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12 Chapter 1/Historical Introduction
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TABLE 1.4 Venous Reconstructive Surgery
The pioneers of venous reconstructive surgery
1816 Travers Sutured a traumatic lesion of the femoral
vein
1830 Guthrie Sutured a traumatic lesion of the jugular
vein
1872 Eck Porto-caval anastomosis
1878 Agnew Lateral suture of traumatized veins
1889 Kummel First termino-terminal anastomosis of
the femoral vein
1901 Clermont First termino-terminal anastomosis of
the inferior vena cava
1912 Carrel & Guthrie Nobel prize for improvements of vascular
surgery techniques
Main steps in venous reconstructive surgery
1950 Wanke Surgical decompression of the left
common iliac vein
1953 Kunlin Veno-venous grafting
1954 Warren & Thayer Great Saphenous Vein bypass of
obstructed femoral veins
1958 Palma & Esperon Cross-pubic bypass for iliac vein
occlusion
1964 Stansel Synthetic graft for caval reconstruction
1970 Husni Sapheno-popliteal bypass for femoral
venous obstruction
1982 Fiore Reconstruction with prosthetic grafts of
superior vena cava
1984 Gloviczki; Dale Reconstruction with prosthetic grafts of
inferior vena cava
1988 Zolliker Endovascular disobliteration and stenting
fi lter. One year later, Eichelter and Schenk proposed a temporary caval fi ltration with a removable balloon.
In order to control symptoms of venous insuffi ciency,
Parona suggested in 1894 to ligate the popliteal vein, whereas
Linton suggested in 1948 to interrupt the femoral vein.
Fundamentals of reconstructive venous surgery were
experienced during the nineteenth century, and in 1912,
Carrel and Guthrie received the Nobel Prize for the improvements they gave to vascular surgery techniques. However,
safe and effective venous interventions for venous obstructions of the trunk and limbs developed only after World War
II (see Table 1.4).
THROMBECTOMY
vein in a patient with phlegmasia coerulea dolens. In 1966,
Fogarthy described how to remove vascular obstruction by
a catheter and affi rmed this is the “most rationale, most
effective and safest way of dealing with iliofemoral
thrombosis.”
SURGERY OF VALVES
The fi rst attempt to restore valvular function was performed in 1953 by Eisemann and Malette, who proposed to
produce valve-like structures by gathering folds at two sites
of the venous wall opposite each other. In 1963, Psathakis
proposed to entwine the tendon of the gracilis muscle
between the popliteal artery and vein in order to obtain the
compression of the vein during contraction of the muscle. A
few years later, Ferris and Kistner proposed a transvalvular
approach for internal repair of venous valve (1968). In 1984,
Raju modifi ed this technique by using a supravalvular
approach. Finally, Sottiurai (1988) proposed an internal
approach, modifying the original technique of Raju for
supravalvular repair of the incompetent venous valves. In
1972, Hallberg proposed the external banding of the incompetent valves of deep veins by sheathing the region with a
plastic tube. An extravenous valve substitute in the popliteal
space was described by Psathakis in 1984. In 1982, Taheri
proposed to transfer a valvulated segment of the axillary
vein into the lower femoral vein to treat chronic venous
insuffi ciency. In 1986, Jessup and Lane developed an external technique of banding incompetent valves with a silastic
cuff. One year later, Kistner developed an external suture
technique to “band” incompetent valves.
Reparative or substitutive surgery of venous valves
improved greatly in the last years. In 1999, Dalsing introduced the use of cryopreserved venous valve allografts for
the treatment of chronic deep venous insuffi ciency.15 One
year later, Raju, Berry, and Neglen16 described a variation
of closed external venous valve repair (transcommissural
valvuloplasty). In 2001, Tripathy and Ktenidis reported a
new technique of exposure of the valve commissure, called
the “trapdoor” internal valvuloplasty.
experimented with small-intestinal submucosa square-stent
bicuspid venous valve in sheep jugular veins and in three
patients. In the same year, Corcos18 proposed a monocuspid
valve reconstruction obtained with an intimal fl ap.
