Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3649_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
30.08.2026
Размер:
53 Мб
Скачать
Chapter
https://t.me/med1917
1 
Anatomy
Type D: The GSV is not visible for a certain distance
from the distal thigh down below the knee, but pierces the superficial fascia to become a subcutaneous CV that distally, usually at the mid-leg, enters again into the saphenous compartment. This arrangement corresponds to the ‘S’ type in Figure 1.23 and was found in 14% = 72/500 of cases. In 58% of these the GSV and the CV were incompetent and the latter visible (Fig. 1.29D).
Type E: Same as the previous but the absent portion
of the GSV was very short and, from just below the knee down along the leg; 14% = 72/500. In 53% of these the GSV was incompetent and with varicose collaterals just distal to the knee (Fig. 1.29E).
In 3% of cases (15/500) the classification according to the
criteria described above was not possible.
These data show that in one-third of subjects the middle portion of the GSV is absent (or hypoplastic) for a variable length (types D and E). In subjects with this pattern, varicose veins were present in 56% of cases, while in subjects where the GSV is present in its entire length (types A, B and C) vari­cose veins were present in 34% of cases. This may indicate that the subcutaneous vein which assumes the role of a saphenous vein becomes more readily varicose, probably because it is not protected by the superficial fascia. In such cases the anatomi­cal pattern classified as types D and E might be a predisposing factor for varicose veins.
42
41% both GSV and AASV were present. In these cases the AASV was invariably thinner than the GSV (average 2.4 vs
4.0 mm). Proximally, the ASV joined the GSV close to the SFJ and only rarely (in 3% of cases) terminated directly into the femoral vein. Following the vein backwards, the AASV pierced the superficial fascia and exited the saphenous compartment at a distance of 7–30 cm (average 16 cm), continuing distally as a subcutaneous collateral in an anterolateral direction in 72% of cases, in a medial or anterior direction in 11%, and as more branches and in more directions in 11%. In 6% of cases the AASV joined the GSV without leaving the saphenous compartment (Fig. 1.31).
38
In the remaining 11% of the 172 observed limbs only one vein was observed in the proximal part of the saphenous compartment, but according to the ‘alignment’ sign this vein was the AASV, while there was no GSV in the expected position (saphenous aplasia) (Fig. 1.19C) distally from the SFJ the AASV curved medially and continued downwards along the typical course of the GSV.
. In these cases, 18–20 cm
38
The AASV is of clinical importance because in patients with varicose veins it may be the only proximal reflux source while the GSV remains competent
3,46
(Fig. 1.32), or alternatively, both GSV and ASV may be incompetent. In a retrospective study of 1450 varicose limbs the AASV was involved in 14% (203/1450) of cases (M. Cappelli, personal communication,
2000). The possible patterns of GSV and/or AASV incompe­tence at the SFJ are described elsewhere.
33
T vein
A very constant tributary vein (known as the T vein), has been described. leg just distal to the knee and joins the GSV at the same level in a right-angle fashion (see Fig. 1.7), running inside the fascial compartment for a long distance (Fig. 1.30). It is con­sistently fed by reflux varicose veins, which are clinically visible in the paratibial region and/or in the lateral aspect of the leg.
48
It runs horizontally from the lateral aspect of the
The anterior accessory saphenous vein
When two veins are present in the proximal third of the great saphenous compartment, the medially situated vein is the GSV while the laterally placed vein is the AASV. AASV is recognized and distinguished from the GSV by the ‘alignment’ sign own ‘eye’ (see Fig. 1.19B).
37
(see Fig. 1.19A), and may also have its
3
The anatomy of the AASV was studied by transverse DUS of the saphenous compartment of the thigh in 172 consecu­tive limbs. In 48% of cases only the GSV was present while in
“T” Vein
33,38–41
The
Small Saphenous Vein
The SSV begins behind the lateral malleolus as a continuation of the lateral marginal foot vein. It ascends up the posterior aspect of the calf to empty into the popliteal vein. The SSV lies for its entire length in an intrafascial compartment delimited deeply by the aponeurotic (muscular) fascia and superficially by the superficial fascia. The distal part of this compartment appears on transverse scan, especially in fat legs, as an ‘eye’ similar to that of the GSV in the thigh. The proximal part of the compartment is typically of a triangular shape and is delimited by the medial and lateral heads of the gastrocne­mius muscle and the superficial fascia that stretches over the
Figure 1.30 A vein can be seen running horizontally from the lateral
aspect of the leg just distal to the knee and joining the great saphenous vein (GSV) at the same level in a right-angle fashion. What is peculiar is that it runs inside the fascial compartment for a long tract.
The
T vein of the leg. EJVES 2003;25:313–18.)
14
GSV
(From Zamboni P et al:
A
Figure 1.31 Anterior accessory saphenous vein (AASV) patterns: Following
the vein backwards, the AASV pierces the superficial fascia of the saphenous compartment at a distance of 7–30 cm. It continues distally as subcutaneous collateral in an anterolateral direction in 72% of cases (A); in a medial or anterior direction in 11%, and as more branches and in more directions in 11% (B). In 6% of cases the AASV joins the GSV without leaving the saphenous compartment (C).
la veine saph Phl
ène accessoire antérieure et de son role dans la maladie variqueuse.
ébologie 57:135–140, 2004).
B C
(From Ricci S, Georgiev M, Cappelli M: Définition de
SE
60
https://t.me/med1917
SI
TV
AASV
SP
PTV
PASV
Figure 1.32 The anterior accessory saphenous vein (AASV) may be the
only proximal reflux source while the great saphenous vein is competent: in these cases the terminal valve (TV) is incompetent while the preterminal valve (PTV) is normally competent. PASV, posterior accessory saphenous vein; SE, superficial epigastric vein; SI, superficial iliac vein; SP, superficial pudendal vein.
(Original sketch courtesy of A Pieri)
SSV
3129
16 13 12 19
Figure 1.34 In about 50% of normal subjects the small saphenous vein has
no popliteal junction at all or is just a tiny communicating vessel (right), the classical junction (the first on the left) being not the most frequent.
der Stricht J. La petite veine saph
GSV
ène existe-t-elle, Phlébologie 3:309–15, 2001).
(From Van
Small Saphenous Vein
GCV
PV
PA
Figure 1.33 In 26% of cases the small saphenous vein merges with the
gastrocnemius vein before joining the popliteal vein.
3,36
intermuscular groove (Figs 1.12B, 1.21).
The SSV may occa­sionally be duplicated, with two (or even three) veins of various lengths running into the saphenous compartment.
