Compartment Syndrome

Chronic exertional compartment syndrome (CECS) is defined as a condition in which exertion increases muscle compartment pressure, interfering with tissue circulation and causing ischemia, pain, and even temporary neurological deficits (Blackman 2000).  Terms such as shin splints, march synovitis, anterior tibial pain syndrome, and medial tibial syndrome, have all been used to describe the symptoms of CECS (Rorabeck 1983).

Acute compartment syndrome is “a condition in which increased pressure within a limited space compromises the circulation and function of the tissues within that space”.  Most commonly occurs in the lower leg, but can occur in the thigh, buttock, and foot.

Acute – occurs following trauma to the lower leg, commonly after intramedullary nailing of long bone fractures, after ischaemic re-perfusion injuries, burns or poor positioning during surgery.
Chronic – reversible, activity related increases in intracompartmental pressure.  Also referred to as exercise-induced compartment syndrome (EICS) or exertional compartment syndrome.

Defining the anatomical compartments is essential in understanding the symptoms and treatment of the various CECS in the lower leg.
The concept of four distinct compartments in the lower leg is well-recognised with anterior, lateral, superficial posterior, and deep posterior compartments (Melberg and Styf, 1989).  More recently, a fifth compartment has been described that is in essence a subdivision of the deep posterior compartment, and contains only tibialis posterior.

1.Anterior compartment:  Comprises the tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneus tertius.  Neurovascular structures include the anterior tibial artery and vein with the deep branch of the common peroneal nerve running along the interosseous membrane deep to the extensor hallucis longus.
2.Lateral compartment: Contains the peroneus longus and brevis with the common peroneal nerve dividing into its superficial and deep branches, the latter continuing into the anterior compartment.
3.Superficial Posterior: The posterior compartments lie surrounded by the deep fascia of the leg with the deep transverse fascia separating the deep from the superficial compartments.  The superficial compartment contains gastrocnemius, plantaris, and soleus.
4.Deep posterior: Contains the flexor digitorum longus, flexor hallucis longus, tibialis posterior, and more proximally popliteus.  Neurovascular structures in the deep compartment include the posterior tibial artery and vein and tibial nerve, entering beneath the arch of soleus proximally then lying on the posterior surface of tibialis posterior and more distally on the posterior tibia.  The fifth compartment is created by a discrete fascial layer over the posterior surface of tibialis posterior, and it is therefore possible that elevation of pressures in the compartment alone may occur (Blackman, 2000).

Pathological Process
The generally accepted pathophysiology of this condition is that raised intracompartmental pressure causes relative ischemia of the involved muscles (Blackman, 2000).
Ateriovenous pressure gradient theory:
Ischaemia begins when local blood flow cannot meet the metabolic demands of the tissue.  As the intracompartmental pressure rises, the intraluminal venous pressures also increase leading to a reduction in the arteriovenous pressure gradient resulting n diminished or absent local perfusion.  This causes a further rise in intersititial tissue pressure with the formation of tissue oedema.  The lymphatic drainage is then increased to protect against the rising interstitial fluid pressure.  Once this has reached its maximum, further increases in the intracompartmental pressure cause deformation and collapse of the lymphatic vessels.  It is only at the late stages that the arterial flow into the compartment is seriously compromised and the continuing flow of blood into the compartment increases swelling and oedema.  Pain may not only occur due to the increases in pressure, but also due to sensory receptor stimulation in the fascia or periosteum, or due to biochemical factors released due to reduced blood flow.
Raised intracompartmental pressure model:

A number of authors use this theory as a basis for fasciotomy, subsequently demonstrating a reduction in intracompartmental pressures post surgery (Puranen and Alavaikko, 1981; Rorabeck et al, 1983).

Other proposed evidence for this concept includes the demonstration of elevated intracompartmental pressures during and after exercise (Puranen and Alavaikko, 1981).

Studies on normal muscle also corroborate this theory.  The findings of these studies include a 20% increase in muscle size due to an increase in blood volume with exercise, and that chronic exercise causes a lasting muscle volume increase due to hypertrophy (Amendola and Rorabeck, 1985).

