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Orthopaedic Surgery - Heel Pain (Plantar Fasciitis)


Basics

Plantar fasciitis is the most common cause of plantar heel pain in adults.

Although commonly called “fasciitis,” the underlying process is predominantly degenerative rather than inflammatory, and the term plantar fasciopathy may more accurately describe the pathology.


Other Causes of Plantar Heel Pain

Not all plantar heel pain is caused by plantar fasciitis.

Important alternative causes include:

Entrapment of the first branch of the lateral plantar nerve, heel-pad atrophy, inflammatory enthesopathy associated with seronegative spondyloarthropathies, tarsal tunnel syndrome, and calcaneal stress fracture.

The first branch of the lateral plantar nerve is also commonly referred to as Baxter’s nerve.


Geriatric Considerations

In older adults, plantar heel pain may result from atrophy of the calcaneal fat pad, degenerative changes at the plantar fascial origin, or both.

Loss of heel cushioning can produce pain directly beneath the calcaneus during standing and walking.


Pediatric Considerations

Heel pain in children is more commonly caused by calcaneal apophysitis, or Sever disease, rather than plantar fasciitis.

Sever disease is related to repetitive traction and loading at the immature calcaneal apophysis, particularly around the Achilles tendon insertion.


Treatment of Sever Disease

Management typically includes:

Relative rest, activity modification, heel-cord stretching, NSAIDs when appropriate, heel cushioning, and temporary restriction from running or jumping sports.

A walking boot or short period of immobilization may be used for severe symptoms.

The disorder is self-limited and resolves after closure of the calcaneal apophysis with skeletal maturity.


Pregnancy Considerations

Heel pain during pregnancy may result from plantar fasciopathy or enthesopathy related to increased mechanical loading, weight gain, and hormonal changes.

Fluid retention may also contribute to compression neuropathies such as tarsal tunnel syndrome or entrapment of Baxter’s nerve.

Symptoms frequently improve after pregnancy.


Prevention

Plantar fasciitis cannot always be prevented, but risk may be reduced by avoiding:

Excessive weight gain, prolonged standing, poorly supportive footwear, and abrupt increases in running, jumping, or other repetitive impact activities.

Gradual progression of exercise and maintenance of calf flexibility may also be helpful.


Epidemiology

Plantar fasciitis is extremely common in adults.

It occurs most frequently during the third through fifth decades of life, although it can affect patients of virtually any adult age.


Risk Factors

Recognized risk factors include:

Restricted ankle dorsiflexion, tight gastrocnemius or Achilles complex, obesity or body mass index greater than 30, prolonged standing, running, jumping sports, diabetes mellitus, thyroid dysfunction, and inflammatory rheumatologic disease.


Etiology and Pathophysiology

The term “plantar fasciitis” suggests inflammation, but chronic cases usually show degenerative changes without substantial histologic inflammation.

Repeated tensile loading at the plantar fascia origin can result in microscopic injury, collagen degeneration, and chronic pain.


Repetitive Microtrauma

The plantar fascia is repeatedly tensioned during standing, walking, and running.

Overuse may produce microscopic tearing near its calcaneal origin.

Repeated loading before adequate healing can lead to chronic degeneration.


Contracture

A tight plantar fascia or heel cord increases tension across the plantar-medial calcaneal origin and may contribute to symptoms.


Associated Conditions

Frequently associated findings include:

Pes planus, cavus foot, Achilles or gastrocnemius contracture, obesity, and inflammatory arthropathies.


Flatfoot

Pes planus can increase tensile load on the plantar fascia by allowing greater elongation of the medial longitudinal arch.


Cavus Foot

A cavus foot may also predispose to plantar heel pain because the plantar fascia and other plantar soft tissues can become relatively tight.


Diagnosis

Plantar fasciitis is usually diagnosed clinically on the basis of a characteristic history and physical examination.

Imaging is not routinely required in a typical presentation.


History

The classic complaint is pain at the plantar-medial heel that is most severe with the first few steps in the morning.

A similar pattern may occur after prolonged sitting or inactivity.


Start-Up Pain

Pain often improves after several minutes of walking as the plantar fascia and surrounding tissues “loosen.”


Later-Day Symptoms

Although symptoms may improve initially with activity, pain can worsen again after prolonged standing, walking, or exercise later in the day.


Character of Pain

Patients may describe the discomfort as:

Aching, soreness, burning, stabbing, or sharp pain.


Physical Examination


Foot Alignment

The examiner should evaluate the foot for pes planus, cavus alignment, hindfoot deformity, and abnormal loading patterns.


Ankle Dorsiflexion

Ankle dorsiflexion should be measured with the knee both flexed and extended.

This helps distinguish isolated gastrocnemius tightness from a combined gastrocnemius-Achilles contracture.


Plantar Fascia Palpation

The most characteristic finding is focal tenderness at the plantar-medial calcaneal tubercle, where the plantar fascia originates.


Toe Dorsiflexion

Passive dorsiflexion of the toes tensions the plantar fascia through the windlass mechanism.

This maneuver may increase tenderness and reproduce the patient’s pain.


Neurologic Examination

The tarsal tunnel and course of the first branch of the lateral plantar nerve should be examined when neuropathic pain is suspected.


Tinel Sign

Percussion over the tarsal tunnel may reproduce tingling or burning into the plantar foot in patients with tibial nerve compression.


Baxter Nerve Entrapment

Tenderness or neuropathic pain deep to the abductor hallucis region may suggest entrapment of the first branch of the lateral plantar nerve.


Heel-Pad Atrophy

Pain centered directly beneath the calcaneal tuberosity rather than along the plantar-medial origin of the fascia may suggest fat-pad atrophy.

The heel pad may feel thin or poorly cushioned.


Calcaneal Stress Fracture

Medial-lateral compression of the calcaneus may reproduce pain in a calcaneal stress fracture.

This finding should prompt further investigation when symptoms are atypical for plantar fasciitis.


Laboratory Tests

Laboratory studies are not routinely required.

They may be considered in chronic, bilateral, recurrent, or atypical cases when systemic disease is suspected.


Potential Studies

Depending on the clinical setting, testing may include:

Rheumatoid factor, antinuclear antibodies, thyroid function studies, fasting glucose, hemoglobin A1C, inflammatory markers, and HLA-B27 testing.

HLA-B27 testing is most relevant when a seronegative spondyloarthropathy is suspected.


Imaging


Plain Radiographs

Weight-bearing radiographs of the foot may be obtained when pain is persistent, atypical, or associated with deformity.

They can help exclude fracture, arthritis, or other structural abnormalities.


Heel Spur

A plantar calcaneal spur is not diagnostic of plantar fasciitis.

Heel spurs are frequently found in asymptomatic individuals.

Their presence therefore does not establish the cause of heel pain.


Bone Scintigraphy

Bone scintigraphy may demonstrate increased uptake near the plantar fascia origin.

More diffuse calcaneal uptake may suggest a stress fracture.

Today, MRI is generally more useful when further imaging is needed.


MRI

MRI can demonstrate thickening and degenerative change of the proximal plantar fascia, with surrounding soft-tissue or adjacent calcaneal marrow edema.


Calcaneal Stress Fracture

A stress fracture generally produces more extensive bone marrow edema and may reveal a distinct fracture line.


Pathological Findings

Chronic plantar fasciitis demonstrates degenerative collagen changes at the plantar fascial origin.

Substantial chronic inflammatory cell infiltration is typically absent.


