Venous Insufficiency


Venous Insufficiency

  1. Primary Venous Insufficiency (Varicose Veins)
    • may involve the greater saphenous vein, lesser saphenous vein, perforating veins, or various combinations of these veins
    • underlying mechanism is venous hypertension leading to valve failure

    Varicose Veins
    1. Pathophysiology
      1. Venous Hypertension
        • hydrostatic pressure from standing is one source of venous hypertension
        • another source of venous hypertension is exercise - high pressures develop in the muscle compartments and if a perforating valve fails, these pressures are transmitted to the superficial veins

    2. Risk Factors
      • increasing age is the most important risk factor
      • additional risk factors include female gender, multiparity, obesity, positive family history, past trauma to the extremity

    3. Clinical Manifestations
      1. Symptoms
        • leg heaviness, aching, fatigue, and swelling are the most common symptoms
        • symptoms are usually relieved by leg elevation or elastic support hose

      2. Physical Exam
        • arterial circulation must be assessed as well as the venous circulation, since arterial and venous insufficiency can coexist
        • venous insufficiency is best assessed with the patient standing
        • hyperpigmentation – hemosiderin deposition – is a sign of advanced venous insufficiency
        • venous stasis ulcers develop around the medial malleolus and are not painful
        • venous stasis dermatitis may involve the ankle region and can mimic eczema

        Venous Stasis Ulcer
        Venous Stasis Ulcer

    4. Diagnosis
      1. Duplex Ultrasound
        • test of choice
        • should be done in the standing position, if possible
        • deep, superficial, and perforator veins must be assessed for compressibility, venous flow, augmentation after reflux, and visibility
        • reflux can be demonstrated by compression and release or a Valsalva maneuver

    5. Initial Treatment of Superficial Varicose Veins
      1. External Compression, Elevation, Exercise
        • compression stockings, 20 – 30 mm Hg, should be worn during the day unless the patient also has arterial insufficiency
        • leg elevation several times/day is helpful
        • frequent walking activates the calf muscle pump and reduces ambulatory venous hypertension

      2. Management of Venous Stasis Ulcers
        • Unna boot: triple-layer graded compression dressing with a zinc oxide paste gauze wrap in contact with the skin
        • must be applied by trained personnel
        • 73% of ulcers heal in 9 weeks with an Unna boot

    6. Surgical Treatment of Superficial Venous Insufficiency
      • correction of superficial reflux is a valuable adjunct in patients with chronic venous stasis ulcers

      1. Vein Stripping
        • requires general anesthesia
        • high ligation of the saphenous vein is performed at its junction with the femoral vein
        • saphenous vein is ligated distally in the proximal, medial calf
        • a vein stripper is then used to remove the greater saphenous vein from the groin to the knee
        • the lesser saphenous vein can be removed in a similar fashion
        • saphenous nerve and sural nerve injuries may complicate the procedure
        • has largely been replaced by endovenous ablation techniques

      2. Percutaneous Vein Ablation
        • outpatient procedure done under local anesthesia
        • associated with less discomfort and quicker recovery than traditional vein stripping
        • venous duplex ultrasound examination is essential in planning the procedure
        • an acute DVT is an absolute contraindication; a chronic DVT with recanalization is a relative contraindication
        • radiofrequency ablation directly injures the vein endothelium, resulting in vein thrombosis
        • laser ablation heats the blood, which in turn injures the endothelium
        • a follow up duplex ultrasound several days after the procedure is necessary to confirm that the deep system is still patent and that the saphenous vein has been ablated

      3. Ultrasound-Guided Sclerotherapy
        • may be used to treat the greater and lesser saphenous veins, as well as perforator branches

      4. Treatment of Secondary Branch Varicosities
        • may be managed by outpatient stab phlebectomy or foam sclerotherapy

  2. Secondary Venous Insufficiency
    • usually results from a DVT

    1. Clinical Manifestations
      • patients may describe venous claudication – a bursting pain in the calf
      • usually have more advanced symptoms than patients with primary venous insufficiency
      • may present with chronic venous ulcers

    2. Nonoperative Management
      • compression therapy is the mainstay of treatment
      • requires a high level of compression (30 – 40 mm Hg) for efficacy

    3. Operative Management
      1. Perforator Vein Interruption
        1. Linton Procedure
          • direct surgical interruption of perforating veins
          • rarely done anymore because of a high incidence of wound complications

        2. Endoscopic Procedures
          • outpatient
          • allows direct visualization and interruption of the subfascial perforating veins

        3. Percutaneous Endovenous Techniques
          • same techniques as described for superficial venous reflux – radiofrequency ablation, ultrasound-guided sclerotherapy

      2. Additional Procedures
        • used when the above procedures fail
        • direct valve reconstruction has good to excellent results in 80% of patients
        • venous segment transfer consists of directing the incompetent venous stream through a competent proximal valve
        • direct venous reconstruction: femorofemoral crossover graft, saphenopopliteal bypass, axillary vein to popliteal vein autotransplantation

Lymphedema

  1. Pathophysiology
    1. Lymphatic System
      • returns protein-rich interstitial fluid back to the venous circulation
      • lymphatic flow is facilitated by skeletal muscle contraction and lymphatic vessels contain valves that prevent retrograde flow
      • majority of the body’s lymph flow enters the circulation through the thoracic duct which is located at the angle between the left subclavian vein and left internal jugular vein

