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10 Venous and lymphatic disease
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Louis. e cobbler was miraculously healed by applying the
Saint’s tomb dust directly onto his ulcer, making this the
rst known case report of DVT.
8
e number of notied DVT cases increased rapidly,
along with proposed pathological hypotheses and treatment
attempts. roughout the middle ages and Renaissance,
physicians widely subscribed to the humoral disease theory,
and it was believed that DVT was caused by an accumulation of “evil humors.” Similarly to many other diseases
in the seventeenth to nineteenth centuries, treatment was
focused on eliminating these evil humors and restoring the
body’s natural humoral balance via bloodletting.8 In spite
of a generally erroneous understanding of pathophysiology,
Renaissance physicians did notice a correlation between
DVT and pregnancy, which was the leading cause of
reported DVT during this era. e advised prophylaxis for
pregnancy-related DVT was breast feeding, since the cause
was suspected to be the retention of unconsumed milk in
the legs, commonly referred to as “milk leg.”
8,19
Eventually, the lack of therapeutic ecacy led to the
abandonment of the humoral theory of disease. Physicians
were puzzled by the large blood clots discovered upon
autopsy in the lungs of patients aer sudden death.
Recognition and scientic interest emerged in 1676 when
Richard Wiseman suggested that DVT was caused by an
alteration of blood.
2,8 ,19
In the mid-nineteenth century, Jean
Cruveilhier, a renowned French pathologist, elaborated on
the exact nature of the blood alteration and published his
theory that “phlebitis dominates all of pathology.”
2,8,20
is notion was widely accepted throughout the nineteenth century, with therapy aimed at the symptomatic treatment of infection and associated venous inammation.8 DVT
management included bloodletting, leech application, cupping, purging, ice application, and cold baths, all in an eort to
reduce limb congestion. Targeted anti-infectious agents were
quinquona (quinine) used for malaria, mercury used for syphilis, and autumn crocus (colchicine) used for gout. Finally,
anti-inammatory medications and general antiseptics such
as zinc chloride were also tried in order to prevent DVT.
8
Known as the father of modern pathology, Rudolph
Virchow (Figure 1.7) made tremendous contributions to our
understanding of VTE pathophysiology and initiated the era
of cellular pathology. Aer graduation from medical school
and surgical appointment, he was instantly attracted to the
autopsy room. At the recommendation of his anatomy professor, he intensely studied Cruveilhier’s theory of phlebitis
as the cause of all disease. He was curious as to exactly how
venous inammation led to clot formation, and was determined to establish a method of discerning clots formed while
living from blood clots formed aer death. Aer extensive
laboratory studies, he accurately identied two distinctly
dierent types of thrombus in 1856: the thrombus that forms
within a vessel at the site of occlusion and the thrombus that
breaks away from its origin and forms an embolus traveling through the bloodstream to occlude pulmonary vessels.
Just two years out of medical school, he had discovered the
relationship between DVT and fatal PE, coining the term
Figure 1.7 Rudolf Virchow, 1902, in the year of his
death at the age of 81. (From Bagot CN, Roopen A.
BrJHaematol, 143(2), 180–190, 2008, four black and
white photographs, two diagrams. Database: Image
Quick View Collection.)
“embolism.” His famous triad (venous stasis, trauma, and
hypercoagulability) is still taught and recognized as the
most comprehensive explanation of VTE etiology.
2
Prior to the discovery of anticoagulants, strict bed rest for
many weeks was the cornerstone of VTE treatment. e rationale behind this treatment was that during the “acute phase”
of DVT, the thrombus was not xed to the vessel and was at
high risk of migration,8 and the thrombus could be secured
in place by restricting movement of the limb. Patients’ lower
limbs were set in iron splints to prevent movement, and special reclining orthopedic beds were used to optimize venous
return. e application of a warm compress was also used
to reduce vasospasm and increase collateral circulation.8
Unfortunately, in addition to actually promoting thrombus
formation and extension, prolonged immobilization was
frequently associated with serious unpleasant consequences,
such as lower extremity joint stiness (ankyloses) and muscle
atrophy (amyotrophia).8 Late in the nineteenth century, aer
observing that supercial vein thrombosis quickly vanished
with the use of compression bandages, two German phlebologists (Fischer and Lasker) started prescribing compression bandages to their DVT patients. Despite their foresight
and the appropriateness of their therapy, their approach was
not popular due to the widespread teaching of prolonged bed
rest as the most important treatment for DVT.
