Popliteal artery entrapment: An evolving syndrome

Transcription

1 Popliteal artery entrapment: An evolving syndrome Paul Steven Collins, MD, FACS, Maj, MC, USA, Paul T. McDonald, MD, FACS, Col, MC (Ret), and Robert C. Lim, MD, FACS, Col, MC~ (USAR), San Francisco and Oakland, Calif. Popliteal artery entrapment can result in daudication and limb-threatening ischemia in the young adult. The purpose of this study was to evaluate prospectively those patients with popliteal artery entrapment. To define the syndrome, the methods used in diagnosis and the type of anatomic anomaly were established for each patient. From 1977 to 1988, 12 patients were found to have popliteal artery entrapment. The average age was 27 years, with all but three patients under age 40 years. All patients complained of calf claudication, and one had acute ischemia. The ankle pulses decreased with maneuvers in 10 patients; four patients had a resting ankle/brachial index less than one. All had diminished ankle/brachial indexes when a treadmill test was performed at 4.2 mph, 10% grade, for 10 minutes. All patients had biplanar arteriography with passive dorsiltexion and active plantar flexion. All results showed abnormal extrinsic compression or occlusion of the popliteal artery. Twenty limbs were affected; eight of 12 patients (67%) had bilateral entrapment. Type IV (37%) lesions were the most common, with type II (32%) and type III (26%) following dosely. One (5%) type I lesion and no type V lesions were found. This is the largest single series of patients with popliteal entrapment in the United States. A treadmill test followed by biplanar arteriography established the diagnosis in all patients. Bilateral involvement was twice that reported in previous studies. Popliteal artery entrapment should be considered in the young adult with claudication and may be seen with greater frequency in an increasingly active population. (J Vase SURG 1989;10: ) Intermittent claudication of the lower extremities in patients with no overt signs or symptoms of atherosclerotic peripheral vascular disease may reflect entrapment of the popliteal artery. A large number of cases of popliteal entrapment have been reported from military medical centers, and attention has been focused on this syndrome as a cause of calf and foot daudication in the otherwise healthy, young, military recruit. Entrapment of the popliteal artery may occur as a result of either a congenital muscular anomaly or an abnormal course of the popliteal artery in the popliteal fossa. This anomalous relationship between From the Uniformed Services University of the Health Sciences, San Francisco, (Dr. Collins), Oakland (Dr. McDonald), and the University of California, San Francisco, (Dr. Lim). Presented at the fourth Annual Meeting of the Western Vascular Society, Kauai, Hawaii, Jan , The opinions or assertions contained herein are the private ones of the authors and are not to be construed as official or as reflecting the views of the Department of Defense, Department of the Army, or the Uniformed Services University of the Health Sciences. Reprint requests: Paul Steven Collins, MD, MaJ, MC, USA, Box 156, Presidio of San Francisco, CA /6/14964 the popliteal artery and other musculotendinous elements in the popliteal fossa was first described by Stuart in 1879 ~ and later by Chambardel-Dubreuil in The first case diagnosed and surgically treated was by Hamming in 1959, 3 and the term popliteal entrapment syndrome was first used by Love and Whelan 4 to describe two cases from Waker Reed General Hospital in Contributions from military surgeons continued with a description by Rich and Hughes s in 1967 of both popliteal artery and vein entrapment by the medial head of the gastrocnemius muscle. As reports of varying congenital anomalies affecting the popliteal artery appeared in the literature, various classification systems arose. In 1970 Insua ct al.6 defined two types of popliteal entrapment, with type I an anomalous course of the popliteal artery and type II an abnormal inscrtion of the medial head of the gastrocnemius muscle. This classification was subsequently modified and added to by Delaney and Gonzalez r and also by Ferrero et al.8 to the greatest extent when he defined 10 types of popliteal entrapment. The classification used in this series was that es- 484

