What is a Varix?
A varix is an abnormally dilated, tortuous vein that develops due to increased wall tension from elevated transmural pressure, often combined with structural weakness of the vessel wall. 1, 2
Pathophysiology
Variceal formation occurs through a complex interplay of mechanical forces and structural changes in the vessel wall. The fundamental mechanism involves:
- Increased transmural pressure (the difference between intravascular pressure and surrounding tissue pressure) causes excessive wall tension that the vessel cannot adequately oppose 1
- Structural wall weakness from degradation of extracellular matrix proteins, mediated by increased matrix metalloproteinase (MMP) activity, compromises the vessel's structural integrity 3
- Valve dysfunction may occur either as a primary event causing reflux, or secondary to focal wall dilation near valve junctions, with the reflux then becoming self-perpetuating 3
The progression is cyclical: increased pressure → wall dilation → valve incompetence → further pressure elevation → progressive venous insufficiency 3.
Clinical Manifestations by Location
Esophagogastric Varices (Portal Hypertension)
Varices develop when hepatic venous pressure gradient exceeds 12 mm Hg, which is the threshold necessary for both formation and bleeding. 1
- Size classification is critical for risk stratification: small varices (≤5mm) versus large varices (>5mm), assessed endoscopically 1
- Bleeding risk factors include variceal size, severity of liver disease (Child-Pugh class), red wale markings (longitudinal dilated venules on the variceal surface indicating microtelangiectasias), and portal pressure 1
- Hemorrhage occurs in 5-15% yearly, with mortality of at least 20% at 6 weeks despite treatment 1
- Endoscopic features such as red spots and wale markings represent changes in wall structure and tension; 80% of patients with blue varices or cherry red spots will bleed 1
Lower Extremity Varicose Veins
Varicose veins result from valvular reflux involving genetic predisposition, incompetent valves, weakened vascular walls, and increased intravenous pressure. 4
- Symptoms include pain, burning, itching, heaviness, cramping, throbbing, restlessness, and swelling that worsen with prolonged standing and improve with leg elevation 4, 5
- Progressive disease leads to skin changes including pigmentation, eczema, lipodermatosclerosis, and potentially ulceration 4
- Risk factors include family history, female sex, older age, chronically increased intra-abdominal pressure, and prolonged standing 4
Other Anatomic Locations
- Orbital/eyelid varices are rare, induced by Valsalva maneuver or prone posture due to increased jugular venous pressure, presenting with fullness or proptosis 2
- Pulmonary vein varix presents as an asymptomatic mass on chest radiograph, representing localized pulmonary vein dilation 6
- Pelvic varices, hemorrhoids, and varicoceles share common pathophysiologic mechanisms of vascular wall remodeling in veins running against gravity 7
Common Pitfalls
- Failing to recognize that variceal wall tension depends on both pressure AND vessel radius—larger varices are at higher bleeding risk even at similar pressures 1
- Overlooking that tissue support surrounding the varix can protect against rupture, explaining why some high-pressure varices don't bleed 1
- Misunderstanding that once rupture occurs, bleeding amount relates to transmural pressure, rupture area, and blood viscosity/coagulation status 1
- Delaying intervention in symptomatic lower extremity varices when valvular reflux is documented—compression therapy alone does not prevent disease progression 4