Varicose Veins

This is a review lecture for final year students attached to the University unit &
students preparing for exams. This is not meant for initial study.
Prepared by Dr Dale Maharaj, Lecturer, UWI (updated 08.11.05)

Etiology:
Primary aplasia of valves
Secondary
o Abdominal pressure on veins (pregnancy, obesity)
o DVT Virchows triad
o Carcinoma
Features:
Inspection
o Note size, site, and extent
o Look for complications (ulceration, lipodermatosclerosis, bleeding,
eczema)
Palpation
o Pitting edema or thickening, redness, and tenderness
o Thrombophlebitis (another complication)
o Conduct tourniquet test (Trendelenburg) determines level of
incompetent valves
Signs of DVT (yet another complication)
o Fegans method
Place tourniquet at mid-thigh
Have patient walk
If sudden pain DVT
Listen for bruits
Investigation:
Duplex scan
Venogram
Management:
General
o Reduce risk factors (lose weight, stop smoking, exercise etc.)
o Moisturize legs
o Use of compression stockings
o Use of venotonic agents (e.g. diflon)
Sclerotherapy for small to medium sized varicosities
o Complications
Bruising

Phlebitis
Unsightly skin staining
Ulceration in gator area
DVT
Surgical (sapheno-femoral ligation aka high tie with avulsions)
o Indications
Hemorrhage
Symptomatic varicosities
Incompetent perforator veins

VARICOSE VEINS AND CHRONIC VENOUS INSUFFICIENCY

by ML Da Costa, MCh, FRCSI, FRCS(Glasg), FRCS(Eng),
Introduction
Varicose veins are tortuous, elongated dilated and thickened veins with nonfunctional
incompetent valves
Main influences on the development of varicose veins:
Heredity:
Female sex
Hormones
Gravitational hydrostatic forces
Hydrostatic dynamic muscular compartment force
Heredity uncertain if dominant or recessive trait
Profound effect of female hormones in pregnancy on development of varicose viens:
70-80% appears in 1st trimester, often within 2-3 weeks of gestation
Indicates that do not develop because of size of a gravid uterus, increased blood
flow or iliac venous occlusion
Two mechanical forces act on the heredity and hormonal substrate to produce the
elongation and dilatation of the veins:
Weight of blood column from right atrium to affected vein through valveless
conduits of abdomen, pelvis and any incompetent valves of proximal limb veins-constant
and called hydrostatic pressure
Pressure exerted by contracting muscles on adjacent veins-hydrodynamic force:
forces blood through open valves in deep veins towards the heart. Incompetence of deep
perforators allows transmission of this huge force to unsupported superficial veins and
venules
Clinical Presentation
Asymptomatic:
Unsightly dilated, tortuous veins
Telangiectatic blemishes
Consultation sought by patient on cosmetic grounds
Symptomatic:
Aching pain usually in the calf
all worsening as day progresses

Leg heaviness
Easy leg fatigue

relieved by elevation & rest

maximal on 1st day of menses

Superficial thrombophlebitis
External bleeding
Ankle hyperpigmentation
Lipodermatosclerosis
Venous ulcers
Signs:
Observation: Performed with patient in standing position. Varicosities are
observed and noted. Look for relationship to GSV or short saphenous vein. Determine
of GSV or SSV is varicosed as well. Look for venous stars and flares which occur
subcutaneously especially at the points of highest venous pressure (ankle).
Cough test: Thrill felt with examining hand placed just below SF junction
when patient coughs-signifies primary SF incompetence
Tap test: Thrill felt with examining hand placed over a bunch of
varicosities as other hand gently taps GSV cephalad to examining hand. Basis for this is
that the fliud thrill set up by taspping the GSV passes retrogradely through incompetent
valves
Trendellenburgs test: For primary SF incompetence. Leg is elevated and
veins drained by milking the leg from foot to thigh with patient in reclining position.
Examining hand or a tourniquet is placed just below SF junction and the patient asked to
stand up off the bed. The bunches of varicosities are examined-if they remain unfilled,
then perforators are competent. If bunches of varicosities fill despite control at SF
junction-perforators below SF junction and bunches of varicosities are incompetent.
Watch as examining hand or tourniquet is removed-if bunches of varicosities fill, primary
SF incompetence and incompetence of all valves along the GSV to the varicosities is
present.
Modified Trendellenburgs test: Can be used to determine level of
perforator incompetence. In thigh Hunterian perforator mid-thigh; Dodd perforator
approximately 1 hands breadth above knee. Below knee, Boyd perforator approximately
1 hands breadth below knee; then Cockett perforators 5, 10 and 15cm above ankle.
Application of a tourniquet at each level just below perforator should control the
incompetence and prevent filling of the bunches of varicosities if SF junction is
competent or controlled. Removal of the perforator-controlling tourniquet will result in
filling of the varicosities.
Fegans method (of demonstrating Boyd and Cocketts perforators and
perforator incompetence): with the patient supine and elevating the leg with one hand and
running an examining finger along the medial border of the tibia-the position of below
knee perforators will be easily palpable as sizable defects or depressions in the deep
fascia in patients with chronic perforator incompetence. Finger-tip control with an
examining finger will be possible and the modified Trendellenburg test can be performed
easily.
Perthes test: To detect significant deep venous occlusion or insufficiency.
If an tourniquet is placed just below the SF junction tight enough to occlude superficial

venous drainage, the patient is asked to push him/her-self up and down on his/her toes for
several minutes. If there is significant deep venous occlusion or insufficiency, there will
be a bursting pain (as classically described) or tightness in the calf (venous
claudication). This is because blood cannot be drained out of the leg through the
tourniquet-occluded superficial venous system.

