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Popliteal Artery Entrapment

Masquerading as Asthma

David Wang, MD, MS

THE PHYSICIAN AND SPORTSMEDICINE - VOL 30 - NO. 8 - AUGUST 2002


In Brief: Patients don't always report symptoms that seem unimportant to them. Symptoms that don't respond to routine medical management, or that can't be fully explained by the signs observed, warrant a closer look and further questioning. Although the condition is uncommon, young athletes can develop functional popliteal artery entrapment. Diagnostic studies include examination of dorsalis pedis and posterior tibial pulses, Doppler ultrasonography, and arteriography. Treatment of functional popliteal artery entrapment usually includes surgical exploration, release of the popliteal artery, and a myomectomy of the medial gastrocnemius head.

Family practice physicians often see athletic patients who report activity-related ailments. Although rare, functional popliteal artery entrapment should be part of the differential diagnosis for patients who have exercise-induced lower-leg pain. In the following case, the patient's initial symptom was respiratory, and she did not mention leg fatigue until the second visit. A somewhat rare condition with an atypical presentation could easily have been missed or misdiagnosed. This case underscores the need to ask enough questions, cast a wide net when making a differential diagnosis, and remain open to unusual possibilities if ordinary treatments fail.

Case Report

History. A 20-year-old female collegiate sprinter who had been diagnosed as having exercised-induced asthma came to our sports medicine clinic for treatment of fatigue and increasing shortness of breath with exercise. The patient described difficulty breathing and diminishing athletic performance that added 10 seconds to her 400-m times. She felt she was not responding to recent changes made in her asthma medication by her primary care physician, and she requested further evaluation. Her medications consisted of long- and short-acting beta-agonists, an inhaled corticosteroid, a leukotriene inhibitor, and a nonsedating antihistamine.

The patient reported that her breathing problems were inspiratory and not expiratory. Because this is atypical for asthma, a graded exercise test was performed. When the patient became symptomatic, pulmonary function tests demonstrated a mild expiratory-flow drop consistent with mild asthma. The severity of her symptoms could not be explained by the mild degree of obstruction observed.

When asked about her breathing at a follow-up visit, she stated that the shortness of breath actually began as "tired legs." The athletic training staff was asked to monitor posterior tibial pulses if she became symptomatic during practice; trainers documented the absence of posterior tibial pulses but strong femoral pulses.

Physical exam. Her ankle-to-brachial blood pressure index was normal at rest (1.02) but decreased after 5 minutes of running to 0.79. A duplex scan of her lower extremity was normal. Doppler ultrasonography measurements of the posterior tibial pulse revealed arterial obstruction with resisted ankle plantar flexion. The posterior tibial pulses returned when active plantar flexion was discontinued. A lower-extremity angiogram demonstrated 100% blockage of the popliteal arteries with passive dorsiflexion of the ankle (figure 1).

Diagnosis. The diagnosis was bilateral functional popliteal artery entrapment.

Treatment. The patient underwent surgical exploration of the popliteal space to release the artery so that it would be less likely to become obstructed (figure 2). Through a popliteal approach, the artery appeared normal but was compressed by the gastrocnemius head. Fibrous bands and medial genicular arteries that tethered the popliteal artery were released to increase the mobility of the artery when it is compressed by the medial head of the gastrocnemius muscle. The medial head of the gastrocnemius was not initially divided because the patient wanted to preserve as much athletic function as possible. Postoperative Doppler studies were normal.

Follow-up. After an uncomplicated 3-month postoperative course, the patient was able to resume full activities and return to competitive running. She discontinued all of her asthma medications except prophylactic use of the short-acting beta agonist. Over the next 2 months, she trained at full intensity, and her performance approached her previous premorbid best.

