6 Venous Disorders

6.1 SUPERFICIAL VEIN THROMBOSIS

DEFINITION
Superficial vein thrombosis (SVT) is defined as thrombosis and inflammation
of inner walls of the greater or lesser saphenous veins or their tributaries.

ETIOLOGY
zz Trauma to the vessel wall—a drip needle or pressure externally due to tight
garments or position of a limb.
zz Circulating toxins from septic wounds.
zz In association with deep venous thrombosis (DVT).
zz It is associated with intravenous catheters and infusions.
zz Occurs with varicose veins.
zz Migrating SVT is often a marker for a carcinoma.
zz May also occur in patients with vasculitides, such as thromboangiitis
obliterans (TAO).

PATHOLOGY
Irritation produced changes in the tunica intima causing a thrombus to form.
The thrombus becomes attached to the vein wall and rarely produces an
embolus.

CLINICAL FEATURES
It can easily be distinguished from those of DVT. Patients complain of pain
localized to the site of the thrombus. Examination reveals a reddened, warm and
tender cord extending along a superficial vein. The surrounding area may be red
and edematous. As the condition resolves, the skin become pigmented (brown)
along the course of the vein.
 Venous Disorders 53

INVESTIGATIONS
Phlebography is used to find out the thrombosis.

TREATMENT
Treatment is primarily supportive:
zz Initially, patients can be placed at bedrest with leg elevation.

zz Application of compression bandage in the form of crepe bandage or stockings

from the toes to beyond the upper limit of the affected area.
zz Nonsteroidal anti-inflammatory drugs (NSAIDs) may be provided to relieve

pain and inflammation.

zz Antibiotics in case of infective phlebitis.

zz Anticoagulant therapy: If a thrombosis of the greater saphenous vein

develops in the thigh and extends toward the saphenofemoral vein junction
and to prevent extension of the thrombus into the deep system and a possible
pulmonary embolism.

6.2 DEEP VENOUS THROMBOSIS

DEFINITION
The presence of thrombus within a deep vein and the accompanying
inflammatory response in the vessel wall is termed as deep venous thrombosis
(DVT) or thrombophlebitis.

INCIDENCE
Deep vein thrombosis occurs less frequently in the upper extremity than in the
lower extremity, but the incidence is increasing, because of greater utilization of
indwelling central venous catheters.

ETIOLOGY
The factors that predispose to venous thrombosis were initially described by
Virchow in 1856 and include stasis, vascular damage and hypercoagulability.

RISK FACTORS
zz Recent surgery
zz Neoplasms
zz Trauma
zz Fractures
zz Immobilization
zz Acute myocardial infarction (MI), congestive heart failure (CHF), stroke
54 Vascular Rehabilitation
zz Postoperative convalescence
zz Pregnancy
zz Estrogen use (for replacement or contraception)
zz Hypercoagulable states
zz Previous DVT.

PATHOGENESIS
Damage to the intima causes platelets to be deposited on the vein wall. Venous
stasis increases the accumulation of platelets, which adds to the size of the
thrombus resulting in occlusion of the vessel lumen. Initially, the thrombus is
composed principally of platelets and fibrin. Red cells become interspersed
with fibrin and the thrombus tends to propagate in the direction of blood flow.
The inflammatory response in the vessel wall may be minimal or characterized
by granulocyte infiltration, loss of endothelium and edema. There is further
extension of the thrombus (propagated thrombus) along the vessel to the next
junction with a vein. A portion may break off giving rise to a pulmonary embolus
or the thrombus may become organized and firmly attached to the vessel wall.
Gradually, it is recanalized and circulation is re-established, but the valves are
often destroyed leaving chronic venous insufficiency (CVI).