8
1.2.11 Evolution of surgical and
endovascular VTE treatments
In 1793, John Hunter proposed that DVTs were caused
by blood clots causing vein occlusion and attempted the
1.2 Varicose veins and chronic venous insufficiency 11
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rst surgical treatment in 1784 utilizing venous ligation
above a thrombus in an eort to prevent extension of the
clot, leading to fatal PE. Subsequently, in 1868, Armand
Trousseau, a French surgeon, suggested ligation of the
inferior vena cava (IVC) in cases of recurrent PE. is
approach was also adopted by Enrico Bottini in 1893.2
Surgical venous ligations continued to be practiced into
the twentieth century, despite their association with a
high fatality rate (14%).8 In 1908, Friedrich Trendelenburg
of Leipzig, Germany, performed the very rst pulmonary
embolectomy via le anterior thoracotomy. is operation
was unsuccessfully performed on two patients who were
dying from massive PEs.
In the early twentieth century, physicians lacked a truly
eective treatment and prophylaxis for fatal PEs. Almost
20 years aer Trendelenburg’s failed attempts, Marin
Kirschner, a student of Trendelenburg, completed the rst
successful pulmonary embolectomy on March 28, 1924,
and thus ushered in the era of surgical PE correction. e
intervention was extremely risky, rarely successful, and very
few cases were performed worldwide over the next 40 years.
However, the invention of the heart–lung machine by John
H. Gibbon, Jr. in 1931 made a surgical PE approach more
realistic.
On April 18, 1961, Denton Cooley (Figure 1.8) from
Houston, Texas, accomplished the rst pulmonary embolectomy under extracorporeal circulation in a 37-yearold woman recovering from abdominal hysterectomy.2
However, even with extracorporeal circulation, there
continued to be a tremendous risk of mortality secondary to
fatal intraoperative embolisms and high rates of rethrom-
8,21
bosis.
It remained a measure of last resort reserved only
for massive, acute PEs or chronic, recurrent PEs resulting in large thrombi wedged in the pulmonary arteries
and causing severe pulmonary hypertension.2 A few years
later, in 1969, Dr. Lazar Greeneld suggested a less invasive
method of pulmonary embolectomy using a catheter introduced into the femoral vein under uoroscopic guidance.
is technique, known as transvenous catheter embolectomy or thrombo-fragmentation, was associated with a
25% mortality rate and similar indications as open pulmonary embolectomy.
2
Although the brinolytic properties of some substances
were studied and reported in the late nineteenth century,
thrombolytic agents have been available for medical use
only during the past 50 years. In 1947, the rst partially
puried streptokinase was produced for the treatment of
myocardial infarctions; however, the associated toxicity of
thombolytics during this era greatly precluded their systemic use.
8,22
In 1953, plasmin and streptokinase were intravascularly infused for the rst time in order to treat acute
thromboses, including isolated DVTs in volunteer cancer
patients with advanced metastasis.8 Currently, pharmacological thrombolytic agents are the main treatment that is
initiated for early thrombus removal. e optimal approach
for catheter-directed versus systemic thrombolytic use has
yet to be dened, and there are ongoing research studies in
this area.
8,23
Figure 1.8 Denton A. Cooley, MD, pioneer-
ing cardiovascular surgeon and founder of the
Texas Heart Institute (http://www.examiner.com/
article/a-tribute-to-dr-denton-cooley).
1.2.12 Therapeutic and prophylactic
progress—the anticoagulant era:
1920s–1950s
e most important advances in the medical management
of DVT occurred in the early twentieth century. Concern
shied from fear of sudden death due to fatal DVT embolism to the less severe complications of VTE, including
recurrence and major bleeding. By this time, physicians
had nally formed a consensus on Virchow’s triad as the
pathologic basis of VTE. Before the revolutionary anticoagulation breakthroughs of the 1920s, numerous other ineffective therapeutic options had been tried. Experimental
use of antibiotics (sulfanilamide, sulfapyradine, and sulfathiazole), application of leeches, X-ray therapy, mecholyl
iontophoresis, and paravertebral lumbar anesthesia, developed by Michael DeBakey in 1939, were all proposed and
abandoned. e pathophysiological rationale for the 1940
lumbar sympathetic block was based on venographic series
images, which suggested that DVT was accompanied by
severe vasospasm.
Ochsner and Michael DeBakey popularized IVC ligation
as the best recurrent PE prophylactic method. However,
the sudden interruption of caval venous ow was associated with profound hemodynamic changes, resulting in the
post-phlebitic syndrome.
