Orthopaedic Surgery - Shoulder Instability

Basics

Shoulder instability describes:

Abnormal symptomatic translation of the humeral head relative to the glenoid

beyond the limits of normal physiologic motion.

It is common in:

Young

Active

and

Athletic patients.

Instability Versus Laxity

It is important to distinguish:

Instability

from

Laxity.

Instability is the patient’s subjective experience of:

Painful slipping

Subluxation

Apprehension

or

Dislocation.

Laxity is an objective finding of:

Excessive joint translation on examination.

A patient may have physiologic laxity without:

Symptoms or true instability.

Classification

Shoulder instability may be classified according to:

Direction

Cause

and

Severity.

Classification by Direction

Instability may be:

Anterior

Posterior

or

Multidirectional.

Classification by Etiology

It may be:

Traumatic

or

Atraumatic.

Classification by Degree

Instability events may consist of:

Subluxation

or complete:

Dislocation.

Multidirectional Instability

Multidirectional instability is defined as symptomatic abnormal translation in:

More than one direction.

It commonly has an element of:

Generalized ligamentous laxity

and may involve:

Both shoulders.

Anterior Instability

Traumatic anterior instability is the:

Most common pattern

and often follows a true:

Anterior shoulder dislocation.

Posterior Instability

Posterior instability may result from:

Trauma

such as seizures or electrical injury

or from repetitive loading in athletes such as:

Football linemen.

It may also occur without a single major traumatic event.

Epidemiology

Shoulder instability is common in:

Young athletic populations.

It is among the most frequent shoulder problems encountered in:

Sports medicine.

Posterior Instability

Posterior instability accounts for approximately:

10% of shoulder instability cases.

It is substantially less common than:

Anterior instability.

Incidence

Anterior shoulder dislocation requiring closed reduction has historically been reported at approximately:

24 per 100,000 persons per year.

Posterior instability has been estimated at approximately:

1.1 per 100,000 persons per year.

Age Distribution

Posterior instability peaks in:

Men aged approximately 20–49 years

and in:

Women older than approximately 70 years.

Multidirectional Instability

The exact incidence is unknown.

It is particularly common in athletes involved in:

Gymnastics

Swimming

Volleyball

and other activities requiring repeated:

Overhead motion.

It often becomes symptomatic during the:

Second or third decade of life.

Risk Factors

Important risk factors include:

Young age

Male sex

Contact or collision sports

Connective-tissue disorders

Generalized hyperlaxity

Previous contralateral instability

Seizure disorder

and selected:

Glenoid morphologies.

Glenoid Morphology

Posterior instability is associated particularly with:

Glenoid retroversion

and

Glenoid hypoplasia.

These abnormalities may reduce posterior containment of the:

Humeral head.

Athletic Risk

Certain sports place the shoulder repeatedly in positions that stress specific stabilizers.

Examples include:

Football

Gymnastics

Swimming

Volleyball

and other overhead activities.

Age

Patients younger than approximately:

20 years

have an increased risk of:

Recurrent instability.

Genetics

Historically, traumatic shoulder instability was not considered a primarily:

Genetic disorder

in patients without connective-tissue disease.

However, altered collagen biology may contribute in selected patients.

Reduced expression of:

COL5A1

has been reported in capsular tissue from some patients with recurrent instability.

Etiology

The shoulder has exceptional mobility but relatively limited inherent:

Bony stability.

Normal stability depends on both:

Static

and

Dynamic stabilizers.

Static Stabilizers

These include:

Glenoid morphology

Labrum

Capsule

Glenohumeral ligaments

and

Negative intra-articular pressure.

Dynamic Stabilizers

These include:

Rotator cuff muscles

Long head of the biceps

and

Periscapular musculature.

Anterior Instability Mechanism

The classic mechanism for traumatic anterior instability involves:

Abduction

External rotation

and often:

Extension

with a force that drives the humeral head:

Anteriorly.

Posterior Instability Mechanism

Posterior instability may result from:

Posteriorly directed force

or an axial load with the arm in:

Internal rotation

and

Adduction.

Multidirectional Instability Mechanism

Multidirectional instability is often produced by a combination of:

Biologic factors

such as ligamentous laxity

and

Environmental or activity-related factors

such as repetitive overhead sports.

Associated Conditions and Lesions

Shoulder instability may be associated with:

Bankart lesions

Bony Bankart lesions

HAGL lesions

ALPSA lesions

GLAD lesions

Labral tears

Hill-Sachs lesions

Reverse Hill-Sachs lesions

Rotator cuff tears

Tuberosity fractures

and

Generalized hyperlaxity.

ALPSA Lesion

An:

Anterior labroligamentous periosteal sleeve avulsion

occurs when the anteroinferior labrum and attached ligamentous structures are stripped medially from the:

Glenoid neck

while remaining attached to the:

Periosteum.

Bankart Lesion

A Bankart lesion involves injury to the:

Anteroinferior labrum and capsuloligamentous complex.

It may be:

Soft tissue

or

Bony.

HAGL Lesion

A:

Humeral avulsion of the glenohumeral ligament

occurs when the inferior glenohumeral ligament is avulsed from its:

Humeral attachment.

GLAD Lesion

A:

Glenolabral articular disruption

involves injury to the:

Labrum

and adjacent:

Glenoid cartilage.

Hill-Sachs Lesion

Anterior instability may produce a:

Posterolateral or posterosuperior humeral head compression defect.

This is known as a:

Hill-Sachs lesion.

Reverse Hill-Sachs Lesion

Posterior instability may produce an:

Anteromedial humeral head impaction defect

known as a:

Reverse Hill-Sachs lesion.

Posterior Instability Pathology

Posterior instability may be associated with:

Posterior labral tearing

Posterior cuff fraying

Posterior capsular injury

and

Glenoid retroversion or hypoplasia.

Diagnosis

Diagnosis depends on:

History

Physical examination

and

Imaging.

The clinician must determine whether observed laxity is:

Physiologic

or

Pathologic and symptomatic.

Signs and Symptoms

Patients may report:

Pain

Apprehension

Sensation of slipping

Recurrent subluxation

or

Frank dislocation.

Tenderness

Tenderness may be present around the:

Shoulder girdle

particularly after an acute instability event.

Range of Motion

Attempted motion may produce:

Pain

or a sense of:

Instability.

Abnormal Arm Position

During an acute dislocation, the arm may be held in a characteristic:

Abnormal posture

depending on the direction of displacement.

Physical Examination

A complete examination should include:

Inspection

Palpation

Range of motion

Rotator cuff strength

Instability testing

Hypermobility assessment

and

Neurovascular examination.

Sulcus Sign

The sulcus sign is produced by applying:

Downward traction

to the relaxed arm.

A visible depression below the acromion indicates:

Inferior humeral translation.

It is particularly useful in assessing:

Inferior laxity

and

Multidirectional instability.

Apprehension Test

The shoulder is placed in:

Abduction

and

External rotation.

A sensation of impending dislocation rather than pain alone suggests:

Anterior instability.

Relocation Test

Posteriorly directed pressure on the humeral head during the apprehension position that reduces:

Apprehension

supports the diagnosis of:

Anterior instability.

Acute Setting

Apprehension and relocation testing should not be performed aggressively during an:

Acute unreduced dislocation.

Beighton Score

The:

Beighton hypermobility score

can be used to assess:

Generalized ligamentous laxity.

This is especially relevant in patients suspected of having:

Multidirectional instability.

Load-and-Shift Test

The examiner stabilizes the scapula and translates the humeral head:

Anteriorly

and

Posteriorly.

Excessive translation or reproduction of symptoms suggests:

Instability.

Posterior Stress Testing

Posterior instability may be evaluated using:

Posterior load-and-shift

Posterior stress test

Jerk test

and

Kim test.

Jerk Test

The arm is elevated to approximately:

90°

with internal rotation and axial loading.

A painful:

Clunk

or sudden posterior translation suggests:

Posterior instability or posterior labral pathology.

Kim Test

The Kim test applies a:

Posteroinferiorly directed force

while elevating the arm.

Pain or a posterior clunk may indicate:

Posteroinferior labral injury.

Rotator Cuff Examination

Assess:

Supraspinatus

Infraspinatus

Teres minor

and

Subscapularis strength.

Cuff injury may coexist with:

Instability, especially in older patients.

Neurovascular Examination

Neurovascular status should be assessed:

Before and after reduction

when a dislocation is present.

Particular attention should be paid to the:

Axillary nerve.

Imaging

Plain Radiographs

A full conventional shoulder series is usually the initial study.

At minimum, obtain:

Anteroposterior

and

Axillary views.

Axillary View

The axillary view is essential for identifying:

Posterior dislocation

and determining the relationship between the:

Humeral head

and

Glenoid.

Posterior dislocations are commonly missed when this view is omitted.

Postreduction Imaging

Postreduction radiographs are necessary to:

Confirm concentric reduction

and identify associated:

Fractures

or

Bony defects.

CT

CT is useful for assessing:

Glenoid bone loss

Hill-Sachs defects

Reverse Hill-Sachs lesions

Fracture morphology

and abnormal:

Glenoid version.

MRI

MRI is useful for evaluating:

Labral tears

Capsular injury

Rotator cuff tears

HAGL lesions

and other:

Soft-tissue abnormalities.

MR Arthrography

MR arthrography can improve detection of:

Subtle labral

and

Capsuloligamentous lesions

in patients with chronic or recurrent instability.

Pathological Findings

Histopathological testing is:

Not routinely required.

The relevant pathology is usually defined by:

Clinical examination

and

Imaging.

Differential Diagnosis

Important alternative diagnoses include:

Acromioclavicular injury

Clavicle fracture

Proximal humerus fracture

Rotator cuff tear

and other causes of shoulder pain or apparent instability.

Treatment

General Principles

Treatment depends on:

Direction

Cause

Frequency

Structural damage

and whether instability is:

Traumatic or atraumatic.

Acute Dislocation

If a true dislocation is present, treatment begins with:

Urgent closed reduction.

The technique depends on the:

Direction of displacement.

Reduction

Reduction should be performed using:

Gentle controlled maneuvers

with appropriate:

Analgesia

and

Muscle relaxation.

Posterior dislocations require techniques different from:

Anterior dislocations.

Immobilization

After uncomplicated anterior dislocation, a sling or immobilizer may be used for approximately:

7–10 days

primarily for:

Pain control.

Posterior Dislocation Immobilization

After posterior dislocation, some patients are placed in an:

External rotation brace

to reduce recurrent posterior translation during healing.

Range of Motion

Gentle shoulder motion may begin after:

Acute pain improves.

The sling can be discontinued gradually as:

Comfort allows.

Return to Sport

Athletes may return when they have:

Full range of motion

Symmetric strength

Minimal pain

and sufficient:

Dynamic stability.

