Venous Disease: How it Relates
to the Lower Extremity?
Parag J. Patel, MD MS FSIR
Associate Professor of Radiology & Surgery
Topics
• Scope of the problem
• Anatomy
• Pathophysiology
• Treatment
Prevalence of Venous Insufficiency / Venous Ulcers
• 3-8% total US population
• 10-15% adult males
• 20-25% adult females
• 1% adults > age 60 with ulceration
• Cost > $1 billion/year
Venous Insufficiency
• >30 Million Americans affected
• 1.9 million seek treatment annually
• Vast majority remain undiagnosed
Venous Hypertension
• Arteries no longer have significantly higher pressure than
veins
• Blood is not pumped effectively
• Blood proteins leak into extravascular space
• Fibrin builds up around vessels preventing oxygen and
nutrients from reaching cells
• WBC accumulate in small vessels releasing inflammatory
factors and free radicals
Clinical Impact
• Organ at risk is skin
– Pain
– Edema
– Pigmentation,
lipodermatosclerosis,
venous eczema
– Ulceration
Venous Anatomy of Lower Extremity
• Made up of 3 anatomic systems
– Deep
– Superficial
– Perforating
• Located in 2 separate
compartments
– Deep Compartment
– Superficial Compartment
Physiologic Function
• Deep System
– Transport system to
return blood to heart
– Drains superficial
system through
perforators
– >90% of venous blood
that leaves the limb goes
through DVS
Physiologic Function
• Superficial System
– Serves as reservoir to fill
DVS
– Helps regulate body temp. by
dilating/constricting
– Can dilate to accommodate
large volumes of blood with
little temp change
Venous Anatomy and Physiology
• Normal veins have valves that
allow uni-directional flow
• Leg muscle pump
• Valves normally close when
muscles relax
Venous Pressure changes
• Walk, Walk, Walk
• Venous Pumps
– Plantar, calf and foot pumps
• Standing has highest venous
pressure
• Walking pressure similar to
laying/sitting up
Ambulatory Venous Pressures
Venous Reflux
• Incompetent valves cause
pathologic retrograde flow
during calf muscle relaxation
• Increased venous
pressure/venous hypertension
• Venous hypertension causes
vvs and skin changes =
chronic venous insufficiency
Ambulatory Venous Pressures
Pathophysiology
• Incompetence of venous valves; Chronic obstruction
• Stasis of blood
• Chronic ambulatory venous hypertension
• Defective microcirculation
• RBCs diffuses into tissue planes
• Lysis of RBCs
• Release of hemosiderin
• Pigmentation
• Dermatitis
• Capillary endothelial damage
• Prevention of diffusion and exchange of nutrients
• Severe anoxia
• Chronic venous ulceration
Classification System
• CEAP: Clinical class, Etiology,
Anatomy, Pathology
0 = Normal
1 = Telangiectasias, spider veins
2 = Varicose veins
3 = Edema
4 = Skin changes
5 = Healed ulceration
6 = Active ulceration
Evaluation
• History
– Reflux vs obstruction, venous claudication
• Physical
– Supine and upright
– Pulse examination
• US
– Supine: anatomy, deep vein thrombosis
– Supine &/or Upright: reflux > 0.5
• CT, MR, venogram
– Assessment central veins (when pelvic source is suspected)
Pain
• Highly variable
• Range from fullness/heaviness, dragging or aching
• Exacerbated by standing, progressive throughout the day
• Typically felt in the calf or thigh
• Relieved with limb elevation
• Venous claudication (rare) during exercise
• Night cramps
Superficial Thrombophlebitis
• Common complication
• Most common associated with trauma or period of bed
rest
• Tender, hot, thickened area along course of varicose vein
• Extremely painful
• Potential for fever and malaise
Edema
• Progresses throughout the day
• Deep system insufficiency is more
severe and may be persistent
• Patients should be evaluated for
deep system incompetence
• Distinguish from lymphedema
(non-pitting) Brawny edema
Skin Changes - Pigmentation
• Prolonged venous hypertension
results in venous dilatation and
passage of RBC’s through the
endothelium into the interstitium
which subsequently breaks down
to hemosiderin.
• Typically located on the lower
medial third of the lower leg.
Skin Changes - Dermatitis
• Chronic inflammatory changes can
result in venous dermatitis or
varicose eczema.
