Overview Risk factor Diagnosis Conservative treatment Interventional Treatment Surgical Treatment

Venous incompetence

This is generally overlooked by most people and there is under-appreciation of the problem.

The common manifestation of CVI is dilated veins – telangiectases, reticular and varicose veins.

Visible Veins
Reticular veins
Visible Veins
Varicose veins



CVI affects the venous system of the legs with venous hypertension responsible for leg pain, swelling, skin changes, and ulceration.

Varicose veins have incompetent valves with increased venous pressure leading to progressive dilatation and tortuosity.


  • Varicose veins are estimated as 5-30% in the adult population.
  • Male to female predominance is 1:3. However recent studies show male to predominate over females especially over 50 years where the male incidence was 21.2% and female only 12%.
  • CVI increases with age and there is no sex difference.

Risk factors associated with CVI Include:

  • Age
  • Sex
  • A family history of varicose veins.
  • Obesity
  • Pregnancy
  • Phlebitis
  • Previous leg injury.
  • Standing and sitting for long periods of time.

Venous ulcers

  • The incidence of ulcers is 1% in the population. 20% of these develop venous ulcers. The prognosis of ulcers is poor with recurrence and delayed healing.
Varicose ulcer
Varicose ulcer
  • 50% of the venous ulcers need prolonged therapy lasting over 1 year.
  • The socioeconomic impact is dramatic with impaired ability to socialize thus reducing the quality of life and being a financial burden on the patient.
  • There is a loss of work productive hours which is over 2 million workdays/year.
  • The patient may take early retirement seen in 12.5% of the people with ulcers.
  • It is a tremendous burden on the health care system being over $ 3 billion annually.

Venous pathophysiology

Normal venous anatomy and function

The peripheral venous system is a reservoir and a conduit to return blood to the heart.

The proper functioning of the peripheral venous system depends on a series of muscle pumps and valves.

Vein anatomy in the lower limb
Normal vein anatomy in the lower limb

The blood in the lower limbs must return to the heart against the pull of gravity and against fluctuating those abdominal pressures to return to the heart while the patient is erect.

The veins of the lower limbs are either superficial or deep which are connected through a series of perforating veins.

The superficial veins are located above the muscle fascial plane. They are an interconnecting network which is the primary collecting system and return the blood to the deep system through multiple truncal veins. The main veins of the superficial system are the long and the short saphenous veins which run from the ankle and join the deeper veins – femoral vein in the groin (Sapheno-femoral junction) and the popliteal behind the knee (saphenopopliteal junction). Other superficial veins, including the posterior arch – lateral accessory saphenous and vein of Giacomini can also develop defects leading to CVI.

The deep venous system is located below the muscular fascia and is the collecting system and the outflow of the leg. This consists of the axial veins which follow the course of the major arteries in the leg and the intramuscular veins. Venous sinusoids within the leg muscles join to form the intramuscular venous plexi. Paired calf veins combine to form the large popliteal vein which passes through the adductor canal accompanying the artery and is called the superficial femoral vein. This is joined by the profound femoris vein and forms the common femoral vein. And continues as the external iliac vein.

The superficial veins are connected with the deep veins by perforating veins and pass through the anatomic fascial spaces.

A series of bicuspid valves are located in the superficial and the deep venous systems to see blood moved in the upward direction towards the heart against gravity pull and does nor reflux downwards. The first of these valves are located in the common femoral vein and rarely in the external iliac vein. The frequency of these valves increases from proximal to the distal part of the leg to prevent an increase in pressure at the ankles due to gravity pull. Perforating valves also contain valves in one direction, directing blood from the superficial to the deep.

The valves work in coherence with the muscles of the calf, thigh, and foot. Muscular contraction squeezes the delicate venous sinusoids forcing blood into the veins. The valve system makes sure the blood is forced in only an upward direction and not reversely. Soon after ambulation, the pressure in the leg veins is low (15-30 mmHg) because the muscles have emptied the venous system. Muscular relaxation then allows blood to fill the venous sinusoids via arterial flow through the superficial and deep venous systems.

Deep Veins
Deep veins within the muscles and superficial veins above towards the skin connected by perforator passing within the muscle

In prolonged standing veins slowly fill and become distended making valves separate and increasing the pressure that is directly proportional to the height of the blood column. Contraction of the muscle pump empties the veins and reduce venous pressure.

Calf muscle pump
The venous system and the calf muscle pump.