In-Season Return

Athletes returning during the same season may use an adjustable brace that limits:

Abduction

and

External rotation.

However, recurrent instability during in-season return is:

Common.

Historical data suggest that only a minority may complete the remainder of the season without another instability event.

Activity Modification

For:

Multidirectional instability

and

Subtle posterior instability

initial treatment centers on:

Activity modification

and

Rehabilitation.

Sport Cessation

Temporary cessation of the provocative sport may be necessary for:

Posterior

or

Multidirectional instability

when symptoms are driven by repetitive athletic loading.

Physical Therapy

Physical therapy is central to treatment, particularly for:

Atraumatic

Posterior

and

Multidirectional instability.

Anterior Instability Rehabilitation

After uncomplicated anterior dislocation, therapy can begin once:

Acute pain subsides.

If fractures or other injuries are present, rehabilitation may need to be:

Delayed.

Posterior Instability Rehabilitation

After posterior dislocation, strengthening may be delayed for several weeks, often approximately:

4–6 weeks

depending on associated injury and stability.

Multidirectional Instability Rehabilitation

Patients with multidirectional instability usually require a prolonged course of:

Dynamic stabilization exercises

often lasting approximately:

4–6 months.

Rehabilitation Goals

Therapy emphasizes:

Rotator cuff strengthening

Scapular stabilization

Proprioception

Neuromuscular control

and

Closed kinetic-chain exercises.

Medication

Symptomatic treatment may include:

NSAIDs

Acetaminophen

and

Ice.

A short course of opioid medication may occasionally be used after an acute dislocation, but prolonged use is generally avoided.

Surgery

Surgical treatment is selected according to the:

Underlying structural lesion.

First-Time Dislocation

Surgery after a first-time anterior dislocation remains:

Individualized.

Young athletes at high risk of recurrence may be considered for:

Early stabilization.

Bankart Repair

Soft-tissue Bankart lesions are commonly treated with:

Arthroscopic labral and capsular repair.

Bony Bankart Repair

Significant glenoid rim fractures may require:

Arthroscopic

or

Open fixation or reconstruction.

Hill-Sachs Lesions

Surgical treatment depends on:

Size

Location

Engagement

and the amount of associated:

Glenoid bone loss.

Bone Loss

Recurrent instability can progressively enlarge:

Glenoid

and

Humeral head bone defects.

Substantial glenoid bone loss may require a:

Bone-augmentation procedure

rather than isolated soft-tissue repair.

Tuberosity Fractures

Associated greater or lesser tuberosity fractures are treated according to:

Displacement

Patient function

and

Rotator cuff integrity.

Rotator Cuff Tears

Rotator cuff tears associated with dislocation, especially in patients older than approximately:

50 years

may require:

Surgical repair

when clinically significant.

Irreducible Dislocation

If the shoulder cannot be reduced by closed methods, urgent:

Open reduction

is indicated.

Posterior Instability Surgery

Procedures may include:

Posterior labral repair

Posterior capsular plication

or correction of substantial:

Bone deficiency or abnormal glenoid morphology.

Multidirectional Instability Surgery

Patients with persistent symptomatic multidirectional instability despite prolonged rehabilitation may undergo:

Capsular plication

or another capsular volume-reduction procedure.

Follow-Up

After a simple dislocation, patients are generally reviewed within approximately:

7–10 days.

Early Follow-Up

The clinician should reassess:

Pain

Neurovascular status

Rotator cuff function

Range of motion

and associated:

Fracture or soft-tissue injury.

Sling Weaning

Patients with uncomplicated dislocations should gradually:

Wean from the sling

as pain improves.

Multidirectional Instability Follow-Up

Patients undergoing nonoperative treatment for multidirectional instability should be seen periodically to evaluate:

Compliance

Strength

Scapular control

and

Response to therapy.

Posterior Instability Follow-Up

After posterior instability or dislocation, immobilization strategy and timing of:

Physical therapy

should be individualized according to:

Structural injury

and

Clinical stability.

Prognosis

Prognosis depends on:

Age

Direction of instability

Athletic demands

Degree of laxity

and associated:

Structural damage.

Recurrence in Young Patients

Recurrent instability is very common in:

Teenagers

and

Young adults.

Historical recurrence rates in teenagers have approached:

80%.

Age Effect

The younger the patient at the first instability event, the greater the likelihood of:

Recurrent episodes.

Structural Risk Factors

Recurrence is more likely when associated with:

Labral tears

Capsular injury

Bone loss

Rotator cuff tearing

or

Fracture.

Posterior Instability Outcomes

Football players treated with arthroscopic posterior labral repair often demonstrate a:

High rate of return to play.

Throwing athletes may have more difficulty returning to their:

Previous performance level.

Multidirectional Instability Outcomes

Many patients improve with:

Structured rehabilitation.

Younger athletes may have less predictable success with therapy alone.

Surgical capsular stabilization can produce:

Good functional outcomes

Low recurrence

and

High return-to-sport rates

in appropriately selected patients.

Complications

Recurrent Instability

The most common long-term complication is:

Recurrent subluxation or dislocation.

Glenohumeral Arthritis

Repeated instability episodes may contribute to:

Progressive cartilage damage

and eventually:

Glenohumeral osteoarthritis.

Nerve Injury

Transient:

Neurapraxia

occurs in a minority of patients.

The:

Axillary nerve

is most commonly involved.

Stiffness

Excessive immobilization or surgery may result in:

Loss of shoulder motion.

Vascular Injury

Vascular injury is:

Rare

but has been reported, particularly after traumatic dislocation.

Abnormal pulses or limb perfusion require:

Urgent assessment.

Patient Monitoring

Long-term follow-up should assess:

Recurrent episodes

Pain

Range of motion

Strength

Scapular control

Apprehension

and the effectiveness of:

Rehabilitation.

Key Principle

Shoulder instability is symptomatic abnormal motion of the humeral head relative to the glenoid and must be distinguished from asymptomatic physiologic laxity.

It may be:

Anterior, posterior, or multidirectional, and may arise from traumatic or atraumatic mechanisms.

Young patients, athletes, patients with:

Hyperlaxity

and those with:

Labral or bony defects

have the greatest risk of recurrence.

Treatment ranges from:

Urgent reduction and short-term immobilization after dislocation

to prolonged:

Rotator cuff and scapular stabilization therapy

for atraumatic or multidirectional disease.

Surgery is reserved for:

Recurrent instability, significant labral or capsular injury, substantial bone loss, persistent posterior instability, multidirectional instability that fails rehabilitation, or irreducible dislocation.

Orthopaedic Surgery - Shoulder Impingement Syndrome

Basics

Shoulder impingement syndrome is a common cause of:

Shoulder pain

particularly during:

Overhead activity.

The most common form is:

External or subacromial impingement.

Spectrum of Disease

Shoulder impingement has traditionally been viewed as a spectrum extending from:

Subacromial bursitis

to

Partial-thickness rotator cuff tearing

and eventually:

Full-thickness rotator cuff tearing.

However, the relationship between actual mechanical contact with the acromion and rotator cuff degeneration is complex.

Both:

Intrinsic tendon degeneration

and

Extrinsic mechanical factors

likely contribute.

Major Types

The two principal categories are:

External impingement

and

Internal impingement.

Less common forms include:

Subcoracoid impingement.

External Impingement

External or subacromial impingement is the:

Most common type.

It involves painful contact or compression of structures within the:

Subacromial space.

Subacromial Space

The subacromial space lies between the:

Acromion superiorly

and

Humeral head inferiorly.

Structures occupying or traversing this space include:

Supraspinatus tendon

Infraspinatus tendon

Long head of the biceps

Joint capsule

Subacromial-subdeltoid bursa

Coracoacromial ligament.

Mechanism of External Impingement

Compression of the rotator cuff against the:

Acromion

and

Coracoacromial arch

has historically been considered an important contributor to:

Rotator cuff disease.

The pathological spectrum may range from:

Inflamed and thickened bursal tissue

to

Bursal-sided partial-thickness cuff tearing.

Acromial Morphology

The acromion is commonly described as:

Flat

Curved

or

Hooked.

Hooked morphology has historically been associated with a higher prevalence of:

Rotator cuff tearing.

However, acromial shape should be interpreted as one factor among several rather than as the sole cause.

Structural Causes of Reduced Subacromial Space

Conditions that may decrease the available space include:

Subacromial osteophytes

Greater tuberosity exostosis

Acromial fracture

Os acromiale

Acromioclavicular osteophytes

Proximal humeral malunion.

Soft-Tissue Causes

The space can also effectively narrow because of enlargement or inflammation of:

Rotator cuff tissue

Subacromial bursa

or deposition of:

Calcium within a tendon.

Internal Impingement

Internal impingement occurs predominantly in:

Overhead throwing athletes.

It involves contact between the:

Articular surface of the posterosuperior rotator cuff

and

Posterosuperior glenoid or labrum.

Throwing Phase

Symptoms typically occur during the:

Late cocking

or

Early acceleration phase

of throwing, when the shoulder is in:

Abduction

and

Maximal external rotation.

Internal Impingement Pathology

Associated abnormalities may include:

Partial articular-sided supraspinatus tears

Posterior rotator cuff fraying

Posterior labral tears

Posterosuperior glenoid cartilage defects

and

Bennett lesions.

Bennett Lesion

A Bennett lesion is a:

Posteroinferior glenoid rim exostosis

or ossific change associated with chronic repetitive throwing.

Peel-Back Phenomenon

Extreme external rotation during throwing can place torsional force on the:

Posterosuperior labrum

through the long head of the biceps.

This may produce the:

Peel-back phenomenon

and contribute to:

Superior or posterosuperior labral tearing.

Contributing Factors in Internal Impingement

Internal impingement is often multifactorial.

Important contributors include:

Posterior capsular contracture

Glenohumeral internal rotation deficit

Scapular dyskinesis

Subtle anterior microinstability

Adaptive remodeling in throwing athletes.

Prevention

External impingement symptoms may be reduced by maintaining:

Rotator cuff strength

Scapular control

and

Shoulder flexibility.

Throwing Athletes

For overhead athletes, prevention emphasizes:

Appropriate throwing mechanics

Posterior shoulder flexibility

Scapular stabilization

and management of:

Training volume.

Epidemiology

Shoulder impingement is among the:

Most common causes of shoulder pain.

Its reported prevalence varies because the term has historically encompassed several overlapping:

Subacromial disorders.

Incidence

The exact incidence is difficult to determine because diagnostic definitions vary.

Nevertheless, subacromial pain and impingement-type symptoms represent a:

Very common source of shoulder dysfunction.

Risk Factors

Important risk factors include:

Increasing age

Repetitive overhead activity

Throwing sports

Swimming

Volleyball

Tennis

Gymnastics

Occupational overhead work.

Genetics

There is no established specific:

Genetic association

for shoulder impingement syndrome.

