Stress Fracture

A stress fracture results from repetitive loading that exceeds the capacity of bone to remodel and repair microdamage.

Pathophysiological classification

Fatigue fracture

Normal bone exposed to abnormal repetitive stress.

Typical patient:

Runner
Military recruit
Athlete after sudden increase in training volume

Insufficiency fracture

Abnormal weakened bone exposed to normal physiological loading.

Causes include:

Osteoporosis
Osteomalacia
Vitamin D deficiency
Chronic corticosteroid exposure
Metabolic bone disease
Previous radiation

Classification by risk

The most clinically important classification divides stress fractures into low risk and high risk based on likelihood of displacement, delayed union and nonunion.

Low risk sites

Examples include:

Posteromedial tibial cortex
Fibula
Calcaneus
Second to fourth metatarsal shafts
Many femoral shaft stress injuries

High risk sites

Examples include:

Superolateral tension side femoral neck
Anterior tibial cortex
Tarsal navicular
Proximal fifth metatarsal
Medial malleolus
Patella

High risk stress fractures require substantially more aggressive protection and sometimes prophylactic fixation.

Fredericson MRI classification

Originally developed for tibial stress injury but commonly used to describe increasing MRI severity.

Grade 1

Periosteal oedema
T1 normal

Grade 2

Periosteal and marrow oedema visible on T2 weighted imaging
T1 remains normal

Grade 3

Marrow oedema visible on both T1 and T2 sequences

Grade 4

Severe oedema with a visible cortical or intracortical fracture line

Some modified systems divide grade 4 into:

4a: severe cortical signal abnormality
4b: definite linear fracture line.

Pain initially occurs only during activity.

As injury progresses:

Pain begins earlier during activity
Persists after exercise
Eventually occurs during normal walking or at rest

Examination shows focal bony tenderness rather than diffuse muscle pain.

High risk femoral neck stress injury may present simply with vague groin pain and pain during hip rotation.

A sudden increase in training volume, running distance, surface hardness or load should be specifically sought.

Assess risk factors for impaired bone health:

Low energy availability
Menstrual disturbance
Low BMI
Vitamin D deficiency
Eating disorder
Smoking
Previous stress fractures
Osteoporosis

Plain radiographs are first line but may remain normal for several weeks.

Do not exclude a stress fracture solely because initial radiographs are normal.

MRI: investigation of choice when clinical suspicion remains high; identifies bone stress injury before a clear fracture line appears.

CT is useful for selected cortical stress fractures and evaluating fracture line morphology or healing.

In recurrent, multifocal or insufficiency fractures, consider:

Serum calcium
Phosphate
Alkaline phosphatase
25 hydroxyvitamin D
Thyroid function where appropriate
Bone density assessment
Endocrine or nutritional investigation according to clinical context

Low risk injury

Stop the provoking activity.

Allow pain free activities that do not load the injured bone excessively.

Protected weight bearing is used when ordinary walking remains painful.

Many low risk injuries require approximately 6 to 8 weeks before gradual return to impact activity, although healing time varies substantially by site and MRI grade.

Return to running only after:

Focal tenderness has resolved
Normal walking is painless
Strength is restored
Progressive loading does not reproduce symptoms

Increase activity gradually rather than immediately returning to the previous training load.

High risk injury

Stop impact loading immediately and obtain orthopaedic assessment.

Use protected or non weight bearing when fracture propagation is a concern.

Surgical fixation may be required for:

Displaced stress fracture
High risk tension side femoral neck fracture
Progressive fracture line despite rest
Established nonunion
Selected high risk anterior tibial, navicular or fifth metatarsal injuries

A displaced femoral neck stress fracture is an emergency because further displacement increases the risk of osteonecrosis and nonunion.

Correct the underlying cause

Treat vitamin D deficiency, osteoporosis or endocrine disease where present.

Address low energy availability and nutritional insufficiency.

Simply resting the fracture without correcting the biological cause leads to recurrence.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Avascular Necrosis of the Femoral Head

Also known as: AVN, Osteonecrosis

Avascular necrosis, more accurately termed osteonecrosis of the femoral head, results from disruption of blood supply to subchondral bone.

Necrotic bone initially retains shape but cannot remodel normally under repetitive load. Subchondral fracture then develops, followed by femoral head collapse and secondary osteoarthritis.

Major causes include:

Corticosteroid exposure
Excessive alcohol use
Femoral neck fracture
Traumatic hip dislocation
Sickle cell disease
Systemic lupus erythematosus
Organ transplantation
Coagulopathy and thrombophilia
Gaucher disease
Dysbarism
HIV associated factors
Idiopathic disease

Nontraumatic disease is frequently bilateral. Both hips should therefore be assessed when one side is diagnosed.

