Keywords
athletes - compartment syndromes - sports injuries - sports medicine
Introduction
Von Volkmann first described compartment syndrome (CS) in 1881. Subsequently, there
were CS reports in several anatomical regions, especially the lower extremities.[1] In addition, although there are rarer and limited CS cases reported in the hand,
forearm, and paravertebral compartments.[1]
[2]
[3]
Compartment syndrome is an increased pressure within a non-expandable fibro-osseous
space, leading to compromised tissue perfusion in that specific area. Reduced perfusion
initially causes ischemic pain, followed by reversible and eventually irreversible
tissue damage within the compartment. The resulting edema creates a vicious cycle,
further aggravating the ischemic injury.[1]
Compartment syndrome manifestation can be acute, characterized by severe symptoms
over a short period, or chronic, lasting for a long time. Acute compartment syndrome
(ACS) is a medical emergency, typically resulting from a severe injury or trauma that
leads to intense pain. On the other hand, chronic CS (CCS) is often not an immediate
medical emergency, and it appears after intense and repetitive athletic activity in
the absence of acute trauma. Its treatment involves rest and recovery.[4]
[5]
Along with other exertion-related conditions, CCS can significantly contribute to
developing exertion-dependent symptoms. Therefore, this condition has particular importance
in sports and physical exercise. One of the first descriptions of CCS occurred during
the British expedition to the South Pole in 1912, in which Edward Wilson described
swelling and pain in the anterior compartment of the leg during long walks in the
Antarctic region. Subsequent historical records have also emphasized the prevalence
of CCS in military cohorts, leading to the nickname “marching gangrene”.[4]
Pathophysiology
Numerous hypotheses have attempted to elucidate CCS pathophysiology. However, the
true etiology and development process of the condition remain undetermined.[6]
We know that intense exercise can lead to substantial increases in muscle volume resulting
from increased metabolic demands, tissue perfusion, and muscle fiber growth. Compartment
syndrome occurs when the pressure within the fascial compartment exceeds the diastolic
pressure. This compromised blood flow causes tissue ischemia, metabolite accumulation,
and pain in the affected area.[4]
Some researchers have suggested that untreated CCS can result in neural compression
and irreversible damage due to fluid leakage and increased intracompartmental pressures.
Decreased capillary density and impaired venous flow have also been implicated in
CCS development.[4]
Chronic CS results from increased intracompartmental pressures potentially triggered
by several precipitating events. Local blood flow, determined by local arterial pressure,
venous pressure, and vascular resistance, impacts pressure within a muscular compartment.
Ischemia occurs when interstitial pressure exceeds capillary perfusion pressure (CPP).
Skeletal muscle ischemia releases a histamine-like substance that increases vascular
permeability, causing the formation of blood thrombi and worsening ischemic conditions.
Myocyte rupture releases proteins, which results in water escaping from the arterial
blood into the compartment.[7]
Other contributing factors associated with CCS involve inadequate training methods,
limb misalignment, leg length discrepancies, running style, and poor neuromuscular
control.[8]
Although the precise underlying mechanism is still debatable, consensus points to
CCS development resulting from muscular effort repetition within a compartment, which
reduces blood perfusion.[8]
Epidemiology and Risk Factors
Epidemiology and Risk Factors
The precise prevalence of CCS remains uncertain due to factors that include self-treatment
or activity modification, errors in clinical diagnosis, and failure to seek medical
care. It is estimated that 14 to 34% of leg pain referred for orthopedic treatment
because of activity or exertion is consistent with CCS.[4] The current prevalence of CCS in the general population is unknown. However, it
has been documented in specific athletic subgroups at a rate of 0.49 cases per one
thousand people per year.[9]
Chronic compartment syndrome primarily affects the leg, with more than 95% of cases
reported in this region. However, there are variable reports of involvement in the
lumbar paravertebral compartment,[1] hand, forearm, thigh, and foot from specific high-risk groups.[4] Among leg compartments, the most affected is the anterior compartment (42–60%),
followed by the lateral (35–36%), deep posterior (19–32%), and superficial posterior
compartments (3–21%). Single-compartment involvement is less common (37%); approximately
40% of symptomatic cases involve 2 compartments, 18% involve 3 compartments, and only
5% affect all 4 compartments. Bilateral involvement is more prevalent, representing
up to 95% of cases, with no differences in laterality.[4]
Anatomical disparities between adolescents and adults increase the risk of CS development
in younger patients.[7] Shadgan et al.[10] noted clinicians often believe that younger subjects have a stiffer/narrower and
stronger fascia, combined with greater muscle density, increasing their vulnerability
to CS. Therefore, CCS diagnosis is frequent, although not limited to, in young athletes
involved in repetitive activities, such as long-distance or cross-country running.[7]
Older studies showed conflicting outcomes regarding the prevalence of CCS in men and
women. Some studies reported a higher CCS occurrence in men, while others have suggested
a potential increased occurrence in women. However, the latest literature investigations
reported a similar incidence of CSS among men and women.[4]
Rothman et al.[11] found that women were less likely than men to return to sports after a surgical
intervention, and factors such as intracompartmental pressures, sports participation,
and postoperative outcomes were not statistically different between genders.
