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Dermis
Supercial
compartment
Deep
compartment
saphenous vein
Supercial
facia
Saphenous
compartment
Deep
facia
Saphenous vein
Figure4.1 is diagram of the saphenous compartment shows its relationships with the super cial and deep compartments as well as the saphenous
vein and nerve and their relationships to the medial, anterior, and lateral accessory saphenous veins. (Redrawn with permission from Caggiati A,
Bergan JJ, Gloviczki P, etal. Nomenclature of the veins of the lower limbs:An international interdisciplinary consensus statement, J Vasc Surg . 2002.
36 :416–422.)
In fact, there are many variations of the small saphenous
vein as it connects both to the popliteal vein and to cranial
extensions of the saphenous vein, as well as connections to
Supercial circumex
iliac artery and vein
Lateral circumex
femoral vein
Anterior cutaneous
branches of femoral nerve
Supercial
epigastric
artery and vein
Supercial
exterior
pudendal arter
and vein
Great saphenous
vein
Mid thigh
perforating vein
the posteromedial circum ex vein (vein of Giacomini).
e third system of veins is called the perforating vein
system. As indicated earlier, they connect the super cial
and deep systems of veins. ere is a fundamental fact that
confuses understanding of perforating veins. is relates to
ow direction. Some perforating veins produce normal ow
from the super cial to the deep circulation, others conduct
abnormal out ow from the deep circulation to the super cial circulation. is is termed perforating vein re ux. Any
of these perforating veins may demonstrate bidirectional
ow (see Table4.1).
In the leg, the principal clinically important perforating
veins are on the medial aspect of the ankle and leg, and are
found anatomically at approximately 6-cm intervals from
the base of the heel through the upper portion of the leg.
ey are therefore at roughly 6, 12, 18, and 24cm from the
Table4.1 SUMMARY OF IMPORTANT CHANGES IN
NOMENCLATURE OF LOWER EXTREMITYVEINS
Anterior tributary of
great saphenous vein
Proximal paratibial
perforators
Saphenous
nerve
Medial knee
perforator
Posterior
arch vein
Great saphenous vein
Supercial peroneal nerve
Figure4.2 is diagrammatic representation of the great saphenous vein
emphasizes it relationship to perforating veins and the posterior arch
vein. (Redrawn with permission from Mózes G, Gloviczki P, Kádár
A, Carmichael SW. Anatomy of the perforating veins. In Gloviczki
P, and Bergan JJ, eds. Atlas of endoscopic perforating vein surgery .
London:Springer.1998.)
Posterior tibial
perforators
Femoral Vein Common Femoral Vein
Super cial Femoral Vein Femoral Vein
Sural Veins Sural Veins
Medial perforators
of the foot
Huntarian Perforator Mid igh Perforator
Cockett’s Perforators Paratibial Perforator
May’s Perforator
Gastrocnemius Point Intergemellar Perforator
38 • BASIC CONSIDERATIONS
OLD TERMINOLOGY NEW TERMINOLOGY
Soleal Veins
Gastrocnemius Veins
(Medial and Lateral)
Posterior Tibial Perforators
Ext. iliac v.
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Great
saphenous v.
Deep
femoral v.
Boyd’s
perforator
Ant. tibial veins
Proximal paratibial
perforator
“24 cm” perforator
Dorsalis pedis v.
© MAYO
1997
Figure4.3 Deep connections of the main thigh and leg perforating veins are
shown in this diagram of the deep veins of the lower extremity. (Redrawn
with permission from Mózes G, Gloviczki P, Kádár A, Carmichael SW.
Anatomy of the perforating veins. In Gloviczki P, and Bergan JJ, eds. Atlas
of endoscopic perforating vein surgery . London:Springer.1998.)
Med. plantar v.
Femoral v.
Hunter’s
perforator
Dodd’s perforator
saphenous v.
Gastrocnemius veins
Popliteal v.
Soleus veins
Muscle perforators
Peroneal veins
Post. tibial veins
Paratibial Perforators:
Cockett III perforator
Cockett II perforator
Cockett I perforator
Lat. plantar v.
oor (see Figure4.3). ese medial perforating veins may
become targets for treatment of severe chronic venous insuf ciency (CVI). Smaller perforating veins can be found along
intermuscular septa and these allow direct drainage of blood
6
from surface veins into the deep venous system.
Conversely,
when they are dysfunctional, they allow muscular compartment pressure to be transmitted directly to unsupported
cutaneous and subcutaneous veins and venules.
VENOUS PHYSIOLOGY
It is estimated that 60 to 75% of the blood in the body is to
be found in the veins. Of this total volume, about 80% is
contained in the veins that are less than 200µm in diameter.
It is important to understand this reservoir function as it
is related to the major components. e splanchnic venous
circulation and the veins of the skin are richly supplied by
the sympathetic nervous system bers, but muscular veins
have little or none of these. e veins in skeletal muscle, on
the other hand, are responsive to catecholamines.
Although arterial pressures are generated by muscular
contractions of the heart, pressures in the venous system
largely are determined by gravity. In the horizontal position, pressures in the veins of the lower extremity are similar
to the pressures in the abdomen, chest, and extended arm.
However, with the assumption of the upright position, there
are dramatic changes in venous pressure. e only point in
which the pressure remains constant is the hydrostatic indifferent point just below the diaphragm. All pressures distal
to this point are increased due to the weight of the blood
column from the right atrium. When assuming the upright
position, there is an accumulation of approximately 500
ml of blood in the lower extremities, largely due to re ux
through the valveless vena cava and iliac veins. ere is some
loss of uid into the tissues, and this is collected by the lymphatic system and returned to the venous system.