Saphenopopliteal junction
The saphenopopliteal junction (SPJ) is situated, typically, within 5 cm proximal to the popliteal crease. In some cases the SSV merges with the gastrocnemius vein before joining the popliteal vein (Fig. 1.33). This has been found in 26% of cases in a series of 83 consecutive limbs with incompetent and dilated SSV. may join the popliteal vein at different sites on its circumfer­ence. In the above-mentioned series the SPJ was lateral in 42%, posteromedial in 30%, posterior in 15%, posterolateral in 12% and even anterolateral in 1% of cases. in normal subjects it has been observed that in about 50% of cases the SSV has no popliteal junction at all (see next para­graph), or is just a tiny vessel (Fig. 1.34). SSV may be hypoplasic or absent.
49
Another point of surgical interest is that the SSV
49
Astonishingly,
50
In some cases, the
Giac
TE
Figure 1.35 Proximally the thigh extension may join the great saphenous
vein as intersaphenous thigh anastomosis (the ‘true’ Giacomini vein); continue straight up into the gluteal area as a single vein or be divided into many deep and superficial branches; join the deep femoral veins as a posterior or posterolateral thigh perforator; or divide into many muscular or subcutaneous branches of the posterior thigh.
Bourgery, Anatomie descriptive. In Delaunay CA, editor, [no title available] Paris, 1835. Courtesy M. Georgiev, MD)
Musc
Perf
SPJ
(From a design taken from
Thigh extension of the SSV
In 1873 Giacomini described in detail the thigh extension (TE) of the SSV (Fig. 1.35). confirmed that the SSV extends into the thigh in about 50% of cases; in a third of these the SSV joins the popliteal vein (Fig. 1.36A) and then continues up into the thigh, while in the remaining two-thirds of cases the SSV continues into the thigh without any connection with the popliteal vein53 (Figs 1.34,
1.36B). The anatomy of the TE of the SSV (also known as vein
of Giacomini or femoropopliteal vein) has been confirmed by USI. The distal portion of the TE is recognized on DUS by its intrafascial position into a triangle-shaped compartment that resembles the GSV compartment and is delimited by the semi-
51,52
Further anatomical dissections
15
Chapter
https://t.me/med1917
1 
Anatomy
TE
SSV
SSV
TE
PV
A
Figure 1.36 Ultrasound imaging aspects of small saphenous vein (SSV)–popliteal arrangement. A, The SSV extends into the thigh in about 50% of cases; in
one-third of these the SSV joins the popliteal vein and then continues up into the thigh (B), while in the remaining two-thirds of cases the SSV continues into the thigh without any connection with the popliteal vein (PV) (TE, thigh extension).
A
Figure 1.37 The thigh extension may transmit reflux from the incompetent
saphenopopliteal junction up to the great saphenous vein and/or varicose veins of the thigh (A), or vice versa, from the incompetent saphenofemoral junction and/or groin, to the small saphenous vein (SSV) (B).
B
B
L
SPJ
A
M
PV
FP
G
P
S
PA
PP
PA
M
GV
tendinous muscle (medially), the long head of the biceps muscle (laterally) and the superficial fascia that stretches over the intermuscular groove (see Figs 1.9, 1.16, 1.21A). Proxi­mally, the TE may join the GSV at various distance from the SFJ as intersaphenous thigh anastomosis (the ‘true’ Giacomini vein); continue straight up into the gluteal area as a single vein or be divided into many deep and superficial branches; join the deep femoral veins as a posterior or posterolateral thigh perforator; or divide into many muscular or subcutaneous branches of the posterior thigh. In many cases the proximal ending of the TE is a combination of the above-mentioned terminations. The possible variants of proximal termination of the TE are presented in Figure 1.35. The TE may transmit reflux from the incompetent SFJ and/or groin, gluteal and thigh perforators and/or collaterals to the SSV, or, vice versa, from the incompetent SPJ up to the GSV and/or varicose veins of the posterior thigh (Fig. 1.37A, B).
3,33
Arrangement of the SSV and its collaterals
As with the GSV the subcutaneous collaterals of the SSV/TE are recognized because they pierce the superficial fascia to enter the saphenous compartment. One particular superficial collateral of the SSV deserves separate description. It is the so-called ‘popliteal area vein’ and was described by Dodd.54 This vein runs subcutaneously along the posterior aspect of
16
Figure 1.38 The so-called ‘popliteal area vein’ runs subcutaneously along
the posterior aspect of popliteal area, calf and leg, sometimes parallel to the small saphenous vein, and typically has a separate junction with the popliteal vein, usually lateral to the saphenopopliteal junction (SPJ).
S, Georgiev M, Goldman MP: Anatomical bases of ambulatory phlebectomy. In: Goldman MP, Georgiev M, Ricci S, Ambulatory phlebectomy, Boca Raton, 2005, Taylor
(Adapted from Ricci
& Francis)
popliteal area, calf and leg, sometimes parallel to the SSV, and typically has a separate junction with the popliteal vein, usually lateral to the SPJ (Fig. 1.38).
3,55
Foot Veins
The arrangement of the superficial veins in two layers sepa­rated by the superficial fascia is also present in the foot and
collat.V
https://t.me/med1917
fascia
V.Marg
Figure 1.39 The dorsal venous arch and the medial and lateral marginal
veins – V. Marg – (anatomic origin of the great and small saphenous veins) are similarly placed under the superficial fascia while the tributaries run more superficially – collat. V.
collat.V
Arch Vein
MI:1.3
2DG
Figure 1.41 Perforating veins connect the superficial veins to the deep
veins; they ‘perforate’ the aponeurotic fascia, giving them their name. The fascial point of perforation is always visible with ultrasound. Also, valves are visible, usually at the level of the fascial hole (arrow).
9.8 0
9.8
cm/s
11L5 T8.4 CF 4.4 21 fps
1
2
2DG
PRF
16.5K Filter
90
DR
75
CG
50
3
90
DR
75
Foot Veins
Figure 1.40 The collateral veins on dorsum of foot are the continuation of
the subcutaneous collaterals of the leg and are also subcutaneous, overcoming the deeper arch vein.
can be demonstrated by DUS. The dorsal venous arch and the medial and lateral marginal veins are the anatomical origin of the great and small saphenous veins, respectively, and are similarly placed under the superficial fascia (Fig. 1.39). The collateral veins on the dorsum of the foot are the continua­tion of the subcutaneous collaterals of the leg and are also subcutaneous (Fig. 1.40).