17
In 2003, Pavcnik
Paré is probably the fi rst to perform a superfi cial vein
thrombectomy in 1545: he suggested performing an incision
along the vein and squeezing it to expel the thrombus. The
fi rst thrombectomy of deep veins was performed by Lawen
in 1937. In 1939, Leriche and Geisendorf associated a periarterial sympathectomy of the nonpulsatile but unoccluded
femoral artery to a successful thrombectomy of the femoral
VENOUS ULCERS—WHY TO
TREAT THEM
Ulcers of venous origins were discriminated by Spender
(1866) in “varicose ulcers” and “venous ulcers” (“. . . ulcers
of the varicose type without varicose veins . . .”), attributing
the latter to failure of deep veins. One year later, John Gay
Ulcer Therapy 13
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fi rst associated induration and bronzing of the skin as circulatory complications of venous disorders, and, having noted
that varicose veins can be present for many years without
any ulcer or bronzing of the skin, affi rmed that “. . . ulceration is not a direct consequence of varicosity, but all of
other conditions of the venous system with which varicosity
is not infrequently a complication . . .” Gay’s intuitions were
already been explained by Fabricius (1603), who affi rmed
that varicose veins carry “fecaloid humours” that cause skin
damage. The “bad humours” could be the hemosiderin that
spreads from the capillary bed into the interstitium,19 or
other substances that produce a pericapillary fi brin cuff,
poorly permeable to gases20 or induce leukocyte trapping,
migration, and release of cytotoxic substances.
21
And Why Not to Heal Them
Only few authors devoted to the Pythagorean theory of
the four humours suggested not to heal ulcers because they
are considered as benefi cial in expelling dangerous substances. Galen of Pergamum (130–200 ad) believed that
black bile would be trapped by a healing ulcer. Thus, black
bile could leak outside while the ulcer remains unhealed. If
the ulcer heals, madness and other disasters would follow.
Avicenna even warned to reopen varicose ulcers if these
spontaneously closed. In modern times, among those reluctant to treat ulcers were Lorenz Heister (1718) and Henry
Françoise Le Dran (1731). Both of them considered the ulcer
to be a drain for humors that caused severe illness if not
expelled. Laufman stated: “. . . A number of British surgeons took up the same cry in the eighteenth century and
even into the nineteenth century(!!) . . .”
ULCER THERAPY
Modern ulcer therapy is based on 1) topical medications;
2) compressive bandage; and 3) surgery of related veins. The
same was true more than two thousand years ago.
In fact, since many centuries bc ago, venous ulcers are
treated by topical applications of substances (like the fi g
pultice used by the Prophet Isaiah), associated to bandages
(Celsus) and local hygienic treatments (Hippocrates). Principles of local treatments were meticulously described in
1446 by an anonymous surgical textbook (quoted by Partsch,
2002), which treated extensively (9000 words) the treatment
of leg ulcers. Four steps are reported: 1) enlargement of the
ulcer mouth, to obtain drainage; 2) mortifi cation (debride-
ment); 3) mundifi cation (cleansing); 4) fl eshing (production
of granulation tissue).
Ulcer therapies based only upon topical remedies were
strongly criticized in 1797 by Everard Home: “. . . It must
appear obvious, that there is no probability that any one
TABLE 1.5 Walking or Bed Rest to Heal Ulcers?
1778 Benjamin Bell Absolute bed rest
1783 Michel Underwood Immediate mobilization
1793 John Hunter Bed rest
1797 Thomas Baynton Walking
1799 Whately “. . . to walk with no scruples . . .”
1861 Hilton Bed rest
1886 Dechambre Walking
medicine can ever be discovered which, whether internally
administered or locally applied, shall have powers adapted
to the cure of all ulcer on the legs; and it would appear, the
idea that such a medicine may exist, has retarded very considerably, the advancement of our knowledge in the treatment of ulcers . . .” In addition, Brodie (1846) warned
against the frequent occurrence of cutaneous sensitization
due to drugs and other remedies used topically to treat
ulcers.
The importance of associating bandages to local treatment of ulcers was well known since Hippocrates and in
1676, the Englishman Richard Wiseman warned that venous
ulcers healed by compression usually recur once the compression is discontinued. In 1771 Else tried to determine
what compression therapy would do in old ulcers of the leg,
without administering any internal medicine, and found it so
exceedingly effi cacious that he believed it will seldom fail
where there is no carious bone. It has been discussed at
length, whether bandaged patients must walk or if it is better
that they rest on the bed (see Table 1.5). Besides clinical
argumentations, ambulatory treatment of venous ulcers was
justifi ed by the analysis of the costs of hospitalization
reported by Underwood in 1783 and by Philip Boyers in
1831.
Besides topical treatments, surgery of the varicose veins,
when present, has been recommended since old times.
Hyeronimus Fabricius of Acquapendente (1603) suggested
to associate compression to double ligation and division of
the varix above the ulcer. In turn, John Gay (1867) randomly
divided all the veins around the ulcers by several incisions.
