Popliteal entrapment as a result of neurovascular compression by the soleus and plantaris muscles William D. Turnipseed, MD, and Myron Pozniak, MD, Madison, Wis. Intermittent claudication may occur in well-conditioned athletes because of an unusual form of popliteal artery entrapment that results from overtraining. These patients complain of calf muscle cramping, rapid limb fatigue, and occasional paresthesias on the plantar surface of the foot when running on inclines or when repetitive jumping is performed. Results of plethysmographic screening tests for popliteal entrapment are positive in these patients. Magnetic resonance angiography and intravenous digital subtraction angiography studies, however, do not demonstrate findings typical of anatomic popliteal entrapment. No evidence exists of aberrant positioning of the popliteal artery in foot neutral positioning, but with forced plantar flexion, the neurovascular brindle is deviated and compressed laterally. Surgical exploration of the popliteal fossa demonstrates no obvious musculotendinous abnormality. Symptoms of claudication and arterial compression are relieved by surgical release of the soleus muscle from its tibial attachments, resection of its fascial band, and resection of the plantaris muscle. (J VAsc
SURG 1992;15:285-94.)
Intermittent claudication, an uncommon complaint in young, healthy adults, may occur because of an unusual form of popliteal entrapment that affects well-conditioned athletes and usually causes deep-calf muscle cramping (soleal), rapid limb fatigue, and occasional paresthesias on the plantar surface of the foot. These symptoms are most predictably aggravated by running up hills or repetitive jumping or both and ,commonly affect athletes participating in sports such as cross country, basketball, and volleyball. The clinical complaints are frequently confusing to trainers and physicians alike, because they are not uniformly reproducible, because findings on physical examinations are usually normal, and because traditional use of physical therapy, rest, and antiinflammatory medications rarely afford symptomatic relief. This report describes the diagnosis and treatment of 12 patients with "functional" popliteal entrapment. PATIENTS A N D M E T H O D S Between 1987 and 1991, 120 patients were evaluated for symptoms of atypical lower extremity From the Departments of Surgery (Dr. Turnipseed) and Radiology (Dr. Pozniak), Universityof Wisconsin. Presented at the Forty-fifth Annual Meeting of the Societyfor Vascular Surgery, Boston, Mass., lune 4-5, 1991. Reprint requests: William D. Tumipseed, MD, Department of Surgery, H4/730A, 600 Highland Ave., Madison, WI 53792. 24/6/33493
clandication. 1 These patients (50 men, 70 women) were young (mean age, 22 years) and had longstanding symptoms (mean duration, 24 months) that would abate or completely disappear after extended rest but would reappear with exercise. Most were recreational or scholarship athletes (108 of 120, 90%) referred from our sports medicine department because of recalcitrant complaints of muscle cramping and paresthesias, which seriously affected competitive levels of performance in athletic events. Unlike patients suffering from overuse injuries such as stress fracture, tendonitis, and periostitis, these patients failed to respond to traditional forms of medical management and rehabilitation (physical therapy, ultrasonography, icing, and use of antiinflammatory medications). These patients were referred to the vascular service to rule out arterial or venous causes for their claudication symptoms and to determine whether chronic compartment syndrome might be present. After a thorough history was taken and physical examination was performed, noninvasive arterial plethysmography was performed, and segmental Doppler pressures were obtained at rest and after standard treadmill exercise (1.5 mph at 10 degrees for 5 minutes) in patients with absent or weak lower extremity pulses to screen for underlying arterial occlusive lesions such as premature atherosclerosis or medial cystic occlusive disease. In addition, all 285
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Fig. 1. The medial approach is routinely used in symptomatic patients suspected of having functional popliteal entrapment. The popliteal fossa is explored to nile out an anatomic form of entrapment. If the semimembranous and semitendinons tendons or gracilis and sartorial insertions must be transected during exploration of the popliteal fossa, they should be repaired before closure.
/I, J/llll/tlllll\\ I ~
~
'~~ ~///-4//-~ / / ~/ f' f ~~ ~
~.'~
Transected PlantarisM.
~e~lec(e Soleus dFaa~arura
Fig. 2. The deep proximal (soleal compartment) is decompressed by lysing the medial attachments of the muscle to the tibia. The dense anterior fascial sling of the soleus is sharply excised laterally to its fibular attachments. The plantaris muscle is resected.
120 patients were screened for possible popliteal entrapment by measuring Doppler pressures and calf plethysmography with the foot in neutral and in forced plantar and dorsiflexion positions? Twelve patients with positive screening tests for popliteal entrapment and symptoms of calf claudication also had duplex and magnetic resonance imaging (MRI) studies of the popliteal vessels performed at rest and with the foot in forced plantar flexion? Dynamic intravenous digital subtraction angiography (IVDSA) was performed in these patients to confirm popliteal artery entrapment. All patients with paresthesias of the foot had electromyography and nerve conduction studies as well. Compartment pressure measurements were performed with use of the hand-held Stryker Digital Computer System
(Stryker Surgical, Kalamazoo, Mich.) in patients with symptoms referable to the anterolateral and posterior superficial compartments. Pressure measurements were not performed in patients with deep posterior compartment symptoms because of the increased chance of neurovascular injury. Medial exploration of the popliteal fossa with resection of the plantaris muscle, and decompression of the deep posterior compartment by surgical release of the tibial attachments of the soleus muscle were performed in symptomatic patients with noninvasive and angiographic evidence of popliteal artery compression. Postoperative plethysmography, duplex scanning, or MRI of the popliteal artery was performed to document surgical correction of the popliteal entrapment.
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Popliteal entrapment 287
R. Ankle BP) Rest
L Ankle BP) Rest
R. ~ . i e i 3 P Y ~
',L Ankle BP) Dorsi
Fig. 3. Screening test in a patient with right-sided soleal claudication demonstrates bilateral popliteal artery compression in both the plantar flexion and dorsiflexion positions.
]Fig. 4. A, Duplex imaging demonstrates a widely patent poptiteal artery and normal flow in ~:he foot in neutral position. B, A popliteal artery in the same patient occludes against the posterior surface of the tibia with forced plantar flexion o f the foot.
288 Turnipseed and Pozniak
Fig. 5. Intravenous digital subtraction angiography demonstrates normal arterial anatomy on the right side with the foot in neutral position. On the left side lateral deviation from the midline position and compression of the popliteal artery occur against the lateral condyle of the femur (arrow).