  1. normal venous pressure. The standing venous pressure is 80 —90 mmHg. With exercise, the calf pressure drops to 20 – 30 mmHg (> 50% decrease). The return pressure is more gradual and takes > 20secs.
  2. Abnormal pressure with deep vein reflux. The drop pressure with exercise is blunted (< 50% decrease). The return venous pressure to resting level is rapid because of a short refill time (< 20 sec).

Venous pathophysiology and dysfunction

  • Venous diseases occur when venous pressure is increased which impairs the return of blood through various mechanisms which include:
  • Valvular incompetence of the deep, superficial or perforator systems.
  • venous obstruction (DVT)
  • Combination of the above
  • Muscle pump dysfunction
Deep vein thrombosis
Deep vein thrombosis
Venous valve incompetence
Venous valve incompetence
  • These all produce venous hypertension on standing or ambulation. This disturbance in the microcirculation brings about changes in the microcirculation.
  • Prolonged venous hypertension may lead to hyperpigmentation, subcutaneous tissue fibrosis (lipodermatosclerosis)  and eventual ulceration.
  • In deep valve failure, normal blood volume is pumped out of the leg but refill occurs by both arterial flow and pathological retrograde flow. The venous pressure immediate after ambulation may be normal or elevated but veins refill quickly and high venous pressure occurs without muscle contraction. The valves are damaged mostly due to past DVT.
  • The incompetence of the valves may be a congenital primary defect due to weakness in the wall or valve leaflets or secondary to direct injury, superficial phlebitis of excessive venous distention due to hormonal effects or venous hypertension.
  • Failure of the valves located at the deep and superficial vein junctions as sapheno-femoral and saphenopopliteal junctions allows high pressure to be transmitted from the deep to the superficial venous systems resulting in varicose veins.
  • High pressure from the deep system can also be transmitted to the superficial system via the perforator valve incompetence. This is aggravated by the contraction of the muscle pump of the legs. The high pressure generated in the superficial veins results in valve incompetence. This is responsible for reflux in the superficial and deep venous systems.
  • Obstruction of the deep veins may result in rising in pressure with contraction of the muscles and secondary muscle pump dysfunction. The obstruction may occur due to the previous DVT with inadequate recanalization, venous stenosis or due to external compression (May-Thurner Syndrome with compression of the left common iliac vein as it passes between the right common iliac artery and the limbo-sacral region). Venous outflow obstruction is responsible for CVI.

images-11          images-12

May-Thurner syndrome

  • Dysfunction of the muscle pump prevents venous blood from being effectively emptied from the distal extremity. The muscle pump failure could occur as a primary disorder as in neuro-muscular conditions or muscle wasting syndromes or as a secondary disorder due to severe reflux or obstruction. In this, the post-ambulatory venous pressures will be nearly as high as the pressures after prolonged standing. Muscle pump dysfunction or failure is mainly responsible for superficial venous incompetence and its complication of stasis venous ulcer.
  • Changes in the hemodynamics of the large veins of the legs are transmitted to the venous microcirculation and finally develops venous microangiopathy. Features of this microangiopathy include – elongation, dilatation, tortuosity of the capillary beds, thickening of the basement membrane with increased collagen and elastic fibers, endothelial damage with a widening of the inter-endothelial spaces and increased peri-capillary edema with ‘halo’ formation.
  • The abnormal capillaries with increased permeability and high venous pressures lead to fluid accumulation, macromolecules, and extravasated RBCs into the interstitial spaces.
  • Besides changes in the blood vessels and connective tissue changes in the lymphatic network and nervous system occur.
  • Fragmentation and destruction of the micro lymphatics further impair drainage from the leg and dysfunction of the local nerve fibers may alter the regulatory mechanism.
  • Several mechanisms for the development of microangiopathy have been put forward and include fibrin cuff formation, growth factor trapping, and white blood cell trapping.
  • The fibrin cuff theory involves the accumulation of fluid containing fibrin into the pericapillary space. This cuff with impaired fibrinolysis increase the diffusion barrier inhibits the repair process and maintains the inflammatory process.
  • Another theory is the trapping of growth factor by fibrin and other macromolecules preventing the healing.
  • Another theory is the trapping of White blood cells in capillaries or post-capillary venules. The adhesion of the white cells with activation releases inflammatory mediators and proteolytic enzymes with endothelial damage which increases permeability or impedes flow leading to occlusion.