Ischemia Model:
There is some debate as to whether these increases in pressure result in clinically significant ischemia, and therefore may not be the main pathological factors linked to pain in CECS (Amendola et al. 1990; Trease et al. 2001)

Evidence Supporting:
Those who support the ischemia hypothesis suggest there are three potential mechanisms to explain the development of tissue ischemia:
1.Increased pressure causes arterial spasm and therefore a decrease in arterial inflow (Matsen, 1975)
2.Increased pressure causes obstruction of the microcirculation (Rorabeck and Macnab, 1975)
3.Increased pressure causes arteriolar or venous collapse leading to ischemia (Matsen, 1975; Black et al, 1990; Hutchinson and Ireland, 1994)

Evidence negating:
In a study by Balduini et al.  (1993) on 26 patients with lower leg pain, 24 patients with positive pressure tests failed to demonstrate signs of ischemia.  The two exceptions (17% of patients with CECS) had evidence of ischemia with associated pressure measurements above 160 mm Hg.  They concluded that, below these very high compartment pressures, ischemia was not a significant factor in the development of CECS.
Amendola et al. (1990) also failed to find any evidence of ischemia in patients with compartment syndrome.  They used nuclear blood flow imaging in their study on magnetic resonance imaging (MRI) in CECS and found that none of the patients with positive pressure studies demonstrated “consistent ischemic changes”.
Alternative explanations for the pain associated with CECS may be:
1.Sensory receptor stimulation in the fascia or periosteum due to increased pressure (Balduini et al. 1993)
2.Biochemical factors released due to minimally reduced blood flow (Balduini et al. 1993; Amendola and Rorabeck, 1985)
3.The symptomatic relief after fasciotomy may be due to the mechanical release of tension or biochemical changes, rather than the reversal of ischemia.

Clinical Presentation

Several months to years history of pain induced by exercise and relieved by rest.
Cramping, burning, or aching pain and tightness in the lower leg with exercise (Black et al. 1990), with continual or progressively increasing pain as exercise continues or intensity is increased (Blackman, 2000).  Eventually causing the individual to stop exercising.
Pain should cease or dramatically reduce within minutes of stopping (Balduini, 1993); however, some authors state that it may continue overnight and into the next day, depending on duration and severity of the condition (Martens and Moeyersoons, 1990)
Maybe bilateral.
Neurological symptoms vary depending on which nerve is involved (Blackman, 2000)

Physical signs are absent at rest, and all patients should therefore be examined post exercise, using the aggravating activity wherever possible (Martens and Moeyersoons, 1990).
This usually reveals a tense, firm compartment that may be painful to deep palpation and passive stretch (Blackman, 2000).
There may be tenderness along the tibial border if it is associated with stress fracture of the tibia, or traction periostitis due to chronic tension of the compartment fascia at the attachment to the tibia (Blackman, 2000)
Neurological examination is essential.  This may reveal patterns suggestive of the specific nerve and, therefore, the compartment involved (Black et al. 1990).
Anterior. Weakness of dorsiflexion and paraesthesia in the first web space (deep peroneal nerve).
Lateral: Weakness of dorsiflexion (deep peroneal nerve) and/or eversion (superficial peroneal nerve), and paraesthesia over the anterolateral distal shin and dorsum of the foot (superficial peroneal nerve) and first web space (deep peroneal nerve).
Deep posterior: involves the tibial nerve and may produce dysaesthesias over the medial arch of the foot and/or cramping of the intrinsic foot muscles. (Blackman, 2000).
Muscle hernias over the anterolateral compartments have been reported, especially at the point where the superficial peroneal nerve pierces the deep fasica (Black et al, 1990).  These hernias are thought to be an indicator of elevated intracompartmental pressure (Beith et al. 1980).
Signs of arterial insufficiency such as distal pulse deficits and poor capillary return are rare and occur only with very high intracompartmental pressures (Balduini et al. 1993)

Diagnostic tests
The most useful test to confirm CECS is a compartment pressure study, using a transducer-tipped probe.  A positive diagnosis requires elevated pressures on exercise which must coincide with reproduction of the patients typical pain (Pedowitz et al. 1990).
Many different pressures have been recorded.  However, the most accepted and predictive values are pre- and post- exercise pressures (Pedowitz et al 1990).  Studies on patients without CECS demonstrate a return to within 1mmHg of resting pressure within 3.4-5 min post exercise (Nkele et al. 1988).  Therefore, a delay of between 6 and 30 min in the return of post-exercise pressure to resting pressure levels must occur to demonstrate a positive test (Rorabeck et al. 1988).
Pedowitz et al. (1990) defined the criteria for diagnosis of anterior CECS in the leg as requiring one or more of the following: pre-exercise >15 mm Hg.  1-min post exercise >30 mm Hg, and 5 min post-exercise >20 mm Hg.  These were based upon a comparison with 210 normal muscle compartments tested using the same protocol.
Other investigations may be indicated in order to make any differential diagnosis, eg. X-ray, MRI, bone scintigraphy, and CT.

