clicking, or popping along the lateral joint line.

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Imaging

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Plain Radiographs

Radiographs are not diagnostic in every case, but AP, lateral, tunnel, and skyline views may reveal secondary skeletal features associated with a discoid lateral meniscus.

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Radiographic Findings

Possible findings include widening of the lateral joint space, lateral joint-line lipping, cupping of the lateral tibial plateau, flattening or squaring of the lateral femoral condyle, hypoplasia of the tibial eminence, and elevation of the fibular head.

These findings may suggest the diagnosis but are not always present.

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MRI

MRI is the preferred imaging study for confirming the morphology of the meniscus and identifying associated tears or instability.

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Sagittal MRI Findings

A discoid meniscus is suggested when continuity between the anterior and posterior horns is visible on three or more consecutive 5-mm sagittal images.

This reflects the abnormal width of the meniscus.

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Coronal MRI Findings

On coronal imaging, the meniscus may demonstrate a broad block-like or bow-tie appearance, with increased meniscal width across the lateral compartment.

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Pathological Findings

The affected meniscus is disc-shaped rather than semilunar.

Histologically, discoid menisci demonstrate reduced collagen content and abnormal orientation of collagen fibers, which may contribute to their increased susceptibility to tearing.

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Stable Variant

A stable discoid meniscus retains normal peripheral and tibial ligamentous attachments.

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Unstable Variant

The unstable variant lacks normal posterolateral meniscotibial attachments, producing excessive mobility of the posterior meniscus.

This is characteristic of the Wrisberg type.

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Differential Diagnosis

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Acute Meniscal Tear

A normal-shaped meniscus with an acute tear can produce similar pain, clicking, locking, and joint-line tenderness.

MRI helps distinguish the underlying anatomy.

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Meniscal Cyst

A meniscal cyst may cause joint-line swelling and pain and is often associated with a meniscal tear.

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Osteochondritis Dissecans

Osteochondritis dissecans may cause knee pain, swelling, catching, or locking and should be considered in younger patients with mechanical symptoms.

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Osteochondral Fracture

An osteochondral fracture can produce acute pain and mechanical blockage, especially after trauma.

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Physeal Fracture

In skeletally immature patients, physeal injury may mimic internal derangement of the knee.

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Tibial Eminence Fracture

A fracture of the tibial eminence can produce pain, swelling, and extension loss and may resemble an ACL-associated injury.

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Anterior Cruciate Ligament Tear

ACL injury may produce swelling, instability, and mechanical symptoms and should be considered particularly after acute trauma.

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Treatment

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General Principles

Many discoid menisci are asymptomatic and require no treatment.

Observation is appropriate when the patient has no pain, locking, swelling, or functional impairment.

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Symptomatic Disease

Patients with persistent pain, locking, swelling, popping, or instability may require surgical treatment.

The operative strategy depends on whether the meniscus is torn and whether it is mechanically stable.

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Nonoperative Treatment

Nonoperative management has a limited role in a persistently symptomatic discoid meniscus.

A short period of immobilization or activity modification may be attempted in patients with acute-onset symptoms, particularly when the diagnosis remains uncertain.

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Return to Activity

Patients may gradually resume normal activities once symptoms have resolved and full motion and function have returned.

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Surgery

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General Surgical Principle

Modern treatment emphasizes preservation of as much functional meniscal tissue as possible.

Total meniscectomy should be avoided whenever feasible because removal of the entire meniscus substantially increases the risk of later osteoarthritis.

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Stable Discoid Meniscus

For a symptomatic stable discoid meniscus, the preferred procedure is arthroscopic partial meniscectomy with saucerization.

Excess central meniscal tissue is removed to recreate a more normal semilunar shape while preserving a stable peripheral rim.

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Meniscal Repair

If a meniscal tear or unstable peripheral attachment is present, repair may be performed at the same time as saucerization.

Preservation of the peripheral meniscus helps maintain normal load transmission across the knee.

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Importance of Meniscal Preservation

Maintaining a functional meniscus allows continued shock absorption, load distribution, and joint stabilization.

This may decrease the risk or delay the development of degenerative osteoarthritis compared with complete meniscectomy.

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Unstable Discoid Meniscus

An unstable meniscus is generally treated with arthroscopic saucerization and stabilization of the remaining peripheral meniscus.

If the posterior attachment is deficient, it may be reattached to create a stable and functional meniscal rim.

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Complete Meniscectomy

Complete meniscectomy is reserved for situations in which the meniscus is not salvageable.

Possible indications include extensive degenerative change, a massive irreparable tear, or severely abnormal meniscal tissue that cannot be reconstructed.

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Follow-Up

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Prognosis

Patients with a stable discoid meniscus generally have good outcomes following appropriately performed saucerization.

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Effect of Age

Younger patients often have better postoperative results than older patients, particularly when the meniscal tissue can be preserved before substantial degenerative change develops.

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Extent of Meniscal Resection

Removal of a larger amount of meniscal tissue is associated with a greater subsequent risk of osteoarthritis.

For this reason, preservation of a stable peripheral rim is preferred whenever technically possible.

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Partial Versus Total Meniscectomy

Partial meniscectomy and saucerization generally produce better clinical and radiographic outcomes than total meniscectomy at both short- and long-term follow-up.

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Complications

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Osteoarthritis

The major long-term complication after excessive meniscal resection is degenerative osteoarthritis of the involved compartment.

This risk is particularly high after complete meniscectomy.

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Recurrent Meniscal Tear

Even after saucerization, the remaining meniscus retains abnormal tissue architecture.

Therefore, the residual discoid meniscus remains more susceptible to future tearing than a normal meniscus.

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Persistent or Recurrent Symptoms

Pain, popping, or locking may recur if residual unstable tissue or a new tear develops.

Repeat arthroscopic evaluation may occasionally be required.

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Patient Monitoring

Patients should be followed until pain, swelling, locking, and mechanical symptoms have resolved and knee motion has returned satisfactorily.

After surgery, follow-up should also assess meniscal stability, range of motion, return to activity, recurrent tearing, and the development of degenerative changes.

Orthopaedic Surgery - Discitis

Basics

Discitis is an infection involving the intervertebral disc space and adjacent vertebral endplates.

The infection may occur through hematogenous spread or after direct inoculation during a spinal procedure.

Although the lower lumbar spine is affected most often, discitis can involve any intervertebral level.

Classification

Discitis may be classified as spontaneous or hematogenous, in which infection reaches the disc through the bloodstream, or iatrogenic, occurring after procedures such as discectomy or discography.

The infecting process may be pyogenic, granulomatous, or, rarely, parasitic.

Pyogenic Infection

Pyogenic discitis is most commonly caused by Staphylococcus aureus.

Other organisms become more important in immunocompromised patients, intravenous drug users, and patients exposed to healthcare-associated infections.

Granulomatous Infection

Granulomatous disc infection may occur with tuberculosis and other chronic infectious processes.

These infections often have a slower course and may cause more extensive adjacent vertebral destruction.

Epidemiology

Hematogenous discitis is uncommon.

The mean age of spontaneous childhood discitis has historically been reported at approximately 7 years, although the condition can occur at any age.

Incidence

The reported incidence of discitis and related spinal infection is approximately 4–24 cases per million people per year.

Risk Factors

Important risk factors include diabetes mellitus, alcohol misuse, organ transplantation, immunosuppression, intravenous drug use, and procedures that enter or approach the disc space.

Examples of iatrogenic risk include discography, discectomy, and spinal procedures.

Etiology

The causative organism varies according to age and host factors.

Staphylococcal species are the most common pathogens in routine pyogenic infection.

In compromised hosts and intravenous drug users, gram-negative aerobic organisms and fungal pathogens such as Candida become more important.

Kingella kingae

In young children, particularly between approximately 6 months and 4 years of age, Kingella kingae is an important cause of osteoarticular infection and may be responsible for discitis.

Pediatric Vascularity

Young children are particularly susceptible because the disc and adjacent endplate region have a richer blood supply than in adults.

Until approximately 8 years of age, vessels may cross the cartilaginous endplate from the adjacent vertebral body, facilitating hematogenous spread into the disc region.

Associated Conditions

Discitis may coexist with or progress into vertebral osteomyelitis.

In advanced disease, the distinction between disc infection and adjacent vertebral infection may become less clear because both structures can be involved.

Diagnosis

General Principles

The diagnosis is established through a combination of clinical findings, laboratory studies, and imaging.

No single test is sufficient in every case.

Signs and Symptoms

The most common symptom is back pain, usually insidious in onset and progressively worsening.

Children may present less specifically, with abdominal pain, reduced appetite, irritability, malaise, or refusal to walk.

Back Stiffness

Spinal stiffness is common.

Patients may avoid flexing the spine because movement increases pain.

Refusal to Walk

Young children may refuse to stand, walk, or sit normally even when they cannot clearly localize their pain.

This can be an important presenting feature.

Pain With Spinal Percussion

Tenderness or pain with percussion over the affected spinal level may be present.

Loss of Lordosis

Lumbar discitis may cause flattening of the normal lumbar lordosis because of protective muscle spasm.

Fever

Fever is often low grade and may be absent.

The lack of fever does not exclude discitis.

Physical Examination

Lumbar Alignment

The examiner should determine whether normal lumbar lordosis is maintained or reduced.

Loss of lordosis may reflect pain and paraspinal muscle spasm.

Forward Flexion

Patients may have pain or refuse to bend forward.

This is often one of the most useful functional signs during examination.

Paraspinal Percussion

Gentle percussion over the spine may reproduce focal pain.

Abdominal Examination

Lumbar discitis can occasionally present with abdominal pain.

The abdomen should therefore be palpated, particularly in children with poorly localized symptoms.

Neurologic Examination

The neurologic examination is usually normal.

Neurologic deficits are more concerning for advanced infection, epidural involvement, abscess, or neural compression.

Laboratory Tests

White Blood Cell Count

The white blood cell count may be mildly elevated but can remain normal.

A normal count therefore does not exclude infection.

ESR and C-Reactive Protein

The erythrocyte sedimentation rate and C-reactive protein are commonly elevated, but the rise may be modest.

Either marker can occasionally be normal, particularly early in the disease course.

Blood Cultures

Blood cultures should be obtained when discitis is suspected.

However, they are positive in fewer than approximately 30% of cases in some series.

Biopsy

Direct biopsy with microbiologic analysis provides the most definitive method of identifying the causative organism.

Biopsy is particularly useful in immunocompromised patients, atypical infections, or cases that fail to respond to empiric treatment.

Imaging

Plain Radiographs

Plain radiographs are often normal early in the disease.

Abnormalities may not become visible until several weeks after symptoms begin.

Radiographic Findings

Later findings include disc-space narrowing, irregularity of the vertebral endplates, and mild adjacent osseous destruction.

MRI

MRI is the preferred imaging modality for suspected discitis because it can demonstrate infection before changes become visible on radiographs.

It provides excellent anatomic detail of the disc, endplates, vertebral marrow, epidural space, and surrounding soft tissues.

Bone Scan

Bone scintigraphy can be used when MRI is unavailable or contraindicated.

However, degenerative changes may cause false-positive findings, and MRI generally provides superior anatomic information.

FDG-PET

FDG-PET may help distinguish spinal infection from degenerative abnormalities in selected cases.

Its use is generally reserved for situations in which conventional imaging is inconclusive.

Pathological Findings

Discitis produces chronic inflammatory change with destruction of the intervertebral disc and adjacent endplates.

As infection progresses, the distinction between discitis and vertebral osteomyelitis may become less pronounced.

Differential Diagnosis

Tuberculous Spondylodiscitis

Tuberculosis should be considered, particularly when there is extensive vertebral body destruction, paraspinal involvement, or a more indolent clinical course.

Tuberculous disease often produces greater bony destruction than routine pyogenic discitis.

Vertebral Osteomyelitis

Vertebral osteomyelitis primarily affects the bone, whereas discitis begins in the disc and adjacent endplates.

In practice, the two processes frequently overlap.

Treatment

General Principles

Treatment usually consists of appropriate antibiotic therapy for approximately 6–8 weeks.

Surgery is reserved for selected patients with neurologic compression, severe pain, major bone destruction, abscess requiring drainage, instability, or failure of medical treatment.

Rest

Relative rest may be helpful during the painful early phase.

Immobilization

A brace may be used when pain is significant or when additional support is needed.

Prolonged unnecessary immobilization should be avoided once symptoms begin to improve.

Antibiotic Therapy

Antibiotics should target the most likely organism initially and then be adjusted if culture results identify a specific pathogen.

The route of therapy depends on illness severity and patient age.

Childhood Spontaneous Discitis

In otherwise healthy children with typical spontaneous discitis, empiric treatment directed against common pathogens is often successful.

Routine biopsy or operative debridement is not always required when the clinical picture is classic and the child responds appropriately.

Intravenous Versus Oral Therapy

Severely ill patients generally require intravenous antibiotics initially.

Mildly affected patients may be treated orally in selected circumstances, with close follow-up.

Compromised Host

In immunocompromised patients or those with atypical risk factors, biopsy and drainage are more strongly indicated because unusual organisms are more likely.

Physical Therapy

Physical therapy is generally not required during the acute painful phase.

In adults with persistent stiffness after infection control has begun, therapy may help restore spinal mobility, strength, and function.

Medication

Routine Antibiotic Coverage

Historically, agents such as oxacillin, dicloxacillin, or cephalosporins have been used for susceptible staphylococcal infection.

Current empiric therapy should reflect local resistance patterns and patient-specific risk factors.

MRSA Coverage

Because methicillin-resistant Staphylococcus aureus (MRSA) is an important pathogen in both hospital and community settings, vancomycin or another appropriate anti-MRSA agent may be required, particularly in severe cases.

Broad-Spectrum Coverage

Complicated infections and infections in compromised hosts may require broader coverage against gram-negative and anaerobic organisms, depending on the clinical scenario.

Pain Control

NSAIDs or short-term mild opioid analgesics may be used for severe pain during the acute phase until the infection comes under control.

Surgery

Indications for Biopsy

Biopsy is especially appropriate in the immunocompromised patient, the patient with atypical infection, or the patient who fails to improve with empiric medical therapy.

Biopsy Approach

Biopsy can be performed through an anterolateral or posterolateral route with imaging guidance.

