Sclerosis is defined as the stiffening of a structure, usually caused by a replacement of the normal organ-specific tissue with connective tissue. In the case of venous pathology, we use term Sclerotherapy to describe the act of injecting a chemical agent directly into the lumen of a vein to purposely cause internal scarring of the veins being treated. Once the vein scars shut, blood reroutes to flow through healthier veins and the sclerosed vein is absorbed back into the body.

After sclerotherapy, treated veins tend to fade within a few weeks, although occasionally it may take a month or more to see the full results. In some instances, several sclerotherapy treatments may be needed.

For sclerotherapy to be fully effective, the use of a compressive garment over the treated area is essential to help promote seal of the vein. Therefore the complete term for this type of treatment is Compression Sclerotherapy.

Compression sclerotherapy is used to treat a variety of venous pathologies. Abnormal veins can be divided into three basic categories: Spider Telangiectasias, Reticular Veins, and Varicose Veins.

Spider Telangiectasias describe clusters of abnormal veins that are typically less than 1 mm in diameter. They reside in the dermal layer of the skin.

Reticular Veins describe abnormal veins between 2 and 4 mm in diameter. They reside in the subdermal layer of the skin. Reticular veins typically feed nests of telangiectasias.

Varicose Veins are abnormal veins greater than 3 mm in diameter. They are subdermal branches of the large truncal sub fascial veins – the greater saphenous or lesser saphenous veins.

Sclerotherapy is currently the treatment of choice for telangiectasias and reticular veins. It is also commonly used as an adjunctive treatment for tributaries of the saphenous vein after saphenous obliteration by endovenous laser, radiofrequency, or surgery. Sclerotherapy (endovenous chemical ablation) can also be used as a primary treatment for nonsaphenous varicosities and saphenous veins, commonly using ultrasound assistance – Foam Sclerotherapy.

Sclerosants include the following:

  • Detergents - Disrupt vein cellular membrane (protein theft denaturation)
    • Sodium tetradecyl sulfate (Tromboject)
    • Polidocanol (Asclera, Aethoxysclerol)
    • Sodium morrhuate (Scleromate)
    • Ethanolamine Oleate (Ethamolin)
  • Osmotic agents - Damage the cell by shifting the water balance through cellular gradient (osmotic) dehydration and cell membrane denaturation
    • Hypertonic sodium chloride solution
    • Sodium chloride solution with dextrose (Sclerodex)
  • Chemical irritants - Damage the cell wall by direct caustic destruction of endothelium
    • Chromated glycerin (Sclermo)
    • Polyiodinated iodine

The most commonly used agents are hypertonic saline, sodium tetradecyl sulfate, and polidocanol.

Hypertonic saline - The principal advantage of this agent is the fact that it is a naturally occurring bodily material with no molecular toxicity. It is not widely accepted as a sclerosing agent because it can cause pain, burning, and leg cramps upon injections; if extravasated, it likely causes significant tissue necrosis; it is highly likely to produce marked postsclerotherapy hemosiderin staining, which is cosmetically unacceptable; and it is difficult to achieve adequate sclerosis of large vessels without exceeding a tolerable salt load.

Sodium tetradecyl sulfate (Tromboject), a synthetic surfactant (soap), is the only approved sclerosant in North America. It is commercially available in 1% or 3% standard concentrations. This sclerosant is reliable, safe, and effective. The main clinical concerns stem out of its tendency to cause postsclerotherapy hyperpigmentation in up to 30% of patients, a high likelihood of tissue necrosis upon extravasation (especially when injected in high concentrations), and occasional cases of anaphylaxis.

Polidocanol is a nonester local anesthetic, popular in Europe, which was approved in March, 2010 by the FDA for use in the United States and more recently in Canada. It is painless upon injection, does not produce tissue necrosis if extravasated, and has a very low incidence of allergic reactions, although few cases of anaphylaxis have been reported. Also, in some patients, it may produce hyperpigmentation.

The lead principle in sclerotherapy is to cause irreversible endothelial injury in the desired vessels while avoiding damage to normal collateral vessels and surrounding tissues. The lowest effective volume and concentration of the most suitable sclerosant should be used to minimize the likelihood of adverse effects. Factors such as sclerosant concentration, volume, mixing, and procedure technique are more important factors than the choice of the sclerosant itself.

Mixing a detergent sclerosing agent with a gas (commonly air) results in foam formation. Foam is obtained after repeated alternate passages from one syringe to another through a connector. Compared to traditional liquid sclerotherapy, foam sclerotherapy has certain advantages including a smaller volume of the sclerosing agent needed for injection, lack of dilution with blood (dilution decreases efficacy), homogeneous effect along the injected veins, and ultrasound echogenicity. The use of foam sclerotherapy is generally reserved for larger vessels and not spider veins.