Venous Insufficiency

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Venous Insufficiency

• Vic V. Vernenkar, D.O.
• St. Barnabas Hospital
• Dept. of Surgery

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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.

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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.

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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.

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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.

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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

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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.

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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.

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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.

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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 (150-200mmHg). 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.

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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.

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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.

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Diagnostic Evaluation

• Physical Examination and History
• Hand-held doppler probe
• Duplex Ultrasound
• Venography

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Vein Stripping
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Treatment

• Conservative and Surgical Measures
• Graduated compression stockings.
• Sclerotherapy

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Treatment

• Phlebectomy for veins4mm (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.

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Treatment

• Endoscopic therapy (SEPS)
• Venous Reconstruction (still experimental)

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Saphenofemoral Ligation
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