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J. Bergan

Venous valves play an important role in trans-

porting blood from the lower extremities to the

heart. Upward movement is contingent upon valve

closure, and in order for valve closure to occur,

there must be a reversal of the normal transvalvular

pressure gradient. Back pressure resulting in ﬂ ow

exceeding 30 cm/s leads to valve closure. Direct

observation of human venous valves via special-

ized ultrasound techniques has revealed that venous

ﬂ ow is not normally in a steady state but is irregu-

larly pulsatile. Venous valves undergo opening and

closing cycles. Even when fully opened, the cross-

sectional area between the lea ﬂ ets is 35% smaller

than that of the vein distal to the valve [ 4 ] . Flow

through the valve separates into a proximally

directed jet and distal ﬂ ow into the sinus pocket

proximal to the valve cusp. The vortical ﬂ ow pre-

vents stasis and ensures that all surfaces of the

valve are exposed to shear stress. Valve closure

develops when the vortical ﬂ ow pressure exceeds

the proximally directed jet ﬂ ow [ 5 ] .

Intuitively, the role of venous valves during mus-

cular exercise is to promote antegrade ﬂ ow from

super ﬁ cial veins to deep veins through perforating

veins while preventing retrograde motion in the

opposite direction. Normally functioning perforat-

ing vein valves protect the skin and subcutaneous

tissues from the effects of muscular contraction

pressure, possibly exceeding 100–130 mmHg,

which may cause pooling of ﬂ uid in the super ﬁ cial

circulation. In particular, volume and pressure

changes in veins within the calf occur with mus-

cular activity. In the resting position, with the foot

ﬂ at on the ﬂ oor, there is no muscle instigated ﬂ 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 [ 6 ] . Properly

functioning valves ensure that blood ﬂ ows from the

foot and ankle into the deep veins of the calf. Then,

calf contraction transports this blood into the deep

veins of the thigh, and henceforth, blood ﬂ ow pro-

ceeds to the pelvic veins, vena cava, and ultimately

to the heart all due to the in ﬂ uence of lower extrem-

ity muscular contraction.

The role of venous valves in an individual qui-

etly standing is not well understood. Pressures in

the super ﬁ cial and deep veins should theoreti-

cally be the same during quiet standing, but as

Arnoldi has found, the pressure in the deep veins

is 1 mm higher, which would tend to keep the

valves in the perforating veins closed [ 7 ] .

Development of ultrasound technology has

uncovered a third compartment to add to the

Super ﬁ cial and Deep compartments of the lower

extremities (Fig. 4.1 ). This is termed the Saphenous

compartment and this encloses the Great and Small

Saphenous veins, their accompanying nerves and

the Saphenous ligaments which tether the veins in

place. In many instances, the Saphenous veins are

thought to transmit the venous hypertension that

triggers the shear stress induced changes that even-

tuate in valve destruction and vein wall weakness of

primary venous insuf ﬁ ciency. This theory is under

current attack.

Pathophysiology of Primary

Venous Insuf ﬁ ciency

Explanations of venous Pathophysiology as pub-

lished in reviews, texts, and monographs of the

past century are currently out of date. Rather than

Table 4.1 Visible and functional chronic venous disease in San Diego study participants

Visible disease Normal Super ﬁ cial disease Deep disease Total

No. % No. % No. % No. %

Normal 978 22.1 5 0.1 36 0.8 1,019 23.0

Spider veins 232 52.5 20 0.5 75 1.7 2,416 54.6

Varicose veins 164 3.7 526 11.9 92 2.1 78 17.7

Trophic changes 53 1.2 107 2.4 45 1.0 205 4.6

Total (legs) 3,516 79.5 658 14.9 248 5.6 4,422 100.0

Adapted from Criqui et al. [

3 ]

In this study, classi ﬁ cation was based on ultrasonographic ﬁ ndings. Of the 782 legs with varicose veins, 697 (89.1%) also

had telangiectatic veins. Of the 205 legs showing trophic changes, 188 (91.7%) also had telangiectases and 141 (68.8%)also

had varicose veins. Of the 248 legs showing deep functional disease, 119 (48.0%) also had super ﬁ cial functional disease

https://t.me/med1917

214 Pathophysiology of Venous Disease

repeat old dogma, we offer in this chapter the

modern theories of venous disease based on new

and rigorous science.

