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VARICOSE VEINS AND
MANAGEMENT
Dr PRASHANTH.S
GENERAL SURGERY RESIDENT
CAIMS
 Superficial veins : located above the muscular
fascia. The saphenous vein rests over the
muscular fascia and appears like a “Egyptian
eye” on duplex scan.
 Deep veins : located in the muscular
compartment, follows the same course as
arteries.
 Perforator veins :these are rich network of
perforating veins that traverse the muscular
fascia between the deep and superficial veins.
They direct the flow from superficial to deep
veins.
Venous valves
 They prevent retrograde flow of blood in a
proximal to distal direction.
 They are found throughout the body, but
highest concentration is located in the lower
extremities.
 They are bicuspid and can form sinusoidal
dilatations due to locally reversed flow.
 Close with velocity-30 cm/sec.
 The inferior vena cava (IVC), common iliac
veins, portal venous system, and cranial
sinuses are valveless
Venous wall structure and
composition
 Composed of 3 layers
 INTIMA: it is a single layer of cells resting on a
thin layer of connective tissue.Valves are lined
on both sides with a layer of intima over thin
connective tissue skeleton.
 MEDIA: consists of smooth muscles and
connective tissue such as collagen. It conveys
protection from dilatation and varicosity
formation.
 ADVENTITIA: its not well differentiated from
media contains of loose connective tissue, vasa
vasorum.
Anatomy of great saphenous
vein
 The great saphenous vein drains the medial end
of the dorsal venous arch of the foot and passes
upwards directly in front of the medial malleolus.
 It then ascends in company with the saphenous
nerve in the superficial fascia over the medial
side of the leg.
 The vein passes behind the knee and curves
forward around the medial side of the thigh.
 It passes through the lower part of the
saphenous opening in the deep fascia and joins
the femoral vein about 1.5 inches below and
lateral to the pubic tubercle.
 The great saphenous vein possesses numerous
valves and is connected to the small saphenous
vein by one or two branches that pass behind the
knee.
 Several perforating veins connect the great
saphanous to the deep veins along the medial
side of the calf.
 At the saphenous opening in the deep fascia, the
great saphenous vein usually receives three
tributaries that are variable in size and
arrangement– superficial circumflex iliac,
superficial epigastric and superficial external
pudendal
Main perforators of the great saphenous vein
 May perforators- at the level of ankle
 Cockett – at 5, 10 and 15 cm
from medial malleolus
 Boyd - below knee
 Dodd - above knee
 Mid thigh perforator
 SFJ
Short saphenous vein
 It arises from the lateral part of the dorsal venous
arch of the foot.
 It ascends behind the lateral malleolus in company
with sural nerve
 It follows the lateral border of the tendo calcaneus
and then runs up the middle of the back of the leg.
 The vein pierces the deep fascia and passes between
the two heads of the gastrocnemius muscle in the
lower part of the popliteal fossa.
 The mode of termination of the small saphenous
vein is subject to variation- may join the popliteal
vein, may join the great saphenous, may split into
two one joins popliteal and one joins great
saphenous.
Pathogenesis
Two theories
 Fibrin cuff theory
 White cell trapping theory
Incompetence of venous valves
Stasis of blood
Chronic ambulatory venous hypertension
Defective microcirculation
RBC’s diffuses into tissue planes
Lysis of RBC’s
Release of haemosiderin
Pigmentation
Dermatitis
Capillary endothelial damage
Prevention of diffusion and exchange of nutrients
Severe anoxia
Chronic venous ulceration
Fibrin cuff theory
White cell trapping theory
Inappropriate activation of trapped leucocytes
release proteolytic enzymes which cause cell
destruction and ulceration.
Fibrin deposition, tissue death, scarring occurs
together called as lipodermatosclerosis
Classification of lower
extremity venous disease
(CEAP)
 C - clinical signs
 E – etiological classification
 A – anatomic distribution
 P – pathological dysfunction
Grading of clinical signs
0-- no visible or palpable signs of venous
disease
1– telangiectases, reticular veins or malleolar
flare
2– varicose veins
3– oedema without skin changes
4– skin changes ascribed to venous diseases
5– skin changes with healed ulcer
6– skin changes with active ulcer
Aetiology
A. Primary varicosities due to:
 Congenital incompetence or absence of
valves.
 Weakness or wasting of muscles- defective
connective tissue and smooth muscle in the
venous wall.