It was only one century later, that selective interruption of
perforating veins below the ulcer was emphasized by Franck
Cockett. Currently, sclerotheraphy is used to obliterate periulcerative varicose veins. Nevertheless, the fi rst to perform
an endovenous treatment of ulcers was Sigismond Johann
Elsholz in 1665, using a chicken bone as a needle and a
bladder of pigeon as a syringe.
At any case, it was suggested to invoke a “divine factor”
to heal ulcers (Fabricius, 1603). On the contrary, the Roman
physician Asclepiade believed that ulcer healing needs
“. . . delicate massages from sweet maiden or boy, according
with own preferences . . .”
14 Chapter 1/Historical Introduction
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TABLE 1.6 Presidents of the IUP
Erich Krieg 1959–1970
Henrik Van Der Molen 1971–1983
Jean Van Der Stricht 1983–1989
André Davy 1989–1995
Georges Jantet 1995–1999
Hugo Partsch 1999–2003
Claudio Allegra 2003–2007
Eberhard Rabe (elect) 2007–2012
ADDENDA: THE INTERNATIONAL
UNION OF PHLEBOLOGY (IUP)
It was on March 24, 1959, at the Château de Meyrargues
in France near Aix-en-Provence, at the close of a joint
meeting of the responsible representatives of the four existing Societies of Phlebology (the French Society of Phlebology created in 1947, the Benelux Society of Phlebology
created in 1957, the German Society of Phlebology created
in 1958, and the Italian Society of Phlebology, which came
into being at the same time) that the foundations of an International Union of Phlebology were laid. Those responsible
were, Tournay and Wallois (France), van der Molen
(Benelux), Krieg (Germany), and Bassi and Comel (Italy).
Actually, the IUP includes the phlebological societies of
more than 40 countries (see Table 1.6).
References
1. Lurie F, Kistner RL, Eklof B, Kessler D. Mechanism of venous valve
closure and role of the valve in circulation: A new concept, J Vasc
Surg. 2003. 38: 955–961.
2. Ono T, Bergan JJ, Schmid-Schonbein GW, Takase S. Monocyte infi l-
tration into venous valves, J Vasc Surg. 1998. 27: 158–166.
3. Caggiati A, Luccichenti G, Pavone P. Three-dimensional phle-
bography of the saphenous venous system, Circulation. 2000. 102:
E33–35.
1
Chronology of main innovations in the fi eld of venous medicine and
surgery occurred during the last decades derived mainly by a PubMed
investigation.
1
4. Uhl JF, Verdeille S, Martin-Bouyer Y. Three-dimensional spiral CT
venography for the pre-operative assessment of varicose patients,
Vasa. 2003. 32: 91–94.
5. Ruehm SG, Zimny K, Debatin JF. Direct contrast-enhanced 3D MR
venography, Eur Radiol. 2001. 11: 102–112.
6. Szendro G, Nicolaides AN, Zukowski AJ, Christopoulos D, Malouf
GM, Christodolou C, Myers K. Duplex scanning in the assessment of
deep venous incompetence, J Vasc Surg. 1986. 4: 237–242.
7. Luizy F, Franceschi C, Franco G. A method of venous study by real time
ultrasonography associated with directional and continuous Doppler
ultrasonography, Ann Med Interne (Paris). 1986. 137: 484–487.
8. Partsch H, Rabe E, Stemmer R. Compression therapy of the extremities, Editions Phlebologiques Francais, Paris. 2002.
9. Ricci S, Georgiev M, Goldman MP. Ambulatory phlebectomy. Mosby
St Louis. 1995.
10. Corcos L, De Anna D, Zamboni P, Gasbarro V, Bresaola V, Procacci
T, Liboni A, Macchi C, Donini I. Reparative surgery of valves in the
treatment of superfi cial venous insuffi ciency. External banding valvuloplasty versus high ligation or disconnection. A prospective multicentric trial, J Mal Vasc. 1997. 22: 128–136.
11. Yamaki T, Nozaki M, Sasaki K. Alternative greater saphenous veinsparing surgery: Valvuloplasty combined with axial transposition of a
competent tributary vein for the treatment of primary valvular incompetence, 18-month follow-up, Dermatol Surg. 2002. 28: 162–167.
12. Mozes G, Gloviczki P, Menawar SS, Fisher DR, Carmichael SW,
Kadar A. Surgical anatomy for endoscopic subfascial division of perforating veins, J Vasc Surg. 1996. 24: 800–808.
13. Labropoulos N, Mansour MA, Kang SS, Gloviczki P, Baker WH. New
insights into perforator vein incompetence, Eur J Vasc Endovasc Surg.
1999. 18: 228–234.