Venous valves play an important role in transporting
blood from the lower extremities to the heart. In order for
valve closure to occur, there must be a reversal of the normal
transvalvular pressure gradient. Apressure and generated
velocity ow exceeding 30 cm/sec leads to valve closure.
Direct observation of human venous valves has been made
7
possible by specialized ultrasound techniques.
Venous ow
is not in a steady state but is normally pulsatile, and venous
valves undergo regular opening and closing cycles. Even
when fully opened, the cross-sectional area between the leaflets is 35% smaller than that of the vein distal to the valve.
Flow through the valve separates into a proximally directed
jet and vortical ow into the sinus pocket proximal to the
valve cusp. e vortical ow prevents stasis and ensures that
all surfaces of the valve are exposed to shear stress. Valve closure develops when the vortical ow pressure exceeds the
proximally directed jet ow.
e role of venous valves in an individual quietly standing is not well understood. Pressures in the super cial and
deep veins are essentially the same during quiet standing,
but, as Arnoldi has found, the pressure in the deep veins is
1mm higher, which would tend to keep the valves in the
8
perforating veins closed.
Normally functioning perforating
vein valves protect the skin and subcutaneous tissues from
the e ects of muscular contraction pressure. is muscular
contraction pressure may exceed 100 to 130mmHg.
Intuitively, the role of venous valves during muscular
exercise is obvious, since their major purpose is to promote
antegrade ow from super cial to deep. Volume and pressure changes in veins within the calf occur with muscular
activity. In the resting position, with the foot at on the
oor, there is no ow. However, in the heel strike position,
the venous plexus under the heel and plantar surface of the
foot (Bejar’s plexus) is emptied proximally. Blood ows
VENOUS ANATOMY, PHYSIOLOGY, AND PATHOPHYSIOLOGY • 39
from the foot and ankle into the deep veins of the calf. en,
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calf contraction transports this blood into the deep veins of
the thigh, and henceforth, blood ow proceeds to the pelvic
veins, vena cava, and ultimately to the heart all due to the
9
in uence of lower extremity muscular contraction.
PATHOPHYSIOLOGY
Abnormal functioning of the veins of the lower extremities
is recognized clinically as venous dysfunction or, more commonly, venous insu ciency. Cutaneous telangiectases and
subcutaneous varicose veins usually are grouped together
under the title “primary venous insu ciency,” and limbs
with skin changes of hyperpigmentation, edema, and healed
or open venous ulceration are categorized asCVI.
ankle. Prolonged venous hypertension initiates a cascade
of pathologic events. ese manifest themselves clinically
as lower extremity edema, pain, itching, skin discoloration,
11
and ulceration.
e earliest signs of venous insu ciency o en are elongated and dilated veins in the epidermis and dermis, called
telangiectasias. Slightly deeper and under the skin are at,
blue-green veins of the reticular (network) system. ese
may become dilated and elongated as well (see Figure4.4).
And nally, still deeper but still super cial to the super cial
fascia are the varicose veins themselves. All of these abnormal veins and venules have one thing in common:they are
elongated, tortuous, and have dysfunctional venous valves.
is implies a common cause, which is in a mm a t i o n .
CVI
PRIMARY VENOUS INSUFFICIENCY
A dysfunctional venous system follows injury to vein walls
and venous valves. is injury is largely due to in amma-
10
tion, an acquired phenomenon.
Factors that are not
acquired also enter into such injury. ese include heredity,
obesity, female gender, pregnancy, and a standing occupation in women. Vein wall injury allows the vein to elongate and dilate thus producing the visual manifestations of
varicose veins. An increase in vein diameter is one cause of
valve dysfunction that results in re ux. e e ect of persistent re ux through axial veins is a chronic increase in distal venous pressure. is venous pressure increases as one
proceeds from the inguinal ligament past the knee to the
Varicose vein
Skin changes of hyperpigmentation, scarring from previous ulceration, and active ulcerations are grouped together
under the term CVI. Numerous theories have been postulated regarding the cause of CVI and the cause of venous
12,13
ulceration.
All the theories proposed in the twentieth
century have been disproved. An example is the theory
of venous stasis, rst proposed in a manuscript by John
14
Homans of Harvard in 1916.
In this treatise on diagnosis and management of patients with CVI, Dr.Homans
coined the term “post-phlebitic syndrome” to describe the
skin changes of CVI. He stated that, “Overstretching of the
vein walls and destruction of the valves . . . interferes with
the nutrition of the skin . . . therefore, skin which is bathed
under pressure with stagnant venous blood will form
Telangiectasias
Dermis
Reticular vein
Supercial fascia
Great saphenous vein
Indirect perforating vein
Deep fascia
Figure4.4 is cross-sectional view of the subcutaneous venous circulation shows how venous hypertension is transmitted to the unsupported veins
of the dermis and subcutaneous tissues from axial veins and the deep veins of the muscular compartments. (Redrawn with permission from Somjen
GM. Anatomy of the super cial venous system, Dermatol Surg . 1995. 21 :35–45.)
Direct perforating vein
Deep vein
40 • BASIC CONSIDERATIONS
permanent open sores or ulcers.” at statement, like many
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others that describe venous conditions and their treatments, is steeped in dogma and is short of observational
fact. e erroneous term “stasis ulcer” honors that misconception, as do the terms “venous stasis disease” and “stasis
dermatitis.”