Etiology

Pain commonly occurs during:

Forward elevation

and

Internal rotation.

Multiple structural and functional abnormalities may contribute.

Proximal Humeral Malunion

Malunion involving the:

Greater tuberosity

or proximal humerus may mechanically narrow the:

Subacromial space.

Coracoacromial Ligament

Thickening of the:

Coracoacromial ligament

may contribute to subacromial contact.

Acromioclavicular Arthritis

Inferiorly projecting osteophytes from the:

AC joint

may reduce the space available for the:

Rotator cuff.

Rotator Cuff Weakness

Weakness or tearing of the rotator cuff may permit:

Superior migration of the humeral head

which can further decrease the:

Subacromial space.

Neurologic Weakness

Rarely, weakness from:

Cervical radiculopathy

or

Suprascapular neuropathy

may impair the supraspinatus and infraspinatus enough to alter shoulder mechanics.

Subacromial Bursitis

Inflammation and thickening of the:

Subacromial bursa

commonly accompany symptomatic external impingement.

Internal Impingement Etiology

Excessive repetitive external rotation in throwers may produce contact between the:

Posterior cuff

and

Posterior-superior glenoid.

Posterior Capsule Contracture

Tightness of the posterior capsule is a common finding and can contribute to:

Glenohumeral internal rotation deficit

and altered humeral translation.

Scapular Dyskinesis

Abnormal scapular motion may reduce:

Effective subacromial clearance

and disturb the normal:

Scapulohumeral rhythm.

Associated Conditions

Common associated abnormalities include:

Glenohumeral internal rotation deficit

Hooked acromion

Os acromiale

Posterior capsular contracture

Partial articular-sided supraspinatus tears

Rotator cuff tears

Scapular dyskinesis

Diagnosis

Diagnosis is primarily based on:

History

Physical examination

and selective:

Imaging.

Signs and Symptoms

Typical symptoms include:

Shoulder pain with overhead activity

Difficulty performing work or sport

and

Night pain or difficulty sleeping.

Activity-Related Pain

Pain commonly occurs during:

Reaching overhead

Throwing

Swimming

Lifting

or repetitive occupational use.

Physical Examination

A complete examination should assess:

Range of motion

Rotator cuff strength

Scapular mechanics

Impingement signs

and associated:

Labral or instability findings.

Neer Impingement Sign

The examiner passively forward elevates the arm.

Reproduction of shoulder pain, often above approximately:

90° of elevation

suggests:

Subacromial pain or impingement.

Neer Impingement Test

Historically, the Neer test refers to repeating the painful maneuver after:

Subacromial local anesthetic injection.

Relief of pain supports the subacromial space as the:

Pain generator.

Hawkins Test

With the shoulder and elbow flexed to:

90°

the examiner forcibly:

Internally rotates the shoulder.

Pain suggests:

Subacromial impingement or rotator cuff pathology.

Jobe Test

The arm is elevated in the:

Scapular plane

and internally rotated or pronated while resistance is applied.

Pain or weakness suggests:

Supraspinatus pathology.

Internal Impingement Examination

Internal impingement may produce posterior shoulder pain with:

Abduction

and

Maximal external rotation.

Range of Motion

Both shoulders should be compared for:

Internal rotation

External rotation

Forward elevation

and

Total rotational arc.

Contracture

Loss of motion may indicate:

Posterior capsular tightness

or another shoulder contracture contributing to symptoms.

Scapular Examination

Observe the scapula during:

Forward elevation

and

Abduction

for:

Winging

Asymmetric motion

or

Dyskinesis.

Imaging

Plain Radiographs

Conventional shoulder radiographs are useful for identifying:

Calcific tendinitis

Arthritis

Acromial abnormalities

Proximal humeral malunion

Os acromiale

and other bony causes of pain.

Acromiohumeral Distance

The distance between the acromion and humeral head can be assessed on radiographs.

A normal interval is generally around:

7–14 mm

depending on technique and patient factors.

Marked narrowing may suggest:

Chronic rotator cuff insufficiency.

Acromial Morphology

Radiographs may also demonstrate:

Flat

Curved

or

Hooked acromial morphology.

MRI

MRI is useful for evaluating:

Rotator cuff tendons

Subacromial bursitis

Labral pathology

Biceps abnormalities

and alternative diagnoses.

Internal Impingement Imaging

MRI or MR arthrography may demonstrate:

Articular-sided cuff tearing

Posterior labral injury

or other changes associated with:

Internal impingement.

Bennett Lesion Imaging

A Bennett lesion may be visible as a:

Posterior glenoid rim exostosis.

Pathological Findings

Possible pathological findings include:

Rotator cuff tendinosis

Interstitial cuff tearing

Partial-thickness tearing

Full-thickness tearing

Thickened inflamed bursa.

Differential Diagnosis

Important alternatives include:

Acromioclavicular arthritis

Biceps tendinopathy

Calcific tendinitis

Cervical radiculopathy

Adhesive capsulitis

Glenohumeral arthritis

Symptomatic os acromiale

Rotator cuff tear

Scapular winging

Scapular dyskinesis

Suprascapular neuropathy

Thoracic outlet syndrome

Treatment

General Principles

Initial treatment is typically:

Nonoperative.

The cornerstone of treatment is:

Physical therapy

combined with:

Activity modification

and symptomatic medication.

Activity Modification

Avoid or temporarily reduce activities that reproduce symptoms, particularly:

Repeated overhead motion

Heavy lifting

or

Throwing.

Throwing Athletes

Athletes with internal impingement should temporarily stop:

Throwing or painful overhead activity

and enter a structured:

Sport-specific rehabilitation program.

Physical Therapy

Rehabilitation should emphasize:

Rotator cuff strengthening

Periscapular strengthening

Scapular stabilization

Range-of-motion restoration

and correction of:

Scapular mechanics.

Rotator Cuff Strengthening

Improving cuff strength helps maintain the humeral head:

Centered within the glenoid

and may reduce abnormal superior translation.

Periscapular Strengthening

Strengthening the:

Trapezius

Serratus anterior

Rhomboids

and other scapular stabilizers can improve:

Scapulothoracic rhythm.

Range of Motion

Any limitation in:

Posterior shoulder flexibility

or

Internal rotation

should be addressed when clinically relevant.

Sleeper Stretch

The:

Sleeper stretch

may be used selectively in throwing athletes with:

Posterior shoulder tightness

or

Glenohumeral internal rotation deficit.

It should be performed carefully to avoid provoking symptoms.

Sport-Specific Rehabilitation

Internal impingement rehabilitation should ultimately address:

Throwing mechanics

Kinetic-chain function

Core strength

Scapular control

and progressive return to:

Overhead activity.

Medication

First Line

Symptomatic treatment may include:

NSAIDs

and

Acetaminophen.

Subacromial Corticosteroid Injection

A subacromial corticosteroid injection may provide:

Temporary pain relief

and can assist participation in:

Physical therapy.

It may also have diagnostic value.

Repeated injections should be used cautiously because of potential adverse effects on:

Tendon tissue.

Surgery

Surgery is reserved for patients with:

Persistent symptoms despite appropriate nonoperative treatment

or those with a specific structural lesion requiring correction.

Acromioplasty

Acromioplasty has historically been used to enlarge the:

Subacromial space

by reshaping the undersurface of the:

Acromion.

Its routine value for isolated subacromial pain without a clear structural indication remains:

Debated.

Distal Clavicle Excision

When symptomatic:

AC joint osteophytes or arthritis

contribute to pain, distal clavicle excision may be considered in selected patients.

Bursectomy

Inflamed:

Subacromial bursal tissue

may be removed arthroscopically when persistent symptoms accompany other surgically treated pathology.

Rotator Cuff Treatment

If a rotator cuff tear is identified, treatment may include:

Débridement

or

Repair

depending on:

Tear depth

Size

Location

and patient factors.

Internal Impingement Surgery

Surgical treatment may include:

Rotator cuff débridement or repair

Labral débridement or repair

and, in selected cases,

Posterior capsular release.

Follow-Up

Patients should be monitored throughout:

Rehabilitation

and after:

Injection or surgery.

Prognosis

Most patients improve with:

Nonoperative treatment.

Historical series suggest successful outcomes in approximately:

70–80%

with a combination of:

Physical therapy

and

Subacromial injection.

Factors Associated With Better Outcome

Historically reported favorable factors include:

Shorter duration of symptoms

Less prolonged work absence

and lack of substantial:

Acromioclavicular degeneration.

These associations should not be interpreted as deterministic for an individual patient.

Surgical Outcome

Patients who undergo surgery after unsuccessful conservative treatment may experience improvements in:

Pain

and

Shoulder function.

Long-Term Decompression Outcomes

Historical long-term follow-up after subacromial decompression has demonstrated acceptable results in many patients, although current practice places more emphasis on:

Rotator cuff pathology

Scapular mechanics

and avoiding unnecessary decompression.

Return to Sport in Internal Impingement

Return-to-play rates are generally favorable, but return to the same performance level depends on:

Extent of cuff injury

Labral involvement

and the athlete’s:

Throwing demands.

Complications

Potential complications of treatment include:

Acromial fracture

Skin discoloration after corticosteroid injection

Infection

Deltoid dysfunction

Neurovascular injury

Seroma

Hematoma

Complex regional pain syndrome

and general:

Medical complications.

Deltoid Dysfunction

Open decompression procedures can rarely injure the:

Deltoid attachment

and lead to impaired:

Shoulder elevation.

Corticosteroid Skin Changes

Subacromial corticosteroid injection may occasionally cause:

Skin depigmentation

or

Subcutaneous fat atrophy

near the injection site.

Patient Monitoring

Follow-up should assess:

Pain

Range of motion

Rotator cuff strength

Scapular control

and ability to resume:

Work or sport.

Internal Impingement Monitoring

In throwing athletes, rehabilitation goals include restoration of:

Full functional range of motion

Strength

Dynamic stability

Scapular mechanics

and

Neuromuscular control.

Return to throwing should occur through a:

Graduated sport-specific progression.

Key Principle

Shoulder impingement syndrome encompasses a group of subacromial and internal contact disorders that produce pain during shoulder elevation or overhead activity.

External impingement most commonly involves the:

Rotator cuff and subacromial bursa beneath the coracoacromial arch, whereas internal impingement primarily affects:

Overhead athletes through contact between the posterosuperior cuff and glenoid.

Treatment begins with:

Activity modification, rotator cuff and scapular rehabilitation, restoration of motion, analgesic therapy, and selective subacromial injection.

Surgery is reserved for:

Persistent symptoms or clearly defined structural pathology, and routine acromioplasty for nonspecific subacromial pain remains:

Controversial.

Orthopaedic Surgery - Shoulder Dislocation

Basics

The shoulder is the:

Most commonly dislocated major joint.

