Popliteal
artery entrapment - diagnosis and treatment. the concept of functional
entrapment.
(Portuguese
PDF version)
José
Dalmo de Araújo1, José Dalmo de Araújo
Filho2, Emerson Ciorlin2, Ana Paula
de Oliveira2, German Eliecer Sanchez Manrique2,
Arlindo Dias Pereira2
1.
Head of the Division of Vascular Surgery, Institute of Cardiovascular
Diseases (Instituto de Moléstias Cardiovasculares - IMC), São
José do Rio Preto, São Paulo, Brazil.
2. Institute of Cardiovascular Diseases (IMC), São José
do Rio Preto, São Paulo, Brazil.
Correspondence:
Dr. José Dalmo de Araújo
Rua Castelo D'Água, 3030
CEP: 15015-210 - São José do Rio Preto - SP.
Tel.: +55 17 230.8522
Fax: +55 17 232.3764
E-mail: imc@imconline.com.br
ABSTRACT
Objectives:
To discuss the diagnosis, complications and treatment of popliteal
artery entrapment and the concept of functional entrapment, giving
special attention to the treatment of "anatomical" and
"functional" cases.
Methods:
Sixty-three patients with popliteal artery entrapment were studied
in the last 25 years. Thirty-one of these patients were submitted
to surgery: nine of them had abnormal muscle insertion ("anatomical
cases"), four presented bilateral popliteal entrapment; eight
of 13 surgically treated limbs showed type II disorders, four of
them, type III, and one limb had type IV disorders. Eight limbs
revealed vascular complications; one presented stenosis; three of
them had chronic obstruction; two had acute obstruction (one with
acute thrombosis and one with embolism) and two limbs presented
aneurysms. Twenty-two patients had functional entrapment (with normal
muscle insertion). Two aneurysms occurred in this group due to compression
at the level of Hunter's canal. The 22 patients were submitted to
section of the internal gastrocnemius tendon, which often showed
hypertrophy and/or lateral insertion. Veins were used as a substitute
for damaged arteries.
Results:
After a follow-up of six months to 25 years (on average six years),
the results were excellent for "anatomical" cases. Among
the "functional" cases, eight patients showed recurrent
compression (25%) and three patients had recurrent symptoms (10%).
These results were attributed to insufficient surgical decompression.
The reduction of symptoms was attributed to the release of the popliteal
sciatic nerve, to the compartment decompression originated from
the surgical treatment and to the change in sports habits in the
postoperative period.
Conclusions:
The "anatomical" cases should be operated on even if they
are asymptomatic. In cases with arterial injury, the injured artery
must be replaced with an autologous vein, which thus prevents endarterectomy.
The "functional" cases must be clinically treated with
alteration of sports habits, exercise therapy, and follow-ups with
duplex ultrasonography every six months. Surgery must be indicated
if symptoms worsen or if there is vascular injury.
Key
words: entrapment syndrome, popliteal vessels, muscle abnormalities
Palavras-chave: síndrome de aprisionamento, vasos
poplíteos, anomalias musculares.
J
Vasc Br 2002;1(1):22-31.
INTRODUCTION
Popliteal
artery entrapment was first described in 1879, in Edinburgh, by a medical
student, while he was dissecting a leg that had been amputated due to
gangrene caused by aneurysmal thrombosis of the popliteal artery in
a 64-year-old patient.1 For a long period,
popliteal artery entrapment was considered to be a very rare condition.
In 1925, Chambardel Dubreuil2 reported an
anatomic variant in which there was external deviation and detachment
of the popliteal artery from its "sentinel vein" due to the
of the internal gastrocnemius tendon.
In 1959,
Hammings3 first described a case of a 12-year-old
patient who was successfully treated with surgery (section of the inner
head of the gastrocnemius and endarterectomy of the popliteal artery).