Differential Diagnosis

Important alternative diagnoses include:

Calcaneal apophysitis in children, calcaneal stress fracture, heel-pad atrophy, tarsal tunnel syndrome, Baxter nerve entrapment, inflammatory enthesopathy, and spinal radiculopathy.


Treatment


General Principles

Nonoperative treatment is the foundation of management.

Surgery is rarely required because the vast majority of patients improve with conservative measures.


Stretching

Stretching of the gastrocnemius-Achilles complex and plantar fascia should be performed regularly.

Stretching can be performed several times daily and before or after athletic activity.


Activity Modification

Activities that aggravate symptoms should be reduced temporarily.

Running, jumping, prolonged standing, and repetitive impact activity may need to be modified during the symptomatic phase.


Footwear and Heel Cushioning

A soft gel heel cup or cushioned heel insert may improve comfort by reducing impact at the plantar heel.

Supportive footwear is preferable to poorly cushioned or worn-out shoes.


Orthotic Arch Support

An arch support may be useful, particularly in patients with pes planus or excessive pronation.

Prefabricated devices are often sufficient initially.


Night Splints

A dorsiflexion night splint may help chronic symptoms by maintaining the ankle and plantar fascia in a gently stretched position overnight.

This may reduce severe first-step morning pain.


Ice and Massage

Ice application and deep-tissue or plantar fascial massage may provide symptomatic relief.

Rolling the plantar foot over a chilled bottle or similar device combines stretching, massage, and cooling.


Immobilization

A walking boot or short period of cast immobilization can be used for severe or recalcitrant symptoms to reduce repetitive loading of the plantar fascia.


Corticosteroid Injection

Local corticosteroid injection may be considered for persistent symptoms that have not responded to other nonoperative measures.

However, injections should be used cautiously because they carry risks including plantar fascial rupture and fat-pad atrophy.

Repeated injections are generally avoided.


Post-Injection Protection

Temporary restriction of high-impact activity after injection is appropriate.

A short period of protected weight bearing or boot use may be considered in selected patients.


Return to Activity

Once symptoms improve, activity should be resumed gradually.

Running and jumping should not be restarted abruptly at full intensity because sudden increases in repetitive stress can provoke recurrence.


Extracorporeal Shock-Wave Therapy

Extracorporeal shock-wave therapy can be considered for chronic plantar fasciitis that persists despite prolonged conservative treatment.

It may offer an alternative before operative intervention in appropriately selected patients.


Calcaneal Stress Fracture

Calcaneal stress fractures are generally treated with:

Activity restriction, protected weight bearing, NSAIDs or other analgesia when appropriate, and temporary immobilization when symptoms are severe.


Sever Disease

Treatment of calcaneal apophysitis similarly emphasizes:

Relative rest, heel-cord stretching, activity modification, heel cushioning, and short-term immobilization for severe cases.

Surgery is not indicated.


Heel-Pad Atrophy

Heel-pad atrophy is managed primarily with well-cushioned footwear, shock-absorbing heel cups, and reduction of repetitive impact loading.


Physical Therapy

Physical therapy can help teach proper calf and plantar fascia stretching, gait mechanics, strengthening, and graded return to activity.

It is particularly useful when tightness or biomechanical abnormalities contribute to symptoms.


Medication

NSAIDs may be used for short-term relief when pain is substantial.

Because the condition is largely degenerative rather than inflammatory, medication primarily provides symptomatic benefit rather than correcting the underlying pathology.


Surgery

Surgery is rarely indicated and is generally reserved for patients with persistent disabling symptoms despite at least 6–9 months of well-performed nonoperative treatment.


Partial Plantar Fascia Release

The usual procedure consists of partial release of the plantar fascia origin.

A complete release should be avoided because it may destabilize the longitudinal arch.


Heel-Spur Removal

Routine removal of a calcaneal spur is generally unnecessary because the spur itself is often not the source of pain.


Nerve Decompression

When persistent tarsal tunnel syndrome or entrapment of Baxter’s nerve contributes to symptoms, decompression may be performed in selected cases, sometimes in combination with partial plantar fascia release.


Contraindication in Sever Disease

Plantar fascia surgery is not appropriate for calcaneal apophysitis.

Sever disease is a self-limited developmental condition.


Follow-Up


Prognosis

The prognosis is excellent.

More than 90% of patients improve with nonoperative treatment and are able to return to normal activities.

Resolution may nevertheless require several months.


Complications


Plantar Fascia Rupture

Plantar fascial rupture may occur after corticosteroid injection or excessive surgical release.


Arch Collapse

Excessive release of the plantar fascia can weaken support of the medial longitudinal arch and contribute to arch collapse.


Lateral Column Overload

Loss of plantar fascial tension may shift mechanical stress toward the lateral midfoot, producing painful lateral column overload.


Fat-Pad Atrophy

Corticosteroid injection may contribute to degeneration or thinning of the heel fat pad, producing persistent plantar heel pain.


Patient Monitoring

Follow-up should assess pain intensity, morning first-step symptoms, tenderness at the plantar fascial origin, ankle dorsiflexion, activity tolerance, and adherence to stretching and footwear modification.

Persistent atypical pain, neurologic symptoms, focal bony tenderness, or failure to improve should prompt reconsideration of the diagnosis and evaluation for alternative causes such as stress fracture, nerve entrapment, or inflammatory disease.


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Orthopaedic Surgery - Hand Anatomy and Examination


Basics

The hand is a highly specialized organ that provides strength, precision, sensation, grasp, and fine motor control, allowing complex activities ranging from heavy manual work to delicate manipulation.

Anatomically, the hand can be divided into volar (palmar) and dorsal surfaces.


Volar Anatomy

The volar aspect contains many of the major structures responsible for hand function, including the digital nerves, major vascular structures, flexor tendons, and intrinsic muscles.

Because these structures are closely packed together, even relatively small palmar lacerations may injure several important tissues simultaneously.


Bony Anatomy

The hand and wrist contain a complex arrangement of bones.

There are:

8 carpal bones, 5 metacarpals, and 14 phalanges.

Each finger contains a proximal, middle, and distal phalanx.

The thumb has only two phalanges: proximal and distal.


History

A thorough history should precede the physical examination.

Important information includes:

Hand dominance, occupation, previous hand injuries or operations, mechanism of trauma, duration of symptoms, and location and character of pain.

Functional complaints such as weakness, loss of grip, numbness, locking, instability, or difficulty with specific activities should also be documented.


General Examination Principles

Understanding normal hand anatomy and biomechanics is essential for identifying injury.

The examiner should use a consistent, systematic examination sequence so that important structures are not overlooked.

The opposite hand provides an extremely useful comparison with the patient’s normal anatomy, strength, motion, and joint laxity.


Inspection

The hand should first be observed at rest.


Resting Posture

The natural posture of the fingers should be assessed.

Abnormal finger position may indicate tendon rupture, nerve injury, fracture, dislocation, or joint contracture.

The normal flexor cascade should also be observed.


Deformity

The examiner should identify any gross angular, rotational, or joint deformity.

Rotational malalignment may become more obvious when the patient makes a fist.


Soft-Tissue Changes

Look for:

Swelling, bruising, erythema, wounds, scars, masses, muscle wasting, and skin abnormalities.


Nail and Fingertip Examination

The nail plate, nail folds, pulp, and surrounding soft tissues should be inspected for:

Subungual hematoma, nail-bed injury, infection, fingertip trauma, vascular compromise, or deformity.


