Chapter 20 discusses Venous Valvular Insufficiency Testing.
Define the conditions related to chronic venous valvular insufficiency, including:
Clinical
Etiologic
Anatomic
Pathophysiologic
Describe noninvasive vascular testing:
Direct testing methods
Indirect testing methods
Outline protocol differences based on testing objectives:
Screening
Definitive diagnosis
Pretreatment mapping
Peritreatment imaging
Procedure/patient follow-up
Define ha duplex ultrasonography's role in evaluating lower extremity venous disorders.
Types of veins:
Great Saphenous Vein (GSV)
Small Saphenous Vein (SSV)
Tributaries include:
Anterior Accessory Saphenous Vein (AASV)
Posterior Accessory Saphenous Vein (PASV)
Vein of Giacomini (VOG)
Veins lie within saphenous fascia layers, giving an "eye" appearance.
Normal positioning of the GSV within the saphenous compartment illustrated.
Arrows indicate fascia surrounding the vein.
GSV courses medially in the thigh and leg.
AASV aligned with the femoral artery in a transverse plane.
PASV may connect with the VOG.
Identified in the GSV below the knee:
Triangle formed by:
Gastrocnemius muscle
Tibial bone
GSV
Helps differentiate the saphenous vein from tributaries.
Mostly segmental; complete duplications are rare.
Duplicated veins must follow the same path and remain parallel.
Terminal valve present at SFJ; second preterminal valve distal to tributaries.
Important landmarks include:
Superficial epigastric vein (SEV)
Superficial external pudendal vein
Superficial circumflex iliac vein
Bicuspid valves identified with B-mode imaging.
Leaflets open with muscular contraction, close with relaxation.
Regulate blood return efficiently; incompetence leads to retrograde flow.
Common finding in the general population.
Varicose veins prevalence rates:
60% in women
56% in men
Associated conditions:
Telangiectasias
Edema
Skin changes
Ulcers
Reflux prevalence in lower extremities is 35%; increases with age.
Visual Signs:
Spider veins
Telangiectasias
Varicose veins
Edema
Skin changes
Ulceration
Temporary swelling may occur after prolonged standing or specific activities.
Sources to differentiate include lymphatic obstruction, cardiac disease, and arterial disease.
Manifestations include:
Localized redness
Atrophic blanche
Lipodermatosclerosis
Ulcerated wounds
C0: No signs/symptoms.
C1: Telangiectasias/reticular veins.
C2: Varicose veins.
C3: Edema.
C4: Skin changes.
C5: Healed ulcers.
C6: Open ulcers.
Different subclasses to explore potential causes of CVI.
Treatments include:
Stripping and ligation
Endovenous thermal ablation
Chemical ablation/sclerotherapy
Phlebectomy
Deep venous disease treatments like anticoagulation and thrombolysis.
Performed with ultrasound guidance; vein is closed from within.
Device used induces thermal injury, causing vein shrinkage.
Standard technology for evaluating CVI includes:
Assessment of deep and superficial veins.
Flow characterization using Doppler assessment.
Photoplethysmography (PPG) for reflux detection.
Air plethysmography (APG) for quantifying CVI.
Near-infrared imaging for visualizing superficial veins.
B-mode Ultrasound Findings:
Normal veins: Thin-walled and compressible.
DVT: Enlarged and incompressible.
Chronic CVI: Enlarged diameter with anechoic lumen and visible valve leaflets.
Emphasizes importance of understanding anatomy and appropriate testing for diagnosing and treating venous insufficiency.