From that year on, several cases were reported.19-20
Servello, in 1962,20 was the first to describe
missing pulses with maneuvers of plantar flexion and dorsiflexion. Love
and Whelan, in 1965, coined the term "Popliteal Artery Entrapment"
and proposed its classification into four types (see further ahead).8
Frequently, vascular surgeons come up with at least one unpublished
case at discussions during meetings. Consequently, this disease could
be no longer regarded as extremely rare and vascular surgeons probably
developed more awareness about it with the advent of less invasive diagnostic
tools, which allowed for more frequent and earlier diagnoses.
In 1967,
Rich and Hughes9 described the concomitant
compression of the popliteal vein, thus adding a new type (V) to the
previous classification proposed by Love and Whelan in 1965.8
Later on, in 1971,14 Delaney and Gonzales
complemented this description. Several studies showed the possible entrapment
of the popliteal vein either separately21,22,23,24
or in association with artery entrapment.16,25
Rich et al., in 197925, coined the term
"Popliteal Vascular Entrapment".
Raju and
Neglen,26 in their excellent study conducted
in 2000, showed incidental venous compression in 42% of venograms (22%
of them consisted of bilateral compression). A limited number of these
compressions have pathological relevance, provided that other causes
are ruled out, for symptoms of Chronic Venous Insufficiency, especially
when the pressure of the popliteal vein is present. In 57% of the cases,
there was concomitant artery entrapment, as diagnosed by photoplethysmography.
The authors observed abnormal insertion of the gastrocnemius in five
of 30 patients and abnormal course of popliteal artery and vein (lateral
gastrocnemius tendon) in two cases. The remaining 23 cases did not show
muscle disorders. In this case, compression was attributed to the perivascular
tissue when the muscles contracted.
In 1985,
Rignault et al.27 described the "functional"
entrapment of the popliteal artery in 53 recruits and 53 asymptomatic
athletes. They observed entrapment in 30% of the whole sample and in
50% of the athletes. After that time, several studies28,29,30
showed asymptomatic arterial and venous compression in the general population
when plantar flexion or dorsiflexion of the foot was performed as occurs
with the subclavian artery as a result of hyperabduction of upper limbs.
In 1999,
Levien and Veller31 drew attention to the
fact that 50% of the population can have "functional" compression
and that, in such cases, the treatment should be primarily clinical.
Surgical treatment should be used in selected and very symptomatic cases
that do not respond to clinical treatment. Therefore, these authors
suggested the addition of type VI to the classic classification proposed
by Delaney and Gonzales.14 Nowadays, we should investigate the cases
of popliteal artery entrapment, by clinical and laboratory analyses,
in young athletic patients who complain of claudication pain in the
lower limbs, without any other etiological explanation (popliteal artery
entrapment) or in cases of patients with signs of chronic venous insufficiency,
especially edema and unremitting pain or pain that increases on walking
(popliteal vein entrapment).
The most
frequently used classification is that proposed by Delaney and Gonzales14
with additions by Rich and Hughes9 and Levien
and Veller.31
I. The
popliteal artery is medially deviated towards the internal gastrocnemius
tendon, which is normally inserted into the femoral condyle.
II. The
prematurely formed popliteal artery partially arrests the migration
of the medial head of the gastrocnemius, which has a more lateral attachment,
thus compressing the artery.
III. Presence
of additional gastrocnemius tendon, which is laterally inserted and
compresses the artery.
IV. Arterial
compression by the popliteal muscle.
V. Concomitant
compression of the popliteal vein. This could occur in types I to IV
Rich and Hughes.9
VI. Functional
compression: the artery and vein are compressed by anatomically normal
but hypertrophic muscles. Levien and Veller.31
Evidently,
not every case can be comprised by these classifications. Therefore,
for example, isolated venous compression and the compressions by Hunter's
canal, as occurred with one of our patients (Figure 1), would be regarded
as special cases.
 Figure
1 - Poststenotic bilateral popliteal
artery aneurysm. Compression by Hunter's canal. Without anomaly of anatomical
insertion. Severe hypertrophy of the gastrocnemius muscle.
