Fracture Principles



Classification: (AO)

Diaphyseal Fractures:

Type A
Simple fractures with cortical disruption for at least 90% of the bone circumference
Type B
Multi-fragmentary, wedge fracture, always some contact however between the two main fragments
Type C
Multi-fragmentary, complex fractures with no contact between the two main fragments
With A, B or C further divided on the basis of the fracture configuration ie
A1 spiral ® C1 complex spiral
A2 oblique ® C2 complex segmental with 50% contact each end
A3 transverse ® C3 complex irregular (number or irregular intermediate fragments)

Articular Fractures:

Type A
Extra-articular, may be intra-capsular but do not involve the joint surface
Type B
Part of the articular surface involved, the remainder being still connected to the diaphysis
Type C
Complete articular fracture with the articular surface disrupted and completely separated from the diaphysis

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Fracture Healing

Unique in that there is reconstruction of the original tissue rather than healing with scar formation as in other tissues.
McKibbin B JBJS (1978) (from Cardiff Royal Infermary)

Stages of Fracture Healing:

Inflammatory Stage:

Fracture ® soft tissue injury and ruptured vessels
Formation of Fracture haematoma
Osteocytes deprived of nutrition at the fracture ends die and play a passive role in the repair process
Presence of necrotic material ® inflammatory response
Increased cell division evident within the first 8 hours reaching a maximum in some 24 hours
Activity first seen in the periosteum and extends along the entire bone to be localised at the fracture site in a few days
Acute Inflammation subsides ® repair phase

Repair Stage:

Organisation of haematoma occurs ® primary callus formation
Micro environment is acidic (moves towards neutrality during repair and becomes alkaline)
Electro negativity is also found in the region of a fresh fracture
Pluripotential mesenchymal cells ® fracture site (cells from cambian layer periosteum, endosteal cells, ? endothelial cells ? monocytes)
Capillary buds grow into the fracture site
Callus is formed made up of fibrous tissue, cartilage and immature fibre bone
Cartilage forms particularly in the periphery of the callus in regions of low O2 tension
Increased movement ® increased cartilage formation
Cartilage is resorbed as enchondral bone formation occurs
Osteoclastic resorption of dead bone occurs
Gradual increase in concentration of collagen and hydroxyappatite ® mineralisation of the matrix as woven bone
Remodelling phase begins

Remodelling Stage:

Once the fracture has been bridged ® functional modification which continues for a prolonged period (years)
Resorption of poorly placed trabeculae and new bone struts are deposited corresponding to lines of force
Cancellous bone ®resorption and replacement takes place on the surface of trabeculae (creeping substitution
Cortical bone ® osteoclasts ream out a tunnel followed by vessels bringing osteoblasts ® lay down lamellar bone to form the new osteon (cutter head)
Process thought to be mediated through electrical variation in zones of tension and compression
Electopositivity (associated with osteoclastic activity) occurring on a convex surface and negativity (associated with osteoblastic activity) on a concave surface

Source of osteogenic tissue:

  1. Osteoprogeniter cells. Cells with a predetermined commitment to bone formation and occur in close association to bone surfaces or the marrow.
    OR
  2. Metaplasia of previously uncommitted fibroblasts which develop the power of osteogenesis given appropriate environmental stimulus. Cells arise from surrounding soft tissue. Osteogenic induction.
This theory is supported by the formation of bone by non specialised cells in extra skeletal sites

Control of Fracture Healing: Bridging by external, medullary or 1o callus

1. External callus:

Dependent on the existence of another fracture fragment (ie no response from an amputation stump)
Continuity of periosteum ® bridging callus ® induction, if no contact is made within a certain time ® primary callus response
Mechanical and humeral influences as attempts to bridge the fracture are not continued indefinitely

2. Medullary callus

Cartilage formation is less prominent in medullary callus
Controlled by similar process and in displaced fractures may unite with the external callus
Develops independently of rigid fixation

3. 1o Bone healing:

May only be possible where there is rigid fixation, evacuation of fracture haematoma and intimate contact of one bone end with the other
Equates with the process of normal bone turnover
Direct bone union occurs when rigid fixation prevents formation of fracture callus. Osteoclasts resorb the dead bone of the fracture ends and osteoblasts form new bone directly across the fracture. The fracture depends on the plate or means of fixation for stability for some time.
Indirect bone union occurs in the absence of rigid fixation through callus formation.

