Olecranon Fracture

An olecranon fracture is an intra articular fracture of the proximal ulna involving the trochlear notch and insertion of the triceps mechanism.

The olecranon performs three major functions:

Forms the proximal trochlear articulation
Provides a posterior buttress preventing anterior translation of the ulna
Serves as the insertion of the triceps tendon

Treatment therefore depends on both articular congruity and integrity of the extensor mechanism.

Mechanisms include:

Direct impact onto the posterior elbow, commonly producing comminution
Indirect injury from sudden triceps contraction, commonly producing a transverse fracture
High energy fracture dislocation

Mayo classification

The Mayo classification is based on displacement, comminution and ulnohumeral stability.

Type I: Nondisplaced

Displacement below approximately 2 to 3 mm and a stable elbow.

Nondisplaced, noncomminuted.

Nondisplaced, comminuted.

Type II: Displaced but stable

The fracture is displaced, but the ulnohumeral articulation remains stable.

IIA

Displaced, noncomminuted.

IIB

Displaced and comminuted.

Type III: Displaced and unstable

The fracture is associated with ulnohumeral instability or fracture dislocation.

IIIA

Unstable, noncomminuted.

IIIB

Unstable and comminuted.

Mayo IIA is the classical simple displaced transverse fracture suitable for compression or tension band principles, whereas IIB and III injuries generally require plate fixation.

Associated injuries

Look for:

Radial head fracture
Coronoid fracture
Monteggia type injury
Elbow dislocation
Collateral ligament injury

A transolecranon fracture dislocation is different from a Monteggia injury. The proximal radioulnar relationship remains intact, but the forearm translates through the comminuted trochlear notch.

Patients present with posterior elbow pain, swelling and haemarthrosis.

A palpable gap may be present.

Assess active elbow extension.

Loss of active extension suggests disruption of the extensor mechanism, although pain can make examination unreliable.

Inspect carefully for an open wound because the olecranon has minimal posterior soft tissue coverage.

Document:

Ulnar nerve function
Median nerve function
Radial nerve function
Radial and ulnar pulses

Nonoperative treatment

Appropriate for:

Mayo type I fractures
Intact extensor mechanism
Stable elbow

Selected frail, low demand older patients with displaced but stable fractures may also be treated nonoperatively when the morbidity of fixation outweighs the benefit. Functional outcomes can remain acceptable despite a fibrous nonunion.

Use brief posterior splint immobilisation followed by early range of motion.

Avoid prolonged immobilisation because the elbow develops stiffness rapidly.

Operative indications

Operate for:

Displaced fracture in an active patient
Loss of active extension
Articular incongruity
Unstable fracture
Open fracture
Fracture dislocation
Failure of nonoperative treatment

Simple transverse fracture

Mayo IIA fractures can be treated with:

Tension band fixation
Intramedullary screw with tension band augmentation
Plate fixation

Tension band constructs rely on an intact anterior cortex and a simple fracture that can be compressed.

Do not use tension band wiring for severe comminution, distal extension or unstable fracture dislocation.

Classic K wire tension bands are effective but frequently produce symptomatic posterior metalwork. Plate fixation has lower rates of hardware related reoperation in several comparative series.

Comminuted fracture

Mayo IIB and most type III fractures require precontoured proximal ulna plate fixation.

Reconstruct:

Trochlear notch
Olecranon length
Proximal ulna alignment
Coronoid where involved

Avoid narrowing or distortion of the trochlear notch.

Small depressed articular fragments may require elevation and support.

Fragment excision

Excision of the proximal fragment with triceps advancement has a limited role.

Consider only when:

Elderly low demand patient
Severe osteoporotic comminution cannot be reconstructed
Less than approximately 50% of the olecranon articular surface would be removed
Elbow remains stable

Avoid this strategy in young or active patients and in fracture dislocations because removal reduces posterior elbow stability.

Postoperative care

Stable fixation should permit early elbow motion.

Protect active resisted extension initially while the fracture heals.