 Stretching of deep fascia
 Inheritance with FOXC2 gene
 Klippel-Trenaunay syndrome
B. Secondary varicosities
 Recurrent thrombophlebitis
 Occupational – standing for long hours
 Obstruction to venous return like abdominal
tumour, retroperitoneal fibrosis,
lymphadenopathy.
 Pregnancy
 A-V malfunctions
 Iliac vein thrombosis
Symptoms in varicose veins
 Dragging pain
 Heaviness in the legs
 Night time cramps
 Oedema of feet
 Discolouration/ ulceration in the feet / painful
walk
Causes of pain / cramps in
varicose veins
 Chronic venous hypertension
 Hypoxia of tunica media due to altered function of
vasa vasorum
 Increased capillary pressure
 Hyper viscosity of red cells
 Platelet hyperaggregation
 Reduced in capillary permeability causing capillary
functional disorder
 Altered cutaneous microcirculation due to leukocyte
adhesion and accumulation into the venous wall,
release of free radicals cause micro vascular lesional
disease.
Venous disability scoring
system
0– asymptomatic
1– symptomatic but able to carry out activities
without any therapy
2– symptomatic can do activities only with
compression or limb elevation
3-- symptomatic – unable to do daily activities
even with compression or limb elevation
Complications of varicose
veins
 Haemorrhage
 Eczema and dermatitis
 Periostitis
 Venous ulcer
 Marjolin’s ulcer
 Lipodermatosclerosis
 Ankylosis of the ankle joint
 Talipes equino varus
 DVT
 Calcification
 thrombophlebitis
 Brodie-Trendelenburg test– vein is emptied by
elevating the limb and a tourniquet is tied just
below the sapheno-femoral junction. Patient
is asked to stand quickly. When tourniquet or
thumb is released, rapid filling from above
signifies sapheno-femoral incompetence.
This isTrendelenburg test 1.
 In Trendelenburg test 2, after standing
tourniquet is not released. Filling of blood
from below upwards rapidly can be observed
within 30-60 seconds. It signifies perforator
incompetence.
 PERTHE’S test: the effected lower limb is
wrapped with elastic bandage and the patient
is asked to walk around and exercise.
Development of severe cramp like pain in the
calf signifies DVT.
 MODIFIED PERTHE’S test: tourniquet is tied just
below the sapheno-femoral without
emptying the vein. Patient is allowed to have
a brisk walk which precipitates bursting pain
in the calf and also makes superficial veins
more prominent. It signifies DVT
 Three tourniquet test: to find out the site of
incompetent perforator, three tourniquet are
tied after emptying the vein.
1 at sapheno-femoral junction
2 above knee level
3 another below knee level
Patient is asked to stand and looked for filling of
veins and site of filling. Then tourniquets are
released from below upwards, again to see
for incompetent perforators.
 SCHWARTZ test: in standing position, when
lower part of the long saphenous vein in leg is
tapped, impulse is felt at the saphenous
junction or at the upper end of the visible part
of the vein. It signifies continuous column of
blood due to valvular incompetence.
 PRATT’S test: Esmarch bandage is applied to the
leg from below upwards followed by a
tourniquet at sapheno-femoral junction. After
that the bandage is released keeping the
tourniquet in the same position to see the
“blow outs” as perforators.
 MORRISEY’S COUGH IMPULSE test: the varicose
veins are emptied. The leg is elevated and
then patient is asked to cough. If there is
sapheno-femoral incompetence, expansile
impulse is felt at saphenous opening. It is a
venous thrill due to vibration caused by
turbulent back flow.
 FEGAN’S test: on standing, the site where the
perforators enter the deep fascia bulges and
this is marked. Then on lying down, button
like depressions in the deep fascia is felt at
the marked out points which confirms the
perforator sites.
Venous Doppler
 With patient standing, the Doppler probe is placed at
sapheno-femoral junction and later wherever required.
 Basically by hearing the changes in sound, venous flow,
venous patency, venous reflux can be very well identified.
1. To find out DVT- very important
2. To find out sapheno-femoral, sapheno-popliteal
incompetence
3. To find out perforator incompetence
4. Uniphasic signals signify flow in one direction-normal
5. Biphasic flow signifies reversal flow with incompetence
Duplex scan
 It is a highly reliable U/S Doppler imaging
technique (high resolution B mode ultrasound
imaging and Doppler ultrasound is used),
which along with direct visualisation of veins,
gives the functional and anatomical
information and also colour map.
 Examination is done in standing, lying down
position and also valsalva manoeuvre.
 DVT is very well identified by this method.
Venography
 Ascending venography was a very common
investigation done before Doppler period.
