1. Vic V. Vernenkar, D.O. St. Barnabas Hospital Dept. of Surgery
Venous Insufficiency
Vic V. Vernenkar, D.O.
St. Barnabas Hospital
Dept. of Surgery

2. 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.

3. 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.

5. 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.

6. 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.

7. 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

8. 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.

10. 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.

12. 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.

13. 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 ( mmHg). 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.

14. Venous Hypertension
If proximal valves become incompetent at saphenofemoral junction, muscular contraction 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….

15. 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.

16. Diagnostic Evaluation
Physical Examination and History
Hand-held doppler probe
Duplex Ultrasound
Venography

17. Vein Stripping

18. Treatment Conservative and Surgical Measures
Graduated compression stockings.
Sclerotherapy

19. 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.

20. Treatment Endoscopic therapy (SEPS)
Venous Reconstruction (still experimental)

23. Saphenofemoral Ligation