Its predisposition to dislocation reflects the combination of:

Extensive range of motion

and relatively limited inherent:

Bony stability.

The glenohumeral joint therefore relies heavily on:

Capsular

Labral

Ligamentous

and

Muscular restraints

to maintain stability.

Classification

Shoulder dislocations are primarily classified according to the:

Direction of displacement of the humeral head.

The major types are:

Anterior

Posterior

and

Inferior dislocation.

Anterior Dislocation

Anterior dislocations account for approximately:

95% of shoulder dislocations.

The humeral head typically moves:

Anterior and inferior to the glenoid.

Posterior Dislocation

Posterior shoulder dislocation is substantially less common but clinically important because it is:

Frequently missed.

Failure to obtain an adequate:

Axillary or equivalent lateral view

is a major reason the diagnosis is overlooked.

Arm Position

The position in which the patient holds the arm often reflects the:

Direction of dislocation.

Anterior and posterior dislocations typically produce different characteristic postures.

Spontaneous Reduction

Some shoulder dislocations:

Reduce spontaneously

at the time of injury or before medical evaluation.

In these patients, residual:

Pain

Instability

Labral injury

or

Fracture

may provide evidence that a dislocation occurred.

Age-Related Injury Pattern

Associated injuries vary considerably with:

Patient age.

Younger Patients

Patients approximately:

30 years or younger

are more likely to sustain injury to the:

Labrum

Capsule

or

Glenoid rim.

Older Patients

Patients older than approximately:

40–50 years

have a higher likelihood of associated:

Rotator cuff tear

Greater tuberosity fracture

and

Neurovascular injury.

Prevention

There is no completely effective method of preventing traumatic shoulder dislocation.

Avoidance of:

Contact and collision sports

may reduce exposure to a common mechanism in younger patients.

Epidemiology

Shoulder dislocation occurs most frequently in:

Young males

with another incidence peak occurring in:

Older adults.

Sex

Historical series report that males account for approximately:

74% of shoulder dislocations.

Age Distribution

The highest incidence occurs in:

Males younger than 20 years.

A second peak occurs in individuals older than approximately:

70 years.

This produces a:

Bimodal age distribution.

Incidence

The overall incidence in the United States has historically been estimated at approximately:

24 per 100,000 persons per year.

Geriatric Considerations

Approximately:

20% of shoulder dislocations

occur in patients older than:

60 years.

Older-Adult Associated Injuries

Compared with younger patients, older individuals have an increased incidence of:

Rotator cuff tears

Greater tuberosity fractures

and

Peripheral nerve injury.

Rotator Cuff Evaluation in Older Patients

Persistent weakness following reduction in an older patient should raise concern for:

Acute rotator cuff tear.

MRI or ultrasound may be appropriate when there is:

Significant weakness

or an abnormal examination after reduction.

Pediatric and Adolescent Considerations

The incidence is particularly high among:

Adolescent boys, especially around 14–16 years of age.

Recurrence following nonoperative treatment may be very high in this group and can resemble that seen in:

High-risk young adults.

Risk Factors

Important risk factors include:

Male sex

Contact sports

Collision sports

Generalized ligamentous laxity

Connective-tissue disorders

Previous shoulder dislocation

Risk Factors for Recurrent Instability

Recurrent dislocation is associated with:

Young age at first dislocation

Male sex

Hyperlaxity

Glenoid bone loss

Humeral head bone loss

Repeated instability episodes

and the amount of time and activity exposure after the:

Initial dislocation.

Early Age at First Dislocation

An initial dislocation before approximately:

20 years of age

is strongly associated with a higher likelihood of:

Recurrent instability.

Genetics

Traumatic shoulder instability has traditionally not been regarded as primarily:

Genetic.

However, alterations in collagen biology may contribute to susceptibility in some individuals with:

Recurrent instability

or underlying connective-tissue laxity.

Reduced expression of:

COL5A1

has been reported in capsular tissue from some patients with recurrent instability.

Etiology

The classic mechanism of an anterior shoulder dislocation is:

Abduction

External rotation

and

Extension

with a force directed so that the humeral head is driven:

Anteriorly.

Predisposing History

Important historical factors include:

Previous shoulder trauma

and

Prior dislocation or instability episodes.

Posterior Dislocation Mechanisms

Posterior dislocations may occur after:

Seizure

Electrical injury

or trauma that produces forceful:

Internal rotation and adduction.

Because the deformity may be subtle, these injuries require a:

High index of suspicion.

Associated Conditions and Injuries

The patient’s age helps predict the pattern of associated damage.

Patients Younger Than 40 Years

Younger patients commonly sustain injuries involving the:

Capsule

Glenoid

and

Labrum.

Bankart Lesion

A Bankart lesion involves injury to the:

Anteroinferior glenoid labrum and capsuloligamentous structures

after anterior dislocation.

Bony Bankart Lesion

When the anterior-inferior glenoid rim is fractured, the injury is termed a:

Bony Bankart lesion.

The lesion may therefore be:

Soft-tissue

Bony

or a combination of both.

Patients Older Than 40 Years

Older patients are more likely to sustain:

Rotator cuff tears

Greater tuberosity fractures

Lesser tuberosity fractures

Articular cartilage injuries

Coracoid fractures

and

Neurovascular injury.

Hill-Sachs Lesion

Anterior shoulder dislocation may create a:

Compression defect of the posterolateral or posterosuperior humeral head

when it impacts the:

Anterior glenoid rim.

This is known as a:

Hill-Sachs lesion.

Reverse Hill-Sachs Lesion

Posterior shoulder dislocation may produce an:

Anteromedial humeral head impaction defect

known as a:

Reverse Hill-Sachs lesion.

Diagnosis

Diagnosis is based on:

History

Physical examination

and

Radiographs.

Signs and Symptoms

Typical findings include:

Severe shoulder pain

Tenderness

Inability or unwillingness to move the shoulder

and visible alteration in:

Shoulder contour.

Arm Support

Patients frequently support the injured arm using the:

Opposite hand

to minimize painful motion.

Neurovascular Symptoms

Patients may develop:

Numbness

Weakness

or other evidence of:

Nerve injury.

The:

Axillary nerve

is the most commonly affected.

Axillary Nerve Findings

Axillary nerve dysfunction may cause:

Reduced sensation over the lateral shoulder

and

Deltoid weakness.

Physical Examination

A careful examination should be performed:

Before and after reduction.

Inspection

Inspect the shoulder girdle for:

Asymmetry

Loss of normal contour

Swelling

Ecchymosis

and deformity.

Anterior Dislocation Appearance

With anterior dislocation, the shoulder may appear:

Squared off

with a prominent:

Acromion

and loss of the normal rounded deltoid contour.

Palpation

The displaced humeral head may occasionally be palpable:

Anteriorly

or

Posteriorly

depending on the direction of dislocation.

Sulcus Sign

The sulcus sign demonstrates:

Inferior laxity

but is more relevant to chronic instability evaluation than to the immediate management of an acute dislocation.

Apprehension and Relocation Tests

These tests are useful after the acute injury has resolved to evaluate:

Anterior instability.

They should not be aggressively performed during the:

Acute dislocation episode.

Neurovascular Examination

Document before and after reduction:

Axillary nerve sensation

Deltoid function

Distal motor function

Peripheral pulses

Capillary refill

and overall:

Limb perfusion.

Range of Motion and Strength

Formal testing of:

Active motion

Passive motion

and

Shoulder girdle strength

should usually be deferred until after:

Reduction

and reduction of acute pain.

Imaging

Plain Radiographs

Conventional radiographs are generally sufficient to confirm the diagnosis.

At minimum, imaging should include:

Anteroposterior view

and

Axillary or equivalent orthogonal view.

Axillary View

The axillary view is particularly important for detecting:

Posterior shoulder dislocation.

If AP and scapular-Y views appear normal but clinical suspicion remains, an:

Axillary view

should be obtained whenever feasible.

Posterior Dislocation Pitfall

Posterior dislocation may be missed when only:

AP radiographs

are obtained.

This is one of the classic diagnostic pitfalls in shoulder trauma.

Scapular Y View

The scapular-Y view can help demonstrate the relationship between the:

Humeral head

and

Glenoid.

However, it does not completely replace the:

Axillary view.

Postreduction Radiographs

Radiographs should be obtained after reduction to:

Confirm concentric reduction

and evaluate for associated:

Fractures

Hill-Sachs lesions

or other bone injury.

CT

CT is useful for assessing:

Glenoid bone loss

Humeral head defects

Fracture configuration

and complex:

Bony instability lesions.

MRI

MRI is useful for evaluating:

Labral tears

Capsular injury

Rotator cuff tears

Biceps pathology

and other:

Soft-tissue injuries.

Pathological Findings

Histopathological testing is:

Not routinely required

for traumatic shoulder dislocation.

Differential Diagnosis

Important alternative or associated diagnoses include:

Acromioclavicular injury

Cervical spine injury

Clavicle fracture

Labral injury

Proximal humerus fracture

Rotator cuff tear

Treatment

General Principles

Acute shoulder dislocation requires:

Prompt closed reduction

after appropriate assessment and imaging.

The direction of the dislocation must be understood because it influences the:

Reduction technique.

Urgency

Reduction should be performed:

Urgently

to relieve pain, reduce neurovascular stretch, and minimize ongoing:

Cartilage and soft-tissue injury.

Analgesia and Sedation

Options include:

Intra-articular local anesthetic

Procedural sedation

Intravenous analgesia

or other appropriate pain-control strategies.

Muscle Spasm

Muscle spasm can prevent easy reduction.

Adequate:

Analgesia

Relaxation

and gentle technique reduce the risk of:

Iatrogenic fracture or soft-tissue injury.

Reduction Principles

Reduction should be:

Slow

Controlled

and

Gentle.

Forceful manipulation should be avoided.

Stimson Technique

The patient lies:

Prone

with the affected arm hanging over the side of the table.

Gentle downward traction, historically sometimes assisted by:

Weights

allows gradual muscle relaxation and reduction.

Traction-Countertraction

With the patient supine, gentle longitudinal traction is applied to the:

Affected arm

while countertraction is applied across the torso using:

A sheet or assistant.

Milch Technique

The arm is gradually:

Abducted

while the examiner controls the humeral head.

Once adequate abduction is achieved, gentle:

External rotation

may assist reduction.

FARES Technique

The:

FARES technique

uses gentle longitudinal traction while the arm is progressively abducted with small:

Vertical oscillations.

It is designed to provide:

Fast, atraumatic reduction

without abrupt force.

Posterior Dislocation Reduction

Posterior dislocations require special caution.

Forceful:

External rotation

should be avoided because it can cause:

Proximal humerus fracture

particularly when a reverse Hill-Sachs lesion is present.

Posterior Reduction Principle

Reduction generally involves:

Gentle traction

Controlled internal rotation

and carefully directed force on the:

Proximal humerus

to disengage the humeral head from the posterior glenoid.