A tourniquet is applied above the malleoli and
vein of the dorsal venous arch of foot is
cannulated. Water soluble dye is injected,
flows into the deep veins.
X-rays are taken below and above knee level.
Any block in deep veins, its extent, perforator
status can be made out by this.
It is good reliable investigation for DVT.
 Descending venogram
It is done when ascending venogram is not
possible and also to visualise incompetent
veins.
Here contrast material is injected into femoral
vein through a cannula in standing position.
X rays pictures are taken to visualise deep veins
and incompetent veins.
Plethysmography
It is a non invasive method which measures
volume changes in the leg.
 Photo plethysmography
 Air plethysmography
Photo plethysmography
 Using probe transmission of light through the
skin, venous filling of the surface venules which
reflects the superficial venous pressure is
measured.
 Initially patient performs dorsiflexion at ankle for
10 times to empty the venules and pressure
tracing falls in photo plethysmography.
 Patient takes rest and refilling occurs. In normal
people, it occurs through arterial inflow in 20-30
seconds.
 In venous incompetence filling also occurs by
venous reflux and refilling time is faster than
normal
 Site of reflux cannot be localised by this method.
Air plethysmography
 Patient is initially in supine position with veins emptied by
elevation of leg. Air filled plastic pressure bladder is placed on calf
to detect volume changes.
 Minimum volume is recorded. Patient is turned to upright
position and venous volume is assessed.
 Maximum venous volume divided by time required to achieve
maximum venous volume gives the venous filling index.
 VFI is a measure of reflux
 Ejection fraction is volume change measured prior and after
single tiptoe manoeuvre which is a measure of calf pump action.
 Residual venous fraction is an index of overall venous function
which is venous volume in the leg after ten tiptoe manoeuvres
divided by venous volume prior to manoeuvre.
 Increased VFT and diminished ejection fraction in patient will
benefit from surgery
Treatment
1. Conservative treatment
 Elastic crepe bandage application from below
upwards or use of pressure stockings to the limb
pressure gradient of 30-40 mmHg is provided.
 Diosmin therapy which increases the venous tone.
 Elevation of the limb- relieves oedema.
 Unna boots- provide non elastic compression
therapy. It comprises a guaze compression
dressings that contain zinc oxide, calamine and
glycerine that helps to prevent further skin break
down. It is changed once a week.
 Pneumatic compression method– provide dynamic
sequential compression.
2. Drugs used for varicose veins
 Calcium dobesilate—500 mg BD. Calcium
dobesilate improves lymph flow; improves
macrophage mediated proteolysis and
reduces edema.
 Diosmin 450 mg + Hesperidin 50 mg
(DAFLON 500 mg). Mainly used in relieving
night cramps but not to improve healing of
ulcers.
3. Injection– sclerotherapy: By injecting
sclerotic agent into the vein, complete
sclerosis of the venous walls can be achieved.
Indication
 Uncomplicated perforator incompetence
 In the management of smaller varices-
reticular
 Recurrent varices
 Isolated varices
 aged / unfit patients
Sclerosants used are—
 Sodium tetradecylsulphate 3%(STDS) –
commonly used
 Sodium morrhuate
 Ethanolamine oleate
 Polidocanol
Mechanism of action
 Causes aseptic inflammation
 Causes perivenous fibrosis leading to block
 Causes approximation of intima leading to
obliteration by endothelial damage
 Alters intravascular pH / osmolality
 Changes surface tension of plasma membrane.
 A 23 gauge needle is inserted into the vein (3-8
mm sized) and vein is emptied. 0.5-1 ml of
sclerosant is injected into the vein and
immediately compression is applied on the vein.
 So as to allow the development of sclerosis and
to have proper endothelial apposition.
 Usually injection is started at the ankle region
and then proceeded upwards along the length of
veins at different points.
 Later pressure bandage is applied for six weeks.
Often injections may have to be repeated at 2-
4weeks intervals for 2-4 sessions. Technique is
called as macrosclerotherapy
Microsclerotherapy
 Very dilute solutions of sclerosing agent like
STDS(0.1% of 0.1 ml dilute) polidoconol is
injected into the thread veins and reticular
veins followed by application of compression
bandage
 Dermal flare will disappear well by this
method
Contraindiactions for sclerotherapy
 Sapheno femoral incompetence
 Deep venous thrombosis
 Huge varicosities– may precipitate DVT
 Peripheral arterial diseases
 Hypersentivity / immobilty
 Venous ulcer– relative contrainidication
Advantages
 It can be done as an outpatient procedure
 It does not require aneasthesia
Disadvantage
 Inadvertent subcutaneous injection can cause
skin necrosis or abscess formation
 Anaphylaxis
 Hyperpigmentation
 Thrombophlebitis
 Deep vein thrombosis can occur
Surgery
A. Trendelenburg operation:
It is juxta-femoral flush ligation of long saphenous
vein (flush with femoral vein), after ligation
superficial circumflex, superficial external
pudendal, superficial epigastric vein, deep
external pudendal vein and unnamed
tributaries.