Percutaneous image-guided techniques are commonly used when feasible.

Drainage and Debridement

Patients who fail to improve with medical treatment or who develop abscess, neurologic compression, or substantial tissue destruction may require surgical drainage and debridement.

Anterior Approach

An anterior approach may provide direct access to the involved disc space and vertebral endplates for decompression and debridement in selected cases.

Reconstruction

Adults with extensive destruction of the disc space or vertebral endplates may require spinal reconstruction to restore stability and alignment.

Minimally Invasive Techniques

Endoscopic or minimally invasive discectomy and drainage may be used in selected adults.

These techniques are less commonly required in children.

Follow-Up

Prognosis

The overall prognosis is generally good once the infection is successfully eradicated.

Children usually recover particularly well.

Childhood Outcome

After childhood discitis, the vertebrae adjacent to the infected disc may undergo spontaneous, painless fusion.

This usually does not cause major long-term functional problems.

Adult Outcome

In adults, spontaneous fusion is less reliable.

Residual chronic back pain or stiffness may persist even after the infection has resolved.

Complications

Persistent Infection

Failure to improve clinically within approximately 1–2 weeks should raise concern for an incorrect organism, inadequate antimicrobial coverage, abscess formation, resistant infection, or the need for debridement.

Neurologic Complications

Although uncommon, advanced infection can cause epidural extension, neural compression, or neurologic deficit.

These findings require urgent evaluation.

Structural Destruction

Severe infection can produce substantial endplate and vertebral destruction, resulting in deformity or instability.

Patient Monitoring

Clinical examination is one of the most useful methods for following recovery.

The examiner should monitor pain, tenderness to percussion, spinal flexibility, gait, and general function.

Laboratory and Radiographic Follow-Up

ESR and radiographic changes often lag behind clinical improvement.

Persistent radiographic abnormalities do not necessarily indicate treatment failure if symptoms and inflammatory markers are improving.

MRI or repeat imaging should be reserved for patients whose clinical course is atypical or worsening.

Orthopaedic Surgery - Developmental Dysplasia of the Hip

Basics

Developmental dysplasia of the hip (DDH) describes a spectrum of abnormal development and instability of the hip joint, ranging from mild acetabular dysplasia and subluxation to complete dislocation of the femoral head.

The femoral head tends to migrate superolaterally, while the acetabulum becomes progressively shallow and deformed.

Most abnormalities develop in utero, although instability may occasionally evolve during early infancy.

Clinical Presentation Across Age Groups

DDH is usually identified during routine newborn or early-childhood screening.

Occasionally, a mild subluxation or acetabular dysplasia is missed during infancy and first becomes apparent during adolescence or early adulthood because of limping, activity-related discomfort, or hip pain.

Classification by Severity

The condition may be classified according to the degree of hip instability.

A subluxable hip is normally reduced but can be partially displaced from the acetabulum with gentle provocative pressure and spontaneously returns to its reduced position.

A dislocatable hip can be completely displaced from the acetabulum during examination and subsequently reduced.

A dislocated hip remains outside the acetabulum at rest and requires a specific reduction maneuver to relocate the femoral head.

Barlow and Ortolani Findings

The Barlow maneuver assesses whether a located hip can be displaced posteriorly from the acetabulum.

A clearly dislocatable hip represents a positive Barlow test.

The Ortolani maneuver assesses whether an already dislocated hip can be reduced into the acetabulum.

A palpable reduction clunk represents a positive Ortolani sign.

Synonyms

Older terminology includes congenital dislocation of the hip, although developmental dysplasia of the hip is preferred because the disorder includes a much broader spectrum than complete congenital dislocation.

Other terms include hip dysplasia and unstable hip.

General Prevention

There is no reliable method for preventing DDH completely.

The most important strategy is early detection, because treatment becomes more difficult and the risk of complications increases as the child gets older.

Children born to parents with hip dysplasia should be examined particularly carefully.

Epidemiology

Females are affected approximately four times more often than males.

This difference is thought to relate partly to greater ligamentous laxity and hormonal influences.

Incidence

When all degrees of neonatal hip instability are included, DDH occurs in approximately 1 in 200 births.

Complete dislocation is less common, occurring in roughly 1 in 1,000 births.

Risk Factors

Important risk factors include breech presentation, first-born status, female sex, oligohydramnios, and a positive family history.

Connective-tissue disorders associated with ligamentous laxity, such as Ehlers–Danlos syndrome and Marfan syndrome, may also increase risk.

Breech Presentation

Breech positioning is one of the strongest recognized risk factors.

The position increases hamstring tension and alters the mechanical forces acting across the developing hip.

First-Born Status

First-born infants may have less available intrauterine space because of greater uterine and abdominal wall tone, increasing the effect of mechanical constraint.

Oligohydramnios

Reduced amniotic fluid limits fetal movement.

Persistent hip adduction can direct the femoral head toward the edge of the acetabulum and interfere with normal acetabular development.

Genetics

A positive family history substantially increases risk, but DDH does not follow a simple established Mendelian inheritance pattern.

The disorder is generally considered multifactorial, with both genetic susceptibility and mechanical factors contributing.

Etiology

DDH is thought to result from unfavorable mechanical forces acting on a susceptible hip during fetal development.

Persistent adduction or abnormal positioning of the femoral head reduces normal concentric contact between the femoral head and acetabulum.

Because normal acetabular development depends on the femoral head remaining well centered, prolonged displacement leads to increasing dysplasia.

Severity and Timing

The earlier abnormal mechanical forces develop during gestation, the more severe the resulting hip dysplasia may be.

Severe early displacement can result in substantial deformity of both the femoral head and acetabulum.

Ligamentous Laxity

Generalized ligamentous laxity can increase hip instability.

This may partly explain the greater frequency in females and the tendency for DDH to cluster within families.

Postnatal Factors

Postnatal positioning can also influence hip stability.

Persistent adduction, a contralateral abduction contracture, or tight swaddling with the hips extended and adducted may interfere with spontaneous stabilization.

Associated Conditions

DDH may occur with other so-called packaging disorders caused by limited intrauterine space.

These include muscular torticollis and metatarsus adductus.

Syndromic Associations

Hip dysplasia may also be seen in genetic disorders, particularly connective-tissue diseases and skeletal dysplasias.

The presence of associated congenital abnormalities should increase clinical suspicion.

Diagnosis

Signs and Symptoms in Infancy

Infants with DDH are usually asymptomatic.

The diagnosis during the first months of life depends primarily on careful physical examination and, when indicated, imaging.

Hip Instability

The most important early finding is a palpable clunk as the femoral head moves out of or back into the acetabulum during the Barlow or Ortolani maneuver.

This should be distinguished from a benign soft-tissue click.

Hip Position

The affected hip may rest in slight adduction.

A deeper proximal thigh crease can sometimes be present, although skin-crease asymmetry alone is neither sensitive nor specific.

Limited Abduction

Reduced hip abduction is an important finding.

The affected hip may abduct less than approximately 50–60°, depending on age and examination technique.

Parents may first notice this limitation while changing diapers.

Hip Click

An isolated hip click without a true clunk is usually nonspecific.

Clicks may arise from the fascia lata, synovial folds, or even structures around the knee and may occur in completely normal infants.

Loss of Instability Clunk With Age

By approximately 6 months of age, the classic Barlow and Ortolani signs may disappear because a chronic dislocation becomes more fixed.

At this stage, limited abduction becomes increasingly important diagnostically.

Walking Development

A child with DDH may begin walking at the expected age or only slightly later.

Therefore, normal timing of walking does not exclude hip dysplasia.

Findings After Walking Age

Once walking begins, asymmetry may become more obvious.

The affected thigh may appear smaller, proximal thigh creases may become more pronounced, and leg-length discrepancy may be evident.

Toe Walking

A child with unilateral dislocation may appear to toe walk on the affected side as compensation for limb shortening.

Trendelenburg Gait

Weakness of the hip abductor mechanism can produce a Trendelenburg limp.

When the child stands on the affected side, the pelvis drops on the opposite side because the displaced hip provides a poor mechanical lever arm for the abductors.

Bilateral DDH

When both hips are dislocated, limb-length asymmetry may be less obvious.

The child may instead develop a waddling gait and increased lumbar lordosis.

Pain

Pain is generally absent during childhood.

Symptoms usually appear only after secondary cartilage degeneration and osteoarthritis develop, potentially beginning in late adolescence but often much later.

Physical Examination

Hip Abduction

Hip abduction should be assessed carefully in every infant.

Asymmetric or restricted abduction is one of the most useful clinical signs of DDH across age groups.

Barlow Test

The infant should be warm, calm, and relaxed.

With one hip examined at a time, the hip is flexed and gently adducted while posteriorly directed pressure is applied through the knee or thigh.

A positive test occurs when the femoral head can be partially or completely displaced from the acetabulum.

Ortolani Test

After the Barlow maneuver, the hip is gently abducted while the examiner lifts the greater trochanter anteriorly.

A palpable clunk as the femoral head reduces into the acetabulum indicates a positive Ortolani sign.

Examination Technique

The examination should be gentle.

Forceful manipulation should be avoided because aggressive testing can cause discomfort and makes the infant less relaxed, reducing examination reliability.

Galeazzi or Allis Sign

With the infant supine, hips and knees are flexed and the feet placed symmetrically.

A difference in knee height indicates apparent femoral shortening and suggests unilateral hip dislocation.

This is known as the Galeazzi or Allis sign.

Gait Examination

Walking children should be observed for limping, Trendelenburg gait, toe walking, waddling, and excessive lumbar lordosis.

Imaging

Ultrasound

Ultrasound is the preferred imaging modality during the first several months of life, before sufficient ossification of the femoral head makes radiographs more informative.

It is particularly indicated when the physical examination is abnormal or important risk factors are present.

Timing of Ultrasound

Ultrasound is most useful during the first approximately 6 months of life.

Interpretation requires experience because neonatal hip anatomy is largely cartilaginous.

Plain Radiographs

Plain radiographs become increasingly useful after approximately 4–6 months, as the femoral head and acetabulum become more readily evaluated radiographically.

Radiographic Assessment

Radiographs should assess both the shape of the acetabulum and the position of the proximal femur relative to it.

Acetabular shallowness, lateral migration, and proximal displacement may all be present.

Shenton Line

The Shenton line is a curved line formed by the medial femoral neck and the superior pubic ramus.

In a normally located hip it forms a smooth continuous arc.

Disruption suggests displacement of the proximal femur.

Femoral Head Position

The proximal femoral epiphysis should lie medial to the outer margin of the acetabulum.

Lateral or superior displacement supports the diagnosis of subluxation or dislocation.

Arthrography

Arthrography can be used during reduction procedures to define the cartilaginous femoral head, acetabulum, and structures that may block reduction.

A small residual space between the femoral head and acetabulum following reduction suggests a better-quality reduction.

CT and MRI

CT and MRI have limited roles in routine screening and diagnosis.

They may be useful in selected cases, particularly after reduction when clarification of hip position is necessary or when complex anatomy must be assessed.

Pathological Findings

Acetabular Changes

The acetabulum becomes shallow and flattened, particularly posterosuperiorly, when the femoral head is not concentrically reduced.

Femoral Head Changes

The femoral head may become flattened anteriorly, and femoral anteversion may increase.

These abnormalities become more pronounced with longstanding displacement.

Degenerative Changes

Chronic dysplasia causes abnormal joint loading.

Cartilage degeneration and secondary osteoarthritis can develop beginning in the second decade of life or later.

Differential Diagnosis

Benign Soft-Tissue Click

A simple hip or knee click caused by fascia or synovial tissue should not be confused with a true instability clunk.

Neuromuscular Hip Dysplasia

Children with cerebral palsy or spina bifida may develop hip subluxation or dislocation because of abnormal muscle forces.

This is a different mechanism from classic developmental dysplasia.

Congenital Femoral Abnormalities

Congenital femoral shortening and coxa vara can produce limb-length discrepancy or altered gait while the femoral head remains located within the acetabulum.

Treatment

General Principles

The goal of treatment is to obtain and maintain a concentrically reduced hip early enough to permit normal development of the acetabulum and proximal femur.

Earlier treatment is generally easier, safer, and more successful.

Early Reduction

When a true dislocation is identified in early infancy, reduction should be achieved promptly, ideally within the first several weeks of life.

Delay allows soft tissues to contract and acetabular deformity to progress.

Treatment by Age

Management varies substantially according to the child’s age and the severity and stability of the hip.

Newborn Management

Mild Instability

A newborn with a mild click or transient subluxability may initially undergo serial examinations, because some unstable neonatal hips stabilize spontaneously during the first days or weeks of life.

A true dislocation or persistent instability requires treatment.

Birth to 6 Months

Pavlik Harness

Persistent instability or a dislocated hip in a young infant is commonly treated with a Pavlik harness or similar dynamic abduction brace.

The harness holds the hips flexed and abducted while allowing controlled movement.

Hip Position

Hip flexion is usually maintained beyond approximately 90°, while excessive forced abduction is avoided.

The goal is to guide the femoral head gently into the acetabulum without compromising its blood supply.

Specialist Supervision

Pavlik harness treatment should be supervised by an orthopaedic surgeon experienced in pediatric hip disorders.

Improper positioning can cause complications.

Confirmation of Reduction

The hip should become reduced within the first few weeks of harness treatment.

Reduction is confirmed using ultrasound or appropriate radiographic imaging.

If the hip remains unreduced, prolonged ineffective harness treatment should be avoided.

Duration of Bracing

The brace is typically worn full-time until the hip becomes clinically and radiographically stable.

It may then be used part-time until acetabular development has normalized sufficiently.

After 6 Months

Closed or Open Reduction

After approximately 6 months of age, treatment frequently requires closed reduction under anesthesia, with open reduction performed when a stable concentric reduction cannot be achieved.

Spica Casting

Following successful reduction, the hip is usually maintained in a hip spica cast for a period of several months.

Age 6–24 Months

Traction

Some surgeons historically use a period of skin traction before reduction to gradually stretch contracted soft tissues.

Its use varies by treatment protocol.

Reduction

Closed reduction is attempted when feasible.

If soft-tissue structures prevent stable reduction, an open procedure is required.

Post-Reduction Immobilization

After reduction, the hip may be maintained in a spica cast for approximately 3–6 months, with cast changes and imaging as required.