CLINICAL FEATURES
zz Most common complaint is cramp-like pain in the calf.
zz Unilateral leg swelling (edema around the joint distal to the area).
zz Local warmth.

zz Erythema.

zz Tenderness may be present along the course of the involved veins.

zz Palpable cord.

zz Increased tissue turgor.

zz Distention of superficial veins.

zz Appearance of prominent venous collaterals.

zz In some patients, deoxygenated hemoglobin in stagnant veins impart a

cyanotic hue to the limb, a condition called phlegmasia cerulea dolens.

zz In markedly edematous legs, the interstitial tissue pressure may exceed

the capillary perfusion pressure, causing pallor, a condition designated as

phlegmasia alba dolens.
zz Unexplained systemic features, e.g. mild pyrexia, pleuritic pain, tachycardia

in a patient recovering from surgery.

zz Severe pulmonary embolus giving signs of extreme distress, breathlessness

and shock may be the first indication of DVT.

Examination may reveal posterior calf tenderness, warmth, increased tissue
turgor or modest swelling and rarely a cord. Cuff test, Homan’s sign and Mose’s
sign will be positive.

INVESTIGATIONS
zz D-Dimer, a degradation product of cross-linked fibrin is often elevated in
patients with venous thrombosis.
 Venous Disorders 55

zz Duplex venous ultrasonography: By imaging the deep veins, thrombus can be

detected either by direct visualization or by inference when the vein does not
collapse on compressive maneuvers.
zz The Doppler ultrasound measures the velocity of blood flow in veins. This
velocity is normally affected by respiration and by manual compression of
the foot or calf. Flow abnormalities occur when deep venous obstruction is
present.
zz Magnetic resonance imaging (MRI): It is useful in patients with suspected
thrombosis of the superior and inferior vena cava or pelvic veins.
zz Venography: Contrast medium is injected into a superficial vein of the foot
and directed to the deep system by the application of tourniquets. The
presence of a filling defect or absence of filling of the deep veins is required
to make the diagnosis.

DIFFERENTIAL DIAGNOSIS
Deep vein thrombosis must be differentiated from a variety of disorders that
cause unilateral leg pain or swelling, including muscle rupture, trauma or
hemorrhage; a ruptured popliteal cyst and lymphedema. It may be difficult to
distinguish swelling caused by the postphlebitic syndrome from that due to
acute recurrent DVT. Leg pain may also result from nerve compression, arthritis,
tendinitis, fractures and arterial occlusive disorders.

TREATMENT
zz Bedrest with a cradle and the end of the bed elevated (15–22 cm) until all the
local signs subside may be up to 7 days.
zz Anticoagulants prevent thrombus propagation and allow the endogenous lytic
system to operate:
—— This includes either unfractionated heparin or low-molecular–weight

heparin (LMWH).
—— A direct thrombin inhibitor, such as lepirudin or argatroban may be

used as initial anticoagulant therapy for patients in whom heparin is

contraindicated, because of heparin-induced thrombocytopenia (HIT).
—— Warfarin is administered during the first week of treatment with heparin

and may be started as early as the first day of heparin treatment.

zz Thrombolytics: Thrombolytic drugs such as streptokinase, urokinase and
tissue plasminogen activator (tpA) may also be used.
zz Vena cava filter (Greenfield filter): To prevent pulmonary embolism.

PROPHYLAXIS
Prophylaxis should be considered in clinical situations where the risk of DVT is
high.
zz Low-dose unfractionated heparin (5,000 units 2 h prior to surgery and then

5,000 units every 8–12 h postoperatively).

zz Warfarin.
56 Vascular Rehabilitation
zz External pneumatic compression (TED antiembolic stockings) applied to the
legs are used to prevent DVT.

COMPLICATIONS
zz Pulmonary embolism
zz Chronic venous insufficiency.

6.3 VARICOSE VEINS

DEFINITION
Varicose veins are dilated, tortuous superficial veins that result from defective
structure and function of the valves of the saphenous veins.

INCIDENCE
zz The most common in 40–50 years
zz Females are more affected than males.

TYPES
Varicose veins can be categorized as primary or secondary. Primary varicose
veins originate in the superficial system and occur two to three times as frequently
in women as in men. Approximately half of patients have a family history of
varicose veins. Secondary varicose veins result from deep venous insufficiency
and incompetent perforating veins or from deep venous occlusion causing
enlargement of superficial veins that are serving as collaterals.

