Home › Pathology › Varicose Veins: Pathophysiology and Complications

Varicose Veins

Varix

For medical students2 min readUpdated 2026-10-10

Varicose veins represent a pathological enlargement of the vascular lumen, tortuosity, and vessel elongation developing under the influence of chronically elevated intravenous pressure. The disease is accompanied by structural remodeling of the venous wall and valve apparatus.

Common sitesLower extremity veins, esophagus, hemorrhoidal plexuses

Vessel wallThinned in areas of dilation, thickened in other segments

Critical complicationEsophageal variceal rupture in 7–20% of patients with cirrhosis

Lower limb epidemiologyAffects 10–20% of adults; women are 4 times more likely

Causes and Pathogenesis

The primary triggering mechanism for varix development is a sustained increase in intravascular pressure caused by impaired venous outflow. A key role in this process is played by congenital or acquired weakness of the venous wall tissues. There are two main forms of the disease:

Primary: Caused by hereditary weakness of vascular structures.
Secondary: Develops due to mechanical obstruction to blood flow, such as vascular occlusion by a tumor or thrombus.

Pathomorphological Changes

At the microscopic and macroscopic levels, varicose veins undergo profound transformation:

In areas of maximal bulging and stretching, the vessel wall becomes thinned.
In other segments, compensatory hypertrophy of smooth muscle elements is observed alongside sclerotic processes.
Venous valves undergo sclerosis and deformation, rendering them incompetent and worsening blood stasis.

This pathology is frequently combined with a dangerous process—phlebothrombosis.

Lower Extremity Varicose Veins

This form predominantly affects superficial vessels that lack rigid fixation by surrounding tissues. The condition is provoked by prolonged standing, heavy lifting, pregnancy, obesity, and tight clothing. Patients experience leg edema and unpleasant trophic skin changes, including dermatitis and ulcers. A characteristic complication is thrombosis of the varicosities, although classic pulmonary thromboembolism is atypical for this condition.

Involvement of Internal Plexuses and Esophagus

The pathological process frequently affects internal organs and venous reservoirs:

Hemorrhoidal veins: Dilation involves the lower and upper plexuses (external and internal hemorrhoids), arising against the background of constipation, pregnancy, or portal hypertension. It is accompanied by a risk of bleeding, inflammation, and incarceration.
Esophageal veins: Develop as portosystemic anastomoses in liver cirrhosis, portal vein thrombosis, or pylephlebitis. The main danger is sudden rupture of altered varices under the impact of food boli, leading to massive hemorrhage.

Frequently asked questions

What trophic skin changes develop in lower extremity varicose veins?

In lower extremity varicose veins, trophic skin changes such as dermatitis and trophic ulcers develop. These pathological processes arise due to progressive chronic venous insufficiency. Overstretching of vessels and valve incompetence lead to venous hypertension and blood reflux into superficial veins. This causes marked microcirculatory disturbances in tissues, ultimately causing trophic skin lesions.

What complications are characteristic of hemorrhoidal varicosities?

Hemorrhoidal varicosities are characterized by inflammatory, hemorrhagic, and mechanical complications. Key pathological conditions include:

Inflammation and ulceration — result from trauma to hemorrhoidal nodes.
Hemorrhoidal thrombophlebitis — develops when infection joins the affected nodes.
Bleeding — can be very intense, resembling arterial bleeding upon mechanical injury.
Incarceration — occurs when internal nodes prolapse through the anal sphincter.

Which venous plexuses act as portosystemic anastomoses in portal hypertension?

In portal hypertension, the venous plexuses of the esophagus, stomach, rectum, and anterior abdominal wall act as portosystemic anastomoses. Blood from the portal system is shunted through the following zones:

Esophageal and gastric veins — anastomoses are localized in the lower third of the esophagus and the cardia of the stomach.
Hemorrhoidal plexus — located in the lower rectum, shunting blood into the inferior vena cava system.
Paraumbilical veins (vv. paraumbilicales) — run in the falciform ligament of the liver and distribute blood to the superficial veins of the anterior abdominal wall, forming the caput medusae sign.

What are the main causes leading to the development of varicose veins?

The main cause is elevated intravenous pressure secondary to impaired venous outflow. A predisposing factor is the congenital or acquired inadequacy of the venous wall tissues.

Why are esophageal varices life-threatening?

Esophageal veins dilate during portal hypertension, acting as portosystemic anastomoses. Rupture of such thinned varices due to food trauma or inflammation causes fatal hemorrhage in 7–20% of patients with liver cirrhosis.

How does primary varicose vein disease differ from secondary?

Primary disease is caused by hereditary weakness of the vascular wall. Secondary varicose veins develop as a consequence of luminal obstruction by a thrombus or tumor.

Go deeper

Pathogenesis of hemorrhoidal nodes and portosystemic anastomoses
Microscopic structure of the venous valve apparatus in varicosities
The role of liver cirrhosis in the formation of esophageal bleeding
Trophic skin changes of the lower extremities in venous stasis
Similarities and differences between phlebothrombosis and thrombophlebitis in varicose disease