SURGICAL T E C H N I Q U E Exploration of the popliteal fossa is performed with the patient under spinal or general anesthesia by means of the medial approach. Patients are placed in the supine position, prepared and draped so as to expose the entire lower extremity, and the surgical incision is made below the knee at the level of the upper midcalf just as though one intended to do a distal popliteal artery bypass (Fig. 1). Care is taken to avoid injury to the saphenous vein and nerve. The gasttocnemius fascia is then incised, and a large ellipse (3 x 6 cm) is removed to release the posterior superficial compartment. Whenever possible, the tendon insertions of the sartorius and the gracilis muscles as well as the semimembranous and semitendinous muscles should be left intact. Blunt and sharp dissection is used to expose the neurovascular and musculotendinous structures of the popliteal fossa. Palpation and direct examination of the popliteal artery is necessary to identify aberrant positioning of the vessels or anomalous muscular bands. If anatomic abnormalities cannot be identified and treated, the surgeon should release the medial tibial attachments of the soleus muscle by placing an index finger into the soleal canal and using the electric cautery. Once the tibial attachments of the soleus muscle have been released, the neurovascular bundle
Journal of VASCULAR SURGERY
is easily identified. The anterior fascia of the soleus muscle thickens to form a fibrous sting that crosses the lower border of the popliteal fossa attaching laterally to the proximal fibula. This fibrous fascial sling is sharply excised including its lateral attachments. The posterior fascia of the popliteus muscle is also excised. The facial excision from the opposing surfaces of the popliteus and soleus muscles make it less likely that rigid scar formation will reentrap the neurovascular bundle as it passes between them. Once the soleal release has been completed, attention is then turned to the plantaris muscle, which often acts in conjunction with the medial head of the gastrocnemius muscle to laterally compress the neurovascular bundle against the lateral margin of the soleal sling when the foot is in plantar flexion. The plantaris tendon, which runs anteromedially to the gastrocnemius muscle, is transected, and the large proximal portion of the muscle is dissected free of its anatomic bed and resected (Fig. 2). The wound is then irrigated and checked for hemostasis. The skin is closed with subcuticular absorbable sutures and steri strips. The patients are discharged the day after operation and instructed to use crutches for ambulatory assistance until normal weight bearing and gait is achieved. Once the skin is healed, rehabilitation is started by use of the stationary bike and kickboard exercises in the pool. Jogging usually begins in 3 to 4 weeks, and complete recovery to athletic levels of performance is achieved in 2 to 3 months. RESULTS None of the 120 patients in this series had physical or noninvasive testing evidence suggestive of intrinsic arterial occlusive disease. Seventy patients had symptoms attributed to the anterolateral compartment (58%), and 50 patients (42%) had symptoms affecting the posterior compartment (10 had superficial gastrocnemius muscle cramping; 12 had proximal soleal cramping and pain; 28 had distal retrotibial tightness and cramping). Plethysmographic screening tests for popliteal entrapment were positive in 30 of the 120 patients (25%) suspected of having possible compartment syndrome. (A positive test was defined as obliteration of the plethysmographic waveforms and/or a drop in ankle index to less than 0.5 with forced plantar flexion or dorsiflexion of the foot) (Fig. 3). Twelve of the 30 patients with positive results on entrapment screening studies had soleal claudication symptoms (11 unilateral, 1 bilateral). The remaining 18 patients with positive popliteal compression tests had no symptoms referable to posterior muscle groups. Furthermore, out-
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Fig. 6. A, Magnetic resonance gradient echo image demonstrates a normally positioned popliteal artery at rest. B, Sagittal MILl shows patient's popliteal artery in neutral position. C, When the foot is plantar flexed, the popliteal artery is occluded by lateral compression against the femoral condyle and the soleal sling. D, Sagittal MRI in plantar flexion demonstrates popliteal artery occlusion.
comes of plethysmographic screening tests performed in 40 asymptomatic age group controls were positive in 53% of those considered to be athletically well conditioned and 30% of those considered to be physically inactive. Duplex imaging with gray scale or color-flow techniques or both, performed on all 12 patients with positive plethysmographic screening tests and symptoms of calf claudication and in 20 asymptomatic control subjects with positive screening tests, confirmed popliteal artery compression at the approximate point where the neurovascular bundle enters the soleal canal (Fig. 4, A and B). Intravenous digital subtraction angiography was performed in eight of
the 12 symptomatic patients with deep calf daudication and positive plantar flexion studies. No angiographic evidence was found of medial arterial displacement or occlusion in the neutral or resting positions. However, with forced plantar flexion, lateral compression and occlusion of the popliteal artery was demonstrated (Fig. 5). Later in our study, IVDSA was discontinued because the same information could be obtained with use of MRI of the popliteal artery. Magnetic resonance imaging of the popliteal vessels and calf muscles suggested that the neurovascular bundle is forced laterally against the angle of the soleal sling and that the plantaris muscle in conjunction with the medial head of the gastroc-
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Table I. Summary of data Diagnostic tests (plantar flexion stress) Name
Age
Sex
RR
19
M
LH
20
M
KW
17
F
TK
25
M
KK
20
SR
Symptom
Pleth. ~
Duplex
Bilateral claud.
Positive
Positive
Positive
Positive
Positive
Positive
Positive
Positive
F
Unilateral claud. and paresthesia Unilateral claud. and paresthesia Unilateral claud. and paresthesia Unilateral claud.
Positive
Positive
20
F
Unilateral claud.
Positive
Positive
JS
19
F
Positive
Positive
JN
32
M
Positive
Positive
MH
26
M
Positive
Positive
DF
17
F
Unilateral claud. and paresthesia Unilateral claud. and paresthesia Unilateral claud. and paresthesia Unilateral claud.
Lateral compressmn popliteal artery Lateral compression popliteal artery Lateral compression popliteal artery Lateral compressmn popliteal artery Lateral compression popliteal artery Lateral compression popliteal artery Lateral compression popliteal artery Lateral compressmn popliteal artery ND
Positive
Positive
ND
JD
26
F
Unilateral claud.
Positive
Positive
ND
JS
16
F
Unilateral claud.
Positive
Positive
ND
IVDSA
.MR/ Lateral compression popliteal artery Lateral compression popliteal artery Lateral compression popliteal artery Lateral compresslon popliteal artery Lateral compression popliteal artery Lateral compressmn popliteal artery Lateral compressmn poptiteal artery Lateral compression popliteal artery Lateral compression popliteal artery Lateral compresslon popliteal artery Lateral compression popliteal artery Lateral compression popliteal artery
~ND, Not done; Clan&, claudication; Pleth, plethysmography.
nemius compresses the popliteal vessels against the lateral condyle of the femur more proximally (Fig. 6, A toD). Six of 12 patients (50%) with symptoms ofsoleal claudication also had intermittent numbness and plantar paresthesias. However, electromyography and nerve conduction studies performed on patients with paresthesias demonstrated minor conduction defects in only one case. Compartment releases (4 anterolateral, 5 distal deep posterior, and i posterior superficial) were performed in five of the 12 patients (40%) with soleal claudication before popliteal entrapment release. One patient was referred to our clinic after bilateral vascular reconstruction for popliteal entrapment syndrome because of persistent claudication symptoms. Postoperative plantar flexion and MRI in this patient demonstrated persistent popliteal artery compression. Thirteen surgical procedures were performed on the 12 patients with symptoms of soleal claudication and evidence of distal popliteal artery entrapment. All popliteal entrapment release procedures were done as first-day operative procedures by means of spinal or general anesthesia.4,5 The medial approach was routinely used, and effort was made to identify aberrant positioning of the popliteal artery or abnormal musculotendinous bands in the popliteal fossa. No
such abnormalities were identified in this group of patients. Entrapment release and posterior compartment decompression was accomplished by resection of the plantaris muscle, take-down of the medial tibial insertions of the soleus muscle, and complete excision of the fascial band that forms the soleal sling. All patients were discharged on the first postoperative day. Crutch assisted ambulation was allowed only until full weight beating and normal gait could be achieved. Physical rehabilitation and reconditioning in most athletes was completed within 2 to 3 months. Most complications were minor. Two patients had wound complications (1 seroma, 1 superficial cellulitis), one had transient reflex sympathetic dystrophy with complete resolution, and new compartment symptoms developed in two in areas remote to the soleal release because of increased physical activity. Clinical follow-up ranged from 3 to 36 m o n t h s (mean, 20 months). Nine of the 12 patients treated surgically (75%) had complete relief from claudication and paresthetic symptoms, and three (25%) were significantly improved. All but one returned to vigorous sports activity. Postoperative plantar flexion tests and duplex imaging performed have shown complete resolution of the popliteal compression and no evidence of recurrence (Fig. 7). Data are summarized in Table I.
