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Don’t Just Blame it on the Veins

An Update on Vascular Exertional Limb Pain

Dyer, Kevin T., MD1; Hogrefe, Christopher P., MD, FACEP1,2,3

Current Sports Medicine Reports: October 2018 - Volume 17 - Issue 10 - p 347–353
doi: 10.1249/JSR.0000000000000527
Sports-Specific Illness and Injury: Section Articles

Exertional limb pain is a common problem encountered in recreational and competitive athletes. Affecting both the upper and lower extremities, this broad entity can be musculoskeletal, vascular, neurologic, oncologic, or infectious in origin. This article focuses on the vascular causes of exercise-related extremity pain, which encompass a cadre of elusive diagnoses. Specifically, we examine arterial endofibrosis, popliteal artery entrapment syndrome, and chronic exertional compartment syndrome of both the upper and lower extremities. For each of these conditions, we offer updates regarding the respective epidemiology, common signs and symptoms, worthwhile diagnostic modalities, and pertinent treatment options, all based on evidence and reports published over the past year.

1Department of Emergency Medicine, Northwestern Medicine, Chicago, IL;

2Department of Medicine-Sports Medicine, Northwestern Medicine, Chicago, IL; and

3Department of Orthopaedic Surgery-Sports Medicine, Northwestern Medicine, Chicago, IL

Address for correspondence: Christopher P. Hogrefe, MD, FACEP, Suite 1300, Lavin Family Pavilion, 259 East Erie, Northwestern Medicine, Chicago, IL 60611; E-mail:

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Exertional limb pain is a common problem encountered in recreational and competitive athletes. This classification of injury can affect both the upper extremities and lower extremities depending upon the type of activity. Exertional arm or hand pain is most commonly seen in motorcycle riders, rowers, kayakers, water skiers, and manual laborers (1). Conversely, exertional leg pain is primarily encountered in runners, soccer players, cyclists, and skaters. Regardless of the location, exertional limb pain can be a disabling condition that often represents a diagnostic challenge due to the associated broad differential (Table 1) and the fact that multiple conditions can coexist in the same athlete (2). While each of these potential etiologies are noteworthy, this article focuses on the vascular causes of exercise-related extremity pain, specifically arterial endofibrosis, popliteal artery entrapment syndrome, and chronic exertional compartment syndrome (CECS) of the upper and lower extremities (1). For each of these conditions, we offer updates regarding the respective epidemiology, common signs and symptoms, worthwhile diagnostic modalities, and pertinent treatment options, all based upon evidence and reports published over the past year.

Table 1

Table 1

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Arterial Endofibrosis

Endofibrosis (EF) is a nonatheromatous, flow-limiting condition that most frequently impacts highly-trained endurance athletes (e.g., cyclists, triathletes, long-distance runners) and is generally only evident during provocative exercise (3,4). The true prevalence of EF is unknown, but it is believed to be underreported with one study citing hemodynamic evidence of endofibrosis in 10% to 20% of elite athletes (5). Endofibrosis symptoms occur only at near-maximal exercise and are typically unilateral. Interestingly, the condition is most common in the left external iliac artery; however, the disease can extend to the common iliac, common femoral, and profunda femoris arteries as well (3,4). Patients endorse muscle cramps followed by the feeling of swelling, numbness, or pain in the calf, thigh, or gluteal region of the affected side (5). Clinical examination findings are usually sparse, but one may identify diminished distal pulses or a femoral bruit with hip flexion or extension (5). Imaging of the iliac arteries in these patients can be vexing, as lesions are often dismissed as normal or insignificant (6). One also should consider that not all endofibrosis is symptomatic. Furthermore, the hemodynamic effects of minor degrees of stenosis are usually only identified with elevated blood flow rates under an intense exercise load. As such, measuring the ankle-brachial pressure index (ABPI) within 1 min of exercise cessation can be a valuable diagnostic tool (6).