2 Volume 10 Number 5 November 1989 Popliteal artery entrapment 485 Fig. 1. Selective left leg arteriogram with leg in active plantar flexion. Arrow marks compression of popliteal artery. Fig. 2. Biplanar arteriogram (lateral view) of left leg in active plantar flexion.arr0w marks compression of the popfiteal artery. tablished by Love and Whelan 4 and modified by Rich et al. 9 in 1979 when they described 14 limbs with popliteal entrapment. Type I is defined as an aberrant medial course of the popliteal artery around the normally placed medial head of the gastrocnemius muscle. Type II is an abnormal lateral attachment of the medial head of the gastrocnemius muscle, which covers a minimally displaced popliteal artery. Type III occurs when an accessory slip or head of the medial gastrocnemius muscle arises more laterally on the head of the femur. Type IV describes entrapment of the popliteal artery by fibrous bands or the popliteal muscle. The popliteal artery may or may not pass medial to the medial head of the gastrocnemius muscle. Finally, type V describes entrapment of both the artery and vein by any of the mechanisms above. In this series patients were evaluated with preestablished noninvasive and arteriographic criteria to establish the diagnosis ofpopliteal artery entrapment. The type of popliteal entrapment was defined at operation. The methods used in diagnosis and the types of anatomic anomalies are presented to define the syndrome of entrapment of the popliteal artery. METHOD All patients had examination performed by Doppler ultrasonography of the posterior tibial artery and dorsal artery of the foot at the ankle. An antde/brachial index (ABI) was then established for each patient) Those patients with ABIs less than one were considered to have fixed arterial occlusive lesions. In those patients with normal ABIs, exercise treadmill testing was then performed as described by McDonald et al.n Initially a 3-minute treadmill test at 3 mph with 0% grade was performed. The ABIs were then again measured, and if less than one with

3 486 Collins, McDonald, and Lira Journal of VASCULAR SURGERY Table I. Patients with popliteal entrapment Ankle/ brachial index (ABI) Rest GXT ~ Patient Age~sex Side R L R L Type Operation Results 1 G.M. 30 M Bilateral a 0.85b 2 A.M. 26 M Right a J.B, 19 M Bilateral b 0.97b 4 S.K. 19 M Bilateral a 0.89a 5 R.G. 22 M Lcft b 6 J.C.? 21 M Bilateral b 0.85b 7 M.T. 53 F Right a D.H. 20 F Bilateral a 0.65a 9 W.E. 36 M Right b W.G. 37 M Bilateral b 0.81b 11 T.C. 28 M Bilateral a 0.89b 12 M.T. 22 M Bilateral b 0.88b TEA, Thromboendarterectomy; SV BPG, saphenous vein bypass graft. a, GXT at 3 mph or 3 minutes at a 0% grade. b, GXT at 4.2 MPH for 10 minutes at a 10% grade (May increase all three variables to elicit symptoms.) *GXT, Graded exercise treadmill test.?reoperated and additional Type IV identified. R-tI TEA, myotomy Good L-II Myotomy R-II Myotomy Excellent refused operation R-I SV BPG, Myotomy Good L-III Myotomy L-II Myotomy Excellent R-II Myotomy Excellent L-II Myotomy R-III TEA, Myotomy Excellent R-III Myotomy Good L-III Myotomy R-IV Lysis of bands Good R-IV Lysis of bands Excellent L-IV Lysis of bands R-III SV BPG, lysis of Excellent bands L-IV Lysis of bands R-IV Lysis of bands Excellent L-IV Lysis of bands reproduction of the patient's symptoms, the test was considered positive for possible poplitcal entrapment. If the ABIs did not decrease, a more strenous treadmill test was performed at 4.2 mph at a 10% grade for at least 10 minutes. Some of the patients stated that their symptoms did not occur until the end of their mandatory 2-mile run, and these patients were exercised accordingly. Also any other exercises that the patient reported caused symptoms were performed and ABIs were determined. Those patients with diminished ABIs at rest and with exercise then had arteriography performed. Standard aortic, pelvic, and runoff films were obtained. If no lesion was found to account for the symptoms, selective injection was then performed of the affected extremity, and biplanar arteriography was obtained with the feet in a neutral position, then with the feet passively dorsiflexed, and finally when they were actively plantar flexed (Figs. 1 and 2). Both legs were studied to determine the incidence of bilateral disease. RESULTS From 1977 to 1988, 12 patients were found to have popliteal artery entrapment (Table I). The average age was 27 years, with a range from 19 to 53 years. All but one patient was under 40 years old. All patients had a chief complaint of calf pain, and two also complained of foot pain with ambulation. The average duration of symptoms was 13 months, with a range from 2 months to 3 years. Most patients had been seen in many clinics before the diagnosis was established. One patient had an acute occlusion of the poplitcal artery and limb-threatening ischemia. All 10 men and two women were white. Four patients had a resting ABI less than one. Ten patients had decreased ankle pulses with passive dorsiflexion and active plantar flexion at rest. Six patients had decreased ABIs, with reproduction of their symptoms at an initial S-minute, 3 mph, 0% grade treadmill test, whereas six had normal ABIs. On performing a treadmill test for 10 minutes at a 10% grade at 4.2 mph these six patients decreased their ABIs, with reproduction of their symptoms. Arteriograms were then obtained on all 12 patients. All had abnormal results of their studies. Sixteen limbs had deviation of the popliteal artery's course or extrinsic compression of the artery with maneuvers or both. Four limbs had occluded vessels. In addition, four limbs on the contralateral side showed no evidence of occlusion, aneurysmal dilation, or extrinsic compression. Thus 20 limbs in 12 patients were shown to be abnormal and two thirds of these patients had bilateral popliteal entrapment.