14. van Neer PA, Veraart JC, Neumann HA. Venae perforantes: A clinical
review, Dermatol Surg. 2003. 29: 931–942.
15. Dalsing MC, Raju S, Wakefi eld TW, Taheri S. A multicenter, phase
I evaluation of cryopreserved venous valve allografts for the treatment
of chronic deep venous insuffi ciency, J Vasc Surg. 1999. 30: 854–864.
16. Raju S, Berry MA, Neglen P. Transcommissural valvuloplasty: Technique and results, J Vasc Surg. 2000. 32: 969–976.
17. Tripathi R, Ktenedis KD. Trapdoor internal valvuloplasty—A new
technique for primary deep vein valvular incompetence, Eur J Vasc
Endovasc Surg. 2001. 22: 86–89.
18. Corcos L, Peruzzi G, Procacci T, Spina T, Cavina C, De Anna D. A
new autologous venous valve by intimal fl ap. One case report. Minerva
Cardioangiol. 2003. 51: 395–404.
19. Zamboni P, Izzo M, Fogato L, Carandina S, Zanzara V. Urine hemosiderin: A novel marker to assess the severity of chronic venous
disease, J Vasc Surg. 2003. 37: 132–136.
20. Browse NL, Burnand KG. The cause of venous ulceration, Lancet,
1982. 2(8292): 243–245.
21. Coleridge Smith PD, Thomas P, Scurr JH, Dormandy JA. Causes of
venous ulceration: A new hypothesis, Br Med J (Clin Res Ed).
1988. 296: 1726–1727.
CHAPTER
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2
Venous Embryology and Anatomy
GEZA MOZES and PETER GLOVICZKI
INTRODUCTION
Substantial knowledge has accumulated in recent years
on development and anatomy of the venous system. Progress in medical genetics resulted in identifi cation of genes
linked to development of circulation and in recognition of
growth factors affecting normal and abnormal development
of blood vessels. Perfection of ultrasound technology combined with an increasing clinical interest in venous disease
resulted in identifi cation of new compartments and clinically
important anatomic structures.1 Finally, a new, clinically
relevant anatomic terminology of the veins of the leg and
pelvis was introduced.2 In this chapter we discuss the embryology of the venous system and present the most frequent
venous anomalies. We describe the histology of large veins
and present a detailed anatomy of the veins of the trunk and
the upper and lower limbs. Discussion of the anatomy of the
visceral and cervical veins is beyond the scope of this review.
The new terminology of veins will be used in this manuscript (see Table 2.1).
EMBRYOLOGY
During embryogenesis the earliest veins develop from
capillary plexuses; these carry blood into the sinus venosus,
the in-fl ow end of the forming heart. The right and left
common cardinal veins drain directly into the sinus venosus
(see Figure 2.1). The common cardinal veins form at the
junction of the anterior and posterior cardinal veins on both
sides. Between this junction and the heart the common cardinal veins receive the vitelline and umbilical veins. The
vitelline veins initially drain the yolk sac and later the intes-
tines. The right umbilical vein regresses completely, the left
drains the placenta.
The anterior cardinal veins drain the cranial part of the
embryo and are connected to each other by a large central
anastomosing channel. The segment of the left anterior cardinal vein located proximal to the anastomosis will regress.
The oblique vein of the left atrium and the coronary sinus
develop from the regressed proximal segment of the left
anterior cardinal vein. The remaining distal segment becomes
the left internal jugular vein and the anastomosis between
the anterior cardinal veins forms the left brachiocephalic
vein. The right internal jugular and brachiocephalic veins
develop from the proximal segment of the right anterior
cardinal vein. The external jugular veins develop secondarily. Failure of the regression of the proximal left anterior
cardinal vein results in double superior vena cava (SVC),
whereas erroneous regression on the right side results in
left-sided SVC (see Figure 2.2a, b).
The posterior cardinal veins run caudal to the heart and
distally develop an interconnecting iliac anastomosis. Contrary to their anterior counterparts, the posterior cardinal
veins regress almost completely. Only a small proximal
segment remains on the right side to form the azygos arch
and the iliac anastomosis to transform into the common,
external, and internal iliac and median sacral veins.
Most veins, caudal to the heart, develop from the sub- and
supracardinal veins, which arise dorsal and ventral to the
regressed posterior cardinal veins, respectively. The subcardinal veins anastomose with each other (subcardinal anastomosis) and with the supracardinal veins (subsupracardinal
anastomosis). The majority of the left-sided cardinal veins
regress. The right subcardinal vein develops to drain most
of the upper, the right supracardinal vein most of the lower
part of the abdomen.