PATIENTS
AND METHODS
Over 25
years, 63 patients were diagnosed with popliteal artery entrapment syndrome.
Thirty-one were operated on and among these, nine had different anatomical
disorders, especially type II (Table 1).
Table
1 - Popliteal artery entrapment (the most frequent anatomical disorders)
 |
| Type
I |
0 |
| Type
II |
07 |
| Type
III |
04 |
| Type
IV |
02 |
| n.
of limbs |
13
(09 patients) |
| n.
of patients |
09 |
|
Three
bilateral occurrences with type II and two occurrences with type III
The remaining
patients did not show anatomical disorders described in the classic
classification; however, all of them had hypertrophic medial head of
the gastrocnemius (five patients), lateral insertion of the gastrocnemius
(five patients) or both conditions (11 patients) (Figure 2).
Figure
2 - Surgical aspect of gastrocnemius tendon hypertrophy, before
and after section.
Among the
anatomical disorders presented by a patient who practiced distance running
and cycling, there was large hypertrophy of the gastrocnemius and adductor
muscles, with stenosis of Hunter's canal and formation of bilateral
aneurysm of the popliteal artery (Figure 1) with distal embolization.
The rest of the arterial tree above Hunter's canal was absolutely normal.
Abnormal muscle insertion was absent. There were vascular complications
in eight limbs: stenosis in one (Figure 3), three chronic obstructions
(Figure 4), two acute obstructions (acute thrombosis in one and embolism
in the other) and two aneurysms (Figure 5) (Table 2). These complications
account for 14% of 57 surgically treated limbs; 46% of the "anatomical"
cases and 4.5% of the "functional" cases.
Figure
3 - Arterial stenosis due to type II
anatomical entrapment. Note the normality of the rest of the artery.
Figure
4 - Obstruction of the popliteal artery
secondary to type II entrapment.
Figure
5 -Surgical aspect of the popliteal
artery aneurysm. Case of Figure 1.
Table
2 - Popliteal artery entrapment - vascular complications
|
| Stenosis |
01 |
| Chronic
obstruction |
03 |
| Acute
obstruction |
02 |
| Aneurysm
|
02 |
| Total
|
08
(14% of 57 surgically treated limbs) |
|
Fifty-seven
limbs were surgically treated in 31 patients. Bilaterality was present
in 87% of the cases. However, when the cases with anatomical disorders
are set apart, bilaterality is reduced to 44% (4/9) (total of 13 limbs).
In cases with no muscle disorder, bilaterality amounted to 100% in 22
patients.
Surgery
was always indicated when arterial compression was present. Up to the
moment, we have not had any indication because of venous compression,
although it is often combined with arterial compression in functional
cases. We have two patients on follow-up who presented chronic venous
insufficiency, possibly related to muscle compression of the popliteal
vein.
The posterior
route was always used (incision in Z to cross the popliteal crease with
the upper internal branch and the lower medial branch, superposed to
the vascular pathway) (Figure 6). The surgery was performed on both
limbs at one time when myotomy and revascularization are required on
one side only. When bilateral vascular repair is necessary, the surgery
is performed in two stages.
Figure
6 - Posterior route to popliteal veins
and nerves.
The patient
is able to walk on the first day after the surgery.
Of 63 patients,
32 have been followed up with clinical counseling and exercise therapy.
Surgical treatment is only recommended if symptoms worsen to an extent
in which social and professional life is hindered or if vascular injuries
appear.
The maximum
follow-up period for surgically treated cases was 25 years and the minimum
was six months (on average six years) (diagnosis was more common in
the last few years).