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Popliteal entrapment
EA/IG ND Positive Negative Negative ND ND Negative Negative Negative ND ND ND
Surgery Soleal release and resection o f plantaris Soleal release and resecnon of plantaris Soleal release and resection o f plantaris Soleal release and resection o f plantaris Soleal release and resection o f plantaris Soleai release and resection of plantaris Soleal release and resection o f plantaris Soleal release and resection o f plantans Soleal release and resection o f plantaris Soleal release and resection o f plantaris Soleal release and resection o f plantaris Soleal release and resection o f plantaris
Follow-up
Outcome
18 m o
Excellent
9 mo
Excellent
18 m o
Excellent
30 m o
Excellent
27 m o
Excellent
36 m o
Excellent
39 m o
Excellent
16 m o
Excellent
6 mo
Excellent
4 mo
Good
25 m o
Fair
12 m o
Good
DISCUSSION
Poplite~d entrapment syndrome has classically been described as an anomalous relationship between the popliteal artery, the medial head of the gastrocnemius muscle, and other musculotendinous elements in the popliteal fossa. 4-8The original anatomic description of this condition was made by T. P. Stuart in 1879. 9 In 1959 Hamming 1° described clinical symptoms associated with the popliteal entrapment and a surgical plan for treating this condition (gastrocnemius transection and thromboendarterectomy of the popliteal artery). In 1965 Love and Whelan 11 coined the term "popliteal entrapment syndrome.''11 Since then several anatomic variants of this condition have been described and classified. The most common anatomic abnormalities include passage of the popliteal artery medial to the medial head of the gastrocnemius muscle (type 1, Insua Whelan), 12,13 normal anatomic positioning of the popliteal artery with compression caused by aberrant origins of the gastrocnemius or plantaris muscles (type II, Insua; type II and type III, Whelan), ~2,~3and compression of the popliteal artery by the popliteus muscle or a fibrous band in the same position (type IV, Whelan, Haimovici et al.). ~3,~4 More recent clinical experience suggests that the phenomenon of popliteal artery compression may be a much more common ew:nt than previously described. As screen-
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ing techniques are more widely used it appears that "functional" popliteal entrapment may occur in the absence of any musculotendinous developmental abnormalities, and that this form of neurovascular compression may represent a normal physiologic variant in well-trained and physically overdeveloped athletes. ~5 It also appears that there may be a significant differencc in the morbidity associated with anatomic and functional forms of popliteal entrapment. Historical accounts suggest that arterial compression associated with deviations in the anatomic course of the popliteal artery or compression by anomalous bands may cause acute arterial occlusions or aneurysmal degeneration. No clinical evidence exists to support the concept that fimctional entrapment, in the absence of any clinical symptoms, requircs surgical intervention. Symptoms associated with the functional-type entrapment are uncommon and occur in only approximately 25% of those individuals with positive plantar flexion screening tests. No clear-cut evidence exists that compression of the popliteal artery in these patients actually causes soleal cramping and/or paresthesias. Physiologic and anatomic information derived from duplex imaging and MRI of the popliteal fossa suggests that lateral displacement of the neurovascular bundle may compress the popliteal nerve as well as the vein and artery against the lateral angle of the soleal sling and the lateral condyle of the tibia. Repeated trauma to the popliteal nerve with repetitive plantar flexion may cause a neuromuscular form of claudication and explain the intcrmittent paresthesias that are commonly associated with this condition. No substantive evidence has been found that arterial insufficiency is the primary cause for symptoms in these patients. All were capable of vigorous cardiovascular effort and exhibited remarkable endurance except in circumstances where accentuated plantar or dorsiflexion were required as in jumping or running up inclines. The rapid onset of symptoms with these specific maneuvers supports the idea that vascular insufficiency may not be the most important factor in the genesis of this symptom complex. Functional popliteal entrapment has many clinical similarities to the thoracic outlet syndrome, in both conditions primary arterial ischemia is uncommon. Although complications from arterial or venous compression are possible, they rarely occur. In both cases symptoms commonly develop when repetitive activity patterns result in netu'ovascular compression. Furthermore, in both conditions the only clinical beneficiaries from surgical intervention appear to be the symptomatic patients.
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Fig. 7. Postoperative pulse volume recording demonstrates release of a functional entrapment on the right side after a deep proximal compartment release and plantar resection. Our data suggest that pulse volume recording screening and duplex imaging tests may not be capable of distinguishing between anatomic and functional forms of this disease. 16 Dynamic "stress" angiography (our preference is IVDSA) and MRI studies are more helpful in analyzing the anatomic relationships of popliteal entrapment.17 Anatomic entrapment caused by abnormal passage of the popliteal artery around or through muscles is often manifest by "medial" deviation or compression of the artery with foot in dorsal or plantar flexion positions. Segmental popliteal artery occlusion also suggests possible anatomic entrapment. Angiography commonly demonstrates "lateral" displacement and compression of the popliteal artery in patients with "functional" entrapment. Intrinsic arterial lesions have not been demonstrated in patients with functional entrapment. The surgeon must be aware that several potential causes exist for popliteal entrapment. The decision to operate, the kind of operation, and the surgical approach should be tailored to information derived from clinical history and preoperative testing, The posterior approach with gastrocnemius muscle transection and arterial repair may be quite appropriate in patients with threatened limbs as a result of anatomic popliteal entrapment. However, the medial approach with resection of the plantaris muscle and proximal release of soleus muscle and excision of its fascia] b a n d is effective for functional forms of the disease and minimizes the rehabilitation efforts in the
competitive athlete. The im-portance of considering this ldnd of release in patients with popliteal entrapment is emphasized by the one patient in our series who remained symptomatic despite traditional vascular repair until the soleal muscle release and plantaris muscle resection was performed. In summary, functional popliteal entrapment syndrome is much more prevalent than originally expected. Symptoms associated with this condition are uncommon and are aggravated by specific physical activities in well-conditioned athletes. Noninvasive tests like plethysmography and duplex imaging may not accurately distinguish anatomic from functional types of popliteal entrapment syndrome. Angiography and MRI tests are more diagnostic. Surgical compamnent release for functional popliteal entrapment is indicated in symptomatic patients and perhaps in patients that remain symptomatic after traditional proximal popliteal repairs for anatomic entrapment syndrome. REFERENCES 1. Tumipseed W, Demler DE, Girdley F. Chronic compartment syndrome. Ann Surg 1989;210:557-63. 2. Darling RC, Bucldey C~, Abbott WM, Raines JK. Intermittent claudication in young athletes: popliteal artery entrapment syndrome. J Trauma 1974;14:543-52. 3. Collins PS, McDonald PT, L i m RC. Popliteal artery entrapment: an evolving syndrome. J VAsc SURG 1989;10: 484-90. 4. Rich NM, Hughes CW. Popliteal artery and vein entrapment. Am J Surg 1967;113:696-8.
