Chronic venous insufficiency (CVI)

Chronic venous insufficiency (CVI) is one of the most common, often unknown and underestimated diseases worldwide. CVI is a chronic disorder of blood flow from the legs to the heart characterized by pain and swelling in the legs or ankles, and varicose veins. This is caused by dysfunction of the venous valves that cause disruption of venous blood flow, so that blood reflux can occur in the veins. CVI is often referred to as varicose veins, namely there are veins that appear enlarged, tortuous, and bluish in color under the surface of the skin which usually occurs in the leg veins, but varicose veins can also occur in other places.

CVI has a significant impact on cosmetic problems. The consequences of cosmetic problems in CVI can affect quality of life and are associated with more serious manifestations. Without proper treatment, the condition can become progressive so that it can become Chronic venous ulcer which has more severe clinical symptoms. Even with treatment, complications can occur if venous hypertension persists. Other complications that can occur such as massive bleeding

The results across studies show that in the general population between 1% to 17% of men and 1% to 40% of women may experience Chronic Venous Insufficiency. Based on some data, developing countries have a lower overall prevalence than developed or industrialized countries. The prevalence of CVI is more common in women than men (3:1). Among all patients with chronic venous insufficiency, about 1% to 2.7% will experience ulcer veins. Ulcer formation will cause a poor prognosis, with about 40% of patients experiencing recurrence despite treatment.

The etiology of CVI can be classified into 3, namely congenital CVI, primary CVI, and secondary CVI: (Patel and Surowiec, 2022). 2.3.1 Congenital CVI The cause of congenital CVI is an abnormality where the valve that should have formed in a segment is not formed at all (aplasia, avalvulia), or its formation is not perfect (dysplasia) (Patel and Surowiec, 2022). 2 2.3.2 Primary CVI The cause of primary CVI is intrinsic weakness of the vein wall, namely the elongation of the valve (elongation) or the valve is too flexible. This condition will cause the valve to close incompletely, so that the valve cannot withstand backflow and reflux occurs. Recent studies have shown that around 70% of patients have primary chronic venous insufficiency and 30% have secondary disease. Studies on primary chronic venous insufficiency have identified reduced elastin content, increased extracellular matrix remodeling, and inflammatory infiltration. The peak changes the integrity of the veins causing dilation and valve incompetence (Patel and Surowiec, 2012). 2.3.3 Secondary CVI Secondary CVI occurs in response to DVT (Deep Vein Thrombosis) which triggers an inflammatory response that then injures the vein wall. Several months or years after the occurrence of venous thrombosis called post-thrombotic syndrome. In this syndrome, scar tissue formation will occur, causing fibrosis, and will also cause shortening of the valve leaflets (shrinkage and valves). If the damage to the valve leaflets is very severe, it is difficult to repair. The specific etiology, chronic venous insufficiency triggers venous hypertension. The most common non-modifiable risk factors are female gender and non-thrombotic iliac vein obstruction (May-Thurner syndrome). Modifiable risk factors include smoking, obesity, pregnancy, prolonged standing, DVT, and venous injury (Patel and Surowiec, 2022).

There are several mechanisms associated with superficial venous valve failure. The most common is a congenital abnormality that causes weakness in the dilated venous valve wall, causing low pressure and secondary valve failure. Congenital abnormalities in the valve can also cause valve incompetence even in low blood pressure conditions. Normal veins and normal valves can also swell due to the influence of hormones such as pregnancy hormones (Youn and Lee, 2018). Increased venous blood pressure will eventually cause venous insufficiency syndrome. Under normal conditions, there are two body mechanisms that prevent venous hypertension. First, the tricuspid valve in the vein prevents backflow and venous adhesion. Deep Vein Thrombosis often blocks the valve and will eventually cause irreversible damage to the valve. Second, in normal ambulation, the calf muscles reduce venous pressure by 70% in the lower extremities. With rest, the pressure returns to normal for 30 seconds. In venous disease, venous pressure only decreases by 20% with movement. When ambulation stops, the pressure in the venous lumen decreases slowly and returns to normal within a few minutes (Youn and Lee, 2018).

Clinical Manifestations

Swelling in the legs or ankles Feet feel heavy or sore, hot and itchy Pain when walking that stops at rest Skin discoloration Varicose veins Leg ulcers (Patel and surowiec, 2022).