Irreducible Dislocation

If closed reduction fails, the patient requires:

Urgent open reduction.

Failure may result from:

Interposed soft tissue

Fracture fragments

or an entrapped:

Humeral head defect.

Immobilization

After uncomplicated reduction, patients are typically placed in a:

Sling

or

Shoulder immobilizer.

Duration of Sling Use

A short period of approximately:

7–10 days

is often sufficient for pain control in simple dislocations.

The exact duration depends on:

Age

Associated injury

and

Comfort.

Early Motion

After acute pain subsides, patients should gradually begin:

Gentle range-of-motion exercises.

Prolonged immobilization should be avoided, especially in:

Older patients

because of the risk of:

Shoulder stiffness.

Return to Sport

Athletes may return when they have:

Full or near-full range of motion

Symmetric strength

Minimal or no pain

and sufficient:

Stability for sport-specific activity.

Bracing for Contact Sports

Some contact athletes use braces that limit:

External rotation

and

Abduction

during return to play.

However, recurrent instability after return to competition remains:

Common.

Physical Therapy

Physical therapy may begin after the:

Acute pain subsides.

Rehabilitation Goals

The goals are to restore:

Range of motion

Rotator cuff strength

Scapular control

and

Symmetric shoulder function.

Associated Injuries

If a patient has an associated:

Fracture

Rotator cuff tear

or other significant injury, rehabilitation may need to be:

Delayed or modified.

Need for Therapy

Not every uncomplicated dislocation requires formal:

Physical therapy.

A structured home program may be sufficient for some patients.

Medication

First-Line Analgesia

Pain may be treated with:

NSAIDs

and

Acetaminophen.

Opioids

A short course of opioid analgesia may occasionally be needed for:

Severe acute pain.

Routine prolonged opioid treatment should be avoided.

Surgery

Surgical treatment after a first-time shoulder dislocation is:

Individualized.

First-Time Dislocation

Many first-time dislocations are initially managed:

Nonoperatively.

However, early surgery may be considered in selected:

Young high-risk athletes

or patients with significant structural injury.

Surgical Target

Surgery should address the specific abnormality responsible for instability, as identified clinically and with:

MRI

CT

or other advanced imaging.

Bankart Repair

Young patients commonly have a:

Bankart lesion.

Soft-tissue Bankart lesions are typically repaired:

Arthroscopically

with restoration of the:

Labrum and capsule.

Bony Bankart Repair

A significant glenoid rim fracture may require:

Arthroscopic

or

Open fixation or reconstruction

depending on the size and configuration of the:

Bone defect.

Hill-Sachs Lesion

Large humeral head defects that engage the glenoid may contribute to:

Recurrent instability.

Remplissage

A:

Remplissage procedure

fills the Hill-Sachs defect using posterior capsulotenodesis, typically involving the:

Infraspinatus tendon and posterior capsule.

This reduces the tendency of the defect to:

Engage the anterior glenoid.

Bone Reconstruction

Very large humeral head defects may occasionally require:

Bone grafting

or other reconstructive procedures.

Greater Tuberosity Fracture

Associated greater tuberosity fractures are treated according to:

Displacement

Rotator cuff function

and

Patient activity level.

Rotator Cuff Repair

Complete rotator cuff tears associated with dislocation in older patients may require:

Arthroscopic

or

Open repair

when medically and functionally appropriate.

Glenoid Bone Loss

Substantial anterior glenoid bone loss is an important cause of:

Recurrent instability.

Latarjet Procedure

The:

Latarjet procedure

transfers the:

Coracoid process

to the anterior glenoid to augment deficient:

Glenoid bone stock

and provide additional dynamic stability.

Other Bone-Block Procedures

Alternative bone-augmentation techniques may be used depending on:

Defect size

Prior surgery

and surgeon preference.

Follow-Up

Patients are generally reassessed within approximately:

7–10 days

after injury.

Early Follow-Up Goals

The clinician should reassess:

Pain

Neurovascular function

Rotator cuff strength

Range of motion

and possible associated:

Fractures or soft-tissue injuries.

Sling Weaning

Patients with uncomplicated dislocations are usually encouraged to:

Gradually discontinue sling use

as pain improves.

Advanced Imaging

Further MRI or CT may be obtained when there is concern for:

Rotator cuff tear

Labral injury

Bone loss

Persistent weakness

or

Recurrent instability.

Prognosis

Prognosis depends heavily on:

Age at first dislocation

Sex

Activity level

and the amount of:

Structural damage.

Recurrence in Young Patients

Recurrent instability is particularly common in patients younger than approximately:

21 years.

Historical studies have reported recurrence rates approaching:

80% in teenagers

after nonoperative treatment.

Effect of Age

The younger the patient at the time of the initial dislocation, the greater the likelihood of:

Recurrence.

Male Sex

Male sex has also been associated with a higher risk of:

Recurrent instability

in several studies.

Associated Pathology

Recurrence risk increases when dislocation is accompanied by:

Labral injury

Capsular injury

Glenoid bone loss

Hill-Sachs lesion

or other structural abnormalities.

Complications

Recurrent Instability

The most common long-term complication in young patients is:

Recurrent dislocation or subluxation.

Glenohumeral Arthritis

Repeated instability episodes may contribute to progressive:

Glenohumeral osteoarthritis.

Even a single traumatic dislocation can occasionally produce:

Long-term chondral damage.

Chondral Injury

Dislocation may damage:

Articular cartilage

of the glenoid or humeral head.

Labral Tears

Labral injury is common, particularly after:

Anterior dislocation in younger patients.

Nerve Injury

Transient nerve injury or:

Neurapraxia

occurs in a minority of patients.

Historical estimates are approximately:

5%.

Axillary Nerve

The:

Axillary nerve

is the most commonly injured nerve.

Patients should be examined for:

Lateral shoulder numbness

and

Deltoid weakness.

Rotator Cuff and Nerve Injury Association

Rotator cuff tears and peripheral nerve injuries may coexist, particularly in:

Older patients.

The presence of one should prompt consideration of the:

Other.

Proximal Humerus Fracture

A shoulder dislocation may occur with:

Greater tuberosity fracture

or other proximal humerus fractures.

Vascular Injury

Vascular injury is:

Rare

but can occur, particularly in:

Older patients

or high-energy trauma.

Loss of pulses, expanding hematoma, or limb ischemia requires:

Urgent vascular assessment.

Patient Monitoring

Follow-up should evaluate:

Pain

Range of motion

Strength

Neurovascular status

Rotator cuff function

and evidence of:

Recurrent instability.

Key Principle

Shoulder dislocation is most commonly anterior and occurs because the glenohumeral joint sacrifices stability in order to achieve exceptional mobility.

Young patients most often sustain:

Labral and capsular injuries, while older patients are more likely to have:

Rotator cuff tears, tuberosity fractures, and nerve injuries.

Diagnosis requires appropriate radiographs, especially an:

Axillary view to avoid missing posterior dislocation.

Treatment begins with:

Urgent gentle reduction, postreduction imaging, short-term sling use, and progressive rehabilitation.

Surgery is considered for:

Recurrent instability, significant Bankart or Hill-Sachs lesions, substantial glenoid bone loss, associated rotator cuff tears, fractures, or irreducible dislocation.

Orthopaedic Surgery - Short Stature

⸻

Basics

Short stature is generally defined as:

Height below the 3rd percentile for age and sex

relative to the general population.

There are many potential causes of short stature. From an orthopaedic perspective, the most important group is:

Skeletal dysplasia.

⸻

Most Common Overall Cause

The most common causes of short stature overall are:

Familial short stature

and

Constitutional growth delay.

These typically produce proportionate short stature without a primary abnormality of:

Bone or cartilage development.

⸻

Skeletal Dysplasia

Skeletal dysplasias are a diverse group of disorders characterized by intrinsic abnormalities of:

Cartilage formation

Bone growth

and

Skeletal remodeling.

Many become apparent at:

Birth

or during:

Early childhood.

⸻

Synonym

The historical term:

Dwarfism

has been used to describe disproportionate short stature, although specific diagnostic terminology is preferred whenever possible.

⸻

Classification

The most widely accepted classification system is the:

International Classification of Skeletal Dysplasias / Osteochondrodysplasias.

⸻

Classification by Body Proportion

Skeletal dysplasias may be broadly grouped according to whether shortening predominantly involves the:

Limbs

or

Trunk.

Thus, patients may demonstrate:

Short-limb disproportion

or

Short-trunk disproportion.

⸻

Classification by Bone Region

Disorders can also be classified according to the part of the long bone most severely affected:

Epiphyseal

Metaphyseal

or

Diaphyseal.

⸻

Epiphyseal Disease

Patients with major epiphyseal involvement are particularly prone to:

Joint contractures

Early degenerative arthritis

and

Reduced range of motion

because the:

Articular surfaces

are directly affected.

⸻

Rhizomelic Shortening

The term:

Rhizomelic

refers to disproportionate shortening that is greatest in the:

Proximal limb segments

such as the:

Humerus

and

Femur.

A classic example is:

Achondroplasia.

⸻

Epidemiology

Skeletal dysplasias collectively are uncommon.

Historical estimates suggest an incidence of approximately:

1 in 3,000 to 1 in 5,000 live births.

⸻

Risk Factors

Potential risk factors include:

Positive family history

Consanguinity

and membership in populations with a relatively high frequency of particular:

Inherited skeletal dysplasias.

⸻

Geographic Clustering

Certain disorders occur more commonly in specific populations because of:

Founder effects.

Examples historically include:

Diastrophic dysplasia in Finland

and selected metaphyseal dysplasias in:

Amish communities.

⸻

Genetics

Many skeletal dysplasias are inherited in:

Autosomal-dominant

or

Autosomal-recessive patterns.

⸻

New Mutations

A substantial number of affected children have:

De novo mutations

despite no family history.

These individuals may subsequently transmit the disorder to their:

Children

depending on the mode of inheritance.

⸻

Genetic Testing

Molecular testing is available for many skeletal dysplasias.

It may help with:

Diagnostic confirmation

Prognostic counseling

and

Family planning.

⸻

Etiology

The molecular cause varies according to the specific disorder.

⸻

Achondroplasia

Achondroplasia results from a pathogenic variant affecting:

FGFR3 – fibroblast growth factor receptor 3.

This produces abnormal regulation of:

Endochondral bone growth.

⸻

Diastrophic Dysplasia

Diastrophic dysplasia is caused by abnormalities involving a cellular:

Sulfate transporter

which affects normal cartilage and skeletal development.

⸻

Mucopolysaccharidoses

Mucopolysaccharidoses result from inherited deficiencies of enzymes involved in:

Glycosaminoglycan metabolism.

Accumulation of undegraded material affects:

Bone

Joints

and multiple organ systems.