All tributaries should be ligated, otherwise
recurrence will occur
Double saphenous vein is the commonest anomaly
occuring near sapheno-venous junction.
B. Stripping of vein: using Myer’s stripper vein is
stripped off. Stripped from below upwards is
technically easier.
Immediate application of crepe bandage reduces the
chance of bleeding and hemotoma formation.
Stripping avulses the vein as well as obliterates the
tributaries.
Babcock’s stripper and rigid metal pin stripper can also
be used.
Stripping of the short saphenous vein is done from
ankle below upward after passing stripper from
above downwards.
Complication is injury to saphenous or sural nerve
causing neuralgia.
Inverting or invaginating stripping using rigid Oesch pin
stripper is better as postoperative pain and
hematoma is less common and also there is tissue
damage.
C. Subfascial ligation of Cockett and Dodd
Perforators are marked out by fegan’s method.
Perforators are ligated deep to deep fascia
through incisions in antero medial side of
the leg.
Radiofrequency ablation
(RFA)
 This is done under general or regional
anaesthesia.
 RFA catheter is passed into long / short
saphenous vein near SFJ or SPJ under guidence.
85 Celsius temperature is used for long period of
time to cause endothelial damage, collagen
denaturation and venous constriction.
 Phlebectomy is done while withdrawing the
catheter. Wall of vein is destroyed through its full
thickness.
 Vein forms a cord, which gets dissolved by
macrophages and immune cells.
Endo venous laser ablation
 It is done as a OP procedure.
 Patient lies in supine with diseased leg flexed, hip
externally rotated and knee flexed.
 With aseptic precaution, under U/S guidance GSV is
cannulated above the knee and a guide wire is
passed beyond SJF and 5- French catheter is passed
over guide wire and tip is placed 1cm distal to the
junction.
 200 ml of 0.1% lignocaine is infilterated along the
length of the GSV.
 Laser fibre is inserted up to the tip of the catheter
and catheter is withdrawn for 2 cm and laser fibre
protrudes for 2 cm.
 Laser fibre is fired step by step using diode laser, one
mm withdrawal in 2 seconds.
 Once procedure is over catheter is removed
and pressure bandage is applied for 2 weeks.
 Heat produced (729 – 1000 Celsius) by the
laser produces steam bubbles with thermal
damage of endothelium leading into
occlusion of the vein.
 Laser therapy has inability to create flush
occlusion allowing tributaries to open up and
cause recurrence.
SUBFASCIAL ENDOSCOPIC
PERFORATOR SURGERY (SEPS)
 First described by Heuer in 1980, it became the most
accepted surgical treatment of advanced stages of chronic
venous insufficiency because it is minimally invasive nature
and safety profile
 Can be performed with one or two endoscopic ports, the
two port technique uses one 10 mm video port for camera
and 5 mm port for instrumentation.
 The limb is elevated and the field is made bloodless by
using a Esmarch bandage, and a thigh tourniquet is inflated
to 300 mmHg.
 10 mm port is placed in the healthy medial aspect of calf, 10
cms distal to tibial tuberosity.
 Avoid large opening because gas may leak and cause poor
visibility.
 The camera is inserted into the 10mm port and then second
5 mm port is inserted under direct vision about 10-20 cm
distal and posterior to the first port.
 CO2 is insufflated to enlarge and optimally visualise the
subfascial space, with pressure maintained at around 30
mmHg.
 All the visible perforators after dissection are interrupted by
using harmonic scalpel, electrocautery or division with
scissors between metallic clips.
 More proximal paratibial perforators are visualised better
by exposing the medial insertion of the soleus on the tibia,
remain close to tibia to avoid damage to posterior tibial
vessels and nerve.
 On completion, the ports are removed, tourniquet is
deflated and CO2 is manually expressed from subfascial
space.
 Local anaesthetic solution is instilled into the subfascial
space to help with postoperative analgesia and
compressive bandage is applied.
Transilluminated phlebectomy
 It is done by passing transilluminating light
under the skin and passing a rotating blade
through another small incision.