At 5 months postsurgery she developed a "deadness" in her legs and a shorter stride length with hard interval training. Clinically, she no longer had dorsalis pedis and posterior tibial pulses with resisted plantar flexion, indicating a return of the popliteal entrapment syndrome. Ankle-to-brachial index testing postexercise again demonstrated a decline, and Doppler studies again showed decreased flow in the popliteal artery. With the ankle in a neutral position, magnetic resonance imaging (MRI) of the popliteal space did not show any abnormalities except the medial gastrocnemius muscle touching, but not impinging on, the popliteal artery. The patient's symptoms rapidly worsened until she had pain in the calves with normal ambulation and could not walk to class without pain.

Additional treatment. The patient underwent a second procedure to free up any scarring from the first procedure and to release the medial head of the gastrocnemius muscle. The medial head of the gastrocnemius was found to be quite large and touching the artery, even with the ankle in a neutral position. Myomectomy of the medial gastrocnemius head almost immediately relieved the patient's ambulatory pain.

Further follow-up. Within 2 months she was active in martial arts and running 30 minutes without pain. She is still occasionally using the short-acting beta- blocker for very mild asthma before exercising.

Background on Artery Entrapment

Stuart1 first described popliteal artery entrapment in 1879, but it was not until 1959 that Hamming2 diagnosed and surgically treated the condition. Since then, there have been several descriptions3,4 of an aberrant popliteal artery through and around the medial head of the gastrocnemius muscle. In 1985, Rignault et al5 described a symptomatic patient who had normal popliteal spaces. They defined this as functional popliteal entrapment syndrome. A recent literature review6 revealed that functional popliteal entrapment was more common than structural popliteal entrapment caused by anatomic variants.

Reports of popliteal artery entrapment syndrome are more common in athletic men, probably because much of the literature describes military populations. With women becoming more active in competitive sports and reports derived from nonmilitary populations, we may see more women diagnosed with this condition.

Most reports of popliteal artery entrapment occur in younger athletes, possibly because younger people are more often involved in vigorous training that can lead to functional hypertrophy of the gastrocnemius.6 Hypertrophy of the gastrocnemius medial head may contribute to functional entrapment of the popliteal artery because of their proximity. The development of functional popliteal entrapment syndrome may also be multifactorial; a tight or immobile, hypersensitive, or spasmodic popliteal artery may be contribute to entrapment.

Clinical Features

Claudication with pain provoked by some level of work is the most common presenting symptom in 90% of patient reports. Repeated popliteal artery compression causes trauma to the arterial wall, leading to premature localized atherosclerosis. As the pathology progresses, acute ischemia can occur if there is an occlusion of the artery or thrombosis within an aneurysm.7 Symptoms of acute or chronic ischemia, such as paresthesias, discoloration, temperature change, pain at rest, or tissue necrosis, account for the remaining 10% of patient reports. Popliteal entrapment is bilateral in 25% to 43% of patients.7,8

In this patient, shortness of breath was a very unusual symptom of popliteal entrapment, and the symptom of "tired legs," discovered only at the second interview, was attributed to exercise-induced ischemia of the lower leg. While pain often accompanies ischemia, this patient was unable to recall any history of lower-leg pain; perhaps because the tiredness occurred before pain and created a perception that she was exercising at near-maximal capacity. The patient may have perceived the oxygen debt of the lower leg as shortness of breath and attributed it to her asthma. Pain may develop as the condition worsens, as in this case when the patient reported pain with ambulation after the first procedure.

Investigation

Diagnosing popliteal entrapment can be difficult. In a study by Deshpande and Denton,6 5 of 8 patients had been treated with posterior compartment decompression for presumed chronic compartment syndrome before the correct diagnosis was made.