56
Perforating veins
Perforating veins were first described in 1803 by Van Loder. They occur from the ankle to the groin, connecting the superficial veins to the deep veins; they ‘perforate’ the aponeu­rotic fascia, giving them their name. The fascial point of per­foration is always visible with USI (Fig. 1.41).
The average number of perforating veins per leg has been
found to be as great as 155
59
or as few as 64.60 They are not distributed regularly along the limb’s surface but increase in density from proximal to distal in a 1 : 2 : 8 proportion between the thigh, the leg, and the foot.
61
Sixty percent of perforating veins, always the ones that are
more important and named, are accompanied by an artery
(Fig. 1.42)
; and usually contain one to three one-way valves, depending on their length (see Fig. 1.41). These one-way valves can be thought of as check valves, which serve to prevent high venous pressure (from muscle contraction) from being transmitted to the superficial veins. Normally, perforat-
57,58
59
Figure 1.42 Perforators are usually accompanied by an artery easily visible
by duplex and color ultrasound.
0
2
11L5
4
T8.4
28 fps
Figure 1.43 The ‘S’ shape of normal perforators is a mechanism helping to
achieve competence.
ing veins are thin walled, varying in diameter from less than 1 mm to 2 mm.62 They may also be valveless, especially when less than 1 mm in diameter.63 In such cases, their competence is maintained by their oblique orientation through muscle, or by the ‘S’ shape that they display (Fig. 1.43).
With muscular contraction, the deep fascia is tightened and the S curves are compressed. This puts the perforator veins under tension, closes the vein and prevents blood from escap­ing from the deep veins of the calf muscle pump into the
2DG
90
DR
75
17
Chapter
https://t.me/med1917
1 
Anatomy
18
Table 1.2 Distribution of incompetent perforator veins on 901 lower limbs
Percentage of Limbs with
Incompetent Veins
Perforator Veins Right Limbs Left Limbs
Saphenofemoral junction 100.00 100.00
Saphenopopliteal junction 15.0 15.5
Mid-Hunterian perforator 7.0 6.7
Genicular perforator 2.9 1.6
Lateral thigh perforators 1.8 1.3
13.5-cm midcalf Cockett 15.9 17.3
18.5-cm midcalf Cockett 34.3 35.2
24-cm midcalf Cockett 20.0 19.6
30-cm midcalf Cockett 13.0 12.7
35-cm midcalf Cockett 6.6 7.0
40-cm midcalf Cockett 4.2 3.1
Calf perforators (other) 12.0 11.2
Gastrocnemius/peroneal muscle perforator
Anterior tibialis/peroneal perforator 3.1 2.9
Lateral tibial perforators 0.02 0.04
Lateral foot perforators 2.0 2.4
Medial foot perforators 3.5 2.9
Modified from Sherman RS: Ann Surg 130:218, 1949.
25.0 24.0
superficial veins. Although variable in location, a number of perforating veins occur with marked regularity (Table 1.2).
Paratibial perforators connect the main trunk or tributaries of the GSV with the posterior tibial veins and course close to the medial surface of the tibia. These correspond to the so-called Sherman PV (at the lower and mid leg) and Boyd PV (at the upper leg). Posterior tibial perforators connect the posterior accessory GSV with the posterior tibial veins. These correspond to the so-called Cockett PV, named first, second, and third. As described by Frank Cockett, they can be indi­cated topographically as upper, middle and lower.
The most important perforators in the thigh are known as the Hunterian and the Dodd perforator(s), which are located in the medial thigh. These connect the GSV to the femoral vein in the middle third of the medial thigh (Hunterian) and the lower third of the thigh (Dodd).
64
Incompetence of the midthigh (Hunterian) perforator is a common cause for medial thigh varicose veins in patients with a competent SFJ.
Perforating veins have also been described in the foot.
65
Raivio
has documented more than 40. One is situated about
2.5 cm below the inferior tip of the medial malleolus. A second occurs approximately 3.5 cm below and anterior to the medial malleolus. The other two are on an arc approximately 3 cm anterior to and below the medial malleolus. Perforating veins in the foot are valveless or have one-way valves that are reversed to allow blood to flow from the deep to the superfi­cial veins.
66
The great number of perforating veins and venous
anastomoses of the foot allows for their safe removal.
Venous valvular system
Fabricius of Aquapendente (1533–1620) is credited with being the first to detail the anatomy of veins and their valves, in
Padua in 1579. He suggested that valves ‘… insure a fair dis­tribution of the blood … prevent distention … and stop blood from flooding into the limb …’.
67
However, a more recent historical review credits the Parisian Charles Estienne with mentioning venous valves in 1545 and Lusitanus and Cannano publicly demonstrating valves in Ferrera, Italy in 1555.
68
The valves appear as translucent, thin structures that vibrate
with blood flow. Numerous bicuspid valves appear down to vein diameters less than 100 micrometers (µm). studies demonstrate valves in venules as small as 40 µm in diameter.
70,71
69
Recent
Studies of the embryologic development of veins show that the number of venous valves decreases in utero with fetal maturity. It has been suggested that this disappearance con­tinues, albeit at a reduced but variable rate, during childhood, adolescence and adult life.
72,73
A morphologic study of normal saphenous veins removed from cadavers has revealed an average of 8.7 valves, with 6.3 of these appearing above the knee and 2.4 below the knee.
74
Aging in itself does not appear to decrease the number of venous valves of the leg, nor does the number of venous valves appear to differ between men and women.
75
The number of venous valves has been found to be fewer in varicose veins than in normal veins. Valvular insufficiency occurs in undamaged valves as well as damaged valves. Com­petent venous valves withstand pressures of up to 3 atmos-
76
pheres.
Therefore, for incompetence to occur, the valve annulus dilates to render the valves incompetent. This obser­vation is supported by investigations that reveal no difference in viscoelastic behavior in perivalvular vein wall tissue. Chronic venous dilation may lead to sclerosis. It is postulated that this is caused by turbulent blood flow.
78
However, sinus wall and valvular defects have been found in autopsy studies in up to 90% of adults without apparent varicosities.
79
There-
77
fore, valve and valvular sinus abnormalities, at best, comprise only one factor in the development of varicose veins. A full explanation of the pathophysiologic significance of valvular deficiency and dysfunction is addressed in Chapter 3.
Nerves of the Leg of Phlebologic Interest
The sural nerve (SuN) and the saphenous nerve (SaN) are interesting in VV treatment because of their proximity to the SSV and the GSV at the leg, respectively.