In addition to ABPI, D’Abate et al. have proposed a Color Doppler Ultrasound (CDU) algorithm capable of detecting EF (Fig. 1) (6). In evaluating 37 athletes referred to them for suspected EF, they performed preexercise and postexercise CDU on the iliac arteries. A total of 24 athletes (29 limbs) were diagnosed with EF. Abnormal waveforms of the stenotic/damped type were present after exercise in the iliac arteries of all 29 limbs. The waveform changes were accompanied by high peak-systolic velocity (>350 cm·s−1) and end-diastolic velocity (>150 cm·s−1). Fifteen patients underwent further imaging with digital subtraction angiography (DSA), computed tomography angiography (CTA), or magnetic resonance angiography (MRA). Of these only eight had findings consistent with EF on imaging, but all 15 had EF confirmed on postoperative histology (6). The authors conclude that CDU is a valuable tool in the evaluation and subsequent diagnosis of patients with suspected iliac EF.

Figure 1

Figure 1

This sentiment was echoed by Peake et al. (7) who discussed their experience with 46 patients (50 limbs) over a 7-yr period, serving as one of the largest case series investing EF. They discuss the evolution of the diagnosis and management of patients with EF, asserting that ABPI and ultrasound (US) are sufficiently sensitive to diagnose EF based upon their experience. The authors opine that cross-sectional imaging yields little value in the diagnosis and instead should be reserved for cases in which there is a diagnostic uncertainty, the proximal extent of disease cannot be visualized on US, or when planning for an intervention (e.g., surgery). The authors recommend a bilateral extremity evaluation regardless of the laterality of symptoms as several of their patients had a degree of asymptomatic disease. Additionally, they recommend a duplex assessment up through the profunda femoris arteries in addition to the external iliac arteries since early identification of increased intima-media thickness (>0.9 mm) and flow limitations can help guide a vascular surgeon regarding the extent of a potential endarterectomy. On that note, surgery remains the primary treatment modality for EF, with an endarterectomy with patch angioplasty commonly pursued. Peake and colleagues report that this approach resulted in a significant portion (85%) of their patients becoming symptom-free and returning to their previous level of competition (5,7). Conversely, angioplasty and stenting have not been shown to be effective, long-term treatment options for EF. The former management strategy did show some short-term functional improvement. However, within 8 wk all of the patients in two particular studies suffered a recurrence of symptoms (8,9). Regarding arterial stenting, the mechanical forces associated with AF may lead to stent migration or fracture. This intervention also may result in intimal hyperplasia (10). For these reasons and due to sparse case reports detailing success with this management approach, stenting for AF is not deemed to be a suitable treatment option.

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Popliteal Artery Entrapment Syndrome

First described in 1879 and officially named in 1965, popliteal artery entrapment syndrome (PAES) is a relatively rare diagnostic conundrum, which is an oft-missed cause of exertional leg pain (11–13). Clinical studies report an incidence of 0.17%, while post mortem studies suggest an incidence of 3.5% (14). Patients with this condition are typically young (early 30s), lack vascular risk factors, and have symptoms that significantly overlap with other causes of exertional leg pain. These factors can combine to lead to an initial misdiagnosis and/or failed interventions (14,15). Further complicating the workup of PAES is the anatomic variation of the condition (Table 2) (16). The site of entrapment can occur in several different locations, may prove to be solely function, or PAES may even involve the popliteal vein rather than the popliteal artery.

Table 2

Table 2

Though a diagnostic challenge, some features of the clinical course can help identify PAES. We recommend an increased suspicion for this condition in patients with leg claudication who present with prolonged symptoms and a lack of therapeutic success (e.g., physical therapy). Corneloup et al. (13) found the mean duration from symptom onset to diagnosis was 34 months, with a range of 3 to 180 months. Although there is no “typical” patient who suffers from PAES, the overwhelming majority of patients (83%) are men in their early 30s (range of 17–52) (13). It is important to note that this male predominance makes an already tough diagnosis even more challenging in the female patient. Otherwise, PAES presents unilaterally 60% of the time. Lastly, in one study this entity possessed an 86% overlap with CECS when intracompartmental pressures (ICP) were measured (13).

Further confounding the identification of PAES, there are no truly diagnostic physical examination findings to aid in this pursuit. However, several maneuvers can prove to be useful. A case report by Wady et al. discussed a 30-year-old female with type IV PAES who had an absent popliteal pulse with weak posterior tibial (PT) and dorsalis pedis (DP) pulses (13). However, as discussed by Hameed, these findings are not 100% sensitive since the abnormal relationship between the gastrocnemius and popliteal artery may only be clinically evident with contraction of the gastrocnemius. Therefore, they recommend assessing the PT and DP pulses and ankle-brachial indices with resisted plantar flexion as this may lead to compression of the vessel by the musculature (15).