Factors affecting fracture healing:

  • Soft tissue injury and local blood supply
  • Radiation, chemical or thermal burns
  • Infection, anaemia or hypoxia
  • Excessive compression ( more than 30lbs) inhibits enchondral ossification but cyclic compression is beneficial
  • Intermittent shear stresses promotes cartilage formation
  • High shear stresses promotes fibrous tissue formation
  • Corticosteroids inhibit osteoblast differentiation ® slow healing
  • Growth hormone increases fracture healing (only if deficient)
  • Denervation retards fracture healing
  • Exercise increases fracture healing
  • Head injury promotes fracture healing by a humoral mechanism
  • Vitamin C is required for normal collagen matrix formation

Union:


Incomplete repair, the bone moves as one but clinically is still a little tender and attempted angulation is painful. The fracture is clearly visible on X-Ray with fluffy callus. Not safe to be unprotected.

Consolidation:

Complete repair, calcified callus is ossified and attempted angulation is painless. Repair is complete and further protection is unnecessary.

Delayed union:

A fracture that has not united in what is considered a reasonable amount of time for a fracture of that type in that location.

Non-union:

A fracture that will not unite without surgical intervention. A Non union is usually non tender.
Incidence of non union said to be 5% in all long bone fractures

Malunion:

Consolidation of a fracture in a deformed position.

Cell induction:

Influence a certain cell, tissue or substance may have on another cell such that the second cell or descendants of that cell exhibit physiological processes that the original cell did not.

Perkins timetable

For normal fracture healing: (Pioneered delayed splintage)
A spiral fracture in the upper limb unites in 3/52
double it for consolidation
double it again for the lower limb
double it again for a transverse fracture

Blood supply of bone;

  1. Nutrient artery ® medullary arteries supplies the marrow and inner 2/3 of diaphysial cortex.
    In areas away from muscle or facial attachments ® supply full thickness of cortex
  2. Multiple metaphyseal arteries which anastomose with terminal branches of the medullary arteries at the junction of metaphysis and diaphysis
  3. Multiple periosteal arterioles supply the outer 1/3 of the cortex
    Periosteal vessels alone are sufficient to support normal fracture repair
  4. All veins drain to the periosteal surface
Increased blood flow secondary to a fracture peaks at 2/52 at six times the normal base line ® 3.5 times the normal baseline at 3/52 which persists until 8-10/52 and returns to normal at about 12/52.
Extra osseous blood supply to external callus develops rapidly after a fracture and perhaps replaces the damaged medullary supply,

Indications for ORIF of fractures:

Absolute:

  1. Unable to obtain an adequate reduction
  2. Displaced intra-articular fractures
  3. Certain types of displaced epiphyseal fractures
  4. Major avulsion fractures where there is loss of function of a joint or muscle group
  5. Non-unions
  6. Re- implantations of limbs or extremities

Relative:

  1. Delayed unions
  2. Multiple fractures to assist in care and general management
  3. Unable to maintain a reduction
  4. Pathological fractures
  5. To assist in nursing care
  6. To reduce morbidity due to prolonged immobilisation
  7. For fractures in which closed methods are known to be ineffective

Questionable:

  1. Fractures accompanying nerve of vessel injury
  2. Open fractures
  3. Cosmetic considerations
  4. Economic considerations

Traction:

Fixed traction
Pull is exerted against a fixed point
Balanced traction
Pull against the weight of the body
Combined traction
Traction fixed to the splint and the splint is suspended against the weight of the body
Skin traction
(Buck's) can pull no more than 4 or 5 kg

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Compound Fractures

Classification

Gustilo and Anderson " Prevention of infection in the treatment of 1025.Open fractures of long bones" JBJS 58A: 453-458, 1976

Type 1

An open fracture with a wound less than 1cm long and clean

Type 2


An open fracture with a wound more than 1 cm long without extensive soft tissue damage,flaps or avulsions

Type 3


An open fracture with extensive soft tissue damage
An open segmental fracture
A traumatic amputation
Gustilo, Mendoza and Williams " Problems in the management of type 3 open fractures: a new classification of type 3 open fractures"
J Trauma 24:742-746, 1984