More than 90% of people diagnosed with CSS participate in athletic activities, with
no difference reported between those participating in elite or recreational levels
of competition. Although several sports have been linked to CCS, including lacrosse,
football, basketball, skiing, and field hockey, the condition is more frequent in
endurance runners, who account for up to 68% of cases.[4] Some rare cases have occurred in weightlifting, American football, and baseball
athletes.[2]
[3]
[12] However, CCS can also affect less active populations.
Intense exercise, including running, although not exclusively, has been associated
with an increased CCS incidence. Physiological and metabolic changes due to significant
physical activity affect muscle volume and compartmental pressures. Eccentric muscle
strengthening in adults is a potential cause for decreased fascial conformity and
CCS development. Patients with CCS often have a thickened fascia and a higher prevalence
of fascial defects compared with asymptomatic individuals. Anabolic androgenic steroids
and other performance-enhancing drugs for muscle growth may also contribute to abnormal
elevations in intracompartmental pressures, and some suggested them as potential risk
factors for CCS.[4] Some evidence indicated that training errors, specifically an abrupt increase in
training volume, intensity, or both, can be the chief risk factor for CCS development.[13]
Anatomy and Clinical Presentation
Anatomy and Clinical Presentation
Chronic CS is the second most common cause of exertion-related leg pain, followed
by medial tibial stress syndrome (MTSS), affecting approximately one third of athletes.
It is critical to consider other potential diagnoses of exercise-induced leg pain,
such as nerve entrapment, bone stress injuries, deep vein thrombosis, MTSS, and miscellaneous
clinical conditions during symptom evalution.[4]
[13]
A comprehensive knowledge of lower limb anatomy is crucial for CCS diagnosis and identification
of the compartments involved. The lower leg anatomically has four compartments, namely,
anterior, lateral, superficial posterior, and deep posterior, with an additional fifth
compartment for the tibialis posterior muscle, which has a fascia ([Fig. 1]).[14]
Fig. 1 A transverse section of the leg shows the four compartments, namely, the anterior
compartment (containing the tibialis anterior, extensor digitorum longus, extensor
hallucis longus, and fibularis tertius muscles), the lateral compartment (composed
of the peroneus longus and brevis muscles), the superficial posterior compartment
(containing the gastrocnemius, soleus, and plantaris muscles), and the deep posterior
compartment (containing the tibialis posterior and the flexor digitorum longus muscles).
The anterior compartment contains the deep peroneal nerve, anterior tibial artery,
anterior tibialis muscle, extensor digitorum longus muscle, extensor hallucis longus
muscle, and fibularis tertius muscle. Increased pressure in this compartment can lead
to sensory loss in the first interdigital space and weakness during toe and ankle
dorsiflexion.[14]
The lateral compartment has the peroneus longus and brevis muscles, the peroneal artery,
and the superficial peroneal nerve. Compression in this compartment can result in
weakness during foot eversion and reduced sensation in the dorsum of the foot.[14]
The posterior superficial compartment contains the posterior tibial artery, gastrocnemius,
soleus, and plantaris muscles, in addition to the distal segment of the sural nerve.