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5. Berkoff HA, Crummy AB. Popliteal artery entrapment syndrome. Vase Surg 1976;10:264-7. 6. Podore PC. Popliteal entrapment syndrome: a report oftibiat nerve entrapment. J VASCSURG 1985;2:335-6. 7. Iwai T, Sato S, Yamada T, et al. Popliteal vein entrapment caused by the third head of the gastrocnemius muscle. Br I Surg I987;74:1006-8. 8. Delaney TA, Gonzalez LL. Occlusion ofpopliteal artery due to muscular entrapment. Surgery I971;69:97-101. 9. Stuart TPA. A note on variation of the course of the popliteal artery. J Anat Physiol 1879;13:162. 10. Hanmxing Jl. Intermittent claudication at an early age due to an anomalous course of the popliteal artery. Angiology
1959;10:369-70. i 1. Love JW, Whelan TJ. Popliteal artery entrapment syndrome. Am J Surg 1965;109:620. i2. Insua JA, Young JR, Humphries AW. Popliteal artery entrapment syndrome. Arch Surg 1970;101:771-5.
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13. Whelan TJ Jr, Popliteal artery entrapment syndrome. In: Haimovici H, ed., Vascular surgery: principles mad techniques. New York: Appleton-Century-Crofts, 1984:55767. 14. Haimovici H, Spragregen J, Johnson F. Popliteal artery entrapment by a fibrous band. Surgery 1972;72:789-92. 15. Rignault DP, Pailler IL, Lunel F. The "functional" popliteal entrapment syndrome. Int Angiol 1985;4:341-3. 16. Williams LR, Flinn WR, McCarthy WJ, Yao JST, Bergan II. Popliteal artery entrapment: diagnosis by computed tomography. J VASCSURG 1986;3:360-3. 17. Greenwood LH, Yrizarry JM, Hallett J-Wlr. Popliteal artery entrapment: importance of the stress runoff for diagnosis. Cardiovasc Intervent Radiol 1986;9:93-9. Submitted June 10, 1991; accepted Aug. 29, 1991.
DISCUSSION
Dr. N o r m a n Rich (Bethesda, Md.). Collectively we have found this report by Turnipseed and his colleagues to be informative and interesting. In general terms, questions could be raised regarding our 1979 report to ISCVS on popliteal vascular entrapment from Walter Reed Army Medical Center and the 1989 report by Collins and associates from Letterman Army Medical Center on why essentially all of the cases identified had anatomic anomalies in comparison with and contrast to the current report where there were none identified. The anthors identified a 1985 report by Rignault and his coworkers from Paris. Dr. Rignault has kindly served on our. faculty in recent years providing us an opportunity for an update regarding his thoughts since we believe that he was the first to use the term "functional" popliteal entrapment. Our current assessment is that considerable confusion exists between popliteal vascular entrapment and the compartment syndrome, as the latter is identified in the current report. We, like others, have found noninvasive testing to have too many false-positive outcomes in athletes who are asymptomatic. Angiography or M R I or both currently provide the best opportunity to distinguish entrapment from compartment syndrome as the authors have stressed. However, we ask the authors to comment on our observation that compartment syndrome can have elevated compartment pressure without interruption in the flow in the popliteal artery, whereas entrapment has definite interruption in major arterial flow and may or may not have high compartment pressure. As originally identified by Rignault, functional entrapment may be, but is usually not, associated with high intercompartmental pressure. The authors stress the importance of compartment decompression in their series of patients. Both their
diagnosis of compartment syndrome and the previous interpretation by Rignault possibly represent even two types of "functional" entrapment adding to even more confusion. In regard to the incision, we remain convinced that the posterior approach provides the best opportunity to identify anatomic variance. We have added the soleus release, as described by the authors, and/or the plantar tendon transection. If these structures appeared to be compressive, and this adds even further to the confusion, which of the therapies really alleviated the symptoms? We are aware of a number of anecdotal cases where anatomic variants have been missed with the medial approach. Could the authors have yet missed any of these anatomic variants? Dr. William Turnipseed. In response to the question of whether pressures were abnormal, I think it might be interesting for you to understand what we described as abnormal compartment pressures. These are significantly different from what you are used to dealing with when you are talking about the subacute or acute compartment syndromes. They are much lower. Abnormal pressures are usually between 15 and 20 m m H g or greater. We, as Dr, Rich has pointed out, have not identified significant compartment pressure elevations in many of the patients that we have talked about. In two cases we actually had an identical pattern o f symptoms in which we did the release procedure without the positive plantar flexion studies and got total relief o f the symptoms. One patient was sent to us from another institution in the Midwest where the traditional lysis and bypass operations had been performed for anatomic forms o f the disease and he still had the symptoms. We did the release and he does not have the symptoms anymore. I still am not sure which operation is most appropriate. There are some clear*cut indications for doing the posterior
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approach, and I think these are the patients who have the anatomic deviations of the popliteal artery that are described either by MRI or by angiography. By and large, if you look at the population we are dealing with, these are not army and air force recruits. These are elite class runners and dedicated athletes. A minimal operation has to be done, and I think this is the appropriate operation for this particular group of highly trained athletes with activityspecific pathologic complaints.
I believe as MRI is more widely used that we will be able to identify more precisely those that have functional forms of the disease and those that clearly have the anatomic form of the disease. I would totally agree with Dr. Rich that in circumstances where anatomic disease is identified, I would use the posterior approach.
E. J. W Y L I E T R A V E L I N G F E L L O W S H I P OF T H E E D U C A T I O N A L F O U N D A T I O N OF T H E S O C I E T Y F O R V A S C U L A R S U R G E R Y The Educational Foundation of the Society for Vascular Surgery (with financial assistance from W. L. Gore & Associates, Inc.) has established an E. J. Wylie Traveling Fellowship. The purpose of the fellowship is to enable young surgeons to visit centers of excellence in vascular surgery in the United States and abroad. The benefits of educational travel for the maintenance and enhancement of excellence in the practice of vascular surgery are obvious. To be considered for selection a candidate must: i. Be younger than 40 years of age at the time the traveling fellowship is awarded 2. Have completed a postgraduate vascular training program or have considerable experience in vascular surgery supplemental to general surgical training 3. Be committed to an academic career in vascular surgery and have obtained an academic appointment in a medical school or freestanding clinic devoted to excellence in medical education 4. Have a demonstrated record of success in pursuing clinical or basic science research sufficient to assure academic excellence in his or her pursuit of a career in vascular surgery Selection will be made without regard to the candidate's geographic location. A candidate submitting documentation for consideration for selection must furnish an up-to-date curriculum vitae and a list of publications, research projects, current research support, and a list of the centers that he or she wishes to visit. Three letters of recommendation are required, including one from the Division Head and another from the Chairman of the Department of Surgery of the institution in which the candidate holds a faculty appointment. A 500-word essay describing the objectives of the candidate's travel plans and linking these to his or her career goals must be appended. The Travel Fellowship Award is $10,000, granted to one person for use during a time limit and for expenses of travel, research, and clerical help. Application for the Fellowship award shall be made in a letter containing the information and documents as detailed. The deadline for receiving applications is March 1, 1992. Letter of nomination or intent should be directed to: Ronald J. Stoney, MD, FACS Chairman, E. J. Wylie Traveling Fellowship Committee Division of Vascular Surgery University of California Medical Center 505 Parnassus Ave., M-488 San Francisco, CA 94143
SURG 1992;15:285-94.)
