Varicose Vein Treatment: Endovenous Laser Therapy

Excerpt

Varicose veins are superficial veins in the subcutaneous tissue that become enlarged upon standing and are a common manifestation of underlying chronic venous disease. Chronic venous disease encompasses a spectrum, presenting as eczema, hyperpigmentation, telangiectasia, superficial thrombophlebitis, lipodermatosclerosis, atrophie blanche, and ulceration. Established risk factors include age, family history, obesity, and previous pregnancy. Other risk factors such as gender, smoking, history of injury to lower extremity, and occupations that require prolonged standing, have not shown a strong or consistent correlation, and require further studies. Symptoms of chronic venous disease include leg heaviness, pedal swelling, and pain that can significantly diminish the quality of life.

The pathophysiology of venous disease is complex and poorly understood. What is known is that inflammation plays a central role in the development and progression of the disease. Mechanically, there is a hemodynamic dysfunction, such as hypertension, that causes valvular reflux resulting in hemostasis or blood pooling in the lower extremities. This sets off a feed-forward cycle of venous wall remodeling and local inflammation. It is believed that high venous pressures cause shear stress, which is sensed by the endothelial cells. In response, growth factors such as vascular endothelial growth factor (VEGF), platelet-derived growth factor, and transforming growth factor-beta 1 (TGF-beta 1) are released and stimulate vascular smooth muscle cell proliferation. In addition, endothelial cells increase the production of adhesion molecules, which promote leukocyte attachment and transmigration. The result is a disruption of collagen homeostasis producing varicose veins, which are less elastic and unable to maintain structural conformation during high-pressure blood flow. Progression of the disease involves further VEGF and TGF-beta 1 mediated vascular remodeling with increased leukocyte infiltration. Ultimately, this pathology culminates in dermal changes and ulcer formation. Taken together, valvular reflux appears to be the critical factor that initiates the cascade of inflammatory cytokines disrupting collagen homeostasis resulting in structural changes to the venous wall.

Chronic venous disease is classified based on CEAP (clinical, etiologic, anatomic, and pathophysiologic) criteria:

Updated 2020 CEAP classification guidelines are as follows:

1. C0: Without any visible or palpable signs of disease

2. C1: Telangiectasia or reticular veins

3. C2: Varicose veins

   1. C2r: Recurrent varicose veins

4. C3: Edema is present

5. C4: Changes in skin and subcutaneous tissue

   1. C4a: Pigmentation or eczema

   2. C4b: Lipodermatosclerosis or atrophie blanche

   3. C4c: Corona phlebectatica

6. C5: Healed ulcers

7. C6: Active ulcers

   1. C6r: Recurrent active venous ulcer

Etiologic classification is based on congenital (Ec), primary (Ep), secondary (Es), or unknown (En). Es is further differentiated into intravenous (Esi) or extra-venous (Ese). Combinations of etiologic states can coexist. Anatomic classification is differentiated based on the affected vein and laterality: superficial (As), perforator (Ap), deep (Ad), or unknown (An). Pathophysiology is defined by whether the cause is due to reflux (Pr), obstruction (Po), both (Pr,o), or neither (Pn).

Although there are many different approaches to treatment ranging from conservative (compression stockings) to invasive (vein stripping) for varicose veins depending on the severity of the disease, this article will focus on the use of endovenous laser ablation. The theory behind venous ablation is using heat to damage the vein wall, which causes fibrosis and collapse of the vein. LASER, which stands for “light amplification by stimulated emission of radiation,” is a device that focuses light energy. For endovenous laser ablation, a fiber optic laser is inserted into the vein and, when activated, will transmit light energy to the laser tip that is distributed radially by a prism and will heat the surrounding tissue. Heat injury to the vein wall will cause disruption to collagen, leading to fibrosis and collapse of the vessel. Tumescent anesthesia, which plays a critical role in this procedure, is given prior to ablation to decrease intravenous blood volume through venous compression, create a barrier between laser and surrounding tissue, and provide local anesthesia. The procedure can be performed in an outpatient setting and does not require general anesthesia. Advantages of endo-ablation include rapid recovery with return to work on average in 1 day and 96.7% of vein obliteration maintained at 3 and 5 years after the procedure.