3,4
The Vein Book
15
All rights of reproduction in any form reserved.
Copyright © 2006, Elsevier Inc.
16 Chapter 2/Venous Embryology and Anatomy
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Majority of the azygos system develops from the cranial
part of the supracardinal veins. The infrarenal segment of
the inferior vena cava (IVC) develops from the caudal right
supracardinal vein. The renal segment of the IVC arises
from the subsupracardinal anastomosis, a venous network
TABLE 2.1 Historic and New Anatomic Terms of Lower
Extremity Veins
Historic term New term
Greater or long saphenous vein Great saphenous vein (GSV)
Smaller or short saphenous vein Small saphenous vein (SSV)
Saphenofemoral junction Confl uence of the superfi cial
inguinal veins
Giacomini’s vein Intersaphenous vein
Posterior arch vein or Leonardo’s Posterior accessory great
vein saphenous vein of the leg
Superfi cial femoral vein Femoral vein
Cockett perforators (I,II,II) Posterior tibial perforators (lower,
middle, upper)
Boyd’s perforator Paratibial perforator (proximal)
Sherman’s perforators Paratibial perforators
24 cm perforators Paratibial perforators
Hunter’s and Dodd’s perforators Perforators of the femoral canal
May’s or Kuster’s perforators Ankle perforators
located circumferentially around the aorta (renal collar).
Eventually, the posterior segment of the collar regresses and
the anterior part gives the left renal vein. Most of the suprarenal segment of the IVC develops from the right subcardinal vein, except for the short hepatic segment, which
originates directly from hepatic sinusoids.5 Variation in the
complex development of IVC and left renal vein is not
uncommon. If the right subcardinal vein fails to connect to
the liver sinusoids, the suprarenal segment of the IVC will
not develop, consequently the lower part of the body will be
drained through the azygos system and the liver will drain
directly into the heart. Double IVC (0.2–3%) occurs due to
the persistence of the left supracardinal vein, therefore it
usually involves only the infrarenal segment (see Figure
2.2).6 Left-sided IVC (<0.5%) develops if persistence of the
left supracardinal vein is associated with regression of the
right supracardinal vein (see Figure 2.2).7 Developmental
variations of the left renal vein include persistent (circumaortic) renal collar (1–9%) and retroaortic left renal vein
(1–2%) (see Figure 2.3).
8
Capillaries of the primitive limb buds initially drain into
the marginal sinuses. In the arm the ulnar portion of the
marginal sinuses dominate over the radial ones, and eventually form the basilic, axillary, and subclavian veins. The
FIGURE 2.1 Embryology of the major veins (adopted from Avery LB. Developmental Anatomy, revised 7
Philadelphia: WB Saunders, 1974).
th
ed.
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subclavian vein drains into the proximal anterior cardinal
vein. The cephalic vein develops secondarily from segments
of the radial marginal sinuses and attaches to the axillary
vein later. In the leg, segments of the primitive marginal
sinuses persist only distally and develop into the peroneal,
anterior tibial, and small saphenous veins. The great saphenous vein originates from the posterior cardinal vein and
later gives off the femoral, popliteal, and posterior tibial
veins.
HISTOLOGY
The venous wall has three layers: intima, media, and
adventitia. The intima is made up by endothelial cells and
an underlying thin connective tissue layer. Valves are formed
by infolding of the intima, therefore they are covered with
endothelium on both sides and have a very thin connective
tissue skeleton. Venous valves are bicuspid. The veins are
distended at the base of the valves, probably secondary to
the effects of local fl ow reversal. The border of the intima
is marked by the internal elastic lamina: a layer of thick
elastic fi bers. The internal elastic lamina is well developed
only in large veins; it is incomplete in medium-sized and
absent in small ones. The media is composed of smooth
muscle cells and connective tissue fi bers, most of which is
collagen. Larger superfi cial veins, such as the GSV, have
thick muscular media with the ability of signifi cant contraction. Smaller tributaries of the GSV have thinner media, and
therefore are more prone to varicosity. Media of the deep
FIGURE 2.2 Developmental anomalies of the superior (SVC) and infe-
rior vena cava (IVC). a. Double SVC (posterior view). b. Left SVC (posterior view). c. Double IVC. d. Left IVC.
calf veins contain plenty of collagen, providing better wall
strength. More central deep veins, such as femoral, iliac,
axillary, and subclavian veins, contain less and less smooth
muscle cell. The media of the superior and inferior vena
cava is built up almost exclusively from connective tissue.
The adventitia is poorly differentiated from the media, in
particular in larger veins. It consists of some loose connective tissue with vasa vasorum and nerve fi bers.