⸻

Other Disorders

Many additional skeletal dysplasias have now been linked to specific abnormalities of:

Receptors

Structural proteins

Enzymes

or

Extracellular matrix pathways.

⸻

Associated Conditions

Depending on the diagnosis, skeletal dysplasias may be associated with:

Neurologic compromise

Respiratory problems

Spinal deformity

Hip dysplasia

Foot deformities

Joint contractures

Early arthritis

⸻

Neurologic and Respiratory Problems

Spinal deformity or narrowing may cause:

Cord compression

Nerve-root compression

Spinal stenosis

or restrictive:

Pulmonary dysfunction.

⸻

Developmental Delay

Some metabolic storage disorders, such as:

Hurler syndrome

may be associated with:

Neurodevelopmental impairment.

⸻

Hip Abnormalities

Hip dysplasia and abnormal proximal femoral development may occur in several skeletal dysplasias and can lead to:

Pain

Instability

and

Early osteoarthritis.

⸻

Clubfoot

Foot deformities, including:

Clubfoot

may occur in disorders such as:

Diastrophic dysplasia

and some forms of:

Spondyloepiphyseal dysplasia.

⸻

Scoliosis

Scoliosis and kyphosis are common complications across many:

Skeletal dysplasias.

⸻

Diagnosis

Diagnosis is based on:

Growth pattern

Body proportions

Physical examination

Radiographic features

and, increasingly,

Genetic testing.

⸻

Achondroplasia

Achondroplasia is the:

Most common skeletal dysplasia.

Typical features include:

Rhizomelic limb shortening

Frontal bossing

Midface hypoplasia

Delayed motor milestones

Thoracolumbar kyphosis

Lumbar spinal stenosis

and

Foramen magnum narrowing.

⸻

Adult Height in Achondroplasia

Adult height is typically markedly reduced and historically has often been:

Below approximately 50 inches

although individual height varies.

⸻

Neurologic Concerns in Achondroplasia

Important neurologic issues include:

Foramen magnum stenosis

in infancy and childhood

and

Lumbar spinal stenosis

later in life.

⸻

Multiple Epiphyseal Dysplasia

Multiple epiphyseal dysplasia is one of the more common skeletal dysplasias.

It is often inherited as:

Autosomal dominant.

⸻

Multiple Epiphyseal Dysplasia Features

Characteristic findings include:

Abnormal ossification of multiple epiphyses

Mild short stature

Short limbs

Prominent joints

Joint pain

Reduced range of motion

and

Angular limb deformity.

⸻

Joints Commonly Involved

The:

Hips

Knees

and

Ankles

are commonly affected.

Because short stature may be relatively mild, diagnosis may not occur until:

Later childhood.

⸻

Adult Height in Multiple Epiphyseal Dysplasia

Historical adult heights have ranged approximately from:

57 to 67 inches.

⸻

Hypochondroplasia

Hypochondroplasia is usually an:

Autosomal-dominant

mild short-limb skeletal dysplasia.

⸻

Hypochondroplasia Features

Possible findings include:

Symmetric limb shortening

Mild frontal bossing

Lumbar lordosis

Mild kyphosis

and features that may overlap with:

Achondroplasia.

⸻

Facial Features

Unlike classic achondroplasia, patients often have little or no:

Midface hypoplasia.

⸻

Diastrophic Dysplasia

Diastrophic dysplasia is an:

Autosomal-recessive

skeletal dysplasia with prominent abnormalities of:

Cartilage

Joints

and

Extremities.

⸻

Diastrophic Dysplasia Features

Typical findings include:

Rhizomelic shortening

Cauliflower ear

Major joint contractures

Hitchhiker thumb

Foot deformity

Scoliosis

and sometimes:

Cervical spinal abnormalities.

⸻

Hitchhiker Thumb

The characteristic:

Hitchhiker thumb

refers to an abducted or unusually positioned thumb associated with:

Diastrophic dysplasia.

⸻

Mucopolysaccharidoses

Common musculoskeletal and systemic features include:

Joint contractures

Organomegaly

Skeletal deformity

and, in some forms,

Cataracts

or

Developmental delay.

⸻

Multiple Osteochondromas

Hereditary multiple osteochondromas is typically:

Autosomal dominant.

⸻

Clinical Features

Patients may have:

Mild short stature

Multiple osteochondromas

Angular limb deformity

Leg-length discrepancy

and mechanical impingement involving:

Tendons

Nerves

or, rarely,

The spinal canal.

⸻

Malignant Transformation

A small percentage of patients develop malignant transformation, most often to:

Secondary chondrosarcoma.

Historical estimates are around:

1%

although reported risk varies.

⸻

Spondyloepiphyseal Dysplasia

Spondyloepiphyseal dysplasia may produce:

Short-trunk disproportion

Cervical instability

Scoliosis

Joint contractures

and

Hip and knee stiffness.

⸻

Cervical Spine Risk

Cervical instability is particularly important because of the potential for:

Spinal cord injury.

⸻

Down Syndrome

Musculoskeletal features may include:

Pes planus

Ligamentous laxity

and characteristic hand and facial findings.

Patients may also demonstrate:

Developmental delay.

⸻

Turner Syndrome

Turner syndrome occurs in:

Females

with complete or partial loss of one:

X chromosome.

⸻

Turner Syndrome Features

Typical findings include:

Short stature

Cubitus valgus

Webbed neck

and

Delayed or abnormal sexual development.

⸻

Osteogenesis Imperfecta

Osteogenesis imperfecta may be associated with:

Broad cranial shape

Shortened and deformed long bones

Frequent fractures

Scoliosis

Kyphosis

and

Basilar invagination.

⸻

X-Linked Hypophosphatemia

X-linked hypophosphatemia results from pathogenic variants involving:

PHEX.

Musculoskeletal findings may include:

Short stature

Lower-extremity deformity

and particularly:

Genu varum or genu valgum, depending on the individual.

⸻

Physical Examination

Evaluation should determine whether short stature is:

Proportionate

or

Disproportionate.

⸻

Birth Length

Document:

Length at birth

because congenital skeletal dysplasias often show disproportion from:

Early infancy.

⸻

Current Growth

Record:

Current height

Growth percentile

and serial:

Growth velocity.

⸻

Body Proportion

Compare:

Trunk length

with

Limb length.

Other useful measurements may include:

Sitting height

Arm span

and

Upper-to-lower segment ratio.

⸻

Dysmorphic Features

Examine for characteristic:

Craniofacial

Hand

Foot

and

Soft-tissue abnormalities

that may suggest a specific diagnosis.

⸻

Neurologic Examination

A complete neurologic assessment is important to identify complications of:

Spinal stenosis

Foramen magnum narrowing

or

Cervical instability.

⸻

Joint Examination

Document:

Range of motion

Contractures

and

Joint stiffness.

⸻

Limb Alignment

Assess for:

Varus

Valgus

Rotational deformity

and

Leg-length discrepancy.

⸻

Spine Examination

Evaluate for:

Scoliosis

Kyphosis

Lordosis

and possible signs of:

Spinal instability.

⸻

Laboratory Tests

Routine laboratory studies are often:

Not diagnostic

for skeletal dysplasia.

Testing should be directed by the suspected alternative or specific disorder.

⸻

Chemistry

A chemistry panel may be useful when there is concern for:

Metabolic bone disease

or other systemic illness.

⸻

Endocrine Evaluation

Endocrine studies may be appropriate when considering:

Growth hormone deficiency

Thyroid disease

or other hormonal causes of proportionate:

Short stature.

⸻

Urinary Testing

Urine testing may help identify selected:

Storage disorders

or metabolic diseases.

⸻

Specialized Testing

More specialized biochemical and genetic testing is often coordinated by a:

Medical geneticist

or

Endocrinologist.

⸻

Imaging

A skeletal survey or targeted radiographic evaluation may help establish the pattern of:

Bone and cartilage abnormality.

⸻

Suggested Radiographs

Common studies include:

Lateral skull

Cervical spine

Lateral thoracolumbar spine

AP pelvis

AP hand and wrist.

Additional imaging depends on:

Clinical findings

and the suspected diagnosis.

⸻

Skull and Cervical Spine

These images may identify:

Foramen magnum narrowing

Cervical instability

Basilar invagination

or abnormal:

Vertebral development.

⸻

Thoracolumbar Spine

Spinal imaging may identify:

Kyphosis

Scoliosis

Vertebral dysplasia

or

Spinal stenosis.

⸻

Pelvis

Pelvic radiographs help evaluate:

Acetabular development

Proximal femoral morphology

and

Hip dysplasia.

⸻

Hand and Wrist

Hand and wrist radiographs may demonstrate:

Epiphyseal abnormalities

Metaphyseal changes

and provide information regarding:

Skeletal maturity.

⸻

Pathological Findings

Histologic abnormalities vary according to the specific disorder.

Many skeletal dysplasias involve altered development of:

Cartilage

Bone

Ligament

and

Tendon.

⸻

Differential Diagnosis

Short stature should not automatically be attributed to:

Skeletal dysplasia.

Evaluation may require consultation with:

Genetics

and

Endocrinology.

⸻

Important Alternatives

Differential diagnoses include:

Familial short stature

Constitutional growth delay

Malnutrition

Endocrine disease

Chronic systemic illness

Long-term corticosteroid use

⸻

Constitutional Short Stature

Children with constitutional growth delay are often:

Proportionately short

and may have delayed:

Bone age

and

Pubertal development.

⸻

Malnutrition

Insufficient caloric or nutrient intake may impair:

Linear growth

and should be considered when body weight is also:

Low.

⸻

Hormonal Disorders

Possible causes include:

Growth hormone deficiency

Hypothyroidism

and other endocrine abnormalities.

⸻

Chronic Disease

Long-standing conditions affecting the:

Heart

Lungs

Kidneys

Gastrointestinal tract

or other systems can impair normal:

Growth.

⸻

Treatment

⸻

General Principles

Orthopaedic management of skeletal dysplasia is primarily directed toward:

Function

Alignment

Stability

and prevention or treatment of:

Neurologic complications.

⸻

Cervical Spine Instability

Cervical instability should be identified and monitored carefully.

Treatment may include:

Bracing

or

Surgical fusion

when instability threatens:

Neurologic function.

⸻

Spinal Stenosis

Patients with symptomatic stenosis and:

Neurogenic claudication

or neurologic deficit may require:

Surgical decompression.

⸻

Scoliosis and Kyphosis

Spinal deformities should be:

Documented

and followed over time.

Progressive deformity may require:

Bracing

or

Surgical correction.

⸻

Genetic Counseling

Accurate:

Genetic counseling

is important for affected individuals and their families.

⸻

Multidisciplinary Care

Management may require coordination among:

Orthopaedics

Medical genetics

Endocrinology

Neurology

Pulmonology

and other specialists depending on the diagnosis.