Alfred Blalock, who later initiated cardiac surgery, dis-
proved the stasis theory by studying oxygen content from
15
varicose veins and normal veins.
He pointed out that the
oxygen content of the femoral vein in patients with severe
CVI was greater than the oxygen content of the contralateral nona ected limb. Because oxygen content was higher,
some investigators felt that arteriovenous stulas caused
16,17
venous stasis and varicose veins.
ough disproved,
that explanation has some basis in fact, since the entire
thermal regulatory apparatus in limbs depends on the
opening and closing of arteriovenous shunts. ese shunts
are important as they explain some terrible accidents that
happen during sclerotherapy when sclerosant entering
a vein is shunted into the arterial system and distributed
18
in its normal territory.
Microsphere investigations have
failed to show any shunting, and the theory of arteriovenous communications has died despite the fact that these
shunts actually exist and do open under the in uence of
venous hypertension.
Hypoxia and its part in causation of CVI was investigated throughout the last 25years of the twentieth century.
English investigators thought that a brin cu , observed
histologically, blocked transport of oxygen and was responsible for skin changes of CVI at the ankles and distally.
19
at theory has been abandoned even though a true periarteriolar cu is easily identi ed histologically.
e two elements that make up all the manifestations of
lower extremity venous insu ciency are failure of the vein
valves and vein walls and skin changes at the ankles, both of
20
which are related to venous hypertension.
FAILURE OF VEIN WALLS ANDVALVES
Our work suggests that venous hypertension causes a shear
stress–dependent leukocyte-endothelial interaction, which
21
has all the manifestations of chronic in ammation.
ese
are leukocyte rolling, rm adhesion to endothelium, and
subsequent migration of the cells through the endothelial
22
barrier into parenchyma of valves and vein walls.
ere,
macrophages elaborate matrix metalloproteases, which
destroy elastin and possibly collagen as well. Vein walls
become stretched and elongated. Vein valves become perforated, torn, and even scarred to the point of near total
absence. ese changes are seen both macroscopically and
23
angioscopically.
Similar changes have been produced in
the experimental animal by constructing an arteriovenous
stula to mimic the venous hypertension of venous dysfunc-
24
tion in humans.
S K I N C H A N G E S
e second manifestation of CVI is expressed in the skin,
where leukocytes also are implicated in the observed
changes. ere is evidence that leukocyte activation in
the skin, perhaps related to venous hypertension, plays a
major role in the pathophysiology of CVI. omas, working with Dormandy, reported that 25% fewer white cells
and platelets le the dependent foot of the patients with
venous hypertension. When the foot was elevated there was
a signi cant washout of white cells but not platelets, suggesting platelet consumption within the microcirculation
25
of the dependent foot.
ey concluded that the decrease
in white cell exodus was due to leukocyte trapping in the
venous microcirculation secondary to venous hypertension. ey further speculated that trapped leukocytes may
become activated, resulting in release of toxic metabolites
causing damage to the microcirculation and overlying skin.
Apparently, the primary injury in the skin is extravasation of
macromolecules and red blood cells into the dermal interstitium. Red blood cell degradation products and interstitial protein extravasations are potent chemoattractants and
represent the initial chronic in ammatory signal responsible for leukocyte recruitment.
e important observations of Dormandy’s group were
historically the rst to implicate abnormal leukocyte activity in the pathophysiology ofCVI.
e importance of leukocytes in the development of dermal skin alterations was further emphasized by Coleridge
26
Smith and his team.
patients with primary varicose veins, lipodermatosclerosis,
ey obtained punch biopsies from
and patients with lipodermatosclerosis and healed ulcers.
ey counted the median number of white blood cells per
high power eld in each group but there was no attempt to
identify the types of leukocytes. In patients with primary
varicose veins, lipodermatosclerosis, and healed ulceration
there was a median of 6, 45, and 217 WBCs per mm
respectively. is demonstrated a correlation between clinical disease severity and the number of leukocytes in the dermis of patients withCVI.
e types of leukocytes involved in dermal venous stasis
skin changes remain controversial. T-lymphocytes, macrophages, and mast cells have been observed on immunohistochemical and electron microscopic examinations.
27,28
variation in types of leukocytes observed may re ect the
types of patients investigated. e London group biopsied
patients with erythematous and eczematous skin changes,
whereas Pappas has evaluated predominantly older patients
with dermal brosis. Patients with eczematous skin changes
may have an autoimmune component to their CVI, whereas
patients with dermal brosis may have experienced pathologic alterations consistent with chronic in ammation and
altered tissue remodeling. Skin biopsies have shown that in
liposclerotic, eczematous skin macrophages and lymphocytes were predominant in such diseased skin. In ltration of
2
e
,
VENOUS ANATOMY, PHYSIOLOGY, AND PATHOPHYSIOLOGY • 41
leukocytes into the extracellular space has been documented
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by observing the localization of these leukocytes around capillaries and postcapillary venules. Accompanying the leukocytes is a disorganized collagen deposition. Clearly, CVI of
the skin and its subcutaneous tissues is a disease of chronic
in ammation, again dependent on venous hypertension.
SUMMARY AND CONCLUSIONS
Knowing the normal anatomy of the venous system of the
lower extremities and the normal functioning of its elements is essential to understanding the pathologic processes
of venous dysfunction. Both processes, valve and vein wall
damage, and the advanced skin changes of CVI are the
result of sterile in ammatory reactions. Both appear to be
triggered by venous hypertension and, therefore, therapy
must be directed at correcting such venous hypertension.