To evaluate and classify the condition, treatment, and consequences or complications of this disease, several assessment scales are used. The CEAP classification is based on clinical signs (Clinical), causes (Etiologic), Anatomic, and Pathophysiology. The etiological classification separates diseases based on congenital, primary, or secondary properties. Anatomy based on the affected veins including superficial, deep, or perforating veins. Pathophysiological classification identifies reflux in superficial, communicating, or deep systems, and outflow obstruction. The main disadvantage of this system is that because of its static nature, this type of classification is difficult to use to assess changes that occur in response to therapy that has been given

Supporting examinations that can be performed are Duplex Doppler ultrasonography A type of ultrasound procedure performed to assess blood vessels, blood flow and the structure of leg veins. 2. Venogram Performed using x-rays and intravenous (IV) contrast dye to visualize blood vessels. Contrast dye causes blood vessels to appear dull on x-ray imaging, which makes it easier to visualize the blood vessels being evaluated. 3. Venous plethysmography The plethysmography technique detects changes in venous blood volume in the legs. Venous obstruction and valve reflux change the normal pattern of venous filling and emptying to ex

Initial management of CVI is conservative measures to reduce symptoms and prevent secondary complications and disease progression. The use of compression stockings is one example of conservative management. Compression stockings help improve symptoms and hemodynamic conditions with varicose veins and eliminate edema. Stockings with a pressure of 20-30 mmHg (grade II) provide maximum results. In the study, it was found that around 37-47% of patients who used compression stockings for 1 year after suffering from DVT prevented leg ulcers. The disadvantages of using stockings are the relatively expensive price, lack of patient education, and poor cosmetics. If conservative measures fail or do not provide changes, further treatment can be carried out. Patients with advanced CVI who are not treated are at risk of ulceration. A healthy lifestyle including maintaining ideal body weight or weight loss if overweight can improve the manifestations of CVI. Obesity is a major risk factor for 10 the development of CVI and its complications. Weight loss after bariatric surgery has been shown to improve the manifestations of CVI, including edema and ulcers. It can be extrapolated that weight loss by other means can also help in the treatment of CVI

Surgery, surgery can be used to treat chronic venous insufficiency including: 1. Ligation The damaged vein is tied so that blood does not pass through the vein. If the vein or valve is severely damaged, the blood vessel will be removed (vein stripping). 2. Surgical repair The vein or valve is repaired surgically, through an open incision or with the use of a catheter. 3. Vein Transplant Replacing the damaged blood vessel with a healthy blood vessel from another part of the body. 4. Subfascial endoscopic perforator surgery Minimally invasive procedures are performed with an endoscope. The perforator vein is cut and tied. This allows blood to flow to healthy blood vessels and improves ulcer healing. (Rabe and Pannier, 2020). 5. One of the minimally invasive varicose vein therapy options is Endovenous Laser Ablation (EVLA). The advantage of using this therapy option is that it can be performed on outpatients under local anesthesia. The EVLA procedure uses a laser fiber inserted into the distal VSM (vena saphena magna) to the SFJ (saphena femoral junction) under ultrasound control. The procedure is first performed by administering local perivenous anesthesia by infiltrating around the VSM extender blood vessels. The goal is not only to provide analgesia but also to provide a pressure effect on the vein so that the vein wall is apposed to the fiber which acts as a "heat sink" to prevent local tissue damage. EVLA does not cause the vein to shrink immediately when compared to when radiofrequency ablation is performed, but the vein will shrink gradually for several weeks until it is not visible after 6 months with an ultrasound examination, then followed by endothelial damage, coagulative necrosis, narrowing and vein thrombosis.

Complications 1 Venous ulcer 2 Leg discoloration 3 Thrombophlebitis 4 DVT 5 Pulmonary embolism 6 Bleeding 7 Secondary lymphedema 8 Chronic pain

Some efforts that can be done to reduce the risk of CVI are: 1. Avoid long periods of standing or sitting 2. Elevate the legs to reduce pressure in the blood vessels in the legs. 3. Exercise regularly. 4. Lose weight 5. Compression stockings to focus pressure on the legs and help blood flow. 6. Antibiotics if needed to treat skin infections