Clinical manifestation

  • CVI has a vast range of presentations form telangiectases to skin fibrosis and venous ulceration.
  • One must realize that the same presentations may be due to different problems like incompetent valves alone, venous obstruction alone, muscle pump dysfunction alone or in combination.
  • The major manifestations of CVI are dilated veins, edema, leg pain, and cutaneous changes.
  • Varicose veins are dilated veins that become progressively tortuous, larger and are prone to thrombophlebitis. Edema begins at the ankle and progresses up the leg and is worse on dependency. Pain and discomfort are worse on standing and relieved by elevation. The pain is due to the edema which increases the intra-compartmental pressure. Tenderness along the distended vein. Obstruction of the deep vein may give venous claudication of severe leg pain with ambulation.
Thrombophlebitis of varicose vein
Thrombophlebitis of varicose vein
  • Skin changes include hyperpigmentation due to hemosiderin deposition and eczematous dermatitis. Fibrosis may develop in the dermis and subcutaneous tissue (lipodermatosclerosis). There is an increased risk of cellulitis, leg ulceration and delayed wound healing.
  • Long-standing CVI may lead to lymphoedema.

Clinical classification of CVI

This is the CEAP classification: Clinical; Etiological; Anatomy; Pathophysiologic classification.

Clinically it has 7 categories (0 – 6) and further categorized by the presence or absence of symptoms.

Etiology is based on the congenital, primary and secondary causes of venous dysfunction.

Anatomic causes are superficial, deep and perforating veins

Pathophysiologic causes describe the underlying mechanism that causes CVI reflux, venous obstruction or both.


The diagnosis is made via history, examination and non-invasive testing.

Invasive testing is performed when surgery is contemplated.

Physical examination

  • Inspection and palpation – shows visible bulges of varicose veins, hyperpigmentation, stasis dermatitis, atrophic blanching (white scaring at the site of previous ulcers with capillaries around it) or lipodermatosclerosis.
  • The patient is evaluated standing to view maximal distention of the veins.
  • Edema is generally pitting in the late stages but initially, it presents as calf fullness Long standing edema leads to brawny edema.
Pitting oedema feet
Pitting edema feet
  • Active or healed ulcers are seen in advanced cases and mostly present on the medial supra-malleolar region at the site of the major perforating veins and the greatest hydrostatic pressure.
  • Trendelenburg test is performed bedside to distinguish superficial from deep reflux. The patient lies and elevates the legs to empty the veins. He stands after applying the tourniquet. If there is superficial disease the veins will remain collapsed if compression is more proximal to the point of reflux. In deep venous reflux, the veins will continue to dilate despite the use of a tourniquet or manual compression. Though the test determines the distribution of venous insufficiency but does not determine the extent of severity or provide the information about the cause.
  • Bedside doppler studies point to the direction of the flow. This is performed by maneuvers like Valsalva or sudden release of thigh or calf compression.

Differential diagnosis

  • Systemic causes of edema like heart failure, renal failure, liver failure, endocrine disorders or side effects of medication like calcium channel blockers, non-steroidal anti-inflammatory or oral hypoglycaemic agents.
  • Other local causes are ruptured popliteal cyst, soft tissue hematoma or mass, chronic exertion compartment syndrome, gastrocnemius tear of lymphoedema
  • With clinical examination and non-invasive testing mostly proper diagnosis is established.

Non-invasive testing

Venous duplex imaging

  • Used for assessing DVT and the etiology and severity of  CVI.
  • In DVT venous compressibility along with flow characteristics are diagnostic. The flow direction is assessed in a 30% reverse Trendelenburg position during maneuvers like Valsalva and augmentation after limb compression. Some use the cuff inflation-deflation method with rapid cuff deflation in the standing position to demonstrate reflux.
Reflux tracing
Colour doppler study showing reflux tracing
  • Reflux is determined by the direction of flow towards the feet. The reflux time is noted and the longer the reflux time the more severe the problem.
  • It can help us to see the valvular function.

Photoplethysmography (PPG)

  • Used to establish the diagnosis of CVI
  • Changes in the blood volume in the dermis of the limb are shown by the backscatter of the light emitted from the diode with a photosensor.
  • The PPG probe is put on the foot and the blood in the foot emptied by calf contractions. The return of blood is shown by increase backscatter of light and the refill time calculated.
  • The refill time is the time needed for the PPG tracing to return to 90% of the baseline after stopping calf contraction.
  • A refill time < 18-20 sec is indicative of CVI while > 20 sec is normal.
  • The use of a low-pressure cuff allows distinguishing superficial from deep reflux.
  • The correction of an abnormal refill time with a low-pressure cuff is indicative of saphenous vein disease.
  • Failure to correct abnormal refill time with low-pressure cuff is indicative of deep venous disease.
  • This test does not provide information about the anatomic distribution.
  • PPG is only for assessing the presence and absence of disease and nothing more.