R E F E R E N C E S
1. Federative International Committee for Anatomical Terminology.
Terminologia Anatomica. Stuttgart: George ieme Verlag . 1998 .
2 . B un de ns W P , B e r g a n J J , H a l a s z N A , M u r r ay J , D re ho b l M . e
super cial femoral vein: A potentially lethal misnomer , JAMA.
1995 . 274 : 1296–1298 .
3. Caggiati A , Bergan JJ , Gloviczki P , etal. Nomenclature of the veins
of the lower limbs: An international interdisciplinary consensus
statement , J Vasc Surg . 2002 . 36 : 416–422 .
4. Weiss RA , Weiss MA . Controlled radiofrequency endovenous
occlusion using a unique radiofrequency catheter under duplex
guidance to eliminate saphenous varicose vein re ux:A2-year follow-up , Dermatol Surg . 2002 . 28 : 38–42 .
5. Bush RG , Hammond KA . Tumescent anesthetic technique for long
saphenous stripping , J Am Coll Surg . 1999 . 189 : 626–628 .
6. Somjen GM . Anatomy of the super cial venous system , Dermatol
Surg . 1995 . 21 : 35–45 .
7. Lurie F , Kistner RL , Eklof B , Kessler D . Mechanism of venous valve
closure and role of the valve in circulation:Anew concept , J Vasc
Surg . 2003 . 38 : 955–961 .
8. Arnoldi CC . Venous pressures in the leg of healthy human subjects
at rest and during muscular exercise in the nearly erect position , Acta
Chir Scand . 1965 . 130 : 520–534 .
9. Gardner AMN , Fox RH . e return of blood to the heart , 2e. London:
John Libbey . 1993 . 81 .
10. Schmid-Schönbein GW , Takase S , Bergan JJ . New advances in the
understanding of the pathophysiology of chronic venous insu ciency , Angiology . 2001 . 52 (Suppl 1 ): S27–S34 .
11. Ballard JL , Bergan JJ , eds. Chronic venous insu ciency:Diagnosis and
treatment . London: Springer-Verlag . 2000 .
12. Homans J . e etiology and treatment of varicose ulcer of the leg ,
Surg Gynecol Obstet . 1917 . 24 : 300–311 .
13. Browse NL , Burnand KG . e cause of venous ulceration , Lancet .
1982. 320 ( 8292 ): 243–245 .
14. Homans J . e operative treatment of varicose veins and ulcers
based on a classi cation of these lesions , Surg Gynec Obst . 1916 .
22 : 143–158 .
15. Blalock A . Oxygen content of blood in patients with varicose veins ,
Arch Surg.
16. Piulachs P , Vidal Baraquer F . Pathogenic study of varicose veins ,
Angiology. 1953 . 4 : 59–100 .
17. Brewer AC . Arteriovenous shunts , Br Med J . 1950 . 2 : 270 .
18. Bergan JJ , Weiss RA , Goldman MP . Extensive tissue necrosis following high-concentration sclerotherapy for varicose veins , Derm Surg .
2000 . 26 : 535–542 .
19. Coleridge Smith PD . Microcirculation disorders in venous leg
ulcer:Microcirculation in CVI , Microcirculation . 2001 . 8 : 1–10 .
20. Takase S , Lerond L , Bergan JJ , Schmid-Schonbein GW . e
in ammatory reaction during venous hypertension in the rat ,
Microcirculation . 2000 . 7 : 41–52 .
21. Takase S , Schmid-Schonbein G , Bergan JJ . Leukocyte activation in patients with venous insu ciency , J Vasc Surg . 1999 . 30 :
148–156 .
22. Takase S , Pascarella L , Lerond L , Bergan JJ , Schmid-Schonbein GW .
Venous hypertension, in ammation, and valve remodeling , Eur J
Vasc Endovasc Surg . 2004 . 28 : 484–493 .
23. Hoshino S , Satokawa H , Ono T , Igari T . Surgical treatment
for varicose veins of the legs using intraoperative angioscopy.
In: Raymond-Martimbeau P , Prescott R , Zummo M , eds. Phlebologie
92. Paris : John Libbey Eurotext . 1992 . 1083–1085 .
24. Takase S , Pascarella L , Lerond L , Bergan JJ , Schmid-Schonbein GW .
Venous hypertension, in ammation, and valve remodeling , Eur J
Vasc Endovasc Surg . 2004 . 28 : 484–493 .
25. omas PR , Nash GB , Dormandy JA . White cell accumulation
independent legs of patients with venous hypertension:A possible
mechanism for trophic changes in the skin , Br Med J (Clin Res Ed).
1988 . 296 ( 6638 ): 1693–1695 .
26. Scott HJ , Smith PDC , Scurr JH . Histological study of white blood
cells and their association with lipodermatosclerosis and venous
ulceration , Br J Surg . 1991 . 78 : 210–211 .
27. Wilkerson LS , Bunker C , Edward JCW , Scurr JH , Coleridge Smith
PD . Leukocytes, their role in the etiopathogenesis of skin damage in
venous disease , J Vasc Surg . 1993 . 27 : 669–675 .
28. Pappas PJ , DeFouw DO , Venezio LM , etal. Morphometric assessment of the dermal microcirculation in patients with chronic venous
insu ciency , J Vasc Surg . 1997 . 26 : 784–795 .
1929 . 19 : 898–904 .
42 • BASIC CONSIDERATIONS
5 .
