Venous Insufficiency Flashcards
Diagnosis
Identification of the underlying pathophys of the wound is critical to development and implementation of a POC
Artery vs. Vein
Size of muscular wall is large in arteries!
Arterial system is a resistance system with more pressure in it
Veins have smaller vascular wall so less pressure associated with it
Vein has what
valves - so blood moves in one direction only
Elastin a vs. vein
the larger the artery, the more recoil the artery will have
veins have elastin but not as much as arteries
so arteries have blood flow into them, they contract, and as blood moves away, the elastic contracts and allows for maintenance of normal pressure on the arteries - this is less true for the veins
Endothelial cells (inside - lumina)
they respond to shear stress
blood flow through the a and v is a shear force
They respond to inc in flow pressures by releasing inflammatory mediators that produce localized ifnlammation in the local areas - happens more in artery side because more pressure there
Endothelial cells also release growth factors
Epidermis vascularization
NONE!!! no vascularization within it
Basement membrane does wht
reduce friction between epidermis and dermis
Beneath the basement membrane is what
Plexus moves into basement membrane Another one between the dermis and the adipose tissue Another layer within subQ tissue Each of these is larger as you go deeper
Deep veins
Run along with arteries that share their name - might be more than one vein that runs along with it
Contained in the same sheath as the artery
Deep veins are thinner and less muscular than the superficial veins - they have less pressure associated with them than the superficial veins do
Because they are so deep though they have a little more pressure related to soft tissue around them
LE venous anatomry - deep veins
Anterior tibial vein Posterior tibial vein Peroneal vein Popliteal vein Femoral vein Deep femoral vein Common femoral vein
Perforating veins do what
connect superficial veins to deep veins
Perforating vein - venous insufficiency theory
Thought is that it might be an issue with the valve not getting the blood to the superficial?
Superficial veins of LE
Great saphenous vein
Small saphenous vein
What happens in the ankle are
The blood moves directly into the deep veins and from the deep veins it moves into the superficial veins which then fills the saphenous veins and then perforating veins and then deep veins further up
This is why we often see venous insufficieicny in the medial ankle region
Venous insufficiency ulcers
Chronic condition
Insidious
Venous hypertension exists!!! - this is the primary cause!
Theories of venous insufficiency ulcers
Fibrin cuff theory of ulcer development
White blood cell trapping
Growth factor trapping (this is outlier of the theories)
Theories of venous insufficiency ulcers - Fibrin cuff
Constant venous hypertension causes widening of capillary pores
This allows large molecules like fibrinogen to move through
Fibrin accumulates around the vascular walls and within the interstitial spaces
Mechanical barrier is built
This is an older theory
Theories of venous insufficiency ulcers - Growth factor trapping
The cuff traps growth factors into its matrix decreasing its availability (of growth factors to health insult to tissue)
Theories of venous insufficiency ulcers - White blood cell trapping AKA ischemia reperfusion injury
Cycling venous pressure allow an accumulation of WBCs in the capillaries
Localized ischemia occurs secondary to dec flow
WBC become activated and release lytic enzymes - other infalmmatory cytokines activate
Skin characteristics in a CVI ulcer
1 Hyperprofileration of the epidermis
2 Thickening of the dermis with the dermal epidermal junction becoming convoluted
3 Dermal tissue changes may impair keratinocyte migration
All of this leads to - Lipodermatosclerosis (sclerosis, skin, fat)
Lipodermatosclerosis
Heardening (sclerosis) of the skin
A form of panniculitis/inflammation of the SubQ tissue
Risk factors
Calf muscle pump failure (weak, sustained standing) Vein dysfunction - varicosities Age over 65 Diabetes Mellitus Trauma
Differential diagnosis
Ischemic ulcer
Diabetic (neuropathic) ulcer
Clinical classification - CO - class
No visible or palpable signs of venous disease
Clinical classification - C6 - class
Skin changes are defined above with active ulceration
Clinical classification - S - clinical presentation class
symptomatic - but not seeing the classic venous signs
Clinical classification - A
asymtomatic
E - etiological classification
Ec = congenital Ep = primary Es = secondary (postthrombotic) En = no venous causes identified
Anatomic classification
As = superficial veins Ap = perforator veins Ad = deep veins An = no venous location identified
Pathophysiologic classifciation
Pr = reflux
Po = obstruction
Pr, O = reflux and obstruction
Pn = no venous pathophys identifiable
Venous insufficiency ulcers -c haracterisitcs
1 hemosiderin deposits 2 lipodermatosclerosis 3 generally on medial aspect of leg above medial malleolus 4 loss of subQ fat 5 dry skin surrounding wound 6 shallow wound 7 irregular wound margins 8 moderate to severe exudate 9 mild pain 10 red round bed may have fibrous yellow or white slough
Venous insufficiency ulcers - general tx guidelines
1 infection prevention, measures needed 2 dec risk of trauma 3 LE exercises 4 promote healing - edema control, compression, dressing to control exxudate) 5 clean and moisturize skin 6 pt education regarding life long care
Venous insufficiency ulcers - general tx guidelines - dressing that control exudate
usual semipermeable semiocclusive
