Chronic compartment syndrome is also known as chronic exertional compartment syndrome (CECS). The pathophysiology of chronic exertional compartment syndrome is multifactorial (Brewer and Gregory 2012). It is thought to differ from acute compartment syndrome in the sense that in CECS tissue pressures are elevated, but not to the extent that tissue ischaemia occurs, as is the case in acute compartment syndrome (Bong et al. 2005).

Some authors have postulated that in CECS increased compartmental pressure is caused by a combination of physiological factors such as increased blood flow, oedema and muscle volume during strenuous exercise, combined with decreased compliance of the fascia surrounding the compartment (Bong et al. 2005). It is still unclear, however, if pain in CECS is caused by subsequent decreased arterial blood supply and relative ischaemia or rather by periosteal nerve compression (Bong et al. 2005).

The lower leg is divided into multiple compartments containing muscles and other anatomic structures and separated by fascia. The contents of these compartments are described below:

The compartments that are most commonly involved are the anterior compartment, in 40–60 % of patients, and the deep posterior compartment, in 32–60 % of patients (Bong et al. 2005; Brewer and Gregory 2012).

Apart from the main patient group of long-distance runners, chronic compartment syndrome is also common in athletes performing sports that require extensive running, such as soccer, football and basketball (Bong et al. 2005). Several studies have observed fascial defects in 20–60 % of patients with chronic compartment syndrome (Pedowitz and Gershuni 1995). These defects are commonly found in the fascia surrounding the lateral compartment (Edwards et al. 2005). Muscle tissue can herniate through a fascial defect, and some authors have considered such herniations to be an indicator of increased compartmental pressure (Blackman 2000).

However, fascial herniations have also been shown to occur in patients without chronic compartment syndrome (Bong et al. 2005).

Patients suffering from chronic compartment syndrome commonly present with a dull ache in the leg within the first thirty minutes of exercise. This is then followed by a cramping, burning or aching pain and tightness occurring with continuing exercise (Pedowitz and Gershuni 1995; Bong et al. 2005). Pain often increases during running and quickly disappears when exercise is ceased. Most often, pain is located over the involved compartment(s). In the vast majority of patients, symptoms are bilateral (Bong et al. 2005). Some patients may experience neurological symptoms as well, such as weakness or sensory abnormalities (Blackman 2000; Bong et al. 2005).

Physical examination at rest often reveals no signs of pathology. Palpation is usually not painful, but in some cases, exercising before physical examination can cause the affected muscles to feel tense and deep palpation or passive stretching to be painful (Blackman 2000; Bong et al. 2005).

Compartment hydrostatic pressure testing is the gold standard for the diagnosis of chronic compartment syndrome, requiring pre-exertional and post-exertional measurements (Bong et al. 2005; Edwards 2005; Brewer and Gregory 2012). Exact methods and techniques and normal values of measuring pressure vary, but measurements should always be done in rest, followed by measurement after exercise similar to the level of exercise in the athlete’s regular routine (Bong et al. 2005). Pedowitz et al. have described criteria for these pressure measurements to be applied in clinical practice (Pedowitz and Gershuni 1995). However, compartment pressure testing is an invasive diagnostic method, which explains why imaging modalities such as MRI and ultrasound also have a valuable role in the diagnosis of chronic compartment syndrome.

The additional value of radiologic imaging in CCS is limited.

In literature, various terms are used for describing stress fractures, such as insufficiency, fatigue, incremental, low-trauma and march fractures (Liong and Whitehouse 2012). The cause is thought to be excessive, prolonged or recurrent loading of the bone producing a misbalance between bone resorption and bone formation processes, which leads to stress injury (Lassus et al. 2002). If overuse with microtrauma is continued, eventually a stress fracture can develop (Lassus et al. 2002; Brewer and Gregory 2012). As much as 80–95 % of all stress fractures are located in the lower extremity, with the majority of these fractures involving the tibia and a minor part concerning the fibula (Brewer and Gregory 2012). Stress fractures of the tibia can be either transverse or longitudinal (Liong and Whitehouse 2012). Transverse fractures are more common, whereas longitudinal fractures are seen in only 10 % of tibial stress fractures. Tibial stress fractures usually affect the distal two-thirds of the posteromedial tibia, categorised as low-risk stress fractures, compared to anterior cortex stress fractures, which are considered high risk (Liong and Whitehouse 2012). Stress fracture of the fibula occurs most often in the lower third part of the fibula, just proximal to the attachment of the tibiofibular ligament (Fredericson et al. 2006).

Stress fractures of the lower leg are common in military recruits, dancers and athletes, especially long-distance runners. Females have a four times higher risk of a stress injury in general (Lassus et al. 2002). Other risk factors for stress fractures include Caucasian race, irregular menses, eating disorders, osteoporosis or osteopenia, and previous stress fractures (Lassus et al. 2002; Edwards 2005). Additionally, multiple concurrent stress fractures are not unusual, as is seen in 10 % of runners and in 20 % of female athletes (Sullivan et al. 1984; Bennell and Brukner 1997).

At first, patients experience only pain during exercise, but later on pain is also present in rest and in some cases even at night (Lassus et al. 2002; Edwards 2005; Fredericson et al. 2006). Swelling of the surrounding soft tissues may be present (Lassus et al. 2002).

On physical examination, the leg commonly appears normal. Palpation or tapping at the site of fracture can produce tenderness if extensive bone marrow involvement is present (Fredericson et al. 1995). In a third of patients, the posterior part of the tibia can be painful (Fredericson et al. 2006). Pain can be accompanied by erythema or localised swelling of the leg (Edwards 2005). The bony tenderness can be more discrete than in chronic compartment syndrome or MTSS (Bong et al. 2005). Vibratory pain at the site/location of the stress fracture is thought to be able to confirm the diagnosis (Edwards 2005).

Imaging has an important role in the diagnosis of lower leg stress fractures, especially because early identification of stress fractures is essential in order to prevent long-term complications.

In some cases, the diagnosis of stress fracture can be made exclusively based on patient history and physical examination. In inconclusive cases, however, imaging can provide additional information that is essential for the diagnosis. The imaging modalities used most commonly in the diagnostic workup of lower leg stress fractures are plain radiographs, CT, MRI and bone scintigraphy.