Type 4

  1. Adequate soft tissue coverage of a fractured bone despite extensive soft tissue laceration or flaps, or, high energy trauma irrespective of the size of the wound
  2. Extensive soft tissue loss with periosteal stripping and bone exposure-usually assoc with massive contamination
  3. Open fracture assoc with arterial injury requiring repair

Management

Emergency room

during initial resuscitation and evaluation, splint fractures, cover open wounds with betadine soaked dressings, take wound swabs
Antibiotics:
type 1+2 wounds cephalothin
type 3 add gentamicin
farm/ tetanus prone add 5 million units penicillin 4/24
administer IV antibiotics for 3 days unless clinically or on culture there is evidence of infection.
Tetanus prophylaxis

Debridement

remove gross debris
pulsed lavage- 5+ L of saline, antibiotics can be added to the solution
surgical debridement - skin, subcut fat, fascia, muscle ( colour, contractility).
fasciotomy if required
remove all devitalised bone
reinspect in ~ 3/7, if after 3-5 days the wound is clean ®DPC

Fracture stabilisation

casts/ braces
external fixation
internal fixation
combination

Wound closure

Type 1 wounds
can be closed immediately as infection rate is same as for closed injuries
Type 2 + 3 wounds
never primarily close
Aim to achieve closure within 7-10 days

Bone grafting

delay for 6-12 wks until soft tissues have healed

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Decision to Amputate

Grade 3C tibial fracture management has a high rate of complications and unsatisfatory functional outcomes

Mangled Extremity Severity Score

ref: Johansen etal "objective criteria accurately predict amputation following lower extremity trauma" J Trauma 30: 568-573, 1990

ASkeletal /soft tissue injuryPoints
Low energy ( stab, simple fracture , "civilian gun-shot wound")1
Medium energy ( open or multiple fractures, dislocation)2
High energy (close range shotgun, "military gunshot, crush)3
Very high energy ( above plus gross contamination)4
BLimb Ischaemia
Pulse reduced or absent but perfusion normal1
Pulseless, paraesthesias, diminished capillary refill2
Cool, paralysed, insensate3
-Score doubled for ischaemia more than 6 hrs
CShock
Systolic BP always more than 900
Hypotensive transiently1
Persistent hypotension2
DAge
less than 300
30-501
more than 502

In this study a score of 7 or more predicted amputation in 100% of 26 pts

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Bone Complications

AVN

Site dependent- scaphoid, talus

Delayed Union

Causes:
  1. Inadequate blood supply
  2. Infection (and in any open fracture)
  3. Insufficient splintage
  4. ? Internal fixation (® loss of fracture haematoma)
  5. Distraction of fragments (traction, intact fellow bone)

Non-union

Causes

  1. Excessive Motion
  2. Gap
  3. Blood supply
All other factors listed below will result in non-union through one or more of these mechanisms

Predisposing Factors

  1. Site (eg distal 1/3 tibia, scaphoid, femoral neck)
  2. Systemic factors: 1o hyperparathyroidism
    Nutrition
    Drugs eg;Steroids
    Anticoagulants
    Radiation
    Burns
    Age
  3. Too large a gap (distraction or bone loss)
  4. Interposition of soft tissue (periosteum, muscle etc)
  5. Soft tissue loss (loss of blood supply)
  6. Intact fellow bone (® gap at fracture site)
  7. Infection (20-25% non unions are infected)
  8. Poor blood supply
  9. Pathological lesion
  10. Movement (poor splintage, fixation or compliance)

Radiological Features

Failure to show progressive change
Sclerosis of bone ends
Bone atrophy above and below the fracture
Hypertrophic ® abundant callus with fracture still evident
Atrophic ® no callus and fracture evident
Bone scan in non union not hot

Classification

  1. Non unions with vital bone ends (vascular on bone scan)
    Hypertrophic ® elephants or horses foot
    Oligotrophic ® no response or callus but vascular
    Rigid fixation alone will probably suffice ® union.
  2. Avascular non union lacks callus (Atrophic)
    Dystrophic ® partial union of butterfly
    Neuetic ® avascular segment
    Gap ® segment missing
    Atrophic (end stage)
    Bone grafting is required to stimulate osteogenesis.
  3. Pseudarthrosis ® synovial lining and joint fluid between fracture ends.
    Cold cleft between hot end on bone scan
    Will not heal without intervention.