⸻

Mobility

With increasing age, some patients develop:

Severe arthritis

or

Spinal disease

that reduces mobility.

Powered mobility devices may become useful for maintaining:

Independence

and reducing excessive energy expenditure.

⸻

Growth Hormone

Growth hormone is generally not an effective treatment for increasing height in many forms of:

Disproportionate skeletal dysplasia.

It may, however, have a role in specific conditions such as:

Growth hormone deficiency

or selected syndromic causes of short stature under endocrine supervision.

⸻

Limb Lengthening

Selected patients with:

Achondroplasia

or other short-limb dysplasias with relatively preserved joint and muscle function may consider:

Limb-lengthening procedures.

⸻

Magnitude of Lengthening

Extensive staged lengthening may increase final height by as much as approximately:

One foot

in highly selected patients.

This involves substantial treatment burden and risk.

⸻

Physical Therapy

Physical therapy cannot correct the underlying:

Skeletal dysplasia

or fixed bony deformity.

However, it may improve:

Strength

Mobility

Endurance

Joint function

and overall:

Independence.

⸻

Medication

No single medication treats all forms of:

Skeletal dysplasia.

⸻

Disorder-Specific Therapy

Some specific disorders now have:

Targeted medical therapies

or metabolic treatments.

Management should be tailored to the:

Underlying diagnosis.

⸻

Surgery

Surgery is performed for:

Spinal instability

Neurologic compression

Progressive deformity

Severe limb malalignment

or

Advanced joint degeneration.

⸻

Spinal Fusion

Fusion with instrumentation may be required for:

Progressive scoliosis

Kyphosis

or

Instability.

⸻

Spinal Decompression

Decompression may be required for:

Lumbar stenosis

Cervical stenosis

or other neurologic compression.

⸻

Osteotomy

Corrective osteotomy may be used for significant:

Varus

Valgus

or other angular deformities of the extremities.

⸻

Joint Replacement

Patients with severe early osteoarthritis due to epiphyseal dysplasia may eventually require:

Total joint arthroplasty.

The:

Hips

and

Knees

are commonly affected.

⸻

Follow-Up

Patients require long-term surveillance because many complications evolve during:

Growth

or later:

Adulthood.

⸻

Monitoring Interval

Children may be reviewed approximately every:

6 months

depending on the specific disorder and clinical severity.

⸻

Developmental Monitoring

Follow:

Motor milestones

Growth

Neurologic function

and

Skeletal deformity.

⸻

Prognosis

The prognosis varies widely according to:

Specific diagnosis

Severity

and associated:

Neurologic

Respiratory

or

Systemic abnormalities.

⸻

Spinal Complications

Many skeletal dysplasias are associated with:

Spinal stenosis

Cervical instability

and

Progressive deformity.

⸻

Arthritis

Early degenerative disease of the:

Hips

and

Knees

is common in several epiphyseal dysplasias.

⸻

Cervical Instability

Cervical instability is particularly associated with:

Spondyloepiphyseal dysplasia

and some:

Mucopolysaccharidoses.

⸻

Basilar Invagination

Basilar invagination may occur in disorders such as:

Osteogenesis imperfecta.

This can result in compression of:

Brainstem

or

Upper cervical neural structures.

⸻

Complications

Complications vary widely but may include:

Degenerative arthritis

Joint contractures

Spinal stenosis

Cervical instability

Scoliosis

Kyphosis

Neurologic compromise

Respiratory restriction

Limb deformity

Leg-length discrepancy

⸻

Patient Monitoring

Follow-up should assess:

Growth

Developmental milestones

Body proportions

Neurologic status

Spinal alignment

Joint range of motion

Contractures

and

Limb deformity.

⸻

Key Principle

Short stature is defined as height below approximately the 3rd percentile for age, but the cause may range from normal familial or constitutional variation to significant skeletal disease.

The most important orthopaedic causes are:

Skeletal dysplasias, which produce intrinsic abnormalities of cartilage and bone growth and often cause disproportionate short stature.

Evaluation should determine:

Body proportions, growth pattern, neurologic status, spinal deformity, joint contractures, and limb alignment, supported by targeted radiographs and genetic evaluation.

Orthopaedic treatment is directed primarily toward:

Maintaining function, correcting deformity, treating spinal instability or stenosis, and managing early joint degeneration, rather than simply increasing height.

Orthopaedic Surgery - Shin Splints

Basics

Shin splints, more accurately termed:

Medial tibial stress syndrome

are a common overuse condition characterized by:

Exercise-related pain along the posteromedial border of the tibia.

They usually develop after repetitive:

Running

Jumping

or other high-impact activity, particularly when training volume or intensity increases too quickly.

Synonyms

Common terms include:

Medial tibial stress syndrome

Tibial periostitis

Runner’s leg

and the traditional term:

Shin splints.

Nature of the Disorder

Medial tibial stress syndrome is best considered part of a:

Bone and periosteal stress response

caused by repetitive mechanical loading of the:

Tibia

and surrounding musculofascial attachments.

The condition differs from a discrete:

Tibial stress fracture, although both lie along the same spectrum of repetitive loading injury.

Epidemiology

Shin splints are especially common among:

Adolescents

Young adults

Runners

and athletes undergoing:

Conditioning programs.

Incidence

Reported incidence among runners is approximately:

13.6–20%.

Rates vary according to:

Training population

Running volume

and the diagnostic criteria used.

Risk Factors

Important risk factors include:

Running or jogging

Recent increase in mileage

Recent increase in speed or intensity

Training errors

Foot pronation

Pes planus

Higher body mass index

Female sex

Poor conditioning

Training Errors

A sudden increase in:

Running distance

Frequency

Hill work

or

Intensity

is a common precipitating factor.

The tissues of the leg may not have sufficient time to adapt to the new:

Mechanical load.

Foot Mechanics

Excessive:

Pronation

or a relatively flat foot may increase rotational and bending forces through the:

Tibia.

These biomechanical factors may contribute to repetitive stress along the:

Medial tibial border.

Etiology

Historically, shin splints were attributed mainly to:

Periostitis

at the muscular attachments of the:

Soleus

and

Posterior tibial structures.

Current concepts also recognize repetitive:

Tibial bone stress

as an important component of the disorder.

Muscular Traction

Repeated traction from muscles attaching along the medial tibia, particularly the:

Soleus

may contribute to irritation of the:

Periosteum

and underlying bone.

Repetitive Impact

Repeated ground-reaction forces generated during:

Running

and

Jumping

produce cyclical bending of the tibia.

When these loads exceed the bone’s capacity to remodel, pain may develop.

Associated Conditions

Medial tibial stress syndrome is commonly seen in:

Athletes undergoing conditioning

especially runners and military recruits.

Lower-Limb Deformity

Any biomechanical abnormality that increases stress through the leg may contribute, including:

Pes planus

Excessive pronation

and selected abnormalities of:

Lower-extremity alignment.

Diagnosis

The diagnosis is primarily:

Clinical.

A careful history and examination are important because shin splints can resemble more serious disorders such as:

Tibial stress fracture

and

Chronic exertional compartment syndrome.

Signs and Symptoms

Pain is usually induced by:

Exercise

and is located along the:

Posteromedial border of the distal tibia.

Character of Pain

The pain is typically:

Dull

Aching

or

Diffuse.

In some patients it may become:

Quite intense.

Timing of Pain

Symptoms often appear:

At the beginning of exercise.

Pain may continue during or after the workout but generally:

Improves with rest.

Progression

With continued training despite symptoms, pain may become:

More persistent

and may eventually limit:

Running performance.

Pain at rest or focal severe pain should raise concern for:

Stress fracture.

Physical Examination

The key finding is:

Diffuse tenderness along the posteromedial tibial border.

Distribution of Tenderness

Tenderness generally extends over a:

Relatively long segment

of the tibia rather than being confined to one very small:

Focal point.

This helps differentiate medial tibial stress syndrome from a:

Stress fracture.

Pain With Muscle Testing

Symptoms may be reproduced with resisted:

Plantarflexion

and

Inversion

because these movements recruit muscles attached near the symptomatic tibial region.

Inspection

There is usually little visible abnormality.

Occasionally there may be mild:

Soft-tissue swelling

or tenderness without marked erythema.

Gait and Foot Examination

Examine:

Foot posture

Arch height

Pronation

Ankle motion

and overall:

Running or walking mechanics.

Stress Fracture Concern

A tibial stress fracture should be suspected when tenderness is:

Highly localized

rather than diffuse.

Other concerning features include:

Pain at rest

Night pain

Pain with walking

and progressively worsening symptoms despite:

Activity reduction.

Chronic Exertional Compartment Syndrome

Chronic exertional compartment syndrome may present with exercise-induced pain but typically has a different pattern.

Symptoms often involve the:

Anterolateral leg

and may include:

Tightness

Neurologic symptoms

or temporary:

Weakness.

Fascial Herniation

Patients with exertional compartment syndrome may occasionally have visible or palpable:

Fascial hernias.

Imaging

Plain Radiographs

Plain radiographs are often:

Normal

in medial tibial stress syndrome.

Their main role is to exclude:

Stress fracture

or another bony abnormality.

Serial Radiographs

Early stress fractures may also be radiographically occult.

Therefore, normal initial radiographs do not completely exclude a:

Bone stress injury.

Bone Scintigraphy

Historically, bone scanning may show:

Diffuse longitudinal uptake

along the posteromedial tibia in medial tibial stress syndrome.

Stress Fracture Bone Scan

A stress fracture more commonly produces:

Focal

or

Transverse increased uptake

rather than a long diffuse pattern.

MRI

MRI is highly useful for distinguishing:

Medial tibial stress syndrome

from

Stress fracture.

It can identify:

Periosteal edema

Bone marrow edema

and, in more advanced stress injury,

A fracture line.

Compartment Pressure Testing

When:

Chronic exertional compartment syndrome

is strongly suspected, compartment pressure measurements before and after:

Exercise

may be considered.

This is most relevant when symptoms are:

Anterolateral

and consistently appear at a reproducible level of exertion.

Pathological Findings

The disorder has historically been associated with inflammation or stress reaction involving the:

Periosteum

and attachment sites of the:

Soleus

and nearby posterior tibial musculature.

Modern evidence also supports an underlying:

Tibial bone stress response.

Differential Diagnosis

The two most important conditions to distinguish are:

Tibial stress fracture

and

Chronic exertional compartment syndrome.

Tibial Stress Fracture

Stress fractures typically cause:

More focal tenderness

and may progress to pain with:

Walking

or

Rest.

MRI is helpful when the diagnosis is uncertain.

Chronic Exertional Compartment Syndrome

This condition typically causes:

Tightness or pain during exercise

that resolves after stopping.

Possible associated symptoms include:

Paresthesia

Weakness

and a feeling of:

Leg fullness or pressure.