A dysfunctional venous system is caused by

injury to vein walls and venous valves. This is

known because such damage is readily demon-

strable on plain light microscopy [ 8 ] . Factors that

enter into such injury include heredity, obesity,

female gender, pregnancy, and a standing occupa-

tion in women (Table

4.2 ). Vein wall injury allows

the vein to elongate and dilate. An increase in vein

diameter is one cause of valve dysfunction and

re ﬂ ux. The effect of persistent valvular re ﬂ ux is a

chronic increase in distal venous pressure. This

venous pressure increases as one proceeds from

the inguinal ligament past the knee to the ankle.

The prolonged venous hypertension initiates a cas-

cade of pathologic events. These manifest them-

selves clinically as lower extremity edema, pain,

itching, skin discoloration, and ulceration [

8 ] .

The earliest signs of venous insuf ﬁ ciency are

often varicose veins in the epidermis and dermis,

called telangiectasias. Slightly deeper are ﬂ at,

blue-green veins of the reticular (network) system.

These may become varicose as well. And ﬁ nally,

deeper yet 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.

Chronic Venous insuf ﬁ ciency

Skin changes of hyperpigmentation, scarring

from previous ulceration, and active, open ulcer-

ations are grouped together under the term

chronic venous insuf ﬁ ciency (CVI). Numerous

theories have been postulated regarding the cause

Skin

superficia

compart

Deep

compar

(Muscul

compart

Cutenous vein

Reticular vein

Sv = Superficial vein

saphenous

vein

Fct

Deep vein

Deep fascia

∗

Deep

arfery

saphenous space

superficial fascia

Fig. 4.1 In this drawing the relationships of the saphen-

ous compartment are clearly indicated. Note the deep,

super ﬁ cial and saphenous compartments. Deep veins are

found deep to the muscular fascia and super ﬁ cial veins

super ﬁ cial to the super ﬁ cial fascia. Dilation of super ﬁ cial

veins results in varicose veins. Perforating veins connect

deep and super ﬁ cial veins and traverse the fascia. Small

veins immediately under the skin are called reticular

veins. Intra-cutaneous veins are normally present; when

dilated they form telangiectasia

Table 4.2 Risk factors for chronic venous disease

Heredity

Female gender (progesterone effect)

Pregnancy (progesterone effect)

Age

Greater height

Prolonged standing (in women)

Obesity

https://t.me/med1917

J. Bergan

of chronic venous insuf ﬁ ciency and the cause of

venous ulceration. All of the theories proposed in

the last century have been disproved.

An example is the theory of venous stasis ﬁ rst

proposed in a manuscript by John Homans at

Harvard in 1917. It was a treatise on diagnosis

and management of patients with chronic venous

insuf ﬁ ciency and in it Homans coined the term

“post-phlebitic syndrome” to describe the skin

changes of CVI. He stated: “Overstretching of

the vein walls and destruction of the valves…

interferes with the nutrition of the skin… there-

fore, skin which is bathed under pressure with

stagnant venous blood will form permanent open

sores or ulcers.” This statement, like many others

that describe venous conditions and their treat-

ments, is steeped in dogma and is short of obser-

vational fact. The term “stasis ulcer” honors that

misconception, as do the terms “venous stasis

disease” and “stasis dermatitis.”

Alfred Blalock, who later initiated and was best

known for cardiac surgery, disproved the theory by

studying oxygen content from varicose veins and

normal veins [

9 ] . He pointed out that the oxygen

content of the femoral vein in patients with severe

chronic venous insuf ﬁ ciency was greater than the

oxygen content of the contralateral non-affected

limb. Because oxygen content was higher, some

investigators felt that arteriovenous ﬁ stulae caused

venous stasis and varicose veins. That theory, though

disproved, has some basis in fact since the entire

thermo-regulatory apparatus in limbs depends on

the opening and closing of arterio-venous shunts.

These shunts are important as they explain some

accidents that happen during sclerotherapy when

sclerosant entering a vein is shunted into the arterial

system and distributed in its normal territory [ 10 ] .

Microsphere investigations have failed to show any

shunting and the theory of arteriovenous commu-

nications has died despite the fact that these shunts

actually exist and do open under the in ﬂ uence of

venous hypertension [ 11 ] .