Major complications include:

Symptomatic hardware
Elbow stiffness
Loss of extension
Ulnar nerve symptoms
Post traumatic arthritis
Infection
Nonunion
Fixation failure

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

Compartment Syndrome

Also known as: Acute compartment syndrome

Compartment syndrome occurs when pressure within a closed osteofascial compartment rises sufficiently to impair local tissue perfusion. Progressive venous obstruction increases interstitial oedema, reduces the arteriovenous pressure gradient and ultimately compromises capillary blood flow, producing muscle and nerve ischaemia.

The clinically important distinction is between acute compartment syndrome, which is a limb threatening surgical emergency, and chronic exertional compartment syndrome, which is exercise induced and usually treated electively.

Acute compartment syndrome most commonly affects the leg and forearm but can occur in the thigh, foot, hand, buttock and upper arm.

Major causes include:

Tibial shaft fracture
High energy tibial plateau fracture
Forearm fractures
Crush injury
Reperfusion after arterial occlusion
Tight casts or circumferential dressings
Intramuscular haemorrhage, particularly with anticoagulation or coagulopathy
Vascular injury
Burns
Prolonged limb compression in an unconscious patient
Extravasation of pressurised IV fluid
Vigorous exercise in susceptible patients

A fracture does not need to be present. Conversely, an open fracture does not protect against compartment syndrome.

Anatomical compartments of the leg

There are four major compartments:

Anterior

Contains:

Tibialis anterior
Extensor hallucis longus
Extensor digitorum longus
Deep peroneal nerve
Anterior tibial vessels

Lateral

Contains:

Peroneus longus
Peroneus brevis
Superficial peroneal nerve

Superficial posterior

Contains:

Gastrocnemius
Soleus
Plantaris

Deep posterior

Contains:

Tibialis posterior
Flexor hallucis longus
Flexor digitorum longus
Tibial nerve
Posterior tibial vessels

The deep posterior compartment is particularly easy to inadequately decompress.

Forearm compartments

The forearm contains:

Volar compartment
Dorsal compartment
Mobile wad containing brachioradialis and radial wrist extensors

The carpal tunnel may require simultaneous decompression when median nerve pressure is clinically significant.

Acute versus chronic exertional syndrome

Acute compartment syndrome

Rapid rise in pressure with threatened muscle and nerve viability. Requires emergency fasciotomy when established.

Chronic exertional compartment syndrome

Reversible exercise induced rise in compartment pressure. Symptoms resolve with rest and there is no ongoing tissue necrosis between episodes.

Diagnosis is primarily clinical and requires repeated examination.

The earliest and most useful findings are:

Pain disproportionate to the apparent injury
Increasing analgesic requirement
Pain with passive stretch of muscles within the affected compartment
Tense or firm compartment
Progressive sensory disturbance

Pain may become less prominent late when nerves and muscle have infarcted. Therefore, sudden improvement in pain in a severely compromised limb is not necessarily reassuring.

The classical five Ps are:

Pain
Paraesthesia
Pallor
Paralysis
Pulselessness

Only pain and paraesthesia are useful early. Paralysis and pulselessness are late findings.

A normal arterial pulse does not exclude compartment syndrome.

Compartment pressure sufficient to destroy microvascular muscle perfusion can exist while major arteries remain patent.

In children, useful warning features include:

Anxiety
Agitation
Increasing analgesic requirement

Patients at particularly high risk of missed compartment syndrome include:

Unconscious trauma patients
Intubated patients
Patients receiving regional anaesthesia or heavy sedation
Children unable to describe symptoms
Patients with neurological injury

Serial examination should be documented.

Do not delay fasciotomy for imaging when clinical compartment syndrome is clear.

Compartment pressure measurement is useful when:

Examination is unreliable
Findings are equivocal
The patient is unconscious
Multiple injuries obscure the pain response

A commonly used parameter is:

Delta pressure = diastolic blood pressure minus measured compartment pressure

A delta pressure of 30 mmHg or less strongly supports clinically important compartment hypoperfusion. No single absolute pressure value should replace clinical judgement, and pressure trends can be more useful than a single measurement.

