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and the perforating veins connecting the two. All these veins have valves with the
exception of soleus venous sinuses. Valves are more numerous in the deep veins and
increase in number progressively from proximal to distal in keeping with greater
hydrostatic pressures in the lower part of the leg. The valves prevent retrograde flow into
the superficial veins, reduce the venous pressure in the superficial and deep systems in
the upright posture and aid in the venous return against gravity by the calf muscle pump.
The superficial venous system consists of an extensive plexus of venules and veins
beneath the skin and the long saphenous vein (LSV) and the short saphenous vein (SSV)
that run on the deep fascia.
Long Saphenous Vein
The LSV (Fig. 1), the longest vein in the body, commences from the medial marginal vein
of the foot and ascends about 2.5–3 cm anterior to the medial malleolus, crosses the distal
third of the medial surface of the tibia obliquely, and runs upwards behind its medial
border to the knee; here it is posteromedial to the medial tibial and femoral condyles
(a hand’s breadth behind the medial border of the patella) and then ascends slightly
forward across the medial aspect of the thigh and passes through the cribriform fascia
covering the saphenous opening to join the femoral vein. It is often duplicated, more
frequently distal to the knee. The surface marking of the sapheno–femoral junction is
1–1.25 inches (2.5–3.5 cm) below and lateral to the pubic tubercle and a line drawn from
this to the femoral adductor tubercle represents the LSV.
Figure 1 Long saphenous vein (LSV): (1) LSV; (2) common femoral vein; (3) saphenous
opening. (a)–(e) Terminal tributaries of the LSV encountered at groin dissection.
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Tributaries. The LSV drains the sole via the medial marginal veins. In the leg, it
connects with the upper of the three ankle perforating veins. Just below the knee, the LSV
receives a vein from the posterior calf communicating with the SSV, the anterior vein of
the leg and the posterior arch vein of Dodd and Cockett formed by the union of the venous
arches connecting the three ankle perforating veins (also called Leonardo’s vein).
Perforating veins join the LSV or its main tributaries in the upper calf (tibial tubercle or
Boyd’s perforator), in the distal thigh (Dodd’s perforator) and in the mid thigh (Hunterian
perforator). In the thigh, the LSV receives several small tributaries. Two large veins—
posteromedial and anterolateral—join the LSV close to its termination. Near its
termination, the LSV receives the superficial circumflex iliac, superficial epigastric, and
superficial and deep external pudendal veins. The LSV is connected to the SSV via
common tributaries in various segments of the leg.
Short Saphenous Vein
The SSV (Fig. 2) begins behind the lateral malleolus as a continuation of the lateral
marginal vein. It ascends in the lower third of the calf lateral to tendo achilles lying
on the deep fascia. In the middle third, it inclines medially to the midline and enters an
intrafascial compartment in the aponeurotic investment of the gastrocnemius muscle, and
in the upper third it penetrates the deep fascia passing between the heads of the
gastrocnemius to enter the popliteal fossa and usually drains into the popliteal vein above
the skin crease of the knee joint. Its termination however is variable, and it may terminate
above, below, or at the level of the knee and may join the popliteal vein, LSV, deep
posterior femoral veins, or deep sural muscular veins. The sural nerve closely follows the
SSV on its lateral aspect in its lower third. At its termination in the popliteal fossa, the SSV
Figure 2 Short saphenous vein (SSV) (1) and popliteal vein (2).
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is closely related to the medial popliteal nerve. Its deep situation renders
the vein inconspicuous even when markedly varicose. The lateral or external ankle
perforating vein at the junction of the lower and middle third of the calf joins the SSV to
the peroneal vein and sometimes a mid-calf perforating vein connects it to the
soleus sinusoids.
Deep Veins
The deep veins are those accompanying the major arteries, the gastrocnemius veins and
the soleus venous arcades and sinusoids which are the main collecting chambers of the
calf-muscle pump.
Perforating Veins
These connect the deep veins to the superficial veins or their tributaries and are valved
such that blood flows only from the superficial to the deep veins.
Upper Limb
The superficial veins in the upper limb are the cephalic and basilic veins. The former runs
along the lateral aspect of the forearm and arm and terminates in the axillary vein. The
latter runs along the medial aspect of the forearm and then accompanies the brachial
artery, finally joining the brachial vein to form the axillary vein. At the outer border of the
first rib the axillary vein continues as the subclavian vein which joins the internal jugular
vein to form the brachiocephalic vein.