Vascular Examination

Adequate perfusion should be confirmed in the hand and each individual digit.


Radial and Ulnar Arteries

The radial and ulnar arteries should be palpated at the wrist.

Doppler examination can be used if pulses are difficult to detect.


Digital Arteries

The digital arteries can be assessed with handheld Doppler when vascular injury is suspected.


Capillary Refill

Capillary refill should be tested in each finger.

Normal refill is generally less than approximately 2 seconds in a warm, well-perfused hand.


Additional Perfusion Assessment

When necessary, finger temperature and pulse oximetry may provide additional information about digital perfusion.

These measurements are particularly useful when vascular compromise is subtle.


Allen Test

The Allen test assesses patency of the radial and ulnar arteries and the completeness of the palmar arterial arch.

The patient repeatedly opens and closes the hand while the examiner compresses both the radial and ulnar arteries.

The hand is then opened and one artery is released.

Rapid return of color indicates adequate flow through that artery and the palmar arch.

The test is then repeated for the opposite artery.

Delayed or absent reperfusion suggests arterial obstruction or incomplete collateral circulation.


Neurologic Examination

Neurologic assessment should include both sensory and motor testing.

The median, ulnar, and radial nerves should be evaluated systematically.


Sensory Examination

Sensation can initially be tested with light touch.

Two-point discrimination provides a more detailed evaluation of digital nerve function.


Two-Point Discrimination

Normal static two-point discrimination at the fingertip is generally approximately 6 mm or less, while moving two-point discrimination is normally somewhat finer.

The result should be compared with the opposite hand and adjacent digits.

A bent paperclip or formal discriminator can be used when dedicated instruments are unavailable.


Motor Examination

Both the extrinsic muscles, originating in the forearm, and the intrinsic muscles, originating within the hand, should be tested.


Extrinsic Flexors

The flexor digitorum superficialis and flexor digitorum profundus tendons should be tested individually in each finger.


Flexor Digitorum Profundus

To test the FDP, hold the PIP joint in extension and ask the patient to flex the DIP joint.

Active DIP flexion indicates continuity of the profundus tendon.


Flexor Digitorum Superficialis

To isolate the FDS, hold the other fingers in extension and ask the patient to flex the finger being tested at the PIP joint.


Extrinsic Extensors

Finger extension at the MCP joints should be tested individually.

Thumb extension should also be assessed.

Weakness may reflect tendon injury or radial nerve dysfunction proximal to the hand.


Intrinsic Muscles

The intrinsic muscles can be assessed by asking the patient to flex the MCP joints while extending the interphalangeal joints.

Finger abduction and adduction should also be tested with the MCP joints extended.

Asking the patient to cross adjacent fingers can further assess intrinsic muscle function.


Median Nerve


Sensory Examination

Median nerve sensation should be tested over the palmar aspect of the thumb, index finger, middle finger, and radial half of the ring finger.


Thenar Eminence

Sensation over the thenar eminence is supplied by the palmar cutaneous branch of the median nerve, which branches proximal to the carpal tunnel.

This area should be tested separately.

Preserved thenar sensation despite numbness in the median-innervated digits can support localization of compression to the carpal tunnel.


Motor Examination

Palmar abduction of the thumb assesses the abductor pollicis brevis and is an important test of recurrent motor branch function of the median nerve.


Ulnar Nerve


Sensory Examination

Sensation should be tested over the little finger and ulnar half of the ring finger, including the volar fingertip.


Motor Examination

The ulnar nerve supplies most of the intrinsic muscles of the hand.

Motor function can be tested by asking the patient to abduct and adduct the fingers or cross the fingers.


Radial Nerve


Sensory Examination

Radial nerve sensation is best assessed over the dorsal first web space.


Motor Examination

The radial nerve does not provide meaningful intrinsic motor innervation within the hand itself.

Motor function is assessed through muscles in the forearm by testing wrist extension, MCP joint extension of the fingers, and thumb extension.


Bones, Tendons, and Ligaments

Every bone and major joint should be palpated systematically when trauma or localized pain is present.


Range of Motion

Both active and passive range of motion should be assessed.

Approximate normal values include:

Thumb IP joint: approximately 0–80° of flexion.

Thumb MCP joint: approximately 0–50° of flexion.

Finger DIP joints: approximately 0–70 to 90°.

Finger PIP joints: approximately 0–100° or slightly greater.

Finger MCP joints: approximately 0–90°.

Wrist flexion: approximately 80°.

Wrist extension: approximately 70°.

Normal motion varies among individuals, so comparison with the opposite side is valuable.


Joint Examination

Each joint should be assessed for:

Tenderness, swelling, effusion, bogginess, instability, crepitus, loss of motion, or hypermobility.


Collateral Ligaments

Excessive side-to-side laxity may indicate injury to a collateral ligament.

Stress testing should be performed carefully and compared with the opposite side.


Important Wrist Structures

Two common sources of wrist pathology are the scapholunate ligament and the triangular fibrocartilage complex (TFCC).


Scapholunate Ligament

The scapholunate interval should be palpated dorsally for tenderness, particularly after wrist trauma.


TFCC

The TFCC lies on the ulnar side of the wrist and contributes to distal radioulnar and ulnocarpal stability.

Tenderness in this region may indicate a TFCC injury.


Special Tests


Tinel Sign at the Carpal Tunnel

Percussion over the median nerve at the volar wrist may produce tingling, numbness, or electric sensations in the median nerve distribution.

A positive test supports median nerve irritation and may be seen in carpal tunnel syndrome.


Flexion-Compression Test

The examiner applies direct pressure over the carpal tunnel while the wrist is held in flexion.

Reproduction of numbness, tingling, or pain in the median distribution within approximately 30 seconds supports the diagnosis of carpal tunnel syndrome.


Phalen Test

The patient holds the wrists in maximal flexion, usually by placing the dorsal surfaces of the hands together.

Development of paresthesias in the median nerve distribution within approximately 60 seconds is considered a positive test.


Wrist Aspiration

Wrist aspiration may be performed when infection, crystal arthropathy, hemarthrosis, or another joint process is suspected.


Dorsal Approach

A common dorsal entry point is between the third extensor compartment, containing extensor pollicis longus, and the fourth compartment, containing extensor digitorum communis and extensor indicis proprius.

Lister’s tubercle can be used as a palpable landmark.

The radiocarpal joint is entered just distal to this region, with slight wrist flexion facilitating access.


Eichhoff Test

The Eichhoff maneuver is frequently, although inaccurately, referred to as the Finkelstein test.

The patient places the thumb within the fist, and the examiner then passively deviates the wrist toward the ulna.

Pain over the first dorsal extensor compartment, containing the abductor pollicis longus and extensor pollicis brevis, supports the diagnosis of de Quervain tenosynovitis.

The true Finkelstein maneuver is performed somewhat differently, but both tests stress the first extensor compartment.


Thumb CMC Grind Test

The thumb carpometacarpal joint is assessed by applying axial compression through the thumb metacarpal while rotating or grinding the joint.

Reproduction of pain, particularly with crepitus, is consistent with trapeziometacarpal or thumb CMC osteoarthritis.


Imaging


Plain Radiographs

The standard hand radiographic series includes:

AP or PA, oblique, and lateral views.

These films help identify fractures, dislocations, joint-space abnormalities, malalignment, and degenerative changes.