Air Plethysmography (APG)

  • It has the ability to measure each component of CVI – reflux, obstruction or muscle pump dysfunction.
  • The limb volume changes during the filling and emptying of the venous circulation and this is picked up by the air displacement in the sensitive APG.
  •   venous outflow is assessed by a venous occlusion cuff when an elevated limb has rapidly deflation of the cuff.
Air plethysmography being performed
  • The outflow fraction at 1 sec is the parameter used to assess the adequacy of outflow. The limb is then placed in a dependent position to assess the venous filling. The rate of filling determines the severity of reflux.
  • The venous filling index is calculated by measuring 90% of the venous volume and dividing by the time needed to achieve this. A normal venous filling index is < 2 ml/sec while 4-7ml/sec correlates with the severity of CVI.
  • This test has a sensitivity of  70-80% and a predictive value of 99%.
  • The ability of the calf muscle pump to eject blood is measured by a single and 10 repetitive contractions during toe raise.
  • The volume of blood ejected with one tiptoe maneuver divided by the venous volume is called ejection fraction.
  • Complications of CVI like ulceration correlate with the severity of reflux assessed with the venous filling index and ejection capacity.

Other techniques

  • Strain gauge plethysmography
  • Foot volumetry

They provide physiological information about the venous function and correlates better with the clinical picture than does duplex imaging.

Invasive testing


This could be ascending or descending.

In ascending phlebography the dye is put into the foot and visualized as it passes up the leg. Though it was considered a gold standard now has been replaced by color doppler study.

Ascending venogram (Phlebography)
Ascending venogram (Phlebography)

It tells us about the anatomy and this knowledge may be helpful in surgical interventions and help distinguish primary from a secondary disease.

In descending phlebography the contrast is injected proximally in a semi-vertical posture on a tilt table using the Valsalva maneuver. It identifies reflux in the common femoral vein at the saphenofemoral junction but could identify other locations also.

It is performed in deep venous reconstructions or in case a duplex scan is not able to identify the problem.

Ambulatory venous pressures (AVP)

It is the hemodynamic gold standard in assessing CVI.

A needle is inserted into the dorsum of the foot and connected to the transducer. The pressures are recorded at rest and after exercise (toe raises). The pressure is also seen before and after applying a tourniquet at the ankle to distinguish between superficial and deep venous reflux.

Ambulatory venous pressures
Ambulatory venous pressures being conducted

It is valuable in assessing severity and clinical outcomes in CVI.

The mean ambulatory venous pressure (normal range 20 – 30 mmHg) and refill time (normal range 18 – 20 secs) are very useful measurements.

It provides information on the global competence of the venous system.

It, however, cannot reflect the pressure in the deep system. It is also invasive and therefore is seldom used in clinical practice.

Selection of studies

  • This depends on the purpose of the study.
  • Mostly non-invasive studies are performed to establish a diagnosis.
  • The anatomic site of disease and its hemodynamic importance is needed for the treatment of CVI.
  • The anatomic site of reflux which is needed to plan an intervention Is best provided by venous duplex reflux evaluation.
  • If quantitative information is needed to assess the severity of the disease to guide the therapy and monitor response to therapy then APG is the right test.

Treatment of CVI

Conservative treatment
  • This involves to relieve the symptoms and prevent complications and progression of the disease.
  • Behavioral measures like leg elevation to reduce edema and reducing intra-abdominal pressure.
  • Use of compression stockings is the mainstay of the treatment.
  • Should conservative measures fail then further treatment is advocated based on anatomic and pathophysiologic features.
  • To decide the course of management color doppler study and perhaps air plethysmography help.
  • Specific treatment is based on CEAP classification. Classes 4 – 6 need invasive treatment. These patients if left uncorrected are at risk of ulceration, recurrent ulceration, non-healing venous ulcers, progressive infection and lymphoedema