8
Also in the early 1940s, Drs. Alton
2
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1.2.13 The evolution of prophylactic
treatment
Heparin became the thromboprophylactic treatment of
choice for DVT in the 1950s, but surgery was still used,
notably in cases of severe VTE.8 In order to reduce surgeryrelated adverse outcomes, various devices were proposed
from the mid-1950s onwards for temporary or partial interruption of the IVC. In the early 1960s, Adams-DeWeese
and Miles developed partial IVC occlusion clips that successfully trapped potentially fatal clots without completely
occluding blood ow. e clips were very popular throughout the 1960s; however, due to complications, including
IVC thrombosis and narrowing, the devices failed to provide substantial clinical improvement. Intraluminal devices
were then designed to act as lters.
the rst intraluminal “harpgrip” lter in 1958, which could
block the transit of emboli without signicantly disturbing the function or dynamics of the venous system.
Although promising results were seen in preventing PE,
lter placement required major surgery under general anesthesia. Finally, this problem was solved with the Mobin–
Uddin umbrella, which was released for general clinical
use in 1970. e device was simply installed via catheter
under local anesthesia.8 Unfortunately, the Mobin-Uddin
umbrella also had a high complication rate. In 1969, a new
generation of intraluminal lters was introduced by Dr.
Lazar Greeneld and Mr. Garman Kimmel, an oil drilling engineer. Modications of their prototype known as
the “Greeneld lter” were widely used for over 25 years.2
e next phase of development involved retrievable lters,
which became available for clinical use only 20 years ago
and are still the objects of therapeutic trials.
Without doubt, the best protection against DVT and PE
continues to be the identication of high-risk patients and
the subsequent implementation of adequate medical anticoagulant prophylactic measures.
2,8
DeWeese constructed
8
8,21
given at home was as safe and eective as hospital-administered unfractionated heparin.
8,26
at same year, a small,
randomized trial provided evidence that early ambulation
with compression stockings improved pain and counteracted edema without increasing the risk of PE.
dence resulted in the recommendation for early ambulation
with compression stockings as a part of standard management.8 In 1997, compression stockings were shown to be
ecacious for preventing post-thrombotic syndrome.
Compared with the conventionally established VTE
medications, new oral anticoagulants (factor Xa inhibitors) have shown equivalent or superior clinical benet with
comparable safety. ey also have the potential to improve
compliance, as they do not need routine monitoring.
1.2.15 Conclusion: Modern economic
implications of VTE treatment
In spite of diagnostic and therapeutic progress, VTE is still a
common and serious medical condition that aects approximately two million people in the United States yearly.
2011, the estimated annual cost of initial and recurrent VTE
events was $13.5–$69.3 billion, of which $4.5–$39.3 billion
is entirely preventable. VTE prevention recently became
a priority of e Joint Commission (TJC), the Centers for
Medicare and Medicaid Services (CMS), and the National
Quality Forum in 2006.
and indirect societal costs related to VTE and its complications are tremendous, and optimizing VTE treatment and
prevention is critical to providing the best possible patient
outcomes and minimizing costs related to treatment and
future complications.
bosis has the unique opportunity of changing the conversation, from VTE management via diagnosis and treatment,
to prophylaxis, in order to improve the quality of health
care and simultaneously reduce the burdensome morbidity,
mortality, and costs associated with preventable VTE.
andprophylaxis
31,34,35
32,36
us, the eld of venous throm-
e direct health care costs
8,28
is evi-
8
8,29–32
32,33
In
1.2.14 The modern era: Ambulatory
management of DVT (since 1950)
Diagnostic progress radically modied DVT management.
Venography was not consistently us ed to diagnose DVT until
it was standardized in the 1970s. is allowed physicians
to treat objectively conrmed DVT. Venography expedited
treatment tremendously, even in clinically asymptomatic
patients.
8,24,25
Heparin signicantly decreased PE mortality,
with both its anti-inammatory and analgesic properties
allowing for shorter bed rest recommendations.
Fear of thrombus migration made most physicians reluctant to recommend immediate patient mobilization. Until
the early 1990s, ambulation was not recommended and bed
rest, oen lasting 5–7 days, was still included in DVT treat-
8,26
ment.
e introduction of low-molecular-weight heparin
(LMWH) in the 1980s enabled simplication of anticoagulant treatment.
