Venous Disease and Chronic Ulcers Flashcards
What is chronic venous disease?
Disease where VR is impaired leading to sustained venous HTN
What are the 3 main pathological mechanisms contributing to the development of chronic venous disease?
ROC:
Reflux
Obstruction
Calf muscle pump failure
Describe the superficial venous system of the lower limb
Greater saphenous vein
Small saphenous vein
Anterior accessory saphenous vein
Vein of Giacomini
Describe the deep venous system of the lower limb
Tibial veins
Popliteal vein
Superficial femoral vein
Common femoral vein
External iliac vein
Common iliac vein
What structures join the superficial and deep venous systems?
Perforating veins (with unidirectional valves to prevent reflux)
Saphenofemoral junction (SFJ)
Saphenopopliteal junction (SPJ)
What is the prevalence of chronic venous insufficiency in the adult population?
10-35%
What % of recognised ulcers have been present for >12 months?
50%
Describe the pathophysiology of venous disease
Blood flows from superficial to deep veins through unidirectional valves During exercise, a combination of the calf muscle pump, vein patency and valvular competence reduces venous pressure from 90 mmHg to 30 mmHg Failure of any or all of these systems results in chronic venous insufficiency Pathway from venous HTN to ulceration not fully understood and still debated (“white cell trapping” and “fibrin cuff” theories are most popular)
Describe the “white cell trapping” hypothesis of venous disease
WBCs are larger and less deformable than RBCs When perfusion pressure is reduced by venous HTN, WBCs plug capillaries and RBCs build up behind WBC activation occurs Endothelial adhesion by WBC releases proteolytic enzymes and oxygen free radicals causing endothelial and tissue damage
Describe the “fibrin cuff” hypothesis of venous disease
Increased venous pressure is directly transmitted to capillaries resulting in capillary elongation and increased endothelial permeability Larger molecules such as fibrinogen become deposited into tissues Fibrinogen is converted to fibrin Accumulation of fibrin acts as barrier to oxygen and causes tissue hypoxia leading to ulceration
CEAP classification for chronic venous disease
Clinical classification Etiologic classification Anatomic classification Pathophysiologic classification
Categories of clinical classification in CEAP
C0: no visible or palpable signs of venous disease C1: telangiectasies or reticular veins C2: varicose veins C3: oedema C4a: pigmentation or eczema C4b: lipodermatosclerosis or atrophie blanche C5: healed venous ulcer C6: active venous ulcer Then can be S: symptomatic or A: asymptomatic
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Telangiectasies or reticular veins (C1)
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Lipodermatosclerosis (C4b)
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Atrophie blanche (C4b)
Symptoms of chronic venous disease
Pain (aching, tightness) Skin irritation Calf heaviness Muscle cramps
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Venous eczema
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Varicose veins
Categories of etiologic classification in CEAP
Ec: congenital Ep: primary Es: secondary (post-thrombotic) En: no venous cause identified
Categories of anatomic classification in CEAP
As: superficial veins Ap: perforator veins Ad: deep veins An: no venous location identified
Categories of pathophysiologic classification in CEAP
Pr: reflux Po: obstruction Pr,o: reflux and obstruction Pn: no venous pathophysiology identifiable
What is a varicose vein?
Elongated, tortuous, dilated vein (thin-walled,, valve deformed, resulting in abnormal blood flow and bulging of the skin)
Distinguish between primary and secondary varicose veins
Primary: affecting superficial veins or perforators in the absence of deep incompetence Secondary: associated with deep venous incompetence from recanalisation of previous DVT (i.e. venous obstruction)
What are the only solid predisposing factors for varicose veins?
Genetics Previous DVT
How much risk does genetics confer for varicose veins?
If both parents affected, risk is 90% If one parent affected, risk is 25% for males and 62% for females
Describe the clinical presentation of varicose veins
Cosmetic issues (e.g. telangiectasia, reticular veins, varices) Pain (general leg ache or heaviness) Swelling (early on causes ankle pitting oedema, later may become indurated) Thrombophlebitis Bleeding Skin changes (varicose eczema, pigmentation, lipodermatosclerosis, atrophie blanche) Ulceration