Just as there is no pathognomonic physical examination finding for PAES, there is no clear consensus on the best diagnostic approach or imaging study. Measuring the ABPI with resisted plantarflexion is an inexpensive and relatively simple first study to use as an adjunct to a thorough physical examination. Gaunder et al. noted that a drop of 30% to 50% should further raise one’s suspicion for PAES (17). If this result is concerning, a reasonable next step is vascular ultrasound given that it is relatively cost-effective and noninvasive. The patient discussed in Wady’s case report lacked a definitive popliteal artery, although the presence of collaterals was noted. These findings are highly suggestive of the presence of PAES (14). Corneloup et al. (13) make a rather strong recommendation for ultrasound as the first-line imaging modality as well. They found that CDU was 76% specific when using complete occlusion of the popliteal artery as a positive test. Unfortunately, the sensitivity (SN) was not calculated in this study, and thus it is unknown if an inability to totally occlude the popliteal artery on a CDU sufficiently rules out PAES.

Additional modalities for diagnosing PAES include MRA and CTA. Some authors advocate for MRA since it can assess the vasculature, surrounding structures, and degree of pathology. It also can rule out other diagnoses and assist with preoperative planning (14). Though more costly, it avoids ionizing radiation, a noteworthy advantage given the typical young age of patients with PAES. Other authors prefer CTA because patients are frequently unable to maintain resisted plantarflexion adequately during the long MRA acquisition times. This technical difficulty can lead to motion artifact, thereby degrading image quality and diagnostic accuracy (13,14,18). Overall, it appears that CTA remains the most common diagnostic modality currently employed in the evaluation of PAES, frequently enhanced with provocative maneuvers during the procurement of such imaging (15).

Recent publications discussing the novel uses of different imaging modalities appear promising and may change the manner in which PAES is evaluated. Thakor et al. (19) employed the use of Steady State MRA with a blood pool agent. This agent binds to albumin and remains in circulation, thereby enabling repeated imaging and provocative testing. Their protocol employed a rapid image sequence acquisition with a 24-s duration, which permitted the patient to carry out provocative maneuvers without causing fatigue or motion artifact. Another potential alternative imaging modality has been proposed by Boniakowski (18), who presented a case report of a patient with signs and symptoms suggestive of PAES yet nondiagnostic CTA and MRA imaging. A DSA with provocative maneuvers was remarkable for an occlusion of a long segment of popliteal artery. However, this imaging modality was unable to identify the specific area of compression. Using intravascular ultrasound (IVUS), the authors successfully identified the site of compression and adequately evaluated the vessel wall, providing valuable information regarding the need for arterial bypass. They proceed to recommend the use of IVUS as a staged procedure in conjunction with DSA during the preoperative evaluation of potential PAES.

With regard to management, a couple of articles published over the past year discussed the use of botulinum toxin A (BTX-A) as a means of nonoperative treatment for functional PAES (Type VI). Hislop et al. conducted a prospective trial with 33 total patients, six undergoing operative management and 27 opting for a local injection of BTX-A (20). All of the participants were reevaluated at 6 and 12 months, and those in the BTX-A cohort were offered additional injections at those subsequent visits. Symptoms were rated on a five-point Likert scale with responses including significantly better, better, no difference, worse, and significantly worse. A “good” outcome was defined as significantly better or better at both 6 and 12 months. A “mixed” outcome entailed improvement at 6 months but no difference at 12 months. And lastly, a “poor” outcome was defined as no change overall or worsening of symptoms at any point. At 12 months, four of the surgical patients reported significantly better symptoms and the other two reported no change. In the BTX-A group, 59% had a “good” outcome, and the other 41% had a “mixed” outcome. None of the patients reported worsening of their symptoms. Also, those who received an additional injection at 6 months were more likely to report a “good” outcome. Lastly, an additional finding the authors highlighted was that the success rate of a BTX-A injection was inversely correlated with the amount of plantarflexion force required to occlude the affected vessel (20).