Graded compressive stockings

  • This is the first line of treatment and the mainstay of therapy. It helps neutralize the hydrostatic forces of venous hypertension.
  • The compression provided ranges from 20 – 50 mmHg. A pressure between 30 – 40 mmHg provides a significant improvement in pain, swelling, skin pigmentation, activity and well being if compliance of 70 – 80% is achieved.
Graded compression stockings
Graded compression stockings
  • In patients with venous ulcers compression stockings and other compression, bandaging modalities are effective in healing and recurrence of ulceration.
  • If properly done most venous ulcers will heal in a mean time of 5.3 months.
  • Compression stockings reduce the residual volume fraction which is an indicator of reducing the calf muscle pump function and to reduce reflux in the veins.
  • The grade of compression prescribed depends on tension and length.Tension is based upon CEAP Classification – Class 2 – 3 are given stockings between 20 – 30 mmHg; class 4 – 6 are give between 30 – 40 mmHg; and for recurrent ulcers 40 – 50 mmHg.
Stockings showing the degree of pressures at various points of the leg
  • The common length is knee length because patient compliance is best and relief of symptoms is adequate.
  • The use of mid-thigh or waist stocking is recommended for patients with edema above the knee but their compliance is more difficult.
  • Stocking should be changed every 6 – 9 months if used daily.

Wound and skin care

  • The compromised skin area must be kept moisturized to prevent skin breakdown and infection.
  • Stasis dermatitis should be treated with topical steroids creams.
  • Venous ulcers – control bacterial overgrowth to reduce infectious complications.
  • Hydrocolloid and foam dressings are needed for fluid drainage macerating the adjacent normal skin.

In infected ulcer bed, silver impregnated dressings control infection and restore tissue integrity.

Pharmacological drugs

Four groups of drugs have been advocated for CVI.

  1. Coumarins (alpha-benzo pines)
  2. Flavonoids (gamma – benzopyrones)
  3. Saphonosides (horse chestnut extract)
  4. Plant extracts
  • These drugs have veno-active properties which may improve venous tone and capillary permeability though the precise mechanism is not known.
  • Flavanoid (Daflon) reduces oedema related symptoms and is used as a primary treatment or in combination with surgery.
  • Studies show that in CVI coumarin + flavonoid with compression given for 12 weeks resulted in less oedema and pain.
  • Horse chestnut seed extract is as effective as compression stockings in short term to reduce oedema and pain of CVI but long term results are not available.
  • The use of pentoxifylline (trental) and antiplatelets like aspirin and platelet-derived growth factor helps in promoting healing and preventing recurrence of venous ulcers.


  • Problems in calf and foot muscle pump function play an important role in the development of CVI.
  • Exercise programs have been conducted to rehabilitate the muscle pump and improve the symptoms of CVI.
Standing tip toe helps
Standing tiptoe helps
  • A study in patients with CEAP grade 4 – 6 disease underwent programs of physical training to improve muscle strength. Venous hemodynamics were assessed by color Doppler and air plethysmography and muscle strength assessed by a dynamometer. After 6 months the calf muscle strength was normalized but there was no change in the venous reflux.
Various exercise that assists muscle pump of the legs
  • Thus exercise to re-establish muscle pump function may prove beneficial as supplementary therapy to medical and surgical treatment in advanced CVI.

Interventional Treatment

  • It is used in obliterating telangiectasis, varicose veins and venous segments with reflux.
  • It is used in conjunction with surgical procedures for correcting CVI.
  • The indications for use of sclerotherapy are:

– spider veins (<1mm)

– venous lakes

– varicose veins (1-4 mm size)

– bleeding varicosities

– small cavernous hemangiomas (venous malformations)

  • Sclerosing agents – hypertonic solution of sodium chloride (23.4% solution), sodium tetradecyl sulfate, polidocanol, sodium morrhuate.
  • They must be diluted to avoid tissue necrosis and inflammation.
  • It improves the hemodynamics in 12 weeks
  • a complication is hyperpigmentation of the surrounding skin from hemosiderin degradation. This complication may be treated by micro thrombectomy where multiple small incisions are used directly over the thromboses varicosity to extrude the thrombus. This results in less hyper-pigmentation within 1 – 3 weeks.

Ablative therapy with endogenous radio frequency and laser.

  • Here thermal energy is used in the form of radio frequency or laser to ablate the vein.
Varicose Vein
Varicose vein being ablated and closing shut
  • Local heat generated damages the intimal vein lining leading to thrombosis and eventually fibrosis.
  • There is complete obliteration n 85% after 2 years  with recanalization rate of 11%
  • 90% were free from saphenous vein reflux.
  • 95% were satisfied and had improved symptoms.
  • Potential complications of radio frequency are:

– saphenous nerve injury.