Treatment

Tibia ® excision of segment of fibula if intact or healed
bone grafting by a variety of techniques
(success in 70-98% of the time)

Scaphoid ® inlay graft / peg graft & screw fixation
External stimulation will not work if defect greater than 1/2 the diameter of the bone

Malunion

Primary
Fracture never reduced
Secondary
Reduction not held
Malunion in a child will remodel provided the fracture is near a bone end and not mal-rotated.
Operation is indicated if the deformity is unsightly, limits function or to prevent development of secondary OA.

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Joint Complications

Instability

Ligamentous laxity, muscle weakness, bone loss

Stiffness

due to:
  1. Inactivity ®adhesions
  2. Infection
  3. Malunion- eg of radius and ulna® decreased rotation
  4. Myositis Ossificans:
    Commonest site the elbow
    ? related to muscle damage ® reduced ROM
    Do not surgically intervene until bone mature
    Activity of lesion indicated by serum Alkaline Phosphatase and activity on bone scan
  5. Reflex Sympathetic Dystrophy (Sudecks' Atrophy):
    Synonyms:Post traumatic osteodystrophy
    Sudecks atrophy
    Post traumatic algodystrophy
    Abnormal reaction to injury characterised by pain, swelling, stiffness, vasomotor changes and osteoporosis of bone of the affected part.
    Incidence
    5% of all nerve injuries
    F more than M
    Whites more than Blacks
    60% of cases involve either the median nerve or tibial component of the sciatic nerve.
    ? Aetiology
    Persistent painful lesion,
    Patient diathesis
    Abnormal sympathetic reflex
    Classification (Lankford)
    Minor causalgia
    Involves purely sensory nerve to distal portion of extremity
    Minor traumatic dystrophy
    Most common type, follows trauma
    Shoulder Hand Syndrome
    Proximal trauma or painful visceral lesion eg shoulder, neck injury, cervical disk, heart attack, stomach ulcer or Pancoast tumour.
    Major traumatic dystrophy
    Trauma that produces swelling, redness, stiffness and dysfunction. Crush injuries and Colles fractures head the list.
    Major causalgia
    Partial injury to major mixed nerve in proximal part of the extremity
    Clinical Features:
    Dramatic description of symptoms
    Aggravated by active or passive motion ® stiffness of joints
    Pain intensified by sudden noises or change in temperature
    Pain lessened if patient distracted
    Fingers become puffy, patch discolouration, unduly moist, hyperaesthetic and stiff
    Swelling most usual, cool, moist, colour red, pale or cyanosed
    Vasomotor instability associated with prolonged capillary return
    Atrophy of subcutaneous tissue with shiny skin and tapering fingers due to atrophy of the tip of the fat pad
    X-Rays
    Patchy rarefaction
    Bone Scans ® may have blood pool increase and increased activity away from the site of the initial injury (whole of limb)
    Treatment:
    Counselling
    Pain control, LA blocks, TENS
    Sympathetic blockade ® 80% success
    1. Stellate ganglion blocks interrupt sympathetic outflow without interfering with somatic nerve function
    2. Guanethidine vascular block, acts as a false transmitter replacing adrenalin from nerve endings ® reduces pain and enables mobilisation
      Prolonged physio ® gradual recovery
  6. Secondary Osteoarthritis
    May follow articular fractures, fractures resulting in AVN of subarticular bone or result from abnormal stress transfer following a fracture around a joint.
  7. Unreduced dislocations

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Venous Thrombosis & PE

Hyper coagulability secondary to activation of Factor X by thromboplastins from damaged tissue in association with stasis.
Secondary to use of a tourniquet or bandage and increased stickiness of platelets due to exposure of damaged tissue etc.
Prophylaxis indicated for prolonged rest in bed or in high risk patients
ie
Previous history of DVT
Obese patients
Patients with malignant disease
Patients on the oral contraceptive
Following pelvic or hip fractures or operations

Contraindicated if tendency to bleed or active peptic ulceration

 

Treatment
Commence once risk of bleeding reduced (~ 72 hours) with subcutaneous heparin (LMW) 2500 units daily and commence Warfarin once risk of secondary bleed reduced (~ 1 week to 10 days) and aim for INR around 2

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Fat Embolism

The pathogenesis of the fat embolism syndrome is the subject of conjecture and controversy