9,10
FIGURE 2.3 Circumaortic renal collar.
ANATOMY OF THE THORACIC VEINS
The superior vena cava (SVC) starts at the confl uence of
the brachiocephalic veins behind the fi rst right costal cartilage, and ends at the level of the third right costal cartilage
where it drains into the right atrium. The SVC is about 7 cm
long and 2 cm wide. Halfway along its course, before it
enters the pericardium, the SVC receives the azygos arch.
The brachiocephalic veins are formed at the confl uence of
the subclavian and internal jugular veins behind the sternoclavicular joints (see Figure 2.4). The right brachiocephalic
vein is short, about 2–3 cm, and lies anterior to the innominate artery.
obliquely behind the manubrium from left to right, anterior
7
The left one is about 6 cm long and courses
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gives the entire right arm of the H, the hemiazygos gives the
left lower and the accesory hemiazygos vein the left upper
segment. The azygos vein starts at T12 to L2 with the confl uence of the right ascending lumbar and subcostal veins.
The azygos vein ascends on the right side up to the level of
T4, then passes anterior to form an arch joining the SVC.
Major tributaries of the azygos vein are the right posterior
fi fth to eleventh intercostal veins and the right superior intercostal vein draining the second to fourth intercostal veins.
The hemiazygos vein starts similar to the azygos vein but
on the left side of the vertebral column at T12–L2. It courses
cranial and at the level of T8 it crosses over to join the
azygos vein. Major tributaries of the hemiazygos vein are
the left posterior eighth to eleventh intercostal veins. The
accessory hemiazygos vein has more variation than the
azygos and hemiazygos veins. Usually it drains the left
superior intercostal vein (which in turn drains the left second
to fourth intercostal veins) and the left posterior fi fth to
seventh intercostal veins. At the level of T7 it either crosses
over to the right and joins the azygos or stays on the left
and joins the hemiazygos vein. If the connection between
the accessory hemiazygos and the rest of the azygoshemiazygos system is not developed, the accessory hemiazygos vein will drain through the left superior intercostal
vein into the left brachiocephalic vein. The azygoshemiazygos system receives several small veins from the
viscera of the chest and freely anastomoses with the vertebral venous plexuses as well. The azygos-hemiazygos
system provides an important collateral pathway in case of
IVC or SVC obstruction.
7
FIGURE 2.4 Thoracic and retroperitoneal veins.
to the left subclavian, common carotid arteries, and superior
to the aortic arch. Major tributaries of the brachiocephalic
veins are the vertebral, internal thoracic, and inferior thyroid
veins. The fi rst intercostal vein drains into the brachiocephalic veins on both sides. The left superior intercostal vein
is connected to the left brachiocephalic vein, whereas on the
right it joins the azygos vein. There are no valves in either
the SVC or the brachiocephalic veins.
The azygos-hemiazygos system forms an H-shaped
network in the posterior mediastinum, anterior to the body
of the thoracic vertebrae (see Figure 2.4). The azygos vein
ANATOMY OF THE UPPER
EXTREMITY VEINS
The dorsal and palmar digital veins join to form the
metacarpal veins, which drain into the superfi cially located
dorsal venous network of the hand. The cephalic and basilic
veins arise from this network on the radial and ulnar side of
the wrist, respectively. The superfi cial veins on the palmar
side of the hand are richly anastomosed to the deep veins.
A superfi cial and a more proximal deep venous arch is
formed from the interconnection of the palmar veins and
parallel the corresponding arterial arches.
The cephalic vein originates at the anatomical snuff box
from the dorsal venous network. It courses over the distal
radius to the ventral aspect of the forearm and ascends on
the lateral side of the arm. The cephalic vein runs in the
deltopectoral groove, it enters the infraclavicular fossa
behind the pectoralis major muscle and pierces the clavipectoral fascia before empting into the axillary vein (see Figure
2.5). The basilic vein begins on the ulnar side of the wrist,
passes along the ulnar aspect of the forearm, and courses
more ventrally at the level of the elbow. Above the elbow
Anatomy of the Abdominal and Pelvic Veins 19
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sponding arteries. The three pairs of deep veins of the
forearm form the brachial veins at the level of the elbow.
The paired brachial veins join the basilic vein to form the
axillary vein at the lower border of the teres major muscle (at
the lateral border of the scapula on an antero-posterior chest
x-ray). The axillary vein is located medial and inferior to the
axillary artery and the medial cord of the brachial plexus lies
between the two vessels. The axillary vein ends at the outer
border of the fi rst rib where it becomes the subclavian vein.