Its compression can cause numbness on the side of the foot and distal calf.[14]
The deep posterior compartment has the tibialis posterior muscle, flexor digitorum
longus muscles, peroneal artery, and tibial nerve. Increased pressure in this compartment
can lead to weakness in plantar flexion and numbness in the sole.[14] Since most cases occur in the lower limbs, we will not discuss anatomical details
from other regions.
The natural progression of CCS is often atraumatic, although some subjects may report
a history of low-energy trauma. Patients usually experience stiffness, pain, or discomfort
in the anterior and lateral part of the leg after prolonged exercise, and symptoms
frequently improve with rest or activity reduction; this particular detail is a specific
criterion for the disease.[13] The symptoms of CCS are bilateral in up to 95% of patients. At the superficial peroneal
nerve distribution, affected subjects may experience reduced vibratory sensitivity
and decreased motor range, leading to lower foot and ankle control loss described
before.[4] Cramps, hyposensitivity, or muscle weakness are evident in approximately one third
of patients.[13]
Diagnosis
The diagnosis of CCS relies on a detailed history and thorough physical examination.
It is vital to document training frequency, volume, duration, and intensity, along
with any patterns for the onset and resolution of reported symptoms. Although patients
may not experience symptoms at rest, exertion can trigger significant symptoms that
limit activity. The top five symptoms frequently reported by patients with CCS include
pain, tightness, cramping, weakness, and decreased sensation in the dorsum of the
foot.[4]
Recently, Vogels et al.[15] proposed five key criteria for CCS diagnosis. Study panel members agreed that CCS
was likely if the patient (I) participates in activities requiring repetitive activation
of the same muscles, (II) reports pain during exercise, (III) reports stiffness/tightness
during exercise, (IV) stops specific activities earlier or avoids them, and (V) presents
symptoms induced by provocative activities at the physical examination.[15]
During the physical examination, passive compartment stretching may elicit pain if
the patient has recently exercised, although pain is uncommon at rest. Palpation of
the affected area can reveal fascial defects in 39 to 46% of subjects with CCS.[4]
Although there is much ongoing debate, the historical standard for diagnosing CCS
has been intracompartmental pressure measurement. Whitesides et al.[16] pioneered the development of a technique for this measurement in a revolutionary
study using objects such as a syringe, needle, saline solution, and plastic tubes
connected to a manometer. Current intracompartmental pressure monitoring can employ
several commercially available devices inspired by Whitesides' invention.[16] This monitoring allows a comparison between affected and unaffected compartments
in both lower limbs. In the diagnostic process, patients undergo a physical stress
test before and after a series of manometry measurements to analyze trends in intracompartmental
pressures in symptomatic compartments. Typical resting intracompartmental pressure
in the leg is usually lower than 10 mmHg, although measurements can vary considerably
between patients and suffer influence by the operator performing the procedure.[4]
A study by Davis et al.[17] monitored 17 patients with CCS during physical stress tests. Analysis revealed that
these subjects experienced leg pain after, on average, 11 minutes of exertion, rating
the pain as an 8 out of 10 on the Visual Analog Scale. Symptoms subsided after about
45 minutes of rest. Approximately 36% of subjects reported numbness or tingling in
addition to pain after exertion. Objective pressure measurements showed significant
increases in the anterior, lateral, deep posterior, and superficial posterior compartments
following physical stress testing.[4]
Pedowitz et al.[18] established diagnostic criteria to confirm exercise-induced CCS. According to them,
the diagnosis requires meeting the following criteria: 1) preexercise pressure higher
than 15 mmHg; (2) pressure 1 minute after exercise higher than 30 mmHg; or 3) pressure
5 minutes after exercise higher than 20 mmHg.