Theories

  1. Bone marrow or fragments have been demonstrated in lung sections, indicating that mechanical fat embolization does indeed occur. (Mechanical Theory)
  2. More recent evidence shows that the fat embolism syndrome can occur by way of other mechanisms without skeletal trauma.
    The blood lipid changes during stress in combination with the changes that occur in the blood coagulation system may result in coalescence of chylomicrons into larger fat droplets.
    This explains how the fat gets past the lungs from the venous system and results in systemic emboli. (Metabolic Theory)

Clinical features

Shortness of breath, restlessness and confusion
Increased temp to 39o or 40o and tachycardia. BP usually within normal limits
Associated with anaemia, thombocytopenia and high ESR
Petechial rash front and back of chest, root of the neck and conjunctiva become evident on the second or third day after injury

Hypoxia is the hallmark of the fat embolism syndrome ® coma potentiated by cerebral emboli ® cerebral oedema.Fat globules obstruct pulmonary capillaries and are hydrolysed to FFA's which accumulate in the lung parynchyma.These cause direct toxic effects on alveolar lining cells and provoke an inflammatory response® decreased lung compliance, shunting
Chest X-Ray ® progressively snowstorm like pulmonary infiltrations.
ECG changes- reflecting cardiac strain- prominent S waves, arrhythmias, RBBB, T- inversion
Fat may be found in venous blood or urine

Treatment

General management principles;

Prevent shock, maintain airway, blood volume, fluid and electrolyte balance, immobilise injured parts
Administer oxygen, ventilatory assistance may be required in order to maintain an adequate arterial oxygen tension.

Use of massive intravenous steroid therapy has been advocated (Stoltenberg & Gustillo) suggesting that improves gas exchange and decreased the inflammatory response in the lungs. Dose used 600 -1,200 mg Methylprednisolone sodium succinate every 24 hours in divided doses.

Heparin has also been used as it increases the serum activity of lipase and hastens the intravascular hydrolysis of ventral fat. It also has anti platelet action helping to prevent platelet aggregation. Dose used is 2,500 units IV every 6-8 hours.
Low molecular weight Dextran inproves microvascular flow- also expands plasma volume, reduces platelet adhesiveness

Prognosis

Mortality reported up to 50% in those with marked resp failure + coma
NB-Prophylaxis - adequate immobilisation of fractures prior to transportation and early fixation of long bone fractures.

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Skin

Fracture blisters
Caused by elevation of superficial layers of skin by oedema.
Sometimes prevented by firm bandaging and should be treated by application of a dry dressing.
Pressure sores and bed sores

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Muscle and Tendon

Adhesions require early mobilisation
Atrophy will recover following return to normal use
Avulsion fractures may need reconstruction
Attrition ruptures following fracture (EPL after distal radius fracture , Biceps after neck of humerus)

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Nerve

Usually neuropraxia, may be secondary to compression from splints
Axonotmesis may be secondary to traction on limb
Neurotmesis rare after fractures

In closed fractures recovery is usual and should be awaited
Humeral fractures, particularly the Halstein Lewis fracture (junction middle and distal 1/3 with a lateral spike) has a high association with radial nerve injury. If develops a nerve palsy after manipulation it should be explored and with other types of humeral shaft fractures ® expectant treatment

Incidence of palsy after a humeral shaft fracture is 10.5% (5% proximal 1/3, 14.6% middle 1/3 and 19.4% distal 1/3) after ORIF 2.5% and after manipulation 2%
Full spontaneous recovery expected in 80% in 4 - 10 months

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Arteries

May be cut, compressed or contused

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Crush Syndrome

Release of myo-haematin into the circulation ® renal problems & low output renal failure.
Severe crush of greater than 2 hours duration or complete tourniquet occlusion of greater than 6 hours should ® amputation (before release of the tourniquet.)

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Compartment Syndrome

A condition in which increased tissue pressure within a limited space compromises the circulation and the function of the contents of that space.
Volkmans Ischaemia of Muscle ® fibrosis and eventually contracture

Classification

Mild
2 - 3 digits only involved
Moderate
Increased flexor involvement
Severe
Contracture of both flexors and extensors
Most common after supra condylar fracture of the humerus in children, proximal 1/3 tibial fractures, fractures of the femur in infants treated in gallows traction and lying or squatting in an unusual position while intoxicated.

Nerves will function for about 2-4 hours and following loss of function peripheral nerves have the potential to recover.

