Menu

Stress Fractures

Stress fractures

 

Can occur in any physically active person

 

I.      Incidence

 

Dependant on the activity;

 

Ø  15% of all stress fractures occur in runners.

Ø  70% of all runners injuries are stress fractures.

Ø  Stress fractures occur in order of injury rate in runners: tibia, fibula, metatarsals and pelvis.

Ø  Sports specific areas for stress fractures: Ribs (golf, boxing, rowing).

Ø  Lumbar spine /pars - cricket, basketball, tennis and soccer.

 

II.    Cause

 

Ø  A stress fracture is a partial or complete fracture caused by an accumulation of stress to a localized area.

Ø  They arise as a result of repetitive application of stresses that are lower than the stress required to fracture the bone in a single loading.

Ø  Bone endures a stress whenever a force is loaded on it. This can come from the pull of a muscle or the shock of a weight - bearing extremity contacting the ground.

Ø  Low levels of force can cause bone to deform or bend known as strain.

Ø  The bones stress/strain response depends on the loads direction, bones geometry, micro-architecture, density and surrounding muscle contractions.

Ø  In most activities when the force is removed the bone elastically rebounds back to its original position.

Ø  The force that a bone can endure and still rebound back without damage to its original state is within the elastic range.

Ø  Forces that exceed the elastic range are in the Plastic Range.

 

î  Once forces reach the plastic range a lower load can cause greater deformation and permanent damage to the bone.

î  Forces can be applied to a bone through compression, tension, torsion and shear.

î  Compression Forces occur through cancellous bone eg Calcanueus/NOF.

î  Tension Forces where bone is being pulled away from bone eg Tibia and fibula.

 

î  As load is applied to the bony shaft through a bend, a tension strain is placed upon the convex surface and a compressive on the concave surface.

î  The muscle attached to the surface of the Compact Bone (exterior) can either increase or decrease intensity of a load.

î  It can act as a shock absorber by controlling bone strain and decreasing intensity or it can increase bone strain by excessive muscular pull.

î  This is common in NWB bone eg Fibula and Ribs.

î  Weak or Fatiguing shock absorbing muscles allow load to be translated to bone = stress fracture.

 

Anatomy of bone

 

Ø  Has both cortical (aka compact) and cancellous components.

 

I.        Cortical

Ø  Outer layer of bones, dense highly organised structure desiged for compression rather than tension. eg shaft of femur and tibia.

Ø  Unit of cortical bone is called the osteon.

Ø  This is concentric layers of Lamellar bone surrounded by small channels called Haversian Canals. These house nerves and blood vessels.

Ø  Osteocyte single bone cell lying inside Lacunae which lies outside Lamellae.

Ø  Canaliculi link Haversian Canals to Osteocytes to transport nutrition via blood vessels.

II.      Cancellous

Ø  Trabecular irregular meshwork of fibres designed to withstands stress according to alignment of the fibres eg tarsals and pelvis.

Ø  Found in the ends and central portion of the shaft.

 

Remodeling

 

Ø  Constant remodeling itself to endure external forces.

Ø  Column Law - the magnitude of stress is greatest on the surface of the column and decreases to the zero at the centre ie most of the remodeling takes place in the outer cortex.

 

How

 

Ø  Osteoclastic - reabsorption of existing bone.

Ø  Ostelblasts - form new bone cells.

 

î  Therefore normal activity stimulates regular remodeling of bone with constant nutritional flow resulting in stronger healthier bone.

î  Conversely a sedentary lifestyle results contributes to bone atrophy.

î 

 

What triggers remodeling?

 

Ø  Activation of Osteoclasts

 

î  One theory is tension or torque/bending created on the CONVEX side causes a electro+VE charge and may lead to Osteoclastic stimulation.

 

Ø  Other mechanisms

 

î  Sensors which recognise increasing and decreasing mechanical strains, hormones, endocrine function, decreased venous flow and decreased oxygen flow.

 

Ø  Role of osteoclasts

        

î  Form cone and secrete protein enzyme which cuts longitudinal tunnels through bone 3-10mm deep.

î  These new canals are filled with osteoblasts and form new matrix to support canals called lamellar bone.

î  This process takes 10 - 14 days to form canal from the onset of remodeling.

î  The conversion of the matrix to mature lamellar bone a further week and up to 90 days. This stage is when the lamellar bone is at its weakest due to the hollow canal.