However, it is worth highlighting that diagnostic cut-off criteria differ substantially
depending on the author,[15] and pressure measurements are not always reliable due to factors such as patient
tolerance, operator technique, and use of different measuring devices. Furthermore,
the invasive nature of the test may be associated with risks of incorrect needle placement,
bruising, and nerve damage.[15]
Aweid et al.[4] reviewed several studies evaluating the usefulness of intracompartmental pressure
measurements for CCS diagnosis. These authors concluded that although pressure measurement
use is widely available, there is limited evidence to validate their accuracy, and
the clinical presentation should be further considered for CCS diagnosis.
Regarding the applicability and diagnostic value of measuring intracompartmental pressure,
it is essential to remember that the clinical history, physical examination, and exclusion
of differential diagnoses are indispensable to the diagnostic process. To overcome
these limitations of the needle technique, new diagnostic protocols have been suggested,
with the recommended systematic use of conventional MRI to exclude differential diagnoses.[19]
Magnetic resonance imaging is the best imaging method for evaluating exercise-related
leg pain, as it detects conditions such as tibial stress syndrome, tibial stress fracture,
neural compressions, muscle and tendon injuries, exercise-related thrombosis, and
fascial hernias.[19]
In clinical practice, conventional MRI sequences initially exclude differential diagnoses.
Subsequently, patients run (or walk) on a treadmill, according to their physical capabilities,
until they can no longer tolerate the activity due to pain. Immediately after stopping
the activity, patients undergo a new MRI for fluid-sensitive and fat-suppressed axial
sequence (T2-weighted/short tau inversion recovery, STIR) acquisition. Some studies
have confirmed the validity of postexercise MRI for CCS diagnosis, using a 1.54-fold
increase in signal intensity as a diagnostic cut-off value with a 96% sensitivity
and 87 to 90% specificity.[19]
Therefore, MRI is a non-invasive method, readily accepted by patients, with good availability
in large medical centers, the best imaging test to rule out differential diagnoses,
and a scientifically validated option for CCS diagnosis.[19]
Treatment
Surgical Treatment
The treatment for CCS comprises several surgical and non-operative management strategies.
Traditionally, surgical treatment has more reports and better outcomes, but there
is increasing evidence that conservative treatment may be an option in selected cases.
In athletes, management consists of surgical intervention. Non-surgical treatment
failure, paresthesia, exertion-induced pain that disappears with rest, tightness,
cramps, ischemia, foot drop, and the patient's desire are the main indications for
surgical treatment.[9]
[20]
In a systematic review of the surgical management of CCS[9] including 1,495 patients from 24 studies, the most used techniques were compartment-specific
open fasciotomy (86%), fasciotomy with partial fasciectomy (12%), and endoscopic fasciotomy
(< 2%). For the anterior compartment, the most commonly affected by CSS, a single
longitudinal incision between the anterior tibial crest and fibula through the skin
and subcutaneous tissue was the most frequent procedure (207 out of 240). However,
the outcomes of this review did not demonstrate a superiority between the techniques
described. Concerning the posterior compartment, the most used surgical technique
was a longitudinal incision slightly medial to the tibial crest with the release of
the solar bridge of the tibia to approach the deep fascia. The success rate of this
intervention was 61% for the deep posterior compartment (44 out of 72) and 100% for
the superficial posterior (3 out of 3). The authors suggested that this compartment
is prone to lower surgical success.
A systematic review including seven articles on surgical intervention in the posterior
compartment found that the techniques differed slightly throughout the studies. However,
the review reached no conclusions since the researchers used different methods for
outcome measurement.[21]
New procedures, such as minimally-invasive or endoscopic procedures, have been gaining
relevance in recent decades. A review by Lohrer et al.[13] concluded the lack of statistical difference between these techniques since the
unweighted average success rate was 86.3% for the endoscopic technique and 80.0% for
the minimally invasive CCS release. D'Amore et al.[22] compared endoscopic procedures and open fasciotomy in elite and amateur athletes
with lower limb CCS. Their results showed that the return to sport rate was 84.6%
in patients undergoing an endoscopic procedure and 72.7% in those undergoing open
fasciotomy, with symptom recurrence rates of 69.2% and 72.7%, respectively, with no
statistical difference. Neither group presented complications or severe outcomes.