– DVT in 16% needing color doppler surveillance.

  • Laser treatment with 810-nm or 940-nm diode has obliterated saphenous vein in 93% at 2 years with no cases of DVT.
  • In both RFA and laser, tumescent anesthesia is used to prevent skin burns and reduce pain with early return to activity.
RFA Ablation
Results before and after RFA ablation


Endovascular therapy

  • This has become increasingly important to restore the venous circulation by removing the obstruction.
  • 10 – 30% of the patients with severe CVI have iliac vein stenosis or occlusion and need stenting which is being increasingly performed now.
  • In a large series with iliac veins stenting:

– 50% were relieved of pain and

– 33% had total resolution of the edema,

– 55% had total ulcer healing.

– The patency of iliac vein stenting at 3 years is 75%.

– Close follow-up is mandatory as restenosis occurs in 23% and should have a re-stent.

Surgical treatment

Ligation, stripping and venous phlebectomy

  • High ligation of saphenofemoral junction and stripping of the LSV is standard for many patients with CVI.

Stripping Vein  Stripped Vein

The procedure of stripping and stripped vein on table

  • The cluster of veins arising from the LSV is avulsed by stab phlebectomy.
  • Transilluminated power phlebectomy (TriVex) removes clusters of veins by fewer stab incisions and in quicker time.
  • Lighting and stripping of the LSV can be performed in all CEAP classes 2 – 6 with venous reflux and improve the venous hemodynamics, eliminating deep venous reflux, providing symptomatic relief of advanced stages of CVI and helping ulcer to heal.
  • In a large study with superficial and deep venous reflux, surgery + compression was compared to compression alone and found the results to be 28% to 12% improvement.

Subfascial endoscopic perforator surgery

  • The importance of perforator incompetence contributing to CVI cannot be overlooked.
  • Surgery has often been performed to ligate perforators contributing to the superficial reflux and CVI. It is often not easy to perform this surgery due to the pre-existing tissue damage in the affected area.

Endoscopic Surgery

SEPS being performed and the perforator cut and clipped

  • Subfascial Endoscopic Perforator Surgery (SEPS) can ligate the incompetent perforators in areas of lipodermatosclerosis of ulcers by entering from a remote site with normal tissue.
  • A study using the SEPS technique found that 88% ulcers healed at 1 year but there was a recurrence rate of 28% at 2 years.
  • SEPS has also been used along with superficial vein ablation and found that 91% ulcers heal at a mean of 2.9 months with significant improvement in symptoms.
  • In another large series of > 800 patients with CEAP clinical classes 4-6 for 9 years 55% underwent surgical ligation with stripping + SEPS – 92% ulcers healed with only 4% recurrence rates.

Valve reconstruction

  • Venous valve injury may lead to the progression of CVI.
  • Venous valvuloplasty has been shown to provide 59% competency and 63% ulcer free time at 30 months.
  • Complications are:

–  bleeding as patients are anticoagulated


– PE

– Ulcer recurrence

– wound infection.

  • Valves destroyed by post-phlebitic valve destruction cannot have venous valvuloplasty and need transposition of the profound femoris vein or saphenous vein valve and axillary vein valve to the damaged popliteal or femoral segments.
  • Cryopreserved vein valves allografts have been used. There is a high incidence of early thrombosis and poor patency and competence and increased patient morbidity. That is why this is not used now.


  • Chronic Venous Disease is a common problem and has a major impact on the individual and the health system.
  • A normal venous function needs axial veins with a series of venous valves and perforating veins to allow communication between the deep and the superficial systems and the venous muscle pump.
  • Dysfunction of any of these may lead to venous hypertension and CVI.
  • The manifestations of CVI range from pain and swelling to venous ulceration.
  • There are a number of invasive and non-invasive techniques that aid in the diagnosis and treatment.
  • The commonest used is the venous color doppler to confirm the diagnosis and provide anatomic details.
  • Air-plethysmography is needed to assess the severity of CVI.
  • Treatment of CVI is based on the severity of the disease and guided by anatomic and pathophysiologic considerations.
  • Graded compression stockings are the mainstay of the treatment of CVI.
  • Surgical and endogenous techniques are required with unsatisfactory medical (non-operative) treatment.
  • Recently early use of endogenous techniques is being recommended.