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ROLE OF PHYSIOLOGIC TESTING IN
VENOUSDISORDERS
Je rey K. Raines and Jose I. Almeida
f the 25 million Americans with venous insuf ciency, approximately 7 million exhibit seri-
O
venous ulcers.
annually and do so for symptoms of venous insu ciency.
Approximately 80% of venous patients are managed conservatively with observation, leg elevation, and support
stockings; while the remainder are treated surgically with
vein stripping or endovenous ablation. Most investigators
acknowledge with the development of safe, less traumatic,
and e ective endovenous techniques for venous insu ciency, more individuals in the population will seek treatment, and physicians will be more inclined to move from
conservative therapy to surgical therapy.
bosis and identify, grade, and follow venous insu ciency.
Since more patients will be presenting for therapy because
of improved outcomes with endovenous techniques over
traditional surgery, physiologic testing will take on increasing importance. For purposes of this chapter, physiologic
testing includes the various devices based on plethysmographic concepts, and color ow duplex imaging. e goal
of these studies is to provide accurate information describing the hemodynamic or anatomic characteristics of the
patient with chronic venous insu ciency, precluding the
need for invasive studies.
Venous insu ciency of the lower extremity is far more frequent than venous insu ciency in any other part of the
human circulation. is chapter will therefore be limited
to the lower extremity. e venous system in the lower
extremities is composed of three interconnected parts:the
deep system, perforating (i.e., communicating) system, and
super cial system. By virtue of the venous muscular pump
and bicuspid/unidirectional valves, in healthy veins, blood
ows toward the right side of the heart (i.e., upward) and
from the super cial system to the deep system (i.e., inward).
ous symptoms such as edema, skin changes, and
1
About 1million seek formal medical advice
Physiologic testing is used to de ne deep venous throm-
2
BACKGROUND
Lower extremity muscle compartments contract dur-
ing ambulation. is contraction compresses the deep
veins, producing a pumping action, which propels blood
upward toward the right side of the heart. is pumping
action is signi cant; transient pressures in the deep system have been recorded as high as 5 atmospheres during
strenuous lower extremity exertion. is pumping action
secondary to ambulation has the e ect of reducing pressure within the super cial system. With this in mind, it is
instructive to comment on the hydrostatic pressure under
which all three venous systems of the lower extremity are
subjected. A uid column has weight and can produce a
pressure gradient. In an individual 6 feet in height, the
distance from the level of the right atrium to the ankle is
120cm and produces a hydrostatic pressure of approximately 90mmHg.
Deep veins can withstand elevated pressure because the
fascia in which they exist limits dilation. In contrast, the
super cial system, surrounded by elastic skin, is constructed
for low pressure; therefore, elevated pressure in the super cial system can produce dilation, elongation, and valve
failure. Dilation increases the diameter of the veins and
elongation causes them to be more tortuous.
Consider the following cascade of events. Because of
valve failure, above-physiologic pressure develops in the
super cial system. With time, nearby super cial valves begin
to fail (i.e., lose their ability to direct ow in one direction).
With dilation and multiple valve failure, venous blood will
ow in the direction of the pressure gradient, which is downward and outward. is ow direction is directly opposite
physiologic ow (i.e., upward and inward). e early result
is varicose veins and telangiectasia, which are visible on the
skin surface.
Early or mild venous insu ciency produces low-level
pain, edema, burning, throbbing, and leg cramping. As the
disease progresses patients can develop venous stasis changes
that can lead to debilitating severe so tissue ulceration. We
know from hemodynamics and clinical experience, on eliminating high pressure or ow in diseased super cial venous
channels, symptoms can improve dramatically.
43
In understanding lower extremity venous hemodynam-
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ics, the following experiment is instructive (see Figure5.1).
First, a super cial vein in the foot of a normal subject is
cannulated and connected to a uid column (sterile saline
with Vitamin Ato add color to the column). With the subject standing erect, the uid column will rise to the level of
the right atrium. is is due to the fact that the pressure
at the right atrium is near zero and therefore, the venous
pressure at the cannulation site is almost entirely based on
the subject’s hydrostatic blood column (the subject’s blood
and the uid in the column have nearly the same speci c
weight). When the subject is asked to perform sustained
ankle exion, the uid column drops to between 50–60%
of its resting height. is simulates walking and the reduction in super cial venous pressure secondary to the ambulatory venous pump. In subjects with venous insu ciency,
the uid column will not drop to normal levels. If a subject’s uid column falls to normal levels while occluding the
super cial system, the observer knows the deep system is
intact and the super cial system is incompetent. If the uid
column remains elevated with exclusion of the super cial
system, the observer knows the deep system is incompetent.
As will be illustrated, physiologic venous testing is based on
the principles outlined in this experiment.
While the morbidity secondary to venous insu ciency
3
and varicose veins is signi cant,
the most devastating consequence is due to life threatening venous thromboembolism to the lungs. In a study from the Mayo Clinic, during
14,629 person-years of follow-up, 1,333 patients died.
Figure5.1 e stick gure on the le illustrates a normal subject erect
and motionless with a venous cannulation in the le foot. Venous
pressures rises to the level of the right atrium. e stick gure on the
right illustrates the e ect of the normal lower extremity venous pump
and the unidirectional valves activated by walking or ankle exion. e
uid column is reduced to between 50–60% of its resting value. Failure
to reduce the height of the uid column results in ambulatory venous
hypertension (i.e., venous insu ciency).
Seven-day, 30-day, and 1-year venous thromboembolism
4
survival rates were 75%, 72%, and 64%, respectively.