The SuN, running along the SSV, is formed by two different branches merging at different leg levels to form the definitive nerve. The tibial branch (nervus cutaneus medialis surae – NCMS) branches from the tibial nerve at the popliteal fossa and runs parallel to the SSV in the groove of the gastrocnemius muscles, ventrally and outside the SSV compartment. Gener­ally at the middle third of the calf (but with large variations) it meets the peroneal branch of the SuN and enters the saphe­nous compartment, coming in straight contact with the SSV, extending down to the foot.
The peroneal branch of the SuN (nervus cutaneus lateralis surae – NCLS) originates from the common peroneal nerve. This nerve comes down laterally to the popliteal fossa along the biceps femoris muscle to the head of peroneus. During this course it sends a ‘communicating branch’, the NCLS, directed distally and medially, to join the NCMS to complete the SuN (Fig. 1.44).
This typical anatomical arrangement (Fig. 1.45), has great variations. The two branches can run independently. point of contact with the SSV may be found by DUS at differ­ent levels of the calf. This point has been called the ‘risk point’ because possible nerve injury during VV treatments probable from this point distally.
82
The SaN takes origin from the femoral nerve 2 cm below the inguinal ligament, comes down along the adductor
80
The
81
is more
canal following the femoral artery, continues behind the sar-
https://t.me/med1917
torius muscle, becoming superficial at the knee where it runs between the sartorius and gracilis muscle tendons. At this point the nerve is visible by DUS behind the GSV and in deeper position. Progressively the SaN becomes superficial and runs anterior to the GSV, coming in close contact with the vein (Fig. 1.46)
at about 2–3 cm below and medial to the tibial tuberosity. From this point down the nerve follows the GSV extending to the foot. It is also possible to identify the ‘risk point’ for the SaN (Fig. 1.47).
83–86
Histology
Vein walls
The first part of the venous system consists of the venule, which serves as a collecting tube for capillaries. The cutaneous
Great saphenous vein
Figure 1.44 The sural nerve is formed by two branches, one coming from
the tibial nerve (TN), the medial sural cutaneous nerve (Med SCN), the other coming from the common peroneal nerve, the lateral sural cutaneous nerve (Lat SCN). Both form the sural nerve that runs in close contact with the distal small saphenous vein.
Small saphenous vein
Common peroneal nerve
Lateral SCN Medial SCN
Sural nerve
Point of contact ‘Risk point’
microcirculation is organized as two horizontal plexuses. One is situated 1–1.5 mm below the skin surface. The other is at the dermal subcutaneous junction. Arterioles ascending into these layers and venules descending are paired while they connect the two plexuses. The arterial capillaries form dermal papillary loops and at the dermal subcutaneous junction col­lecting veins contain bicuspid valves oriented to prevent ret­rograde flow of blood.
87
The venule is approximately 20 µm
in diameter and consists of an endothelium surrounded by a fibrous tissue composed of a thin layer of collagenous fibers. The venule increases in diameter, with smooth muscle cells appearing within the fibrous sheath when the diameter is approximately 45 µm. At a diameter of 200 µm, the muscular layer becomes better defined. At a clinically recognizable diameter consistent with small phlebectasia (venectasia), the vessels are composed of a thick media with myocytes. Colla­genous fibers are clearly organized into bundles, and elastic fibers can be observed.
88
Larger diameters contain elastic fibers
and a more organized structure.
Telangiectasias commonly seen in the skin of lower extremities can be explained by abnormalities in the organiza­tion and ultrastructure of the cutaneous microvasculature rather than by neovascularization. The telangiectasias seen in essential telangiectasia and in scleroderma are clearly a dila­tion of the postcapillary venules of the upper horizontal
89
plexus.
Microscopically, the normal young internal saphenous vein is a musculofibrous conduit with both passive and active func­tions. The normal vein is slightly oval, with the short axis perpendicular to the skin. In response to an increase in intra­luminal pressure, the diameter increases and the vein loses its oval appearance. Veins tend to assume an elliptical shape, particularly at low transmural pressures. These qualities of shape deformability allow veins to change volume with very little force, thus aiding their role as a high-capacitance
90,91
system.
With continued increases in venous pressure or progression of varicose disease, the vein increases in both length and diameter and becomes tortuous. Whether normal or varicose, the saphenous vein is composed of three tunics: intima, media and adventitia.
The intima is a thin structure consisting of a layer of endothelial cells and a deep fenestrated basement membrane bounded by a thin, fragmented elastic lamina.
92
The central portion of the cell containing the nucleus bulges into the lumen and, on its free surface, exhibits multiple small micro­villi. Although endothelial cells are easily destroyed by chemi­cal and physical insults, they demonstrate a marked capacity for regeneration.
93
The media is composed of three layers of muscle bundles.
The inner layer consists of small bundles of longitudinally
Histology
Risk point
V.S.E.
N.S.T.
N.S.E.
A
N.S.T. N.S.T. N.S.T. N.S.T.
B C D E
V.S.E. V.S.E. V.S.E. V.S.E.
N.S.P.N.S.P.N.S.P.
N.S.P.
N.S.P.
Figure 1.45 Different anatomical combinations of
the two branches of the sural nerve and different levels of nerve-to-vein contact (‘risk point’). (NSE, sural nerve; NSP, lateral sural cutaneous nerve; NST, medial sural cutaneous nerve; VSE = SSV)
(Adapted from Payen B: Rappel anatomique de la veine saph
ène externe, Phlébologie 38:453, 1985)
19
Chapter
https://t.me/med1917
1 
Anatomy
0
GSV
1
2
3
Figure 1.46 The saphenous nerve, initially in a deeper position, becomes
superficial and anterior to the GSV, coming in close contact with the vein (‘risk point’) at about 2–3 cm below and medially to the tibial tuberosity. The nerve is visible using ultrasound with a high frequency probe (12–18 Mhz).
most cells of the longitudinal layer to improve contractile efficiency.
94
The amount of muscle within the vein wall is not uniform throughout the venous system. There is an increasing smooth muscle content from the proximal to the distal and the deep to the superficial veins.
95
The obvious functional importance is to counteract hydrostatic pressure. In addition, the greatest extent of circular muscle occurs at the level of insertion of the valve leaflets. This composition helps to prevent valvular dila­tation and incompetence and is the last region to dilate in a varicose vein.
96
This area is known to be dilated in primary
valvular insufficiency.
The adventitia is the thickest portion of the vein wall. It is primarily composed of collagen, with interlacing fibers ori­ented in longitudinal, spiral, and circular fashions. vessels of the thigh, a considerable network of elastic fibers occurs and stretches from valve to valve. merges with the perivenous connective tissue and contains the vasa vasorum and adrenergic nerve fibers.