In a separate publication, Murphy discussed the use of BTX-A in an elite male athlete with functional PAES who received this intervention prior to his 2016 season (21). He experienced a decrease in strength and performance at 1 wk postinjection (measured by single leg hop distance, eccentric ankle plantarflexion work, and peak torque), but he did return to baseline levels at a 4-wk follow-up visit. Furthermore, an US at the 4-wk evaluation suggested medial gastrocnemius denervation and atrophy with increased arterial diameter and decreased arterial flow velocity. With that said, a post-season analysis revealed that his distance sprinted per game had significantly increased (21). While both of the aforementioned recent publications have their limitations, they suggest that BTX-A may be an effective, minimally invasive treatment for functional PAES. However, as Murphy points out, this treatment should be properly timed due to the potential transient decrease in performance.

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Lower-Extremity CECS

Chronic exertional compartment syndrome was first described by Mavor in 1956 when he detailed the case of a professional soccer player who experienced recurrent anterior leg pain and muscle herniation (22). The athlete was subsequently treated with a fasciotomy and fascia lata graft, which resulted in resolution of his symptoms and a return to his previous high level of function.

With regard to the epidemiology of this condition, CECS has long been thought to be a disease of younger males involved in either sports or the military. However, this assertion has been questioned recently due to bias in earlier studies. de Bruijn et al. (23) conducted a large study of patients looking to identify factors predictive of CECS. They determined that the diagnosis of CECS was more likely in males with bilateral symptoms (74%). Interestingly, they found the mean age for CECS to be 25 years, but there was an increased prevalence at age 50 years as well. This was discussed further in another study from de Bruijn in which one out of seven patients diagnosed with CECS was older than 50 years (24). In addition to age and sex, they also reproduced other studies illustrating an increased likelihood with specific activities, particularly running and skating. The authors created a nomogram (Fig. 2) that can be used to approximate risk and guide additional, more invasive testing (23). While not a standalone diagnostic tool, it is worthwhile to review this nomogram since it details the factors that may positively correlate with CECS. Otherwise, patients themselves may report leg pain that occurs after a specific volume or duration (especially after a change in training). This pain is often described as a pressure, fullness, burning, or cramp-like sensation. The astute physician should recall that CECS pain abates with decreased intensity or cessation of the activity.

Figure 2

Figure 2

Much like PAES, CECS is a challenging diagnosis, one with no consensus regarding the diagnostic criteria. The most widely utilized and accepted means of diagnosing CECS is via ICP measurement at rest and again at both 1 min and 5 min postexercise (2,25,26). Pedowitz and colleagues (27) have provided the criterion most often utilized to make the diagnosis of CECS. If any one of the following three criteria are achieved CECS should be suspected: preexercise pressure ≥ 15 mm Hg, 1 min postexercise pressure ≥ 30 mg, or 5 min postexercise pressure ≥ 20 mm Hg. It is worth noting that others have subsequently suggested that slightly modifying Pedowitz’s criterion (i.e., to ≥14 mm Hg, ≥ 35 mm Hg, and ≥ 23 mm Hg, respectively) would significantly improve the SN and specificity (SP) of ICP testing when assessing for CECS (28).

It is worth mentioning that there also are other modalities that have been described when evaluating possible cases of CECS. These tests include MRI, infrared spectroscopy, ultrasound imaging, and Thallium 201 chloride scintigraphy with SPECT scanning. However, these assessments appear insufficient for reaching a definitive diagnosis, and further evidence is needed before they are routinely implemented in the clinical setting (2,26).

Surgical and nonsurgical options for the treatment of CECS exist, and reports of novel nonsurgical methods have been published of late. Collins et al. presented a case in which a 34-year-old male triathlete with CECS was treated with a comprehensive approach to Functional Manual Therapy (FMT) (26). This patient underwent 23 sessions over the course of three and a half months, returning to pain-free running and training at the conclusion of this treatment regimen. ICP was measured at 4 months post-therapy and found to be within the normal range at rest (<15 mm Hg) and 1 min postexercise (<30 mm Hg). Six months following the aforementioned treatment he completed an Olympic Triathlon without pain, and at 3 years posttreatment the patient was pain-free at rest and with low-impact activity. With that said, he did report a 2/10 pain with high-impact exercise, although it did not necessitate modification of his activity (26). While “only” a case report involving a single patient, it suggests that CECS may be treated adequately with FMT and result in a sustained positive outcome.