The endoscopic technique would have benefits over open fasciotomy, such as lower risk
of infection, shorter time to activity return due to the lower soft-tissue manipulation,
less postoperative hematoma, limited fibrosis, better visualization of compartmental
structures, and fascial release extension.[9]
[22] It is an adequate alternative treatment for CCS release from the anterior and lateral
compartments, with a good success rate and no inferiority in the literature.[22]
Conservative Treatment
Exercise-induced CCS conservative treatment remains poorly documented in scientific
research. Rest, interrupting symptom-triggering activity, and analgesic agents seem
essential. However, few documented guidelines or specific procedures describe how
to optimize them and the population most benefited from those interventions. In a
systematic review of the literature on new non-surgical management, Rajasekaran et
al.[6] found little evidence of techniques, which included gait shifting, chemodenervation,
ultrasound-guided fascia fenestration, and massage.
Nevertheless, a case series by Diebal et al.[23] on different running techniques and how they affect compartment pressure and pain
in CCS patients showed promise, and it was included in a military non-surgical management
program.[23]
[24] This protocol involves several treatments described in the literature, with a greater
focus on walking and running re-education. In one study, these authors reported that,
after a 2-year follow-up in a population of 50 patients undergoing their protocol,
57% were still on active duty without surgery, 43% returned to their original military
post, 36% left military service, 48% remained with symptoms, and 12% of patients underwent
fasciotomy.[24] This study showed moderate outcomes, which could decrease the need for surgical
procedures. Although there is little evidence on the results of gait retraining in
athletes, this research's focus may be an alternative to fasciotomy or an attempt
to prevent it.
In 2022, a clinical consensus panel of experts discussed conservative CCS treatment
and its efficacy. It concluded that gait retraining and cessation of provocative activities
are critical when attempting a non-surgical approach. The literature cites physical
therapy, botulinum injections, and shoe modifications as less significant and mainly
adjacent measures depending on the patient's symptoms.[15]
Conservative versus Surgical Treatment
Conservative versus Surgical Treatment
Although there are no randomized clinical trials to compare surgical and conservative
treatments, some studies reported a superiority of interventional procedures, mainly
in patients with CCS of the anterior compartment and amateur and elite athletes. In
a retrospective cohort, Vogels et al.[25] found that the success rate considered by patients was significantly higher in those
who underwent fasciotomy (42% compared with a 17% success rate in the group undergoing
conservative treatment), and a lower frequency of pain and tightness during sports
was also noted. However, there was no difference between these two groups regarding
the return to the same level of performance before each intervention.
In contrast to these findings, Thein et al.[26] observed significantly better outcomes in returning to sports and maintaining the
same physical activity level per the Tegner score in patients undergoing surgical
treatment. The rate of return to presymptomatic athletic level was 25% in patients
who did not undergo fasciotomy and 77.4% for those who did, with p = 0.001.
It is worth highlighting that none of these studies have the gold standard regarding
the methodological procedure, with several inherent biases in their conduction, and
no standardized conservative treatment, which was mostly performed by physical therapists
or clinicians. However, they corroborate the hypothesis that the surgical procedure
seems to be a better treatment, with higher patient satisfaction, in athletes.[25]
[26]
Final Considerations
Chronic CS is the second most common cause of exertion-induced lower limb pain, followed
by MTSS. Although it is rarely urgent and symptoms are relieved by rest and cessation
of triggering activities, accurate assessment of intracompartmental pressure remains
challenging, and gold-standard treatment is imprecise. Furthermore, the authors suggest
that untreated CCS can lead to neural compression and irreversible damage due to elevated
intracompartmental pressures.
The true prevalence of CCS remains uncertain, but it is estimated to account for approximately
14 to 34% of physical activity-related leg pain. Intense exercise, particularly running,
has been linked to an increased incidence of CCS. However, military personnel are
also usually affected by CCS.