97
The collagen layer
98,99
93
In larger
The vasa vasorum provides the arteriovenous circulation in the wall of the blood vessel. These vessels arise as branches from arterioles present in perivenous connective tissue that are fed by neighboring arteries.
100
Venous capillaries of the vasa vasorum form venules that empty into veins running in the loose perivenous con­nective tissue. As discussed in Chapter 3, alterations of the vasa vasorum may lead to the development of arteriovenous fistulas.
Great saphenous vein
Saphenous nerve
Point of contact ‘Risk point’
Figure 1.47 Intimate association of the saphenous nerve with the great
saphenous vein below the knee joint. The saphenous nerve originates from the femoral nerve, follows the femoral artery in the adductor canal, becomes superficial at the knee passing between the sartorius and gracilis muscle tendons, getting in close contact with the great saphenous vein (GSV). From this point down the nerve follows the GSV until it reaches the foot. It is also possible to identify the ‘risk point’ for the saphenous nerve.
arranged muscle fibers. Loose connective tissue and small elastic fibrils separate the muscle bundles.
92
The middle layer is composed of wide bundles of smooth muscle in a circular orientation. The muscle bundles may be separated by thin or thick layers of elastic fibrils.
92
In addition, the outer layer is quite variable, being composed of longitudinal muscle bundles spread out through thick fibrous tissue. The outer­most cells of the circular layer interdigitate with the inner-
20
Venous valves
Venous valves are composed of a thin layer of collagen and a variable amount of smooth muscle covered on both surfaces by endothelium.
101
An increase in muscle fibers is found at the base of the valve cusp running circumferentially and longitu­dinally for a variable distance along the length of the valve
97,102
cusp.
Elastic fibers extend along the whole length of the cusp and lie close to the endothelium. Collagen fibers are concentrated at the base, thinning out toward the free edge of the cusp. The valve is avascular and thus dependent on humeral blood for its oxygen supply.
103,104
Fegan97 proposes that the muscle fibers play an active role in regulating blood flow. Through an evaluation of anatomi­cal dissection of multiple valves, he believes that contraction of the circular muscles at the base of the valve reduces the vein diameter, and contraction of the longitudinal fibers shortens and thickens the cusp. This type of coordinated muscle action maintains tone in the vein wall in the face of increased pres­sure from retrograde blood flow.
The valve cusp changes with age.
105
In the parietal layer, collagen becomes thicker and denser with an increase in the elastic lamellae. The luminalis develops deep, narrow depres­sions. The vein wall at the valve sinus thickens with an increase in adipose tissue, muscle cells and connective tissue. These changes produce less flexibility of the valve cusp, which may produce abnormal blood flow currents and eddies that could lead to valvular incompetence.
Vein wall variation
The composition of vein walls varies with the type and loca­tion of the veins. Depending on their location, veins assume many different functions, and the muscular content of the vein wall varies accordingly. They are used as pumps and reservoirs and must withstand variations in gravitational and intravascular pressure demands. The percentage of smooth muscle increases with distal locations. Veins in the lower extremities are the only veins that are composed of more than 40% smooth muscle, with veins in the foot having 60–80% smooth muscle compared with 5% in axillary veins. the hydrostatic pressure within the vein also correlates with
95
However,
smooth muscle content and superficial veins have more
https://t.me/med1917
smooth muscle than deep veins.
106
The differences in vein wall content may affect sclerotherapy treatment, as described in Chapter 7.
The function of the vein wall collagen is to prevent overd­istension, whereas elastin produces elastic recoil. With advanc­ing age, multiple changes may occur in the vessel wall. The intima thickens, increasing and disorienting elastic fibers.
92
The media develops a more disorganized arrangement of muscle bundles and hypertrophy of the outer muscular layer. Elastic fibers become more irregular and dystrophic and the elastic lamina becomes more fragmented, atrophic, thin and irregular.
92
The adventitia becomes increasingly fibrous. Thus the lack of an organized elastic support and smooth muscle degeneration in an aged vein render it more susceptible to pressure-induced distension.
Some histologic studies demonstrate that fibrotic wall changes are a common finding in the GSV in all age groups without venous disorders.
106
The incidence of fibrotic change increases from 25% to 50% in the population under 40 years of age to 100% in those over 70 years of age.
Other studies have confirmed the fact that varicose saphen­ous veins have significantly larger wall areas and larger amounts of collagen. This is true more so in the proximal GSV compared with the distal GSV. Also there is excess smooth muscle and elastin in varicose veins proximally compared with distally. This has suggested to some that varicose veins are a dynamic response to venous hypertension. Others believe that the vein wall in varicose disease is thinned rather than dynamically responsive.
107
In saphenous veins subjected to biopsy during arterial bypass surgery, intimal thickening has been found to be common. Smooth muscle hyperplasia, elastosis and fibrosis contribute to this intimal thickening. In addition, medial longitudinal muscle hypertrophy is seen.
108
Venules
Venules in the upper and mid dermis usually run in a hori­zontal orientation. The diameter of the postcapillary venule ranges from 12 mm to 35 mm. Collecting venules range from 40 mm to 60 mm in the upper and mid dermis and enlarge to become 100 to 400 mm in diameter in the deeper tissues.
109
One-way valves are found at the subcutis (dermis)–adipose junction on the venous side of the circulation.70 Valves are usually found in the area of anastomosis of small to large venules and also within larger venules unassociated with branching points. The free edges of the valves are always directed away from the smaller vessel and toward the larger and serve to direct blood flow towards the deeper venous system. The structure of these valves is identical to that of the valves found in deep and larger veins.
Postcapillary venules are composed of endothelial cells covered by a basement membrane, some collagen fibers, and, rarely, smooth muscle cells. Collecting veins in the deep dermis gradually receive more muscle cells until they become veins with a continuous muscle coat (see Fig. 1.48).
110,111
Telangiectasias
Histologic examination of simple telangiectasias demonstrates dilated blood channels in a normal dermal stroma with a single endothelial cell lining, limited muscularis, and adven-
112
titia.
Therefore, such vessels probably evolve from capillaries
or early venules.
Blue-to-red arborizing telangiectasias of the lower extremi­ties are probably dilated venules, possibly with intimate and direct connections to underlying larger veins of which they are direct tributaries.