Older Than 24 Months

Open Reduction

Older children more commonly require open reduction because the capsule, muscles, and intra-articular structures have become contracted and dysplastic.

Femoral Osteotomy

A femoral osteotomy may be performed to shorten, derotate, or realign the proximal femur.

Shortening can decrease excessive pressure on the reduced femoral head and may reduce the risk of avascular necrosis.

Pelvic Osteotomy

An iliac or other pelvic osteotomy may be needed to improve acetabular coverage of the femoral head.

The choice depends on age and the specific acetabular deformity.

Adductor Tenotomy

An adductor tenotomy may be performed when tight adductor muscles limit the safe range of hip abduction after reduction.

The goal is to enlarge the stable zone in which the hip remains reduced without excessive pressure.

Age and Surgical Outcome

The results of surgical reduction generally become less predictable as the child gets older.

Nevertheless, reduction may still provide worthwhile functional improvement in selected children up to approximately 6–8 years of age.

Physical Therapy

Routine physical therapy is usually limited.

Young children generally regain strength and hip motion naturally after reduction and immobilization.

Therapy may be used selectively when stiffness, weakness, or gait abnormalities persist.

Follow-Up

Long-Term Surveillance

Children treated for DDH require follow-up until skeletal maturity.

Even after successful reduction, acetabular and femoral development may remain abnormal.

Residual Dysplasia

Approximately 10–25% of successfully reduced hips may fail to remodel completely.

Persistent acetabular or proximal femoral dysplasia may eventually require an osteotomy.

Prognosis

Early Treatment

When DDH is identified and treated successfully during infancy, the hip may develop nearly normally and long-term function can be excellent.

Untreated Complete Dislocation

Untreated complete dislocation results in abnormal hip mechanics and usually produces a permanent waddling or Trendelenburg gait.

Pain and degenerative change frequently develop by approximately 30–50 years of age, sometimes earlier.

Subluxated Hip

A persistently subluxated hip may develop symptomatic osteoarthritis earlier than a completely dislocated hip because the remaining articular surface is exposed to highly concentrated abnormal loading.

Complications

Femoral Nerve Palsy

Excessive hip flexion in a Pavlik harness can produce transient femoral nerve palsy.

Historically, this has been reported in approximately 2.5% of treated infants.

Redislocation

Redislocation may occur after reduction, with reported rates around 5%.

Stable maintenance of reduction and careful follow-up are therefore important.

Residual Dysplasia

Residual acetabular dysplasia may persist despite successful reduction.

Historical rates have been reported around 25%, depending on age and treatment method.

Avascular Necrosis

Avascular necrosis of the proximal femoral epiphysis is one of the most serious complications of treatment.

It may occur if blood supply to the femoral head is compromised by excessive positioning, forceful reduction, or other treatment-related factors.

Historical rates have been approximately 10%, although incidence varies substantially by technique and severity.

Consequences of Avascular Necrosis

Growth disturbance following AVN can produce femoral head deformity, shortening, altered neck-shaft relationship, joint incongruity, and later degenerative arthritis.

Once established, these changes may not be fully reversible.

Patient Monitoring

Patients require regular examination and imaging after treatment to ensure that the hip remains reduced and the acetabulum continues to develop normally.

Monitoring should include hip range of motion, limb length, gait, acetabular development, femoral head growth, and signs of avascular necrosis or recurrent instability.

Because incomplete remodeling may not become apparent until later childhood, surveillance should continue through skeletal maturity.

Orthopaedic Surgery - Denosumab

Basics

Denosumab is a fully human IgG2 monoclonal antibody directed against receptor activator of nuclear factor-kappa B ligand (RANKL).

By binding RANKL, denosumab prevents activation of the RANK receptor on osteoclast precursors and mature osteoclasts. This inhibits osteoclast formation, activity, and survival, thereby reducing osteoclast-mediated bone resorption.

Indications

Denosumab is used in disorders associated with excessive osteoclast activity or increased bone turnover.

Important indications include metastatic bone disease, multiple myeloma, postmenopausal osteoporosis, and giant cell tumor of bone.

Giant Cell Tumor of Bone

In giant cell tumor of bone, denosumab may be considered when the lesion is unresectable, metastatic, or when tumor reduction may facilitate a less morbid operation and preservation of bone or an adjacent joint.

Its therapeutic effect is related to inhibition of the RANK/RANKL pathway that is central to formation of the osteoclast-like giant cells within these tumors.

Treatment

Dosing for Giant Cell Tumor and Malignant Bone Disease

For giant cell tumor of bone and selected oncologic indications, denosumab is commonly administered at 120 mg subcutaneously every 4 weeks.

Additional loading doses may be given on days 8 and 15 during the first month of therapy.

Osteoporosis Treatment

Denosumab is also used at a lower cumulative dose for osteoporosis.

The exact regimen depends on the indication and formulation, and treatment should follow the appropriate prescribing protocol for osteoporosis rather than the higher-dose oncologic regimen.

General Measures

Activity

Denosumab itself does not usually require restriction of routine physical activity.

Activity limitations, when present, are generally related to the underlying skeletal disease, fracture risk, or associated treatment rather than to the drug alone.

Dental Procedures

Invasive dental procedures should ideally be addressed before therapy begins whenever feasible.

Elective dental extractions and other procedures involving substantial manipulation of the jaw should be approached cautiously during treatment because of the risk of osteonecrosis of the jaw.

Mechanism of Action

RANKL is required for normal development and activation of osteoclasts.

Denosumab binds RANKL and prevents interaction with the RANK receptor, resulting in a marked decrease in osteoclast-mediated bone turnover.

Unlike bisphosphonates, denosumab does not become permanently incorporated into bone, so its pharmacologic effects diminish after treatment is discontinued.

Complications

Osteonecrosis of the Jaw

One of the most important complications is osteonecrosis of the jaw (ONJ).

The risk generally increases with greater cumulative exposure and is higher in patients receiving high-dose treatment for malignancy.

Risk Factors for Osteonecrosis of the Jaw

Factors associated with greater ONJ risk include longer treatment duration, multiple myeloma, corticosteroid use, diabetes mellitus, antiangiogenic therapy, poor oral hygiene, and invasive dental procedures such as tooth extraction.

Preventive dental care before starting treatment is therefore important.

Dental Evaluation

Patients should undergo an appropriate dental examination before denosumab is initiated, particularly when high-dose oncologic therapy is planned.

Active dental infection or necessary invasive dental treatment should be addressed when possible before exposure.

Atypical Femoral Fracture

Long-term suppression of bone turnover may rarely be associated with atypical femoral fractures.

These fractures may occur in the subtrochanteric region or femoral shaft, extending from just below the lesser trochanter toward the supracondylar region.

Prodromal Femoral Pain

Patients may experience thigh, groin, or hip pain with weight-bearing before an atypical fracture becomes complete.

New unexplained pain in these locations should prompt evaluation for a stress reaction or incomplete fracture.

Reversibility

The antiresorptive effects of denosumab are reversible after treatment is stopped.

Bone turnover can rise substantially after discontinuation, so cessation or interruption of therapy should be planned carefully according to the underlying indication and subsequent osteoporosis or oncologic management.

Hypocalcemia

Denosumab can lower serum calcium because of reduced osteoclastic release of calcium from bone.

Hypocalcemia may be particularly important in patients with renal impairment, vitamin D deficiency, or other disturbances of calcium metabolism.

Patient Monitoring

Dental Examination

A dental assessment should be performed before therapy when clinically appropriate.

During treatment, patients should maintain good oral hygiene and report persistent dental pain, exposed bone, or delayed healing following dental procedures.

Serum Calcium

Serum calcium should be checked before and during treatment.

Calcium and vitamin D supplementation should be provided when indicated to reduce the risk of treatment-associated hypocalcemia.

Symptoms of Hypocalcemia

Patients should be educated about symptoms suggesting low serum calcium.

These may include muscle spasms, twitching, numbness or tingling around the mouth or fingers, facial twitching, and seizures in severe cases.

Monitoring for Stress Fracture

Patients should report new thigh or groin pain during weight-bearing.

When symptoms are suspicious, imaging should be obtained to assess for an incomplete or atypical femoral stress fracture.

Pregnancy

Denosumab should not be used during pregnancy.

Patients with reproductive potential should receive counseling regarding pregnancy avoidance during therapy and for the appropriate period after treatment according to the prescribed regimen.

Patient Teaching

Patients should understand the important warning symptoms associated with therapy, particularly those of hypocalcemia, jaw osteonecrosis, and atypical femoral fracture.

Good dental hygiene, appropriate calcium and vitamin D intake, and prompt reporting of new skeletal pain are important components of treatment.

Frequently Asked Questions

How Long Can Denosumab Be Used?

Treatment duration depends on the underlying indication, fracture or oncologic risk, treatment response, and adverse effects.

Long-term therapy requires periodic reassessment.

Unlike some bisphosphonate regimens, denosumab should not be stopped casually or followed by an unsupervised drug holiday, because rapid rebound in bone turnover can occur after discontinuation.

Can a Patient Become Pregnant While Taking Denosumab?

No. Denosumab is not approved for use during pregnancy.

Patients with reproductive potential should avoid conception during treatment and follow the recommended post-treatment contraception interval.

What Is an Important Contraindication?

Pre-existing hypocalcemia is a major contraindication to starting denosumab.

Serum calcium abnormalities should be corrected before treatment is initiated.

Orthopaedic Surgery - De Quervain (Radial Styloid) Tenosynovitis

Basics

De Quervain tenosynovitis, also called radial styloid tenosynovitis, is a stenosing disorder involving the first dorsal extensor compartment of the wrist.

This compartment contains the abductor pollicis longus (APL) and extensor pollicis brevis (EPB) tendons.

Patients typically complain of pain and tenderness over the radial side of the wrist, particularly near the radial styloid.

Epidemiology

De Quervain tenosynovitis can occur in either sex and at almost any age, but it is especially common in middle-aged women.

Among working-age adults, the reported incidence is approximately 1.3% in women and 0.5% in men.

Risk Factors

Important risk factors include female sex, middle age, repetitive wrist use, and repetitive thumb motion.

The condition is also frequently seen in new mothers, often because of the repetitive wrist and thumb positions used while lifting and caring for an infant.

Etiology

The disorder is generally considered more of a tendinopathy and stenosing tenosynovial condition than a classic inflammatory tendinitis.

Repeated mechanical stress causes thickening and irritation of the tendon sheath and narrowing of the fibro-osseous tunnel through which the APL and EPB tendons pass.

Repetitive Activities

Activities involving repeated thumb abduction, thumb extension, or wrist deviation may provoke symptoms.

Commonly associated activities include racquet sports, fly fishing, golf, and repetitive infant care.

In golfers, the nondominant wrist may be affected because of the mechanical stresses generated during the swing.

Associated Conditions

De Quervain tenosynovitis may occur in association with rheumatoid arthritis and other inflammatory disorders involving the tendon sheaths.

Diagnosis

Signs and Symptoms

The typical presentation is pain and tenderness along the radial aspect of the wrist, usually directly over the first dorsal compartment near the radial styloid.

The discomfort may radiate proximally into the forearm or distally toward the thumb.

Aggravating Movements

Symptoms are commonly worsened by thumb extension or abduction combined with ulnar deviation of the wrist.

Repetitive gripping, lifting, twisting, and thumb use may be particularly painful.

Physical Examination

Examination may demonstrate localized tenderness, swelling, bogginess, or crepitus over the first dorsal compartment.

The most characteristic area of tenderness lies over the radial side of the radial styloid.

Eichhoff Test

The Eichhoff test, which is frequently mislabeled as the Finkelstein test, is performed by having the patient place the thumb within the palm and close the fingers around it.

The wrist is then deviated toward the ulna.

Reproduction of sharp pain over the first dorsal compartment constitutes a positive test.

Finkelstein Maneuver

The true Finkelstein maneuver involves the examiner gently pulling the patient’s thumb distally and directing the wrist into ulnar deviation.

Pain localized over the first dorsal compartment supports the diagnosis.

WHAT Test

The wrist hyperflexion and abduction of the thumb (WHAT) test is another provocative maneuver.

The patient hyperflexes the wrist and actively abducts the thumb against the examiner’s resistance.

Reproduction of the characteristic radial wrist pain indicates a positive test.

Thumb CMC Examination

The first carpometacarpal joint should also be examined because thumb CMC osteoarthritis may coexist with or mimic de Quervain tenosynovitis.

Range of motion and a CMC grind test should be assessed.

Intersection Syndrome

Intersection syndrome is an important alternative diagnosis.

It is less common than de Quervain tenosynovitis and often produces pain and crepitus approximately 4 cm proximal to the wrist, rather than directly over the radial styloid.

Laboratory Tests

Routine laboratory testing is not required for uncomplicated de Quervain tenosynovitis.

Laboratory studies may be considered only when a systemic inflammatory or rheumatologic disorder is suspected.

Imaging

Plain Radiographs

AP and lateral wrist radiographs may be obtained when there is concern for associated osseous pathology.

Dedicated views of the first carpometacarpal joint may help identify degenerative arthritis that could account for similar symptoms.

Role of Imaging

Imaging is not usually required to establish the diagnosis when the history and examination are classic.

Its primary role is to exclude alternative or concomitant pathology.

Pathophysiology

The APL and EPB tendons pass through a relatively rigid fibro-osseous tunnel within the first dorsal compartment.

Thickening of the tendon sheath and narrowing of the tunnel impair normal tendon gliding.

This produces friction, pain, and progressive irritation with repetitive thumb or wrist movement.

Anatomic Variations

Considerable anatomic variation exists within the first dorsal compartment.

The APL may consist of multiple tendon slips, while the EPB may travel within a separate subsheath.

These variations are important because an unrecognized separate compartment can cause failure of injection or incomplete surgical release.

Differential Diagnosis

Thumb CMC Osteoarthritis

Degenerative disease of the first carpometacarpal joint can produce pain near the base of the thumb.

Pain with the CMC grind test and radiographic degenerative changes favor arthritis.

Intersection Syndrome

Intersection syndrome causes pain where the first dorsal compartment tendons cross the second dorsal compartment tendons.

The tenderness is usually several centimeters proximal to the radial styloid.

