Tendon Rupture

Tendon rupture is partial or complete structural failure of a tendon, producing loss of normal force transmission from muscle to bone.

Rupture may be:

Acute traumatic
Degenerative
Spontaneous through diseased tendon
Open tendon laceration

Clinically, the most useful distinctions are:

Partial versus complete

A partial rupture retains some continuity and function.

A complete rupture produces full structural discontinuity.

Acute versus chronic

Acute tears have relatively mobile tendon ends and better potential for direct primary repair.

Chronic neglected tears progressively develop:

Retraction
Adhesion
Muscle atrophy
Fatty degeneration
Tendon gap

and may require reconstruction rather than direct repair.

Risk factors for spontaneous or low energy rupture include:

Increasing age
Chronic tendinopathy
Diabetes
Renal disease
Hyperparathyroidism
Systemic inflammatory disease
Fluoroquinolone exposure
Systemic or local corticosteroid exposure
Previous tendon injury

Patients often describe:

Sudden snap or pop
Acute pain
Immediate weakness
Loss of a previously normal movement
Palpable tendon defect

The examination must assess function, not merely tenderness.

Examples:

Quadriceps tendon

Loss of active knee extension and inability to perform straight leg raise.

Patellar tendon

Same extensor mechanism failure, usually with a high riding patella.

Distal biceps

Loss of flexion strength and particularly supination strength.

Triceps

Weak or absent resisted elbow extension.

Achilles

Loss of plantar flexion power with positive Thompson test.

Partial ruptures can preserve enough function to make the diagnosis less obvious.

Management depends heavily on the tendon involved.

Partial rupture

A partial tear with preserved function can often be treated with:

Relative rest
Short protective immobilisation where necessary
Progressive physiotherapy
Correction of precipitating factors

Progress loading according to pain and function.

Failure to regain strength or progression to complete rupture requires reassessment.

Complete rupture

A complete rupture causing major functional loss usually requires either:

Structured functional rehabilitation

Surgical repair

depending on the tendon.

Not all complete tendon ruptures require surgery. Acute Achilles rupture is the important example where modern functional nonoperative treatment can produce results close to operative repair in appropriately selected patients.

Extensor mechanism rupture

Complete quadriceps or patellar tendon rupture with loss of active knee extension generally requires early surgical repair.

Repair is easier during the first several weeks before:

Tendon retraction
Scar formation
Patellar migration
Quadriceps shortening

Acutely, use strong nonabsorbable or high strength sutures with:

Transosseous tunnels

Suture anchors

according to tear location.

Chronic extensor mechanism disruption may require:

V Y advancement
Tendon autograft
Allograft
Synthetic augmentation

Distal biceps rupture

A complete distal biceps rupture in an active patient generally benefits from repair because nonoperative treatment leaves substantial loss of supination strength.

Repair is ideally performed during the early period before major tendon retraction and scarring.

Older low demand patients may accept nonoperative treatment.

Open tendon injury

Open laceration requires:

Wound assessment
Irrigation and debridement when contaminated
Neurovascular examination
Primary tendon repair when tissue is suitable

A contaminated open tendon injury should not be closed around devitalised tissue merely to obtain immediate repair.

Rehabilitation principle

Tendon healing requires protection from excessive tensile load but also benefits from controlled progressive mechanical stimulation.

Prolonged rigid immobilisation causes:

Adhesion
Joint stiffness
Muscle atrophy
Reduced tendon mechanical quality

Rehabilitation should therefore progress from protected motion to controlled strengthening according to the repaired tendon and strength of the construct.

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

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.

Tendon Rupture

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management