8
8,27
In 1996, it was demonstrated that LMWH
1.3 THE LYMPHATIC SYSTEM AND
LYMPHEDEMA
1.3.1 Ancient understanding of the
lymphatic system
e rst recorded lymphatic system descriptions are attributed to the ancient Greeks. Many of the same scientists who
made signicant contributions to the discovery of varicose veins and chronic venous insuciency also advanced
our understanding of the lymphatic system. In the fourth
century , Aristotle described “bers which take a position between blood vessels and nerves and which contain a
colorless liquid.” Later in 400 , Hippocrates discovered
axillary lymph nodes as “vessels containing white blood.”
Galen (129–199 ) and Paul of Aegina (607–690 ) continued the observations of lymphatics. Hundreds of years
37
References 13
https://t.me/med1917
then passed before there was any notable progress in the
study of the lymphatic system.
1.3.2 Fifteenth to seventeenth centuries
Nicola Massa (1499–1569), an Italian human anatomist,
described the renal lymphatic vessels and pondered their
function.37 Eustachius found a white structure while dissecting a horse in 1552, and subsequently named it the “vena
alba thoracis.”37 In the seventeenth century, the founder of
microanatomy and the rst histologist Marcello Malpighi
(1628–1689) identied capillaries that linked the arteries and
veins in the lungs. He also noted conglobate glands (nodes)
positioned beside the course of lymphatics. Later, Henri
Francois LeDran (1685–1770) was the rst to note the spread
of cancer throughout the lymphatic system.37 e discovery of mesenteric lymphatics was made in 1622 by Gasparo
Aselli (1581–1626), a professor of anatomy and surgery. Aselli
coincidentally noticed what he later named “lacteal vessels”
(“venae albae aut lacteae”) while dissecting alive dogs in both
fed and unfed states.37 Initially, he believed that the network
of ne, lightly colored cords were nerves; however, some
started leaking a milky, white uid, prompting his further
attention and investigation.37 He also noted valves within
the lacteal vessels.37 Johann Vesling (1598–1694), a German
anatomist, published in 1634 some of the earliest human lymphatic system illustrations, including of the thoracic duct.
37, 38
Other subsequent investigators demonstrated that lymphatic
vessels were widely distributed throughout the body.
e term “lymphatics” was rst used by omas
Bartholin (1616–1680). Interest in the anatomy and function of the newly discovered lymphatic system continued
to increase among scientists and anatomists, and the lymphatic system was proposed as having an important role in
the development of ascites and edema.
37
1.3.3 Eighteenth- to nineteenth-century
discoveries
William Hunter (1718–1783) and his younger brother John
Hunter, the infamous “father of modern surgery” (1728–
1793), both researched and dened the course of the lymphatic system from their dissections of animals and human
cadavers.
37
An atlas of the human lymphatic system published
in 1787 by an anatomy professor from Italy, Paolo Mascagni,
was more complete, emphasizing the lymphatic origins as
completely separate entities from blood vessels in the tissue.
37
1.3.4 Nineteenth and twentieth centuries
e lymphatic system was recognized as central to the
immune system of the body. Lymphography was rst
introduced in 1931 by Hernani Monteiro in order to
study the lymphatic system in vivo. Servelle in Paris was
already using direct contrast lymphangiography in 1943.
Kinmonth in 1952 used blue dye to stain the lymphatics
and then directly injected radio-opaque contrast in order
to investigate lymphatic diseases. Today, contrast magnetic
resonance lymphangiography is the most commonly performed test (although it is still used only rarely).39 In our
era of digitalized technology and new contrast agents, the
eld of lymphatic imaging continues to evolve and progress as a powerful tool for future diagnostic and therapeutic
advancements.
40
1.3.5 Treatment options for lymphedema
Patients can develop debilitating lymphedema of the upper
or lower extremities due to congenital or acquired causes.
Surgica l options have been slow to develop and have not been
widely adopted because of their mixed results. Lymphatic
reconstruction via microsurgery, lymph node transplant,
and excisional surgery (the Charles procedure) have been
the mainstays of therapeutic modalities. ese options will
be discussed in a later chapter.
1.4 CONCLUSIONS
e history of venous disease is rich, fascinating, and farreaching. e discoveries in past centuries were tremendous. e explosion of recent developments is adding to the
intriguing and interesting stories that should be recorded
for future generations.
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10. Wiseman R. Several Chirurgical Treatises. Flesher:
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12. Moore W. The operative treatment of varicose
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13. Bergan J. Conrad Jobst and the development of
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15. Alguire PC and Scovell S. Overview and management of lower extremity chronic venous disease.