Radiocarpal Arthritis

Degenerative disease of the radiocarpal joint can cause radial-sided wrist pain and stiffness.

Radiographs and joint-specific examination help distinguish it from de Quervain disease.

Wartenberg Syndrome

Wartenberg syndrome results from entrapment or irritation of the superficial branch of the radial nerve.

It typically causes burning pain or sensory disturbance over the dorsoradial hand rather than isolated tendon pain.

Treatment

General Principles

Initial management is nonoperative.

A trial of conservative treatment for approximately 3–6 months is appropriate in most patients unless symptoms are unusually severe or persistent.

Activity Modification

Patients should avoid or reduce repetitive movements that aggravate symptoms, particularly repeated thumb abduction, extension, forceful gripping, and sustained wrist deviation.

Thumb Spica Splint

Immobilization of the wrist and thumb in a thumb spica splint may reduce tendon motion and allow symptoms to settle.

Splinting is particularly useful during activities that provoke pain.

NSAIDs

Nonsteroidal anti-inflammatory drugs may be used for symptomatic relief when medically appropriate.

They may decrease pain but do not directly correct the mechanical stenosis.

Corticosteroid Injection

Corticosteroid injection into the first dorsal compartment is highly effective in many patients.

Reported success rates may be as high as approximately 91%.

Injection Technique

Accurate placement within the tendon sheath is important.

Injection failure may occur if an unrecognized EPB subsheath or another septum prevents medication from reaching all involved tendons.

Ultrasound-Guided Injection

Ultrasound guidance can improve visualization of the tendon sheath and anatomic septations.

This may improve injection accuracy, particularly when variant anatomy is present.

Injection Complications

Potential complications include skin depigmentation and subcutaneous fat atrophy at the injection site.

Patients should be counseled about these cosmetic risks.

Physical Therapy

Splinting and activity modification are often the most useful rehabilitation measures.

Therapy may also include gentle stretching, ergonomic modification, and education regarding movements that increase friction within the first dorsal compartment.

Medication

Medical treatment primarily consists of NSAIDs and corticosteroid injection.

Repeated injections should be considered cautiously because of local tissue risks.

Surgery

Indications

Surgery is considered when significant symptoms persist or recur despite appropriate nonoperative treatment.

A previous temporary improvement after corticosteroid injection supports the first dorsal compartment as the source of pain before proceeding with surgery.

Surgical Release

The operation consists of release of the first dorsal extensor compartment.

A radial-sided incision is made over the compartment while carefully protecting the superficial radial sensory nerve branches.

Superficial Radial Nerve Protection

The dorsal sensory branches of the radial nerve frequently cross the surgical field.

They must be identified and protected because direct injury can cause persistent numbness or a painful neuroma.

Release of the Fibro-Osseous Tunnel

The constricting fibro-osseous sheath is opened to allow unrestricted gliding of the APL and EPB tendons.

All internal septa and separate tendon subsheaths must be identified and released.

Dorsal-Sided Release

The sheath is commonly opened along its dorsal margin.

This leaves a volar portion of the retinaculum intact and may help prevent postoperative volar subluxation of the tendons.

Anatomic Variations During Surgery

The surgeon should specifically search for multiple APL slips and a separate EPB compartment.

Failure to recognize these variants is one of the most common reasons for persistent symptoms after surgery.

Postoperative Immobilization

Patients are commonly placed in a thumb spica splint for a short period after surgery.

Motion is then gradually resumed according to wound healing and symptoms.

Follow-Up

Prognosis

The prognosis is generally excellent.

Most patients improve with splinting, corticosteroid injection, or surgical decompression when required.

Follow-Up Schedule

Patients may be reviewed at approximately 3-month intervals until symptoms resolve or a decision regarding operative treatment is made.

Complications

Superficial Radial Nerve Injury

The most serious operative complication is injury to the superficial radial sensory nerve.

Because the nerve lies close to the first dorsal compartment, careful surgical dissection is essential.

Sensory Loss

Nerve injury may result in a localized area of numbness or diminished sensation over the dorsoradial wrist and hand.

Painful Neuroma

More severe nerve injury may lead to formation of a painful neuroma.

This can produce significant chronic pain and may require additional surgery.

Persistent Symptoms

Persistent symptoms after surgical release are most commonly caused by an unreleased septum or an unrecognized separate EPB subsheath.

Revision decompression may be required.

Tendon Subluxation

If the compartment is released improperly, the APL and EPB tendons may subluxate volarly during wrist movement.

A dorsal-sided release technique helps reduce this risk.

Patient Monitoring

Follow-up should assess radial wrist pain, tenderness, thumb and wrist motion, response to splinting or injection, and any sensory changes in the superficial radial nerve distribution.

After surgery, monitoring should also include wound healing, tendon stability, recurrence of symptoms, and evidence of nerve irritation.

Orthopaedic Surgery - Cubital Tunnel Syndrome

Basics

Cubital tunnel syndrome (CuTS) is an ulnar nerve entrapment neuropathy at the elbow caused by compression, traction, or both as the ulnar nerve passes through the cubital tunnel.

Patients typically experience pain, numbness, and paresthesias along the ulnar side of the forearm and hand. More advanced disease may produce weakness and wasting of muscles supplied by the ulnar nerve.

Synonym

Cubital tunnel syndrome is sometimes referred to as ulnar tunnel syndrome, although the term should be distinguished from compression of the ulnar nerve at Guyon canal in the wrist.

Epidemiology

Cubital tunnel syndrome is the second most common upper-extremity entrapment neuropathy, after carpal tunnel syndrome.

Men and women are affected at approximately similar rates, with reported incidences of about 25 per 100,000 person-years in men and 19 per 100,000 person-years in women.

Risk Factors

Important risk factors include diabetes mellitus and previous trauma around the elbow.

Degenerative changes, repetitive elbow flexion, local structural abnormalities, and prolonged external pressure may also contribute.

Etiology

Symptoms result from a combination of compression and traction on the ulnar nerve, particularly during elbow flexion.

Flexion decreases the volume of the cubital tunnel while simultaneously stretching the ulnar nerve around the medial epicondyle.

Potential Sites of Compression

The ulnar nerve may be compressed at several locations around the elbow.

These include the Arcade of Struthers, medial intermuscular septum, cubital tunnel proper, and the interval between the two heads of the flexor carpi ulnaris.

Cubital Tunnel Proper

The most common site of compression is the cubital tunnel itself, where the ulnar nerve passes behind the medial epicondyle and beneath Osborne’s ligament.

External and Structural Causes

Potential causes of compression include an enlarged medial head of the triceps, previous trauma, recurrent ulnar nerve subluxation, osteophytes from arthritis, ganglion cysts, and anomalous muscles such as an anconeus epitrochlearis.

Associated Conditions

Cubital tunnel syndrome may coexist with other compressive neuropathies, including carpal tunnel syndrome and thoracic outlet syndrome.

More than one site of nerve compression may therefore be present in the same patient.

Diagnosis

General Principles

The diagnosis is primarily clinical, based on the characteristic history and physical examination.

Nerve conduction studies can support the diagnosis, although false-negative electrodiagnostic studies may occur.

Signs and Symptoms

Patients commonly report a vague aching pain around the medial elbow that may extend into the ulnar aspect of the forearm, wrist, or hand.

Numbness and paresthesias commonly involve the ring and small fingers.

Sensory Symptoms

Altered sensation may occur in the ulnar distribution of the hand and sometimes the medial forearm.

Symptoms are often aggravated by prolonged elbow flexion, such as during sleep, driving, or telephone use.

Physical Examination

Sensory Examination

The examiner should identify sensory abnormalities in the ulnar nerve distribution but should also examine other dermatomes and peripheral nerves.

This is important for excluding cervical radiculopathy, additional peripheral nerve entrapment, or double-crush syndrome.

Dorsal Ulnar Hand Sensation

Numbness over the dorsal ulnar aspect of the hand suggests that ulnar nerve compression is proximal to Guyon canal because the dorsal sensory branch arises before the nerve enters the wrist canal.

Intrinsic Muscle Strength

Intrinsic hand strength should be assessed carefully.

Weakness may affect pinch, finger abduction and adduction, and other fine motor functions.

Froment Sign

The Froment test evaluates weakness of the adductor pollicis.

The patient grasps a piece of paper between the thumb and index finger while the examiner attempts to pull it away.

Positive Froment Sign

If the adductor pollicis is weak, the patient compensates by flexing the thumb interphalangeal joint using the flexor pollicis longus.

This compensatory thumb flexion constitutes a positive Froment sign.

Wartenberg Sign

A Wartenberg sign occurs when the small finger rests persistently in an abducted position.

This reflects weakness of the intrinsic muscles responsible for finger adduction.

Muscle Wasting

The hand should be inspected for intrinsic muscle atrophy.

Wasting is often especially visible in the first dorsal interosseous muscle and along the hypothenar region.

Tinel Sign

Tapping over the ulnar nerve at the cubital tunnel may reproduce tingling or electric sensations into the ring and small fingers.

This constitutes a positive Tinel sign at the elbow.

Elbow Flexion Test

The elbow is held in maximal flexion for approximately 1 minute, usually with the wrist maintained neutral or slightly extended.

Reproduction of ulnar-sided numbness or paresthesias supports the diagnosis.

Keeping the wrist neutral helps avoid provoking coexisting carpal tunnel syndrome.

Scratch Collapse Test

The scratch collapse test has been described as an additional provocative maneuver.

The patient resists shoulder internal rotation while the examiner lightly scratches the skin over the suspected compression site.

Transient loss of resistance has been described in association with compressive neuropathy, although this maneuver should be interpreted together with the rest of the examination.

Ulnar Nerve Subluxation

The ulnar nerve should be palpated while the elbow moves from extension into flexion.

Subluxation or dislocation of the nerve over the medial epicondyle may affect surgical planning and can favor anterior transposition in selected patients.

Imaging and Diagnostic Testing

Plain Radiographs

Elbow radiographs may be obtained when there is concern for a bony cause of compression, previous trauma, deformity, or osteoarthritis.

Radiographs are not required in every uncomplicated case.

Nerve Conduction Studies

Nerve conduction velocity studies may demonstrate slowing of ulnar nerve conduction across the elbow.

The above-elbow and below-elbow conduction velocities are compared.

Electrodiagnostic Criteria

Findings supporting cubital tunnel syndrome include a conduction velocity drop of more than approximately 10 m/s across the elbow or an absolute conduction velocity of less than approximately 50 m/s across the involved segment.

Electrodiagnostic findings should be correlated with clinical symptoms.

Pathological Findings

During surgical decompression, one or more specific areas of nerve constriction may be visible.

All potential sites of compression should be inspected to ensure complete release.

Differential Diagnosis

Cervical Radiculopathy

Compression of the C8 or T1 cervical nerve roots can produce hand numbness, weakness, and intrinsic muscle dysfunction similar to CuTS.

A cervical examination is therefore important when symptoms are atypical.

Thoracic Outlet Syndrome

Thoracic outlet syndrome may produce ulnar-sided paresthesias and upper-extremity discomfort.

The distribution and associated vascular or proximal neurologic findings can help distinguish it from isolated cubital tunnel syndrome.

Guyon Canal Syndrome

Ulnar nerve compression at Guyon canal in the wrist can produce sensory and motor abnormalities in the ulnar hand.

Preserved dorsal ulnar hand sensation favors compression at the wrist rather than the elbow.

Carpal Tunnel Syndrome

Carpal tunnel syndrome affects the median nerve rather than the ulnar nerve but may coexist with CuTS.

The sensory distribution and provocative examination findings help distinguish the two.

Neurologic Disorders

Systemic neurologic conditions such as Guillain–Barré syndrome and amyotrophic lateral sclerosis can produce weakness or sensory changes that mimic peripheral entrapment neuropathy.

Medial Epicondylitis

Medial epicondylitis causes pain over the medial elbow but does not usually produce ulnar nerve sensory loss or intrinsic muscle weakness unless associated CuTS is also present.

Ulnohumeral Osteoarthritis

Degenerative arthritis of the elbow can cause medial elbow pain and osteophyte formation.

Large osteophytes may also contribute directly to ulnar nerve compression.

Treatment

General Measures

Initial treatment is usually nonoperative in patients with mild or moderate symptoms and no progressive motor deficit.

The primary goals are to reduce nerve compression and minimize prolonged elbow flexion.

Night Splinting

A nighttime elbow splint, brace, or soft wrap can be used to prevent excessive flexion during sleep.

Keeping the elbow from flexing beyond approximately 50° may reduce nocturnal symptoms.

Activity Modification

Patients should avoid prolonged elbow flexion and repetitive activities that provoke symptoms.

Direct pressure over the cubital tunnel, such as leaning the medial elbow on a desk or armrest, should also be minimized.

Duration of Conservative Treatment

A trial of nonoperative treatment for approximately 1–3 months is reasonable in patients without severe weakness or progressive neurologic impairment.

Surgery

Indications

Surgery should be considered when symptoms persist despite appropriate conservative care, when numbness is worsening, or when weakness of ulnar-innervated muscles is present.

Progressive muscle wasting is a particularly important indication for surgical evaluation.

Surgical Options

Operative techniques include in situ decompression, anterior ulnar nerve transposition, and medial epicondylectomy.

The optimal procedure depends on nerve stability, anatomy, previous surgery, and the specific site of compression.

In Situ Decompression

Simple decompression releases constricting structures while leaving the ulnar nerve in its native position.

The procedure can be performed through an open or endoscopic approach.

Anterior Transposition

Anterior transposition relocates the ulnar nerve from behind the medial epicondyle to a position anterior to it.

The nerve may be placed subcutaneously, intramuscularly, or submuscularly.

Indications for Transposition

After decompression, the nerve is examined dynamically.

If it is unstable, subluxates, or dislocates over the medial epicondyle, anterior transposition may be performed.

Medial Epicondylectomy

Medial epicondylectomy removes part of the medial epicondyle to reduce tension and compression on the ulnar nerve.

Care must be taken to protect the medial collateral ligament of the elbow.

Medial Antebrachial Cutaneous Nerve

Branches of the medial antebrachial cutaneous nerve cross the operative field during medial elbow surgery.

These branches should be carefully identified and protected because injury can produce painful neuroma or numbness.