 Veins are grasped and removed by rotating
movements.
AMBULATORY PHLEBECTOMY
Done through small incisions using special
phlebectomy instruments.
ELECTRODESSICATION
Using weak electric current through a fine
needle directly into the spider veins.
THANK YOU

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Varicose veins and management 1

  • 1. VARICOSE VEINS AND MANAGEMENT Dr PRASHANTH.S GENERAL SURGERY RESIDENT CAIMS
  • 2.  Superficial veins : located above the muscular fascia. The saphenous vein rests over the muscular fascia and appears like a “Egyptian eye” on duplex scan.  Deep veins : located in the muscular compartment, follows the same course as arteries.  Perforator veins :these are rich network of perforating veins that traverse the muscular fascia between the deep and superficial veins. They direct the flow from superficial to deep veins.
  • 3. Venous valves  They prevent retrograde flow of blood in a proximal to distal direction.  They are found throughout the body, but highest concentration is located in the lower extremities.  They are bicuspid and can form sinusoidal dilatations due to locally reversed flow.  Close with velocity-30 cm/sec.  The inferior vena cava (IVC), common iliac veins, portal venous system, and cranial sinuses are valveless
  • 4. Venous wall structure and composition  Composed of 3 layers  INTIMA: it is a single layer of cells resting on a thin layer of connective tissue.Valves are lined on both sides with a layer of intima over thin connective tissue skeleton.  MEDIA: consists of smooth muscles and connective tissue such as collagen. It conveys protection from dilatation and varicosity formation.  ADVENTITIA: its not well differentiated from media contains of loose connective tissue, vasa vasorum.
  • 5. Anatomy of great saphenous vein  The great saphenous vein drains the medial end of the dorsal venous arch of the foot and passes upwards directly in front of the medial malleolus.  It then ascends in company with the saphenous nerve in the superficial fascia over the medial side of the leg.  The vein passes behind the knee and curves forward around the medial side of the thigh.  It passes through the lower part of the saphenous opening in the deep fascia and joins the femoral vein about 1.5 inches below and lateral to the pubic tubercle.
  • 6.  The great saphenous vein possesses numerous valves and is connected to the small saphenous vein by one or two branches that pass behind the knee.  Several perforating veins connect the great saphanous to the deep veins along the medial side of the calf.  At the saphenous opening in the deep fascia, the great saphenous vein usually receives three tributaries that are variable in size and arrangement– superficial circumflex iliac, superficial epigastric and superficial external pudendal
  • 7. Main perforators of the great saphenous vein  May perforators- at the level of ankle  Cockett – at 5, 10 and 15 cm from medial malleolus  Boyd - below knee  Dodd - above knee  Mid thigh perforator  SFJ
  • 8. Short saphenous vein  It arises from the lateral part of the dorsal venous arch of the foot.  It ascends behind the lateral malleolus in company with sural nerve  It follows the lateral border of the tendo calcaneus and then runs up the middle of the back of the leg.  The vein pierces the deep fascia and passes between the two heads of the gastrocnemius muscle in the lower part of the popliteal fossa.  The mode of termination of the small saphenous vein is subject to variation- may join the popliteal vein, may join the great saphenous, may split into two one joins popliteal and one joins great saphenous.
  • 9. Pathogenesis Two theories  Fibrin cuff theory  White cell trapping theory
  • 10. Incompetence of venous valves Stasis of blood Chronic ambulatory venous hypertension Defective microcirculation RBC’s diffuses into tissue planes Lysis of RBC’s Release of haemosiderin Pigmentation Dermatitis Capillary endothelial damage Prevention of diffusion and exchange of nutrients Severe anoxia Chronic venous ulceration Fibrin cuff theory
  • 11. White cell trapping theory Inappropriate activation of trapped leucocytes release proteolytic enzymes which cause cell destruction and ulceration. Fibrin deposition, tissue death, scarring occurs together called as lipodermatosclerosis
  • 12.
