VARICOSEVEINS
DR. MD. SHERAJUL ISLAM
FCPS (Surgery), FACS(USA)
Assistant Professor, Surgery
Sheikh Sayera Khatun Medical College
ANATOMY OFVEINS OF LOWER LIMB
DeepVeins
•Tibial, popliteal and femoral veins are called “veins of
conduits” which drain blood into iliac veins and then to IVC
• Pumping veins:They are venous sinuses existing in the calf
muscles which pump blood towards major veins.They are
better termed as musculovenous pumps.They are also
called as the peripheral heart
SuperficialVeins
• Long saphenous vein/Great Saphenous vein:
Subcutaneous vein over the inner aspect of the leg and thigh, joins
into femoral vein at fossa ovalis
Tributaries are:
 posterior arch vein
anterior vein of leg
 anterolateral vein
 posteromedial vein
sometimes accessory saphenous vein
SuperficialVeins
• Short saphenous vein:
It is over the lateral and posterior aspect of the leg enters the
deep fascia in the upper calf region and later joins popliteal
vein at variable distance
• Posterior arch vein of Leonardo
• Anerior arch vein to peroneal veins
Superficial veins
•Superficial veins have got multiple valves
which facilitates blood flow towards heart.
Superficial veins usually drain about 10% of
lower limb blood i.e. from skin and
subcutaneous tissues
PerforatorVeins
They are the veins which connect superficial to deep veins
• They travel from superficial fascia through an opening in the
deep fascia before entering the deep veins
• The direction of blood flow here is from superficial to deep veins
•These perforators are also guarded by valves so that the blood
flow is unidirectional
•Reversal of flow occurs due to incompetence of perforators
which will lead to varicose veins
Types of perforators
• Ankle perforators (May or Kuster)
• Lower leg perforators: I, II, III (of Cockett)
• Gastrocnemius perforators (of Boyd)
• Mid thigh perforators (Dodd)
• Hunter’s perforator in the thigh
PHYSIOLOGY OFVENOUS BLOOD
FLOW IN LOWER LIMB
• Veins are thin-walled vessels with collapsible walls, that
assume an elliptical configuration in collapsed state and
circular configuration in the filled state
• Venous valves are abundant in the distal lower extremity
and the number of valves decreases proximally, with no
valves in superior and inferior vena cava.
Venous Return :
• 1. Arterial pressure across the capillary increases the pumping action of vein
• 2. Calf musculovenous pump: During contraction phase of walking, pressure
in the calf muscles increases to 200-300 mmHg.This pumps the blood
towards the heart.
During relaxation phase of walking, pressure in the calf falls and allows blood
to flow from superficial to deep veins through perforators. Normally while
walking, pressure in the superficial system at the level of ankle is 20 mmHg
• 3. During walking, foot pump mechanism propels blood from plantar veins
into the leg
• 4. Gravity. Note: Pressure in arteriolar end of the capillary is 32 mmHg;
venular end of capillary is 12 mm Hg
Factors responsible for venous return
•1. Negative pressure in thorax
• 2. Peripheral pump—calf muscles
• 3.Vis-a-tergo of adjoining muscles
• 4. Nonrefluxing valves in course of veins
VARICOSEVEINS
•They are dilated, tortuous, elongated veins in the
leg
•There is reversal of blood flow through its faulty
valves
Types:
• 1. Long saphenous vein varicosity
• 2. Short saphenous vein varicosity
• 3.Varicose veins due to perforator incompetence
• 4.Thread veins are small varices in the skin usually around ankle which
look like dilated, red or purple network of veins
• 5. Reticular varices (1-3 mm in size): Are slightly larger varices than
thread veins located in subcutaneous region
• 6. Combinations of any of above. Small varicose vein is < 3 mm in
diameter. Large varicose vein is > 3 mm in diameter
Pathogenesis:
TwoTheories:
• Fibrin cuff theory
•White cell trapping theory
Pathogenesis:
• Incompetence of venous valves
• ↓↓ ↓↓ ↓
• Stasis of blood
• ↓↓ ↓↓ ↓
• Chronic ambulatory venous hypertension
• ↓↓ ↓↓ ↓
• Defective microcirculation
Pathogenesis:
•↓↓ ↓↓ ↓
•RBC diffuses into tissue planes
• ↓↓ ↓↓ ↓
• Lysis of RBC’s
• ↓↓ ↓↓ ↓
• Release of haemosiderin
•↓↓
Pathogenesis:
•Pigmentation
•↓↓ ↓↓ ↓
•Dermatitis
•↓↓ ↓↓ ↓
• Capillary endothelial damage
Pathogenesis:
• ↓↓ ↓↓ ↓
•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—White cell trapping
theory
•Fibrin deposition, tissue death, scarring occurs
together, called as lipodermatosclerosis.