113–115
Electron microscopic examination of
‘sunburst’ varicosities of the leg has demonstrated that these vessels are widened cutaneous veins.88 They are found 175 to 382 µm below the stratum granulosum. The thickened vessel walls are composed of endothelial cells covered with collagen and muscle fibers. Elastic fibers are also present. Electron microscopy reveals an intercellular collagenous dysplasia, lattice collagen and some matrix vesicles. These findings suggest that telangiectatic leg veins, like varicose veins, have an alteration of collagen metabolism of their walls. Therefore, like varicose veins, these veins are dysplastic.
Alternatively, arteriovenous anastomoses may result in the pathogenesis of telangiectasias. These were demonstrated by de Faria and Moraes
115
in 1 of 26 biopsy specimens of leg
telangiectasias.
Skin biopsy of more unusual forms of telangiectasia, such as unilateral nevoid telangiectasia, may show an accumulation of mast cells. induced by the chronic release of one or more products of mast cells, particularly heparin.
116
In these cases permanent vasodilation may be
117,118
Innervation
Innervation of the vein plays an important part in the regula­tion of venous tone. Different stimuli are known to produce venous constriction: pain, emotion, hyperventilation, deep breathing, Valsalva’s maneuver, standing and muscular exer-
119
cise.
Although muscular veins have little or no sympathetic
innervation, cutaneous veins are under hypothalamic ther­moregulatory control and have both α receptors.
120
Because the outermost media and adventitia contain the nerve endings, myogenic conduction contributes to the neurogenic activation by coordinating venous contrac-
102,121
tion. of muscle cells from nerve endings is rarely less than 1000 Å (0.1 nm).
Even in the outer layers of the media, the separation
122
Therefore, an intact smooth muscle layer is impor­tant in vein physiology.
Venous constriction and dilation occur through both
central and local nervous stimuli.
123
when veins are used as arterial conduits. One report describes spasms of a vein graft 14 months after operation, causing anginal symptoms.
124
Localized cooling provides both a potentiation of adrenergic stimulation and a direct stimulus for venous smooth muscle contraction; is reduced by warming.
126
Venoconstriction also occurs with infusions of norepinephrine (noradrenaline), (adrenaline), phenylephrine, serotonin and histamine. Veins dilate in response to phenoxybenzamine, phentolamine, reserpine, guanethidine, barbiturates and many anesthetic
129
agents.
Therefore, circulating adrenergic and pharmacologic substances influence vein diameter and this may explain why central mechanisms may also be responsible for venous tone. Evidence for a central sympathetic control of venoconstriction has been demonstrated by the failure of such venoconstriction to occur with the tilting of sympathectomized patients. the stress of mental arithmetic or unpleasant thoughts has been shown to activate adrenergic nerves connected to cutane­ous veins. because of a change in either respiration or nerve stimula­tion.
119
Veins may become more distensible during sleep
131
This is one reason for recommending continuous com­pression of sclerotherapy-treated veins during the endosclerotic stages after treatment (see Chapter 8).
Local chemical changes produced through exercise also provide for the distribution of blood flow in accordance with local metabolic needs. Venous smooth muscle is also sensitive to endothelium-derived vasoconstrictor substances and pep­tides such as endothelin.
124
Finally, the increasing smooth muscle content from proximal to distal veins, and a thicker muscular media in superficial veins compared with muscular deep veins, supports the physiologic concept of increasing venous contractility in the distal venous system.
- and β-adrenergic
This may be problematic
125,126
venoconstriction
127
epinephrine
130
128
Even
Histology
21
Chapter
https://t.me/med1917
References
1 
1. Federative Commitee on Anatomical Terminology. Terminologia Anatomica. Stuttgart – New York: Thieme; 1998.
Anatomy
22
2. Caggiati A, Bergan JJ, Gloviczki P, et al. Nomenclature of the veins of the lower limbs: an international interdisciplinary consensus statement. J Vasc Surg 2002;36:416.
3. Ricci S, Georgiev M. Ultrasound anatomy of the superficial veins of the lower limb. J Vasc Technol 2002;26:183.
4. Eklof B, Rutherford RB, Bergan JJ, et al. American Venous Forum International Ad Hoc Committee for Revision of the CEAP Classification: Revision of the CEAP classification for chronic venous disorders: consensus statement. J Vasc Surg 2004;40:1248.
5. Allegra C, Antignani P-L, Bergan JJ, et al. The ‘C’ of CEAP: suggested definitions and refinements: an International Union of Phlebology conference of experts. J Vasc Surg 2003;37:129.
6. Bundens WP, Bergan JJ, Halasz NA, et al. The superficial femoral vein: a potentially lethal misnomer. JAMA 1995;274:1296.
7. Pieri A, Gatti M, Santini M, et al. Ultrasound anatomy of the deep veins of the lower limb extremity. J Vasc Technol 2002;26:201.
8. Franceschi C, Zamboni P. Principles of hemodynamics. New York: Nova Science Publishers Inc.; 2009.
9. Kubik S. Das Venensystem der unteren Extremitat. Eine anatomische Ubersicht-Anwendungsmoglichkeiten fur die Praxiz. Der informierte Arzt, 1985;4:31.
10. Lejars C. Les veines de la plante du pied chez l’homme et les grands animaux, Arch Physiol. XXII, Ser.V TomeII/I, 1890, p 89–103.
11. Gillot C. La semelle de Lejars. Phlébologie 1993;46:173.
12. Tibbs DJ, Sabiston DC, Davies MG, et al. Varicose veins, venous disorders, and lymphatic problems in the lower limbs. Oxford University Press; 1997.
13. Caggiati A. Anatomia clinica del circolo venoso degli arti inferiori, Ch
4. In: Agus G: Chirurgia delle varici, EDRA 2006, Milano.
14. Caggiati A, Bergan JJ. The saphenous vein: derivation of its name and its relevant anatomy. J Vasc Surg 2002;35:172.
15. Somjen GM. Anatomy of the superficial venous system. Dermatol Surg 1995;21:35.
16. Berry SM, Susman B, Ibrahim IM, et al. Determination ‘good’ saphenous vein for use in in-situ bypass grafts by real-time, B-mode imaging. J Vasc Technol 1988;12:184.
17. Browse NL, Burnand G, Thomas ML. Diseases of the veins: pathology,
diagnosis, and treatment. London: Edward Arnold; 1988.
18. Sherman RS. Varicose veins: anatomy re-evaluation of Trendelenburg tests and operating procedure. Surg Clin North Am 1964;44:1369.
19. Kupinski AM. The lesser saphenous vein: an under-utilized arterial bypass conduit. J Vasc Technol 1987;11:145.
20. Dodd H, Cockett FB, editors. The pathology and surgery of the veins of the lower limb. 2nd ed. Edinburgh: Churchill Livingstone; 1976.