Muscle can last 6-8 hours but has no potential for regeneration once ischaemic ® fibrous scar.

Ischaemic muscles fibrose and contract, ischaemic nerves may recover ® deformity but inconsistent numbness. Extension of the fingers may only be possible with flexion of the wrist.

Established contracture in the upper limb can be treated with distal advancement of the flexor origin, may decrease deformity but not necessarily improve function.

Effect of limb elevation ® lowers local arterial pressure and decreases tissue PO2. Once blood flow is reduced elevation of the limb or compression (bandage, POP) ® further reduction in blood flow

Syndrome may develop 2o to

  1. Arterial injury & ischaemia
  2. Direct tissue trauma

Clinical Presentation

The first and most important symptom of an impending acute compartment syndrome is pain that is greater than expected from the primary problem, such as a fracture or contusion.

Patient has a swollen, palpably tense compartment

Pain on stretching the involved muscles (may also be present due to the injury)

Paresis or weakness may be secondary to nerve involvement, primary ischaemia, or guarding secondary to pain

Paraesthesia is nearly always present as each compartment or the arm or leg has at least one nerve passing through it

Unless major arterial injury or disease is present peripheral pulses are palpable and capillary refill is routinely present, skin pink and viable due to shunting of blood from the compartments through the superficial circulation

Diagnosis and differentiation from nerve or vascular injury based on the presence of increased intra compartmental pressure.

Treatment

® fasciotomy if pressures greater than 30-40 mmHg (Normal resting pressure ~5 mmHg, increases to ~ 50mmHg with exercise and will return to near normal levels after ~ 5 mins in most cases)

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Growth Arrest

Osseous bridging of the physis may occur after any injury to the physis, the most common being physeal fracture. Other causes include infection, tumour, therapeutic irradiation, burn, frostbite, electrical injury, metabolic or haematological abnormality, sensory neuropathy, micro vascular ischaemia or the insertion of metal

Distal radius physis is injured most frequently but is an uncommon site of physeal arrest.

The distal femur and proximal tibia account for only 3% of physeal injuries but are the most frequent sites of physeal damage and growth disturbance.

Physeal fracture of the distal femur has at least a 30% chance of developing a growth arrest, 36% have a leg length discrepancy of more than 2cm.
33% have angulation more than 5o

Deformity is usually detected within 6 months of injury

Growth disturbance may not become evident for several / many years after the insult, particularly if the injury occurred when the physis was small.

The site of the bony bridge and the rate of growth of the patient will determine the type and extent of any deformity. The younger the patient is at the time of the injury the more likely that it will lead to a significant clinical problem.

 

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Classification of Physeal Injuries

Salter-Harris classification of physeal fractures has been expanded to six types.
Ogden (J Ped Orthop; 1982) from his series of 443 physeal fractures has added another three.

Salter-Harris I

Salter-Harris II

Salter-Harris III

Salter-Harris IV

Salter-Harris V

Salter-Harris VI

Ogden VII

Ogden VIII

Ogden IX
Ogden VII
Epiphyseal fractures not involving physis
Ogden VIII
Metaphyseal fractures affecting later growth
Ogden IX
Periosteal damage affecting later growth

 

Aetiology of premature partial growth plate arrest

  1. Trauma: 80%
    Salter-Harris Type 1: 5%
    Salter Harris Type 2: 5%
    Salter Harris Type 3: 5%
    Salter Harris Type 4: 85%
    Salter Harris Type 5: 0% ?
  2. Infection: 10%
  3. Tumour: 5%
  4. Iatrogenic (pins, stapes): 2%
  5. Irradiation: 2%
  6. Burns: 1%

Location of physeal arrest

  1. Distal Femur: 39%
  2. Proximal Tibia: 18%
  3. Distal Tibia: 30%
  4. Distal Radius: 5%
  5. Distal Ulna: 3%
  6. Distal Fibula: 1%
  7. Proximal Humerus: 1%
  8. Proximal Phalanx Great Toe: 1%
  9. Pelvis (tri-radiate): 1%

Types of Bridge formation

1. Peripheral
Involves the zone of Ranvier, important in latitudinal growth of the physis.
May ® severe angular deformity ® surgical approach from the periphery excising the overlying periosteum.
2. Linear
Osseous bridge extends as a linear structure across the physis. Most common site is the medial malleolus. May also lead to significant angular deformity ® may remove making a tunnel through the bone.
3. Central
The most severe type of injury and the most difficult to rectify surgically. Bridge is completely surrounded by normal cartilage. Affects longitudinal growth predominantly. Needs to be approached from the metaphysis. Do not replace bone excised from the bridge in filling the metaphyseal defect.
Harris lines appear after restoration of growth following a physeal injury, the line being due to slowing of growth for a variable period following injury. If these lines are parallel to the physis then damage to growth is unlikely
Excision of an osseous bridge that constitutes 50% or more of the entire area of the physis usually gives a poor result.