Lateral View

For evaluation of individual digits, the fingers may be splayed or separated on the lateral projection to prevent overlap and allow clearer visualization of each phalanx and joint.


General Examination Approach

A complete hand assessment should proceed systematically through:

Inspection, vascular examination, sensory testing, motor testing, tendon assessment, joint range of motion, ligament stability, palpation, special tests, and appropriate imaging.

Because the structures of the hand are small and closely related, comparison with the opposite hand and careful documentation are especially important for detecting subtle abnormalities.


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Orthopaedic Surgery - Hamstring Strain



Basics


The hamstrings are a group of long muscles located in the posterior thigh. They extend from the pelvis toward the knee and play an important role in hip extension, knee flexion, gait, sprinting, and deceleration.


A hamstring strain is a stretch-induced or forceful contraction injury of the muscle-tendon unit.


The injury commonly occurs when the hamstrings are required to change rapidly from controlling limb motion eccentrically to generating force concentrically, particularly during sudden acceleration or deceleration.



Mechanism


Hamstring strains frequently occur during quick starts, sudden stops, sprinting, jumping, or other explosive movements that produce a powerful contraction while the muscle is lengthened.



Classification


Hamstring strains are traditionally divided into three grades according to severity.



Mild Strain


A mild strain produces pain and muscle spasm without a substantial structural tear.


There is minimal loss of strength and usually only mild functional limitation.



Moderate Strain


A moderate injury involves partial tearing of muscle fibers.


Pain is more pronounced, and measurable weakness and functional limitation are present.



Severe Strain


A severe injury represents a complete or near-complete tear of the muscle or tendon, sometimes including avulsion from its bony attachment.


Marked weakness and immediate loss of function are typical.



Limitations of Grading


Traditional strain grading provides a useful description of injury severity, but clinical classification systems do not consistently predict the exact time required for return to sport.



Prevention


Prevention programs focus on improving hamstring strength, flexibility, fatigue resistance, and neuromuscular control.



Stretching


Regular hamstring stretching may be beneficial, particularly as part of a structured conditioning program.


Stretching should be performed carefully when the muscles are fatigued.



Conditioning


Anaerobic interval training and sport-specific drills can improve the ability of the hamstrings to tolerate repeated high-speed loading.



Strengthening


Eccentric hamstring strengthening is particularly important because the hamstrings undergo substantial eccentric loading during sprinting and deceleration.



Epidemiology


Hamstring strains are among the most common injuries encountered in athletes.


They are particularly associated with sports requiring sprinting, jumping, kicking, sudden acceleration, and ballistic lower-extremity movements.



Frequency


Hamstring injuries have been reported to account for a substantial proportion of sports-related injuries, reaching approximately 29% in some athletic populations.


They account for approximately 12% of injuries among professional football players in some series.



Associated Sports


Activities commonly associated with hamstring injury include running, football, skiing, dancing, skating, jumping, and weight lifting.



Recurrence


Recurrence is a major clinical problem.


Approximately one-third of hamstring injuries may recur, particularly when return to sport occurs before full recovery of strength and flexibility.



Risk Factors


Important risk factors include:


Increasing age, previous hamstring injury, muscle weakness, imbalance between quadriceps and hamstring strength, reduced lower-extremity flexibility, impaired trunk or core stability, fatigue, and dehydration.


The strongest predictor of future hamstring injury is often a previous hamstring strain.



Anatomy and Pathophysiology


The principal hamstring muscles are the biceps femoris, semitendinosus, and semimembranosus.



Proximal Origin


The semitendinosus, semimembranosus, and long head of the biceps femoris originate from the ischial tuberosity.


The short head of the biceps femoris originates from the posterior femur rather than the pelvis.



Distal Insertions


The biceps femoris inserts primarily on the fibular head.


The semitendinosus inserts medially on the proximal tibia as part of the pes anserinus, while the semimembranosus inserts on the posteromedial proximal tibia.



Function


The hamstrings flex the knee and contribute to hip extension.


During running and gait, they contract eccentrically to decelerate knee extension and absorb kinetic energy.



Common Site of Injury


Muscle strain most often occurs near a musculotendinous junction, frequently involving the biceps femoris, especially during high-speed running.



Pediatric and Adolescent Considerations


In children and adolescents, the tendon may be stronger than the immature apophysis.


A forceful hamstring contraction can therefore produce an ischial tuberosity avulsion fracture rather than a purely tendinous injury.



Adult Considerations


In adults, the same mechanism may produce a partial or complete proximal hamstring tendon avulsion.



Etiology


Hamstring strains usually occur when the muscle is rapidly lengthened while simultaneously generating substantial force.



Predisposing Factors


Predisposing factors include:


Poor flexibility, inadequate warm-up, fatigue, dehydration, muscle weakness, impaired coordination between opposing muscle groups, and quadriceps-to-hamstring strength imbalance.



Common Injury Mechanisms


Typical mechanisms include:


Sprinting from starting blocks, clearing a hurdle, forceful jumping or take-off, sudden acceleration, rapid deceleration, and water-skiing falls.



Water-Skiing Injury


A classic water-skiing mechanism occurs when the hips are suddenly flexed while the knees remain extended, sometimes producing substantial proximal hamstring injury.



Associated Conditions


Hamstring injuries may coexist with other musculoskeletal problems, including lumbar strain and groin strain.



Diagnosis



History


The usual presentation is sudden posterior thigh pain during running, jumping, or another explosive activity.



Sudden Onset


Most patients describe an abrupt onset of pain and tenderness.


A smaller proportion may develop symptoms more gradually.



Pop


More severe injuries may be accompanied by a sudden pop or tearing sensation, followed by immediate weakness or inability to continue activity.



Signs and Symptoms


Common symptoms include:


Posterior thigh pain, tenderness, weakness, swelling, bruising, and difficulty walking or running.


Pain is generally aggravated by stretching the hamstrings or activating them against resistance.



Physical Examination



Gait


Patients may demonstrate a stiff-legged gait because they attempt to avoid simultaneous hip flexion and knee extension, which places the hamstrings on stretch.



Inspection


The posterior thigh should be examined for:


Swelling, bruising, ecchymosis, hematoma, contour abnormality, or a palpable defect.


Marked bruising may indicate a more substantial tear.



Palpation


The entire hamstring muscle-tendon complex should be palpated from the ischial tuberosity to the distal insertions.


The location of maximal tenderness helps identify the injured structure.



Resisted Knee Flexion


Pain or weakness with resisted knee flexion supports the diagnosis of hamstring injury.



Resisted Hip Extension


Pain with resisted hip extension may also occur, especially with proximal injury.



Stretch Testing


Passive hip flexion combined with knee extension stretches the hamstrings and may reproduce symptoms.



Pathological Findings


The injury spectrum ranges from microscopic muscle-fiber disruption to a partial or complete tear of the biceps femoris, semitendinosus, semimembranosus, or associated tendons.



Imaging


Imaging is not routinely required when the history and examination clearly indicate an uncomplicated muscle strain.



Plain Radiographs


Radiographs should be obtained when fracture or avulsion is suspected.



Pelvic Radiographs


In adolescents, pelvic radiographs may demonstrate an ischial tuberosity avulsion fracture.



Knee Radiographs


If symptoms are concentrated near the distal biceps femoris insertion, knee radiographs may demonstrate an associated fibular head avulsion fracture.



Femoral Radiographs


Plain films of the femur may be helpful when a fracture is suspected after significant trauma.