  • 13. Classification of lower extremity venous disease (CEAP)  C - clinical signs  E – etiological classification  A – anatomic distribution  P – pathological dysfunction
  • 14. Grading of clinical signs 0-- no visible or palpable signs of venous disease 1– telangiectases, reticular veins or malleolar flare 2– varicose veins 3– oedema without skin changes 4– skin changes ascribed to venous diseases 5– skin changes with healed ulcer 6– skin changes with active ulcer
  • 15. Aetiology A. Primary varicosities due to:  Congenital incompetence or absence of valves.  Weakness or wasting of muscles- defective connective tissue and smooth muscle in the venous wall.  Stretching of deep fascia  Inheritance with FOXC2 gene  Klippel-Trenaunay syndrome
  • 16. B. Secondary varicosities  Recurrent thrombophlebitis  Occupational – standing for long hours  Obstruction to venous return like abdominal tumour, retroperitoneal fibrosis, lymphadenopathy.  Pregnancy  A-V malfunctions  Iliac vein thrombosis
  • 17. Symptoms in varicose veins  Dragging pain  Heaviness in the legs  Night time cramps  Oedema of feet  Discolouration/ ulceration in the feet / painful walk
  • 18. Causes of pain / cramps in varicose veins  Chronic venous hypertension  Hypoxia of tunica media due to altered function of vasa vasorum  Increased capillary pressure  Hyper viscosity of red cells  Platelet hyperaggregation  Reduced in capillary permeability causing capillary functional disorder  Altered cutaneous microcirculation due to leukocyte adhesion and accumulation into the venous wall, release of free radicals cause micro vascular lesional disease.
  • 19. Venous disability scoring system 0– asymptomatic 1– symptomatic but able to carry out activities without any therapy 2– symptomatic can do activities only with compression or limb elevation 3-- symptomatic – unable to do daily activities even with compression or limb elevation
  • 20. Complications of varicose veins  Haemorrhage  Eczema and dermatitis  Periostitis  Venous ulcer  Marjolin’s ulcer  Lipodermatosclerosis  Ankylosis of the ankle joint  Talipes equino varus  DVT  Calcification  thrombophlebitis
  • 21.  Brodie-Trendelenburg test– vein is emptied by elevating the limb and a tourniquet is tied just below the sapheno-femoral junction. Patient is asked to stand quickly. When tourniquet or thumb is released, rapid filling from above signifies sapheno-femoral incompetence. This isTrendelenburg test 1.  In Trendelenburg test 2, after standing tourniquet is not released. Filling of blood from below upwards rapidly can be observed within 30-60 seconds. It signifies perforator incompetence.
  • 22.  PERTHE’S test: the effected lower limb is wrapped with elastic bandage and the patient is asked to walk around and exercise. Development of severe cramp like pain in the calf signifies DVT.  MODIFIED PERTHE’S test: tourniquet is tied just below the sapheno-femoral without emptying the vein. Patient is allowed to have a brisk walk which precipitates bursting pain in the calf and also makes superficial veins more prominent. It signifies DVT
  • 23.  Three tourniquet test: to find out the site of incompetent perforator, three tourniquet are tied after emptying the vein. 1 at sapheno-femoral junction 2 above knee level 3 another below knee level Patient is asked to stand and looked for filling of veins and site of filling. Then tourniquets are released from below upwards, again to see for incompetent perforators.
  • 24.  SCHWARTZ test: in standing position, when lower part of the long saphenous vein in leg is tapped, impulse is felt at the saphenous junction or at the upper end of the visible part of the vein. It signifies continuous column of blood due to valvular incompetence.  PRATT’S test: Esmarch bandage is applied to the leg from below upwards followed by a tourniquet at sapheno-femoral junction. After that the bandage is released keeping the tourniquet in the same position to see the “blow outs” as perforators.
  • 25.  MORRISEY’S COUGH IMPULSE test: the varicose veins are emptied. The leg is elevated and then patient is asked to cough. If there is sapheno-femoral incompetence, expansile impulse is felt at saphenous opening. It is a venous thrill due to vibration caused by turbulent back flow.  FEGAN’S test: on standing, the site where the perforators enter the deep fascia bulges and this is marked. Then on lying down, button like depressions in the deep fascia is felt at the marked out points which confirms the perforator sites.
  • 26. Venous Doppler  With patient standing, the Doppler probe is placed at sapheno-femoral junction and later wherever required.  Basically by hearing the changes in sound, venous flow, venous patency, venous reflux can be very well identified. 1. To find out DVT- very important 2. To find out sapheno-femoral, sapheno-popliteal incompetence 3. To find out perforator incompetence 4. Uniphasic signals signify flow in one direction-normal 5. Biphasic flow signifies reversal flow with incompetence
  • 27. Duplex scan  It is a highly reliable U/S Doppler imaging technique (high resolution B mode ultrasound imaging and Doppler ultrasound is used), which along with direct visualisation of veins, gives the functional and anatomical information and also colour map.  Examination is done in standing, lying down position and also valsalva manoeuvre.  DVT is very well identified by this method.