Substances used to fill defect

Fat
Autogenous, no need to remove
May need second incision to get graft
May float out with release of tourniquet
Shown to enlarge as growth occurs
Silastic
Inert, mouldable to cavity and easily removed
Need special authorisation for use
Must be sterilised, infections reported
Fractures at site of insertion reported
PMMA
Light, inert, non-conductive, transparent (no barium)
Mouldable to defect, good haemostasis,
No fractures reported
No need to remove later but may be difficult if necessary
Packed sterile, no infections reported

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Pathological Fractures

  1. Those occurring in normal bone (stress fractures)
  2. Those occurring in bone which is clearly abnormal

1. Stress Fractures

Patient usually healthy
Fracture site often tender and pain elicited on springing the fracture, may present with a lump which turns out to be fracture callus.
May not be evident on X-Ray, only becoming evident as callus begins to form but is hot on a bone scan.
Most need only avoidance of the aggravating activity, femoral neck fractures require ORIF.

2. Abnormal Bone

Defective Bone Disused Bone Diseased Bone Displaced Bone Disordered Bone
Brittle Bones Post Traumatic Pagets Cysts Osteoporosis
Marble Bones Paralysis Osteomyelitis Deposits Osteomalacia
Congenital Pseudarthrosis Rheumatoid Syphilitic Fibrous Dysplasia Hyper-parathyroidism

54% are secondary to metastatic disease
5% are due to primary bone tumours
41% are secondary to benign bone conditions
Breast Ca leading cause of pathological fracture41%
Other tumours (kidney, lung, prostate, bowel and thyroid)43%
Myeloma or lymphoma account for 16%
More than half of the secondary deposits are in the femur
Secondary deposits distal to either the knee or elbow are uncommon except in pre terminal disease.
Survival of cancer patients after their first pathological fracture
(1960) 50% survive 6/12. 22% 1 year
(1977)69% survive 6/12. 55% 1 year

Indications for ORIF of metastatic lesions

  1. Life expectancy greater than 1 - 2 months
  2. Continued pain after radiotherapy
  3. Lesion greater than 2.5 cm diameter (described for the femur)
  4. Destruction of 50% or more of the cortex of a long bone
  5. Adequate bone quality
  6. Procedure would ® mobilisation and independence
more than 50% cortical erosion ® 60% go on to fracture
less than 50% cortical erosion ® 4% go on to fracture(Filder 1981)
Type of primary tumour ® affect union rate reported between 14-50%
(breast, prostate, myeloma & lymphoma unite more frequently than those due to lung, kidney & gut)

Secondary deposits in the spine

Vertebral bodies 4-7 times more common to be involved than the pedicles but pedicular involvement more easily seen.
Thoracic spine commonest site for secondary deposits ® neurological or cord complications but the lumbar spine is the commonest site for involvement.

Harrington classification of spinal involvement (1986 Current Concepts)

  1. No neurological loss or bone involvement
  2. Involvement of bone without collapse or instability
  3. Neurological impairment without significant involvement of bone
  4. Vertebral collapse and mechanical back pain / instability without significant neurological compromise
  5. Vertebral collapse / instability with neurological compromise
I & II: Analgesics, chemotherapy / hormonal therapy
III: Radiotherapy
IV & V: Surgery

There is no difference in the outcome of laminectomy & radiotherapy and radiotherapy alone. Complete block / compromise do poorly, and incomplete blocks do well in both groups (Harrington)
Radiotherapy 30% no recurrence of symptoms
Laminectomy 50% no recurrence of symptoms
Anterior decompression 90% no recurrence of symptoms
59% of those with an incomplete block will have a lesion at another level as well
NB:Use PMMA only if less than 1 year life expectancy and should use posterior stabilisation to supplement anterior decompression if unstable.

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