Classification of lower-extremity venous
diseases
CEAP classification
C — Clinical signs (grade 0-6); (A) for asymptomatic or (S)
for symptomatic presentation
E — Etiologic classification (congenital, primary,
secondary)
A — Anatomic distribution (superficial, deep or
perforator)
P — Pathophysiologic dysfunction (reflux or obstruction)
Aetiology ofVaricoseVeins
• Varicosities are more common in lower limb because of erect posture and long
column of blood has to be supported which can lead to weakness and
incompetency of valves
• Incidence is 5% of adult population
• A. Primary varicosities
• B . Secondary varicosities
A. Primary varicosities
A. Primary varicosities due to:
•1. Congenital incompetence or absence of valves
•2.Weakness or wasting of muscles—defective
connective tissue and smooth muscle in the venous wall
•3. Stretching of deep fascia
•4. Inheritance (family history) with FOXC2 gene
• 5. Klippel –Trenaunay syndrome.
B. Secondary varicosities
• 1. Recurrent thrombophlebitis
• 2. Occupational – standing for long hours (traffic police,
guards)
• 3. Obstruction to venous return like abdominal tumour,
retroperitoneal fibrosis, lymphadenopathy
• 4. Pregnancy (due to progesterone hormone).
• 5. AV malformations—Congenital or acquired.
• 6. Iliac vein thrombosis
Sites where varicosities can occur
i. Lower limb
ii. Pampiniform plexus of veins
iii.Vulva
iv. Sites of portosystemic anastomosis
Predisposing factors for varicose veins
are:
• age
•Sex
• race
•Obesity
• height
• left > right
• occupation
•family history
•erect posture
Clinical Features
Symptoms in varicose veins
• Dragging pain
• Heaviness in the legs
• Night time cramps – usually late night
• Oedema feet
• Discolouration/ulceration in the feet/painful walk
Signs:
•1.Visible dilated veins in the leg with pain, distress, nocturnal
cramps, feeling of heaviness, pruritus
•2. Pedal oedema, pigmentation, dermatitis, ulceration, tenderness,
restricted ankle joint movement
• 3. Bleeding, thickening of tibia occurs due to periostitis
• 4. Positive cough impulse at the sapheno-femoral junction.
Saphena varix – a large varicosity in the groin, which becomes
visible and prominent on coughing
Signs:
• 5. Brodie-Trendelenburg test:Vein is emptied by elevating the limb and
a tourniquet is tied just below the sapheno-femoral junction (or using
thumb, sapheno-femoral junction is occluded)
• Patient is asked to stand quickly
• When tourniquet or thumb is released, rapid filling from above
signifies saphenofemoral incompetence
• This isTrendelenburg test I
• InTrendelenburg test II, after standing tourniquet is not released.
Filling of blood from below upwards rapidly can be observed within 30-
60 seconds. It signifies perforator incompetence
Signs:
•6. Perthe’s test:The affected 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
• 7. Modified Perthe’s test:Tourniquet is tied just below the
sapheno-femoral junction 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.
