VARICOSE VEINS

RISK FACTORS

Female gender Heridity

h/o trauma to extremity

Hormonal : estrogen & progesterone

Occupation

Pathophysiology

calf muscle augments return of blood to heart from extrimities

Calf muscle contracts →gastrocnimeus & soleus sinuses compressed→propels blood towards heart

Normal valves aid in retrograde flow

When one or more incompetant valves occurs ➔symptoms of venous insufficiency develops

Two source of developing varicose veins

1.Gravitational ; hydrostatic pressure

2.Dynamic ; force of muscle contraction

 

Incompetant valves of perforators→Compartment pressure increases (150 to 200mm Hg)→

Transmitted directly into superficial venous system→Sudden increase in pressure→Dilatation and lengthening of superficial veins

 

Cellular changes

  • Macrophage & monocytic infiltration in valves of veins with venous insufficiency
  • In regions of advanced venous insufficiency  capilliary proliferation occurs increased capilliary permeabilityleakage of fibrinogen
  • Fibrin remains in extravascular space pevents exchange of nutrients &oxygen to surrounding cells

 

Clinical features

Aching in veins – prolonged standing,relieved by elevation of limb

Ankle swelling

Cutaneous burning – venous neuropathy

pruritis – excess hemosiderin deposition

 

SKIN CHANGES

1)Lipodermatosclerosis : prolonged amulatory venous hypertension & c/c inflammation

Characterised by ; Brawny edema of distal calf,champagne bottle leg,fibrotic ,hypertrophic skin & hyperpigmentation

Advanced cases; fibrosis of achillis tendon

2)Atrophic blanche ; pale hue visualised around medial malleolus

3)Corona phlebectasia ; tiny telengiectasia usually at medial malleolus

Investigations

DOPPLER EXAMINATION

Emits sound when blood flows fast the transmitting & receiving channels

Unipasic signal :flow one direction

Biphasic flow : blood refluxing through incompetent valves

VARICOSE VEINS

VARICOSE VEINS

DUPLEX

Probe has multiple emitting & receiving crystals Direction of flow shown as colour image

B mode grey scale image; vein can be traced to termination

Perforators visualised

PHLEBOGRAPHY

Done preoperatively when deep venous reconstruction planned

Ascending & descending types

Indication for surgery

1)Cosmesis

2)Bleeding from vein

3)Superficial thrombophlebitis

3)Lipodermatosclerosis

4)Venous stasis ulcer

TRENDELENBURG’S PROCEDURE

Saphenofemoral junction ligation & greater saphenous vein stripping

Incision : oblique 2.5cm below & lateral to pubic tubercle

GSV is traced upwards to its termination blunt dissection

Ligated

GSV retrogradely stripped to knee using Babcock’s intraluminal stripper or Rigid metal pin stripper

Invagination of vein is done

 

Stirpping done from above downwards to avoid lymphatic and cutaneous nerve damage and avulsion of tribitaries

Incision : along langer’s line

Vein teased out of sucutaneous tissue using small hook/mosquito forceps

 

Saphenopopliteal junction ligation & leese   saphenous vein stripping

Incision ; transverse skin incision in popliteal fossa below termination of vein

Deep facia divided vertically

Vein identified & traced to saphenopopliteal junction,vein divided stripper passed upwards from ankle,carefully dissecting off sural nerve

 

Injection therapy

Fogan’s method

Detergent injected into superficial veins

Sodium tetradecyl sulphate – destroys lipid membrane of endothelial cells,shedding of cells →thrombosis,fibrosis,obliteration

Local compression applied after sclerosant injection

Patient asked  to walk frequently  to avid sup.thrombophlebitis

  • Allergic to sod tetradecyl ,use hypertonic saline

USG guided foam sclerotherapy

Needle introduced into vein under duplex USG guidance

Polidocanol sclerosant used

Top of saphenous vein compressed with probe to prevent foam entering deep vein

 

Endovenous therapy

Recent advances in ablation of incompetant great & small saphenus vein

radiofrequency closure

endovenous laser ablation

Can be done both are duplex guided percutaneous access

 

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