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10/28/2014 1 Venous Insufficiency Is a multifactorial disorder Abnormal circulatory condition characterized by decreased return of the venous blood from the legs to the trunk of the body manifested by edema, pain, varicosities and skin changes Objectives: Improved understanding of venous insufficiency disease Implications to quality of life and patient care Improved identification of venous pathologies Current treatment recommendations and options

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Page 1: Buterbaugh, Jill - Powerpoint - c.ymcdn.com · PDF fileVenous Insufficiency Is a multi‐factorial disorder Abnormal circulatory condition characterized by ... Treatment of venous

10/28/2014

1

Venous Insufficiency Is a multi‐factorial disorder

Abnormal circulatory condition characterized by decreased return of the venous blood from the legs to the trunk of the body manifested by edema, pain, varicosities and skin changes

Objectives: Improved understanding of venous insufficiency disease

Implications to quality of life and patient care

Improved identification of venous pathologies

Current treatment recommendations and options

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The earliest known depiction of varicose veins is this sculpture on the west side of the Acropolis in Athens, from the 4th Century B.C.

0 5 10 15 20 25

Heart Valve Disease

Cardiac Arrhythmias

Stroke

Congestive Heart Failure

Peripheral Arterial Disease

Coronary Heart Disease

Venous Reflux Disease

Venous Insufficiency Prevalence

Risk factors for venous insufficiency

Family History

Female (40%) vs. Male (25%)

Advancing Age

Venous Malformations

History of clotting disorders or thrombus

Trauma/Surgery

Pregnancy/Multi‐parity

Occupation (standing or sedentary)

Hormonal therapies including birth control

Obesity

Smoking

Page 3: Buterbaugh, Jill - Powerpoint - c.ymcdn.com · PDF fileVenous Insufficiency Is a multi‐factorial disorder Abnormal circulatory condition characterized by ... Treatment of venous

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Venous Insufficiency = Impaired Venous Return…..

Calf Muscle Pump

Thoracic Excursion & Cardiac Function

Intravenous Valves

Intra‐abdominal Pressure

Neurohormonal Influence

Increased Intravascular Volume

Vein Wall Integrity

Venous Obstruction

Gravity

Calf Muscle Pump• Heel strike• Gastrocnemius muscle contraction

• Failure can result from• Neuromuscular disorders• Muscle wasting• Absent/fallen foot arch• Ankle fusion• Sedentary lifestyle (sitting or 

standing)• High heels• Prolonged immobility• Corrective casting

Thoracic & Cardiac Implications

Diaphragmatic excursion

Preload/Afterload

Systemic Arterial Pressure

Pressure gradient

Congestive Heart Failure

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Intravenous valves

Prevents blood from refluxing in the opposite direction of venous return

No valves in portal, hepatic and internal jugular veins.

Valve failure Increased intravenous pressures Venous dilation Valve leaflet weakening Valve leaflet failure Injury from thrombus Injury from trauma

Congenitally missing or defective valves

Intra‐abdominal Pressure

• Pregnancy• Parity

• Obesity• Ascites• Chronic Constipation

Neurohormonal Influence Neuro (Sympathetic)

Cardiac output

Peripheral resistance

Hormonal

Progesterone

Pregnancy

Normal menstrual cycles

Obesity‐stores in adipose

Decreases smooth muscle contractility

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Increased Intravascular Volume

30% more during pregnancy

Congestive Heart Failure

Renal Failure

Medication side effects

The venous system normally contains 64% of the total body blood volume

Vein Wall Integrity Generally oval Intima

thin layer of endothelial cells and deep fenestrated basement membrane

fragmented elastic lamina contain small micro‐villi tremendous ability to regenerate

Media 3 layer of muscle bundles separated by loose connective tissue and elastic fibrils

variability in the amount of muscle in the vein walls

Adventitia thickest portion of the vein wall composed of collagen with interlacing fibers in longitudinal, spiral and circular fashions