Signs:
• 8.Three tourniquet test:
• To find out the site of incompetent perforator, three tourniquets
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
Signs:
• 9. Schwartz test
•10.Pratt’s test:
•11.Morrissey’s cough impulse test
•12.Fegan’s test
•13. Ian-Aird test
•14.Examination of the abdomen has to be done to look for
pelvic tumours, lymph nodes, which may compress over the
veins to cause varicosity
Investigations
•1.Venous Doppler
•2. Duplex scan
•3.Venography
•4. Plethysmography
•5. Ambulatory venous pressure (AVP):
•6. Arm-Foot venous pressure
Investigations:
• 7. U/S abdomen, peripheral smear, platelet count, other relevant
investigations are done depending on the cause of the varicose veins
• 8. If venous ulcer is present, then the discharge is collected for
culture and sensitivity, biopsy from ulcer edge is taken to rule out
Marjolin’s ulcer
• 9. Plain X-ray of the part is taken to look for periostitis
• 10.Varicography: Here non-ionic, iso-osmolar, nonthrombogenic
contrast is injected directly into the variceal vein to get a detailed
anatomical mapping of the varicose veins. It is used in recurrent
varicose veins.
Differential diagnosis
• Lymphoedema
• A-V malformation
• Orthostatic oedema
• Renal and cardiac disease
• Hepatic causes
Vasculitis
• Metabolic diseases like gout, myxoedema, and morbid obesity
• Chronic infections like tuberculosis, syphilis
Treatment
1. Conservative treatment:
• Elastic crepe bandage application from below upwards or use of pressure
stockings to the limb— pressure gradiant of 30-40 mmHg is provided.
• Diosmin therapy which increases the venous tone.
• Elevation of the limb—relieves oedema.
• Unna boots—provide nonelastic compression therapy. It comprises a gauze
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
Treatment
2. Drugs used for varicose veins:
• Calcium dobesilate—500 mg BD. Calcium dobesilate improves
lymph flow; improves macrophage mediated proteolysis; and
reduces oedema.
• Diosmin—450 mg BD • Diosmin 450 mg + Hesperidin 50 mg
(DAFLON 500 mg). Mainly used in relieving night cramps but not to
improve healing of ulcers
•Toxerutin 500 mg BD,TID. Anti erythrocyte aggregation agent
which improves capillary dynamics. Benefits of all these drugs are
doubtful.
Treatment
3. Injection—sclerotherapy: (Fegan’s technique)
By injecting sclerosants into the vein, complete sclerosis of the venous walls
can be achieved
Indications
• Uncomplicated perforator incompetence
• In the management of smaller varices—reticular veins, thread veins
(telangiectasis)
• Recurrent varices
• Isolated varicosities
• Aged/unfit patients.
Treatment
Sclerosants used are—
• Sodium tetradecyl sulphate 3% (STDS)–commonly used
• Sodium morrhuate
• Ethanolamine oleate
• Polidocano
Treatment
Contraindications for sclerotherapy
• Sapheno femoral incompetence
• Deep venous thrombosis
• Huge varicosities – may precipitate DVT
• Peripheral arterial diseases
• Hypersensitivity/immobility
•Venous ulcer – relative contraindication
Treatment
4. Surgery:
•a.Trendelenburg operation
•b. Stripping of vein
•c. Subfascial ligation of Cockett and Dodd
•d. Ligation of short saphenous vein at saphenopopliteal
junction
•e. Removal of superficial varicose veins by hook
phlebectomy
Treatment
•f. Linton’s vertical approach—subfascial ligation of
perforators
•g. Stab avulsion of varicose vein and perforators
•h. Subfascial endoscopic perforator ligation surgery (SEPS)
•i. Radiofrequency ablation (RFA) method (VNUS closure
method
•j.Trivex method
•k. Endo venous laser ablation (EVLA)
Complications ofVaricoseVeins
• Haemorrhage:Venous haemorrhage can occur from the
ruptured varicose veins or sloughed varicose veins, often
torrential, but can be controlled very well by elevation
and pressure bandage
• Eczema and dermatitis
• Periostitis causing thickening of periosteum
Complications ofVaricoseVeins:
•Venous ulcer
• Marjolin’s ulcer
• Lipodermatosclerosis
• Ankylosis of the ankle joint
•Talipes equino varus
• Deep venous thrombosis
• Calcification
•Thrombophlebitis
Varicose vein

Varicose vein

  • 1.