Baria et al. (29) reported a case highlighting their experience with onabotulinum toxin A (oBTX-A) as a surgical alternative for CECS. Their patient was a 20-yr-old recreational runner who was diagnosed with CECS in her left lower leg both by ICP measurement and US. She was treated with proximal and distal injections of 20 units of oBTX-A into the tibialis anterior, extensor hallucis longus, extensor digitorum longus, fibularis longus, and fibularis brevis. The patient experienced improvement of her pain within 1 wk and continued to endorse symptomatic improvement at a 14-month follow-up visit. Furthermore, she denied any subjective weakness or other adverse effects (29). This case report suggests that oBTX-A may be a viable potential treatment in certain contexts. However, with a relative lack of data pertaining to this intervention, the ideal patient selection criteria and optimal treatment protocol remain a mystery. Future studies assessing these aspects of oBTX-A may provide evidence to justify it as another low-risk treatment option for patients with CECS.

Another nonsurgical option for the treatment of CECS involves gait modification. Forefoot running in particular has shown promise in this regard. Diebal et al. (30) showed that this particular running technique was effective in treating anterior compartment CECS, both in decreasing the number of symptoms in addition to reducing the severity of symptoms. These patients were able to avoid a surgical intervention (31). Based on this work and others, it is reasonable to pursue gait re-training as a means to effectively treat CECS.

Despite the aforementioned discussion, surgery is still considered the definitive treatment for CECS. However, a 6% to 11% recurrence rate has previously been cited, and a recent case series by van Zantvoort et al. (32) identified a recurrence rate as high as 26% (28). Surgical treatment entails an open or endoscopic fasciotomy (with or without fasciectomy) and resection of any fascial bands (2). While most surgeries are performed using a double incision technique, an alternative approach with a single minimal incision fasciotomy also has been described. Drexler et al. (33) published a retrospective case series in which 54 patients (95 legs) were followed for 4.6 to 97.5 months (mean, 50.1 months) after a single minimal incision fasciotomy of the anterior compartment (63.2%), lateral compartment (31.5%), or lateral and peroneal compartments (2.1%). Of this cohort, 8.4% of the legs experienced a recurrence of symptoms, and 4.2% of legs experienced nerve injury. These rates are in line with those reported from previous studies using the same approach as well as studies implementing the more traditional techniques. While this single minimal incision fasciotomy method is not novel, the case series from van Zantvoort and colleagues suggests that it does not seem to be inferior and that future rigorous studies should be conducted.

While most cases of lower-extremity CECS involve the anterior and lateral compartments, Lui (34) and Lavery et al. (35) described their surgical approaches to the posterior compartment in two separate articles. Lui (34) used an endoscopic approach to a fasciotomy of the superficial and deep posterior compartments in which the operative field is away from the saphenous vein and nerve, which are the two structures most commonly injured during a posterior compartment fasciotomy. Lavery et al. (35) used a mini-open technique to optimize visualization and limit iatrogenic injury. Although these articles involve only a single patient each and neither comment on the long-term outcomes, we include them to raise awareness of newly described approaches to the treatment of posterior compartment CECS.

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Upper-Extremity CECS

Although significantly rarer, CECS also can occur in the upper extremity as well. Specifically, this entity has been described in the forearm and hand. Common offending activities include rowing, kayaking, weightlifting, water skiing, motocross, and softball. Additionally CECS has been described in manual laborers and military soldiers (1,36).

Similar to its lower-extremity counterpart, there is no consensus on the diagnostic approach; the diagnosis is usually made based on historical features and ICP measurements. Clinical signs and symptoms suggestive of upper extremity CECS include: hard and painful volar forearm muscles, decreased ability to extend the fingers or wrist, pain with passive extension of the fingers, and cramping of finger flexor and wrist muscles (37). These symptoms usually resolve within 15 to 30 min of concluding the offending activity and quickly recur when activity resumes. A complicating factor in the evaluation for this condition is that the symptom-inciting activity can be tough to replicate in the office. Consequently, Humpherys et al. (37) recommend the use of repetitive forearm muscle contractions by rolling a weight attached to a stick or hanging by both arms to reproduce the symptoms.