  • 28. Venography  Ascending venography was a very common investigation done before Doppler period. A tourniquet is applied above the malleoli and vein of the dorsal venous arch of foot is cannulated. Water soluble dye is injected, flows into the deep veins. X-rays are taken below and above knee level. Any block in deep veins, its extent, perforator status can be made out by this. It is good reliable investigation for DVT.
  • 29.  Descending venogram It is done when ascending venogram is not possible and also to visualise incompetent veins. Here contrast material is injected into femoral vein through a cannula in standing position. X rays pictures are taken to visualise deep veins and incompetent veins.
  • 30. Plethysmography It is a non invasive method which measures volume changes in the leg.  Photo plethysmography  Air plethysmography
  • 31. Photo plethysmography  Using probe transmission of light through the skin, venous filling of the surface venules which reflects the superficial venous pressure is measured.  Initially patient performs dorsiflexion at ankle for 10 times to empty the venules and pressure tracing falls in photo plethysmography.  Patient takes rest and refilling occurs. In normal people, it occurs through arterial inflow in 20-30 seconds.  In venous incompetence filling also occurs by venous reflux and refilling time is faster than normal  Site of reflux cannot be localised by this method.
  • 32. Air plethysmography  Patient is initially in supine position with veins emptied by elevation of leg. Air filled plastic pressure bladder is placed on calf to detect volume changes.  Minimum volume is recorded. Patient is turned to upright position and venous volume is assessed.  Maximum venous volume divided by time required to achieve maximum venous volume gives the venous filling index.  VFI is a measure of reflux  Ejection fraction is volume change measured prior and after single tiptoe manoeuvre which is a measure of calf pump action.  Residual venous fraction is an index of overall venous function which is venous volume in the leg after ten tiptoe manoeuvres divided by venous volume prior to manoeuvre.  Increased VFT and diminished ejection fraction in patient will benefit from surgery
  • 33. Treatment 1. Conservative treatment  Elastic crepe bandage application from below upwards or use of pressure stockings to the limb pressure gradient of 30-40 mmHg is provided.  Diosmin therapy which increases the venous tone.  Elevation of the limb- relieves oedema.  Unna boots- provide non elastic compression therapy. It comprises a guaze compression dressings that contain zinc oxide, calamine and glycerine that helps to prevent further skin break down. It is changed once a week.  Pneumatic compression method– provide dynamic sequential compression.
  • 34. 2. Drugs used for varicose veins  Calcium dobesilate—500 mg BD. Calcium dobesilate improves lymph flow; improves macrophage mediated proteolysis and reduces edema.  Diosmin 450 mg + Hesperidin 50 mg (DAFLON 500 mg). Mainly used in relieving night cramps but not to improve healing of ulcers.
  • 35. 3. Injection– sclerotherapy: By injecting sclerotic agent into the vein, complete sclerosis of the venous walls can be achieved. Indication  Uncomplicated perforator incompetence  In the management of smaller varices- reticular  Recurrent varices  Isolated varices  aged / unfit patients
  • 36. Sclerosants used are—  Sodium tetradecylsulphate 3%(STDS) – commonly used  Sodium morrhuate  Ethanolamine oleate  Polidocanol Mechanism of action  Causes aseptic inflammation  Causes perivenous fibrosis leading to block  Causes approximation of intima leading to obliteration by endothelial damage  Alters intravascular pH / osmolality  Changes surface tension of plasma membrane.
  • 37.  A 23 gauge needle is inserted into the vein (3-8 mm sized) and vein is emptied. 0.5-1 ml of sclerosant is injected into the vein and immediately compression is applied on the vein.  So as to allow the development of sclerosis and to have proper endothelial apposition.  Usually injection is started at the ankle region and then proceeded upwards along the length of veins at different points.  Later pressure bandage is applied for six weeks. Often injections may have to be repeated at 2- 4weeks intervals for 2-4 sessions. Technique is called as macrosclerotherapy
  • 38. Microsclerotherapy  Very dilute solutions of sclerosing agent like STDS(0.1% of 0.1 ml dilute) polidoconol is injected into the thread veins and reticular veins followed by application of compression bandage  Dermal flare will disappear well by this method
  • 39. Contraindiactions for sclerotherapy  Sapheno femoral incompetence  Deep venous thrombosis  Huge varicosities– may precipitate DVT  Peripheral arterial diseases  Hypersentivity / immobilty  Venous ulcer– relative contrainidication Advantages  It can be done as an outpatient procedure  It does not require aneasthesia
  • 40. Disadvantage  Inadvertent subcutaneous injection can cause skin necrosis or abscess formation  Anaphylaxis  Hyperpigmentation  Thrombophlebitis  Deep vein thrombosis can occur
  • 41. Surgery A. Trendelenburg operation: It is juxta-femoral flush ligation of long saphenous vein (flush with femoral vein), after ligation superficial circumflex, superficial external pudendal, superficial epigastric vein, deep external pudendal vein and unnamed tributaries. All tributaries should be ligated, otherwise recurrence will occur Double saphenous vein is the commonest anomaly occuring near sapheno-venous junction.