VENOUS PHYSIOLOGY AND PATHOPHYSIOLOGY
Knowledge of the physiology of venous return is crucial to the understanding of the
fundamental factors responsible for the development of chronic venous hypertension and
the changes that accompany it. In the supine position the venous return occurs evenly
along the superficial and deep veins propelled by the capillary hydrostatic pressure (about
20 mmHg). In the erect posture the main mechanism of venous return is the muscle pump
or “peripheral heart” (9). The venous drainage of the superficial tissues in the erect
exercising leg is inwards to the deep veins via the perforating veins.
Calf-Muscle Pump (Musculo-Venous Pump)
The valved intra- and inter-muscular deep veins constitute a series-parallel arrangement
of reciprocating pumps (10). The chambers of the pump receive blood from the distal
deep veins and plantar veins aided by the foot pump during walking, from the superficial
veins via the ankle perforators, but the greatest supply is from the muscle capillary bed.
The tight deep fascia that invests the calf muscles causes high pressure within the
musculo-fascial compartment during muscle contraction, forcing the venous blood
upward against the hydrostatic pressure gradient. The pump also reduces the mean
hydrostatic pressure both in the superficial and deep veins which, in turn, increases the
arteriovenous pressure gradient in the tissues and facilitates arterial inflow in the
exercising limb. Thus the “peripheral heart” achieves a substantial increase in peripheral
blood flow with a modest energy input than the alternative of a significant increase in
cardiac output. During muscle relaxation, the superficial venous pressure also falls and
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blood is sucked in from the superficial tissues into the deep veins through the perforating
veins. Thus the skin of the lower leg is protected during exercise against
venous hypertension by the ability of the musculo-venous pump to lower the superficial
venous pressure at the ankle and the competence of the valves in the perforating veins
that maintain unidirectional flow into the deep veins.
Ambulatory Venous Hypertension and Leg Ulceration
Chronic venous insufficiency (CVI) results from venous obstruction or reflux, calf
muscle pump dysfunction or a combination of these factors. The effect of venous
incompetence is to prevent the fall in superficial venous pressure during exercise. This is
called ambulatory venous hypertension and is the main cause of leg ulceration. Patients
with an ambulatory venous pressure (AVP) of less than 40 mmHg have a minimal
incidence of venous ulceration compared with an 80% incidence of ulceration in those
with an AVP of greater than 80 mmHg (11). Incompetence of the deep veins has a more
severe effect on the skin around the ankle than does superficial venous incompetence.
Reflux in the popliteal and infrapopliteal veins is more important than proximal deep
reflux to the development of advanced CVI (12). However, signs of CVI, including
ulceration, can result from superficial incompetence alone (13–17).
RISK FACTORS
The most important risk factors for primary varicose veins are female sex, a family history
of varicose veins and a history of phlebitis (18). Increasing age (19), Caucasian race,
prolonged standing and pregnancy are also reported as risk factors. Progesterone secreted
from the corpus luteum inhibits smooth muscle contractility causing relaxation of the vein
wall, which may cause varicose veins to appear in the first trimester of pregnancy in the
presence of inherent predisposition.
The principal risk factors for venous ulceration are age, male sex, obesity and
a history of deep vein thrombosis and serious lower extremity trauma (18).
The important risk factors for deep vein thrombosis are prolonged immobilisation,
recent surgery, trauma, malignancy, age, hypercoagulable states, pregnancy, oral
contraceptive pill and a history of venous thromboembolism.
SYMPTOMATOLOGY
Symptoms of venous disease are usually non specific and it is often the accompanying
physical signs that help to confirm the diagnosis. Symptoms do not correlate well with the
presence, size or extent of varicosities. They are often worse towards the end of the day or
after prolonged standing or walking and are usually relieved by elevation of the leg. This
is a characteristic feature of venous disease and helps to differentiate it from other causes
of leg pain arising from arterial, neurologic or musculoskeletal pathology. Relief of
symptoms with compression stockings may indicate that they are of venous origin. A poor
cosmetic appearance is often the only complaint. Not infrequently, complications of the
disease such as superficial thrombophlebitis, haemorrhage or ulceration may be the first
manifestation. Even in the presence of varicosities, many lower limb symptoms have a non
venous cause and surgical treatment is unlikely to ameliorate symptoms in these patients
(20). Nevertheless, a careful evaluation of the presenting symptoms may yield valuable
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diagnostic clues. The three most common symptoms of venous disease are pain, swelling
and changes in the skin of the lower leg, particularly ulceration.