Intermittent claudication, an uncommon complaint in young, healthy adults, may occur because of an unusual form of popliteal entrapment that affects well-conditioned athletes and usually causes deep-calf muscle cramping (soleal), rapid limb fatigue, and occasional paresthesias on the plantar surface of the foot. These symptoms are most predictably aggravated by running up hills or repetitive jumping or both and ,commonly affect athletes participating in sports such as cross country, basketball, and volleyball. The clinical complaints are frequently confusing to trainers and physicians alike, because they are not uniformly reproducible, because findings on physical examinations are usually normal, and because traditional use of physical therapy, rest, and antiinflammatory medications rarely afford symptomatic relief. This report describes the diagnosis and treatment of 12 patients with "functional" popliteal entrapment. PATIENTS A N D M E T H O D S Between 1987 and 1991, 120 patients were evaluated for symptoms of atypical lower extremity From the Departments of Surgery (Dr. Turnipseed) and Radiology (Dr. Pozniak), Universityof Wisconsin. Presented at the Forty-fifth Annual Meeting of the Societyfor Vascular Surgery, Boston, Mass., lune 4-5, 1991. Reprint requests: William D. Tumipseed, MD, Department of Surgery, H4/730A, 600 Highland Ave., Madison, WI 53792. 24/6/33493
clandication. 1 These patients (50 men, 70 women) were young (mean age, 22 years) and had longstanding symptoms (mean duration, 24 months) that would abate or completely disappear after extended rest but would reappear with exercise. Most were recreational or scholarship athletes (108 of 120, 90%) referred from our sports medicine department because of recalcitrant complaints of muscle cramping and paresthesias, which seriously affected competitive levels of performance in athletic events. Unlike patients suffering from overuse injuries such as stress fracture, tendonitis, and periostitis, these patients failed to respond to traditional forms of medical management and rehabilitation (physical therapy, ultrasonography, icing, and use of antiinflammatory medications). These patients were referred to the vascular service to rule out arterial or venous causes for their claudication symptoms and to determine whether chronic compartment syndrome might be present. After a thorough history was taken and physical examination was performed, noninvasive arterial plethysmography was performed, and segmental Doppler pressures were obtained at rest and after standard treadmill exercise (1.5 mph at 10 degrees for 5 minutes) in patients with absent or weak lower extremity pulses to screen for underlying arterial occlusive lesions such as premature atherosclerosis or medial cystic occlusive disease. In addition, all 285
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Fig. 1. The medial approach is routinely used in symptomatic patients suspected of having functional popliteal entrapment. The popliteal fossa is explored to nile out an anatomic form of entrapment. If the semimembranous and semitendinons tendons or gracilis and sartorial insertions must be transected during exploration of the popliteal fossa, they should be repaired before closure.
/I, J/llll/tlllll\\ I ~
~
'~~ ~///-4//-~ / / ~/ f' f ~~ ~
~.'~
Transected PlantarisM.
~e~lec(e Soleus dFaa~arura
Fig. 2. The deep proximal (soleal compartment) is decompressed by lysing the medial attachments of the muscle to the tibia. The dense anterior fascial sling of the soleus is sharply excised laterally to its fibular attachments. The plantaris muscle is resected.
120 patients were screened for possible popliteal entrapment by measuring Doppler pressures and calf plethysmography with the foot in neutral and in forced plantar and dorsiflexion positions? Twelve patients with positive screening tests for popliteal entrapment and symptoms of calf claudication also had duplex and magnetic resonance imaging (MRI) studies of the popliteal vessels performed at rest and with the foot in forced plantar flexion? Dynamic intravenous digital subtraction angiography (IVDSA) was performed in these patients to confirm popliteal artery entrapment. All patients with paresthesias of the foot had electromyography and nerve conduction studies as well. Compartment pressure measurements were performed with use of the hand-held Stryker Digital Computer System
(Stryker Surgical, Kalamazoo, Mich.) in patients with symptoms referable to the anterolateral and posterior superficial compartments. Pressure measurements were not performed in patients with deep posterior compartment symptoms because of the increased chance of neurovascular injury. Medial exploration of the popliteal fossa with resection of the plantaris muscle, and decompression of the deep posterior compartment by surgical release of the tibial attachments of the soleus muscle were performed in symptomatic patients with noninvasive and angiographic evidence of popliteal artery compression. Postoperative plethysmography, duplex scanning, or MRI of the popliteal artery was performed to document surgical correction of the popliteal entrapment.
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Popliteal entrapment 287
R. Ankle BP) Rest
L Ankle BP) Rest
R. ~ . i e i 3 P Y ~
',L Ankle BP) Dorsi
Fig. 3. Screening test in a patient with right-sided soleal claudication demonstrates bilateral popliteal artery compression in both the plantar flexion and dorsiflexion positions.
]Fig. 4. A, Duplex imaging demonstrates a widely patent poptiteal artery and normal flow in ~:he foot in neutral position. B, A popliteal artery in the same patient occludes against the posterior surface of the tibia with forced plantar flexion o f the foot.
288 Turnipseed and Pozniak
Fig. 5. Intravenous digital subtraction angiography demonstrates normal arterial anatomy on the right side with the foot in neutral position. On the left side lateral deviation from the midline position and compression of the popliteal artery occur against the lateral condyle of the femur (arrow).