4 Volume 10 Nmnber 5. November 1989 Popliteal artery entrapment 487 Fig. 3. Normal B-mode ultrasound scan of the popliteal artery. Once a diagnosis of popliteal entrapment was made, all limbs were explored by means of the posterior approach to the popliteal fossa. Four arterial reconstructions were performed-two popliteal artery thromboendarterectomies and two saphenous vein interposition grafts. Type I popliteal artery entrapment was found in one limb (5%), type II in six limbs (32%), type III in five limbs (26%), and type IV in seven limbs (37%). There were no type V popliteal anomalies. One patient refused surgery and could not be classified. After surgery all patients were evaluated with exercise treadmill tests at 1 month, and eight of 12 patients had complete relief of their symptoms and no decrease in their ABIs. Two of four patients classifted as having good results had normal treadmill test results and improved leg symptoms, however they were unable to remain on active duty (Table I). The other two patients had occlusions of their arterial reconstructions on long-term follow-up yet showed mild symptoms. Seven months after surgery one patient again had symptoms similar to his initial complaints, and on reevaluation he was found to have decreased ABIs with exercise and narrowing of the popliteal artery on repeat arteriography. At reoperation, fibrous bands were found compressing the popliteal artery. There was no evidence of the type II entrapment found at the original operation. These bands were released, and again the patient had no symptoms with exercise and had normal exercise treadmill test results. DISCUSSION In discussing the syndrome of popliteal entrapment it must be emphasized that all classification systems are based on a congenital anomaly of the medial head of the gastrocnemius muscle and its relationship to the popliteal artery and other structures within the popliteal fossa. Normally the medial head of the gastrocnemius muscle migrates from an inferior centrolateral a~achment on the femoral epiphyses to a superior medial attachment on the femoral shaft. 12 All of the classifications are simply variations on the anomalous migration of this muscle and its tendinous attachments. The most common congenital anomaly was type IV (37%) in this series, with type II (32%) and type III (26%) close behind. Type I popliteal entrapment was identified in only one patient (5%). This and type II lesions have been the most common lesions so far discussed in the literature. The greater incidence of type III and type IV lesions in this series may be explained by the use of maneuvers with biplanar arteriography to identify, what would ordinarly have been in the past, normal arteriograms. Type I lesions are represented by medial deviation of the vessel and will be obvious to the observer. However, the popliteal artery may be located in its

5 488 Collins, McDonald, and Lim ~oumal of VASCULAR SURGERY Fig. 4. Occlusion of the same, normal popliteal artery with active plantar flexion. Arrow marks compression of the popliteal artery. normal position in Types II, III, and IV, and only through maneuvers during biplanar arteriography will extrinsic compression of the vessel be seen. Therefore, past series may not accurately reflect the true incidence of the types of entrapment. Particularly if they did not perform surgery on those patients having no medial deviation of the vessel, thrombosis, compression at rest, or aneurysmal dilation of the popliteal artery on their arteriograms. This finding may also explain the increased incidence of bilateral lesions found in this series. Two thirds (67%) of the patients had bilateral popliteal entrapment. Only three patients had symptoms in both legs. All three complained of bilateral calf clandication. The other five patients with bilateral entrapment had both limbs studied to determine the incidence of bilateral lesions despite having symptoms in only one leg. The practice of studying both limbs, even the asymptomatic extremity, differs from previous studies and may explain the increased incidence of bilateral lesions. Those patients who showed no symptoms in the contralateral extremity, yet had angiographic evidence of popliteal artery entrapment, were examined, and myotomy or transection of fibrous bands was performed. This policy was to prevent the young, healthy, active adult from becoming disabled later in life as a result of occlusion of the popliteal artery by known disease. In fact, four patients or one third of the series population had an occluded poptiteal artery as their initial presentation. A large number of reports describing popliteal entrapment have come from military medical centers. Does this disease occur in the civilian population? In an autopsy series in 1977 Gibson et al.