The subclavian vein runs posterior and superior to the subclavian artery and recives its only major tributary, the external jugular vein. The subclavian vein ends at the medial
border of the scalenus anterior muscle where it joins the
internal jugular vein to form the brachiocephalic vein.
There are valves in the superfi cial and deep veins of the
arm, although they are not so numerous as in the leg. Valves
in the axillary vein usually are located proximal to the
junction with the brachial and cephalic veins. The subclavian vein has a valve just proximal to the confl uence of the
external jugular vein. Upper extremity venous return is
maintained mainly by the work of the heart without signifi cant contribution of a muscle pump. Therefore the valves
are less important from a functional standpoint. Perforators
between the deep and superfi cial veins are scarce.
FIGURE 2.5 Upper extremity superfi cial veins.
the basilic vein runs medial to the biceps and at about
midway in the upper arm it perforates the deep fascia and
joins the brachial vein. After receiving the brachial vein, the
basilic vein continues in the axillary vein. The median
cubital vein connects the cephalic and basilic veins in the
antecubital fossa. The medial antebrachial vein originates
from the superfi cial palmar venous plexus and runs on the
ventral side of the forearm. It joins either the cephalic or
basilic vein or both in the proximal forearm. The accessory
cephalic vein originates from the dorsal venous plexus on
the ulnar side and crosses over dorsally to join the cephalic
vein in the forearm. Variations in the anatomy of superfi cal
arm veins are countless.
Deep veins of the hand join to form the paired radial,
ulnar, and interosseus veins, which accompany the corre-
ANATOMY OF THE ABDOMINAL AND
PELVIC VEINS
The inferior vena cava (IVC) begins at the confl uence of
the common iliac veins and ascends on the right side of the
vertebral column, passes through the tendinous portion of
the diaphragm, and after a short course (approximately
2.5 cm) in the chest it terminates in the right atrium at the
level of T9. In the upper abdomen the IVC is located posterior to the duodenum, the head and neck of the pancreas,
the lesser sac, and the liver. The intrahepatic portion of the
IVC lies in a groove along the posterior aspect of the caudate
lobe. Tributaries of the IVC are the paired lumbar and renal
veins and the hepatic veins, additionally on the right side the
right gonadal, suprarenal, and inferior phrenic veins also
drain into the IVC (see Figure 2.4). The left gonadal and
suprarenal veins join the left renal vein, the left inferior
phrenic vein drains into the left suprarenal vein. In case of
IVC obstruction, communication between the veins of the
thoracic and abdominal wall (thoracoepigastric, internal thoracic, and epigastric veins), the lumbar-azygos anastomosis,
and the vertebral plexuses provide important collateral
pathways.
The common iliac veins begin at the sacroiliac joint on
both sides and end at L5, where they form the IVC. The only
tributary of the right common iliac vein is the right ascending lumbar vein; the left common iliac vein drains the left
ascending lumbar and median sacral veins (see Figure 2.4).
20 Chapter 2/Venous Embryology and Anatomy
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FIGURE 2.6 Relationship between the fascia and veins of the lower extremity. The fascia covers the muscle and
separates the deep from the superfi cial compartment. Superfi cial veins (a) drain the subpapillary and reticular venous
plexuses, and are connected to deep veins through perforating veins (b). The saphenous fascia invests the saphenous
vein. The saphenous compartment is a subcompartment of the superfi cial compartment.
The right common iliac vein lies postero-lateral to the right
common iliac artery. The distal segment of the left common
iliac vein is medial and posterior to the left common iliac
artery, the proximal segment is posterior to the right iliac
artery and distal aorta. Compression of the proximal left
common iliac vein may occur due to the overlying arterial
structures. The external iliac vein starts at the level of the
inguinal ligament, it courses along the pelvic brim and ends
anterior to the sacroiliac joint where the external and internal
iliac veins form the common iliac vein. On the right the
distal external iliac vein is medial to the artery; however, as
it ascends, more proximally, it courses posterior to it. The
left external iliac vein remains medial to the artery along its
entire course. Tributaries of the external iliac vein are the
inferior epigastric, deep circumfl ex iliac, and pubic veins.
The internal iliac vein runs postero-medial to the internal
iliac artery on both sides. The short trunk of internal iliac
vein is formed by the confl uence of extra and intrapelvic
venous tributaries. The extrapelvic tributaries include the
gluteal (superior and inferior), internal pudendal, and obturator veins, which drain the pelvic wall and the perineum.
Intrapelvic tributaries of the internal iliac vein are the lateral
sacral and visceral (middle rectal, vesical, uterine, and
vaginal) veins, which drain the presacral and pelvic visceral
venous plexuses (rectal, vesical, prostatic, uterine, and
vaginal).