    VARICOSEVEINS DR. MD. SHERAJULISLAM FCPS (Surgery), FACS(USA) Assistant Professor, Surgery Sheikh Sayera Khatun Medical College
  • 2.
  • 3.
    DeepVeins •Tibial, popliteal andfemoral veins are called “veins of conduits” which drain blood into iliac veins and then to IVC • Pumping veins:They are venous sinuses existing in the calf muscles which pump blood towards major veins.They are better termed as musculovenous pumps.They are also called as the peripheral heart
  • 4.
    SuperficialVeins • Long saphenousvein/Great Saphenous vein: Subcutaneous vein over the inner aspect of the leg and thigh, joins into femoral vein at fossa ovalis Tributaries are:  posterior arch vein anterior vein of leg  anterolateral vein  posteromedial vein sometimes accessory saphenous vein
  • 6.
    SuperficialVeins • Short saphenousvein: It is over the lateral and posterior aspect of the leg enters the deep fascia in the upper calf region and later joins popliteal vein at variable distance • Posterior arch vein of Leonardo • Anerior arch vein to peroneal veins
  • 9.
    Superficial veins •Superficial veinshave got multiple valves which facilitates blood flow towards heart. Superficial veins usually drain about 10% of lower limb blood i.e. from skin and subcutaneous tissues
  • 10.
    PerforatorVeins They are theveins which connect superficial to deep veins • They travel from superficial fascia through an opening in the deep fascia before entering the deep veins • The direction of blood flow here is from superficial to deep veins •These perforators are also guarded by valves so that the blood flow is unidirectional •Reversal of flow occurs due to incompetence of perforators which will lead to varicose veins
  • 11.
    Types of perforators •Ankle perforators (May or Kuster) • Lower leg perforators: I, II, III (of Cockett) • Gastrocnemius perforators (of Boyd) • Mid thigh perforators (Dodd) • Hunter’s perforator in the thigh
  • 12.
    PHYSIOLOGY OFVENOUS BLOOD FLOWIN LOWER LIMB • Veins are thin-walled vessels with collapsible walls, that assume an elliptical configuration in collapsed state and circular configuration in the filled state • Venous valves are abundant in the distal lower extremity and the number of valves decreases proximally, with no valves in superior and inferior vena cava.
  • 13.
    Venous Return : •1. Arterial pressure across the capillary increases the pumping action of vein • 2. Calf musculovenous pump: During contraction phase of walking, pressure in the calf muscles increases to 200-300 mmHg.This pumps the blood towards the heart. During relaxation phase of walking, pressure in the calf falls and allows blood to flow from superficial to deep veins through perforators. Normally while walking, pressure in the superficial system at the level of ankle is 20 mmHg • 3. During walking, foot pump mechanism propels blood from plantar veins into the leg • 4. Gravity. Note: Pressure in arteriolar end of the capillary is 32 mmHg; venular end of capillary is 12 mm Hg
  • 14.
    Factors responsible forvenous return •1. Negative pressure in thorax • 2. Peripheral pump—calf muscles • 3.Vis-a-tergo of adjoining muscles • 4. Nonrefluxing valves in course of veins
  • 15.
    VARICOSEVEINS •They are dilated,tortuous, elongated veins in the leg •There is reversal of blood flow through its faulty valves
  • 16.
    Types: • 1. Longsaphenous vein varicosity • 2. Short saphenous vein varicosity • 3.Varicose veins due to perforator incompetence • 4.Thread veins are small varices in the skin usually around ankle which look like dilated, red or purple network of veins • 5. Reticular varices (1-3 mm in size): Are slightly larger varices than thread veins located in subcutaneous region • 6. Combinations of any of above. Small varicose vein is < 3 mm in diameter. Large varicose vein is > 3 mm in diameter
  • 17.
    Pathogenesis: TwoTheories: • Fibrin cufftheory •White cell trapping theory
  • 18.
    Pathogenesis: • Incompetence ofvenous valves • ↓↓ ↓↓ ↓ • Stasis of blood • ↓↓ ↓↓ ↓ • Chronic ambulatory venous hypertension • ↓↓ ↓↓ ↓ • Defective microcirculation
  • 19.