î  This is called the ‘weak third week’ when the cortex is vulnerable to breakdown and stress fracture.

î  The cortex is given protection by the periostium becoming inflamed. This bolsters the weakened cortex until maturity. This however can take up to 20 days therefore leaving the remodeling area still vulnerable at the 3 week mark.

 

Stress fracture

 

A true stress fracture is a visible cortical fracture on X- Ray, CT or MRI.

 

Ø  Stress fractures are classified into 2 types - fatigue or insufficiency.

î  Fatigue fractures are caused by abnormal stress to a normal elastic bone.

î  They occur at different sites depending on age, sex and activity level.

î  Fatigue fractures occur in the physically active population due to abnormal forces caused by increased training, hard surfaces, poor shoes, poor anatomical foot alignment such as a Pes Planus or a Pes Cavus type.

 

Cause of stress fracture was thought to be only due to repetitive loading. However this requires large forces particularly if the tibia. Therefore as stress fractures can occur in the first week of training mechanical stress can not only be the cause.

 

Ø  Insufficiency fractures arise from the application of a normal stress on a bone that is mineral deficient.

î  These fractures are most common in nutrient deficient (osteomalacia).

î  They also occur in the older population in whom osteoporosis and RA are prevalent.

 

 

Perfusion and reperfusion of bone

 

Ø  This is where a temporary Oxygen debt occurs due to bone deformity under load.

Ø  This decrease in Oxygen triggers an increase in osteoclast bone reabsorption and increase in remodeling and a decrease in a bone density.

 

Risk factors

 

Apply to both fatigue and insufficiency stress fractures

 

Ø  Normal bone may be weakened by cysts, surgical or medical procedures eg pin and plates, screws, tendon transfers, joint replacement or radiation.

Ø  Females are more at risk than males particularly teenage girls. This may be due to lower bone density, lean body mass particularly the lower limb, low fat diet , menstrual irregularity.

Ø  Foot type as previously mentioned.

Ø  Most common cause is a change in training.

 

III.   Management

 

Prompt identification essential.

 

Ø  Once diagnosed the injury can be managed with a cyclic management protocol based on the physiology of the bone remodeling and a strategy for prevention.

Ø  Symptoms that resemble a stress fracture are actually due to advanced bone remodeling.

Ø  This stress reaction may only be a point along the continium of remodeling before the onset of a true stress fracture.

 

Intervention

 

May be in the form of casting, splinting or surgical fixation.

 

Diagnosing stress fractures can be difficult as the symptoms are similar to other injuries. Common diagnostic techniques include clinical examination, x-ray, bone scan, MRI.

Management

Ø  ? ? after abnormal reactions to stress in a stress fracture is suspected. Since an x-ray may not be ? for 10 – 21 days after onset of symptoms, a delay in intervention may allow the accelerated remodeling to progress to a true stress fracture.

Ø  The priority is a period of rest or active rest still allowing the athlete to exercise in a pain free manner versus present muscle atrophy.

Ø  An acronym for goals of stress fracture management:

R    Removal of the abnormal stress.

E    Exercise to maintain cardiovascular fitness v prevent atrophy.

S    Safe, pain free return to previous level of activity.

T    Time for bone maturity v catch up of peel remodeling.

Phase I; 1 – 3 weeks

Remove stress from area

Control pain

Prevent deconditioning

Haversian level for mation

Osteoblasts lay down new core ? to buttress weakened bone area.

Last splints, crutches, aircast support area ie pre…. Air support ortho….

Daily ie manage, TENS, contrast

DUS

Crutches to FWB as pain ves

Exercise - …..

Phase II: 3 weeks plus

Pain still guide to overload.

As phase I and walking up to 30 minutes.

Phase III: 5 weeks plus

Use a cyclic training to prevent stress fractures ie limiting 1st 2 weeks of training to / if high impact and high repetition then excluding impact in critical 3rd week, therefore allows new bone formation.

When asymptomatic – running

Walk ? 1 k

15 – 20% á per week     rest day                                à 3 x weeks

0.5 km á per week

Jogging at 1.5 km <span lang="EN-US" style="FONT-SIZE: 11pt; FONT-FAMILY: Wingdings; mso-fareast-language: JA; mso-ascii-font-family: Calibri; mso-hansi-font-family: Calibri; mso-char-type: symbol;