As mentioned above, ICP measurement is a cornerstone in making the diagnosis of CECS. Despite this fact, there is no agreed upon set of criteria for upper extremity CECS. The Whitesides and Heckman criteria are commonly utilized for this purpose. With these guidelines, the diagnosis of CECS is made if the ICP is >30 mm Hg at 5 min after exercise and/or if there is a > 30 mm Hg difference between measured ICP and the diastolic blood pressure 5 min postexercise (accompanied by a history that is typical for the condition) (37). While these criteria are accepted, it is important to note that they are not 100% sensitive. This fact was reiterated by Cole et al. (36) who published a detailed case report on a 21-year-old female who suffered from forearm CECS secondary to softball participation. The authors comment that her forearm ICP never exceeded 30 mm Hg. From this experience they recommend an approach featuring three components: clinical history and physical examination, ICP measurements, and preexercise and postexercise MRI.

A new diagnostic variable proposed in the evaluation of CECS is “TRest,” which is defined as the recovery time between the maximum ICP and a return to resting compartment pressure. This was initially analyzed in 124 male athletes with a diagnosis of CECS, comparing the SN, SP, positive predictive value (PPV), and negative predictive value (NPV) of TRest to the standard ICP diagnostic criteria (1). If the ICP remained >10 mm Hg for more than 14.5 min, TRest was found to be superior across the board in each assessment (SN = 100% vs 73.5%; SP = 94.7% vs 84.2%; PPV = 99.3% vs 97%; NPV = 100% vs 31.4%) (38). This study suggests that TRest may be a useful component in the diagnosis of forearm CECS. Further studies should be considered to validate this variable, potentially looking to evaluate its applicability in patients suspect to have lower-extremity CECS as well.

Upper-extremity CECS treatment options include both nonsurgical and surgical options. For motorcycle riders, Humpherys recommends a 3-month trial of two distinct types of therapies: “bike setup therapies” and “patient-based therapies.” Bike setup therapies focus on grip modifications that can decrease muscle force, in turn limiting tissue swelling and ICP. Meanwhile, patient-based therapies work on increasing core and leg strength (37). If these therapies fail, a surgical intervention with fascial release is advised. Miller et al. (39) describe an endoscopic approach performed on two patients, both of whom resumed motocross riding 1 wk after surgery. The first patient was reportedly symptom free at 3 years, but unfortunately no follow-up information was provided for the second patient.

CECS of the hand also has been reported in approximately a dozen cases. Anatomically, the hand consists of ten compartments: four dorsal interossei, three palmar interossei, hypothenar, thenar, and adductor pollicis compartments. Of the case reports available, the first dorsal interosseous compartment is involved in about 90% of cases with 78% possessing isolated first dorsal interosseous compartment involvement (40). These patients are likely to be manual laborers (e.g., carpenters, mechanics) and present with chronic activity-induced pain. Additionally, they may exhibit significant hypertrophy of the muscles in the affected compartment (41).

Treatment for CECS of the upper extremity has traditionally entailed a release of the affected compartment. But a recent case report describing the use of incobotulinum toxin A (IBTX-A) suggests that this may be a viable alternative to surgery. Orta et al. (41) treated a patient with hand pain located along both the first dorsal and ventral space between the thumb and index finger. The authors injected 10 units of IBTX-A into the first dorsal interosseous muscle and adductor pollici. The patient experienced a subjective loss of strength starting the day following the injection and noted difficulties with writing for 10 d. These symptoms eventually resolved; he endorsed full strength without any symptoms 15 months postinjection. This method appears to show some promise, yet much like the use of BTX-A for lower-extremity CECS future studies investigating the ideal patient selection criteria and optimal treatment protocol should be investigated.

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Exertional limb pain is a relatively common and often significantly painful condition that affects athletes of all skill levels. The vascular causes of exertional limb pain can be particularly elusive to pinpoint since there is frequently symptom overlap with other etiologies. This fact is compounded by the absence of standardized diagnostic criteria. While numerous different entities fall under the vascular category of exertional limb pain, there have been noteworthy developments with regard to the diagnosis and treatment of arterial endofibrosis, popliteal artery entrapment syndrome, and CECS of both the upper and lower extremities. However, confirming these diagnoses still remains a complicated clinical endeavor. Further work lies ahead aimed at refining both the evaluation and treatment of vascular exertional limb pain.