MRI


MRI can define the location, extent, and severity of muscle or tendon injury.


It is particularly useful when a complete tendon avulsion, substantial tear, or alternative diagnosis is suspected.



Stress Fracture


MRI can also differentiate a hamstring strain from an occult stress fracture.



Bone Scintigraphy


Bone scintigraphy can help distinguish stress fracture from soft-tissue injury, although MRI is generally preferred when available.



Differential Diagnosis


Important differential diagnoses include:


Acute fracture, stress fracture, muscle contusion, proximal hamstring tendon avulsion, ischial apophyseal avulsion, and other posterior thigh muscle injuries.



Referred Pain


In more chronic or atypical presentations, referred symptoms from the lumbar spine or hip should also be considered.



Treatment



General Principles


Most musculotendinous hamstring strains are treated nonoperatively.


Treatment progresses through phases according to pain, strength, flexibility, and functional recovery rather than following a rigid timeline.



Acute Phase


During approximately the first week, treatment focuses on controlling pain and swelling.



Initial Measures


Relative rest, ice, compression, and elevation may be used during the early symptomatic period.


Gentle pain-free motion should begin as tolerated.



Subacute Phase


As acute inflammation and pain improve, progressive rehabilitation begins.



Concentric Strengthening


Concentric strengthening can be introduced gradually, together with low-impact cross-training.


Exercises should remain below the threshold that produces significant pain.



Remodeling Phase


During subsequent weeks, rehabilitation emphasizes restoration of muscle length, strength, and neuromuscular control.



Stretching


More progressive hamstring stretching can be introduced once acute pain has settled.



Eccentric Strengthening


Eccentric strengthening is a central component of rehabilitation because the hamstrings must tolerate high eccentric loads during running.



Agility and Trunk Stabilization


Progressive agility drills and core or trunk stabilization exercises are useful for restoring dynamic lower-extremity control.



Functional Phase


Running and sport-specific training can resume gradually when the patient is pain free and has recovered adequate strength and motion.



Return to Sport


Return should be based on functional criteria rather than time alone.


The patient should demonstrate full or near-full range of motion, minimal or no tenderness, symmetric strength, and the ability to sprint and perform sport-specific tasks without pain.



Competitive Phase


Once full activity resumes, continued strengthening, flexibility training, and neuromuscular conditioning are important to reduce recurrence.



Activity


Initial rest should be followed by a gradual progression of activity according to symptoms and functional recovery.


Premature return to sprinting increases the risk of reinjury.



Physical Therapy


Physical therapy is useful for restoring motion, strength, flexibility, and sport-specific function.



Ice Massage


Ice massage may be used for short-term symptomatic relief during the early phase.



Therapeutic Modalities


Modalities such as ultrasound have historically been used, although rehabilitation should focus primarily on progressive exercise and functional restoration.



Aquatic Exercise


Water-based exercise may permit range-of-motion and conditioning work while reducing loading on the injured muscle.



Exercise Progression


Once soreness has improved, active range of motion can progress to resisted knee flexion, hip-extension exercises, eccentric loading, running drills, and sport-specific movements.



Medication



NSAIDs


NSAIDs such as ibuprofen or naproxen may provide short-term relief of pain and swelling.


They have not been shown to accelerate muscle healing and should be used primarily for symptomatic control.



Acetaminophen


Acetaminophen may be used as an alternative analgesic.



Biologic Treatments


Platelet-rich plasma and other biologic therapies have been investigated for hamstring injuries.


Evidence supporting routine use remains limited, and these treatments should not replace structured rehabilitation.



Surgery


Surgery is generally not indicated for uncomplicated musculotendinous junction strains.



Ischial Tuberosity Avulsion Fracture


Adolescent avulsion fractures require assessment of displacement and functional impairment.



Displacement


Historically, displacement greater than approximately 2 cm has been considered a possible indication for operative fixation, particularly in active patients.


Significantly displaced fractures have a greater risk of painful nonunion and persistent functional limitation.



Tendon Avulsion


Complete proximal hamstring tendon avulsions, particularly those involving multiple tendons with substantial retraction, may be considered for surgical repair.


Treatment depends on age, activity level, chronicity, degree of retraction, and functional deficit.



Referral


Evidence of complete tendon rupture, proximal tendon avulsion, substantial weakness, or a significantly displaced ischial avulsion fracture should prompt referral to an orthopaedic sports-medicine specialist.



Follow-Up



Prognosis


Most hamstring strains heal successfully with appropriate rehabilitation.


Recovery time depends on injury severity, location, previous injury, and functional demands.



Mild Strains


Mild strains may improve within several days to approximately 1 week.



Moderate Strains


Moderate injuries may require approximately 1–3 weeks or longer, depending on the size and location of the tear.



Severe Injuries


Severe injuries, tendon avulsions, or displaced ischial tuberosity avulsion fractures may require many weeks to several months before full return to high-level sport.



Complications



Recurrent Strain


Previous hamstring injury significantly increases the risk of another strain.


Recurrence is especially common when flexibility, eccentric strength, and sprinting capacity have not been fully restored.



Chronic Weakness


A significant untreated tendon injury may lead to persistent weakness, reduced endurance, and difficulty with high-speed activity.



Scar Formation


Healing may produce scar tissue that alters normal muscle-tendon mechanics and contributes to recurrent symptoms.



Symptomatic Nonunion


Substantially displaced ischial tuberosity avulsion fractures may fail to unite and produce chronic pain, weakness, or sitting discomfort.



Patient Monitoring


Patients should be followed according to symptom severity and athletic demands.


Monitoring should include pain, tenderness, range of motion, hamstring strength, gait, flexibility, running tolerance, and ability to perform sport-specific movements.


A long-term program of eccentric strengthening, flexibility work, trunk stabilization, and graded athletic conditioning should be continued after return to sport to reduce the risk of recurrence.

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Orthopaedic Surgery - Growth-Plate Injury


Basics

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

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


Common Sites

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

The growth plates most commonly injured include the:

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


Sites at Greatest Risk of Growth Disturbance

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


Synonyms

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

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


Epidemiology

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

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


Age

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


Sex

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


Remaining Growth

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

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


Risk Factors

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


Prevention of Sequelae

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


Physeal Bar

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

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

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


Other Corrective Options

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

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


Contralateral Epiphysiodesis

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


Etiology

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

Other processes may also damage the physis.


Nontraumatic Causes

Potential causes include:

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


Classification

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

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


Salter-Harris Type I

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

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


Salter-Harris Type II

Type II is the most common physeal fracture pattern.

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


Salter-Harris Type III

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

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


Salter-Harris Type IV

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

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


Salter-Harris Type V

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

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


Rang Type VI

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

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


Risk by Classification

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

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


Associated Injuries

Physeal trauma may occur with other injuries, including:

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


Diagnosis

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

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


Signs and Symptoms

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

Visible deformity may be present if the fracture is displaced.


Lower-Extremity Injuries

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


Upper-Extremity Injuries

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


Crepitus

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


Physical Examination

The entire injured limb should be examined carefully.


Skin

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

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


Neurovascular Status

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


Pathological Findings

The physis is organized into several histologic zones:

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


Site of Fracture Propagation

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


Permanent Physeal Injury

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

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


Imaging


Plain Radiographs

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

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


Comparison Views

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


CT

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

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


MRI

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

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


Acute MRI Findings

Possible findings include:

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


Physeal Bar Mapping

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

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


Ultrasound

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


Differential Diagnosis

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

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


Infection

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


Other Causes

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


Treatment


Initial Measures

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


Nondisplaced Fractures

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


Displaced Fractures

Displaced injuries generally require reduction under suitable analgesia or anesthesia.