    2. Lymphedema
      • defined as the abnormal accumulation of interstitial fluid and fibroadipose tissue in the subcutaneous tissues
      • occurs when the lymphatic load exceeds the transport capacity of the lymphatic system
      • accumulation of interstitial proteins causes an osmotic movement of water into the interstitium
      • persistent stasis and fluid accumulation leads to an inflammatory response that results in chronic fibrosis and fibroadipose tissue deposition

  2. Etiology
    1. Primary Lymphedema
      • rare condition that results from an inherited disorder
      • usually presents at birth or early in childhood

    2. Secondary Lymphedema
      • worldwide, the most common etiology is filariasis, which is transmitted by mosquitos
      • in the U.S., the most common cause is from cancer treatment
      • other rare causes include trauma, chronic venous insufficiency, and morbid obesity

  3. Risk Factors
    1. Lymphadenectomy
      • incidence of lymphedema is 17% after axillary node dissection for breast cancer
      • groin dissection for melanoma has a 28% incidence of lymphedema
      • most patients who develop lymphedema do so within 3 years of surgery
      • obesity is also an independent risk factor for lymphedema in cancer patients

    2. Radiation Therapy
      • in breast cancer patients, the incidence of lymphedema is significantly higher in patients treated with both axillary dissection and radiation compared with surgery alone

  4. Diagnosis
    1. Symptoms
      • slowly progressive swelling of the extremity following an axillary node dissection or groin dissection
      • heaviness, tightness, and discomfort are also common complaints

    2. Physical Exam
      • early on, ‘pitting’ edema is common
      • with disease progression, the skin becomes firm and the dermis thickens

      1. Limb Circumference
        • circumferential measurements of the affected and nonaffected extremity is a simple way to estimate edema
        • measurements can be taken at any point on the extremity as long as they are reproducible
        • a difference > 2 cm between the affected and unaffected extremity is significant

    3. Imaging
      • lymphatic imaging – lymphoscintigraphy, MR lymphangiography – is not necessary for diagnosis, but may help plan any proposed surgical procedure

  5. Staging
    • developed by the International Society of Lymphology
    • based on 2 criteria: the ‘softness’ and ‘firmness’ of the limb and the response to elevation

    1. Stage 0
      • subjective feeling of heaviness
      • no obvious edema
      • may last for months or years before progression

    2. Stage I
      • pitting edema
      • no dermal fibrosis
      • resolves with limb elevation

      Stage I Lymphedema
    3. Stage II
      • dermal fibrosis
      • pitting edema may progress to nonpitting edema
      • does not resolve with elevation alone

      Stage II Lymphedema
    4. Stage III
      • nonpitting edema
      • significant fibrosis
      • trophic skin changes – fat deposits, acanthosis, warty overgrowths
      • lymphostatic elephantiasis

      Stage III Lymphedema
  6. Conservative Management
    1. General Measures
      • self-monitoring for changes in color, temperature, size
      • limb elevation
      • maintenance of an ideal body weight
      • exercise is safe and recommended
      • avoid skin infection and injury
      • prompt treatment of cellulitis
      • avoid constricting garments

    2. Compressive Therapy
      • used mostly for ISL stage I patients
      • compression bandages
      • fitted compression sleeves or stockings
      • simple lymphatic drainage (light massage)

    3. Decongestive Therapy
      • used for ISL stage II and III patients
      • manual lymphatic drainage performed by trained physical therapists
      • compression garments
      • intermittent pneumatic pumps

    4. Other Treatments
      • diuretics are often prescribed but offer no benefit
      • stem cells, growth factors, and gene therapy to promote lymphangiogenesis have shown promise in animal models

  7. Surgical Treatment
    • advances in microsurgical techniques are making surgery more useful
    • there are 2 main approaches: physiologic interventions and debulking procedures
    • physiologic interventions are designed to restore lymphatic circulation and improve the antegrade flow of lymph
    • debulking procedures aim to remove the excess fibro-fatty subcutaneous tissue

    1. Physiologic Procedures
      • indicated in early stages of lymphedema

      1. Lymphovenous Anastomosis
        • subdermal lymphatics are identified intraoperatively using lymphangiography
        • microsurgical anastomoses are made between the lymphatics and small venules

      2. Lymph Node Transplantation
        • procedure harvests healthy fat, lymph nodes, and vessels and transfers these into the affected site
        • common donor sites are the supraclavicular area, groin, and omentum
        • for the upper extremity, the wrist is the recipient site and microvascular anastomoses are made to the radial artery and cephalic vein

    2. Debulking Procedures
      • more useful in the later stages of lymphedema

      1. Liposuction
        • promotes better lymphatic flow by immediately decreasing the volume and pressure of the lymph fluid
        • used to remove large fat deposits

      2. Radical Excision
        • several different procedures have been described
        • the Charles procedure is a radical excision of skin and subcutaneous tissue down to the muscle fascia with skin graft closure
        • the Sistrunk procedure is a staged excision of subcutaneous tissue, allowing primary closure of the skin







References

  1. Cameron, 13th ed., pgs 1088 – 1097, 1097 – 1101
  2. Sabiston, 20th ed., pgs 1830 – 1841
  3. Schwartz, 10th ed., pgs 929 – 936
  4. UpToDate. Approach to Treating Symptomatic Superficial Venous Insufficiency. Marc A. Passman, MD. Oct 28, 2019. Pgs 1 – 30
  5. UpToDate. Clinical Features and Diagnosis of Peripheral Lymphedema. Babak Mehrara, MD. Oct 16, 2019. Pgs 1 – 21
  6. UpToDate. Clinical Staging and Conservative Management of Peripheral Lymphedema. Babak Mehrara, MD. Jan 13, 2021. Pgs 1 – 42