Follow-Up

Nonoperative Prognosis

In patients with mild cubital tunnel syndrome, nonoperative management has historically produced excellent results in approximately 58% of cases, excluding many post-traumatic neuropathies.

Surgical Prognosis

Surgical treatment produces good to excellent outcomes in approximately 70–90% of patients.

The degree of recovery depends partly on the severity and duration of preoperative nerve dysfunction.

Decompression Versus Transposition

In the absence of ulnar nerve instability or hypermobility, outcomes after simple decompression are generally comparable with those following anterior transposition.

This allows a less extensive procedure in appropriately selected patients.

Recovery of Weakness

Sensory symptoms may improve earlier than motor weakness.

When severe intrinsic muscle atrophy has been present for a prolonged period, complete strength recovery may not occur even after adequate decompression.

Complications

Postoperative Nerve Irritation

Persistent or new nerve irritation may occur after surgery.

Scar formation, incomplete decompression, nerve instability, or iatrogenic injury may contribute.

Complex Regional Pain Syndrome

Complex regional pain syndrome, historically termed reflex sympathetic dystrophy, may rarely occur after surgery and can produce disproportionate pain, stiffness, and autonomic changes.

Untreated Severe Neuropathy

Progressive untreated ulnar neuropathy can lead to intrinsic muscle atrophy, persistent sensory loss, and clawing of the ring and small fingers.

Ulnar Clawing

Loss of intrinsic muscle function allows imbalance between the extrinsic flexors and extensors.

This can produce hyperextension at the metacarpophalangeal joints and flexion at the interphalangeal joints of the ring and small fingers.

Joint Contractures

Longstanding muscle imbalance and clawing can eventually produce fixed joint contractures.

Early treatment of progressive motor dysfunction may reduce this risk.

Patient Monitoring

Follow-up examinations should document motor strength, sensory function, intrinsic muscle bulk, provocative findings, and progression or improvement of symptoms.

Patients treated surgically should also be monitored for wound problems, recurrent nerve instability, persistent compression, and recovery of hand function.

Orthopaedic Surgery - Computed Tomography

Basics

Computed tomography (CT) is a noninvasive imaging technique that uses a rotating X-ray source and detectors to generate cross-sectional images of the body.

It is particularly useful in musculoskeletal imaging because the acquired data can be reconstructed into multiple planes and displayed as three-dimensional or volume-rendered images.

CT is especially valuable for evaluating complex osseous anatomy, fractures, joint surfaces, cortical bone, mineralization, and postoperative hardware.

Historical Development

CT was introduced in 1972, with the first clinical scanners installed between approximately 1974 and 1976.

By 1980, CT had become widely available.

During the mid-1980s, newer applications were introduced, including dynamic scanning, multiplanar reformations, and three-dimensional CT reconstruction with volume rendering and shaded-surface display.

Routine spiral or helical CT scanning became established around 1989 and subsequently developed into modern multidetector CT technology.

Advantages

Rapid Image Acquisition

One of the major advantages of CT is its speed.

Rapid image acquisition is particularly valuable for trauma patients, seriously ill patients, and children, because scanning can often be completed before significant movement occurs and may reduce the need for sedation.

Complex Anatomic Regions

CT provides excellent visualization of areas that may be difficult to evaluate completely with plain radiographs.

Examples include the spine, pelvis, scapula, wrist, ankle, and other small or anatomically complex joints.

Multiplanar Reconstruction

Modern multidetector CT scanners acquire a volumetric data set that can subsequently be reconstructed in multiple planes.

Images can therefore be generated in the axial, sagittal, coronal, or oblique planes without repeating the scan.

Three-Dimensional Reconstruction

Three-dimensional and volume-rendered reconstructions can clarify complex relationships between fracture fragments, joints, implants, and reconstructed bone.

These techniques are particularly useful for preoperative planning and evaluation of complicated skeletal anatomy.

Imaging Around Hardware

CT may provide useful assessment around metallic implants.

Modern reconstruction and artifact-reduction techniques can substantially decrease metal-related streak artifact, allowing better visualization of bone, implants, graft-host junctions, and surrounding structures.

MRI may be limited by artifact in some patients with extensive metallic hardware.

Patients Unable to Undergo MRI

CT can be performed in patients who cannot safely undergo MRI because of certain implanted devices or metallic foreign bodies.

Examples may include selected non-MRI-compatible cardiac devices, particular aneurysm clips, or metallic orbital foreign bodies.

The actual MRI compatibility of modern implants should always be verified because many contemporary devices are MRI conditional.

Availability and Cost

CT is widely available, rapid, and relatively cost-effective for many clinical problems.

It can often answer important skeletal questions more efficiently than other advanced imaging modalities.

Disadvantages

Soft-Tissue Limitations

CT is generally inferior to MRI for evaluation of bone marrow, spinal cord, peripheral nerves, ligaments, tendons, and many other soft tissues.

MRI is therefore preferred when detailed soft-tissue characterization is the primary goal.

Ionizing Radiation

CT exposes the patient to ionizing radiation.

Radiation dose is greater than with most conventional radiographic examinations, making appropriate patient selection and dose optimization important.

Cost Compared With Radiographs

CT is more expensive than plain radiography and should be used when the additional cross-sectional information is likely to influence diagnosis or treatment.

Intravenous Contrast Risks

When iodinated intravenous contrast is required, potential complications include hypersensitivity reactions and renal adverse effects in susceptible patients.

The indication for contrast should therefore be considered carefully.

CT Technique

Skeletal Imaging

Bone pathology is generally evaluated using thin-section acquisition.

Modern multidetector scanners can obtain very thin slices, allowing high-resolution multiplanar and three-dimensional reconstructions.

Postprocessing

The acquired data can be processed at a workstation to create coronal, sagittal, oblique, three-dimensional, and volume-rendered images.

These reconstructions are especially valuable when evaluating fractures and complex skeletal deformity.

Soft-Tissue Imaging

Extremely thin sections are less critical when the principal target is soft tissue rather than bone.

Reconstructed slice thicknesses of approximately 2–3 mm may be adequate for many soft-tissue applications.

Intravenous Contrast

Evaluation of a soft-tissue mass, abscess, inflammatory process, or vascular injury commonly requires intravenous iodinated contrast.

Contrast improves visualization of vascular structures and patterns of tissue enhancement.

Contrast Administration

Contrast administration protocols vary according to the examination.

High-flow injection may be required for vascular or contrast-enhanced studies, with the exact rate determined by the clinical indication and scanner protocol.

Renal Impairment

Iodinated contrast should be used carefully in patients with significant renal impairment.

Renal function, hydration status, indication for contrast, and alternative imaging methods should be considered before administration.

Previous Contrast Reaction

Patients should be questioned about prior reactions to iodinated contrast.

Those with previous significant reactions may require alternative imaging, a modified contrast strategy, or premedication according to institutional protocol.

Postoperative Applications

Hardware Complications

CT is useful for identifying complications related to orthopedic hardware.

These may include fracture, implant loosening, malposition, surrounding bone destruction, and selected manifestations of infection.

Osteomyelitis

CT may demonstrate cortical destruction, sequestra, gas, or other changes associated with osteomyelitis, particularly in postoperative patients.

MRI is often more sensitive for early marrow infection, but CT can provide valuable structural detail.

Tumor Recurrence

CT may help evaluate possible tumor recurrence in patients with metallic hardware, particularly when MRI is significantly degraded by artifact.

Foreign Bodies

CT is effective for detecting and localizing many retained foreign bodies.

Its cross-sectional nature allows accurate determination of the object’s relationship to bone, joints, vessels, and other structures.

Orthopaedic Oncology Applications

Tumor Mineralization

CT is highly sensitive for detecting calcification and ossification within a lesion.

The pattern of mineralization can help characterize a tumor and narrow the differential diagnosis.

Myositis Ossificans

CT may help distinguish myositis ossificans from neoplasm by demonstrating the characteristic distribution and maturation pattern of peripheral ossification.

Cortical and Periosteal Changes

CT provides excellent visualization of the cortex and periosteal surface.

Patterns of cortical thinning, erosion, destruction, expansion, sclerosis, or periosteal reaction may help distinguish benign from aggressive lesions.

Bone Destruction

The degree of osseous destruction can be assessed accurately with CT.

This information can help estimate structural integrity and risk of pathologic fracture.

Osteoid Osteoma

CT is particularly useful for identifying the small nidus of an osteoid osteoma.

It can also provide image guidance for definitive minimally invasive treatment, such as CT-guided radiofrequency ablation.

Neurovascular and Compartment Involvement

CT can demonstrate tumor extension into adjacent compartments and may identify involvement of major neurovascular structures.

MRI is generally superior for detailed evaluation of these soft-tissue relationships.

Trauma Applications

Occult or Equivocal Fractures

CT is extremely useful when a fracture is suspected clinically but plain radiographs are equivocal or nondiagnostic.

It can reveal subtle fracture lines that are difficult to appreciate on conventional imaging.

Axially Oriented Fractures

Multiplanar and three-dimensional reconstructions are particularly useful for fractures that are oriented in a plane poorly visualized on plain radiographs.

Fracture Extent

CT can accurately determine the extent, displacement, comminution, articular involvement, and physeal involvement of a fracture.

This information is frequently essential for operative planning.

Intra-Articular Fragments

CT can identify small fracture fragments within a joint and define areas of articular depression or step-off.

Nonunion

CT is useful for evaluating suspected fracture nonunion, particularly when overlapping anatomy or implanted hardware makes plain radiographs difficult to interpret.

It can demonstrate persistent fracture gaps and the amount of osseous bridging.

Cervical Spine Trauma

CT is a principal imaging modality for evaluating the cervical spine in moderate- and high-risk trauma patients.

It provides rapid assessment of fractures, alignment, facet injuries, and other bony abnormalities.

Complex Skeletal Regions

CT is particularly useful in trauma involving the pelvis, scapula, wrist, ankle, and spine, where overlapping structures can limit the accuracy of radiographs.

Infection Applications

Postoperative Infection

In postoperative patients, CT may help evaluate new symptoms and identify structural complications after treatment.

It can demonstrate collections, gas, cortical destruction, or other changes suggesting infection.

Extent of Infection

CT can help determine whether infection involves bone, muscle, fascia, or subcutaneous tissue.

Defining the compartments involved may assist in deciding whether medical management alone is adequate or surgical intervention is required.

Response to Treatment

Serial imaging may occasionally be useful for monitoring structural changes during treatment of musculoskeletal infection, although clinical findings and laboratory markers remain important.

Pediatric Applications

Skeletal Dysplasias

CT can be useful in skeletal dysplasias when a large and anatomically complex region must be defined accurately.

It may also be valuable after reconstructive surgery.

Developmental Dysplasia of the Hip

Developmental dysplasia of the hip is usually diagnosed using physical examination, ultrasound, and plain radiographs.

CT may be used in difficult cases or with carefully optimized low-dose protocols.

Evaluation After Hip Reduction

CT has historically been useful for confirming successful hip reduction after placement of a spica cast.

Low-dose imaging protocols are important in these young patients.

Slipped Capital Femoral Epiphysis

CT can demonstrate the orientation of the proximal femoral physis and may help identify contralateral abnormalities with coronal and sagittal reconstructions.

However, routine diagnosis of slipped capital femoral epiphysis is usually based on radiographs, with MRI used in selected early or occult cases.

Alternative Causes of Pediatric Hip Pain

Cross-sectional imaging can also help identify alternative diagnoses such as osteoid osteoma when the source of hip pain is uncertain.

Legg–Calvé–Perthes Disease

CT may occasionally be used for preoperative definition of femoral head deformity and disease severity.

Because of radiation exposure, its use is selective.

Pectus Deformity

CT can define thoracic anatomy in patients with pectus excavatum or other chest-wall deformities.

It may be particularly useful for surgical planning or after unsuccessful previous repair.

Tarsal Coalition

CT is highly effective for characterizing osseous tarsal coalitions.

Multiplanar reconstructions accurately demonstrate the location, orientation, and extent of the coalition and may assist in operative planning.

Pediatric Considerations

Radiation Sensitivity

Children are more sensitive to ionizing radiation than adults.

Because they also have a longer remaining lifespan, the potential lifetime risk of radiation-induced malignancy is greater.

Dose Optimization

CT parameters should therefore be adjusted according to the child’s size, age, and clinical indication.

Only examinations that are likely to provide meaningful clinical information should be performed.

Avoid Multiphase Studies

Unnecessary multiphase CT examinations should be avoided in children.

Obtaining both noncontrast and postcontrast scans without a specific indication can substantially increase radiation dose.

Multidetector CT

Modern multidetector technology allows a single volumetric acquisition to be reconstructed in multiple planes, reducing the need for repeated scanning.

Pregnancy Considerations

Limiting Scan Volume

When CT is necessary during pregnancy, the scan should be restricted to the smallest anatomical region required to answer the clinical question.

Unnecessary multiphase imaging should be avoided.

Radiation Optimization

Protocols should use the lowest radiation exposure that still produces diagnostically adequate images.

Departments should maintain quality-assurance programs and appropriate dose protocols.

Alternative Imaging

When clinically appropriate, ultrasound or MRI should be considered because these techniques do not use ionizing radiation.

However, a necessary CT examination should not be withheld when the expected diagnostic benefit outweighs the potential radiation risk.

Iodinated Contrast in Pregnancy

Iodinated contrast crosses the placenta and should therefore be administered only when it is expected to provide important additional diagnostic information.

No consistent teratogenic effect has been established from routine diagnostic exposure, but use should remain clinically justified.

Abdominal and Pelvic Protection

Radiation exposure outside the imaged region should be minimized through appropriate collimation and modern dose-reduction techniques.

Routine external lead shielding is no longer universally recommended because contemporary CT systems rely primarily on optimized scan parameters and shielding may occasionally interfere with automatic exposure control.

Breastfeeding After Contrast

Modern recommendations generally do not require interruption of breastfeeding after routine iodinated intravenous contrast administration, because only very small amounts reach breast milk and an even smaller amount is absorbed by the infant.

Follow-Up and Complications

Contrast Reactions

Iodinated contrast can produce hypersensitivity reactions ranging from mild symptoms to rare severe reactions.

Patients with a previous contrast reaction have the greatest risk of another reaction.

Asthma may also increase susceptibility.

Premedication

Selected high-risk patients may undergo premedication using corticosteroids and antihistamines according to institutional protocols.