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

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


Early Follow-Up

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


Splint to Cast Conversion

A splint is often used initially because it accommodates swelling.

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


Weight Bearing

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

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


Duration of Immobilization

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

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


Medication

Analgesia should be provided according to pain severity.

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


Surgery


Goal of Reduction

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

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


Repeated Reduction Attempts

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


Delayed Reduction

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

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


Open Reduction

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


Internal Fixation

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


Crossing the Physis

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

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


Open Fractures

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


Follow-Up


Prognosis

Most growth-plate fractures heal without major difficulty.

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


Effect of Salter-Harris Type

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


Effect of Skeletal Maturity

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


High-Risk Anatomic Sites

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


Lower-Risk Sites

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


Complications


Growth Arrest

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

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


Growth Disturbance

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


Limb-Length Discrepancy

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


Malunion

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


Growth Acceleration

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

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


Patient Monitoring

Children at increased risk of growth disturbance require prolonged surveillance.

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


Duration

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


Clinical Assessment

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


Radiographic Assessment

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

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

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

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


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Orthopaedic Surgery - Growing Pains



Basics


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


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



Typical Pattern


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


Children may occasionally awaken from sleep because of the discomfort.



Resolution of Episodes


Each episode resolves completely.


The child is generally normal and pain free between episodes.



Location


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


Pain is usually vague rather than sharply localized.



Frequency


Episodes occur unpredictably.


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


Some severely affected children may experience symptoms almost daily.



Physical Findings


Growing pains produce no persistent objective abnormalities.


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



Synonyms


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



Epidemiology


Growing pains are very common.


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



Age


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



Sex


Girls may be affected slightly more often than boys.



Risk Factors



High Activity Level


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


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



Family History


A positive family history is common.


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



Etiology


The precise mechanism remains uncertain.


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



Possible Contributing Factors


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


None of these explanations completely accounts for the syndrome.



Diagnosis


Growing pains are a clinical diagnosis of exclusion.


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



Signs and Symptoms



Relationship to Activity


Pain frequently occurs after periods of increased activity.


Symptoms most often develop in the evening or at night.



Nocturnal Pain


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


Persistent morning pain is not typical.



Duration


Individual attacks may last from several minutes to several hours.



Laterality


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



Character


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



Severity


Pain intensity varies considerably.


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



Episodic Course


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


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



Physical Examination


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



Observation of Gait


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


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



Palpation


The lower extremities should be palpated systematically.


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



Range of Motion


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



Hip Examination


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


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



General Findings


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


Any such finding should prompt investigation for another diagnosis.



Laboratory Tests


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



Atypical Presentation


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


Further testing should be directed toward the suspected alternative diagnosis.



Imaging


Routine imaging is unnecessary for classic growing pains.



Plain Radiographs


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



Advanced Imaging


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


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



Differential Diagnosis


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


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



Other Concerning Diagnoses


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



Red Flags


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


These findings require further evaluation.



Treatment



Reassurance


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


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



Stretching


A regular stretching program may decrease the frequency of symptoms.


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



Home Program


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



Activity Modification


Most children can remain active.


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



Orthoses


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


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



Physical Therapy


Formal physical therapy is generally unnecessary.


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



Medication


Simple analgesics may be used occasionally for troublesome episodes.


Examples include acetaminophen or NSAIDs when appropriate.


Continuous routine medication is usually unnecessary.



Follow-Up


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


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



Prognosis


The prognosis is excellent.


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



Patient Monitoring


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


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


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


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

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Orthopaedic Surgery - Giant Cell Tumor


Basics

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

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


Typical Location

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

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

Other common sites include the:

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


Flat Bones

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

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


Multifocal Disease

Multifocal giant cell tumor is rare.

Most patients have a single lesion.


Classification

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

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


Stage I: Latent

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

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

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

The tumor may demonstrate relatively little activity on bone scintigraphy.

Histologically, it remains benign.

Pathologic fracture can occasionally occur.


Stage II: Active

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

Patients are usually symptomatic.

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

Bone scintigraphy is generally active.

Pathologic fracture may occur.

Histologically, the tumor remains benign.


Stage III: Aggressive

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

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

Imaging demonstrates cortical destruction with extension into surrounding soft tissues.

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

The tumor may appear markedly hypervascular on angiographic studies.

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


Epidemiology


Age

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

The tumor is uncommon after approximately 55 years of age.


Skeletal Maturity

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

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

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

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


Frequency

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

It is among the more common primary osseous neoplasms.


Sex

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


Risk Factors

Paget disease of bone is a rare predisposing condition.


Etiology

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

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


Associated Conditions


Paget Disease

Giant cell tumor can rarely complicate Paget disease.

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


Secondary Aneurysmal Bone Cyst

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

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


Diagnosis


Signs and Symptoms

Clinical presentation is often nonspecific.

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


Pain

Approximately 90% of patients complain of pain.

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


Pathologic Fracture

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


Joint Symptoms

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


Physical Examination

There is no pathognomonic physical examination finding.

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


Swelling

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


Joint Effusion and Motion

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


Laboratory Tests

Routine serum chemistry studies are generally normal.


Calcium and Phosphate

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

Evaluation may also include parathyroid hormone testing when clinically appropriate.

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


Imaging


Plain Radiographs

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

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


Epiphyseal Involvement

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

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


Cortical Expansion

The cortex may become progressively thinned and expanded.

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


Reactive Sclerosis

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


Spinal Involvement

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


Multicentric Disease

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


Chest Imaging

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

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


Bone Scintigraphy

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

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


Pathological Findings

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


Mononuclear Cells

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

They have relatively large nuclei and inconspicuous nucleoli.

These stromal cells represent the neoplastic component of the tumor.


Giant Cells

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

Their nuclei often resemble those of the surrounding stromal cells.


Mitotic Activity

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

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


Aneurysmal Bone Cyst Component

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


Vascular Invasion

Tumor cells may occasionally extend into blood vessels.


Involutional Changes

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


Differential Diagnosis


Brown Tumor of Hyperparathyroidism

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

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


Giant Cell Reparative Granuloma

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


Nonossifying Fibroma

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


Benign Fibrous Histiocytoma

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


Aneurysmal Bone Cyst

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


Telangiectatic Osteosarcoma

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

Biopsy and careful histopathologic interpretation are essential.


Treatment


General Principles

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

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


Radiotherapy

Radiotherapy is generally avoided whenever complete surgical treatment is feasible.

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

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


Physical Therapy

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


Surgery

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


Curettage

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


High-Speed Burr

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


Local Adjuvant Treatment

Local adjuvants may be used to reduce residual tumor cells.

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

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


Polymethylmethacrylate Cement

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

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


Bone Grafting

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


Subchondral Reconstruction

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


Internal Fixation

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


Wide Resection

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


Reconstruction

Large periarticular resections may require complex reconstruction.

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


Amputation

Amputation is rarely necessary.

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


Follow-Up


Prognosis

Giant cell tumors have a substantial tendency to recur locally.


Simple Curettage

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


Modern Extended Curettage

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


Timing of Recurrence

Most recurrences occur within the first 2 years following treatment.

