Venous_Insufficiency-1

Venous_Insufficiency-1 - Venous Insufficiency Vic V....

Info iconThis preview shows page 1. Sign up to view the full content.

View Full Document Right Arrow Icon
This is the end of the preview. Sign up to access the rest of the document.

Unformatted text preview: Venous Insufficiency Vic V. Vernenkar, D.O. St. Barnabas Hospital Dept. of Surgery Introduction Introduction Venous disorders are divided into acute thromboembolic events or chronic stasis. Chronic includes varicose veins, venous incompetence (superficial and deep). Primary varicose veins can be treated for cure. Chronic is treatable but not curable Varicosities are a symptom of venous disease, not just a cosmetic problem. Introduction Introduction ½ adult men, 2/3 adult women have them. Severe chronic insufficiency seen in 20% of working men and women. Varicosities can range in severity from venectasias to protuberant tortuous varicosities, with associated dermatitis, ulcers, severe pigmentation. Causes Causes Linked to genetics, changes in hormonal milieu. Probably multifactorial Appearance in childhood rare, although some adolescents with FHX of it have valves that are incompetent. Primary varicose vein in young adult are common, cause difficult to pinpoint. Symptoms Symptoms Primary varicosities are elongated, tortuous superficial veins that are protuberant and contain incompetent valves. Mild swelling, heaviness, easy fatigue. Skin should be normal, edema when present is mild. Symptoms Symptoms Primary varicosities merge into more severe chronic venous insufficiency. Swelling is moderate to severe, increasing heaviness with larger varicosities, pigment changes, induration “liposclerosis” When severe, marked swelling, calf pain after standing, sitting, or ambulation. Heavy pigmentation laterally, medially Female Hormones Female Hormones Progesterone (2nd phase menstruation) and principle hormone of pregnancy causes passive dilatation of varicosities. Women will find that the achiness, heaviness is worse in the 2nd 14 days of the cycle than the first. Exacerbation of symptoms with pregnancy also may be noted. Pathogenesis Pathogenesis Deficiencies in elastin and collagen Gandhi found that there is an increase in collagen and decrease in elastin of varicose veins. No difference in proteolytic activity however, so no degradation. Pathogenesis Pathogenesis Anatomic differences in the location of superficial veins of the lower extremities may contribute to pathogenesis. For example, the main saphenous trunk is not always affected by varicosities because it has a well developed medial fibromuscular layer, and is supported by connective tissue to the deep fascia. In contrast the tributaries to it are less supported in the sub Q fat, have less muscle mass in their walls. Add an incompetent valve here and the tributary will dilate from the pressure of the greater saphenous vein. Failure of the protective valve is the mechanism for development of the varicosities here. Communicating veins connecting the deep with the superficial system may have valve failure as well. Venous Hypertension Venous Hypertension Gravitational and Dynamic Gravitational is hydrostatic and caused by the weight of the column of blood from the right atrium. The highest pressure is noted from this at the foot and ankle. Dynamic is caused by forceful muscular contractions (150­200mmHg). If perforating vein fails, high pressures elicited by the contractions are transmitted to the superficial system, causing dilation of superficial veins. Progressive valvular failure may occur down the line. Venous Hypertension Venous Hypertension If proximal valves become incompetent at saphenofemoral junction, muscularcontraction pressure is supplemented by the weight of the static column of blood from the heart. This column becomes a barrier. Blood flowing from the femoral vein spills into the saphenous vein and flow distally. As it refluxes distally thru progressively incompetent valves, it is returned through the perforators to the deep veins, from where it goes back to the femoral vein and starts over again…. Pathogenesis Pathogenesis Changes also occur at the cellular level. Capillary proliferation is seen, extensive capillary permeability as a result of widening of interendothelial cell pores. Transcapillary leakage, principally fibrinogen. There is also some diminished fibrinolytic activity in chronic venous stasis, allowing the extravascular fibrin to remain. Diagnostic Evaluation Diagnostic Evaluation Physical Examination and History Hand­held doppler probe Duplex Ultrasound Venography Vein Stripping Vein Stripping Treatment Treatment Conservative and Surgical Measures Graduated compression stockings. Sclerotherapy Treatment Treatment Phlebectomy for veins>4mm (stab avulsion, stripping. Endovenous Laser Therapy: Use of lasers has become an accepted alternative to surgical stripping to treat varicose veins. A thin laser fiber is inserted into the diseased vein, through a small puncture in the leg above where the visual symptoms appear. The physician then delivers laser energy through the fiber, which causes the vein to close as the fiber is gradually removed. Endovenous laser therapy can be performed in a physician's office in less than one hour and the patient is encouraged to walk immediately following the procedure. Treatment Treatment Endoscopic therapy (SEPS) Venous Reconstruction (still experimental) Saphenofemoral Ligation Saphenofemoral Ligation ...
View Full Document

This note was uploaded on 12/27/2011 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

Ask a homework question - tutors are online