Ficat and Arlet classification

Stage 0

No symptoms and normal imaging, usually historical concept only.

Stage I

Symptoms may be present
Plain radiographs normal
MRI or bone scan abnormal

Stage II

Sclerosis
Cysts
Focal osteopenia
No subchondral collapse

Stage III

Crescent sign
Subchondral fracture
Beginning collapse or flattening
Joint space remains relatively preserved

Stage IV

Advanced femoral head collapse
Joint space narrowing
Acetabular degenerative change
Secondary osteoarthritis

Revised ARCO classification

The current practical staging system is:

ARCO I

Radiographs normal
MRI demonstrates osteonecrosis

ARCO II

Radiographs show sclerosis, focal osteoporosis or cysts
No subchondral fracture or femoral head flattening

ARCO III

Subchondral fracture or collapse is present.

IIIA

Femoral head depression 2 mm or less

IIIB

Femoral head depression greater than 2 mm

ARCO IV

Secondary osteoarthritis with joint space narrowing and acetabular degeneration.

Lesion size

Stage alone does not determine prognosis.

The risk of collapse rises greatly when the necrotic segment:

Is large
Extends laterally into the weight bearing dome

Lesions involving more than approximately 30% of the femoral head and the lateral weight bearing surface have a particularly poor natural history.

Early disease may be asymptomatic.

Typical symptoms are:

Groin pain
Buttock pain
Anterior thigh pain
Pain with weight bearing
Reduced hip internal rotation
Limp

Pain can precede radiographic abnormalities.

Advanced collapse produces:

Rest pain
Night pain
Significant loss of hip movement
Shortening
Secondary osteoarthritis

Ask specifically about:

Current and previous corticosteroid dose
Alcohol exposure
Previous hip trauma
Sickle cell disease
Autoimmune disease
Organ transplantation

Treatment is determined primarily by:

Collapse versus precollapse
Lesion size
Lesion location
Age
Symptoms
Underlying cause

Risk factor modification

Where possible:

Minimise unnecessary corticosteroid exposure
Stop excessive alcohol consumption
Optimise sickle cell management
Treat metabolic and coagulation disorders where identified

Risk modification is important but does not reverse established structural necrosis.

Small asymptomatic lesion

A small medial non weight bearing lesion can be observed with:

Activity modification
Serial imaging
Clinical follow up

Not every MRI lesion requires surgery.

ARCO I and II

These are precollapse stages and therefore the main window for femoral head preservation.

Core decompression is the most established joint preserving operation.

The procedure:

Drills one large or multiple small channels into the necrotic segment
Reduces intraosseous pressure
Promotes revascularisation and bone repair

Best results occur with:

Early disease
Small lesions
No subchondral collapse

Core decompression alone is less reliable with large lateral lesions.

Biological augmentation

Core decompression may be combined with:

Bone marrow aspirate concentrate
Cancellous bone graft
Synthetic bone substitute

Current evidence suggests possible reduction in collapse with bone marrow augmentation compared with decompression alone, but the evidence remains limited and heterogeneous.

Bone grafting

Options include:

Nonvascularised bone graft

Provides structural and biological support.

Vascularised fibular graft

Provides:

Structural support
Vascularised bone
Potential revascularisation

It is technically demanding and most suitable for younger patients in specialist centres.

Osteotomy

Selected young patients with a medium sized necrotic lesion can undergo proximal femoral osteotomy to rotate intact cartilage into the major weight bearing zone.

This is technically demanding and can complicate later total hip arthroplasty.

It has a specialised rather than routine role.

ARCO III

Once subchondral fracture has developed, success of conventional decompression falls sharply.

Very early IIIA disease in a young patient may still be considered for advanced joint preserving reconstruction in specialist practice, but prognosis is significantly poorer than in stage I or II disease.

ARCO IIIB and IV

Established collapse and secondary arthritis are usually treated with total hip arthroplasty.

Do not persist with repeated decompression after major structural collapse.

Sickle cell disease

Sickle cell associated osteonecrosis often affects younger patients and can be bilateral.

Perioperative management requires:

Hydration
Oxygenation
Avoidance of hypothermia
Careful haematological planning
Appropriate transfusion strategy according to haemoglobin and sickling risk

Follow up

Monitor for:

Progressive collapse
Secondary osteoarthritis
Contralateral disease

Persistent increase in pain in a precollapse lesion should trigger repeat imaging rather than waiting for major radiographic deformity.

Stress Fracture

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management