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


Complications


Local Recurrence

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


Pathologic Fracture

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


Pulmonary Metastasis

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

These metastases may behave relatively indolently but require specialist assessment.


Secondary Malignant Giant Cell Tumor

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


Postirradiation Sarcoma

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

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


Sarcomatous Transformation Without Radiation

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


Patient Monitoring

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

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


Chest Surveillance

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

Historically, annual chest radiography has been used.


Long-Term Monitoring

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


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Orthopaedic Surgery - Friedreich Ataxia


Basics

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

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


Systems Involved

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

Endocrine abnormalities, particularly diabetes mellitus, may also occur.


Classification

There are no major orthopaedic subclassifications of Friedreich ataxia.

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


Epidemiology

Friedreich ataxia is rare.

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


Age at Presentation

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

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


Sex

Males and females are affected approximately equally.


Population Distribution

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


Genetics

Friedreich ataxia is inherited in an autosomal recessive pattern.

Affected individuals generally inherit a pathogenic allele from each parent.


Frataxin Gene

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


GAA Trinucleotide Repeat

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

This reduces expression of frataxin.


Relationship to Disease Severity

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


Frataxin Function

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

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


Associated Conditions

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


Diagnosis

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

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


Clinical Features


Classic Neurologic Findings

A characteristic clinical combination includes:

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


Ataxia

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

Gait becomes broad-based and unstable as disease advances.


Areflexia

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


Babinski Sign

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


Additional Signs

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


Symptoms

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

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


Physical Examination


Gait and Coordination

Gait should be observed carefully.

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

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


Spine Examination

Standing alignment should be assessed for excessive kyphosis and scoliosis.

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


Reflexes

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

Plantar responses should also be assessed.


Foot Examination

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

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


Muscle Strength

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

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


Laboratory Tests


Creatine Kinase

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


Glucose Testing

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


Cardiac Assessment

Because cardiomyopathy is common, cardiac evaluation is important.

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


Cardiomyopathy

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


Electrodiagnostic Testing

Electromyography may demonstrate polyphasic potentials.

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


Imaging


Spine Radiographs

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


Long-Term Spinal Surveillance

Spinal deformity can continue to progress even after skeletal maturity.

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


Foot Radiographs

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


Differential Diagnosis


Cerebellar Tumor

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


Chiari Malformation

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


Muscular Dystrophy

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


Spinal Dysraphism

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


Treatment


General Principles

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

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


Orthopaedic Surveillance

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

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


Ambulation

Walking should be maintained safely for as long as possible.

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


Foot Deformity

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

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


Scoliosis Bracing

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

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


Physical Therapy

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

It is also essential after orthopaedic surgery.


Stretching

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


Medication

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

Symptomatic medications may be required for associated problems.


Muscle Spasms

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


Scoliosis Surgery


Preoperative Evaluation

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


Risk of Progression

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


Surgical Indications

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


Curves of 40–60°

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

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

Bracing or surgery may be appropriate depending on these factors.


Fusion Levels

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

Modern segmental instrumentation is used to obtain correction and stability.


Severe Rigid Curves

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

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


Spinal Cord Monitoring

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

Both sensory and motor modalities should be used when feasible.


Postoperative Immobilization

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


Cavovarus Foot Surgery

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


Soft-Tissue Procedures

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

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


Arthrodesis

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


Follow-Up


Specialist Coordination

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


Prognosis

Friedreich ataxia is a progressive disorder.

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


Scoliosis Prognosis

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


Ambulation

Progressive neurologic deterioration commonly leads to loss of independent walking.

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


Survival

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

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


Complications


Cardiomyopathy

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


Foot Skin Problems

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


Respiratory Complications

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


Progressive Loss of Mobility

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


Patient Monitoring

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

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


Scoliosis Monitoring

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

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


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Orthopaedic Surgery - Freiberg Disease (Freiberg Infraction)


Basics

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

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


Anatomic Distribution

The second metatarsal head is affected most frequently.

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

Disease may be unilateral or bilateral.


Disease Progression

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

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

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

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


Epidemiology

Freiberg disease occurs more commonly in females than males.

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


Age

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


Risk Factors

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

These factors increase mechanical stress across the affected metatarsal head.


Etiology

The exact cause is likely multifactorial.

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


Vascular Factors

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


Acute Trauma

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


Repetitive Microtrauma

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


Second Metatarsal Anatomy

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

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


Diagnosis


Signs and Symptoms

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

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


Swelling

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

Swelling may become more noticeable after prolonged activity.


Stiffness

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


Physical Examination


Range of Motion

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

Motion can become progressively restricted in later stages.


Tenderness

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


Swelling

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


Toe-Rise Test

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


Imaging


Plain Radiographs

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

Radiographic appearance varies according to the stage of disease.


Early Radiographic Findings

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

Radiographs can occasionally appear normal in very early disease.


Progressive Disease

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

Subchondral cystic changes and osteophytes may also develop.


End-Stage Disease

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


MRI

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

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


Bone Scintigraphy

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

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


Pathological Findings

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


Metatarsal Head Necrosis

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

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


Cartilage Damage

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


Classification

Several classification systems have been proposed.

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

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


Natural History

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

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

Others develop persistent deformity or degenerative arthritis.


Differential Diagnosis


Idiopathic Synovitis

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


Inflammatory Arthritis

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


Acute Fracture

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


MTP Sprain

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


Metatarsal Stress Fracture

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


Morton Neuroma

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


Treatment


General Principles

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

Early disease is generally treated nonoperatively.


Activity Modification

Activities that reproduce pain should be reduced or temporarily avoided.

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


Immobilization and Footwear

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


Metatarsal Pad

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


Taping

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


Medication

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


Corticosteroid Injection

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

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


Surgery

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


Synovectomy

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


Joint Debridement

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

This can improve motion and reduce mechanical symptoms.


Bone Grafting

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


Dorsiflexion Osteotomy

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

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


Resection Arthroplasty

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

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


Prosthetic Joint Replacement

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

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


Follow-Up


Prognosis

The prognosis is generally favorable.

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


Long-Term Outcome

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

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


Complications


Articular Collapse

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


MTP Arthritis

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


Transfer Metatarsalgia

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

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


Patient Monitoring

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

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


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Orthopaedic Surgery - Fracture Treatment


Basics

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

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


Nondisplaced Fractures

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

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

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


Displaced Fractures

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

Precise description is important for communication and treatment planning.


Angulation

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

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


Translation

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


Rotation

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

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


Shortening

Shortening results from fracture overlap or loss of bone length.

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


Open Versus Closed Fracture

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

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

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


Initial Management of an Open Fracture

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

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


Gustilo-Anderson Classification

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

Definitive grading is best assigned after operative debridement.


Type I

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


Type II

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


Type III

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

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


Type IIIA

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


Type IIIB

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


Type IIIC

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


Fracture Location


Diaphyseal Fractures

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


Metaphyseal Fractures

Metaphyseal fractures occur near the ends of long bones.

Some extend into the adjacent joint surface.


Intra-Articular Fractures

Intra-articular fractures disrupt the joint surface.

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


Fracture Patterns


Transverse Fracture

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


Oblique Fracture

An oblique fracture crosses the bone at an angle.


Spiral Fracture

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


Comminuted Fracture

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

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


Segmental Fracture

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


Impacted Fracture

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


Avulsion Fracture

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


Compression Fracture

Compression fractures occur when bone is crushed under axial load.

They are particularly common in osteoporotic vertebral bodies.