Investigations
The key issue here are the sites and extent of venous valvular incompetence as this will
determine the type and extent of surgery.
Duplex scanning has become the most widely used mode of investigation of both arterial
and venous disease.
It is cheap, non-invasive, involves no radiation, is reproducible and has a well-established
accuracy.
This enables the technician to map the superficial and deep venous systems and provide
the following information that is relevant to the surgeon:
Deep venous system:
Presence/absence of DVT
Competence of deep venous valves
Competence of perforators
Superficial venous system:
Competence of short and long saphenous vein junctions (primary saphenofemoral or sapheno-popliteal incompetence)
Competence of valves along the long and short saphenous veins
The information provided allows the surgeon to address the actual problem at hand and
decide the best surgical procedure for the patient
Very helpful in recurrent varicosities
Management:
Conservative or Operative
Conservative:
High risk patients for general anaesthesia; elderly patients with relatively minor
symptoms, no ulceration or debilitating chronic venous hypertension
Graded compression stockings that can be either above (full length) or below knee
Stockings provide a gradient that is highest at the ankle and falls progressively as
it ascends up the leg
Helps to support column of blood in veins and assist upward flow as well as
reducing the hydrostatic effect of stasis at rest
Below knee found to be as effective as above knee stockings and patient more
compliant and less problems with slippage down leg with time

Operative:
Small incision over surface marking of sapheno-femoral junction in groin or
marked junction of sapheno-popliteal junction (located by Duplex scanning as this
junction can vary considerably)
Dissection of junction and ligation and division of all named tributaries (failure to
do this is the commonest cause for recurrence)
Flush ligation, division and stripping of the long saphenous vein to the knee
(unnecessary to strip below knee as this can cause saphenous nerve injury and does not
increase benefit)
Stab incisions over marked varicosities and avulsion of these veins
Sclerotherapy may be used in combination to eradicate high pressure, feeding
reticular vessels in combination with injection of their targets, the epidermal veins,
telangiectasias
Sclerotherapy is the introduction of a foreign substance into the lumen of a vessel
causing thrombosis and subsequent fibrosis
Detergent substances produce endothelial damage through interference with cell
surface lipids:
Sodium tetradecyl sulphate
Sodium morrhuate
Ethanolamine oleate
Polidocanol
Hypertonic saline and glucose solutions produce dehydration of endothelial cells
through osmosis
Chemical irritants or caustic agents such as chromated glycerin and
polyiodinated iodine produce direct destruction of endothelial cells

TREATMENT OF CHRONIC VENOUS INSUFFICIENCY WITHOUT

ULCERATION
Education
Very important to prevent progression to severe insufficiency and recurrent ulceration
Importance of preventing chronic oedema which leads to ulceration
Limb elevation
Compression therapy
Prevention of injury
Skin care
Pharmacological therapy
Medication that reduces oedema and capillary permeability Daflon (micronized
flavinoid fraction)
Decreases venous capacitance and distensibility and reduces venous emptying time in
patients with significant oedema
Also found to accelerate ulcer healing time when combined with compression therapy
Hydroxyethylrutosides-semi-synthetic flavinoids-act on endothelium to reduce capillary
permeability
Horse chestnut seed extract (HCSE) found to benefit patients with chronic venousd
insufficiency and oedema
Compression Therapy
Mainstay and treatment of choice
Always assess arterial status of limb first as there can be mixed venous and arterial
disease and compression therapy will aggravate arterial disease
Class II (up to 30mmHg) or Class III (up to 40mmHg) benefical for chronic venous
insufficiency
Patients often started on Gr II first as may not be compliant if started with stockings that
are too tight
No added haemodynamic benefit with above knee stockings as compar3ed with below
knee stockings
Massive oedema may not allow use of stockings at first-compression bandaging to reduce
oedema over first few weeks then followed up with stockings
TREATMENT OF CHRONIC VENOUS INSUFFICIENCY WITH ULCERATION
Need to differentiate from other causes of ulceration
Venous stasis may occur in combination with other causes of ulceration also
Sharp debridement of ulcer to reveal clean base
If significant cellulitis-admit for iv antibiotics, elevation and wound care until cellulitis
resolves
Note that patients often appear to have cellulitis but actually have a dermatitis which
resolves once oedema is treated
Compression is the mainstay of treatment

A large number of applications to ulcers to accelerate healing have been described from
cheap saline gauze to expensive hydrocolloid dressings-no one dressing has been shown
to be uniformly superior to others
Dressings applied and then compression either with graded compression stockings or
compression therapy with layered bandaging
So called Charing Cross compression bandaging is a 4-layered bandage system
providing 40mmHg at ankle
Has a high rate of healing venous stasis ulcers: one study 93% healing rate with no
amputations in 134 patients over a 2-year period; 61% healed at 10 weeks and 82% at 20
weeks
Patients are assessed with Duplex scanning and ligation of perforators and stripping of
superficial veins offered to reduce abnormal reflux
Correction of deep venous insufficiency with surgery only offered to good candidates
with severe recurrent ulceration (beyond scope of these notes)
Adjuncts to compression for ulcer healing
Any adjuncts must be compared to gold standard of compression therapy to merit
widespread clinical use
Cost efficacy-many forms of expensive therapies:
Hyperbaric oxygen
Skin grafting
Cultured skin substitutes
Have their places in carefully selected patients