~2 found three cases of popliteal entrapment in 86 cadavers. This represented an incidence of 3.5%. It was also significant that when these patients' histories were reviewed it was found they had complained of claudication for several years before their death. Young adults, who in civilian life may have otherwise led a sedentary existence or who avoided exercise that brought on leg pain, are forced to run and march while in military service thereby bringing out the syndrome of popliteal entrapment. Thus there may be more patients in the population who have popliteal entrapment but are not diagnosed or recognized. It is important to differentiate the patient with a true disease process and those who might be malingering, especially in the military. Determination of the ankle pulses with mad without manueuvers does not adequately evaluate the presence of popliteal artery entrapment and may be abnormal in up to 50% of individuals in good health. 13 Pulse volume recordings have also been shown not to be diagnostic for popliteal entrapmcnt.14 Duplex ultrasonography of the popliteal artery to diagnose popliteal entrapment is just now being investigated; however, this

6 Volume 10 Number 5 November 1989 PopIiteal artery entrapment 489 too can be abnormal in otherwise healthy individuals. This can be seen in Figs. 3 and 4 where a normal popliteal artery becomes completely obliterated with active plantar flexion. One noninvasive test that was useful in this series was the exercise treadmill test. A decrease in the ABI with the standard 3 minute, 3 mph, 0% grade was sufficient to submit the patient to arteriography. A negative result was followed by increasing the time (I0 minutes), speed (4.2 mph), and grade (I0%) of the treadmill. This technique, as established by McDonald et al. 11 led to reproduction of the symptoms and a decrease in the ABI in all patients. The mechanism by which this occurs may be related to increasing muscle mass in a closed compartment, such as the popliteal fossa, thus increasing pressure on the fixed artery by the abnormal musculotendinous attachments. Another pathophysiologic mechanism occurs when a greater degree of exercise is performed, which results in repeated trauma to the vessel by the entrapping structures. The vessel in time becomes stenotic but briefly develops vasospasm, which results in a decrease in the ankle/bracial index after the treadmill tcst or exercise. However, even in the presence of a normal treadmill test, a convincing history and physical examination may be enough to warrant arteriography to explore the presence ofpopliteal artery entrapment or other arterial occlusive disorders. This is the largest single series of patients with popliteal artery entrapment in the United States. A 10-minute, 4.2 mph, 10% grade exercise treadmill test followed by biplanar artcriography with maneuvers were the most sensitive tests to establish the diagnosis in patients suspected of having popliteal entrapment. Bilateral entrapment was twice that previously reported. Popliteal artery entrapment should be considered in all aduks with claudication who have no other cause for arterial insufficiency. This syndrome may be seen with greater frequency in an increasingly active population where walking, jogging, and rtmning to ensure cardiovascular fimess becomes commonplace. REFERENCES 1. Stuart T. A note on a variation in the course of the popliteal artery. J Anat Physiot 1879;I3: Chambardel-Dubreuil L. Variations des Arteres du Pelvis et du Membre Inferieur. Paris: Masson & Cie, Hamming JI. Intermittent claudication at an early age, due to an anomalous course of the popliteal artery. Angiology 1959;10: Love JW, Whelan TJ. Popliteal entrapment syndrome. Am J Surg 1967;109: Rich N, Hughes C. Popliteal artery and vein entrapment. Am J Surg 1967;113: Insua JA, Young JR., Humphries AW. Politeal artery entrapment syndrome. Arch Surg 1970;101: Delaney TA, Gonzalez LL. Occlusion of the popliteal artery due to muscular entrapment. Surgery 1971;69: Ferrero R, Barile C, Buzzacchino A, Bretto P, Ponzio, F. La sindrome da costrizone dell'arteria poplita. Minerva Cardioangiol. 1978;26: Rich N, Collins G, McDonald PT, Kozloff L, Clagett P, Collins J. Popliteal vasular entrapment. Arch Surg 1979; 114: Yao ST, Hobbs IT, Irvine WT. Ankle systolic pressure measurements in arterial disease affecting the lower extremities. Brit I Surg 1969;56: McDonald PT, Easterbrook JA, Rich N, et al. Popliteal artery entrapment syndrome: clinical, noninvasive, and anglographic diagnosis. Am J Surg 1980; Gibson MH, Mills MS, Johnson GE, Downs AR. Popliteal entrapment syndrome. Ann Surg 1977;185: Rignault DP, Pailler JL, Lunel F. The "fimctional" popliteal entrapment syndrome. Int Angiol 1985;4: Darling RC, Buckley CJ, Abbot WM. Intermittant claudication in young athletes: popliteal artery entrapment syndrome. J Trauma 1974;14: DISCUSSION Dr. Whelan (Honolulu, Hawaii). Certain points in this article should be emphasized: (1) the increasing recognition of the bilateral nature of the anomaly--67% in this series compared to 30% to 40% in earlier series; (2) the use of noninvasive Doppler segmental ankle pressure measurements with and without