Premedication reduces but does not completely eliminate the possibility of a reaction.

Renal Adverse Effects

Patients with significant pre-existing renal disease are at greatest risk for renal complications related to iodinated contrast.

Other relevant factors may include dehydration, diabetes, severe systemic illness, and concurrent nephrotoxic medications.

Renal Protection

When contrast is necessary in a patient at increased renal risk, appropriate hydration, avoidance of unnecessary nephrotoxic exposures, and use of the minimum effective contrast dose may reduce risk.

Modern low- or iso-osmolar contrast agents are typically used.

Overall Role in Orthopaedics

CT is an especially valuable orthopaedic imaging modality when detailed evaluation of cortical bone, fracture anatomy, joint surfaces, complex skeletal regions, calcification, reconstruction, or implanted hardware is required.

Its major limitations are ionizing radiation and relatively inferior soft-tissue contrast compared with MRI, so the imaging modality should be selected according to the specific clinical question.

Orthopaedic Surgery - Compartment Syndrome of the Foot

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Basics

Foot compartment syndrome (FCS) occurs when hemorrhage and interstitial edema increase pressure within the closed muscle compartments of the foot, resulting in impaired capillary perfusion.

If pressure remains elevated, progressive ischemia of muscles and nerves may lead to myoneural necrosis and permanent functional impairment.

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General Prevention

The most important factor in preventing the long-term consequences of foot compartment syndrome is maintaining a high index of clinical suspicion.

The diagnosis can be difficult because severe foot trauma itself commonly causes pain and swelling.

Early recognition and treatment are essential.

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Epidemiology

Foot compartment syndrome is uncommon and represents less than 5% of limb compartment syndromes.

Its incidence varies according to the mechanism and severity of injury.

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Calcaneus Fractures

FCS has been reported in up to approximately 10% of patients with calcaneal fractures.

The risk is greater with high-energy, displaced, and markedly swollen injuries.

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Crush Injuries

When a crush mechanism is combined with a forefoot injury, compartment syndrome may occur in as many as approximately 18% of cases.

Crush injuries produce extensive soft-tissue damage, hemorrhage, and edema, making them particularly high risk.

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Isolated Foot Injuries

Among isolated foot injuries overall, compartment syndrome is considerably less common, occurring in approximately 2% of cases.

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Pathophysiology

As intracompartmental pressure rises, the pressure gradient required for capillary perfusion decreases.

When local tissue pressure becomes sufficiently high relative to arterial pressure, blood flow becomes inadequate and tissue ischemia develops.

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Myoneural Ischemia

Continued ischemia damages both muscle and peripheral nerves.

If untreated, this progresses to myonecrosis, nerve injury, fibrosis, contracture, and permanent deformity.

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Long-Term Consequences

Late consequences can include chronic pain, paresthesias, stiffness, claw-toe deformity, cavus or cavovarus alignment, and other structural foot deformities.

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Etiology

Foot compartment syndrome most often follows high-energy trauma.

Common causes include calcaneus fractures, midfoot and forefoot injuries, severe crush injuries, and Lisfranc fracture-dislocations.

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Open Injuries

An open wound does not exclude compartment syndrome.

Open foot injuries may still have intact deeper fascial compartments in which dangerously elevated pressures develop.

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Association With Tibial Fractures

FCS can occasionally occur after a tibial fracture.

This may be related to communication between the deep posterior compartment of the leg and the calcaneal compartment of the foot, allowing swelling or hemorrhage to extend distally.

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Diagnosis

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General Principles

Because FCS is relatively uncommon and the injured foot is often painful and swollen even without compartment syndrome, diagnosis requires careful correlation of the mechanism of injury, serial examination, and compartment pressure measurements when necessary.

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Signs and Symptoms

Typical findings include severe pain, tense swelling, and pain with passive stretching of the toes.

The clinical pattern should be assessed repeatedly because symptoms may evolve over time.

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Severe Pain

Pain is often intense and may appear excessive for the apparent injury.

Persistent or progressively worsening pain despite appropriate immobilization and analgesia should raise concern.

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Tense Swelling

The foot may become markedly swollen and tense.

Because substantial swelling commonly accompanies calcaneal and crush injuries, this finding alone is not diagnostic.

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Pain With Passive Toe Stretch

Pain produced by passive movement of the toes is a common feature.

However, it is not specific for compartment syndrome because fractures and severe soft-tissue injuries can also produce pain with passive motion.

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Sensory Changes

Paresthesias or diminished sensation may develop as nerve ischemia progresses.

Sensory findings can be inconsistent and are less reliable than the overall clinical picture.

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Pulses

Diminished or absent pulses are unreliable for early diagnosis.

Foot pulses may remain present despite critically elevated compartment pressures because larger arteries can remain patent while microvascular perfusion is compromised.

Pulselessness is therefore a late and concerning finding.

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Imaging

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Plain Radiographs

Plain radiographs of the foot and ankle should be obtained to identify fractures or dislocations responsible for the swelling and trauma.

Imaging helps define the underlying skeletal injury but does not diagnose compartment syndrome itself.

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Compartment Pressure Measurement

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Diagnostic Role

Invasive measurement of intracompartmental pressures is useful when the diagnosis is uncertain and has traditionally been considered the objective diagnostic standard for FCS.

Pressure findings should always be interpreted together with the clinical examination.

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Medial Compartment

The medial, or abductor hallucis, compartment may be accessed by placing the pressure needle directly inferior to the first metatarsal.

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Deep Compartment

The deep compartment may be reached by advancing the needle approximately 1 cm deeper from the medial compartment beneath the arch of the foot.

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Interosseous Compartments

Interosseous pressures can be measured from the dorsal foot, commonly by inserting the needle between the third and fourth metatarsals.

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Lateral Compartment

The lateral compartment can be assessed by inserting the needle plantar to the fifth metatarsal.

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Pressure Threshold

Historically, an absolute compartment pressure greater than approximately 30 mm Hg has been considered concerning.

In modern practice, pressure is often interpreted in relation to the patient’s diastolic blood pressure, and the complete clinical picture remains essential.

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Limitations of Pressure Measurement

An elevated isolated pressure value does not necessarily establish compartment syndrome.

Pressure measurements may vary according to technique, location, blood pressure, and injury pattern.

When measured pressures do not correlate with the physical findings, repeated examination and reassessment are important.

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Treatment

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Initial Stabilization

Circumferential or constrictive dressings should be avoided when compartment syndrome is suspected.

Any tight bandage, splint, or dressing should be loosened or removed because external compression may further increase tissue pressure.

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Limb Position

The injured foot should generally be maintained at approximately the level of the heart while the patient is being observed.

Excessive elevation may reduce arterial perfusion, whereas allowing the foot to hang dependently can worsen swelling.

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Serial Examination

Repeated clinical examinations are essential.

Changes in pain intensity, analgesic requirement, swelling, sensory findings, and pain with passive toe motion should be documented.

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Pressure Monitoring

If the diagnosis remains uncertain, invasive pressure measurements should be obtained promptly.

Repeated measurements may be required if symptoms are evolving.

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Swelling Control

Measures to reduce swelling may be used while the diagnosis is being clarified, provided they do not delay definitive treatment.

Pneumatic foot pumps have historically been described for early post-traumatic swelling in selected situations.

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Diuretics

Diuretic therapy has historically been described as a means of reducing generalized edema, but it does not substitute for decompression when true compartment syndrome is present.

Once FCS is diagnosed, treatment is surgical.

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Early Fasciotomy

The most reliable method of preventing irreversible consequences is early surgical fasciotomy.

Once the diagnosis is established, decompression should not be delayed.

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Surgical Planning

The fasciotomy approach should be selected with future fracture fixation and reconstruction in mind.

Incisions that interfere with later definitive fixation should be avoided whenever possible.

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Activity

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Bed Rest

Patients with massive swelling or suspected FCS should generally remain at bed rest during acute evaluation.

The foot should be kept at heart level and protected from weight-bearing.

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Nursing Care

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Frequent Monitoring

Patients with severe foot trauma require close nursing observation.

Increasing, persistent, or inadequately controlled pain should prompt immediate reassessment by the treating clinician.

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Passive Stretch Testing

Pain with passive toe movement should be reassessed frequently.

A worsening response may indicate increasing compartment pressure.

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Change in Clinical Status

Any deterioration in swelling, pain, sensation, or motor function should prompt urgent physician evaluation and consideration of compartment pressure measurement or operative decompression.

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Physical Therapy

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Late Rehabilitation

Physical therapy may be useful for patients who develop residual problems following FCS.

Treatment can include stretching, range-of-motion exercises, strengthening, gait rehabilitation, and desensitization.

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Desensitization

Desensitization techniques may be useful for patients with persistent hypersensitivity or neuropathic symptoms after severe crush injury or compartment syndrome.

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Surgery

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Fasciotomy

Once foot compartment syndrome has been diagnosed, urgent surgical fasciotomy is required.

The goal is complete decompression of the involved compartments before irreversible myoneural injury occurs.

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Three-Incision Technique

A commonly described approach uses three incisions.

Two dorsal incisions are made over the second and fourth metatarsals, while a separate medial incision is made along the arch.

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Dorsal Incisions

The dorsal incisions provide access to the interosseous compartments and can assist with decompression of adjacent spaces.

One incision is positioned over the second metatarsal region and the other over the fourth.

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Medial Arch Incision

The medial incision allows decompression of the abductor hallucis and deeper central muscle compartments.

This approach provides access to important plantar structures not adequately reached from the dorsum.

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Alternative Single Medial Approach

An alternative technique uses a single medial incision.

The abductor hallucis and deep compartments are released, after which the muscles can be reflected plantarly to gain access to additional compartments.

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Interosseous Release Through Medial Approach

Using the single medial technique, the interosseous compartments may be approached internally after mobilization of the plantar musculature.

This avoids multiple dorsal incisions but is technically demanding.

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Plantar-Based Single-Incision Technique

Another described approach uses a plantar-medial incision beginning approximately 5 cm distal to the posterior heel on the non-weight-bearing instep and extending distally.

The intent is to decompress the intermediate and lateral compartments through a single incision.

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Pie-Crusting Technique

A minimally invasive “pie-crusting” technique has also been described.

Multiple small stab incisions are made over the intermetatarsal spaces, followed by blunt fascial release with a hemostat.

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Purpose of Pie-Crusting

The theoretical advantage of this approach is reduction in the size of open wounds and therefore a lower need for skin grafting.

However, complete compartment release remains the overriding surgical priority.

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Wound Management

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Delayed Closure

Fasciotomy wounds are usually left open initially because severe swelling makes immediate closure unsafe.

Closure is commonly attempted approximately 5–7 days later, after edema has substantially decreased.

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Skin Grafting

If the wound edges cannot be approximated without excessive tension, a split-thickness skin graft may be required.

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Follow-Up

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Referral

Severe foot trauma, substantial swelling, or suspected compartment syndrome requires urgent orthopaedic consultation.

Delay in specialist assessment can result in permanent disability.

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Prognosis

The prognosis of a missed or untreated foot compartment syndrome is poor.

Patients frequently develop chronic pain, stiffness, deformity, and impaired walking ability.

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Chronic Pain

Persistent pain may result from muscle necrosis, nerve injury, scar formation, joint stiffness, or abnormal loading of the foot.

It can be significantly disabling.

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Cavus and Cavovarus Deformity

Necrosis and subsequent fibrosis of the intrinsic foot muscles can alter muscle balance.

This may lead to cavus or cavovarus foot deformity.

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Claw Toes

Intrinsic muscle fibrosis and imbalance can produce claw-toe deformities.

Severe fixed claw toes may eventually require operative release or reconstruction.

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Complex Regional Pain Syndrome

Complex regional pain syndrome may develop after severe crush injury or compartment syndrome.

It can cause persistent pain, hypersensitivity, autonomic changes, stiffness, and substantial functional impairment.

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Complications

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Pain

Chronic pain is one of the most frequent consequences of delayed or severe FCS.

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Paresthesias

Nerve ischemia can produce persistent paresthesias, numbness, or sensory disturbance.

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Stiffness

Fibrosis, prolonged immobilization, and joint injury may lead to significant foot and toe stiffness.

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Claw-Toe Deformity

Loss of normal intrinsic muscle function may result in progressive clawing of the toes.

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Foot Deformity

Permanent structural abnormalities may include cavus, cavovarus, toe contractures, abnormal gait, and altered weight-bearing.

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Patient Monitoring

Patients at risk for FCS require repeated assessment of pain, swelling, sensation, motor function, passive stretch discomfort, and compartment pressures when indicated.

Following fasciotomy, monitoring should include wound condition, neurovascular function, edema, fracture healing, toe alignment, range of motion, and the development of chronic deformity or pain.

Orthopaedic Surgery - Compartment Syndrome

Basics

Compartment syndrome occurs when pressure rises within a closed fascial space, reducing tissue perfusion and compromising the function and viability of the muscles, nerves, and vessels contained within that compartment.

Acute compartment syndrome is a limb-threatening surgical emergency. In contrast, chronic or exertional compartment syndrome is usually an exercise-related condition that is symptomatic but not immediately limb threatening.

Tissue Ischemia

As intracompartmental pressure increases, local blood flow falls below the metabolic requirements of the tissues.

Continued ischemia can lead to muscle necrosis, nerve injury, ischemic contracture, weakness, numbness, or irreversible loss of limb function.

Systemic Consequences

Extensive muscle necrosis can produce rhabdomyolysis.

Release of intracellular contents may lead to myoglobinuria, hyperkalemia, acute tubular necrosis, and acute kidney failure.

For this reason, severe compartment syndrome can become a systemic as well as a local emergency.

General Prevention

A high index of suspicion is essential.

Diagnosis is particularly difficult in obtunded trauma patients, sedated or anesthetized patients, patients with drug intoxication, and young children, because pain and other clinical findings may be unreliable.

Anatomic Locations

The leg and forearm are the most commonly involved regions.

However, compartment syndrome can also occur in the thigh, hand, foot, arm, fingers, and gluteal region.

Epidemiology

Acute compartment syndrome is associated most frequently with fractures and high-energy extremity trauma.

Reported incidence includes approximately 1–5% of tibial fractures, 0.25% of distal radius fractures, 3% of forearm fractures, and up to 10% of displaced calcaneal fractures.