Hypoxia and its role in chronic venous

insuf ﬁ ciency was investigated throughout the

last 25 years of the twentieth century. English

investigators thought that a ﬁ brin cuff, observed

histologically, blocked transport of oxygen and

was responsible for skin changes of CVI at the

ankles and distally [

12 ] . This theory has since

been abandoned.

There are two elements that interact to cause

all of the manifestations of lower extremity

venous insuf ﬁ ciency. These are failures of the

vein valves and vein walls, and skin changes at

the ankles; both of which are related to venous

hypertension and the in ﬂ ammatory cascade. Our

work suggests that venous hypertension causes

a shear stress-dependent leukocyte–endothelial

interaction, which has all of the manifestations

of chronic in ﬂ ammation [

13 ] . This includes leu-

kocyte rolling, ﬁ rm adhesion, and subsequent

migration (diapedesis) through the endothelial

barrier into the parenchyma of valves and vein

walls [ 13 ] . There, macrophages elaborate matrix

metalloproteinases (MMPs), which destroy elas-

tin and possibly collagen as well. Vein walls

become stretched and elongated. Vein valves

become perforated and even scarred to the point

of total destruction. These changes are seen both

macroscopically and angioscopically [ 14 ] .

Similar changes have been produced in the

experimental animal by constructing arteriovenous

ﬁ stulae. This produces a localized venous hyperten-

sion which causes the venous valve changes seen

pathologically in man.

The second manifestation of chronic venous

insuf ﬁ ciency, also an in ﬂ ammatory cascade, is

seen in the skin [ 15 ] . Skin biopsies have shown

that liposclerotic eczematous skin demonstrates

macrophage in ﬁ ltration [ 16 ] . Activation of leu-

kocytes promotes the expression of CD11b, an

important cell surface integrin for capillary adhe-

sion. Leukocyte diapedesis into the extracellular

space is facilitated by the induction of endothelial

intercellular adhesion molecule-1 (ICAM-1) with

their subsequent transgression into post-capillary

venules. This has come to be known as the “leu-

kocyte trapping hypothesis” and is veri ﬁ ed by a

number of ultra structural studies. Accompanying

this leukocyte in ﬂ ux and trapping is the disor-

derly activation of dermal ﬁ broblasts through

TGF- b 1 deposition [

17, 18 ] . The result is dermal

ﬁ brosis. Clearly, chronic venous insuf ﬁ ciency of

the skin and its subcutaneous tissues is a disease

of chronic in ﬂ ammation, dependent upon venous

hypertension.

https://t.me/med1917

234 Pathophysiology of Venous Disease

The primary injury is extravasation of macro-

molecules and red blood cells into the dermal

interstitium. The hyperpigmentation of skin in

lipodermatosclerosis may not be just a byproduct

of capillary hyperpermeability. The extravasation

of red cells leads to elevated levels of ferritin and

ferric iron in affected skin [

19 ] . This leads to fur-

ther oxidative stress and the development of a

microenvironment that exacerbates tissue dam-

age and delays healing.

Thus the causes of the disparate pathologic pro-

cesses which eventuate in varicose veins and the

skin changes of chronic venous insuf ﬁ ciency are

beginning to be explained by the triggering effect

of shear stress which initiates the in ﬂ ammatory

cascade, which in turn lies at the bottom of pri-

mary venous insuf ﬁ ciency and the effects of severe

chronic venous insuf ﬁ ciency.

Clinical Duplex Doppler scanning has served

to allow mapping of venous insuf ﬁ ciency in order

to guide therapy. Such mapping has shown the

futility of routine Saphenous stripping, the impor-

tance of preserving re-entry perforating veins and

the frequency of super ﬁ cial venous aneurysms.

Conclusions

Traditional thinking about venous physiology

and Pathophysiology is giving way to new

concepts. These, in turn are changing the way

that patients and their venous insuf ﬁ ciency are

treated. New concepts are brie ﬂ y summarized

in this modern chapter.

References

1. van Bemmelen PS, Bedford G, Beach K, Strandness

DE. Quantitative segmental evaluation of venous val-

vular re ﬂ ux with duplex ultrasound scanning. J Vasc

Surg. 1989;10:425–31.