exercise stress to supplement the previously described passive dorsiflexion and active plantar flexion stress tests, and (3) with greater awareness of the entity, fewer presentations with popliteal arterial occlusion or aneurysm. Our first two cases had midpopliteal artery occlusion. In this series only four of 20 extremities showed an occluded popliteal artery requiting reconstruction, and myotomy alone was the only procedure necessary in the other 16. As more cases have been described, the classic medial deviation or compression of the proximal popliteal artery has been found not to be necessary in suspecting the diagnosis. Lateral deviation may also occur. An anomalous or hypertrophied semimembranosus muscle that is pushing the artery laterally in such cases has been previously identiffed. The entrapment has usually been an anomalous plantar muscle. Finally, an entity has been described as "functional" popliteal entrapment syndrome, described by Rigneault et al. in France, where in hypertrophy of the gastrocnemius muscle in a highly trained athlete has caused compression of the artery and claudication. Contrary to most observers, who feel the diagnosis has been missed frequently in the past, these authors question whether the entity is now

7 490 Collins, McDonald, and Lira Jo~nal of" VASCULAR SURGERY being over-diagnosed. 'They performed both clinical examinations and noninvasive Doppler examinations in 53 normal average draftees and 53 highly trained athletes. Positive results with decrease in pulse and pressure at the ankle with passive dorsiflexion or active plantar flexion was noted in 30% of the former and 50% of the latter, suggesting that the popliteal artery under provocative stress, may be compressed in patients in good health who show no symptoms. It appears that hypertrophic muscles in the popliteal space might predispose an individual to just such a positive test. In the series of Collins et al. all patients had symptoms on one or both sides, positive arteriography results when stressed by the usual provocative maneuvers, and all had anomalous muscles or arteries found on surgical exploration. I would like to ask two questions of the authors: (1) Do you feel, from the nature of the disease found, that operation on an asymptomatic contralateral limb is worthwhile? I gather you operated on all limbs in which the Doppler stress test and stress arteriogram results were positive. In view of the findings of Rigneault et al.,13 which suggest that normal individuals may show compression on the popliteal artery and not have an organic entrapment, did all of your patients with no symptoms show a true entrapment at operation? (2) When myotomy is performed to decompress the popliteal vessel, do the authors reattach the muscle in a noncompressing position, resect the offending muscle, or merely cut it? Dr. Paul S. Collins (dosing). We explored the asymptomatic contralateral limb when it met the nonlnvasive and aniographic criteria, which were established for the symptomatic limb before operation. In all instances, a cause for the positive Doppler stress test and angiographic abnormality was found. Myotomy or transection of fibrous bands was then per~brmed, t agree that individuals in good heakh can obliterate their popliteal pulse, and this was evident in the duplex scan of the patient with no symptoms. However, in the context of a known contralateral entrapment mad the fact that a pathologic entrapment was found on exploration of the asymptomatic limb, we continue to support this approach. Depending on the degree of entrapment, resection or simple myotomy or both were performed. Reartachment of the muscle was not deemed necessary, and no patient experienced limb dysfunction with this approach. Recent experience with duplex scanning of the popliteal artery in normal subjects has shown that all vessels can be narrowed and some totally occluded with active plantar flexion and passive dorsiflexion of the foot. Repeated trauma in this manner to the popliteal arte W by individuals performing strenous activity may result in scarring of the vessel and occlusion. This may be a pathologic mechanism that will appear more in an increasingly active population. A 3.5 % incidence ofpopliteat artery entrapment shown by Gibson et al.~2 in an autopsy series, may lead one to suspect a much greater incidence of this musculotendinous abnormality in the general population. What may be a disease that some are calling over-diagnosed may in fact be underdiagnosed. The disease underlying the popliteal artery occlusion will be missed unless the popliteal artery is exposed in the popliteal fossa. This is not done in most reconstructive cases because a medial approach to bypass surgery is used routinely. Thus the elderly patient with a popliteal or superficial artery occlusion and minimal systemic atherosclerotic disease may represent the end result of years of popliteal artery entrapment and not the progression of atherosclerotic changes in the vessel.