    Pathogenesis: •↓↓ ↓↓ ↓ •RBCdiffuses into tissue planes • ↓↓ ↓↓ ↓ • Lysis of RBC’s • ↓↓ ↓↓ ↓ • Release of haemosiderin •↓↓
  • 20.
  • 21.
    Pathogenesis: • ↓↓ ↓↓↓ •Prevention of diffusion and exchange of nutrients • ↓↓ ↓↓ ↓ •Severe anoxia • ↓↓ ↓↓ ↓ Chronic venous ulceration (Fibrin cuff theory)
  • 22.
    White cell trappingtheory: •Inappropriate activation of trapped leucocytes release proteolytic enzymes which cause cell destruction and ulceration—White cell trapping theory •Fibrin deposition, tissue death, scarring occurs together, called as lipodermatosclerosis.
  • 23.
    Classification of lower-extremityvenous diseases CEAP classification C — Clinical signs (grade 0-6); (A) for asymptomatic or (S) for symptomatic presentation E — Etiologic classification (congenital, primary, secondary) A — Anatomic distribution (superficial, deep or perforator) P — Pathophysiologic dysfunction (reflux or obstruction)
  • 24.
    Aetiology ofVaricoseVeins • Varicositiesare more common in lower limb because of erect posture and long column of blood has to be supported which can lead to weakness and incompetency of valves • Incidence is 5% of adult population • A. Primary varicosities • B . Secondary varicosities
  • 25.
    A. Primary varicosities A.Primary varicosities due to: •1. Congenital incompetence or absence of valves •2.Weakness or wasting of muscles—defective connective tissue and smooth muscle in the venous wall •3. Stretching of deep fascia •4. Inheritance (family history) with FOXC2 gene • 5. Klippel –Trenaunay syndrome.
  • 26.
    B. Secondary varicosities •1. Recurrent thrombophlebitis • 2. Occupational – standing for long hours (traffic police, guards) • 3. Obstruction to venous return like abdominal tumour, retroperitoneal fibrosis, lymphadenopathy • 4. Pregnancy (due to progesterone hormone). • 5. AV malformations—Congenital or acquired. • 6. Iliac vein thrombosis
  • 27.
    Sites where varicositiescan occur i. Lower limb ii. Pampiniform plexus of veins iii.Vulva iv. Sites of portosystemic anastomosis
  • 28.
    Predisposing factors forvaricose veins are: • age •Sex • race •Obesity • height • left > right • occupation •family history •erect posture
  • 29.
    Clinical Features Symptoms invaricose veins • Dragging pain • Heaviness in the legs • Night time cramps – usually late night • Oedema feet • Discolouration/ulceration in the feet/painful walk
  • 30.
    Signs: •1.Visible dilated veinsin the leg with pain, distress, nocturnal cramps, feeling of heaviness, pruritus •2. Pedal oedema, pigmentation, dermatitis, ulceration, tenderness, restricted ankle joint movement • 3. Bleeding, thickening of tibia occurs due to periostitis • 4. Positive cough impulse at the sapheno-femoral junction. Saphena varix – a large varicosity in the groin, which becomes visible and prominent on coughing
  • 31.
    Signs: • 5. Brodie-Trendelenburgtest:Vein is emptied by elevating the limb and a tourniquet is tied just below the sapheno-femoral junction (or using thumb, sapheno-femoral junction is occluded) • Patient is asked to stand quickly • When tourniquet or thumb is released, rapid filling from above signifies saphenofemoral incompetence • This isTrendelenburg test I • InTrendelenburg test II, after standing tourniquet is not released. Filling of blood from below upwards rapidly can be observed within 30- 60 seconds. It signifies perforator incompetence
  • 33.
    Signs: •6. Perthe’s test:Theaffected 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 • 7. Modified Perthe’s test:Tourniquet is tied just below the sapheno-femoral junction 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.
  • 35.
    Signs: • 8.Three tourniquettest: • To find out the site of incompetent perforator, three tourniquets 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
  • 37.