2. Vasdekis SN, Clarke GH, Nicolaides AN. Quanti ﬁ cation of

venous re ﬂ ux by means of duplex scanning. J Vasc Surg.

1989;10:670–7; 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;38:955–61.

3. Criqui MH, Jamosmos M, Fronek A, Denenberg JO,

Langer RD, Bergan J, Golomb BA. Chronic venous

disease in an ethnically diverse population: the San

Diego Population Study. Am J Epidemiol. 2003;158:

448–56.

4. Lurie F, Kistner RL, Eklof B. The mechanism of

venous valve closure in normal physiologic condi-

tions. J Vasc Surg. 2002;35:713–7.

5. Coleridge Smith PD. The microcirculation in venous

hypertension. Vasc Med. 1997;2:203–13.

6. Weijers RE, Kessels AG, Kemerink GJ. The dampen-

ing properties of the heel region of the foot during

simulated heelstrike. J Biomech. 2005;38:2423–30.

7. Arnoldi CC. The function of the venous pump in

chronic venous insuf ﬁ ciency: a phlebographic study.

J Cardiovasc Surg. 1961;2:116–27.

8. Schmid-Schönbein GW, Takase S, Bergan JJ. New

advances in the understanding of the pathophysiology

of chronic venous insuf ﬁ ciency. Angiology. 2001;52

Suppl 1:S27–34.

9. Blalock A. Oxygen content of blood in patients with

varicose veins. Arch Surg. 1929;19:898–904.

10. Bergan JJ, Weiss RA, Goldman MP. Extensive tissue

necrosis following high-concentration sclerotherapy

for varicose veins. Dermatol Surg. 2000;26:535–42.

11. Ahren K, Janson PO, Selstam G. Search for arterio-

venous shunts in the rabbit ovary in situ using perfusion

of microspheres. J Reprod Fertil. 1974;41:133–42.

12. Browse NL, Burnand KG. The cause of venous ulcer-

ation. Lancet. 1982;1998(ii):243–5.

13. Takase S, Lerond L, Bergan JJ, Schmid-Schönbein

GW. The in ﬂ ammatory reaction during venous hyper-

tension in the rat. Microcirculation. 2000;7:41–52.

14. Hoshino S, Satokawa H, Ono T, Igari T. Surgical treat-

ment for varicose veins of the legs using intraoperative

angioscopy. In: Raymond-Martimbeau P, Prescott R,

Zummo M, editors. Phlebologie 92. Paris: John Libbey

Eurotext; 1992. p. 1083–5.

15. Coleridge Smith PD. Treatment of microcirculation dis-

orders in venous leg ulcer. In Messmer K (ed):

Microcirculation in Chronic Venous Insuf ﬁ ciency. Prog

Appl Microcirc. Basel, Karger, 1999;23:121–141.

16. Bergan JJ. Leucocytes and venous valve damage in chronic

venous desease. Medicographia. 2006;28(2):101–8.

17. Pappas PJ, You R, Rameshwar P, et al. Dermal tissue

ﬁ brosis in patients with chronic venous insuf ﬁ ciency

is associated with increased transforming growth fac-

tor- b 1 gene expression and protein production. J Vasc

Surg. 1999;30:1129–45.

18. Sansilvestri-Morel P, Rupin A, Jaisson S, et al. Synthesis

of collagen is dysregulated in cultured ﬁ broblasts derived

from skin of subjects with varicose veins as it is in venous

smooth muscle cells. Circulation. 2002;106:479–83.

19. Ackerman Z, Seidenbaum M, Loewenthal E, Rubinow

A. Overload of iron in the skin of patients with vari-

cose ulcers: possible contributing role of iron accu-

mulation in progression of the disease. Arch Dermatol.

1988;124:1376–8.

https://t.me/med1917

N.S. Sadick et al. (eds.), Practical Approach to the Management and Treatment of Venous Disorders,

DOI 10.1007/978-1-4471-2891-5_5, © Springer-Verlag London 2013

History

General Considerations

A number of patient historical risk factors can

in ﬂ uence the development of super ﬁ cial venous

disease. Among those considered to be of fairly cer-

tain signi ﬁ cance are: family history, age, pregnancy,

and female gender [ 1 ] . Other factors of probable

signi ﬁ cance are: occupation requiring prolonged

standing, obesity, physical activity involving heavy

straining (exaggerated Valsalva’s maneuver), sed-

entary occupation and/or lifestyle, neuromuscular

disorder causing foot/calf muscle pump impair-

ment, history of leg trauma, history of deep vein

thrombosis, and connective tissue laxity [ 2, 3 ] .