Risk Factors

Important risk factors include high-energy trauma, crush injury, prolonged pressure on a dependent limb, anesthesia, drug overdose, altered mental status, fractures, osteotomies, vascular injury, reperfusion, burns, tight casts, constrictive dressings, and tight surgical closure.

High-Risk Patients

Young adult males with tibial or forearm fractures are particularly vulnerable.

Children with displaced supracondylar humerus fractures also require careful surveillance.

Prolonged Procedures and Positioning

Long surgical procedures can produce compartment syndrome because of prolonged external pressure or positioning.

An unconscious or anesthetized patient cannot report progressive pain, making recognition more difficult.

Vascular and Reperfusion Injury

Ischemic injury followed by restoration of blood flow can produce marked tissue edema.

This reperfusion injury may rapidly increase intracompartmental pressure after vascular repair.

Soft-Tissue Causes

Soft-tissue injury alone can produce compartment syndrome.

Examples include severe contusions, crush injury, snake bites, and extensive muscle damage with hemorrhage and edema.

Iatrogenic Causes

Iatrogenic causes include tight casts, restrictive dressings, infiltration of intravenous fluid, intraosseous infusion, antishock garments, and overly tight surgical closure.

Intracompartmental Hemorrhage

Bleeding into a closed compartment can elevate pressure significantly.

Patients with coagulopathy or anticoagulation may therefore be at increased risk.

Pathophysiology

The central mechanism is failure of local tissue perfusion to satisfy metabolic demand.

As tissue pressure rises, the arteriovenous perfusion gradient decreases, resulting in progressive ischemia.

Ischemic Cascade

Muscle ischemia causes cellular swelling, which further increases compartment pressure.

This produces a vicious cycle of increasing pressure, worsening perfusion, greater edema, and progressive tissue necrosis.

Etiology

Any condition that either increases the volume within a compartment or decreases the size of the compartment can produce compartment syndrome.

External Compression

External compression may result from casts, splints, dressings, body positioning, or other constrictive devices.

Removing the external source of compression is an immediate priority when compartment syndrome is suspected.

Fracture-Related Hemorrhage

Fractures may produce substantial bleeding and swelling within a compartment.

Pressure can rise after the initial injury or following fracture manipulation.

Both open and closed fractures can be associated with compartment syndrome.

Vascular Injury

Arterial or venous injury can cause bleeding into a closed space.

Reperfusion following vascular repair can further increase swelling.

Crush Injury

Severe crush injury causes direct muscle damage, hemorrhage, and cell death.

Leakage of intracellular and extracellular fluid then contributes to rapid compartment expansion and pressure elevation.

Associated Conditions

Conditions associated with compartment syndrome include coagulopathy and altered mental status.

Both can increase risk or make diagnosis more difficult.

Diagnosis

Signs and Symptoms

The traditional findings are described as the five P’s: pain, pallor, paresthesia, paralysis, and pulselessness.

However, not all of these findings are present early.

Pain and pain with passive stretch are generally more useful early findings, whereas paralysis and pulselessness are late and ominous signs.

High Index of Suspicion

Clinical findings alone may be unreliable.

This is especially true in children, unconscious patients, heavily sedated patients, and those with distracting injuries.

Serial examinations are therefore essential.

Pain Out of Proportion

The classic early symptom is pain that appears excessive compared with the apparent severity of the injury.

The patient may report escalating discomfort despite appropriate immobilization and analgesia.

Increasing Analgesic Requirement

An increasing requirement for pain medication can be an important warning sign.

This may be particularly useful in children, who may show increasing agitation or analgesic requirements before other findings appear.

Loss of Pain

The disappearance of pain does not necessarily indicate improvement.

If nerves become ischemic and lose function, pain may diminish despite worsening tissue necrosis.

Thus, absence of pain in advanced compartment syndrome is a late and poor prognostic sign.

Paresthesias

Numbness or tingling may develop as sensory nerves become ischemic.

Paresthesias can precede frank sensory loss.

Physical Examination

Mental Status

The patient’s level of consciousness should be documented.

A reliable examination requires the patient to be awake and able to describe symptoms accurately.

Vital Signs

Vital signs should be assessed, with particular attention to the diastolic blood pressure, because the relationship between diastolic pressure and compartment pressure is used in determining tissue perfusion.

Motor Examination

Motor function of muscles within and distal to the involved compartment should be tested and documented serially.

New weakness may indicate progressive nerve or muscle ischemia.

Sensory Examination

Sensation should be examined carefully in the distribution of nerves passing through the affected compartment.

New sensory changes are concerning for nerve compromise.

Hand Compartment Syndrome

Hand compartment syndrome may not cause obvious sensory loss because the major digital sensory nerves are relatively superficial and may lie outside the affected muscle compartments.

Therefore, a normal sensory examination does not exclude compartment syndrome of the hand.

Compartment Tenseness

The involved compartment may feel firm, swollen, or tense to palpation.

This finding can support the diagnosis but is subjective.

Deep Posterior Compartment

The deep posterior compartment of the leg is difficult to assess by palpation because of its location.

A clinically soft superficial compartment does not exclude elevated pressure in the deep posterior compartment.

Pain With Passive Stretch

Pain produced by passively stretching muscles that cross the involved compartment is an important early sign.

For example, passive toe movement may stretch ischemic muscles in the leg and reproduce severe pain.

Pulses

Distal pulses should be assessed and compared with the opposite extremity.

However, preserved pulses do not exclude compartment syndrome because arterial pressure can remain sufficient to maintain flow even when microvascular perfusion is critically impaired.

Pulselessness is generally a late finding.

Compartment Pressure Measurement

General Principles

Direct measurement of intracompartmental pressure is useful when the diagnosis is uncertain or the patient cannot provide a reliable examination.

Pressure measurement should not delay surgery when the clinical diagnosis is clear.

Leg Compartments

The leg contains four major compartments that may require assessment:

Anterior compartment

Lateral compartment

Superficial posterior compartment

Deep posterior compartment

Thigh Compartments

The thigh contains anterior, posterior, and medial compartments.

Hand Compartments

Relevant hand compartments include the thenar, hypothenar, interosseous, adductor pollicis, and carpal tunnel compartments.

Foot Compartments

The foot contains several compartments, including medial, lateral, central, and intrinsic muscle compartments.

Forearm Compartments

The forearm includes volar, dorsal, and mobile-wad compartments.

Arm Compartments

The upper arm contains anterior and posterior compartments, with the deltoid region also considered when clinically appropriate.

Gluteal Compartment

Gluteal compartment syndrome typically involves the gluteus maximus region and may occur after prolonged unconsciousness or high-energy trauma.

Fingers

Compartment syndrome of the fingers is primarily a clinical diagnosis.

Pressure measurements are less commonly used.

Pressure Thresholds

Historically, an absolute compartment pressure of approximately 40 mm Hg has been considered concerning.

More commonly, the delta pressure, calculated as diastolic blood pressure minus compartment pressure, is used.

A delta pressure of 30 mm Hg or less is generally considered an indication for urgent decompression when consistent with the clinical setting.

Serial Pressure Monitoring

When the diagnosis remains uncertain, pressure measurements may be repeated every few hours.

The measurement should be obtained close to the suspected site of injury because pressures may vary within the compartment.

Chronic Compartment Syndrome

Chronic exertional compartment syndrome is characterized by elevated pressure during exercise or delayed normalization after activity.

Its diagnosis and treatment differ from those of acute compartment syndrome.

Laboratory Studies

Basic Metabolic Panel

Electrolytes should be checked when extensive muscle injury is suspected.

Particular attention should be paid to serum potassium, because muscle necrosis may cause life-threatening hyperkalemia.

Creatine Kinase

Serial creatine kinase measurements may help quantify the extent of muscle breakdown when significant rhabdomyolysis is suspected.

Marked elevations support substantial muscle injury but do not diagnose compartment syndrome by themselves.

Urine Myoglobin

Urinalysis can identify myoglobinuria caused by muscle necrosis.

Dark urine may occur when myoglobin levels are high.

Hematocrit

Hematocrit may be useful when substantial hemorrhage into a large compartment, such as the thigh, is suspected.

Preoperative Tests

Standard preoperative laboratory studies are obtained according to the clinical condition and urgency of surgery.

They should not delay decompression in a limb-threatening emergency.

Imaging

Plain Radiographs

Radiographs are used mainly to identify associated fractures or other skeletal injuries.

Imaging is supportive and should never delay treatment when acute compartment syndrome is clinically evident.

Pathological Findings

At fasciotomy, affected muscle may bulge outward once the fascia is opened because of the high intracompartmental pressure.

If diagnosis has been delayed, areas of ischemic or necrotic muscle may be present.

Differential Diagnosis

Arterial Occlusion

Acute arterial occlusion can also produce pain, pallor, paresthesia, weakness, and pulselessness.

However, arterial occlusion does not necessarily produce a tense compartment or elevated intracompartmental pressure.

Neurapraxia

Peripheral neurapraxia can produce weakness or numbness after trauma.

Unlike compartment syndrome, it is not associated with increased compartment pressure or marked compartment tenseness.

Treatment

General Measures

Acute compartment syndrome is a surgical emergency.

Once the diagnosis is established, treatment requires prompt decompression to prevent irreversible muscle and nerve injury.

Remove External Compression

Any cast, splint, dressing, or circumferential bandage should be split, loosened, or removed immediately if compartment syndrome is suspected.

Padding beneath a cast may also need to be completely divided.

Limb Position

When a developing compartment syndrome is being observed, the extremity should generally be maintained at approximately the level of the heart.

Excessive elevation may further reduce arterial perfusion, while dependent positioning can worsen venous congestion and swelling.

Bed Rest

Patients with suspected acute compartment syndrome should remain at rest while urgent assessment proceeds.

Activity that increases tissue demand or swelling should be avoided.

Nursing Care

Frequent neurovascular examinations are essential.

Changes in pain, motor function, sensation, compartment firmness, and analgesic requirements should be reported promptly.

Medical Management

Rhabdomyolysis

When myoglobinuria or major muscle necrosis is present, intravenous fluids may be administered to maintain renal perfusion.

Urine alkalinization may be considered in selected cases, depending on the clinical context.

Hyperkalemia

Hyperkalemia should be treated urgently because of the risk of cardiac arrhythmia.

Electrolytes should be monitored serially in patients with extensive muscle injury.

Treatment of Underlying Conditions

Associated problems may require separate treatment.

Examples include antibiotics for an open fracture or contaminated wound and anticoagulation for a confirmed deep vein thrombosis when appropriate.

Such treatment does not replace surgical decompression of an acute compartment syndrome.

Surgery

Fasciotomy

Definitive treatment consists of longitudinal opening of the fascia surrounding the involved compartment or compartments.

This allows swollen tissues to expand and restores the pressure gradient necessary for adequate perfusion.

Wound Management

Fasciotomy wounds are usually left open initially because immediate closure may recreate elevated compartment pressure.

Delayed primary closure or skin grafting is performed after swelling has subsided.

Negative-Pressure Wound Therapy

Postoperative wounds may be managed with moist dressings or negative-pressure wound therapy.

The choice depends on wound size, swelling, contamination, and institutional practice.

Postoperative Elevation

After decompression, the limb is usually elevated appropriately to reduce swelling while maintaining adequate perfusion.

Leg Fasciotomy

Two-Incision Technique

The leg is commonly decompressed through one lateral and one medial incision.

The lateral incision releases the anterior and lateral compartments.

The medial incision releases the superficial and deep posterior compartments.

Thigh Fasciotomy

Lateral Approach

A lateral incision is commonly used to release the anterior compartment.

The posterior compartment can often be released through the same exposure if necessary.

Medial Compartment

A separate medial incision may be required to decompress the medial thigh compartment.

Hand Fasciotomy

Dorsal Incisions

Two dorsal incisions, commonly placed over the second and fourth metacarpals, can be used to decompress the interosseous compartments.

Palmar Incisions

Additional palmar incisions may be required to decompress the thenar compartment and carpal tunnel.

A separate incision may be used for the hypothenar compartment when necessary.

Forearm Fasciotomy

Volar Release

The volar compartment is commonly released through an extended lazy-S incision.

This approach can be continued distally to release the carpal tunnel if necessary.

Dorsal Compartment

A separate dorsal release may be required when the dorsal compartment is involved, although it is not always necessary.

Foot Fasciotomy

Medial and Dorsal Approaches

The foot may be decompressed through a medial incision, with additional dorsal incisions over the second and fourth metatarsals as required.

Because compartment anatomy of the foot is complex, complete decompression requires careful surgical planning.

Arm Fasciotomy

Medial Approach

The arm may be decompressed through a medial approach, particularly when associated vascular exploration is required.

Both anterior and posterior compartments should be addressed when involved.

Finger Decompression

For digital compartment syndrome, release is generally performed on the ulnar side of the index and middle fingers and the radial side of the ring and little fingers to reduce risk to the dominant neurovascular structures.

Gluteal Fasciotomy

Gluteal compartment syndrome is treated with decompression through an incision over the gluteus maximus region, with release of the involved compartments.

Rehabilitation

Physical Therapy

Postoperative rehabilitation depends on the severity of the soft-tissue, nerve, muscle, and bony injuries.

Physical therapy may focus on range of motion, strengthening, gait training, mobility, and prevention of contracture.

Occupational Therapy

Occupational therapy is particularly useful after upper-extremity compartment syndrome.

Treatment may include hand strengthening, dexterity training, adaptive equipment, and specialized splinting.

Orthotic Referral

Persistent weakness such as foot drop may require an ankle-foot orthosis or another supportive brace.

Prosthetic Referral

If irreversible tissue damage results in limb loss, early prosthetic rehabilitation may improve long-term functional recovery.

Plastic Surgery

Plastic surgical consultation may be required for difficult fasciotomy wounds, soft-tissue coverage, skin grafting, or reconstructive procedures.

Follow-Up

Prognosis

The best outcomes occur when diagnosis is made rapidly and fasciotomy is performed before irreversible muscle and nerve injury develops.

Delay in treatment substantially increases the risk of permanent disability.

Fasciotomy Morbidity

Fasciotomy itself is not a minor procedure.

Large open wounds, painful scars, skin grafting, infection, and chronic venous problems may occur.