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16. Scovell S. Liquid, foam, and glue sclerotherapy
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18. Carroll C, Hummel S, Leaviss J etal. Systematic
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Development and anatomy of
https://t.me/med1917
thevenoussystem
PETER GLOVICZKI
2
2.1 Development of the venous system 15
2.2 Anatomy 17
2.3 Histology 24
In the last two decades, progress in modern imaging studies, such as with duplex scanning, three-dimensional computed tomography, and magnetic resonance imaging, has
provided improved insight into our understanding of the
a natomy of the venous system.
invasive catheter-based therapies has furthermore required
a more thorough knowledge of the venous anatomy in order
to optimize outcome and minimize thromboembolic complications. Since the current Terminologia Anatomica4 suggests terms that are frequently dierent from those used
in clinical practice, a new international anatomic terminology has been developed in order to avoid confusion for
those clinicians who treat patients with acute deep vein
thrombosis and chronic venous disease.
eorts have also resulted in a consensus document on
theduplex anatomy of the venous system of the lower limbs.
is chapter includes a review of the development of the
venous system, followed by a description of the anatomy
of the veins of the lower limb and pelvis. We also discuss
relevant venous anatomy of the trunk and the upper limbs.
e goal of the American Venous Forum is to entice venous
specialists around the world to adopt the new terminology
of leg veins in order to improve the safety and outcomes of
treatments for venous disease and to permit international
collaboration and communication among scientists who are
interested in clinical venous research.
1–3
Increasing u se of mini mally
5–7
International
2
2.1 DEVELOPMENT OF THE VENOUS
SYSTEM
Primitive vascular channels in the limb rst appear in
the third week of gestation. During development, the vascular system undergoes dierentiation through multiple
stages, rst described by Woolard in 1922.8 Stage 1 is the
Acknowledgment 25
References 25
undierentiated stage, with only a capillary network being
present. Stage 2 is the retiform stage when large plexiform structures can be seen. Stage 3, the maturation stage,
includes the development of large channels, arteries, and
veins. Vascular endothelial growth factor (VEGF) secreted
by keratinocytes has been found to induce the penetration
of capillary vessels into the avascular epidermis.
e venous system rst appears in the trunk as bilaterally symmetrical vessels, with the le vessels regressing and
the right vessels dominating as the superior and inferior
vena cavae.10 ese patterns of development lend themselves
to the anatomic variants found among individuals.
9
2.1.1 Veins of the trunk
2.1.1.1 SUPERIOR VENA CAVA AND TRIBUTARIES
Blood is initially returned to the heart tube via the paired
sinus venosus.11 e portion of the body that is cranial to the
developing heart drains through the bilateral anterior cardinal veins, and the caudal portion of the body drains forward
through the bilateral posterior cardinal veins (Figure 2.1).
e anterior and posterior cardinal veins join to form the
common cardinal veins, with the right and le common
cardinal veins draining centrally into the sinus venosus. e
common cardinal veins also receive the vitelline and umbilical veins; the vitelline veins later form into the hepatic portal
system.
e anterior cardinal veins connect the le anterior
cardinal vein with the right anterior cardinal vein. is
le to right channel becomes the le brachiocephalic
vein. e portion of the le anterior cardinal vein that
is caudal to this anastomosis regresses but does not disappear; it forms the oblique vein of the le atrium (vein
15
16 Development and anatomy of thevenoussystem
(a) (b) (c) (d)
L. common
Median sacral v.
suprarenal
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Sinus venosus
Vitelline
and
umbilical
vv.
Ant. cardinal
v.
Common
cardinal
v.
Subcardinal
v.
Subcardinal
anastomosis
Post
cardinal
v.
Sub-
supracardinal
anastomosis
(Renal collar)
IIiac anastomosis
of postcardinal vv.
Subclavian
v.
Supracardinal
v.
Prerenal
segment
(Subcardinal)
Renal segment
(Subsupracardinal
anastomosis)
Postrenal
segment
(Supracardinal)
Hypogastric v.
Ant. cardinal
v.
Hepatic
segment
of
Inf. vena
cava
R. ext.
jugular
v.
Subclavian
v.
Azygos
Post.
cardinal
v.
R. suprarenal
Renal v.
R. spermatic
or ovarian
Gonadal v.
Inf. vena cava
External iliac v.
Sup.
vena
cava
v.
v.
R. renal
v.
v.
R. int. jugular v.
L. brachiocephalic v.
Int. iliac v.
Oblique
v.
Inf.
vena
cava
Hemiazygos
v.