  • 42. B. Stripping of vein: using Myer’s stripper vein is stripped off. Stripped from below upwards is technically easier. Immediate application of crepe bandage reduces the chance of bleeding and hemotoma formation. Stripping avulses the vein as well as obliterates the tributaries. Babcock’s stripper and rigid metal pin stripper can also be used. Stripping of the short saphenous vein is done from ankle below upward after passing stripper from above downwards. Complication is injury to saphenous or sural nerve causing neuralgia. Inverting or invaginating stripping using rigid Oesch pin stripper is better as postoperative pain and hematoma is less common and also there is tissue damage.
  • 43. C. Subfascial ligation of Cockett and Dodd Perforators are marked out by fegan’s method. Perforators are ligated deep to deep fascia through incisions in antero medial side of the leg.
  • 44. Radiofrequency ablation (RFA)  This is done under general or regional anaesthesia.  RFA catheter is passed into long / short saphenous vein near SFJ or SPJ under guidence. 85 Celsius temperature is used for long period of time to cause endothelial damage, collagen denaturation and venous constriction.  Phlebectomy is done while withdrawing the catheter. Wall of vein is destroyed through its full thickness.  Vein forms a cord, which gets dissolved by macrophages and immune cells.
  • 45. Endo venous laser ablation  It is done as a OP procedure.  Patient lies in supine with diseased leg flexed, hip externally rotated and knee flexed.  With aseptic precaution, under U/S guidance GSV is cannulated above the knee and a guide wire is passed beyond SJF and 5- French catheter is passed over guide wire and tip is placed 1cm distal to the junction.  200 ml of 0.1% lignocaine is infilterated along the length of the GSV.  Laser fibre is inserted up to the tip of the catheter and catheter is withdrawn for 2 cm and laser fibre protrudes for 2 cm.  Laser fibre is fired step by step using diode laser, one mm withdrawal in 2 seconds.
  • 46.  Once procedure is over catheter is removed and pressure bandage is applied for 2 weeks.  Heat produced (729 – 1000 Celsius) by the laser produces steam bubbles with thermal damage of endothelium leading into occlusion of the vein.  Laser therapy has inability to create flush occlusion allowing tributaries to open up and cause recurrence.
  • 47. SUBFASCIAL ENDOSCOPIC PERFORATOR SURGERY (SEPS)  First described by Heuer in 1980, it became the most accepted surgical treatment of advanced stages of chronic venous insufficiency because it is minimally invasive nature and safety profile  Can be performed with one or two endoscopic ports, the two port technique uses one 10 mm video port for camera and 5 mm port for instrumentation.  The limb is elevated and the field is made bloodless by using a Esmarch bandage, and a thigh tourniquet is inflated to 300 mmHg.  10 mm port is placed in the healthy medial aspect of calf, 10 cms distal to tibial tuberosity.  Avoid large opening because gas may leak and cause poor visibility.
  • 48.  The camera is inserted into the 10mm port and then second 5 mm port is inserted under direct vision about 10-20 cm distal and posterior to the first port.  CO2 is insufflated to enlarge and optimally visualise the subfascial space, with pressure maintained at around 30 mmHg.  All the visible perforators after dissection are interrupted by using harmonic scalpel, electrocautery or division with scissors between metallic clips.  More proximal paratibial perforators are visualised better by exposing the medial insertion of the soleus on the tibia, remain close to tibia to avoid damage to posterior tibial vessels and nerve.  On completion, the ports are removed, tourniquet is deflated and CO2 is manually expressed from subfascial space.  Local anaesthetic solution is instilled into the subfascial space to help with postoperative analgesia and compressive bandage is applied.
  • 49.
  • 50. Transilluminated phlebectomy  It is done by passing transilluminating light under the skin and passing a rotating blade through another small incision.  Veins are grasped and removed by rotating movements.
  • 51. AMBULATORY PHLEBECTOMY Done through small incisions using special phlebectomy instruments. ELECTRODESSICATION Using weak electric current through a fine needle directly into the spider veins.