SURGICAL T E C H N I Q U E Exploration of the popliteal fossa is performed with the patient under spinal or general anesthesia by means of the medial approach. Patients are placed in the supine position, prepared and draped so as to expose the entire lower extremity, and the surgical incision is made below the knee at the level of the upper midcalf just as though one intended to do a distal popliteal artery bypass (Fig. 1). Care is taken to avoid injury to the saphenous vein and nerve. The gasttocnemius fascia is then incised, and a large ellipse (3 x 6 cm) is removed to release the posterior superficial compartment. Whenever possible, the tendon insertions of the sartorius and the gracilis muscles as well as the semimembranous and semitendinous muscles should be left intact. Blunt and sharp dissection is used to expose the neurovascular and musculotendinous structures of the popliteal fossa. Palpation and direct examination of the popliteal artery is necessary to identify aberrant positioning of the vessels or anomalous muscular bands. If anatomic abnormalities cannot be identified and treated, the surgeon should release the medial tibial attachments of the soleus muscle by placing an index finger into the soleal canal and using the electric cautery. Once the tibial attachments of the soleus muscle have been released, the neurovascular bundle
Journal of VASCULAR SURGERY
is easily identified. The anterior fascia of the soleus muscle thickens to form a fibrous sting that crosses the lower border of the popliteal fossa attaching laterally to the proximal fibula. This fibrous fascial sling is sharply excised including its lateral attachments. The posterior fascia of the popliteus muscle is also excised. The facial excision from the opposing surfaces of the popliteus and soleus muscles make it less likely that rigid scar formation will reentrap the neurovascular bundle as it passes between them. Once the soleal release has been completed, attention is then turned to the plantaris muscle, which often acts in conjunction with the medial head of the gastrocnemius muscle to laterally compress the neurovascular bundle against the lateral margin of the soleal sling when the foot is in plantar flexion. The plantaris tendon, which runs anteromedially to the gastrocnemius muscle, is transected, and the large proximal portion of the muscle is dissected free of its anatomic bed and resected (Fig. 2). The wound is then irrigated and checked for hemostasis. The skin is closed with subcuticular absorbable sutures and steri strips. The patients are discharged the day after operation and instructed to use crutches for ambulatory assistance until normal weight bearing and gait is achieved. Once the skin is healed, rehabilitation is started by use of the stationary bike and kickboard exercises in the pool. Jogging usually begins in 3 to 4 weeks, and complete recovery to athletic levels of performance is achieved in 2 to 3 months. RESULTS None of the 120 patients in this series had physical or noninvasive testing evidence suggestive of intrinsic arterial occlusive disease. Seventy patients had symptoms attributed to the anterolateral compartment (58%), and 50 patients (42%) had symptoms affecting the posterior compartment (10 had superficial gastrocnemius muscle cramping; 12 had proximal soleal cramping and pain; 28 had distal retrotibial tightness and cramping). Plethysmographic screening tests for popliteal entrapment were positive in 30 of the 120 patients (25%) suspected of having possible compartment syndrome. (A positive test was defined as obliteration of the plethysmographic waveforms and/or a drop in ankle index to less than 0.5 with forced plantar flexion or dorsiflexion of the foot) (Fig. 3). Twelve of the 30 patients with positive results on entrapment screening studies had soleal claudication symptoms (11 unilateral, 1 bilateral). The remaining 18 patients with positive popliteal compression tests had no symptoms referable to posterior muscle groups. Furthermore, out-
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Fig. 6. A, Magnetic resonance gradient echo image demonstrates a normally positioned popliteal artery at rest. B, Sagittal MILl shows patient's popliteal artery in neutral position. C, When the foot is plantar flexed, the popliteal artery is occluded by lateral compression against the femoral condyle and the soleal sling. D, Sagittal MRI in plantar flexion demonstrates popliteal artery occlusion.
comes of plethysmographic screening tests performed in 40 asymptomatic age group controls were positive in 53% of those considered to be athletically well conditioned and 30% of those considered to be physically inactive. Duplex imaging with gray scale or color-flow techniques or both, performed on all 12 patients with positive plethysmographic screening tests and symptoms of calf claudication and in 20 asymptomatic control subjects with positive screening tests, confirmed popliteal artery compression at the approximate point where the neurovascular bundle enters the soleal canal (Fig. 4, A and B). Intravenous digital subtraction angiography was performed in eight of
the 12 symptomatic patients with deep calf daudication and positive plantar flexion studies. No angiographic evidence was found of medial arterial displacement or occlusion in the neutral or resting positions. However, with forced plantar flexion, lateral compression and occlusion of the popliteal artery was demonstrated (Fig. 5). Later in our study, IVDSA was discontinued because the same information could be obtained with use of MRI of the popliteal artery. Magnetic resonance imaging of the popliteal vessels and calf muscles suggested that the neurovascular bundle is forced laterally against the angle of the soleal sling and that the plantaris muscle in conjunction with the medial head of the gastroc-
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Table I. Summary of data Diagnostic tests (plantar flexion stress) Name
Age
Sex
RR
19
M
LH
20
M
KW
17
F
TK
25
M
KK
20
SR
Symptom
Pleth. ~
Duplex
Bilateral claud.
Positive
Positive
Positive
Positive
Positive
Positive
Positive
Positive
F
Unilateral claud. and paresthesia Unilateral claud. and paresthesia Unilateral claud. and paresthesia Unilateral claud.
Positive
Positive
20
F
Unilateral claud.
Positive
Positive
JS
19
F
Positive
Positive
JN
32
M
Positive
Positive
MH
26
M
Positive
Positive
DF
17
F
Unilateral claud. and paresthesia Unilateral claud. and paresthesia Unilateral claud. and paresthesia Unilateral claud.
Lateral compressmn popliteal artery Lateral compression popliteal artery Lateral compression popliteal artery Lateral compressmn popliteal artery Lateral compression popliteal artery Lateral compression popliteal artery Lateral compression popliteal artery Lateral compressmn popliteal artery ND
Positive
Positive
ND
JD
26
F
Unilateral claud.
Positive
Positive
ND
JS
16
F
Unilateral claud.
Positive
Positive
ND
IVDSA
.MR/ Lateral compression popliteal artery Lateral compression popliteal artery Lateral compression popliteal artery Lateral compresslon popliteal artery Lateral compression popliteal artery Lateral compressmn popliteal artery Lateral compressmn poptiteal artery Lateral compression popliteal artery Lateral compression popliteal artery Lateral compresslon popliteal artery Lateral compression popliteal artery Lateral compression popliteal artery
~ND, Not done; Clan&, claudication; Pleth, plethysmography.
nemius compresses the popliteal vessels against the lateral condyle of the femur more proximally (Fig. 6, A toD). Six of 12 patients (50%) with symptoms ofsoleal claudication also had intermittent numbness and plantar paresthesias. However, electromyography and nerve conduction studies performed on patients with paresthesias demonstrated minor conduction defects in only one case. Compartment releases (4 anterolateral, 5 distal deep posterior, and i posterior superficial) were performed in five of the 12 patients (40%) with soleal claudication before popliteal entrapment release. One patient was referred to our clinic after bilateral vascular reconstruction for popliteal entrapment syndrome because of persistent claudication symptoms. Postoperative plantar flexion and MRI in this patient demonstrated persistent popliteal artery compression. Thirteen surgical procedures were performed on the 12 patients with symptoms of soleal claudication and evidence of distal popliteal artery entrapment. All popliteal entrapment release procedures were done as first-day operative procedures by means of spinal or general anesthesia.4,5 The medial approach was routinely used, and effort was made to identify aberrant positioning of the popliteal artery or abnormal musculotendinous bands in the popliteal fossa. No
such abnormalities were identified in this group of patients. Entrapment release and posterior compartment decompression was accomplished by resection of the plantaris muscle, take-down of the medial tibial insertions of the soleus muscle, and complete excision of the fascial band that forms the soleal sling. All patients were discharged on the first postoperative day. Crutch assisted ambulation was allowed only until full weight beating and normal gait could be achieved. Physical rehabilitation and reconditioning in most athletes was completed within 2 to 3 months. Most complications were minor. Two patients had wound complications (1 seroma, 1 superficial cellulitis), one had transient reflex sympathetic dystrophy with complete resolution, and new compartment symptoms developed in two in areas remote to the soleal release because of increased physical activity. Clinical follow-up ranged from 3 to 36 m o n t h s (mean, 20 months). Nine of the 12 patients treated surgically (75%) had complete relief from claudication and paresthetic symptoms, and three (25%) were significantly improved. All but one returned to vigorous sports activity. Postoperative plantar flexion tests and duplex imaging performed have shown complete resolution of the popliteal compression and no evidence of recurrence (Fig. 7). Data are summarized in Table I.