Nevertheless, these risks are outweighed by the consequences of untreated acute compartment syndrome.

Motor Recovery

Established paresis caused by prolonged nerve or muscle ischemia frequently has limited recovery.

Motor deficits that are already present at the time of delayed decompression may become permanent.

Sensory Recovery

Persistent numbness from advanced nerve ischemia may also fail to improve.

Sensory loss can predispose the limb to secondary injuries.

Complications

Motor Deficit

Permanent motor complications include weakness, paresis, and foot drop.

These deficits may result from muscle necrosis, nerve injury, or both.

Volkmann Ischemic Contracture

Untreated or inadequately treated forearm compartment syndrome can lead to Volkmann ischemic contracture.

Fibrosis and shortening of necrotic flexor muscles produce a characteristic fixed deformity of the wrist and hand.

Sensory Deficit

Permanent sensory loss may leave the extremity insensate.

Patients are then at increased risk of pressure ulcers, burns, infections, and repetitive unnoticed trauma.

Kidney Failure

Severe rhabdomyolysis can produce myoglobin-mediated renal injury and acute kidney failure.

Aggressive recognition and systemic management are therefore important.

Infection

Necrotic muscle and large fasciotomy wounds increase the risk of infection.

Repeated debridement may be required when nonviable tissue is present.

Chronic Venous Stasis

Chronic swelling and venous insufficiency may develop after severe compartment syndrome or fasciotomy.

Limb Loss

Extensive irreversible ischemia, infection, or vascular injury may ultimately require amputation.

Complex Regional Pain Syndrome

Some patients develop complex regional pain syndrome, historically referred to as reflex sympathetic dystrophy.

This may cause persistent pain, autonomic disturbance, stiffness, and functional impairment.

Patient Monitoring

Intraoperative Monitoring

Compartment pressures can be remeasured after fasciotomy when necessary to confirm that adequate decompression has been achieved.

The surgeon should also directly assess muscle viability.

Post-Closure Monitoring

After delayed wound closure, continued monitoring is necessary because recurrent swelling can recreate elevated compartment pressures.

Serial Neurovascular Examination

Ongoing assessment should include pain, motor strength, sensation, compartment firmness, pulses, capillary refill, renal function, and evidence of systemic rhabdomyolysis.

Any deterioration requires immediate reassessment.

Orthopaedic Surgery - Clubfoot

Basics

Clubfoot, also known as talipes equinovarus, is a complex congenital deformity of the foot that is present at birth.

The deformity consists of three major components: equinus of the heel, varus with internal rotation of the hindfoot, and adduction of the forefoot.

Components of the Deformity

Equinus describes a plantarflexed position of the ankle and heel.

Varus refers to inward turning of the hindfoot, while forefoot adduction causes the front of the foot to deviate medially.

Together, these abnormalities cause the foot to point downward and inward.

Weight-Bearing Pattern

If the deformity remains untreated, the child may bear weight along the lateral border or even the dorsolateral aspect of the foot rather than on the plantar surface.

This abnormal loading can eventually lead to callus formation, pain, and gait difficulty.

Classification

Clubfoot can be divided broadly into two categories.

The first is isolated or idiopathic clubfoot, in which no other congenital abnormality is identified.

The second is syndromic or secondary clubfoot, occurring in association with other congenital or neuromuscular disorders.

Syndromic Clubfoot

Associated conditions include amniotic band syndrome, arthrogryposis, myelodysplasia, diastrophic dysplasia, Larsen syndrome, Freeman–Sheldon syndrome, Möbius syndrome, and Loeys–Dietz syndrome.

Clubfeet associated with these conditions are usually more rigid, more severe, and more resistant to nonoperative treatment than idiopathic clubfeet.

They therefore have a greater likelihood of requiring surgical correction.

Bony Anatomy

The talar neck is characteristically directed medially and plantarward.

The talonavicular relationship is also abnormal, contributing substantially to the medial and plantar displacement of the foot.

Foot Size

The involved foot is usually smaller than normal.

In unilateral cases, the affected foot may be slightly shorter than the contralateral side, generally by less than approximately 1 cm.

The calf may also remain smaller because of associated muscle hypoplasia.

Epidemiology

Clubfoot occurs in approximately 1 in every 1,000 live births.

Males are affected about twice as often as females, producing a male-to-female ratio of roughly 2:1.

Risk Factors

A positive family history substantially increases the likelihood of clubfoot.

Important risk factors include having an affected parent or sibling and the presence of congenital disorders known to be associated with clubfoot.

Associated Congenital Disorders

Conditions linked with clubfoot include amniotic band syndrome, arthrogryposis, myelodysplasia, Möbius syndrome, Freeman–Sheldon syndrome, Larsen syndrome, diastrophic dysplasia, and Loeys–Dietz syndrome.

Certain teratogenic drug exposures during pregnancy, historically including aminopterin, have also been associated with congenital foot deformities.

Genetics

Idiopathic clubfoot is believed to have a multifactorial or polygenic inheritance pattern with variable penetrance.

No single genetic abnormality explains most idiopathic cases.

Familial Risk

When one child has clubfoot, the risk to a subsequent sibling has historically been estimated at approximately 2–6%.

If a parent has clubfoot, the risk to each child has been estimated at approximately 10%.

Etiology

The exact cause of idiopathic clubfoot remains uncertain.

A genetic contribution is strongly suspected, although environmental and developmental factors may also participate.

Associated Conditions

Clubfoot may occur together with other congenital musculoskeletal or neurologic abnormalities.

The presence of other deformities should prompt evaluation for an underlying syndrome or neurologic disorder.

Diagnosis

Signs and Symptoms

The diagnosis is usually evident from the appearance of the newborn foot.

The foot is excessively turned downward and inward, often with a deep medial crease.

Older Children

Untreated clubfoot in an older child can cause difficulty walking, poor shoe fit, painful callosities, and abnormal weight-bearing.

Severe untreated cases may result in walking on the lateral or dorsal aspect of the foot.

Pain

Pain is uncommon in infancy but may develop in older children or adults if the deformity remains uncorrected or becomes rigid.

Physical Examination

The typical examination demonstrates heel equinus, hindfoot varus or supination, and adduction of the midfoot and forefoot.

Together, these findings produce the characteristic appearance of a curved or “kidney-shaped” foot.

Medial Crease

A prominent medial or plantar crease is commonly present.

The foot projects medially from the leg and may resemble the shape of a club.

Flexibility

The examiner should determine how much of the deformity can be passively corrected.

Flexibility is important for assessing severity and planning treatment.

Muscle Function

Ankle and toe muscle activity should be evaluated.

The absence of active toe dorsiflexion may indicate more severe neuromuscular involvement and is associated with a less favorable prognosis.

Calf Hypoplasia

A smaller calf is a characteristic feature.

Even after successful correction of the foot position, some degree of calf hypoplasia usually persists.

Imaging

General Role of Radiographs

Radiographs are not routinely necessary for the diagnosis or early treatment of typical idiopathic clubfoot.

They may be useful when there is concern for underlying bony fusion, atypical anatomy, or when operative treatment is being planned.

Simulated Weight-Bearing Views

When imaging is obtained in a young child who cannot stand, simulated standing AP and lateral radiographs may be used.

Obtaining adequate images can be difficult because of the rigid deformity.

Positioning

The foot should be corrected as close to neutral as possible during imaging.

A Plexiglas plate or similar device may be used to hold the foot in position.

AP Radiograph

On the AP view, the forefoot is typically markedly adducted.

In a normal foot, the talus roughly aligns with the first metatarsal and the calcaneus with the fifth metatarsal.

Kite Angle

The angle between the longitudinal axes of the talus and calcaneus is known as the talocalcaneal or Kite angle.

On an AP radiograph, the normal angle is approximately 20–40°.

Kite Angle in Clubfoot

In clubfoot, the talus and calcaneus are nearly parallel.

As a result, the AP talocalcaneal angle is substantially reduced.

Lateral Radiograph

The lateral view demonstrates the equinus position of the foot.

In a normal foot, the lateral talocalcaneal angle is approximately 35–50°.

Lateral Talocalcaneal Angle in Clubfoot

In clubfoot, the talus and calcaneus remain relatively parallel in the sagittal plane, producing a markedly decreased talocalcaneal angle.

These angular relationships can help assess the adequacy of correction.

Pathological Findings

The principal bony abnormality is medial deviation of the talar neck with subluxation of the talonavicular joint.

Soft-tissue abnormalities are also prominent.

Muscle Abnormalities

Histologic studies have demonstrated that muscle fibers on the affected side may be smaller than normal.

This contributes to the characteristic calf hypoplasia.

Soft-Tissue Contracture

The fascia, tendons, and joint capsules on the medial and posterior aspects of the foot are thickened and contracted.

These soft-tissue abnormalities contribute to the rigidity of the deformity.

Differential Diagnosis

Metatarsus Adductus

Severe metatarsus adductus can resemble clubfoot because the forefoot is turned inward.

The key difference is that metatarsus adductus does not have the fixed hindfoot equinus component characteristic of true clubfoot.

Treatment

General Principles

Treatment should begin as soon as practical after birth.

The current standard for most idiopathic clubfeet is serial manipulation and casting using the Ponseti method.

Ponseti Method

The Ponseti technique gradually corrects the deformity through a specific sequence of gentle manipulations followed by long-leg casting.

Correction proceeds progressively rather than attempting to force the foot immediately into a normal position.

Correction Sequence

The forefoot is gradually abducted while the heel and talus are stabilized.

This corrects the cavus, adduction, and hindfoot varus components.

Equinus is corrected last, after the foot has been brought into appropriate alignment.

Long-Leg Casting

A cast is applied from the toes to above the knee to maintain each stage of correction.

The cast is typically changed at approximately weekly intervals until adequate correction is achieved.

Duration of Casting

Correction often requires approximately 6–8 weeks, although the number of casts varies with the severity and rigidity of the deformity.

Achilles Tenotomy

Persistent equinus is very common after correction of the other components.

A percutaneous Achilles tenotomy is therefore frequently performed to obtain adequate ankle dorsiflexion.

Post-Correction Bracing

After successful correction, maintenance bracing is essential to reduce recurrence.

A foot-abduction brace, commonly consisting of shoes attached to a Denis Browne-type bar, is used.

Brace Schedule

The brace is generally worn essentially full-time during the initial post-correction period and subsequently during sleep and naps for several years.

Adherence to bracing is one of the most important factors in preventing recurrence.

Physical Therapy

Stretching

Stretching of the heel cord and medial soft tissues may be helpful.

However, stretching alone is usually insufficient to correct a true clubfoot.

Maintenance of Correction

Exercises are most useful after casting as an adjunct to preserve ankle and foot flexibility.

They should not substitute for appropriate casting and bracing.

Medication

Medication has little role in the routine correction of clubfoot.

Botulinum toxin has been investigated as an adjunct to casting and splinting in selected cases, but it is not a standard substitute for established Ponseti treatment.

Surgery

Indications

Surgery is reserved primarily for persistent or recurrent deformity that cannot be adequately corrected with repeat casting and less invasive measures.

Modern Ponseti treatment has substantially reduced the need for extensive surgical release.

Treatment of Relapse

Recurrent deformity can frequently be managed with repeat casting, repeat Achilles tenotomy, or anterior tibialis tendon transfer.

The specific treatment depends on the pattern and flexibility of the recurrence.

Anterior Tibialis Tendon Transfer

An anterior tibialis tendon transfer may be useful in a child with recurrent dynamic supination after initial successful correction.

The tendon is repositioned to rebalance the foot during gait.

Extensive Surgical Release

If casting fails completely, more extensive surgery may be necessary.

The goal is to release contracted structures while avoiding excessive dissection that could lead to stiffness and scarring.

Medial Release

Medial procedures may include lengthening or release of the posterior tibial tendon and flexor tendons, together with release of contracted medial structures.

Posterior Release

Posterior correction may require Achilles tendon lengthening and release of contracted posterior joint capsules.

Minimize Capsular Dissection

Extensive capsular release should be minimized whenever possible because over-dissection increases the risk of postoperative stiffness, scarring, weakness, and later pain.

Temporary Fixation

Pins may occasionally be used to maintain correction after surgical release.

When used, they may remain in place for several weeks while the soft tissues heal.

Repeat Surgery

A minority of children treated surgically may require additional procedures later because of recurrent deformity or residual imbalance.

Historically, repeat surgery has been required in approximately 10–20% of surgically treated patients.

Follow-Up

Referral

Children with suspected clubfoot should be referred to an orthopaedic surgeon experienced in pediatric foot deformity and Ponseti treatment.

Early specialist management improves the likelihood of successful nonoperative correction.

Prognosis

With appropriate treatment, most children achieve a plantigrade, functional foot that allows normal or near-normal walking and activity.

Residual Differences

Certain features cannot be fully corrected.

The affected foot often remains somewhat smaller, the calf may remain thinner, and slight limb or foot shortening may persist.

These differences usually have little effect on overall function.

Complications

Residual Deformity

Incomplete correction may leave persistent equinus, varus, adduction, or cavus.

Residual deformity may interfere with shoe wear or gait.

Rocker-Bottom Foot

Overly forceful correction, particularly dorsiflexion before adequate correction of hindfoot and forefoot alignment, can produce a rocker-bottom deformity.

This should be avoided through proper sequential correction.

Overcorrection

Excessive correction can result in hindfoot valgus or other alignment abnormalities.

Stiffness

Extensive surgical treatment may result in a stiff foot.

This is one reason modern management emphasizes serial casting and limited procedures whenever possible.

Pain

Pain can develop later in childhood or adulthood, particularly if residual deformity, overcorrection, stiffness, or degenerative changes are present.

Patient Monitoring

Long-Term Follow-Up

Children require regular follow-up for several years because recurrence may occur even after an initially successful correction.

Timing of Recurrence

Idiopathic clubfoot may recur through approximately 6–7 years of age, although most relapses occur during the first several years of life.

Monitoring for Relapse

Follow-up should assess ankle dorsiflexion, hindfoot alignment, forefoot adduction, dynamic supination, brace adherence, gait, and shoe fit.

Management of Recurrence

Early recurrence can often be successfully treated with repeat Ponseti casting, Achilles tenotomy, or anterior tibialis tendon transfer, avoiding the need for extensive surgery.