Differential diagnosis
Differential diagnosis must include periostitis and stress fracture of the tibia or fibula (Hannaford et al, 1988).  Less common possibilities include: tenosynovitis, vascular and neurological entrapment syndromes, ventral nervous system disorders, primary muscular disorders, infection, and tumours (Styf, 1989).

Often occurs bilaterally (Blackman, 2000)
Equal incidence in male and females (Hutchinson and Ireland, 1994; Wiley et al, 1987; Veith et al. 1980)
Anterior CECS tends to be more common than posterior CECS (Veith et al 1980; Amendola and Rorabeck 1985).
Patients are often described as young and physically active, often runners, reporting recurrent exertion-related pain in the affected muscle compartment (Avramovitz and Schepsis 1994).
However, in a study by Edmundsson et al (2007) most cases had a sedentary lifestyle with leg pain even during walking.
Few predisposing factors for CECS have been reported, although a history of trauma has been mentioned (Tubb and Vermillion 2001).


Early diagnosis is essential, if ischemia has occurred due to trauma, then open and extensive fasciotomies with decompression of all the affected compartments is the treatment of choice.
Many statements discussing conservative methods appear to be based on anecdotal information alone; and more scientific data is required to draw any firm conclusions (Blackman, 2000)
In a retrospective analysis (Blackman et al. 1994), rest from exercise, even for a lengthy period, was not found to be associated with any improvement in pain on resumption of activity.
Modification of intrinsic and extrinsic contributing factors is required; which may include modification of footwear, adjusting training programs, massage, orthotics, strengthening and stretching exercises.
Surgical management for CECS is based on the premise that there is a need to decrease intracompartmental pressure (Blackman, 2000).
This is done by releaseing the fascial barrier of the involved compartment, either through fasciotomy or fasiectomy (Black et al. 1990; Rorabeck et al. 1983; Schepsis et al. 1993; Wiley et al, 1987).
Results for CECS surgery are generally good, with reports demonstrating good functional improvement or symptomatic cure in a high proportion of cases (Puranen and Alavaikko, 1981; Rorabeck et al, 1983; Schepsis et al, 1993; Wiley et al, 1987).
Most reports found a better long-term outcome for anterolateral compared with posterior decompression (Puranen and Alavaikko, 1981; Rorabeck et al, 1983; Schepsis et al, 1993; Wiley et al, 1987).
Postoperatively, anterior compartment releases tend to recover faster, in contrast to deep posterior decompressions (Schepsis et al, 1993; Hutchinson and Ireland, 1994).
Crutches are used until weight bearing is comfortable (usually 3-5 days), although some authors prefer to allow the patient to walk immediately postoperatively (Wallensten, 1983)
Early mobilisation of the affected limb as soon as possible is recognised by many authors as important (Black et al, 1990; Rorabeck et al, 1983; Hutchinson and Ireland, 1994) to prevent excessive scarring and adhesions.  Active range of movement exercises at the knee and ankle are recommended and immediately postoperatively by Hutchinson and Ireland (1994).
Transitional activities such as cycling and swimming (after wound healing) are introduced over the following weeks, and running is commenced between 3 and 6 weeks postoperatively. (Blackman 2000)
Return to full activity usually occurs between 6 and 12 weeks (Black et al, 1990; Rorabeck et al, 1983; Schepsis et al 1993)

The end result of an unidentified acute compartment syndrome can be catastrophic and include nerological deficit, muscle necrosis, ischaemic contracture, severe infection, delayed healing of a fracture, loss of the limb, or even death!  Acute compartment syndrome can lead to the ‘crush syndrome’, marked by acute renal failure as a result of the precipitation of myoglobin released from the damaged muscle in the distal convoluted tubules in the kidney.  Acidic hyperkalaemic blood is also released from the damaged muscle, resulting in cardiac arrythmias and further precipitation of myoglobin in the kidneys.  Extensive muscle damage can result in the need to amputate the limb.
The incidences of complications is strongly related to the timing of fasciotomies, and therefore early diagnosis is essential to prevent irreversible damage occurring.  In acute cases fasciotomy performed within 24hrs gives ‘acceptable’ results as long as the compartment pressure does not exceed 40 mmHg.
Chronic vases may return to running at 6 weeks and competitive sport at 3 months following fasciotomy.  Commonly patients will be pain free following surgery but may continue to experience up to a 20% decrease in strength of the affected compartment.  Studies have shown that men have more successful outcomes than women.


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