L.
v.
L. renal
v.
L.
spermatic
or ovarian
v.
iliac v.
Figure 2.1 (a–d) Stages in development of the major veins. (Redrawn from Avery LB. Developmental Anatomy, revised 7th
Edition. Philadelphia, PA: W.B. Saunders Co., 1974.)
of Marshall) and the coronary sinus. e persistence of
the le caudal anterior cardinal vein results in a double
superior vena cava (Figure 2.2a).3 In the absence of the
right proximal superior vena cava, the blood from the
right upper body is drained into a le superior vena cava
(Figure 2.2b).
forming behind the common iliac arteries. At the level of
the kidneys, the inferior vena cava is formed from the right
sub-supracardinal anastomosis (renal segment), thereby
becoming more anterior in position. Above the kidneys,
the inferior vena cava is formed from the right subcardinal
vein (prerenal segment), which is still more anterior, as it
demonstrated by the inferior vena cava diverging anterior
2.1.1.2 INFERIOR VENA CAVA AND TRIBUTARIES
e inferior vena cava develops from multiple segments.12
e paired posterior cardinal veins originally extend into
the region that will become the pelvis, and are joined
together at the iliac anastomosis (Figure 2.1). Most of the
posterior cardinal veins disappear; the most cranial portion on the right persists as the arch of the azygos. e
very caudal portion of the posterior cardinal veins and
iliac anastomosis form the common, external, and internal
iliac veins and the median sacral vein. e posterior cardinal veins are mostly replaced by the ventral subcardinal
and the dorsal supracardinal veins. Drainage of the more
cranial region of the abdomen goes mostly into the subcardinal veins, and that of the more caudal portion goes into
the supracardinal veins. Most of the azygos system develops from the supracardinal veins. Lastly, the veins of the
le side generally regress, resulting in a right-sided inferior
vena cava.
e most inferior portion of the inferior vena cava—the
postrenal segment—develops from the right supracardinal
vein; therefore, it is relatively posterior in position. is is
demonstrated by the conuence of the common iliac veins
to the aorta. e hepatic segment of the inferior vena cava is
formed directly by hepatic sinusoids.
Since the inferior vena cava develops from bilateral veins,
with the right veins usually persisting, variations are to be
expected, although they are unusual. If the right subcardinal vein fails to make connection with the liver, absence of
the suprarenal inferior vena cava occurs, such that the inferior vena cava drains into the arch of the azygos and the
hepatic veins drain independently through the diaphragm
to the right atrium.3 Double inferior vena cavae (0.2%–3%)
usually occur in the infra-renal portion due to bilateral
persistence of both the right and le supracardinal veins
(Figure 2.2c).13 A le inferior vena cava (0.2%–0.5%) results
from caudal regression of the right supracardinal vein with
persistence of the le supracardinal vein (Figure 2.2d).
Renal vein anomalies include the persistent (circumaortic)
renal collar (1.6%–14%)
le renal vein (3.2%)14 (Figure 2.3).
Congenital absence of the inferior vena cava is a rare but
important anomaly, since it is a cause of deep vein thrombosis in young patients, especially in those without risk factors
for thrombosis.
14,1 5
and the posterior (retroaortic)
12
Aneurysmal changes of retroperitoneal
2.2 Anatomy 17
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(a) (b)
R. brachiocephalic v.
L. sup. vena cava
R. sup. vena cava
Pulmonary
vv.
Coronary
sinus
Inf.
vena
cava
(c)
Figure 2.2 Anomalies of the vena cava. (a) Double supe-
rior vena cava.
inferior vena cava.
posterior views; c and d: anterior views).
Inf. vena cava
L. renal v.
R. renal v.
Gonadal vv.
L. inf. vena cava
(b) Left superior vena cava. (c) Double
(d) Left inferior vena cava (a and b:
(d)
Aorta
2.1.2 Veins of the limbs
e general pattern for the development of the vasculature
of the limbs begins as a ne capillary network arising from
several segmental branches of the aorta. As the limb begins
to extend from the body, a channel from within this network
predominates as the axia l or central artery. e blood returning to the body from capillary networks is rst collected
in a marginal sinus that extends around the apex of the
limb bud, just deep enough to reach the apical ectodermal
ridge. e capillary networks and the marginal sinus itself
send out new vascular sprouts in response to growth of the
limbs. Early on, blood drains from the marginal sinuses of
the limbs into the supercial venous plexuses of the body,
but the blood is progressively shunted into deeper channels as development progresses and deep veins—frequently
paired—develop along major arteries. Valves form in the
veins relatively early. It is thought that the denitive number
of valves is reached by the sixth month of fetal life.