A compartment pressure around or above 30 mmHg is concerning, particularly in a hypotensive patient.

Pressure should be measured in each clinically relevant compartment and close to the level of injury.

Laboratory abnormalities such as elevated creatine kinase, myoglobinuria and metabolic acidosis indicate muscle injury but are too late and nonspecific to establish or exclude the diagnosis.

Immediate measures

While preparing for definitive treatment:

Remove circumferential casts and tight dressings completely
Release constrictive splints
Correct systemic hypotension
Maintain the limb approximately at heart level

Do not elevate the limb substantially above the heart when acute compartment syndrome is suspected because this can further reduce arterial perfusion pressure.

Do not rely on analgesia and observation when symptoms continue to progress.

Fasciotomy

Established acute compartment syndrome requires emergency complete fasciotomy.

Delay progressively increases irreversible muscle and nerve injury.

Muscle can sustain reversible ischaemia for only a limited period. After prolonged complete ischaemia, muscle necrosis, neurological deficit, contracture, rhabdomyolysis and renal injury become increasingly likely.

Leg fasciotomy

The standard technique is a two incision four compartment fasciotomy.

Lateral incision

Decompress:

Anterior compartment
Lateral compartment

Identify and protect the superficial peroneal nerve.

Medial incision

Decompress:

Superficial posterior compartment
Deep posterior compartment

The soleus must be released adequately from its tibial origin to expose and decompress the deep posterior compartment.

Incomplete release of the deep posterior compartment is a recognised technical failure.

Forearm fasciotomy

A generous volar fasciotomy should decompress the flexor compartments.

Extend decompression proximally or distally according to the injury.

Add:

Carpal tunnel release when indicated
Dorsal fasciotomy when the dorsal compartment remains tense after volar decompression

The skin must remain open if primary closure creates tension.

Muscle assessment

At surgery, evaluate muscle viability using:

Colour
Contractility
Consistency
Capacity to bleed

Clearly necrotic muscle should be excised.

Muscle of uncertain viability is better reassessed at planned second look surgery rather than aggressively sacrificed during the first operation when viability is genuinely uncertain.

Second look and wound closure

Return to theatre commonly at approximately 24 to 48 hours for:

Repeat muscle assessment
Further debridement
Wound irrigation
Planning of closure

Do not close swollen fasciotomy wounds under tension.

Options include:

Delayed primary closure
Gradual dermatotraction
Split thickness skin graft

Rhabdomyolysis

Extensive muscle necrosis can produce:

Hyperkalaemia
Hypocalcaemia early
Metabolic acidosis
Myoglobinuria
Acute kidney injury

Monitor:

Potassium
Creatinine
Calcium
Phosphate
Creatine kinase
Urine output

Use aggressive isotonic IV fluid resuscitation when rhabdomyolysis is present while avoiding uncontrolled volume overload.

Treat dangerous hyperkalaemia immediately.

Late presentation

When presentation is extremely delayed and muscle and nerve are clearly irreversibly necrotic, routine fasciotomy can expose large amounts of dead tissue and substantially increase infection and systemic complications. Management must be individualised according to tissue viability, systemic toxicity and reconstructive potential rather than automatically opening every late compartment.

Chronic exertional compartment syndrome

Typical symptoms are predictable pain, tightness, paraesthesia or weakness beginning after a reproducible duration of exercise and resolving after activity stops.

The anterior and lateral leg compartments are commonly involved.

Pressure criteria traditionally used include one or more of:

Resting pressure 15 mmHg or greater
Pressure 30 mmHg or greater at 1 minute after exercise
Pressure 20 mmHg or greater at 5 minutes after exercise

These thresholds should be interpreted alongside the clinical history rather than used in isolation.

Initial treatment includes:

Activity modification
Alteration of training load
Running gait assessment where relevant
Correction of biomechanics

Persistent function limiting disease despite conservative treatment can undergo elective compartment fasciotomy.

Unlike acute compartment syndrome, this is not an emergency.

Olecranon Fracture

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management