Pain
Aching pain is quite common in patients with varicose veins and is due to direct pressure
of the distended veins on the adjacent somatic nerves. Hence this pain is usually localized
to the site of varicosities. Symptoms such as ache, discomfort, heaviness, tightness or
fatigue in the leg that are poorly localized usually result from valvular incompetence.
Proximal venous outflow obstruction produces a characteristic “bursting pain” in the leg
on exercise that is not relieved quickly by rest. This is due to sudden venous hypertension
from exercise-induced hyperemia and outflow resistance and is called venous
claudication. Apart from this claudication, severe pain is unusual in venous disease.
Thrombophlebitis causes pain and tenderness along the length of the involved superficial
or deep vein.
Swelling
The causes of leg swelling are outlined in Table 1. The most common cause is venous
hypertension. The associated skin changes around the ankle and the pattern of distribution
of the edema often help in the diagnosis. In primary uncomplicated varicose veins ankle
swelling is uncommon, and when it appears is mild and more pronounced toward the
end of the day. Acute onset of edema is associated with sudden venous outflow obstruction.
Ankle edema is more typical of CVI and is often the first manifestation of the post-phlebitic
limb. This venous edema is typically brawny, predominantly affecting the lower part of
the leg and the ankle and tends to spare the feet. It is characteristically associated with
skin changes of chronic venous hypertension. It usually involves one limb more than the
other and is relieved by elevating the leg. Varicose veins may or may not be present.
Table 1 Causes of Leg Swelling
Local Systemic
Venous incompetence Hypoproteinemia
Deep veins Secondary hyperaldosteronism
Perforating veins Right heart failure
Superficial veins
Venous outflow obstruction
Intraluminal
Extraluminal
Calf muscle pump dysfunction
Intrinsic muscular disease
Neurologic disease
Joint disease or surgery
Lymphedema
Primary
Secondary
Cellulitis
Posture dependent
Physiologic
Ischemic limb
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Lymphedema usually involves the feet first and spreads proximally. It is not brawny in
nature; and in advanced cases the skin is often hypertrophic, thickened, and folded over
rather than atrophic, resembling an elephant hide, hence the term “elephantiasis.” Failure
to pinch a fold of skin at the base of the second toe is characteristic of lymphedema—
Kaposi-Stemmer sign (21). The edema from systemic disease characteristically pits on
pressure and the surrounding skin is normal. It is usually generalised and symmetrically
affects both legs.
Ulceration
The causes ofleg ulceration are outlined in Table 2.The common causes are chronic venous
hypertension, ischemia or neuropathy. The underlying cause can usually be diagnosed from
the site and appearance of the ulcer, i.e., from inspection. Venous ulceration typically affects
the lower third of the leg, the so called “gaiter area,” in the vicinity of the medial malleolus
and is always associated with the skin changes of chronic venous hypertension. The ulcer is
painful initially but when it becomes chronic the severity of pain subsides. It is usually
shallow with its floor covered by granulation tissue and the base fixed to the deeper tissues.
Long-standing ulcers may cause an equinus deformity of the ankle joint. A chronic ulcer
with raised, thickened or rolled irregular edges and associated with inguinal adenopathy
suggests malignant change and is known as Marjolin’s ulcer. Ischemic ulcer on the other
hand usually affects the most distal part of the extremity and is associated with continuous
rest painthat is relieved by dependency. Neuropathic ulcersusually occur at pressure points
and are associated with some degree of sensory deficit.
SKIN CHANGES OF CHRONIC VENOUS INSUFFICIENCY
Chronic venous hypertension induces characteristic changes in the skin and subcutaneous
tissues above the ankle or the “gaiter area” (Fig. 3). The sustained high venous pressure at
the ankle forces red blood cells out of the skin capillaries, where the hemoglobin is broken
Table 2 Causes of Leg Ulceration
Venous insufficiency
Primary
Secondary
Arterial insufficiency
Neuropathy
Central nervous system
Peripheral nervous system
Malignancy
Cutaneous
Hematologic
Miscellaneous
Infections
Vasculitis
Connective tissue disorders
Hypertension
Hemolytic anemia
AV malformations
Pyoderma gangrenosum
Traumatic
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down to hemosiderin giving rise to a brown pigmentation of the skin. This is an early sign
of skin injury. Eczema may develop as a dry, pigmented, scaly patch over enlarged varices
or over the malleolar area. Exudation of protein-rich fluid and red blood cells sets up an
inflammatory reaction in the subcutaneous tissues leading to fibrosis of the skin and
subcutaneous tissues. This is called lipodermatosclerosis and may be the precursor
of ulceration. The combination of a narrow ankle and prominent calf gives the appearance
of an inverted “champagne bottle.” Reductions in capillary numbers in areas of prior
ulceration causes white patches in the skin called atrophie blanche (22). In primary
uncomplicated varicose veins, eczema with pigmentation is usually confined to the skin
overlying prominent varicosities.
