As chronic venous disease (CVD) progresses, clinical manifestations and CEAP classification grades tend to advance [1]. The progression of CVD is highly variable, following diverse pathways among patients. For instance, some individuals with saphenous reflux may exhibit symptoms without visible varicose veins, whereas others with visible varicose veins may present with or without accompanying venous symptoms. This variability arises because venous hypertension plays a more critical role in symptom development than venous reflux or vein dilatation. A comprehensive understanding of venous hypertension is, therefore, essential for the effective management of varicose veins. Accordingly, this review explores treatment approaches for varicose veins, emphasizing the role of venous hypertension.

Fluid movement is governed by the combined effects of hydrostatic and oncotic pressures. In the context of CVD, hemodynamic disturbances arise, leading to the failure of venous pumps and conduits to sustain normal pressure and flow toward the heart. These disturbances are primarily attributable to venous reflux, obstruction, a combination of reflux and obstruction, or the presence of an arteriovenous fistula. Compensatory mechanisms for obstruction include the extent of collateral circulation and the capacity of the lymphatic system to maintain adequate drainage [2]. The clinical manifestation of symptoms and signs results from the interplay of these forces and compensatory mechanisms. However, the inability to precisely quantify these factors in individual patients hinders a complete understanding of CVD pathophysiology, creating significant management challenges.

In human studies, the mean ambulatory venous pressure (AVP) ranges from 10 to 20 mmHg. Intermediate venous hypertension is classified as 31–45 mmHg, while severe venous hypertension exceeds 45 mmHg. Edema is rarely observed when venous pressure is below 20 mmHg, whereas leg edema consistently develops when venous pressure exceeds 50 mmHg [3]. Patients with severe venous hypertension frequently experience significant symptoms.

The calf muscles and valves of the veins play an important role in venous hypertension. Calf muscle contraction facilitates the closure of venous valves. In a standing position, however, venous valves remain open. Consequently, prolonged standing results in hydrostatic pressure exceeding 90 mmHg, even in individuals without underlying venous pathology, making leg swelling a common occurrence during extended periods of standing. Conversely, during ambulation, the muscle-venous pump rapidly reduces venous pressure through the closure of venous valves, a process referred to as dynamic pressure fractionation [4].

We can easily understand hydrostatic pressure through a simple example. Consider two columns of water: the taller column exerts greater pressure due to its height (Fig. 1). In the same way, the fractionation of pressure by venous valves reduces the effective height of the water column, thereby decreasing the hydrostatic pressure.

Figure 1. There are water columns of the same diameter but different heights. The higher the water column, the higher the pressure, so the water stream comes out more powerfully.

Consider four test tubes of varying shapes. If the water level is identical in all tubes, the hydrostatic pressure remains the same, as hydrostatic pressure is determined solely by the height of the fluid column. This relationship is expressed as P (hydrostatic pressure, Pa)=ρ (density of the fluid)×g (acceleration due to gravity, 9.81 N·kg^–1)×h (height of the fluid column). This phenomenon is known as the hydrostatic paradox (Fig. 2). Increased hydrostatic pressure resulting from venous valve insufficiency plays a more critical role in the pathophysiology of venous disease than the shape of varicose veins. This indicates that the diameter of the vein is less critical in determining treatment indications. Instead, venous hypertension resulting from valve insufficiency constitutes a more significant factor in the pathophysiology of venous disease.

Figure 2. Hydrostatic paradox. In various test tubes, if the water level is the same, the hydrostatic pressure measured at the bottom remains constant.

An increase in venous pressure precedes the dilation of veins. Vein wall dilation is driven by the force exerted by elevated hydrostatic pressure, making venous diameter directly proportional to the applied pressure. When venous pressure exceeds 20 mmHg, the vein walls begin to stretch. This phenomenon is reversible; as the pressure decreases, the vein diameter correspondingly reduces. It is important to highlight that in patients with varicose veins, elevated hydrostatic pressure plays a pivotal role in inducing vein wall dilation [2].

A study directly measuring venous pressure in patients with varicose veins revealed two distinct cases [5]. In the one case, after applying a below-knee tourniquet, venous pressure decreased to below 40 mmHg, and venous refill time (VRT) normalized. In this instance, great saphenous vein (GSV) ablation effectively improved venous pressure. In the other case, however, both AVP and 90% VRT did not normalize with the application of a below-knee tourniquet. This suggests that perforator veins may serve as an additional source of venous hypertension. Normalization of pressure (i.e., >15 s and <45 mmHg, respectively) was achieved following the application of an ankle tourniquet. In this case, below-knee saphenous ablation or removal of the below-knee perforator vein may be required. From a hemodynamic perspective, it can be recommended that treatment of the below-knee saphenous vein could be considered if venous pressure is not effectively reduced by above-knee GSV ablation.

In clinical practice, directly measuring venous pressure in outpatient settings is often challenging. However, venous hemodynamics can be indirectly assessed using air plethysmography. The venous volume graph produced by this method shows patterns that closely mirror changes in pressure during variations in motion [2]. Venous volume measures the calf venous reservoir, which is typically 100–150 mL in healthy individuals, but can increase to 350 mL in patients with chronic venous insufficiency (CVI). The venous filling index (VFI) represents the rate at which 90% of venous volume is filled. An elevated VFI is associated with a higher incidence of venous ulceration. Both venous volume and VFI exhibit a strong correlation with calf vein diameter, but a weaker correlation with superficial veins. These parameters are linked to venous dilatation due to increased venous pressure in the standing position. Notably, venous diameter did not show a significant correlation with clinical presentation [6]. In contrast, the residual volume fraction (RVF) demonstrated a strong correlation with AVP [7]. Therefore, RVF, as measured by air plethysmography, can serve as an indirect indicator of AVP. A previous study involving 112 lower extremities found that RVF was greater than 40% in patients with CEAP classification C4–C6, concluding that RVF correlates well with venous hypertension [8].

CVD leads to hemodynamic disturbances, resulting in the inability of venous pumps and conduits to function effectively. Venous hypertension due to valve insufficiency is the primary underlying mechanism of varicose veins. Treatment for varicose veins should be guided by hemodynamic principles. Below-knee GSV ablation may be warranted if AVP is not adequately reduced by above-knee GSV ablation. AVP can be indirectly measured using air plethysmography.

The author declares no conflicts of interest.