Pediatric Considerations

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


Greenstick Fracture

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

This produces an incomplete fracture with angular deformity.


Buckle or Torus Fracture

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

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


Physeal Injuries

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


Salter-Harris Type I

Type I extends transversely through the physis alone.


Salter-Harris Type II

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


Salter-Harris Type III

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

It is therefore an intra-articular fracture.


Salter-Harris Type IV

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

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


Salter-Harris Type V

Type V is a crush injury of the physis.

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


Perichondral Ring Injury

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


Prevention

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


Pathophysiology

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

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


Diagnosis


History

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

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


Suspected Pathologic Fracture

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

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

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


Nonaccidental Injury

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

Any concern should trigger a formal multidisciplinary safeguarding evaluation.


Physical Examination

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

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


Neurovascular Examination

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


Soft-Tissue Examination

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


Imaging


Plain Radiographs

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

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


CT

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

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


MRI

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

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


Bone Scintigraphy

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


Initial Treatment


Ice and Elevation

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


Immobilization

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


Reduction

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


Principles of Definitive Fracture Treatment

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

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


Splinting

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

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


Casting

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


Cast Valving

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

This reduces circumferential pressure.


Three-Point Mold

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


Functional Bracing

Functional braces permit controlled motion while maintaining fracture alignment.

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


Activity

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

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


Nursing Care

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


Medication


Open Fracture Antibiotics

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

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

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

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


Farm or Grossly Contaminated Injuries

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


Tetanus Prophylaxis

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


Analgesia

Pain control should be tailored to injury severity.

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


Surgery

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


Intra-Articular Fractures

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

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


Diaphyseal Fractures

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


Plates and Screws

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

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


Intramedullary Nails

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

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


External Fixation

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

It may also be used definitively in selected injuries.


Damage-Control Orthopaedics

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

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

Definitive fixation is performed later after resuscitation and physiologic stabilization.


Referral and Safeguarding

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


Prognosis

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

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


Complications


Delayed Union

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

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


Nonunion

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

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


Malunion

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


Osteonecrosis

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

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


Osteomyelitis

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


Compartment Syndrome

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

It is a surgical emergency.

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


Pulmonary Complications

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


Acute Respiratory Distress Syndrome

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


Fat Embolism Syndrome

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


Venous Thromboembolism

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


Complex Regional Pain Syndrome

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

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


Post-Traumatic Arthritis

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


Geriatric Considerations

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

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

Early mobilization is often particularly important in this population.


Patient Monitoring

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

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


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Orthopaedic Surgery - Foot and Ankle Anatomy and Examination


Basics

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

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


Extrinsic Muscles

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


Dorsiflexors

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

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

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


Evertors

The primary evertors are the peroneus longus and peroneus brevis.

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

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


Plantarflexors and Invertors

Several important tendons pass posteromedial to the ankle.

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

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


Extrinsic Toe Flexors

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

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


Intrinsic Foot Muscles

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

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


Muscle Imbalance

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


Bony Anatomy

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

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


Ankle Joint

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

It primarily permits plantarflexion and dorsiflexion.


Range of Motion

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


Ankle Ligaments


Syndesmotic Ligaments

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

Injury to this complex produces a high ankle sprain.


Deltoid Ligament

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

They provide important medial ankle stability.


Lateral Ligament Complex

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

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


Hindfoot

The hindfoot consists principally of the talus and calcaneus.

These bones articulate at the subtalar joint.


Subtalar Motion

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

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


Talus

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

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


Calcaneus

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

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


Midfoot

The midfoot is organized into two principal rows.

Proximally, the navicular and cuboid articulate with the hindfoot.

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


Tarsometatarsal Complex

Ligaments connect most adjacent metatarsal bases.

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


Lisfranc Ligament

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

It is a key stabilizer of the tarsometatarsal complex.


Forefoot

The forefoot consists of five metatarsals and 14 phalanges.

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


Gait Cycle

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


Stance Phase

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


Heel Strike

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

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


Foot Flat

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

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


Toe-Off

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

This produces plantarflexion and propels the body forward.


Windlass Mechanism

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

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

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


Swing Phase

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


Clinical History

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


Acute Injury

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


Pain

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


Mechanical Symptoms

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


Neurologic Symptoms

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


Relevant Medical History

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


Surgical History

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


Functional History

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


Physical Examination

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

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


Standing Examination


Alignment

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

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


Too-Many-Toes Sign

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

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


Gait

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


Heel Rise

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

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


Seated Examination


Vascular Examination

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

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


Venous Status

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


Sensory Examination

Sensation should be assessed according to peripheral nerve distribution.


Superficial Peroneal Nerve

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


Deep Peroneal Nerve

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


Saphenous Nerve

The saphenous nerve supplies the medial border of the foot.


Sural Nerve

The sural nerve supplies the lateral border of the foot.


Tibial Nerve

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


Protective Sensation

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

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


Neurologic Examination

Deep tendon reflexes should be assessed when appropriate.

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


Motor Examination

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


Ankle Dorsiflexion

Dorsiflexion primarily tests the tibialis anterior.


Ankle Plantarflexion

Plantarflexion is generated mainly by the gastrocnemius-soleus complex.


Eversion

Eversion evaluates the peroneal muscles.


Inversion

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


Great Toe Motion

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


Range of Motion

Both active and passive motion should be evaluated.


Ankle Motion

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


Subtalar Motion

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


Chopart Joint

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


Lisfranc Joint

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

Pain or instability may indicate a Lisfranc injury.


Metatarsophalangeal and Toe Joints

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


Palpation

Systematic palpation helps localize pathology.


Malleoli

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


Ankle Joint

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


Posterior Tibial Tendon

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

Tenderness may indicate posterior tibial tendinitis or tendon dysfunction.


Navicular Tuberosity

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

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


Achilles Tendon

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

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


Peroneal Tendons

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

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

Tenderness may reflect tendinitis or associated fifth-metatarsal pathology.


Peroneal Subluxation

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


Sinus Tarsi

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

Tenderness may suggest subtalar joint inflammation or instability.


Syndesmosis

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


Plantar Fascia

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

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


Lisfranc Region

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

Plantar ecchymosis in this region is particularly significant.


Sesamoids

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


Lesser Metatarsal Heads

Tenderness beneath the lesser MTP joints may indicate metatarsalgia.


Intermetatarsal Spaces

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


Special Tests


Anterior Drawer Test

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

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

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

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


Thompson Test

The Thompson test evaluates integrity of the Achilles tendon.

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

An intact Achilles tendon produces plantarflexion of the foot.

Failure of plantarflexion strongly suggests Achilles tendon rupture.


Lesser-Toe Deformities

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


Calluses

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


Flexibility

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


MTP Stability

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


Hallux Valgus Examination


Calluses and Medial Eminence

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


MTP Motion

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

This helps identify associated arthritis or stiffness.


First Tarsometatarsal Hypermobility

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

Excessive mobility suggests first tarsometatarsal joint hypermobility.


Lesser-Toe Deformities

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


Laboratory Tests

Laboratory testing is generally guided by the suspected diagnosis.


Suspected Infection

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


Joint Aspiration

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


Imaging


Plain Radiographs

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


Acute Trauma

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


Weight-Bearing Radiographs

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

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


Stress Radiographs

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


CT

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

It is valuable for evaluating articular congruity and planning reconstruction.


MRI

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

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


Bone Scintigraphy

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

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


General Examination Principles

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

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


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