Diagnostic studies are needed if the history or clinical exam suggests popliteal artery entrapment. Initially, blood pressures of the dorsalis pedis and posterior tibial arteries should be obtained with Doppler ultrasonography. Evaluation of ankle pulses with active plantar flexion and passive dorsiflexion can be helpful, because the pulses are significantly diminished or absent in patients who have entrapment. The knee should be at or near full extension to put more stress on the gastrocnemius muscle, which increases the sensitivity of these maneuvers. Pulse disappearance with provocative maneuvers of the ankle can also occur in unaffected, asymptomatic athletes.9

Duplex scanning can also be used and may be quite sensitive and specific for arterial occlusion in elderly patients. Arteriography can confirm positive Doppler or duplex studies.8 Arteriographs often appear normal when the ankle is in a neutral position; therefore, evaluations must be done with the ankle actively plantar flexed.

MRI can distinguish a structural entrapment (caused by an aberrant course of the popliteal artery) from a functional entrapment, but in either case the treatment will be surgical.

Surgical Choices

Several surgical approaches can be used, but the least invasive surgery for functional entrapment is exploration and release of the fibrous bands and arterial branches tethering the artery. After the medial head of the gastrocnemius was surgically divided, 7 of 8 patients in the Deshpande and Denton study6 had complete relief. In this patient, the initial surgery was conservative compared with most procedures described in the literature (ie, divisions of the medial head of the gastrocnemius and release of the artery). Unfortunately, the less invasive procedure provided only short-term relief, and, ultimately, the patient needed a myomectomy of the medial gastrocnemius head.

Other approaches mentioned in literature include plantaris muscle resection and surgical release of the medial soleus from its tibial attachments.10 If arterial damage or occlusion is found, more invasive procedures, such as a saphenous vein bypass, may be needed.

Expecting the Unexpected

This case illustrates a very unusual presentation of a rare condition; however, sports medicine physicians often see patients who are young, very active, and at risk for popliteal entrapment. This condition should be suspected in patients who experience claudication or ischemic symptoms of the lower extremity. In this case, shortness of breath and fatigue were the initial complaints, perhaps representing an earlier phase of the condition. Early identification of popliteal entrapment is important to prevent more severe arterial disease.

References

  1. Stuart TP: Note on a variation in the course of the popliteal artery. J Anat Physiol 1879;13:162-165
  2. Hamming JJ: Intermittent claudication at an early age due to an anomalous course of the popliteal artery. Angiology 1959;10:369-371
  3. Radonic V, Koplic S, Giunio L, et al: Popliteal artery entrapment syndrome: diagnosis and management, with report of three cases. Tex Heart Inst J 2000;27(1):3-13
  4. Takase K, Imakita S, Kuribayashi S, et al: Popliteal artery entrapment syndrome: aberrant origin of gastrocnemius muscle shown by 3D CT. J Comput Assist Tomogr 1997;21(4):523-528
  5. Rignault DP, Pailler JL, Lunel F: The 'functional' popliteal entrapment syndrome. Int Angiol 1985;4(3):341-343
  6. Deshpande A, Denton M: Functional popliteal entrapment syndrome. Aust N Z J Surg 1998;68(9):660-663
  7. Stager A, Clement D: Popliteal artery entrapment syndrome. Sports Med 1999;28(1):61-70
  8. di Marzo L, Cavallaro A, Mingoli A, et al: Popliteal artery entrapment syndrome: the role of early diagnosis and treatment. Surgery 1997;122(1):26-31
  9. Akkersdijk WL, de Ruyter JW, Lapham R, et al: Colour duplex ultrasonographic imaging and provocation of popliteal artery compression. Eur J Vasc Endovasc Surg 1995;10(3):342-345
  10. Turnipseed WD, Pozniak M: Popliteal entrapment as a result of neurovascular compression by the soleus and plantaris muscles. J Vasc Surg 1992;15(2):285-293

Special acknowledgment and thanks to William Omlie, MD, for his expertise in the management of this case.

Dr Wang is an assistant professor in the Department of Family Practice, director of the sports medicine clinic at Boynton Health Service, and a team physician at the University of Minnesota in Minneapolis. Address correspondence to David Wang, MD, MS, Boynton Health Service, 410 Church St, Minneapolis, MN 55455.

Disclosure information: Dr Wang discloses no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.


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