The authors declare no conflict of interest and do not have any financial disclosures.

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1. Harrison JW, Thomas P, Aster A, et al. Chronic exertional compartment syndrome of the forearm in elite rowers: a technique for mini-open fasciotomy and a report of six cases. Hand (NY). 2013; 8:450–3.
2. Hogrefe CP, Terry MA. Chronic exertional compartment syndrome. In: Miller M, Thompson S, editors DeLee and Drez’s Orthopaedic Sports Medicine: Principles and Practice. 5th ed. Philadelphia (PA): Saunders. In print.
3. Peach G, Schep G, Palfreeman R, et al. Endofibrosis and kinking of the iliac arteries in athletes: a systematic review. Eur. J. Vasc. Endovasc. Surg. 2012; 43:208–17.
4. Feugier P, Chevalier JM. Endofibrosis of the iliac arteries: an underestimated problem. Acta Chir. Belg. 2004; 104:635–40.
5. Veraldi GF, Macri M, Criscenti P, et al. Arterial endofibrosis in professional cyclists. G. Chir. 2015; 36:267–71.
6. D’Abate F, Paraskevas KI, Oates C, et al. Color Doppler ultrasound imaging in the assessment of iliac endofibrosis. Angiology. 2017; 68:225–32.
7. Peake LK, D’Abate F, Farrah J, et al. The investigation and management of iliac artery endofibrosis: lessons learned from a case series. Eur. J. Vasc. Endovasc. Surg. 2018; 55:577–83.
8. Giannoukas AD, Berczi V, Anoop U, et al. Endofibrosis of iliac arteries in high-performance athletes: diagnostic approach and minimally invasive endovascular treatment. Cardiovasc. Intervent. Radiol. 2006; 29:866–9.
9. Wijesinghe LD, Coughlin PA, Robertson I, et al. Cyclist’s iliac syndrome: temporary relief by balloon angioplasty. Br. J. Sports Med. 2001; 35:70–1.
10. Schep G, Bender M, van de Tempel G, et al. Detection and treatment of claudication due to functional iliac obstruction in top endurance athletes: a prospective study. Lancet. 2002; 359:466–73.
11. Stuart TP. Note on a variation in the course of the popliteal artery. J. Anat. Physiol. 1879; 13(Pt 2):162.
12. Love JW, Whelan TJ. Popliteal artery entrapment syndrome. Am. J. Surg. 1965; 109:620–4.
13. Corneloup L, Labanère C, Chevalier L, et al. Presentation, diagnosis, and management of popliteal artery entrapment syndrome: 11 years of experience with 61 legs. Scand. J. Med. Sci. Sports 2018; 28:517–23.
14. Wady H, Badar Z, Farooq Z, et al. Avoiding the trap of misdiagnosis: valuable teaching points derived from a case of longstanding popliteal artery entrapment syndrome. Case Rep. Med. 2018; 2018:3214561.
15. Hameed M, Coupland A, Davies AH. Popliteal artery entrapment syndrome: an approach to diagnosis and management. Br. J. Sports Med. 2018; 52:1073–4 [Epub ahead of print].
16. di Marzo L, Cavallaro A. Popliteal vascular entrapment. World J. Surg. 2005; 29(Suppl. 1):S43–5.
17. Gaunder C, McKinney B, Rivera J. Popliteal artery entrapment or chronic exertional compartment syndrome? Case Rep. Med. 2017; 2017:6981047.
18. Boniakowski AE, Davis F, Campbell D, et al. Intravascular ultrasound as a novel tool for the diagnosis and targeted treatment of functional popliteal artery entrapment syndrome. J. Vasc. Surg. Case. Innov. Tech. 2017; 3:74–8.
19. Thakor AS, Chung J, Patel P, et al. Use of blood pool agents with steady-state MRI to assess the vascular system. J. Magn. Reson. Imaging. 2017; 45:1559–72.
20. Hislop M, Brideaux A, Dhupelia S. Functional popliteal artery entrapment syndrome: use of ultrasound guided Botox injection as a non-surgical treatment option. Skeletal Radiol. 2017; 46:1241–8.
21. Murphy M, Charlesworth J, Koh E. The effects of Botulinum toxin injection in an elite sportsman with functional popliteal artery entrapment syndrome: a case report. Phys. Ther. Sport. 2017; 27:7–11.