For nearly all patients presenting with signs and

symptoms of super ﬁ cial venous insuf ﬁ ciency, care-

ful patient questioning will reveal a ﬁ rst- or second-

degree relative with signi ﬁ cant venous disease. It is

impossible to over-emphasize the importance of

obtaining historical information from the patient.

Repetition of this exercise prior to the institution of

treatment modalities will often uncover further

information of importance in determining which

methods are appropriate. When a history is ﬁ rst

taken, patients often forget or minimize symptoms.

At each subsequent stage of questioning, patients

are reminded of symptoms that might have been

long forgotten or, more commonly, ignored. If his-

torical questioning is allowed at intervals over sev-

eral weeks, patients will have an opportunity to

re ﬂ ect on these questions and begin to notice symp-

toms of which they may have been only minimally

aware. These historical factors become important

not only for establishing the chronicity and severity

of symptoms and in helping to determine appropri-

ate methods of treatment, but also in developing and

meeting the criteria necessary for reimbursement by

insurance carriers or governmental agencies.

Lower extremity scars or incisions should

prompt further investigation, as they may indi-

cate previous surgical resection for melanoma, a

previously excised vascular malformation (with

the attendant rami ﬁ cations), or an incompletely

excised truncal vein requiring further treatment.

During the course of treatment, it is important

not to lose sight of the patient’s chief complaint.

A simple question, “What is the concern about

your legs that you consider most important to the

overall success of your treatment?” should be

addressed at each visit to ensure that progress is

being made toward resolution and that the chief

complaint has been successfully eliminated. If

the chief complaint is cosmetic appearance, and

there has been little or no cosmetic improvement

following treatment, all the explanation in the

world regarding the improved circulatory health

Clinical Evaluation of Patients

with Chronic Lower Extremity

Venous Disorder

Neil M. Khilnani and Nick Morrison

N. M. Khilnani , M.D.

Weill Cornell Vascular,

Weill Medical College of Cornell University ,

New York , NY , USA

e-mail: nmkhilna@med.cornell.edu

N. Morrison , M.D. ()

Morrison Vein Institute ,

AZ , USA

e-mail: nickmorrison2002@yahoo.com

https://t.me/med1917

N.M. Khilnani and N. Morrison

of the legs will do little to convince the patient

that a good result has been achieved.

Also, addressing and managing patient expecta-

tions is critical in achieving good results for patients,

which in turn will be important in maintaining a

successful phlebology practice. Fundamental to

this process is a determination whether the patient’s

complaints are likely related to a venous disease

problem. For example, even on initial evaluation,

one can explain to a patient that sciatic pain most

likely is of an origin other than venous. Patients are

usually quite aware of the effects of other disease

states, such as arthritis, which often exhibits cross-

over symptoms and is more likely the cause of knee

and ankle joint complaints than is venous disease.

Creating realistic patient expectations from the out-

set will lead to the perception by the patient of much

better results than if outcome explanations are left

to the latter portion of the treatment program.

Routine Historical Information

Routine health information should be recorded,

including height and weight (measured, not

related), age and gender. Historical information

should be recorded as well. This includes posi-

tive family history of venous or arterial disease,

allergic history, diabetes, hypertension, cardiac

valvular disease, migraine (especially with aura),

arthritis, back pain, previous allergic reactions,

pregnancy history (including any history of mis-

carriage) and future plans, hormone manipulation

(birth control, replacement therapy), occupations

requiring prolonged standing, effects of rest on

signs and symptoms, and any other factors consid-

ered by the patient or examiner to be in any way

related to symptoms of venous disease. Many of

these factors might become important in the future

if the patient develops new symptoms and if there

are questions as to whether the new symptoms are

related to a progression of the venous disease, side

effects of treatment or entirely unrelated to the

patient’s venous disease.