Vein Wall IntegrityVenous hypertension

Shear‐stress dependent leukocyte‐endothelial interaction

Chronic Inflammation

Migration through endothelial barrier

Macrophages & matrix metalloproteases respond

Destroys elastin & collagen

Over dilation and fibrin formation

**Vein segment volume is three times greater  and compliance is 30 times greater than that of an arterial segment

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Age related vein wall changes Intima thickens

disorientation of elastin fibers

Media  

hypertrophy of the outer muscular layer 

elastic fibers become more irregular and dystrophic 

Adventitia

increasingly fibrous

Vein Obstruction Intrinsic

Thrombus

Arterial Compression

Phlebitis

Tumors

Extrinsic

Restrictive clothing

Positioning

Travel

Gravity 20 mmHg venous pressure when supine

100 mmHg venous pressure when erect

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Increased dermal capillary hypertension

VasodilationIncreased Capillary 

Permeability

WBC Activation

Venous rupture

Venous Hypertension

Decrease in arterial venous pressure gradient

Ischemia

Ulceration Infection Inflammation

Fibrin Accumulation

SclerosisDecreased microvascular 

transport

Venous Reflux

Increased lymph edemaProtein & nutrient loss into interstitial compartment

CEAP Classification

C= Clinical Signs

C0 = No clinical signs 

E= Etiology

A= Anatomy

P= Physiology

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C1 –Telangiectasia & Reticular veins

C2‐Varicose Veins

C3‐Edema

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C4a‐ Venous pigmentation or dermatitis

C4b – Lipodermatosclerosis or atrophie blanche

C5 – Healed Ulcer

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C6 – Active Ulcer

Before & After……

CEAP ClassificationsE=Etiology

Ec – Congenital

Strong family history

Ep – Primary

No family history but no causative factors identified

Es – Seconday

Post thrombotic syndrome

Post trauma

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Deep vein thrombosis

Precipitating event

Immobility

Trauma

Hypecoagulable state

Hormonal therapy

Pregnancy

Hereditary disorders

Post thrombotic syndrome:  edema, skin changes, healed or active ulcer

Post Thrombotic Syndrome

• 3o% to 70% will have within 3 years• 50% to 100% will have within 5 to 10 years

CEAP ClassificationsA = Anatomic Classification

As – Superficial venous system  SSV, GSV, AAGSV, PAGSV, Vein of Giacomini, A/P circumflex veins of 

the thigh & calf, tributaries, reticular and telangiectasia

Ap – perforator veins Connect the superficial system to the deep system

Ad – Deep venous system Peroneal, Soleus, Gastrocnemius, Posterior Tibial, Anterior Tibial, 

Popliteal, Femoral, Common Femoral, External & Internal Iliac, Pudendal, Gluteal, Obturator, Common Iliac, Inferior Vena Cava

Ao – Failure to identify

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Perforating Veins

CEAP ClassificationsP = Pathophysiology

Pr – Reflux

Pathologic > 0.5 seconds, symptomatic

Po – Obstruction

Thrombus

Anatomical Occlusion

May‐Thurner syndrome

Outflow obstruction – obesity, pregnancy

Pro – Reflux & Obstruction

Pn – No identifiable cause

May‐Thurner Syndrome• Also known as iliac vein compression syndrome

• Typically presents with left leg DVT• Caused when the high pressure right iliac artery crosses over the low pressure left iliac vein compressing it

• Treatment• Anticoagulation• Catheter directed Thrombolytic treatment

• Angioplasty or stenting• IVC Filter

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Klipple‐Trenaunay Syndrome

Rare congenital disorder also known as Nevus Varicosus OsteoHypertrophicus

Etiology unknown‐ theories include mesodermal abnormalities during fetal development or pathologic gene for vascular remodeling or tissue overgrowth

Parks‐Weber Syndrome is similar but with AV malformations and shunting

Klipple – Trenaunay Syndrome

Lipedema Syndrome• Waist down• Feet & Toes 

spared• Hormonal 

Influence• Lymphedema 

treatment essential

• Weight loss ineffective

• Liposuction life threatening

• No good treatment options

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Clinical evaluation Cosmetic appearance – psychological impact and may affect 

quality of life Physical symptoms most often associated with veins meeting 

pathological criteria – 3 mm in size; 0.5 seconds of reflux Pain Edema Tingling Aching Burning Muscle cramps Throbbing Heaviness Restless legs Fatigue