21. Hoffman HM, Staubesand J. Die venosen Abflussverhaeltnisse des Musculus triceps surae. Phlebologie 1991;20:164.
22. Georgiev M, Myers K, Belcaro G. The thigh extension of the lesser saphenous vein: from Giacomini’s observations to ultrasound scan imaging. J Vasc Surg 2003;37:558.
23. Georgiev M. The femoropopliteal vein: ultrasound anatomy, diagnosis, and office surgery. Dermatol Surg 1996;22:57.
24. Caggiati A. Fascial relationships of the short saphenous vein. J Vasc Surg 2001;34:241.
25. Taylor GI, Caddy CM, Watterson PA, Crock JG. The venous territories (venosomes) of the human body: experimental study and clinical implications. Plast Reconstr Surg 1990;86:185.
26. Delis KT, Knaggs AL, Khodabakhsh P. Prevalence, anatomic patterns, valvular competence, and clinical significance of the Giacomini vein. J Vasc Surg 2004;40:1174.
27. Albanese AR, Albanese AM, Albanese EF. The lateral subdermic venous system of the legs. Vasc Surg 1969;3:81.
28. Caggiati A, Ricci S, The long saphenous vein department. Phlebology 1997;12:107.
29. Bailly M. Carthographie CHIVA. In: Encyclopedie Médico-chirurgicale, Paris 43–161-B, 1993. p 1–4.
30. Cruveilhier J. Traité d’anatomie descriptive, 2°, Tome troisième. Paris: Ancienne Maison Béchet Jeune; 1843. p. 96–101.
31. Bayle, Hollard, Lauth: Trattato elementare d’Anatomia generale, descrittiva e topografica, Napoli: Federico Stikler, 1843. p 279.
32. Thomson H. The surgical anatomy of the superficial and perforating veins of the lower limb. Ann R Coll Surg Engl 1979;61:198.
33. Ricci S, Georgiev M, Goldman MP. Anatomical bases of ambulatory phlebectomy, Ch 2. In: Taylor ED, editor. Ambulatory phlebectomy. Boca Raton: Taylor & Francis; 2005.
34. Zamboni P, Cappelli M, Marcellino MG, et al. Does a saphenous
varicose vein exist? Phlebology 1997;12:74.
35. Lemasle P, Baud JM, Lefebvre­Villardebo M, Uhl JF. Proposition d’une définition échographique de la grande saphène et des saphènes accessoires à l’étape crural. Phlébologie 1996;49:279.
36. Cavezzi A, Labropoulos N, Partsch H, et al. Duplex ultrasound investigation of the superficial veins and perforators in chronic venous disease of the lower limbs, part II: Anatomy. Eur J Vasc Endovasc Surg 2006;31:288.
37. Bailly M, Nasso C, Ballo M. Ecografia venosa ed esperienza CHIVA. Flebologia 1997;8:117.
38. Ricci S, Georgiev M, Cappelli M. Définition de la veine saphène accessoire antérieure et de son role dans la maladie variqueuse. Phlébologie 2004;57:135.
39. Sherman RS. Varicose veins. Further findings based on anatomic and surgical dissections. Ann Surg 1949;130:218.
40. Shah DM, Chang BB, Leopold PW, et al. The anatomy of the greater saphenous venous system. J Vasc Surg 1986;3:273.
41. Kupinski AM, Evans SM, Khan AM, et al. Ultrasonic characterization of the saphenous vein. Cardiovasc Surg 1993;1:513.
42. Ricci S, Cavezzi A. Echo-anatomy of long saphenous vein in the knee region: proposal for a classification in five anatomical patterns. Phlebology 2002;16:111.
43. Georgiev M. The femoropopliteal vein: ultrasound anatomy, diagnosis and office surgery. Dermatol Surg 1996;22:57.
44. Caggiati A. Fascial relationships of the short saphenous vein. J Vasc Surg 2001;34:241.
45. Ricci S, Caggiati A. Echoanatomical patterns of the long saphenous vein in patients with primary varices and in healthy subjects. Phlebology 1999;14:54.
46. Pieri A, Vannuzzi A, Duranti A, et al. Ròle central de la valvule pré-ostiale de la veine saphène interne dans la genèse des varices tronculaires des membres inférieurs. Phlébologie 1995;48:227. plus errata Phlébologie 48:V, VI, 1995.
47. Cavezzi A, Carigi V, Collura M. Colour flow duplex scanning as a preoperative guide for mapping and for local anaesthesia in varicose vein surgery. Phlebology 2000;15:24.
48. Zamboni P, De Palma M, Carandina S, et al. The ‘T’ vein of the leg. Dermatol Surg, 2004;30:750.
49. Lemasle PH, Uhl JF, Lefebre-Vilardebo M, et al. Confrontation écho­chirurgicale de la terminaison de la saphéne externe dans le cadre de la
chirurgie d’exerèse. Résultats
https://t.me/med1917
préliminaires. Phlébologie 1995;48:321.
50. Van der Stricht J. La petite veine saphène existe-t-elle. Phlébologie 2001;3:309.
51. Giacomini C. Osservazioni anatomiche per servire allo studio della circolazione venosa delle estremità inferiori. Giornale della reale Accademia di Medicina di Torino 1873;13:109.
52. Georgiev M, Myers K, Belcaro G. Giacomini’s observations ‘on the superficial veins of the abdominal limb and principally the external saphenous’. Int Angiol 2001;20:225.
53. Hoffman HM, Staubesand J. Die venosen abflussverhaeltnisse der musculus triceps surae. Phlebologie 1991;20:164.
54. Dodd H. The varicose tributaries of the popliteal vein. Br J Surg 1965;52:350.
55. De Palma M, Carandina S, Mazza P, et al. Perforator of the popliteal fossa and short saphenous vein insufficiency. Phlebology 2005;20:170.
56. Ricci S. Phlébectomie des varices du pied. Phlébologie 2000;53:223.
57. Von Loder JC. Anatomische Tafeln zur Beforderung der Kenntniss des menschichen Korpers. Waimar 1794.
58. Caggiati A, Mendoza E. The discovery of perforating veins. Ann Vasc Surg 2004;18:502.
59. Van Limborgh J. L’anatomie du systeme veineux de l’extremite inferieure en relation avec la pathologie variqueuse. Folia Angiol 1961;8:240.
60. Thompson H. The surgical anatomy of the superficial and perforating veins of the lower limb. Ann R Coll Surg Engl 1979;61:198.