Treatment

General Principles

Treatment is primarily:

Nonoperative.

The cornerstone of management is reducing mechanical loading until symptoms improve.

Activity Modification

Training should be reduced to:

Below the level that provokes symptoms.

This may require decreasing:

Mileage

Speed

Running frequency

or temporarily stopping:

Impact exercise.

Relative Rest

Complete inactivity is usually unnecessary.

Athletes may maintain fitness with low-impact activities such as:

Cycling

Swimming

or other exercises that do not reproduce pain.

Ice

Ice may be applied after activity for:

Symptomatic relief.

Physical Therapy

Physical therapy may assist with:

Calf flexibility

Lower-extremity strengthening

Core strengthening

Foot and ankle mechanics

and gradual return to:

Running.

Stretching

Once acute symptoms improve, stretching may focus on the:

Gastrocnemius

Soleus

and other lower-extremity structures.

Strengthening

Rehabilitation may include strengthening of:

Calf muscles

Foot intrinsic muscles

Hip abductors

Core musculature.

Gait Analysis

Running-form assessment can help identify:

Biomechanical abnormalities

or training patterns that increase repetitive tibial loading.

Orthotics and Footwear

Selected patients with excessive pronation may benefit from:

Orthotic inserts

or

Shoe modification.

The goal is to reduce excessive:

Foot pronation

and improve load distribution.

Training Modification

Long-term prevention requires identifying and correcting:

Training errors.

Mileage and intensity should increase:

Gradually.

Extracorporeal Shock-Wave Therapy

Extracorporeal shock-wave therapy has been studied for persistent medial tibial stress syndrome.

Some studies have suggested:

Earlier symptom improvement

but it is not required for most patients.

Medication

NSAIDs

NSAIDs may provide short-term relief of:

Pain

and

Inflammation.

Analgesics

Other simple analgesics, including:

Acetaminophen

may also be used when appropriate.

Medication should not be used to allow continued training through:

Significant pain.

Surgery

Surgery is:

Rarely required.

Surgical Indications

Only patients with persistent symptoms despite a documented course of:

Maximal nonoperative treatment

should be considered for operative management.

Fascial Release

A:

Posteromedial fascial release

has occasionally been used for refractory cases.

Results are variable, and surgery is reserved for:

Highly selected patients.

Follow-Up

Patients should be reassessed if symptoms:

Persist

Become focal

or worsen despite appropriate:

Activity modification.

Return to Running

Return to impact activity should be:

Gradual.

The athlete should first be able to:

Walk pain free

Hop without pain

and perform basic strengthening exercises without significant:

Tibial discomfort.

Training Progression

Mileage and intensity should be increased:

Incrementally

rather than returning immediately to the previous training level.

Prognosis

The prognosis is generally:

Good.

Most patients improve with:

Nonoperative treatment.

Recurrence

Recurrence is common when the athlete returns too rapidly to:

High training volume

or fails to correct the underlying:

Training error or biomechanical problem.

Prevention of Recurrence

Helpful measures include:

Gradual training progression

Appropriate footwear

Correction of excessive pronation when clinically relevant

Strength and flexibility training

and adequate:

Recovery time.

Complications

The most important potential complication is failure to recognize a:

Tibial stress fracture.

Complete Fracture

An untreated stress fracture may progress to a:

Complete fracture

with possible:

Displacement

and substantially prolonged recovery.

Missed Compartment Syndrome

Failure to identify chronic exertional compartment syndrome may result in:

Persistent exercise limitation

and ongoing:

Neurologic or muscular symptoms.

Patient Monitoring

Monitor:

Pain location

Extent of tenderness

Walking tolerance

Running progression

and response to:

Training modification and rehabilitation.

Development of focal pain, rest pain, or worsening symptoms should prompt evaluation for:

Stress fracture or another diagnosis.

Key Principle

Shin splints, or medial tibial stress syndrome, are an overuse injury characterized by diffuse exercise-related pain and tenderness along the posteromedial tibial border.

The most important precipitating factors are:

Rapid increases in running volume or intensity and repetitive impact loading.

Treatment is usually successful with:

Activity modification, ice, stretching, strengthening, gait and footwear assessment, and gradual return to running.

Persistent focal pain or worsening symptoms should prompt investigation for:

Tibial stress fracture, while anterolateral exertional pain with tightness or neurologic symptoms should raise concern for:

Chronic exertional compartment syndrome.

Orthopaedic Surgery - Shin Splints

Basics

Shin splints, more accurately termed:

Medial tibial stress syndrome

are a common overuse condition characterized by:

Exercise-related pain along the posteromedial border of the tibia.

They usually develop after repetitive:

Running

Jumping

or other high-impact activity, particularly when training volume or intensity increases too quickly.

Synonyms

Common terms include:

Medial tibial stress syndrome

Tibial periostitis

Runner’s leg

and the traditional term:

Shin splints.

Nature of the Disorder

Medial tibial stress syndrome is best considered part of a:

Bone and periosteal stress response

caused by repetitive mechanical loading of the:

Tibia

and surrounding musculofascial attachments.

The condition differs from a discrete:

Tibial stress fracture, although both lie along the same spectrum of repetitive loading injury.

Epidemiology

Shin splints are especially common among:

Adolescents

Young adults

Runners

and athletes undergoing:

Conditioning programs.

Incidence

Reported incidence among runners is approximately:

13.6–20%.

Rates vary according to:

Training population

Running volume

and the diagnostic criteria used.

Risk Factors

Important risk factors include:

Running or jogging

Recent increase in mileage

Recent increase in speed or intensity

Training errors

Foot pronation

Pes planus

Higher body mass index

Female sex

Poor conditioning

Training Errors

A sudden increase in:

Running distance

Frequency

Hill work

or

Intensity

is a common precipitating factor.

The tissues of the leg may not have sufficient time to adapt to the new:

Mechanical load.

Foot Mechanics

Excessive:

Pronation

or a relatively flat foot may increase rotational and bending forces through the:

Tibia.

These biomechanical factors may contribute to repetitive stress along the:

Medial tibial border.

Etiology

Historically, shin splints were attributed mainly to:

Periostitis

at the muscular attachments of the:

Soleus

and

Posterior tibial structures.

Current concepts also recognize repetitive:

Tibial bone stress

as an important component of the disorder.

Muscular Traction

Repeated traction from muscles attaching along the medial tibia, particularly the:

Soleus

may contribute to irritation of the:

Periosteum

and underlying bone.

Repetitive Impact

Repeated ground-reaction forces generated during:

Running

and

Jumping

produce cyclical bending of the tibia.

When these loads exceed the bone’s capacity to remodel, pain may develop.

Associated Conditions

Medial tibial stress syndrome is commonly seen in:

Athletes undergoing conditioning

especially runners and military recruits.

Lower-Limb Deformity

Any biomechanical abnormality that increases stress through the leg may contribute, including:

Pes planus

Excessive pronation

and selected abnormalities of:

Lower-extremity alignment.

Diagnosis

The diagnosis is primarily:

Clinical.

A careful history and examination are important because shin splints can resemble more serious disorders such as:

Tibial stress fracture

and

Chronic exertional compartment syndrome.

Signs and Symptoms

Pain is usually induced by:

Exercise

and is located along the:

Posteromedial border of the distal tibia.

Character of Pain

The pain is typically:

Dull

Aching

or

Diffuse.

In some patients it may become:

Quite intense.

Timing of Pain

Symptoms often appear:

At the beginning of exercise.

Pain may continue during or after the workout but generally:

Improves with rest.

Progression

With continued training despite symptoms, pain may become:

More persistent

and may eventually limit:

Running performance.

Pain at rest or focal severe pain should raise concern for:

Stress fracture.

Physical Examination

The key finding is:

Diffuse tenderness along the posteromedial tibial border.

Distribution of Tenderness

Tenderness generally extends over a:

Relatively long segment

of the tibia rather than being confined to one very small:

Focal point.

This helps differentiate medial tibial stress syndrome from a:

Stress fracture.

Pain With Muscle Testing

Symptoms may be reproduced with resisted:

Plantarflexion

and

Inversion

because these movements recruit muscles attached near the symptomatic tibial region.

Inspection

There is usually little visible abnormality.

Occasionally there may be mild:

Soft-tissue swelling

or tenderness without marked erythema.

Gait and Foot Examination

Examine:

Foot posture

Arch height

Pronation

Ankle motion

and overall:

Running or walking mechanics.

Stress Fracture Concern

A tibial stress fracture should be suspected when tenderness is:

Highly localized

rather than diffuse.

Other concerning features include:

Pain at rest

Night pain

Pain with walking

and progressively worsening symptoms despite:

Activity reduction.

Chronic Exertional Compartment Syndrome

Chronic exertional compartment syndrome may present with exercise-induced pain but typically has a different pattern.

Symptoms often involve the:

Anterolateral leg

and may include:

Tightness

Neurologic symptoms

or temporary:

Weakness.

Fascial Herniation

Patients with exertional compartment syndrome may occasionally have visible or palpable:

Fascial hernias.

Imaging

Plain Radiographs

Plain radiographs are often:

Normal

in medial tibial stress syndrome.

Their main role is to exclude:

Stress fracture

or another bony abnormality.

Serial Radiographs

Early stress fractures may also be radiographically occult.

Therefore, normal initial radiographs do not completely exclude a:

Bone stress injury.

Bone Scintigraphy

Historically, bone scanning may show:

Diffuse longitudinal uptake

along the posteromedial tibia in medial tibial stress syndrome.

Stress Fracture Bone Scan

A stress fracture more commonly produces:

Focal

or

Transverse increased uptake

rather than a long diffuse pattern.

MRI

MRI is highly useful for distinguishing:

Medial tibial stress syndrome

from

Stress fracture.

It can identify:

Periosteal edema

Bone marrow edema

and, in more advanced stress injury,

A fracture line.

Compartment Pressure Testing

When:

Chronic exertional compartment syndrome

is strongly suspected, compartment pressure measurements before and after:

Exercise

may be considered.

This is most relevant when symptoms are:

Anterolateral

and consistently appear at a reproducible level of exertion.

Pathological Findings

The disorder has historically been associated with inflammation or stress reaction involving the:

Periosteum

and attachment sites of the:

Soleus

and nearby posterior tibial musculature.

Modern evidence also supports an underlying:

Tibial bone stress response.

Differential Diagnosis

The two most important conditions to distinguish are:

Tibial stress fracture

and

Chronic exertional compartment syndrome.

Tibial Stress Fracture

Stress fractures typically cause:

More focal tenderness

and may progress to pain with:

Walking

or

Rest.

MRI is helpful when the diagnosis is uncertain.

Chronic Exertional Compartment Syndrome

This condition typically causes:

Tightness or pain during exercise

that resolves after stopping.

Possible associated symptoms include:

Paresthesia