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Popliteal entrapment
EA/IG ND Positive Negative Negative ND ND Negative Negative Negative ND ND ND
Surgery Soleal release and resection o f plantaris Soleal release and resecnon of plantaris Soleal release and resection o f plantaris Soleal release and resection o f plantaris Soleal release and resection o f plantaris Soleai release and resection of plantaris Soleal release and resection o f plantaris Soleal release and resection o f plantans Soleal release and resection o f plantaris Soleal release and resection o f plantaris Soleal release and resection o f plantaris Soleal release and resection o f plantaris
Follow-up
Outcome
18 m o
Excellent
9 mo
Excellent
18 m o
Excellent
30 m o
Excellent
27 m o
Excellent
36 m o
Excellent
39 m o
Excellent
16 m o
Excellent
6 mo
Excellent
4 mo
Good
25 m o
Fair
12 m o
Good
DISCUSSION
Poplite~d entrapment syndrome has classically been described as an anomalous relationship between the popliteal artery, the medial head of the gastrocnemius muscle, and other musculotendinous elements in the popliteal fossa. 4-8The original anatomic description of this condition was made by T. P. Stuart in 1879. 9 In 1959 Hamming 1° described clinical symptoms associated with the popliteal entrapment and a surgical plan for treating this condition (gastrocnemius transection and thromboendarterectomy of the popliteal artery). In 1965 Love and Whelan 11 coined the term "popliteal entrapment syndrome.''11 Since then several anatomic variants of this condition have been described and classified. The most common anatomic abnormalities include passage of the popliteal artery medial to the medial head of the gastrocnemius muscle (type 1, Insua Whelan), 12,13 normal anatomic positioning of the popliteal artery with compression caused by aberrant origins of the gastrocnemius or plantaris muscles (type II, Insua; type II and type III, Whelan), ~2,~3and compression of the popliteal artery by the popliteus muscle or a fibrous band in the same position (type IV, Whelan, Haimovici et al.). ~3,~4 More recent clinical experience suggests that the phenomenon of popliteal artery compression may be a much more common ew:nt than previously described. As screen-
291
ing techniques are more widely used it appears that "functional" popliteal entrapment may occur in the absence of any musculotendinous developmental abnormalities, and that this form of neurovascular compression may represent a normal physiologic variant in well-trained and physically overdeveloped athletes. ~5 It also appears that there may be a significant differencc in the morbidity associated with anatomic and functional forms of popliteal entrapment. Historical accounts suggest that arterial compression associated with deviations in the anatomic course of the popliteal artery or compression by anomalous bands may cause acute arterial occlusions or aneurysmal degeneration. No clinical evidence exists to support the concept that fimctional entrapment, in the absence of any clinical symptoms, requircs surgical intervention. Symptoms associated with the functional-type entrapment are uncommon and occur in only approximately 25% of those individuals with positive plantar flexion screening tests. No clear-cut evidence exists that compression of the popliteal artery in these patients actually causes soleal cramping and/or paresthesias. Physiologic and anatomic information derived from duplex imaging and MRI of the popliteal fossa suggests that lateral displacement of the neurovascular bundle may compress the popliteal nerve as well as the vein and artery against the lateral angle of the soleal sling and the lateral condyle of the tibia. Repeated trauma to the popliteal nerve with repetitive plantar flexion may cause a neuromuscular form of claudication and explain the intcrmittent paresthesias that are commonly associated with this condition. No substantive evidence has been found that arterial insufficiency is the primary cause for symptoms in these patients. All were capable of vigorous cardiovascular effort and exhibited remarkable endurance except in circumstances where accentuated plantar or dorsiflexion were required as in jumping or running up inclines. The rapid onset of symptoms with these specific maneuvers supports the idea that vascular insufficiency may not be the most important factor in the genesis of this symptom complex. Functional popliteal entrapment has many clinical similarities to the thoracic outlet syndrome, in both conditions primary arterial ischemia is uncommon. Although complications from arterial or venous compression are possible, they rarely occur. In both cases symptoms commonly develop when repetitive activity patterns result in netu'ovascular compression. Furthermore, in both conditions the only clinical beneficiaries from surgical intervention appear to be the symptomatic patients.
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Fig. 7. Postoperative pulse volume recording demonstrates release of a functional entrapment on the right side after a deep proximal compartment release and plantar resection. Our data suggest that pulse volume recording screening and duplex imaging tests may not be capable of distinguishing between anatomic and functional forms of this disease. 16 Dynamic "stress" angiography (our preference is IVDSA) and MRI studies are more helpful in analyzing the anatomic relationships of popliteal entrapment.17 Anatomic entrapment caused by abnormal passage of the popliteal artery around or through muscles is often manifest by "medial" deviation or compression of the artery with foot in dorsal or plantar flexion positions. Segmental popliteal artery occlusion also suggests possible anatomic entrapment. Angiography commonly demonstrates "lateral" displacement and compression of the popliteal artery in patients with "functional" entrapment. Intrinsic arterial lesions have not been demonstrated in patients with functional entrapment. The surgeon must be aware that several potential causes exist for popliteal entrapment. The decision to operate, the kind of operation, and the surgical approach should be tailored to information derived from clinical history and preoperative testing, The posterior approach with gastrocnemius muscle transection and arterial repair may be quite appropriate in patients with threatened limbs as a result of anatomic popliteal entrapment. However, the medial approach with resection of the plantaris muscle and proximal release of soleus muscle and excision of its fascia] b a n d is effective for functional forms of the disease and minimizes the rehabilitation efforts in the
competitive athlete. The im-portance of considering this ldnd of release in patients with popliteal entrapment is emphasized by the one patient in our series who remained symptomatic despite traditional vascular repair until the soleal muscle release and plantaris muscle resection was performed. In summary, functional popliteal entrapment syndrome is much more prevalent than originally expected. Symptoms associated with this condition are uncommon and are aggravated by specific physical activities in well-conditioned athletes. Noninvasive tests like plethysmography and duplex imaging may not accurately distinguish anatomic from functional types of popliteal entrapment syndrome. Angiography and MRI tests are more diagnostic. Surgical compamnent release for functional popliteal entrapment is indicated in symptomatic patients and perhaps in patients that remain symptomatic after traditional proximal popliteal repairs for anatomic entrapment syndrome. REFERENCES 1. Tumipseed W, Demler DE, Girdley F. Chronic compartment syndrome. Ann Surg 1989;210:557-63. 2. Darling RC, Bucldey C~, Abbott WM, Raines JK. Intermittent claudication in young athletes: popliteal artery entrapment syndrome. J Trauma 1974;14:543-52. 3. Collins PS, McDonald PT, L i m RC. Popliteal artery entrapment: an evolving syndrome. J VAsc SURG 1989;10: 484-90. 4. Rich NM, Hughes CW. Popliteal artery and vein entrapment. Am J Surg 1967;113:696-8.