A carefully detailed surgical history can reveal

information important to the phlebologist, such as

previously treated skin cancer (which may result in

edema secondary to lymphatic interruption); a

“tumor” removed from a lower extremity (which

may have been a vascular or lymphovascular mal-

formation); or previous venous surgical intervention

(which might alter treatment options and recom-

mendations). One must keep in mind that even a

carefully obtained history may still be inaccurate

because of the patient’s memory or understanding

of previous diagnoses and treatment. It is not infre-

quent that a patient feels certain of a previous “strip-

ping” procedure on one extremity, while surgical

incisions can only be identi ﬁ ed on the opposite

extremity. Or a patient relates a “stripping” when

the surgical incisions are found in places other than

along the saphenous trunks, indicating rather, per-

haps, a previous avulsion phlebectomy procedure.

Vascular-Speci ﬁ c Historical Factors

In the experience of some, a family history of

venous disease is nearly always discoverable [ 3 ] .

However, evidence for this clinical impression is

not incontrovertible [ 4 ] . Commonly, patients will

relate a history of trauma with resultant localized

development of abnormal veins. Other vascular-

speci ﬁ c factors might include: onset of edema

(especially unilateral left leg edema associated

with iliac vein compression syndrome); previous

history of super ﬁ cial thrombophlebitis or deep

vein thrombosis (another common point of confu-

sion for patients); a history of spontaneous preg-

nancy interruptions; or a family history of deep

vein thrombosis or “paradoxical” strokes which

may indicate a thrombophilia disorder requiring

more investigation prior to treatment. Noting the

history of onset and duration of venous disease

signs and symptoms will be important not only to

provide patients with realistic expectations for

control of their venous problems, if not complete

and permanent resolution, but also for documenta-

tion required for insurance reimbursement.

Symptoms

In patients with chronic venous disorder, the

most common symptoms are listed in Table 5.1

and are often associated with prolonged standing,

https://t.me/med1917

275 Clinical Evaluation of Patients with Chronic Lower Extremity Venous Disorder

menstrual period or pregnancy, generally wors-

ening later in the day.

The severity of symptoms does not always

correlate with the extent of physical ﬁ ndings of

venous insuf ﬁ ciency. For example, patients who

participate in a vigorous exercise program will

routinely describe fewer and less severe symp-

toms, as well as exhibit fewer or less severe

physical ﬁ ndings, of chronic venous disorder

than sedentary patients with a similar degree of

severity. Men will often be completely asymp-

tomatic, even up to the point that they suffer a

signi ﬁ cant complication of their venous disease,

such as spontaneous venous rupture, ulceration,

or super ﬁ cial thrombophlebitis.

Burning may be signi ﬁ cant and is frequently

localized to areas of telangiectasias. Pain radi-

ating down the posterior thigh or posterolateral

calf is more commonly neurogenic rather than

of venous origin. An exception is a patient

with sciatic nerve varices who may experience

symptoms of sciatica indistinguishable from

pain of nerve root origin [ 5 ] . Symptoms com-

mon in patients suffering from venous disor-

ders are legs that fatigue easily, lower leg or

ankle swelling, nocturnal cramping (or follow-

ing exercise, not during), and leg heaviness.

Less commonly, patients may experience rest-

less leg, pruritus (especially following exer-

cise), and continually cold or warm feet. These

symptoms should not be discounted in the

evaluation, especially if they are noted in con-

cert with physical signs of venous disorders, as

they often improve with treatment.

Symptoms are frequently relieved by leg ele-

vation, activity, graduated compression hose, or

application of cold compresses or ice.

Physical Signs

The progressive signs of venous insuf ﬁ ciency

resulting from venous hypertension are telangi-

ectasia; tortuous or dilated reticular veins; vari-

cose veins; edema (lower leg, foot, and/or ankle);

“gaiter area” skin changes (discoloration, rash,

eczema, induration); and healed or active ulcer-

ations [ 6 ] . Not uncommonly these changes will

be asymmetric, even unilateral. Scars may be

seen following ulceration or from previous surgi-

cal intervention (the location of surgical incisions

will be an excellent adjunct to con ﬁ rm the

patient’s history). In a patient with swollen

limb(s), one must not forget causes other than

venous, such as lymphatic obstruction/disrup-

tion, proximal obstructing lesion, infection, vas-

cular malformation, or history of lower extremity

trauma. Many medications such as anti-

in ﬂ ammatory agents induce peripheral edema as

a side effect.