ACUTE PRESENTATIONS OF VENOUS DISEASE
Superficial Thrombophlebitis
The affected vein is painful and is felt as a firm, palpable, tender cord with signs of
localized inflammation. It may result from trauma, cellulitis, varicose veins, intravenous
infusions, polycythaemia, autoimmune diseases like Behcet’s syndrome, thromboangiitis
obliterans, or Buerger’s disease, or it may be idiopathic. Occasionally, the thrombus may
extend to involve the adjacent deep vein. Episodes of thrombophlebitis that are transient
and recur spontaneously at different sites is called phlebitis migrans and may indicate an
occult malignancy.
Deep Vein Thrombosis
This can occur with or without demonstrable risk factors. The majority of cases of
deep vein thrombosis (DVT) are clinically silent. 75% of outpatients who present with
clinical features suggestive of DVT do not have the disease (23). In the majority of cases,
the thrombus originates in the calf veins and either spreads proximally or remains
localized to the calf. A more proximal origin of thrombus may occur following pelvic or
hip surgery or trauma. The more proximal the extension of thrombosis, the more severe
the symptomatology.
Figure 3 Chronic venous ulceration with pigmentation and lipodermatosclerosis. (See color
insert.)
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Clinical features cannot be relied upon to make a correct diagnosis (24,25). Pain or
swelling in the leg, or low-grade pyrexia in a post-operative setting, should arouse
suspicion. Pain and tenderness usually indicate significant associated inflammation. The
onset is fairly sudden, and in an ambulant patient pain is severe enough to limit walking.
Fullness ortightness of the calf is acommon complaint. Significant outflow obstruction will
cause a ‘bursting’ pain in the leg when attempting to walk called venous claudication.
Associated pulmonary embolism may produce symptoms of pleuritic pain, dyspnea,
haemoptysis or collapse. One or more of the following signs may be elicited on careful
examination. However, rough manipulation can dislodgea clot with resultant embolisation.
† Swelling of the leg is the most significant and sometimes the only sign. Its
distribution depends on the extent of thrombus. Ankle edema is pitting in nature.
† Dilated veins are seen over the dorsum of the foot and across the front of tibia.
† Muscles that contain the thrombosed veins feel hard and stiff and are tender.
† The entire course of the deep veins from behind the medial malleolus to the groin
should be palpated for tenderness.
† Homan’s sign: If the posterior tibial veins are involved, dorsiflexion of the foot
exerts traction on them to produce calf pain.
† Bancroft’s sign: If the posterior tibial veins are involved, tenderness can be
elicited by pressing forwards the main muscle belly of the calf forwards but not
from side to side.
Duplex ultrasonography is the imaging modality of choice in clinically suspected
DVT. However Wells et al. have shown that DVT can be ruled out in patients with a low
clinical probability of DVT and a negative d-dimer test (26). Ultrasound testing can be
safely omitted in such patients.
Extensive thrombosis involving all the major venous channels in the leg is
characterized by a massively swollen, painful and tender limb that is cold and pale. This
condition is called phlegmasia alba dolens (white leg; milk leg). The femoral artery may
go into spasm, and this, along with the overlying edema, makes it difficult to feel the
femoral pulse and then it may be confused with acute ischemia especially in the initial
stages. When the thrombosis extends to involve the collateral venous channels to cause
complete venous outflow obstruction, the condition is called phlegmasia cerulea dolens
(blue leg). Venous gangrene ensues when the thrombosis involves even the small veins
and capillaries and the high venous pressure and edema significantly reduces arterial
inflow into the limb (27).
Axillary vein thrombosis follows unusual and excessive use of the arm above head
or extrinsic compression of the vein by pathology in the axilla or thoracic outlet. The
clinical features are similar to DVT affecting the lower limb.
OUTPATIENT CLINICAL ASSESSMENT
Venous disease may result from reflux disease, outflow obstruction or both. The aim
of clinical assessment is to detect and localize it and possibly identify the causative or
pre-disposing factor (Table 3). Quantification of the underlying pathophysiology requires
special investigations but is not necessary in all cases. The continuous wave hand-held
Doppler probe has become an indispensable adjunct to clinical assessment and has largely
replaced traditional examination methods using a tourniquet. Duplex ultrasonography
helps to detect the underlying pathophysiology and to assess the severity and extent of the
disease process, factors that are vital in choosing the most appropriate form of treatment.