Venous Clinical Severity ScoreAttribute Absent=0 Mild=1 Moderate=2 Severe=3

Pain None Occasional Daily, moderately limiting

Severe, limits activities or requires regular analgesic

Varicose Veins None Few Multiple: upper or lower

Extensive:  upper and lower

Edema None Evening ankles Afternoon above ankles

Morning

Pigmentation None or focal Diffuse but limited in area and brown

Diffuse, gaiter distribution, purple or brown

Wider distribution, recent changes

Inflammation None Mild cellulitis Moderate cellulitis Severe cellulitis

Induration None Focal Medial or Lateral 1/3 of leg or more

Active Ulcers None 1 2 >2

Ulcer Duration None <3 months > 3 mo but < 1 yr > 1 year

Ulcer Size None < 2 cm 2‐6 cm >6 cm

Compression Therapy

None or non‐compliant

Intermittent Most days Full compliance

Diagnosis

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Vein Diameter Measurements

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Duplex Ultrasound

RIGHT LEFTSize Degree of Reflux  Size  Degree of Reflux 

COMMENTS 9.2mm  2.72sec  GSV at SFJ  7.9mm  1.34sec 11.3mm  2.76sec  GSV at mid thigh  3.6mm  none 10.5mm  2.16sec  GSV at knee  6.4mm  2.02sec 9.6mm  2.12sec  GSV at calf  6.1mm  2.57sec 

GSV at ankle AASV  5.8mm  none PASV 

3.9mm  none  SSV at thigh 4.4mm  none  SSV at SPJ  4.9mm  none 4.5mm  none  SSV at mid calf  3.9mm  none 

SSV at ankle 

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RIGHT LEFTSIZE  Degree of Reflux  SIZE  Degree of Reflux 

COMMENTS 5.5mm  2.96sec  GSV at SFJ  9.8mm  2.9sec 7.7mm  3.33sec  GSV at mid thigh 8.2mm  2.78sec ‐ Not seen  GSV at knee  7.5mm  2.6sec 4.6mm  3.93sec  GSV at calf  4.1mm  2.79sec 

GSV at ankle AASV PASV 4.6mm  none 

8.0mm  1.93sec  SSV at thigh ‐ Hx of Sclero  SSV at SPJ  ‐ Hx of sclero ‐ Hx of Sclero  SSV at mid calf  ‐ Hx of sclero 

SSV at ankle 

Treatment of vein disease Treat the comorbidities

Diabetes

Hypertension

Neuropathy

Lymphedema

Congestive heart failure

Fibromyalgia

Clotting disorders

Etc

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Treatment of venous disease

Treatment of vein disease• Endovenous Radiofrequency Ablation

• Endovenous Laser Ablation

• Phlebectomy

• Sclerotherapy• Clarivein

• Verithena

• Superficial laser or radiofrequency therapy

Endovenous  Laser Ablation &Radiofrequency Ablation

Catheter based procedures

Ultrasound guided

Uses tumescent anesthesia

Uses heat to ablate the diseased vein 

Laser = 1200 centigrade

Radiofrequency = 120 centigrade

Closure rates the same

Aftercare the same

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Endovenous Ablation

Endovenous Ablation

Endovenous Ablation

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Catheter positioned at highest treatment point Vein treated in 7cm vein segments

Until entire length of vein is treated

The VNUS Closure ProcedureUsing the ClosureFAST™ Catheter

Catheter withdrawn from marker to marker..

VNUS Closure® Procedure using the ClosureFAST™ Catheter

Example of Closure on US

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Risks of ablation

Other Risks….. Bleeding

Infection

Vein fails to close

May develop angioneogenesis surrounding the area

May not relieve the symptoms

Chance of permanent nerve injury

Chance of permanent skin discoloration

Sclerotherapy Injection of a chemical agent into a vein to produce endothelial damage producing localized inflammation

Relies on the bodies own inflammatory response to close the vein

Larger veins may need treated more than once Trapped blood resulting in superficial thrombophlebitis is common

If foamed (off label), risk of air embolism, migraine or dyspnea

Permanent discoloration Telangiectasia development Skin ulceration

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Sclerotherapy

Cosmetic Vein Treatment

Superficial laser or radiofrequency ablation 

Veingogh, Veinwave, surface lasers

Microscaring

Permanent discoloration

Telangiectasia development

Skin ulcerations

Results not immediate

Considered cosmetic

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ClariVein® device

VarithenaVarithena™ (polidocanol injectable foam) 1% is a drug/device combination that generates injectable foam for intravenous injection using ultrasound guidance