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5. Berkoff HA, Crummy AB. Popliteal artery entrapment syndrome. Vase Surg 1976;10:264-7. 6. Podore PC. Popliteal entrapment syndrome: a report oftibiat nerve entrapment. J VASCSURG 1985;2:335-6. 7. Iwai T, Sato S, Yamada T, et al. Popliteal vein entrapment caused by the third head of the gastrocnemius muscle. Br I Surg I987;74:1006-8. 8. Delaney TA, Gonzalez LL. Occlusion ofpopliteal artery due to muscular entrapment. Surgery I971;69:97-101. 9. Stuart TPA. A note on variation of the course of the popliteal artery. J Anat Physiol 1879;13:162. 10. Hanmxing Jl. Intermittent claudication at an early age due to an anomalous course of the popliteal artery. Angiology
1959;10:369-70. i 1. Love JW, Whelan TJ. Popliteal artery entrapment syndrome. Am J Surg 1965;109:620. i2. Insua JA, Young JR, Humphries AW. Popliteal artery entrapment syndrome. Arch Surg 1970;101:771-5.
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13. Whelan TJ Jr, Popliteal artery entrapment syndrome. In: Haimovici H, ed., Vascular surgery: principles mad techniques. New York: Appleton-Century-Crofts, 1984:55767. 14. Haimovici H, Spragregen J, Johnson F. Popliteal artery entrapment by a fibrous band. Surgery 1972;72:789-92. 15. Rignault DP, Pailler IL, Lunel F. The "functional" popliteal entrapment syndrome. Int Angiol 1985;4:341-3. 16. Williams LR, Flinn WR, McCarthy WJ, Yao JST, Bergan II. Popliteal artery entrapment: diagnosis by computed tomography. J VASCSURG 1986;3:360-3. 17. Greenwood LH, Yrizarry JM, Hallett J-Wlr. Popliteal artery entrapment: importance of the stress runoff for diagnosis. Cardiovasc Intervent Radiol 1986;9:93-9. Submitted June 10, 1991; accepted Aug. 29, 1991.
DISCUSSION
Dr. N o r m a n Rich (Bethesda, Md.). Collectively we have found this report by Turnipseed and his colleagues to be informative and interesting. In general terms, questions could be raised regarding our 1979 report to ISCVS on popliteal vascular entrapment from Walter Reed Army Medical Center and the 1989 report by Collins and associates from Letterman Army Medical Center on why essentially all of the cases identified had anatomic anomalies in comparison with and contrast to the current report where there were none identified. The anthors identified a 1985 report by Rignault and his coworkers from Paris. Dr. Rignault has kindly served on our. faculty in recent years providing us an opportunity for an update regarding his thoughts since we believe that he was the first to use the term "functional" popliteal entrapment. Our current assessment is that considerable confusion exists between popliteal vascular entrapment and the compartment syndrome, as the latter is identified in the current report. We, like others, have found noninvasive testing to have too many false-positive outcomes in athletes who are asymptomatic. Angiography or M R I or both currently provide the best opportunity to distinguish entrapment from compartment syndrome as the authors have stressed. However, we ask the authors to comment on our observation that compartment syndrome can have elevated compartment pressure without interruption in the flow in the popliteal artery, whereas entrapment has definite interruption in major arterial flow and may or may not have high compartment pressure. As originally identified by Rignault, functional entrapment may be, but is usually not, associated with high intercompartmental pressure. The authors stress the importance of compartment decompression in their series of patients. Both their
diagnosis of compartment syndrome and the previous interpretation by Rignault possibly represent even two types of "functional" entrapment adding to even more confusion. In regard to the incision, we remain convinced that the posterior approach provides the best opportunity to identify anatomic variance. We have added the soleus release, as described by the authors, and/or the plantar tendon transection. If these structures appeared to be compressive, and this adds even further to the confusion, which of the therapies really alleviated the symptoms? We are aware of a number of anecdotal cases where anatomic variants have been missed with the medial approach. Could the authors have yet missed any of these anatomic variants? Dr. William Turnipseed. In response to the question of whether pressures were abnormal, I think it might be interesting for you to understand what we described as abnormal compartment pressures. These are significantly different from what you are used to dealing with when you are talking about the subacute or acute compartment syndromes. They are much lower. Abnormal pressures are usually between 15 and 20 m m H g or greater. We, as Dr, Rich has pointed out, have not identified significant compartment pressure elevations in many of the patients that we have talked about. In two cases we actually had an identical pattern o f symptoms in which we did the release procedure without the positive plantar flexion studies and got total relief o f the symptoms. One patient was sent to us from another institution in the Midwest where the traditional lysis and bypass operations had been performed for anatomic forms o f the disease and he still had the symptoms. We did the release and he does not have the symptoms anymore. I still am not sure which operation is most appropriate. There are some clear*cut indications for doing the posterior
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approach, and I think these are the patients who have the anatomic deviations of the popliteal artery that are described either by MRI or by angiography. By and large, if you look at the population we are dealing with, these are not army and air force recruits. These are elite class runners and dedicated athletes. A minimal operation has to be done, and I think this is the appropriate operation for this particular group of highly trained athletes with activityspecific pathologic complaints.
I believe as MRI is more widely used that we will be able to identify more precisely those that have functional forms of the disease and those that clearly have the anatomic form of the disease. I would totally agree with Dr. Rich that in circumstances where anatomic disease is identified, I would use the posterior approach.
E. J. W Y L I E T R A V E L I N G F E L L O W S H I P OF T H E E D U C A T I O N A L F O U N D A T I O N OF T H E S O C I E T Y F O R V A S C U L A R S U R G E R Y The Educational Foundation of the Society for Vascular Surgery (with financial assistance from W. L. Gore & Associates, Inc.) has established an E. J. Wylie Traveling Fellowship. The purpose of the fellowship is to enable young surgeons to visit centers of excellence in vascular surgery in the United States and abroad. The benefits of educational travel for the maintenance and enhancement of excellence in the practice of vascular surgery are obvious. To be considered for selection a candidate must: i. Be younger than 40 years of age at the time the traveling fellowship is awarded 2. Have completed a postgraduate vascular training program or have considerable experience in vascular surgery supplemental to general surgical training 3. Be committed to an academic career in vascular surgery and have obtained an academic appointment in a medical school or freestanding clinic devoted to excellence in medical education 4. Have a demonstrated record of success in pursuing clinical or basic science research sufficient to assure academic excellence in his or her pursuit of a career in vascular surgery Selection will be made without regard to the candidate's geographic location. A candidate submitting documentation for consideration for selection must furnish an up-to-date curriculum vitae and a list of publications, research projects, current research support, and a list of the centers that he or she wishes to visit. Three letters of recommendation are required, including one from the Division Head and another from the Chairman of the Department of Surgery of the institution in which the candidate holds a faculty appointment. A 500-word essay describing the objectives of the candidate's travel plans and linking these to his or her career goals must be appended. The Travel Fellowship Award is $10,000, granted to one person for use during a time limit and for expenses of travel, research, and clerical help. Application for the Fellowship award shall be made in a letter containing the information and documents as detailed. The deadline for receiving applications is March 1, 1992. Letter of nomination or intent should be directed to: Ronald J. Stoney, MD, FACS Chairman, E. J. Wylie Traveling Fellowship Committee Division of Vascular Surgery University of California Medical Center 505 Parnassus Ave., M-488 San Francisco, CA 94143