The general
characteristics of surgically treated patients are shown in Table 3
Table
3 - Popliteal artery entrapment - general characteristics of surgically
treated patients
|
| Surgically
treated patients |
31 |
| Surgically
treated limbs |
57 |
| Male
|
28
(44%) |
| Female
|
35
(56%) |
| Mean
age |
33.8
years |
| Bilateral |
87% |
| Bilateral
in functional cases |
100% |
| Bilateral
in "anatomical" cases |
44% |
| Follow-up
period |
6
years (6 months to 25 years) |
| Total
of diagnosed patients |
63
(32 patients under clinical follow-up) |
|
Since most
patients were young, only one died during the study period (56 years
old at the time of surgery - death occurred 18 years after the surgery,
with no recurrence of symptoms). The patient who was operated on 25
years ago was 21 years old at the time of surgery. This patient was
submitted to reverse saphenous vein interposition graft due to occlusion
and has remained asymptomatic up to now.
Among the
remaining patients, only two missed follow-up, but they had two or three
follow-ups within a six-month period, with good results. These two patients
belong to the "functional" group. Therefore, of 31 patients,
28 are on regular follow-up. The patients are submitted to duplex ultrasonography
of popliteal arteries with plantar flexion force. The first exam is
done 30 days after the surgery, six months afterwards and then once
a year.
The indication
of surgical treatment follows an algorithm (Figure 7) that involves
only symptomatic patients. In case of negative entrapment maneuvers
or negative duplex ultrasonography results, another etiology should
be taken into consideration (Compartment Syndrome or postural disorders).
Figure
7 - Management of popliteal artery
entrapment.
In case
of positive maneuvers, duplex ultrasonography is performed with entrapment
maneuvers. If compression is partial, clinical follow-up and duplex
ultrasonography should be done every six months. If compression increases
and/or symptoms worsen or if vascular injuries appear, angiography (AG)
(arteriography and venographies), nuclear magnetic resonance (NMR) or
computed tomography (CT) and decompressive surgery should be carried
out.
If the
maneuver produces total occlusion, AG and/or NMR or CT are carried out
with maneuvers that can minimize compression. If no vascular injury
or muscle disorders are present, clinical follow-up and duplex ultrasonography
should be performed every six months. If symptoms and exams are stable,
clinical follow-up should be done. If the vascular injury is visible
on initial duplex ultrasonography, AG and/or MNR or CT should be performed
and surgery should follow. If muscle insertion is abnormal, surgery
is mandatory.
The types
of surgeries available are shown in Table 4.
Table
4 - Types of surgery
|
| Myectomy |
36 |
| Myotomy |
15 |
| Myotomy
+ saphenous vein graft* |
06 |
| n.
of surgically treated limbs |
57 |
|
* In five
cases saphenous vein interposition graft was carried out and in one
case there was femoro-popliteal bypass below the knee
RESULTS
The results
of surgically treated cases (Table 5) showed recurrent vascular compression
in eight limbs (25%), which occurred in "functional" cases.
However, of these eight patients, only three (10%) presented recurrent
symptoms.
Table
5 - Popliteal artery entrapment - surgical results
|
|
Compression
relapse |
Symptoms
relapse |
|
| n.
of patients (31 ) |
8
(25%) |
3
(10%) |
| Surgically
treated limbs (57 ) |
16
(28%) |
6
(10%) |
| n.
of "functional" patients (22
) |
8
(36%) |
3
(13%) |
| n.
of "functional" limbs (44 )
|
16
(36%) |
6
(13%) |
|
All relapses
were bilateral. The 13 limbs surgically treated due to anatomical disorder
(including six limbs with vascular complications) presented great results.
When only
the functional group is taken into account, the recurrence rates obviously
increase (Table 5). Relapses are always bilateral.
Surgical
complications include paresthesia and transient edemas. The esthetic
aspect of the scar of the posterior route is not good, especially in
female patients.
Functional
repair is perfect, despite the partial section and/or resection of the
gastrocnemius. Muscle reconstruction was not carried out in any case.
DISCUSSION
It is well
defined that the entrapment of popliteal arteries due to anatomical
disorder should be distinguished from functional entrapment, whose causes
are still under discussion. In these cases, no anatomical disorders
are present,2-31 however, there might be
vascular injuries in the long run.32 Turnipseed
and Posniak33 stated that vascular injuries
occur in 25% of symptomatic functional cases. Levien and Veller31
reported three cases of obstruction in 30 limbs with functional compression
(10%). In our series, there is only one case of bilateral aneurysm in
22 patients (4.5%).
