The Insidious Spectre – a short discourse on lower extremity stress fractures. (Part One)


The gradual onset of lower-extremity pain in runners is unfortunately often a scatter-gun approach in terms of differential diagnosis. In the case of fatigue bone injury, the sheer volume of symptoms and pain classifications to analyse can certainly prove laborious to identify early onset. Particularly in manual therapy and Osteopathic practice, whereby quick turn-around diagnostic imaging for early interpretation of injury is sparse.

A suppositional diagnosis in the initial phases of stress-induced bone injury is, however inadequate, the first port of call for clinicians. Taking into account not only presentation of pain, but most importantly, pain patterns. Does the pain radiate elsewhere at all? Is it purely localised to the upper shin? Is it alleviated with rest? At which point during exercise does it first present or worsen? First stage pain presentation in stress bone injury can occasionally cause direct and cramping pain in the soleus and gastrocnemius, and occasionally directly downwards to the achilles tendon. All of these symptoms can be indicative of other injury and difficult to link early on, following initial patient presentation.

It is clear then, that early and clear diagnosis of a bone injury caused as a direct result of frequent and repetitive sub-maximal skeletal loading is a rather murky diagnostic minefield.

At the top of this post is a coronal MRI of my own left leg, approximately 14 months subsequent to a spiral fracture of the tibia. Following two weeks of road running I began to develop a slow and insidious ‘burning’ pain in the anterior proximal left shin, and a feeling of general muscular weakness in the left calve. This sensation presented only upon a sudden change in pace during running (sprint intervals) or around the 30 minute mark of a run at slower pace. After appointments with two separate physiotherapists, it was diagnosed as a strain of the calf muscle – despite the anterior shin pain there was no clinical suspicion of stress-related microtrauma in skeletal architecture – or even disruption to normal cortical structure for that matter.

A week following this diagnosis, the leg failed completely as a support at around mile 7 at fast jogging speed, causing a fall at pace which caused no other injury. The sudden sharp ‘electric shock’ type pain was new to me and utterly crippling, immediately causing a complete inability to weight-bear on the left leg and two months of crutch support. The muscular atrophy in the left calf following the period of rehabilitation is quite visible on the above MRI, and amounted to approximately 4 inches diameter of lean muscle loss.

I presented to the fracture clinic at the University Hospital of North Tees, upon which further tests were conducted to confirm an oblique fracture of the tibia, and multiple stress fractures of the anterior cortex (visible on the MRI above as a localised cluster of bright white lines).  The MRI showed a quite linear abnormally wide high signal in the localised bone marrow along the medial anterior surface of the tibia, this was more clearly identifiable on the coronal image but also remarkably apparent on sagittal projection. This injury included soft-tissue as well as bone changes, with quite clear periosteal edema (which refused to abate for around 2 months post recovery), visibly detectable fracture line which was present on radiographic image as well as MRI, and focused cortical abnormalities.

The diagnostic outcome, according to the Fredericson Classification for TSI was a grade 4b stress fracture of the tibia (anterior proximal third) with linear intracortical fracture line and notable periosteal edema.

As a reflective experience, this case shows clearly that early imaging of the affected limb as well as provocative testing may have elicited a diagnostically clear pain response. Could the crack initiation, propagation and resulting damage to the bone have been prevented? Quite possibly. Although the sheer diversity of symptoms leading up to skeletal fatigue – and ultimately complete bony failure, could conceivably have been ten other musculoskeletal conditions.

Speaking now from the other side of the curtain as a practitioner, I find it imperative that my own patient care upon clinical suspicion of a possible stress fracture is not anchored purely on the most salient aspect of the presenting symptoms. An injury which is hallmarked by bony microfailure without a visible fracture line is, by nature, never going to be easily identifiable as part of a ‘pre-emptive strike’ treatment – particularly for an Osteopath.

Thus the spectre of gradual onset bone failure and stress fracture continues to occasionally elude even the most pinpoint diagnostic physical examinations.

To be continued… 


  1. Kijowski R, Choi J, Shinki K, Del Rio AM, De Smet A. (2012). Validation of MRI classification system for tibial stress injuries.. Department of Radiology, University of Wisconsin, Clinical Science Center, Madison. 194 (4), 878-84.
  2. Knapp TP. Garrett WE Jr. Stress fractures: General Concepts, Clinics in Sports Medicine. 16(2):339-56, 1997 Apr.