61. Thulesius O, et al. Blood flow in perforating veins of the lower extremity. In: May R, Partsch H, Staubesand J, editors. Perforating veins. Munich: Urban & Schwarzenberg; 1981.
62. Bjordal RI. Circulation patterns in incompetent perforating veins in the calf and in the saphenous system in primary varicose veins. Acta Chir Scand 1972;136:251.
63. Sarin S, Scurr JH, Coleridge Smith PD. Medial calf perforators in venous disease: the significance of outward flow. J Vasc Surg 1992;16:40.
64. Dodd H. The varicose tributaries of the superficial femoral vein passing into Hunter’s canal. Postgrad Med J 1959;35:18.
65. Raivio EVL. Untersuchungen uber die venen der unteren extremitaten mit besonderer Berucksichtigung der gegenseitigen Verbindungen zwischen den oberflachlichen und tiefen Venen. Ann Med Exp Fenn 1948;26(Suppl):1.
66. Askar O, Kassem KA, Aly SA. The venographic pattern of the foot. J Cardiovasc Surg 1975;16:64.
67. Laufman H. Surgery: the veins. Austin, Texas: Silvergirl; 1986.
68. Scultetus AH, Villavicencio JL, Rich NM. Facts and fiction surrounding the discovery of the venous valves. J Vasc Surg 2001;33:435.
69. Aharinejad S, Lametschwandtner A. Microvascular corrosion casting in scanning electron microscopy: techniques and applications. New York: Springer-Verlag; 1992.
70. Braverman IM, Keh-Yen A. Ultrastructure of the human dermal microcirculation. IV. Valve-containing collecting veins at the dermal­subcutaneous junction. J Invest Dermatol 1983;81:438.
71. Dunn RM, Fudem GM, Walton RL, et al. Free flap valvular transplantation for refractory venous ulceration. J Vasc Surg 1994;19:523.
72. Myers TT. Varicose veins. In: Allen EV, Barker NW, Hines EA, editors. Peripheral vascular diseases. 3rd ed. Philadelphia: Saunders; 1962.
73. Thurner J, Mar R. Probleme der phlobopathologie mit besonderer berucksichtigung der phlebosklerose. Zentralbl Fuer Phlebologie 1967; 6:404.
74. Ortega F, Sarmiento L, Mompeo B, et al. Morphological study of the valvular distribution in the long saphenous vein. Phlebology 1994;9:59.
75. Kosinski C. Observation on the superficial venous system of the lower extremity. J Anat 1926;60:131.
76. Last RJ. Anatomy: regional and applied. 6th ed. Edinburgh: Churchill Livingstone; 1978.
77. Psaila JV, Melhuish J, Conboy V, et al. Do varicose veins have abnormal viscoelastic properties? In: Davy A, Stemmer R, editors. Phlébologie ’89. Blanche, France: John Libbey Eurotext;
1989. p. 77–79.
78. Cotton LT. Varicose veins: gross anatomy and development. Br J Surg 1961;48:589.
79. Eger SA, Wagner FB Jr. Etiology of varicose veins. Postgrad Med 1949;6:234.
80. Payen B. Rappel anatomique de la veine saphène externe. Phlébologie 1985;38:453.
81. Sam RC, Silverman SH, Bradbury AW. Nerve injuries and varicose vein. Eur J Vasc Endovasc Surg 2004;27:113.
82. Ricci S, Moro L, Antonelli Incalzi R. Ultrasound imaging of the sural nerve: ultrasound anatomy and rationale for investigation. Eur J Vasc Endovasc Surg 2010;39:636–641.
83. Ricci S, Moro L, Antonelli Incalzi R. Visualisation ultrasonique des nerfs du membre inférieur d’intérêt phlébologique. Phlébologie 2010;63:110.
84. Holme JB, Holme K, Sorensen LS. The anatomic relationship between the long saphenous vein and the saphenous nerve. Acta Chir Scand 1988;154:631.
85. Price C. The anatomy of the saphenous nerve in the lower leg with particular reference to its relationship to the long saphenous vein. J Cardiovasc Surg 1990;31:294.
86. Garnjobst W. Injuries to the saphenous nerve following operations for varicose veins. Surg Gynecol Obstet 1964;119:359.
87. Braverman IM. The cutaneous microcirculation: ultrastructure and microanatomic organization. Microcirculation 1997;4:329.
88. Wokalek H, Vanscheidt W, Martay K, Leder O. Morphology and localization of sunburst varicosities: an electron microscopic and morphometric study. J Dermatol Surg Oncol 1989;15:149.
89. Braverman IM. Ultrastructure and organization of the cutaneous microvasculature in normal and pathologic states. J Invest Dermatol 1989;93(Suppl 2):2S.
90. Moreno AH, Katz AI, Gold LD, Reddy RV. Mechanics of distention of dog veins and other very thin-walled tubular structures. Circ Res 1970;20:1069.
91. Strandness DE Jr, Thiele BI. Selected topics in venous disorders: pathophysiology, diagnosis, and treatment. New York: Futura; 1981.
92. Bouissou H, Julian M, Piraggi M, Louge L. Vein morphology. Phlebology 1988;3(Suppl 1):1.
93. Farber EM, Bates EE. Pathologic physiology of stasis dermatitis. Arch Dermatol 1954;70:653.
94. Rhodin Johannes AG. Histology: a text and atlas. New York: Oxford University Press; 1974.
95. Kugelgen AV. Uber das Verhaltnis von Ringmuskulatur und Innendruck in menschlichen grossen Venen. Zeitschr Zellforsch 1955;43:168.
96. Barrow DW. The clinical management of varicose veins. 2nd ed. New York: Hoeber-Harper; 1957.
97. Fegan G. Varicose veins: compression sclerotherapy. London: William Heinemann; 1967.
98. Vanhoutte PM. The role of systemic veins: an update. Phlebology 1988;3(Suppl 1):13.
99. Ehinger B, Falck B, Sporrong B. Adrenergic fibers to the heart and to peripheral vessels. Bibl Anat 1996;8:35.
100. O’Neill JP. The effects on venous endothelium of alterations in blood flow through the vessels in vein walls, and the possible relation to thrombosis. Ann Surg 1947;126:
270.
101. Edwards JE, Edwards AE. The saphenous valves in varicose veins. Am Heart J 1940;19:338.
102. Butterworth DM, Rose SS, Clarki P, et al. Light microscopy, immunohistochemistry and electron microscopy of the valves of the lower limb veins and jugular veins. Phlebology 1992;7:27.
References
23