Stress fractures refer to fractures occurring in bone due to a mismatch of bone strength and chronic mechanical stress placed upon the bone. Fractures can either be:
- fatigue fracture: abnormal stresses on normal bone
- insufficiency fracture: normal stresses on abnormal bone
A pathological fracture, although a type of insufficiency fracture, is a term in general reserved to fractures occurring at the site of a focal bony abnormality.
Some authors use the term stress fracture synonymously with fatigue fractures, and thus some caution with the term is suggested.
Stress fractures normally present with worsening pain with a history of minimal or no trauma. In the lower (weight bearing) limb, there is often a history of recent increase of physical activity or significant alteration in the the type or duration of normal athletic activity.
Stress fractures are far more common in the bones of the lower limb than the upper limb.
High risk sites of stress fractures are locations at greatest risk of fracture propagation, displacement or non union. These sites include:
- posterior tubercle of calcaneus
- base of 5th metatarsal
- neck of 2nd to 4th metatarsal
- great toe sesamoids (hallux sesamoids)
- talar neck
- tarsal navicular
- anterior cortex of tibia
- medial malleolus
- superior side of femoral neck
- femoral head
- pars interarticularis of the lumbar spine
Low risk sites of stress fracture are at low risk of complications. They include:
- pubic rami
- proximal humerus/humeral shaft
- posterior medial tibial shaft
- 2nd to 4th metatarsal shafts
Plain radiographs have poor sensitivity in detecting stress fractures, as positive findings may take months to appear. During the first few weeks after the onset of symptoms, x-rays of the affected area may look normal.
Positive findings include sclerosis, periosteal reaction/elevation, cortical thickening and a fracture line.
Bone scans can show evidence of stress fracture within a few days upon onset of symptoms. It is represented as a focus of increased radioisotope activity ('hot spot') due to increased bone turnover at the site of new bone formation. However increased uptake can also be due to osteomyelitis, bone tumours or avascular necrosis, and as such specificity is low.
The appearances are similar to those on plain radiograph with sclerosis, new bone formation, periosteal reaction and fracture lines in long bones. It is also useful in differentiating stress fractures from bone tumour or osteomyelitis if the plain radiographs are negative and bone scans are positive.
On MRI the low signal fracture line usually extends through the cortex and into the medullary canal and is elucidated with surrounding bone oedema in the surrounding marrow. MRI is also useful to differentiate ligamentous/cartilaginous injury from bone injury.
Treatment and prognosis
Treatment is determined by the site of the stress fracture and suitability for rehabilitation.
Fractures at low risk sites are managed conservatively with analgesia, ice, reduced weight bearing and modification of activities until pain resolves.
At high risk sites or in patients where long term rehabilitation is detrimental to their livelihood (i.e. athletes or labourers), orthopaedic consultation is required.
Risk factors such as diet, vitamin D and calcium should be addressed to prevent recurrence. Other factors such as gradual return to training and biomechanical evaluation of gait may be required. Bone density evaluation can be considered in patients with recurrent stress fractures, family history of oesteoporosis or in stress fractures unexplained by exercise activity.
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