Varithena™ injectable foam delivers a 1% polidocanol solution. Each mL of Varithena™injectable foam contains 1.3 mg of polidocanolOne canister of Varithena™ yields 45 mL of usable foam for injection when following instructions for use 

Use up to 5 mLper injection and no more than 15 mLper session

Once activated, the canister of Varithena™ must be used within seven (7) days

Manufactured in accordance with FDA Current Good Manufacturing Practices (cGMPs)

Local anesthetic may be administered prior to cannula insertion, but neither tumescent anesthesia nor patient sedation is required 

Alternative therapies….. Diosmin (Vasculara 630 mg) – Protects from microcirculatory damage Naturally occurring flavonoid glycoside than is vascular protecting exhibiting anti‐inflammatory, free‐radical scavenging, and antimutagenic properties.

Half‐life 26‐43 hours; renal elimination

No known interactions

Appears safe long term

Mechanism of action: Prostaglandin E2  & thromboxane A2 inhibition

Inhibits leukocyte activation, migration, and adhesion

Reduces neutrophil activation

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Alternative therapies….. Horse Chestnut Seed Extract

Has been shown to decrease inflammation, thin the blood and improve vein wall integrity

Only recommended for short term use, long term use not adequately studied

Has a diuretic effect Can interact with medications such as lithium, diabetes medications and anticoagulation/antiplatelet therapy

Precaution recommended with diabetes, liver disease, kidney disease, digestive disease

Not recommended for use during pregnancy & breast‐feeding Raw horse chestnut seed, bark, flower and leaf are unsafe and may cause death

Reference List Gloviczki P, et al. The care of patients with varicose veins and associated chronic venous 

diseases:  Clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum  J Vasc Surg. 2011;53(suppl 5):2S‐48S

Khilnani NM, et al. Multi‐society Consensus Quality Improvement Guidelines for the Treatment of Lower‐extremity Superficial Venous Insufficiency with EndovenousThermal Ablation from the Society of Interventional Radiology, Cardiovascular Interventional Radiological society of Europe, American College of Phlebology, and Canadian Interventional Radiology Association. J Vasc Interv Radiol. 2010;21:14‐31.

Kern P, et al. Compression after sclerotherapy for telangiectasias and reticular leg veins:  A randomized controlled study. J Vasc Surg. 2007;45:1212‐1216

Thorne Research Inc.  Diosmin Monograph.  Alternative Medicine Review. 2004; 9:3:308‐311.

Moneta G, Nicoloff A and Porter J.  Compression treatment of chronic venous ulceration:  A review.  Phlebology. 2000; 15:162‐138.

Schuren J, Vos A and Allen JO.  Venous leg ulcer patients with low ABPIs:  How much pressure is safe and tolerable.  EWMA Journal.  2010; 10: 29‐34.

Humphreys ML, et al.  Management of mixed arterial and venous leg ulcers.  Br J Surg.  2007; 9:1104‐1107.

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Reference List Anderson E, Hansson C and Swanbeck G.  Leg and foot ulcer prevalence and 

investigation of the peripheral arterial and venous circulation in a randomized elderly population:  An epidemiological survey and clinical investigation.  Acta Derm Venereol1993; 73: 57‐61

Rabe E, Pannier F.  Indications, contraindications and performance:  European Guidelines for Sclerotherapy in Chronic Venous Disorders.  Phlebology 2014; 29:26‐33.

GuexxJJ.  Endovenous chemical (and physical) treatments for varices:  What’s new?  Phlebology 2014; 29: 45‐48.

Kahn SR, et al.  Long‐term Outcomes After Deep Vein Thrombosis:  PhostphleboticSyndrome and Quality of Life.  J Gen Intern Med 2000; 15:425‐429.

Caprini JA.  Deep vein thrombosis outcome and the level of oral anticoagulation therapy.  J Vasc Surg 1999; 30:805‐812.

Pittler MH, Ernst E. Horse chestnut seed extract for chronic venous insufficiency (Cochrane Review). In:  The Cochrane Library, Issue 3, 2004.  Chichester, UK:  John Wiley & Sons, Ltd.