Some authors27,28
suggested that, in "functional" cases, the hypertrophy of
the internal gastrocnemius bundle alone is responsible for compression
during muscle contraction. Other authors suggest that the lateralized
insertion of the internal gastrocnemius tendon is more important than
hypertrophy, which would explain its incidence among patients without
remarkable muscle hypertrophy. In fact, Hoffmann et al.34
showed that the incidence of functional compression is the same in highly
trained asymptomatic patients in comparison with patients whose physical
activity is ordinary. Still other authors37,40
suggested both factors, which is in agreement with our study.
Turnipseed
and Posniak33 suggested that compression,
in functional cases, occurs because of the contraction of the internal
gastrocnemius tendon in tandem with the plantaris muscle. These muscles
press the neurovascular bundle outwards against the external femoral
condyle and the canal of the soleus muscle. The diagnosis can be confirmed
by angiography or resonance angiography, which should show laterally
deviated popliteal artery and vein. This was observed in the arteriographies
of several of our cases (Figure 8). In such cases, the plantaris muscle
and the soleus muscle canal should be sectioned and the upper part of
this muscle should be detached from the inner border of the tibia.
Figure
8 - Arteriographic aspect of the lateral
deviation of the popliteal artery, in case of functional entrapment.
According
to Raju and Neglen,26 functional venous
compression could be produced by the perivascular fibrous tissue pulled
during the contraction of adjacent muscles or by abnormal insertion
of the internal gastrocnemius tendon. This venous compression, even
if functional, could cause venous thrombosis in patients who are submitted
to long surgeries and remain with their leg extremely extended or in
patients that have to stay in bed for long periods of time, also with
hyperextension of their lower limbs.31,36
This reminds of axillosubclavian effort thrombosis, which occurs after
hyperextension of the arm in patients with costoclavicular compression.
The compression
of the tibial nerve could be responsible for some of the symptoms, according
to other authors.33
Some studies
suggested that the hypertrophy of both gastrocnemius tendons is the
cause for popliteal artery compression.37
Postural
disorders, such as hyperlordosis or hyperextension of posterior knee
ligaments, are also mentioned as possible causes.35
Regardless
of the cause of compression, we still have doubts with respect to the
treatment:
1. Should
we use clinical or surgical treatment?
2. If surgical,
what kind of procedures should be taken?
3. What
is the access route?
Our experience
allowed us to build a diagram to solve any doubts about the treatment
or procedures in these cases (Figure 7).
It is essential
that duplex ultrasonography38 and AG, NMR30
and CT39 be used.
AG is used
to show compression and/or deviations of the popliteal artery, in addition
to existing vascular injuries (stenosis, obstructions, aneurysms) and
it is also used to analyze the distal vascular bed in case revascularization
is deemed necessary. On the other hand, AG allows observing the lateral
deviation of the popliteal artery or vein in functional entrapments
(Figure 8), since MNR and CT are not always available. However, if they
are available, it is possible to analyze the adjacent muscles and their
possible insertion disorders. Contrast enhanced resonance angiography
and computed tomography angiography allow investigating the vessels.
Perhaps, with the improvement of techniques and equipment, we will be
able to eliminate the use of AG, which is more invasive.
This diagram
only includes symptomatic patients. Sometimes, the symptoms are somewhat
unusual. For example, claudication when walking but no claudication
when running (possibly because walking does not require greater extension
of the popliteal fossa muscles);33 one
of our patients would feel pain in her calf whenever she wore high heels;
another patient only felt pain in the second half of the soccer game
or during the second weekly training (cumulative trauma disorder?).
Couzan
et al.35 suggested standing on tip-toes
every three minutes: a patient with remarkable compression cannot do
that more than 20 times.