ETIOLOGY
zz Failure of development of valve in the vein
zz Damage to the valve due to thrombosis
zz From intrinsic weakness of the vein wall
zz From high intraluminal pressure
zz Rarely from arteriovenous fistulas.

PREDISPOSING FACTORS
zz Pregnancy:
—— Compression of pelvic vein due to enlarged womb (Fig. 6.3.1)

—— Estrogens relax the muscles in the veins and this also increases the

tendency of the veins to expand.

zz Occupation necessitating constant standing, e.g. shop assistant, traffic police,
teachers, etc.
 Venous Disorders 57

Fig. 6.3.1 Uterus pressing the pelvic veins

zz Low-fiber diet, which results in constipation. If the bowel is loaded with

constipated stool it compresses the large (iliac) veins in the pelvis, which in
turn dilates the veins of the leg.
zz Constipation: Staining during constipation builds up pressure and transmits
the pressure to the legs. This increased pressure build-up in the leg veins
over the years will lead to a deterioration of the valves and hence, will lead
to varicose veins.
zz Tight corsets or garters.
zz Contraceptive pills which have estrogen.
zz Family history.
zz Secondary to DVT.

PATHOLOGY (FIG. 6.3.2)

The vein wall dilates at weak areas and the valves become incompetent. Normally
as the calf muscle contracts, there is pressure on deep veins which forces
the blood proximally. This pressure is not transmitted to the superficial
veins, because of valves in communicating veins. When these valves become
incompetent the pressure pushes the blood into a superficial vein, which
dilates and lengthens. A vicious cycle is set up, the ineffectual valves permitting
regurgitation and the increasing amount of blood thus left in the veins still
further dilating them and making the valves more incompetent.
During standing, the force of gravity tends to keep the blood in lower parts
of the body, aggravating the condition. There is loss of elastic tissue, muscle
atrophy of the media layer and hypertrophy of the outer layer. Dilated veins
and abnormally high pressure in the capillaries increases exudation of lymph,
which results in edema.
58 Vascular Rehabilitation

Fig. 6.3.2 Varicose vein caused by valve failure

CLINICAL FEATURES
zz Patients with venous varicosities are often concerned about the cosmetic
appearance of their legs.
zz Patient may complain of a dull ache, pain or pressure sensation in the legs

after prolonged standing; it is relieved with leg elevation.

zz Fatigue in the legs with difficulty in walking.

zz Cramp in the calf muscles, especially at night.

zz The legs feel heavy and mild ankle edema develops occasionally.

zz The skin of the leg may become pigmented and indurated (Figs 6.3.3A and B).

zz Extensive venous varicosities may cause skin ulcerations near the ankle.

zz Superficial venous thrombosis may be a recurring problem.

zz Rarely, a varicosity ruptures and bleeds.

Visual inspection of the legs in the dependent position usually confirms the
presence of varicose veins.

INVESTIGATIONS
zz Doppler ultrasound scan: It can easily identify reflux or back-flow of blood in
the veins.
zz Varicogram: A cuff will be placed around the lower calf and the dye injected
into the veins on the back of the foot. Usually, the site of connection of
the varicose vein to the deep venous system need to be identified and the
 Venous Disorders 59

A B
Figs 6.3.3A and B (A) Varicose vein on female’s leg, black arrows: dilated vein;
white arrow: skin changes; (B) Varicose vein on female’s thigh, white arrow: spider vein

Fig. 6.3.4 Varicose veins caused by deep vein damage

needle is then placed within the varicosity. If the test is done to look at
whether the valves in the leg are working, the needle may be placed either
in the foot or in the groin, and the table will be tilted to see if the dye passes
backwards through the valves (Fig. 6.3.4).
60 Vascular Rehabilitation