Telangiectasias (intradermal veins <1 mm)

(Fig.

5.1 ) are usually the result of localized venous

hypertension only, but may well be associated

with more clinically signi ﬁ cant venous problems.

Only a carefully performed duplex scan by a

fully quali ﬁ ed sonographer will identify patients

with more underlying venous disease than is

readily apparent [ 7 ] . While it is arguably not eco-

nomically justi ﬁ able to perform duplex scans on

all patients with asymptomatic telangiectasias,

it is surprising how often clinically signi ﬁ cant

ﬁ ndings are identi ﬁ ed when duplex is done.

Table 5.1 Symptoms associated with venous disorders

Aching

Tiredness, heaviness in legs

Pain: throbbing, burning

Cramping (nocturnal, post exercise)

Swelling (patient report)

Burning

Itching

Restless legs

Fig. 5.1 Telangiectasias (spider veins) of lower extremity

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N.M. Khilnani and N. Morrison

These ﬁ ndings may well change treatment rec-

ommendations for such patients and help prevent

poor cosmetic outcomes.

Venulectasias (Fig. 5.2 ) are dilated intrader-

mal veins which should raise the suspicion of

underlying venous incompetence even more than

telangiectasia, as this ﬁ nding is related to more

advanced venous hypertension.

Reticular varicosities (Fig.

5.3 ) indicate fur-

ther advancement of venous hypertension and are

described as dilated (1–3 mm) subdermal reticu-

lar veins blue-green in color [ 6 ] .

Corona phlebectasia (“blue crown”) (Fig.

5.4 )

is the ﬁ nding of telangiectasia or reticular vari-

cosities in the malleolar areas of the ankle and

is nearly pathognomonic of truncal incompe-

tence [ 8 ] . No patient with this ﬁ nding, whether

symptomatic or not, should undergo treatment

without a thorough duplex evaluation to uncover

the cause.

Varicose veins (Fig. 5.5 ) are familiar to medi-

cal providers and patients alike, the source of

which must be thoroughly investigated prior to

treatment in order to provide the patient the most

ef ﬁ cient, effective, and durable control of their

venous disease.

Edema (Fig. 5.6 ) associated with venous

insuf ﬁ ciency (sometimes referred to as “phle-

boedema” or “phlebolymphedema”) [ 9 ] must

be distinguished not only from other common

causes of lower extremity edema – cardiac, renal,

hepatic, obstructive, or drug-related, to name but

a few – but also from lipedema and lymphedema.

Lipedema does not characteristically involve

the foot, as do both lymphedema and edema of

venous origin, and is nearly always bilateral and

painful. A positive Stemmer’s sign (“pinch” skin

at base of 2nd toe) will help differentiate the

lymphedematous patient from the patient with

phleboedema.

Severe venous insuf ﬁ ciency can lead to pig-

mented skin changes (Fig. 5.7 ) in the distal lower

legs and ankles.

Acute lipodermatosclerosis (Fig. 5.8 ), often

mistaken for cellulitis, is an in ﬂ ammatory process,

not an infectious one. It may be precipitated by

a connective tissue or autoimmune disorder, but

is more frequently seen with worsening chronic

venous insuf ﬁ ciency and is frequently associated

with eczema, lymphorrhea and/or edema [

6 ] .

Absent appropriate treatment, this acute pro-

cess can eventually progress to chronic lipoder-

matosclerotic changes with discolored skin,

severely indurated skin and subcutaneous tissue,

and edema, and eventually ulcerations and atro-

phie blanche (Fig. 5.9 ).

Fig.5.2 Venulectasia posterior calf

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295 Clinical Evaluation of Patients with Chronic Lower Extremity Venous Disorder

Fig. 5.3 Reticular

varicosities posterior calves

Fig. 5.4 Medial malleolar

corona phlebectasia

indicative of underlying

venous insuf ﬁ ciency

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N.M. Khilnani and N. Morrison

Fig. 5.6 Edema right ankle – posterior view

Fig. 5.5 Patient with moderate varicose veins of truncal origin Fig. 5.7 Patient with advanced varicose veins and pig-

mented skin changes indicative of chronic venous

insuf ﬁ ciency

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