The signs
of chronic venous insufficiency in a young patient with no history of
deep vein thrombosis sometimes suggests venous compression that occurs
either separately or in combination with arterial compression.26
The high
incidence among our female patients (56%) (compared to10-20% in the
literature) is due to the inclusion of "functional" cases
and to the fact that women currently go to fitness centers and end up
developing their calf muscles. Such habit causes functional compression
and also triggers off symptoms in "anatomical" cases that
used to be asymptomatic.
The high
rate of bilaterality also results from the inclusion of functional cases.
Actually, it was expected, since the development of muscles by exercises
is always bilateral and simultaneous.
The type
of surgery required depends on preoperative information obtained from
complementary exams: AG, MNR and CT. In short, it is necessary to decompress
the popliteal artery and vein at their full extension: from Hunter's
canal to the soleus canal; in addition, both of these canals must be
sectioned. As already mentioned, the section of the plantaris muscle
and, occasionally, of the medial head of the gastrocnemius may be necessary.
Evidently, if vascular injury is already present, it should be treated
and the injured artery should be replaced with an autologous vein, thus
avoiding the use of endarterectomy, which has bad results in the long
run.31 If any other muscle insertion disorders exist, they have to
be corrected, which is usually done by sectioning the anomalous tendons.
To establish the diagnosis of compressions caused by muscle insertion
disorders is extremely important and, in these cases, surgery is recommendable
even if vascular injuries and symptoms are nonexistent. Both MNR and
CT are very useful in this case.
Finally,
the access route is another controversial point. Most authors argue
that the posterior route offers enhanced visualization of all popliteal
fossa structures. Other authors33,40
affirm that the medial route is more esthetic and allows treating the
problem more properly.
In this
study, we always used the posterior route. We agree, however, that the
postoperative scar is esthetically bad and that the medial route should
be used as an alternative, especially in "functional" cases.
Regarding
the high rate of recurrence among our "functional" cases (36%),
we believe it is due to the insufficient release of the popliteal artery
and also to the retraction of the postoperative scar. The latter hypothesis
can be explained by relapse after the third or fourth follow-up visit
in most of the cases. Recently, we have adopted myectomy (resection
of a segment of the medial head of the gastrocnemius) in order to correct
this problem.
The decompression
of the popliteal artery should be complete, that is, from Hunter's canal
(which is sectioned) to the soleus canal (which is also sectioned).
If necessary, sections of the plantaris muscle, semimembranous muscle
and popliteal muscle (even if it is in normal anatomical position, anterior
to the popliteal artery) should be performed. In addition, the soleus
muscle should be detached from the upper third of the tibia. This decompresses
the deep posterior compartment.
As for
the lower rate of recurrent symptoms (three patients - 13%), if compared
to the compression recurrence rate (eight patients - 36%), can be explained
by the release of the popliteal sciatic nerve associated with certain
decompression of the compartment by means of the surgery and also by
the change in sports habits of the patients after the surgery.
The excellent
results obtained in the "anatomical" cases are a consequence
of replacing the injured artery with saphenous vein instead of trying
to preserve the injured artery by means of "plasty" or similar
procedures.31
All the
surgically treated patients in this group were symptomatic. In addition,
we were always concerned with ruling out other concomitant diseases,
such as spinal cord disorders (disc herniation, scoliosis, hyperlordosis)
and knee postural disorders (hyperextension of the posterior ligament)
and foot disorders (flat or claw feet).
The treatment
of functional cases should be primarily clinical, with alteration of
sports habits and exercise therapy to encourage proper muscle development.
If surgical treatment is necessary, it should be done completely, as
already mentioned.
Cases with
abnormal muscle insertion are formally recommended for surgical treatment,
even if they are asymptomatic, in order to avoid vascular injuries,
which could worsen and cause limb loss. Today, with the improvement
of diagnostic tools, diagnosis can be established earlier and provide
sufficient anatomical information, which differs from the first published
cases that were often diagnosed by means of those vascular complications.
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