Venous Insufficiency Flashcards
Klippel Trenaunay Syndrome
Port wine stain
VV
Bone and soft tissue hypertrophy involving extremity
Venous hypertensive skin changes
Corona phlebatactica Atrophic blanche Pigmentation (hemosiderin deposition) Lipodermatosclerosis Ezcema
CEAP classification categories
Clinical
Etiology
Anatomy
Pathophysiology
Clinical classification of CEAP C0 C1 C2 C3 C4 C5 C6
C0 no visible disease C1 telengectasia, reticular vein C2 varicose veins C3 edema C4 skin changes C5 healed ulcers C6 active ulcers
Etiology classification of CEAP Ep Es Esi/Ese Ec
Ep: primary Es: secondary Esi: intravenous Ese: extravenous Ec: congenital
Anatomy classification of CEAP
As: superficial vein
Ad: deep vein
Ap: perforator vein
An: none identified
Pathophysiology classification of CEAP
Pr reflux
Po obstruction
Pro reflux + obstruction
Pn normal
Risk factors for varicose vein
Obesity Pregnancy Previous DVT Family history Posture (standing for prolonged periods of time)
Course of long saphenous vein
Medial end of dorsal venous arch Pass anterior to medial malleolus Runs along anteriomedial aspect of calf Passes patella to anteromedial aspect of thigh Joins saphenous vein at SFJ
Course of short saphenous vein
Lateral end of dorsal venous arch
Passes behind lateral malleolus
Joins popliteal vein in popliteal fossa
SSV is accompanied by which nerve?
Sural nerve
PE for VV
Abdominal exam: r/o VV secondary to abdominal mass
Peripheral pulse: r/o concomitant PVD
LL exam:
Look: skin changes, atrophic signs, ulcers
Trendelenberg test: SFJ incompetence
Tourniquet’s test: perforator incompetence
Perthe’s test: deep venous incompetence
European classification of compression hosiery
Class I
Class II
Class III
I: 14-17mmHg (light)
II: 18-24mmHg (medium)
III: 25-35 mmHg (strong)
CI in ABI < 0.9
Daflon
micronised purified flavonoid fraction
Phlebotonic drug: reinforces venous tone by prolonging parietal NA
Vascular protecting agents: combats venous inflammation by decreasing leukocyte activation
Treatment options for varicose veins
Medical Endovascular -Sclerotherapy -Radiofrequency ablation (RFA) -Endovascular laser ablation (EVLA) -Mechanico-chemical endovenous ablation Open
DDX of chronic leg swelling
Venous: -primary vv -primary deep vein incompetence -post thrombotic syndrome -AVM Lymphoedema General: -Fluid overload (CHF, liver failure, nephrotic syndrome) -Pretibial myxoedema Tumor Drug Dependency (postural)
Pathophysiology of CVI
Fibrin cuff hypothesis
White cell trapping hypothesis
Proliferation of capillary
Fibrin cuff hypothesis
Venous hypertension lead to increase porosity
Extravasation of blood constituents including fibrin
Fibrin induced tissue ischemia and cell death
White cell trapping hypothesis
Venous hypertension leads to white cell migration to interstitial space
release proteolytic enzymes and free radicals leading to tissue damage
Aim of CVI management
Correct any underlying causes
Prevention and treatment of complications
Management of CVI
Limb elevation
Exercise
Multilayered graduated elastic compression stockings
Medication - pentoxyfylline (Trental)
Surgery:
-superficial: endovenous
-deep: no definite guidelines, limited experience, highly subspecialized
Layers in multilayered graduated elastic compression stocking
Layer 1: orthopaedic wool/ Velband Layer 2: cottone crepe (Steroplast) Layer 3: elastic, extensible bandage (Elastoplast) Layer 4 Cohesive bandage (Coban)
Pentoxyfylline
Phosphodiesterase inbhitior
For better ulcer healing (RCTs)
Benefits of multilayered graduated elastic compression
symptomatic relief
promote ulcer healing
prevent ulcer recurrence
Evidence: Cochrane review