Two statements may summarize this section. First, the
culprit in venous insu ciency syndrome is elevated pressure
when limbs are dependent or ambulating. Measuring and
understanding venous hemodynamics is the cornerstone of
this diagnosis. Second, deep venous thromboembolism may
result in venous insu ciency and may develop independently. is diagnosis is less hemodynamically oriented and
more focused on sonographic visualization of thrombi.
PLETHYSMOGRAPHY
Plethysmographs are devices that measure volume change.
Over the last 50years plethysmographs that employ completely di erent principles have been developed and used
clinically. e impedance plethysmograph (IPG), based on
a fundamental principle of electronics, is not widely used.
5,6
e strain-gauge plethysmograph (SGP) measures circumference of a selected limb segment and estimates volume.
7,8
Like IPG, this technique is not in widespread use and will
not be more completely de ned.
P H O T O P L E T H Y S M O G R A P H P P G
Photoplethysmographs are not true plethysmographs
because the measure they provide is qualitative and cannot
be used to determine volume. Despite this limitation, PPG
9,10
is used in many clinics to assess venous insu ciency.
e
device measures phenomena limited to the microvasculature of the cutaneous skin. PPG instrumentation includes a
surface transducer, which is taped to the lower leg just above
the medial malleolus and connected to an electrical circuit.
e electrical circuit excites the transducer and records and
interprets the returning signal.
e PPG transducer is designed with an infrared light–
emitting diode and a photosensor. e transducer transmits
light to the skin, which is both scattered and absorbed by the
tissue in the illuminated eld. Blood is more opaque than
surrounding tissue and therefore attenuates the re ected
signal more than other tissue in the eld. e intensity of
re ected light is reduced with more blood in the eld. If the
electrical circuit lters the higher frequency arterial pulsations it is possible to register a signal, which qualitatively
corresponds to venous volume in the segment of interest. PPG is therefore able to detect changes in venous lling secondary to various patient maneuvers, which will be
described below. PPG has found a role in the clinical assessment of venous insu ciency.
AIR PLETHYSMOGRAPHAPG
Properly designed air plethysmographs more accurately
measure true volume than IPG, SGP, or PPG and are easier
44 • BASIC CONSIDERATIONS
to use in the clinical setting.
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11–14
e instrumentation is
characterized by three major components. e rst component is the transducer, which is a form of closed air bladder
used to surround the limb segment of interest. e second
component is a pressure sensor, which can accurately measure the pressure in the air bladder as a function of time.
e third component is the electrical circuit necessary to
control the pressure sensor and display the measured results.
As mentioned above, use of the APG is relatively simple.
e air bladders are generally self-contained units similar to
standard blood pressure cu s and are designed for speci c
limb segments. e connection to the console is generally
limited to a single rubber tube with connector. With the
air bladder surrounding the limb segment of interest, any
change in volume in the limb segment will cause the pressure
within the bladder to change. For example if limb volume
increases the bladder volume with decrease. Since the bladder is a closed system, this will cause the bladder pressure
to increase. Accurate APG carefully correlate bladder state
(i.e., mean bladder pressure and volume), instantaneous
change in bladder pressure, and limb volume change. APG
is able to detect changes in venous limb volume secondary
to various patient maneuvers. e maneuvers and outputs
are similar for all plethysmographs described in this chapter
and are given below. APG is used in the clinical assessment
of venous insu ciency and deep venous thrombosis.
DEFINITION OF PARAMETERS AND
MANEUVERS USED IN GENERIC
PLETHYSMOGRAPHY FOR VENOUS
INSUFFICIENCY
× 10
Volume
EV
VV
VRT
Figure5.2 is gure illustrates parameter de nitions and maneuvers
used generically in plethysmographic studies for venous insu ciency.
Time
RV
the venous re lling time (VRT). is is the time measured
from when the baseline volume begins to increase to its plateau. With the subject in the erect position, the operator
instructs the subject to perform a single brisk ankle exion.
is will produce a momentary reduction in Y-axis volume.
is change in volume is called the ejection olume (EV).
To calculate the ejection action (EF), the operator divides
EV by VV. e subject is then instructed to perform 10
brisk ankle exions. is will produce a reduction in Y-axis
volume, which will be larger than the volume reduction
experienced with one exion. is allows the operator to
measure residual olume (RV). is is de ned as the di er-
ence between the volume a er 10 exions and the baseline
volume. Finally, the operator can calculate the residual ol-
15–17
ume action (RVF) by dividing RV by VV.
Venous insu ciency causes the three venous systems in
the lower extremity to misdirect venous blood volume.
erefore, the goal of this testing is to characterize misdirection of venous blood volume, if present.
Our test subject is placed in the supine position. is
will lower venous pressure in the lower extremities to a value
only slightly above right atrial pressure (~ 0mmHg). Using
a plethysmograph an operator can obtain a baseline volume
in the segment of interest. When the subject is placed in the
erect position lower extremity venous pressure increases due
to the hydrostatic column of blood extending from the right
atrium to the segment of interest. Since veins are compliant
(i.e., increase volume with increased internal pressure), vein
blood volume in the segment of interest increases. is volume increase is displayed on a graph from which measurements may be taken. e Y-axis is volume and the X-axis is
time. Since all measurements are either times or ratios, the
Y-axis is not required to be strictly calibrated as volume.
