Clin Med - Venous Insufficiency Flashcards
Venous Vascular Diseases (5)
- Venous Insufficiency/Chronic Venous Insufficiency
- Varicose Veins
- Superficial Venous Thrombophlebitis
- Deep Vein Thrombosis (DVT)
- Arterial vs Venous Ulcers
Venous Insufficiency definition
venous blood refluxes backwards rather than following a normal antegrade path of flow, thereby resulting in venous congestion of the lower extremities
Venous insufficiency risk factors
- increasing age (women 40-49 y/o and men 70-79 y/o)
- family hx
- smoking
- prior h/o DVT
- prolonged standing
- female gender/pregnancy
- obesity
Venous Insufficiency Pathophysiology
-High venous pressure is responsible for many manifestations of venous insufficiency syndrome.
-Most commonly, congenitally weak/ abnormal vein walls may become incompetent and dilate under normal pressures to cause secondary valve failure
(direct injury or superficial phlebitis may cause primary valve failure).
Affect of hormonal influence on normal veins/valves
Normal veins and normal valves may also become excessively distensible under hormonal influence or pressure of the uterus over the abdominal veins (as in pregnancy).
Primary varicose veins result from…
Recent research shows that primary varicose veins may result from an intrinsic genetic defect of collagen synthesis.
Superficial veins - venous insufficiency
The superficial veins are a network of subcutaneous veins that are superficial to the deep fascia of the lower extremity and include the long saphenous and short saphenous veins.
Etiology of superficial venous insufficiency
- the deep veins are normal, but venous blood escapes from a normal deep system and flows backwards through dilated superficial veins in which the valves have failed.
- valve failure can be spontaneous in patients with congenitally weak valves
- congenitally normal valves can fail as a consequence of direct trauma, obesity, thrombophlebitis, or chronic environmental insult (prolonged standing)
Perforating veins - venous insufficiency
- The perforating veins communicate between the deep and superficial venous systems.
- They contain one-way valves to direct the blood from the superficial system to the deep system.
- -Cockett Perforators
- -Boyd’s Perforators (common site for varicose veins)
- -Dodd’s Perforators
- -Hunterian Perforator
Deep veins - venous insufficiency
The deep veins are located deep to the deep fascia. The deep veins, which accompany the lower extremity arteries, include the:
- -anterior tibial
- -posterior tibial
- -peroneal (fibular)
- -Popliteal
- -Femoral veins
Etiology of deep venous insufficiency
- Deep venous insufficiency can be due to congenital valve or vessel abnormalities.
- Most commonly occurs when the valves of the deep veins are damaged as a result of DVT.
- With no valves to prevent deep system reflux, the hydrostatic venous pressure in the lower extremity increases dramatically.
Chronic Venous Insufficiency Pathophys
Chronic Venous Insufficiency (CVI) refers to morphological and/or functional changes that may occur in the lower extremity due to persistent elevation of venous pressures.
CVI is commonly secondary to…
1) venous reflux due to faulty valve function developing as a long term sequel of DVT and recanalization or, 2) primary valvular incompetence without previous DVT.
Venous hypertension in diseased veins is thought to cause CVI through the following sequence of events (6)
1) Increased venous pressure capillary hypertension
2) Low-flow states within the capillaries cause leukocyte trapping
3) leukocytes release proteolytic enzymes and oxygen free radicals, which damage capillary basement membranes (this makes the capillaries permeable)
4) Plasma proteins leak into the surrounding tissues, forming a fibrin cuff
5) Interstitial fibrin and resultant edema decrease oxygen delivery to the tissues, resulting in local hypoxia
6) Leg edema/inflammation leads to skin changes in the form of tissue loss/ulceration
CVI History
- Patient will c/o swelling in lower legs/feet
- Leg fatigue, aching and/or discomfort
- Sensation of “heavy legs”
- Leg cramps
- Dry scaly skin
- Burning/itching of skin
- Ulcers
- Dilated veins
CVI Physical Exam
Corona phlebectatica (malleolar flare) –the presence of four components:
- ”Venous cups”
- Blue and 3. red telangiectasia
- Capillary “stasis spots”
CVI Physical Exam Cont.
- Leg/ankle 2+/3+ pitting edema
- Hyperpigmentation (reddish-brown discoloration/brawny edema)
- Lipodermatosclerosis (fibrotic changes)
- Atrophie blanche (round white, shiny atrophic patches surrounded by dilated capillaries/ hyperpigmentation)
- Leg ulcers (located in the gaiter area of the calf, proximal and posterior to the medial malleolus and superior to the lateral malleolus, non-painful)
- Telangiectasias (<1 mm), reticular veins (<3mm), dilated tortuous veins (<3 mm)
CVI Labs
- Consider PT/INR and PTT if pt is anti-coagulated
- HgbA1c
- Factor V Leiden mutation (strongly associated with venous ulcers)
CVI Imaging
- Duplex US (will show retrograde or reversed flow, valve closure time >0.5 seconds)
- CT venography (reveals detailed venous anatomy)
- Magnetic resonance venography
- Ascending phlebography
- Air plethysmography (APG)
- Measures venous congestion
CVI Procedures
- Biopsy of wound that will not heal/suspicion of malignancy/atypical location (Marjolin’s ulcer)
- ABI for evidence of arterial disease
- An ABI< 0.8 is a relative contradiction to compression therapy
- Used for compression stocking so that the patient doesn’t end up losing the limb
CVI Edema Treatment
- Short stretch multilayer bandages are ideal for acute phase until edema is stable and the patient can be fitted with compression stockings
- Graduated compression stockings worn during day and evening (have patient take off before bedtime; Aim for a minimum pressure 20-30 mm Hg, preferably 30-40 mm Hg)
- Elevation of legs to heart level for 30 min 3 to 4 x a day
- Exercise to strengthen calf muscle pump
- Moisturizer
- Weight loss/exercise plan
- Diuretics
- Control chronic health conditions – HTN, DM, etc
Stasis dermatitis/ulcers Treatment Wound Care
- Graded compression stockings
- Wound dressing – maintain moist wound environment
- Consider barrier ointment/cream
- Hydrogel if wound is dry
- Diosmin and hesperidin (Anti-oxidant flavonoids administered orally)
- Debride necrotic tissue
- Treat cellulitis
- Exercise
- Pentoxifylline orally
- Horse chestnut seed extract – administered PO to decrease leg pain
How do you treat cellulitis in CVI wound care?
-Cover for gram-positive bacteria, suspect infection if pt has pain, no improvement in wound after 2 weeks of compression
Organisms: Staph and Strep, MRSA is also a possibility
CVI Referrals
- Lymphedema therapist
- Wound clinic/care – intermittent compression pump or Vacuum assisted closure (VAC)
- Vein clinic/vascular specialist
- Home health/PT/OT – can have home health nurse come out and change patients dressings
CVI Treatment - Surgery
- Endovenous Ablation
- Sclerotherapy
- Bypassing blocked veins
- Valve repair
- Angioplasty and stenting of proximal blocked veins (Iliac vein stenting)
Varicose Veins Definition
- Superficial venous abnormality causing permanent dilation and tortuosity of superficial veins.
- Subcutaneous, permanently dilated veins 3 mm or more in diameter when measured in a standing position
- Occurs primarily in the superficial veins of the anterior thigh, calf, and ankle.
Varicose Veins Risk Factors
Increasing age, pregnancy, obesity, prolonged standing and positive family hx.
Varicose Veins Etiology
Caused by systemic weakness in the vein wall due to congenitally incomplete valves or valves that have become incompetent post-DVT, trauma, or increased venous pressure from any other cause.