• Dry, scaly or vesicular and weeping
• Venous ulceration may develop
Skin Changes - Lipodermatosclerosis
• AKA fat necrosis, folliculitis, or chronic cellulitis
• Progressive fibrosis of the skin and subcutaneous tissues
• Acute form is painful and disabling– Thickened raised red-brown area
– Hot
• Chronic form is stiff and shiny skin– Fixed, hard, indurated, contracting
– Inverted bottle shape
Skin Changes – Atrophie Blanche
• Skin necrosis with replacement by
scar tissue
• No ulceration or sloughing
• Small areas or patches that are
gray-white in color and only few
millimeters in size.
• Depression of the skin surface
• Halo of fine dilated venules
Skin Changes - Ulceration
• Previous mentioned conditions are
precursors
• Lead to impairment of tissue
nutrition and oxygenation
• 300k – 400k pts suffer from
venous ulcers in North America
Treatment Options
• Conservative management
– Compression hose therapy
• Excellent functional results
• Poor patient compliance
• Leg elevation
• Wound Care
– Debridement
– Infection Control
– Hyperbaric oxygen
• Surgical stripping
• IR: Endovascular Treatments
• Reflux
– Sclerotherapy
– Thermal ablation
• Obstruction
– Venous Stent Placement
Goal of Therapy
Eliminate or reduce reflux /
obstruction at its highest point
Saphenous Reflux
Min et al, JVIR 2003;14
Conservative Management
• Graduated compression
hose 1st line tx
– Compressing blood out of
superficial veins into deep
system
– Reduction of venous
pressure and subsequently
decreased swelling
• Graduated compression,
higher at the ankle
Classic Treatment
• High ligation
• Saphenous vein stripping
• Perforator interruption
• Deep system valve replacement
/ reconstruction
Downsides to stripping and ligation
• Done under general anesthesia in a hospital setting
• Post-operative pain requiring prescription drugs
• Severe bruising/ tenderness along the treated vein
• Typical recovery is between 2-4 weeks
Thermal Ablation
• Transmural injury
– Radiofrequency or laser
• Acute thrombosis
• Fibrosis
• Permanent obliteration of vein lumen
– Proximal tributaries may remain patent
Thermal Ablation GSV
• Outpatient procedure
• Local anesthetic
• US guided
– Fluoroscopy can be helpful in certain cases
• Immediate ambulation
• Quick return to normal activity
Laser Procedure
Laser Procedure
Laser Procedure
Pre Post
Endovenous Ablation
• Advantages to thermal ablation (RFA and Laser)
– Outpatient procedure
• iv sedation not necessary
– Quick return to normal activity (less patient discomfort)
• 93-95% closure at 2 years in published studies
When to treat obstructive component?
• Persistent Significant limb symptoms
– Pain, swelling, venous dermatitis, venous ulcer, recurrent
cellulitis
• Failed conservative management
– Compression therapy
• Severity of symptoms, NOT venographic findings
EW
• 44-year-old male with a history of extensive DVT
extending from the infrarenal IVC to the bilateral popliteal
veins. He was previously on Coumadin for
anticoagulation, and presented with left lower extremity
phlegmasia.
Outcomes of Venoplasty with Stent Placement for Chronic
Thrombosis of the Iliac and Femoral Veins: Single-Center
Experience
• 89 patients (91 limbs) included in study (189 patients
reviewed)
• 90/91 limbs patent at 30 days
• Primary patency/Primary assisted patency
– 1 year: 81%/94%
– 3 year: 71%/90%
• Study designed to primarily evaluate patency
Kurklinsky et al JVIR 2012;23:1009-15
Percutaneous Recan of Total Occlusion of
Iliac Vein• 139/167 (83%) successfully recanalized
• Stent patency at 4 years: 66%
• Symptom relief at 3 years
– Pain: 79%
– Swelling: 66%
• Venous ulcer healing
– 56% at 33 months
Raju and Neglen JVS 2009;50:360-8
Summary
• Venus ulcers are a significant burden to the healthcare
system
• Reflux and obstruction contribute to elevated ambulatory
venous pressures Venous Hypertension
• Endovascular treatments targeted at sites of venous
insufficiency and venous obstruction will relieve venous
hypertension
• Contributes to healing of venous ulcers
• IRs are a natural partner for podiatry