    Signs: • 9. Schwartztest •10.Pratt’s test: •11.Morrissey’s cough impulse test •12.Fegan’s test •13. Ian-Aird test •14.Examination of the abdomen has to be done to look for pelvic tumours, lymph nodes, which may compress over the veins to cause varicosity
  • 38.
    Investigations •1.Venous Doppler •2. Duplexscan •3.Venography •4. Plethysmography •5. Ambulatory venous pressure (AVP): •6. Arm-Foot venous pressure
  • 39.
    Investigations: • 7. U/Sabdomen, peripheral smear, platelet count, other relevant investigations are done depending on the cause of the varicose veins • 8. If venous ulcer is present, then the discharge is collected for culture and sensitivity, biopsy from ulcer edge is taken to rule out Marjolin’s ulcer • 9. Plain X-ray of the part is taken to look for periostitis • 10.Varicography: Here non-ionic, iso-osmolar, nonthrombogenic contrast is injected directly into the variceal vein to get a detailed anatomical mapping of the varicose veins. It is used in recurrent varicose veins.
  • 40.
    Differential diagnosis • Lymphoedema •A-V malformation • Orthostatic oedema • Renal and cardiac disease • Hepatic causes Vasculitis • Metabolic diseases like gout, myxoedema, and morbid obesity • Chronic infections like tuberculosis, syphilis
  • 41.
    Treatment 1. Conservative treatment: •Elastic crepe bandage application from below upwards or use of pressure stockings to the limb— pressure gradiant of 30-40 mmHg is provided. • Diosmin therapy which increases the venous tone. • Elevation of the limb—relieves oedema. • Unna boots—provide nonelastic compression therapy. It comprises a gauze 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
  • 42.
    Treatment 2. Drugs usedfor varicose veins: • Calcium dobesilate—500 mg BD. Calcium dobesilate improves lymph flow; improves macrophage mediated proteolysis; and reduces oedema. • Diosmin—450 mg BD • Diosmin 450 mg + Hesperidin 50 mg (DAFLON 500 mg). Mainly used in relieving night cramps but not to improve healing of ulcers •Toxerutin 500 mg BD,TID. Anti erythrocyte aggregation agent which improves capillary dynamics. Benefits of all these drugs are doubtful.
  • 43.
    Treatment 3. Injection—sclerotherapy: (Fegan’stechnique) By injecting sclerosants into the vein, complete sclerosis of the venous walls can be achieved Indications • Uncomplicated perforator incompetence • In the management of smaller varices—reticular veins, thread veins (telangiectasis) • Recurrent varices • Isolated varicosities • Aged/unfit patients.
  • 44.
    Treatment Sclerosants used are— •Sodium tetradecyl sulphate 3% (STDS)–commonly used • Sodium morrhuate • Ethanolamine oleate • Polidocano
  • 45.
    Treatment Contraindications for sclerotherapy •Sapheno femoral incompetence • Deep venous thrombosis • Huge varicosities – may precipitate DVT • Peripheral arterial diseases • Hypersensitivity/immobility •Venous ulcer – relative contraindication
  • 46.
    Treatment 4. Surgery: •a.Trendelenburg operation •b.Stripping of vein •c. Subfascial ligation of Cockett and Dodd •d. Ligation of short saphenous vein at saphenopopliteal junction •e. Removal of superficial varicose veins by hook phlebectomy
  • 47.
    Treatment •f. Linton’s verticalapproach—subfascial ligation of perforators •g. Stab avulsion of varicose vein and perforators •h. Subfascial endoscopic perforator ligation surgery (SEPS) •i. Radiofrequency ablation (RFA) method (VNUS closure method •j.Trivex method •k. Endo venous laser ablation (EVLA)
  • 48.
    Complications ofVaricoseVeins • Haemorrhage:Venoushaemorrhage can occur from the ruptured varicose veins or sloughed varicose veins, often torrential, but can be controlled very well by elevation and pressure bandage • Eczema and dermatitis • Periostitis causing thickening of periosteum
  • 49.
    Complications ofVaricoseVeins: •Venous ulcer •Marjolin’s ulcer • Lipodermatosclerosis • Ankylosis of the ankle joint •Talipes equino varus • Deep venous thrombosis • Calcification •Thrombophlebitis