However, its display on the graph must correlate with volume change (see Figure5.2).
e measurement between the supine baseline volume
and the erect volume plateau is known as the venous olume
(VV). From this same curve the operator can determine
SIMPLIFIED DIAGNOSTIC CRITERIA
FOR VENOUS INSUFFICIENCY
ese criteria may be applied to any plethysmograph. e
only restriction is that the volume measurements be taken
accurately. In order to simplify the diagnostic criteria for
venous phlethysmographic studies we have focused on three
parameters. e rst is VRT. In patients with signi cant
venous insu ciency, venous re lling develops secondary
to venous re ux and clearly reduces the time necessary to
complete the process. If VRT is >20 seconds, the limb is not
demonstrating signi cant re ux. If VRT is <20 seconds,
17
the diagnosis of venous re ux should be considered.
e
cial venous insu ciency or deep venous thrombosis, EF is
reduced. If EF is >60% the limb is presenting with normal
venous hemodynamics. For super cial venous insu ciency
the average EF is 50%. Average EF is reduced to 40% in subjects with deep venous insu ciency and 35% in deep venous
obstruction. e third measurement is RVF. If RVF is elevated, the limb is demonstrating venous ambulatory hypertension. Anormal value for RVF is <35%. Subjects with
RVF > 35% should be evaluated further for venous disease.
17
ROLE OF PHYSIOLOGIC TESTING IN VENOUS DISORDERS • 45
D E E P V E N O U S T H R O M B O S I S
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DVTEXAMINATION BY
PLETHYSMOGRAPHY
e four plethysmographs described above have been used
for the identi cation and monitoring of DVT. For purposes
of this text a generic procedure for DVT will be described.
DVT is a life-threatening disease; for that reason alone
accurate diagnosis and therapy is essential. e deep venous
system is not only a conduit for returning blood to the right
side of the heart; it is also a storage or capacitant system.
is means its volume changes rapidly as pressure within
the deep system changes. If one examines a vein at low pressure the walls are nearly fully collapsed and only a small ow
channel is present. It takes very little increase in internal
uid pressure to expand the ow channel of a vein. Finally,
if there is obstruction in a segment of deep vein, despite
rich venous collateral channels, venous pressure distal to the
obstruction will increase. Examination by plethysmograph
makes use of these two principles (i.e., volume change with
increased pressure and resistance).
Typically a plethysmograph transducer is placed at the
calf or distal thigh with the patient lying supine on a table.
In the case of APG the transducer is an air bladder in ated
to 5mmHg; in the case of PPG the transducer is a light
emitting diode. Proximal to the transducer a method of rapidly occluding the deep system must be used. For all transducers this can be a thigh cu in ated rapidly by hand bulb
or automatic in ator.
With the transducer recording a stable venous signal at
5mm/sec chart speed, the pressure in the proximal occluding cu is rapidly elevated to 50mmHg. e transducer is
measuring absolute levels of volume.
With the increased pressure in the proximal cu , venous
blood in the deep system cannot pass under the cu until
the venous pressure reaches approximately occluding cu
pressure. is increase in venous pressure (i.e., pooling)
develops because the proximal cu does not obstruct the
arterial in ow. A er about 20 to 40 seconds, pressure in
the distal venous system reaches the pressure in the occluding cu and venous volume reaches a plateau. Once the
plateau has been reached, the operator rapidly releases the
pressure in the occluding cu . e pooled venous blood
can then return to the right side of the heart via the larger
veins upstream. Two measures of venous hemodynamics
are taken during this test. First, there is the volume increase
from the baseline to the plateau. is is known as segmen-
tal venous capacitance (SVC) and represents the blood storage capacity of the segment vein. is is generally quoted
in millimeters of de ection, or milliliters if the system is
calibrated to volume. e second measurement is the slope
of the volume-time curve immediately a er the pressure in
the occluding cu is released. is is known as maximum
venous out ow (MVO) and represents resistance to blood
ow in the deep system. is may be quoted in millimeters
of de ection per second or milliliters per second if the system is calibrated to volume. e next two sections de ne
the diagnostic use of these parameters.
Segmental Venous Capacitance(SVC)
With experience, vascular technologists and physicians are
able to identify a normal range of SVC with their speci c
plethysmographic equipment. With the subject supine,
normal veins have signi cant capacitance. If proximal deep
venous obstruction is present, pressure distal to the obstruction increases and SVC is markedly reduced. erefore, if
SVC reduces more than 25% when compared with normal
11
levels, venous abnormality is suggested.
It is recommended
that SVC always be measured bilaterally. In the case of unilateral disease, the normal limb can serve as a control, which
increases both sensitivity and speci city.
Maximum Venous Out ow(MVO)
As in the case of SVC, vascular technologists and physicians
are able to identify a normal range of MVO with their speci c
plethysmographic equipment. Normal veins exhibit a very
rapid decrease in volume on de ation of the occluding cu .
When deep system resistance is increased due to deep venous
obstruction the reduction in MVO is dramatic. Again, in the
case of unilateral disease, the normal limb can serve as a control.
Adi erence in MVO between limbs of 25% is abnormal.
When continuous-wave venous Doppler measurements,
SVC, and MVO are performed as a diagnostic package, sensitivity and speci city of the combined testing reaches 85%
11
respectively.
It should be acknowledged duplex venous
Doppler ultrasonic imaging, which requires more expensive
equipment, clearly demonstrates a higher sensitivity and speci city. Further, ultrasound is able to more accurately localize
obstruction and age thrombus. For this reason, plethysmographic methods have limited diagnostic use. ere is one
area in venous disease where SVC and MVO provide unique
and important information. is is in the determination of
venous collaterization following a DVT. Patients that normalize SVC and MVO rapidly have an improved prognosis when
compared with subjects in which normalization is prolonged.