e development of the veins of the limb is likely preceded by the development of major nerves. Gillot proposed
that venous development is induced by major nerves; in the
embryo, these angioguiding nerves are the femoral, the sciatic, and the posterior femoral cutaneous nerves.
the embryonic veins regress during development; their persistence (of the sciatic vein, lateral margina l vein, etc.) is, however,
frequently seen in patients with venous malformations.
e axial artery of the upper limb forms the brachial
artery in the arm and the interosseous artery in the forearm, with the ulnar and radial arteries forming later. Asthe
digits are forming, the apical marginal sinus regresses, but
the proximal marginal channels persist as the cephalic and
basilic veins.
3,19
Many of
20–23
Sup. mesenteric a.
L. renal v.
Retroaortic
L. renal v.
Gonadal v.
Figure 2.3 Circumaortic renal collar.
collaterals have been observed, rupture has been reported,16
and some patients have presented with severe back ache due
to venous congestion.
17
Previous deep vein thrombosis or
retroperitoneal brosis should be considered in the dierential diagnosis.
18
2.2 ANATOMY
2.2.1 Veins of the lower extremity
e veins of the lower extremity are composed of the supercial, the deep, and the perforating veins (PVs). PVs connect
the supercial to the deep venous system. ey pass through
the deep fascia which separates the supercial compartment
from the deep. Communicating veins connect veins within
the same system. e recent development of the evaluation
of the veins with duplex scanning resulted in the recognition of the saphenous sub-compartment and the saphenous
1,2,7
fascia.
e saphenous fascia covers the saphenous subcompartment and separates the great saphenous vein (GSV)
from other veins in the supercial compartment. Bicuspid
valves are important structures in the leg veins, assisting
unidirectional ow in the normal venous system.
2.2.2 Cutaneous microcirculation
e cutaneous branches of arteries reach the skin either
directly or following the penetration of skeletal muscles.
In the skin, the arterioles form a reticular and a more
18 Development and anatomy of thevenoussystem
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Epidermis
Dermis
Supercial
compartment
c
Deep veins
Subpapillary
venous plexus
Reticular
venous plexus
Saphenous
fascia
Great
saphenous
vein
Saphenous
compartment
Deep
compartment
Subcutis
Fascia
Muscle
DISTAL
a
a
b
PROXIMAL
b
c
Figure 2.4 Venous networks in the lower extremity. Capillaries of dermal papillae are drained by the subpapillary venous
plexus, which in turn joins to the reticular venous plexus. Superficial veins
axial veins through direct perforating veins
(b). Perforating veins communicate with each other through small branches.
(a) drain dermal veins and empty into the deep
Muscular venous sinuses fill from the superficial veins or from the reticular venous plexus through indirect perforating
(c) and they are drained into the deep axial veins.
veins
supercial subpapillary dermal plexus.24 Capillary loops of
the dermal papillae emerge from the latter plexus and drain
through venules into the subpapillary venous plexus, which
again drains into the deeper reticular venous plexus at the
dermal–subcutaneous junction (Figure 2.4). Vertically
oriented, small-valved veins connect the reticular venous
plexus to the supercial veins.
the thigh and the leg. e veins lie either anterior, posterior,
or supercial to the main trunk. e posterior accessory
GSV of the leg (Leonardo’s vein or posterior arch vein) is
a common tributary, which begins posterior to the medial
malleolus and ascends on the posteromedial aspect of the
calf to join the GSV distally to the knee (Figure 2.6). e
anterior accessory GSV of the leg drains the anterior aspect
of the leg below the knee. e posterior accessory GSV of
2.2.3 Superficial veins of the leg
the thigh, if present, drains the medial and posterior thigh.
e anterior accessory GSV of the thigh collects blood from
Few veins of the human body have more variability in
their gross anatomy than the supercial veins of the leg.
Supercial veins—the GSV and the small saphenous
the anterior and lateral side of the thigh (Figure 2.6). e
anterior and posterior accessory GSVs join the GSV just
before it ends at the conuence of supercial inguinal veins
vein (SSV) and their tributaries—course in the subcutaneous fat outside the deep fascia and drain blood from
the skin and subcutaneous tissues (Figures 2.5 and 2.6,
Table2.1).
