The year is racing by, and in Australia summer is fast approaching. This means warmer weather, longer days, and increased chance to exercise. Overuse injuries are a common problem, and this month we discuss stress fractures, the bane of every serious (and not so serious) runner. While stress fractures can occur in any bone, the lower limb is particularly susceptible. Early diagnosis and management is the key, as well as strategies that they do not happen again! Happy exercising!
Overload stress can be applied to bone through two mechanisms:
- The redistribution of impact forces resulting in ↑ stress at focal points in bone
- The action of muscle pull across bone.
Histological changes resulting from bone stress occur along a continuum beginning with vascular congestion and thrombosis→ osteoclastic and osteoblastic activity leading to rarefaction, weakened trabeculae and micro-fracture→ complete fracture. Similarly, bony remodelling occurs along a clinical continuum.
The majority of stress fractures heal within 6 weeks of relative rest. Healing is assessed by an absence of local tenderness and by being able to return to activity without pain.
Radiographs are initially normal for the first 2-3 weeks of symptoms and may reveal no findings for several months. In cortical bone (long bones like tibia, metatarsals and the femur) periosteal reaction, cortical lucency, or a fracture line may be appreciated on later films. In cancellous bone (e.g. calcaneus, navicular) the findings are more subtle and consist of a band-like area of focal sclerosis without periosteal reaction.
In the early stages of a stress #, before any changes on plain radiographic films, bone scans are highly sensitive for detecting stress injuries. Acute stress #s reveal discrete, localized areas of ↑ uptake on all three phases of a technetium-99 bone scan.
Soft tissue injuries are characterized by ↑ uptake in the first two phases only, and shin splints are typically positive only on delayed images. As healing of the stress # occurs, the flow phase (phase I), followed by the blood pool or soft tissue phase (phase II), reverts to normal. The intensity of activity on delayed images (phase III) ↓ over 3-18 months as the bone remodels, often lagging behind the clinical resolution of symptoms.
MRI is helpful in grading the stage of certain stress #s and predicting the time to recovery. In long bones, early stress injury (stress reaction or response) manifests as a spectrum from periosteal oedema, to marrow oedema, to a discrete fracture line.
In general, fat-suppressed T2-weighted images are the most sensitive for detecting a stress reaction or fracture. In stress reactions involving cancellous bones, such as the sacrum, MRI shows relatively low signal intensity in the marrow space on T1-weighted images and relatively high signal intensity on fat-suppressed T2-weighted images. When an actual fracture line is present, T1- or T2-weighted images show linear areas of low signal intensity centered in the geographic zone of bone oedema.
Extrinsic risk factors
- Training errors – increase activity at rate that exceeds bone remodelling
- Muscle fatigue – loss of attenuation of ground reaction force. (intensity, duration)
- Terrain: hard → reduced attenuation; Cambered/uneven → compensatory change in muscle activity and alteration in loading balance
- Equipment – adequate cushioning, appropriate to foot type
In military, females suffer a greater incidence of stress #s than males, but this has not been verified in athletic populations, except in elite rowers with rib stress #’s.
Intrinsic risk factors
- Bone density :reduced strength results in more micro-damage
- Poor evidence of risk in males
- Athletic females with stress # are lower than counterparts, but still higher than controls
- Bone geometry – small cross sectional area
- Alignment: Pes planus common, but equally common in those without stress #; Leg length discrepancy does correlate with risk; Foot type alone not predictive; Varus/valgus knee, Q angle, anteverted femoral neck
- Body size and composition – not predictive in athletic cohort (all similar) but it is predictive in the military.
- Bone turnover– serum measures not predictive
- Flexibility & joint ROM – ↓ ankle joint dorsiflexion in navicular & MT stress #’s.
- Muscle strength and endurance
- Hormonal: short luteal phase; Menstrual abnormalities relative risk 2-4; OCP not protective if eumenorrhoeic, unsure if ↓s risk in menstrual disturbance; Testosterone less associated with risk; Late menarche may be a marker for ↑ risk (PTH/GH/glucocorticoids/thyroid hormones)
- Nutrition: Calcium above RDI is not protective- supplementations may help if diet deficient; Restrictive eating is associated with ↑ risk, but causality not proven
Tibia> fibula> Metatarsal> Navicular> Femur> Pelvis
The first step in treating stress fractures is identifying and correcting any predisposing factors. Most low-risk stress fractures can be successfully treated with rest followed by a gradual resumption of activity. For lower extremity low-risk stress fractures, a rest period of 2-6 weeks of limited weight-bearing progressing to full weight-bearing may be necessary. This is followed by a phase of low-impact activities, such as biking, swimming, or pool running. Once the patient can perform low-impact activities for prolonged periods without pain, high impact exercises may be initiated.
High risk stress #s require individual assessment and often prolonged cast immobilization and non-weight bearing +/- surgical fixation.
Treatment of risk factors
Although there has been no proven causality of any risk factors, there have been positive associations found, and therefore these factors should be addressed if present.
- Menstrual disorders
- Caloric restriction
- Muscle weakness
- Leg length discrepancy
- Training volume, intensity, surfaces
- Resumption of normal menses is best.
- OCP if osteopenic
- Medroxyprogesterone – not helpful
- Calcium supplementation – not enough evidence to support its use