CONTINUOUSWAVE VENOUS
DOPPLER CW DOPPLER
CW Doppler instruments are widely available, relatively
inexpensive, and used extensively to rapidly investigate the
peripheral vascular system. CW Doppler measurements can
be used independently or, as mentioned above, combined
with measurements from a plethysmograph. e purpose
of this section is to outline how CW Doppler is used to
facilitate the diagnosis of venous insu ciency of the deep
system, speci cally deep vein re ux andDVT.
11
46 • BASIC CONSIDERATIONS
D V T
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Strandness and Baker introduced CW Doppler in the
18
1960s.
Its initial application was peripheral arterial assessment. With the development of additional maneuvers the
instrumentation was applied rst to the diagnosis of DVT
and later to deep vein insu ciency.
We recommend that the subject be studied on a at
examining table in which the lower extremities may be
placed in the dependent position at approximately 15
degrees. is slight angle dilates the deep system, which
makes the identi cation of veins easier and improves the
velocity signals. We recommend that target veins include
the common femoral vein at the inguinal ligament, popliteal vein at the popliteal fossa, and the posterior tibial vein
just behind the medial malleolus.
With the pencil-like probe positioned toward the
venous ow and at 60 degrees to the ow streamline, the
target velocity is optimized. e fact that a velocity is identi ed means the vein is patent at the target level, and this
is the rst of three major diagnostic criteria. e second
diagnostic criterion is associated with the spontaneous and
phasic nature of the signal. When veins are not obstructed
proximal to the target vein, the local pressure is low and local
velocity changes as a function of respiration. Low-pressure
veins collapse and local velocity is o en reduced to zero
shortly a er inspiration. is is due to the fact that when
the diaphragm moves down on inspiration, pressure in the
closed abdominal cavity increases and collapses veins at low
pressure. With proximal obstruction this phasic velocity is
disturbed in the sense that velocity is no longer phasic with
respiration and in fact may be continuous. e third criterion is associated with velocity response secondary to distal compression. When veins are unobstructed proximal to
the target and compression is performed distally, the local
velocity will increase in response to compression. In a high
resistance proximal venous system, distal compression will
not evoke increased velocity.
If a subject demonstrates at the femoral, popliteal, and
posterior tibial veins good velocity signals that are phasic with respiration and augment with distal compression,
the chance of DVT involving the iliac, common femoral,
femoral, or popliteal veins is very low. DVT limited to the
calf veins is more problematic due to vein duplication at
this level. As mentioned above, when CW Doppler is combined with venous plethysmography (SVC and MVO) the
sensitivity and speci city of the combined package is 85%
11
respectively.
VENOUS INSUFFICIENCY
e main use of CW Doppler in venous insu ciency is in
assessing re ux in the major deep veins of the lower extremity (common femoral, femoral, and popliteal veins). is
procedure is most e ectively performed with the subject
standing. To the extent possible, weight should be shi ed
to the contralateral leg. A bidirectional CW Doppler
with a stereo audio signal and printout is recommended.
For venous work an ultrasound frequency range of 5 to
7 MHz is suggested. As a quick review, the pencil-like
probe of the CW Doppler should be aligned toward the
ow and at an angle of approximately 60 degrees to the
anticipated ow streamline. Unlike duplex ultrasound,
with CW Doppler the exact path of the target vein is not
well de ned. erefore, in practice the operator will have
to manually adjust the probe angle to obtain the maximum signal (audio level and velocity level). e concept
is quite simple; target veins are assessed for reversal of ow
velocity a er rapid manual limb compression and release.
e more reversal, the more re ux. In terms of diagnostic
criteria, a normal vein demonstrates no evidence of re ux
using this technique. Flow reversal can be assessed both
by audio signal and by examination of velocity versus time
17
printouts.
ASSESSMENT OF THE DEEP AND
SUPERFICIAL VENOUS SYSTEMS
USING DUPLEX ULTRASOUND
e two sections preceding this text described pure physiologic measures. is section will focus on the combination
of physiologic and imaging measures. Further, duplex ultrasound has become the “gold standard” in the diagnosis of
both deep venous thrombosis and venous insu ciency. e
method is so pervasive that it has replaced in most venous centers the use of venous plethysmographs and CW Dopplers.
It should also be stated that the accuracy, speed, and cost of
this procedure to diagnose deep venous thrombosis has been
so attractive that venography is rarely indicated or necessary.
Power Color Pulsed-Wave Doppler and HighResolution B-mode Imaging characterize state-of-the-art
duplex ultrasound. Descriptions of these devices are found
elsewhere in this book and are commonplace in medical
literature. e remaining sections describe our approach
to the assessment of the deep and super cial systems using
duplex ultrasound.
RISK FACTORS, VASCULAR HISTORY,
PRESENTING SIGNS AND SYMPTOMS,
AND CEAP CLASSIFICATION
In addition to demographic data we suggest risk factors and
associated history be recorded. is includes parameters
like obesity, pregnancy, hormone use, and hypercoagulability. Also recorded for each leg are presenting signs and
symptoms like edema, pain/tenderness, skin changes, varicose veins, and previous DVT. We have found the CEAP
classi cation to be helpful in describing degree of disease
19
and in developing management plans.
ROLE OF PHYSIOLOGIC TESTING IN VENOUS DISORDERS • 47
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