24–2 7
e supercial venous system of the foot is divided into
the dorsal and plantar subcutaneous venous networks
(Figure 2.5). Supercial vein tributaries drain blood into the
dorsal venous arch on the dorsum of the foot at the level of
Superf. peroneal n.
Small
saphenous v.
Lateral
perforating vv.
Great
saphenous v.
Saphenous n.
Medial
perforating vv.
the proximal head of the metatarsal bones. e medial and
lateral end of this arch continues through the medial and
lateral marginal vein into the GSV and SSV, respectively.
e GSV begins just anterior to the medial ankle, crosses
in front of the tibia and ascends medially to the knee
(Figure2.6). Proximal to the knee, the GSV ascends on the
medial side of the thigh and enters the fossa ovalis at 3 cm
Sural n.
Lateral
marginal v.
Dorsal
venous arch
Medial marginal v.
Deep peroneal n.
inferior and 3 cm lateral to the pubic tubercle. e GSV is
doubled in the calf in 25% of the population and in the thigh
25
in 8%.
e saphenous nerve runs in close proximity to the
GSV in the distal two-thirds of the calf. e accessory GSVs
are frequently present and run parallel to the GSV in both
Figure 2.5 Superficial and perforating veins of the foot.
28
Superf. circumflex
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iliac a. & v.
Anterior accessory
great saphenous v.
Anterior accessory
great saphenous v.
Paratibial
perforators
Great saphenous v.
Superf. peroneal n.
Superf. epigastric a. & v.
Common femoral v.
Pudendal a. & v.
Posterior accessory
great saphenous v.
Great saphenous v.
Perforators of the
femoral canal
Saphenous n.
Posterior accessory
great saphenous v.
Upper
Posterior
Middle
tibial (Cockett)
perforator
Lower
2.2 Anatomy 19
(a) (b)
Common femoral v.
Superf.
epigastric v.
Superf.
circumex
iliac v.
External
pudendal v.
Anterior accessory
great saphenous v.
Great saphenous v.
(c) (d)
Common femoral v.
Superf.
epigastric v.
Superf.
circumex
iliac v.
External
pudendal v.
Anterior accessory
great saphenous v.
Great saphenous v.
Medial ankle perforators
Figure 2.6 Medial superficial and perforating veins of
theleg.
Table 2.1 New terminology of lower extremity veins
Old, historic terms or
eponyms “New” terms
Superficial femoral vein Femoral vein
Greater or long
Great saphenous vein
saphenous vein
Lesser or short
Small saphenous vein
saphenous vein
Saphenofemoral
junction
Confluence of the superficial
inguinal veins
Giacomini’s vein Intersaphenous vein
Posterior arch vein or
Leonardo’s vein
Cockett perforators
(I,II, and III)
Posterior accessory great
saphenous vein of the leg
Posterior tibial perforators
(lower, middle, and upper)
Boyd’s perforator Paratibial perforator (proximal)
Sherman’s perforators Paratibial perforators
“24-cm” perforators Paratibial perforators
Hunter’s and Dodd’s
perforators
May’s or Kuster’s
Perforators of the femoral
canal
Ankle perforators
perforators
Figure 2.7 Most common anatomic variations of the
confluence of superficial inguinal veins (a: 33%; b: 15%;
c:15%; d: 13%).
(saphenofemoral junction) (Figure 2.7). e supercial
circumex iliac, supercial epigastric, and external pudendal veins join each other and the distal GSV in order to form
the conuence of supercial inguinal veins (saphenofemoral junction) (Figure 2.8). Rarely, the GSV terminates high
on the lower abdomen or joins the femoral vein very low,
and the supercial inguinal veins empty individually into
the femoral vein. Other occasional tributaries of the GSV in
the groin include the posterior and anterior thigh circumex veins.
e SSV lies lateral to the Achilles tendon in the distal
calf (Figures 2.9 and 2.10). In the lower two-thirds of the
calf, the SSV runs in the subcutaneous fat and then pierces
the fascia to run between the two heads of the gastrocnemius muscle.27 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 a cephalad direction
(Figure 2.9). Uncommonly, the main trunk of the SSV
continues without draining into the popliteal vein and
eventually empties into the femoral vein or GSV. e intersaphenous vein (vein of Giacomini) is a communicating
vein connecting the SSV to the GSV in the posterior–medial
thigh; this vein, which is present in two-thirds of limbs with
venous disease, usually ascends subfascially and perforates
the fascia to join the supercial system.
29
e sural nerve courses along the SSV in the distal
calf. Supercial veins of the lateral leg and thigh form the
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