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History and physical examination are, however, important in clinical assessment and often
help to choose the most appropriate test for further assessment.
History
A young patient with varicose veins with no history of deep vein thrombosis or positive
family history usually indicates primary disease. The following points should be recorded
meticulously:
† Age and sex of the patient—Varicose veins or venous ulceration in the very
young suggest a congenital abnormality.
† Presenting complaint—pain, ache, heaviness of the legs, ankle swelling, night
cramps, restlessness, heat or burning sensation, throbbing, itching, pins and
needles or tingling sensation, cosmesis, etc.
† Duration and mode of onset—Swelling often precedes the onset of varicose
veins in the post-phlebitic limb.
† Aggravating factors—prolonged standing or walking, worse towards the end of
the day.
† Relieving factors—leg elevation, compression stockings.
† History of complications of the disease—thrombophlebitis, bleeding, ulceration.
† Details of previous treatment.
† History of deep vein thrombosis, swelling or significant trauma to the leg, or
leg fracture.
† History of thrombophilia.
† The type of occupation, overall health status, way of life and the impact of the
problem on activity and life style.
† History of abdominal or pelvic symptoms and pregnancy status if a secondary
cause for varicose veins is suspected.
† Family history of varicose veins or deep vein thrombosis or thrombophilia.
Physical Examination
This is best done in the standing position. Comparison of the two limbs may be useful.
Both lower limbs are exposed from the umbilicus to the toes and inspected over the
Table 3 Causes of Varicose Veins
Primary—unknown cause, often familial
Secondary
Reflux disease due to valve destruction, dysfunction or both following recanalization of deep vein
thrombosis causing deep, perforator or superficial vein incompetence
Nonthrombotic venous outflow obstruction
Pelvic tumors—benign or malignant
Pelvic lymphadenopathy
Pregnancy
Thrombotic venous occlusion
Rare causes
Arteriovenous fistulae
Klippel-Trenaunay syndrome
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front and the back. Examination is carried out methodically by inspection, palpation,
ausculation and insonation.
Inspection
† Distribution of varicosities: This may indicate the superficial venous system
involved. Varicosities in unusual areas such as the pubis or the lower abdominal
wall or bilateral varicose veins should raise the possibility of secondary varicose
veins due to deep venous obstruction. Incompetent perforating veins may
produce a characteristic bulge along the varicosity.
† Presence of telangiectases (also known as thread veins or dermal flares) or
reticular veins both of which can be signs of venous dysfunction.
† Ankle swelling—mild edema can be detected by comparing with the other leg.
† Skin changes of chronic venous insufficiency in the lower third of the leg, e.g.,
pigmentation, eczema, lipodermatosclerosis, healed or active ulceration,
atrophie blanche.
Palpation
Many clinical tests to assess venous disease have been described. These include the cough
impulse test and the percussion or tap sign to detect groin reflux and long saphenous vein
incompetence, Brodie-Trendelenburg test using single or multiple tourniquets to detect the
site or sites of superficial venous reflux, Fegan’s method of seeking the sites of perforators
and Perthe’s test for patency of the deep veins (21,28). Although these tests are based
on the anatomical and physiological principles underlying the development of venous
disease, they have been largely replaced by the hand-held Doppler because of its ease of
use and the accuracy and extent of information that can be obtained. The principles of
testing, however, remain the same. A palpation of the leg is routinely performed prior to
Doppler testing.
† Palpate the texture of the skin and subcutaneous tissues of the lower leg and for
any tenderness or pitting edema.
† Palpate over the varicosities for tenderness and along the course of the long and
short saphenous vein. Varicose veins may be felt lying in a subcutaneous gutter
when they are not visible.
† Palpate the peripheral pulses, as venous and arterial disease of the lower limb
often co-exist, especially in the elderly.
† Examine the innervation of the leg, if there is ulceration.
† Palpate for inguinal lymphadenopathy if there is chronic ulceration, particularly
if there is suspicion of malignant change.
† Examination of the abdomen should be performed (including a rectal and
vaginal or testicular examination when an intra-abdominal or pelvic pathology is
suspected).
Auscultation
Varicosities that remain prominent on lying down may indicate an underlying
arteriovenous fistula and ausculatation may reveal the characteristic “machinery” murmur.
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