22. Mavor GE. The anterior tibial syndrome. J. Bone. Joint. Surg. Br. 1956; 38-B:513–7.
23. de Bruijn JA, van Zantvoort APM, van Klaveren D, et al. Factors predicting lower leg chronic exertional compartment syndrome in a large population. Int. J. Sports Med. 2018; 39:58–66.
24. de Bruijn JA, van Zantvoort APM, Winkes MB, et al. Lower leg chronic exertional compartment syndrome in patients 50 years of age and older. Orthop. J. Sports Med. 2018; 6:2325967118757179.
25. Liu B, Barrazueta G, Ruchelsman DE. Chronic exertional compartment syndrome in athletes. J. Hand. Surg. Am. 2017; 42:917–23.
26. Collins CK, Gilden B. A non-operative approach to the management of chronic exertional compartment syndrome in a triathlete: a case report. Int. J. Sports Phys. Ther. 2016; 11:1160–76.
27. Pedowitz RA, Hargens AR, Mubarak SJ, Gershuni DH. Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am. J. Sports Med. 1990; 18:35–40.
28. Roberts AJ, Krishnasamy P, Quayle JM, et al. Outcomes of surgery for chronic exertional compartment syndrome in a military population. J. R. Army Med. Corps. 2015; 161:42–5.
29. Baria MR, Sellon JL. Botulinum toxin for chronic exertional compartment syndrome: a case report with 14 month follow-up. Clin. J. Sport Med. 2016; 26:e111–3.
30. Diebal AR, Gregory R, Alitz C, Gerber JP. Effects of forefoot running on chronic exertional compartment syndrome: a case series. Int. J. Sports Phys. Ther. 2011; 6:312–21.
31. Diebal AR, Gregory R, Alitz C, Gerber JP. Forefoot running improves pain and disability associated with chronic exertional compartment syndrome. Am. J. Sports Med. 2012; 40:1060–7.
32. van Zantvoort APM, de Bruijn JA, Winkes MB, et al. Role of repeat muscle compartment pressure measurements in chronic exertional compartment syndrome of the lower leg. Orthop. J. Sports Med. 2017; 5:2325967117711121.
33. Drexler M, Rutenberg TF, Rozen N, et al. Single minimal incision fasciotomy for the treatment of chronic exertional compartment syndrome: outcomes and complications. Arch. Orthop. Trauma. Surg. 2017; 137:73–9.
34. Lui TH. Endoscopic fasciotomy of the superficial and deep posterior compartments of the leg. Arthrosc Tech. 2017; 6:e711–5.
35. Lavery KP, Bernazzani M, McHale K, et al. Mini-open posterior compartment release for chronic exertional compartment syndrome of the leg. Arthrosc Tech. 2017; 6:e649–53.
36. Cole A, Hiatt JL, Arnold C, et al. Chronic exertional compartment syndrome in the forearm of a collegiate softball pitcher. Sports Med. Open. 2017; 3:11.
37. Humpherys J, Lum Z, Cohen J. Diagnosis and treatment of chronic exertional compartment syndrome of the forearm in motocross riders. JBJS Rev. 2018; 6:e3.
38. Barrera-Ochoa S, Correa-Vazquez E, Gallardo-Calero I, et al. TRest as a new diagnostic variable for chronic exertional compartment syndrome of the forearm: a prospective cohort analysis of 124 athletes. Clin. J. Sport Med. 2017; [Epub ahead of print].
39. Miller EA, Cobb AL, Cobb TK. Endoscopic fascia release for forearm chronic Exertional compartment syndrome: case report and surgical technique. Hand (NY) 2017; 12:NP58–61.
40. Dwyer CL, Soong MC, Kasparyan NG. Chronic exertional compartment syndrome of the hand: case report and literature review. Hand. 2017; 12:NP43–5.
41. Orta C, Petit J, Gremeaux V. Chronic exertional compartment syndrome in hands successfully treated with botulinum toxin-a: a case. Ann. Phys. Rehabil. Med. 2018; 61:183–5 [Epub ahead of print].
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