CONSERVATIVE TREATMENT
zz External compression stockings has to be worn which provide a counter­
balance to the hydrostatic pressure in the veins.
zz Walking is encouraged.
zz Avoid prolonged standing.
zz Symptoms often decrease when the legs are elevated periodically.
zz Laser therapy: The laser pulse is of a very short duration and destroys the
veins, which are broken into very small particles. These are then removed
by the body’s immune system. There may be some reaction to the laser for
the first 24 hours, with redness at the site, but this resolves quite quickly.
This treatment is given on an out-patient basis and does not require any
anesthesia. The complications of this therapy include pigmentation at the
site and loss of pigment at the site. There is usually loss of hair growth in
the area if the laser treatment is repeated. Very occasionally, there may be
some crusting of the skin together with blistering. But these side-effects do
not last long.
zz Endovenous obliteration of the saphenous vein: A newer treatment for
varicose veins is to insert a long, thin catheter that emits energy (most
commonly heat, radiowaves or laser energy). The released energy collapses
and scleroses the vein. A variety of techniques and protocols are used.
Because it is easier to insert a catheter through a vein in the same direction
that the valves open, the catheter is most commonly inserted into a more
distal portion of the vein and threaded proximally. Energy is released from
the catheter tip. As the catheter is pulled out, the vein lumen collapses.
Bruising, tightness along the course of the treated vein, recanalization and
paresthesia are possible complications.

SURGICAL MANAGEMENT
Surgical therapy may also be indicated for cosmetic reasons:
zz Sclerotherapy: It is a procedure in which a sclerosing solution is injected

into the involved varicose vein and a compression bandage is applied.

The sclerosant solution produces inflammation in the vein so that no blood
can pass through causing the lumen to be obliterated.
zz Surgical therapy usually involves extensive ligation and stripping of the

greater and lesser saphenous veins and should be reserved for patients,
who are very symptomatic, suffer recurrent superficial vein thrombosis,
and/or develop skin ulceration.

COMPLICATIONS
zz Hemorrhage: Bleeding following rupture of a vein.
zz Ulceration: Venous ulcer due to devitalized skin.
zz Phlebitis: Superficial venous thrombosis.
zz Edema particularly of the foot and ankle.
zz Pigmentation.
 Venous Disorders 61

6.4 PULMONARY EMBOLISM

DEFINITION
The term ‘pulmonary embolism’ implies clinically significant obstruction of a
part or the whole of the pulmonary arterial tree, usually by thrombus that
becomes detached from its site of formation outside the lung and is swept
downstream until arrested at points of intrapulmonary vascular narrowing.

TYPES
zz Thrombotic pulmonary embolism
zz Nonthrombotic pulmonary embolism.

Thrombotic Pulmonary Embolism

As a complication of deep venous thrombosis: If a thrombosis breaks off in a
deep vein it travels in the venous system to the right side of the heart, where it
enters the pulmonary artery and passes into the pulmonary circulation where
it blocks a vessel, the lumen of which is too narrow to let it pass through.
The factors that predispose to a deep vein thrombosis also predispose to a
pulmonary embolism. Stasis being the most important initiating factor in
initiating and venous thrombi rather than any damage to vessel wall.
Other: A small proportion of pulmonary emboli may arise from the pelvic veins
including the prostatic venous plexus in men and also from the right side of the
heart (following myocardial infarction and in right ventricular failure).
Septic pulmonary emboli may arise from bacterial endocarditis in patients
with septal defects, from the tricuspid valve in drug abusers, and from foreign
material such as central venous lines, ventriculoatrial and arteriovenous shunts,
internal cardiac defibrillators and pacemaker wires.

Nonthrombotic Pulmonary Embolism

Fat embolism: It is probably a common subclinical event following bony trauma.
Following such trauma, neutral fat may pass into the circulation from injured long
bones, be carried to the lungs and become lodged in the pulmonary vasculature.
Tumor emboli: Pulmonary vessels are occluded by macroscopic emboli, but it
differs in its lack of responsiveness to anticoagulation. Tumors that have been
implicated most frequently include carcinoma of the breast, stomach, colon and
cervix, hepatomas, choriocarcinomas and hypernephromas.
Air embolism: It may be the result of faulty cannulation of the neck veins,
therapeutic insufflation of air into a fallopian tube or intrauterine manipulations,
including criminal abortion in which a frothy solution may be introduced into
the uterus under pressure. Small amount of air are reabsorbed without harm,