Presentation is loading. Please wait.

Presentation is loading. Please wait.

Venous Stasis Joon Ho Jang MD. Incidence/Prevelance & JOBST Coverage It is estimated that more than 80 million Americans suffer from some form of venous.

Similar presentations


Presentation on theme: "Venous Stasis Joon Ho Jang MD. Incidence/Prevelance & JOBST Coverage It is estimated that more than 80 million Americans suffer from some form of venous."— Presentation transcript:

1 Venous Stasis Joon Ho Jang MD

2 Incidence/Prevelance & JOBST Coverage It is estimated that more than 80 million Americans suffer from some form of venous disorder. Up to 13 million people in the U.S. suffer from CVI Peak incidence occurs in women aged 40-9 and men aged years Statistics show one in three Americans over the age of 45 is affected by vein disease, and of those, only 4% are being treated. Annual health care cost in the US to treat CVI is about $3billion; about 2 million workdays are lost per year due to venous ulcers Varicose Veins More than 24 million Americans have varicose veins Up to 50% of women have varicose veins while 24% of men aged and 43% of men over 70 have varicose veins DVT / PTS There are over 200,000 new cases of DVT each year in the U.S. The incidence of pulmonary embolism in patients with DVT ranges from 5 – 20% and can be fatal After an episode of DVT, 20 – 50% of patients develop Post Thrombotic Syndrome within the first 2 years Venous Stasis Ulcers Affect 2.5 million people in the U.S. An estimated 500,000 persons are newly diagnosed each year

3 Venous Stasis…How? Mechanics Structure Inflammation Pressure Obstruction- DVT

4 Function Transport blood back to the heart Prevent intravascular volume overload

5 Anatomy Tunica intima: endothelium with BM and elastic lamina –Produces endothelium derived relaxing factor and prostacyclin Tunica media: Circumferential SM –Maintains venous pressure gradient Tunica externa: Collagen –Stability

6 Valves Venous valves: –One way –Two cusps of CT skeleton covered by endothelium –Closure at > 30cm/s –Exception: IVC, common iliacs, portal, cranial sinus

7 Lower Extremity

8 Venous Hypertension –Hydrostatic pressure vs Mechanical/muscular pressure A. K. Tassiopoulos et al cases of ulcerated legs and venous disease Reflux in superficial, deep, and perforating veins Incompetent valves

9 Valvular Dysfunction Physical damage: splitting, tearing, thinning, adhesion to wall Reduction in number –Not age related Monocyte and macrophage infiltration –Overexpression of Intracellular adhesion molecules –Wall hypertrophy, disruption of collagen synthesis, and destruction of extracellular matrix proteins

10 Shear Stress and Inflammation Pulsatile venous blood flow Valve closes: P vortical > P luminal –Minimal shear stress Low shear stress starts cascade of inflammatory signals

11 Risk Factors Genetic More in females Hormones –Progesterone, estrogen Pregnancy Age: >50 Greater height Prolonged standing Obesity

12 Signs and Symptoms Telangiectasias Reticular veins Varicosity Thrombophlebitis Hyperpigmentation Bleeding from clusters Ulceration Aching Heaviness Early fatigue Edema Itching Restless legs Cramps

13

14

15 Physical Exam, Diagnostic Tests Palpable veins Perthes Test –For deep venous patency –Tourniquet and walk Brodie-Trendelenburg Test –For superficial vein and valve patency –Venous filling time: normal- within 35 secs Duplex Ultrasound Venography

16 Classification: CEAP *Eklof et al. J of Vasc Surg 2004 Clinical classification C0: no visible or palpable signs of venous disease C1: telangiectasies or reticular veins C2: varicose veins C3: edema C4a: pigmentation or eczema C4b: lipodermatosclerosis or atrophie blanche C5: healed venous ulcer C6: active venous ulcer S: symptomatic, including ache, pain, tightness, skin irritation, heaviness, and muscle cramps, and other complaints attributable to venous dysfunction A: asymptomatic

17 CEAP Etiologic classification Ec: congenital Ep: primary Es: secondary (post-thrombotic) En: no venous cause identified Anatomic classification As: superficial veins Ap: perforator veins Ad: deep veins An: no venous location identified Pathophysiologic classification Basic CEAP Pr: reflux Po: obstruction Pr,o: reflux and obstruction Pn: no venous pathophysiology identifiable

18 Treatment Compression Therapy –Stockings, Unna’s Boot Drug Therapy Surgery

19 Compression Stockings Worn during the day Elastic stockings with adjustments in pressure Lower pressure stockings (20-30mm Hg) for edema and DVT prophylaxis Higher pressure ( mm Hg) for ulcers and significant venous disease Operator dependent –Difficult to put on –Physical impediments/Co- morbidities 50% of patients were unable to them on alone 30-65% noncompliance noted in clinical trials in venous centers

20 Efficacy of Compression Therapy 1.22 trials comparing healing of venous ulcers using compression stockings Compressive therapy more effective than non-compression Higher pressure were more effective than lower Multilayer compression was better than single layer bandaging patients with a healed ulcer Continued use of compression stocking reduced reoccurrence within 3-5 year 3.ESCHAR study: 500 limb trial that compares surgery and compression vs. compression alone for ulcer treatment Combination therapy had lower rates of reoccurrence of ulcer at year 4 (24% vs. 52%)

21 Drug Therapy Pentoxifylline –PDE 4 inhibitor that increases intracellular cAMP and stimulates protein kinase A activity –Reduces blood viscosity and decreases platelet aggregation and thrombus formation –Variable efficacy

22 More invasive Sclerotherapy –0.2% sodium tetradecyl injected directly into spider angiomas and smaller superficial varicosities Complications (<5%): allergic reaction, hypo/hyper-pigmentation, local skin necrosis Endovenous laser ablation of saphenous vein (EVLT) Surgical excision of veins (“Stripping”)

23 Efficacy Meta-analysis of 64 studies (12,320 legs) –Anaylzed ablation via Duplex US –Follow upto 5 years –Success rate of EVLT highest after 5 years –Complications: DVT (<3%), local bruising and pain, paresthesias, foam emboli, stroke

24 Works Cited Raju et al. Chronic venous insufficiency and varicose veins. NEJM 2009;360: Bergan et al. Chronic venous disease. NEJM 2006;355: Tassiopoulos et al. Current concepts in chronic venous ulceration. Euro J Vasc Endovasc Surg 2000;20: Ono et al. Monocyte inflitration of venous valves. J Vasc Surg 1998;27: Sansilvestri-Morel et al. Imbalance in the synthesis of collagen type I and collagen type III in smooth muscle cells derived from human varicose veins. J Vasc Res 2001;28: Jacob et al. Extracellular matrix remodeling in the vascular wall. Pathol Biol 2001;49: Eklof et al. Revision of the CEAP classification for chronic venous disorders: Consensus statement. J Vasc Surg 2004;40: Cullum et al. Copression bandages and stockings for venous leg ulcers. Cochrane Database Syst Rev 2000;2: CD Mayberry et al. Fifteen-year results of ambulatory compression therapy for chronic venous ulcers. Surgery 1991;109: Barwell et al. Comparison of surgery and compression with compression alone in chronic venous ulceration (ESCHAR study): randomised controlled trial. Lancet 2004;363: Van den Bos et al. Endovenous therapy of lower extremity varicosities: a meta- analysis/ J Vasc Surg 2009;49:230-9.


Download ppt "Venous Stasis Joon Ho Jang MD. Incidence/Prevelance & JOBST Coverage It is estimated that more than 80 million Americans suffer from some form of venous."

Similar presentations


Ads by Google