Both the IVC and the common iliac veins are valveless.
There is usually one valve in the external iliac vein, however
often it is without any valves.
ANATOMY OF THE LOWER
EXTREMITY VEINS
Thorough knowledge of the fascial compartments of the
leg is a prerequisite of understanding the relationship
between superfi cial and deep veins. The fascia surrounding
the calf and thigh muscles separates two compartments: the
superfi cial compartment, consisting of all tissues between
the skin and the fascia, and the deep compartment, which
includes all tissues between the fascia and the bones (see
Figure 2.6).11 Superfi cial veins run in the superfi cal, deep
veins in the deep compartments. Perforating veins pierce
through the fascia and connect the superfi cial to deep veins.12
Communicating veins connect veins within the same compartment: superfi cial to superfi cial or deep to deep veins.
The saphenous veins are covered by a fi brous sheath, the
saphenous fascia. The saphenous fascia is thinner than the
deep fascia and it is more pronounced in the upper-mid
thigh, than more distally.
nous and muscular deep fascia is the saphenous compartment. The saphenous compartment is a subcompartment of
the superfi cial compartment.
The superfi cial venous system of the foot is divided into
the dorsal and plantar subcutaneous venous network (see
Figure 2.7). Superfi cial vein tributaries drain blood into the
dorsal venous arch on the dorsum of the foot at the level of
the proximal head of the metatarsal bones. The medial and
lateral end of this arch continues through the medial and
1,13
The space between the saphe-
Anatomy of the Lower Extremity Veins 21
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FIGURE 2.7 Superfi cial and perforating veins of the foot and ankle.
lateral marginal vein into the great (GSV) and small saphenous veins (SSV), respectively.
Small superfi cial veins drain the subpapillary and reticular plexuses of the skin and subcutaneous tissues to form
bigger tributaries, which eventually all connect to the saphenous veins.
14,15
The GSV begins just anterior to the medial
ankle, crosses in front of the tibia, and ascends medial to the
knee (see Figure 2.8).
16–18
Proximal to the knee, the GSV
ascends on the medial side of the thigh and enters the fossa
ovalis 3 cm inferior and 3 cm lateral to the pubic tubercle.19
The GSV is doubled in the calf in 25% of the population, in
the thigh in 8%.20 The saphenous nerve runs in close proximity to the GSV in the distal two-thirds of the calf. Accessory
great saphenous veins are frequently present and they run
parallel to the GSV both in the thigh and in the leg; they lie
either anterior, posterior, or superfi cial to the main trunk.
The posterior accessory GSV of the leg (Leonardo’s vein or
posterior arch vein) is a common tributary, it begins posterior to the medial malleolus, ascends on the posteromedial
aspect of the calf, and joins the GSV distal to the knee (see
Figure 2.8). The anterior accessory GSV of the leg drains
the anterior aspect of the leg below the knee. The posterior
accessory GCV of the thigh, if present, drains the medial
and posterior thigh.
11
The anterior accessory GSV of the
thigh collects blood from the anterior and lateral side of the
thigh (see Figure 2.8). The anterior and posterior accessory
GSVs join the GSV just before it ends at the confl uence of
superfi cial inguinal veins (saphenofemoral junction). The
superfi cial circumfl ex iliac, superfi cial epigastric, and exter-
FIGURE 2.8 Superfi cial and perforating veins of the leg.
nal pudendal veins join each other and the distal GSV to
form the confl uence of superfi cial inguinal veins (sapheno-
21
femoral junction) (see Figure 2.9).
Rarely, the GSV terminates high on the lower abdomen or joins the femoral vein
very low and the superfi cial inguinal veins empty individually into the femoral vein.22 Other occasional tributaries of
the GSV in the groin include the posterior and anterior thigh
circumfl ex veins.
The small saphenous vein (SSV) lies lateral to the
Achilles tendon in the distal calf (see Figure 2.10).
23
In the
lower two-thirds of the calf the SSV runs in the subcutaneous fat, then it pierces the fascia and runs between the two
heads of the gastrocnemius muscle. In the popliteal fossa at
about 5 cm proximal to the knee crease, the main trunk of
the SSV drains into the popliteal vein. A smaller vein, the
cranial extension of the SSV, frequently continues in cephalad direction (see Figure 2.10).24 Uncommonly the main
trunk of the SSV continues without draining into the popliteal vein and eventually empties into the femoral vein or
GSV.11 The intersaphenous vein (vein of Giacomini) is a
communicating vein connecting the SSV to the GSV in the
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