Varicose veins can be accompanied by several symptoms. Pain can cause vague and unpleasant pain by stimulating pain sensory receptors of Ad or C fibers through local inflammatory mediators when venous hypertension is transmitted to the microcirculation. Throbbing is believed to be caused by a hemodynamic mechanism. Tightness is thought to be related to increased pressure in the lower extremity compartment. Venous claudication manifests as severe venous outflow obstruction when the arterial inflow exceeds venous outflow. Heaviness and swelling are thought to be edema related to microcirculation. Itching is often associated with skin changes, but can also be a solitary symptom, and inflammation, cytokines, and MMP activation are implicated in pathophysiology. In addition, the exact causes of cramping, restless legs, tingling, and burning are not well known. However, these symptoms may appear in general and are not specific to chronic venous disease (CVD). Conversely, the absence of these symptoms does not exclude CVD (
Venous pain that can be experienced clinically can be triggered by physical stimuli (such as a needle, cathete-rization, or pulling a vein) or by chemical stimuli (such as hyperosmolar fluid injections or acidic or alkaline liquid solutions). Pain may also be caused by venous thrombosis and phlebitis (
Although patients with varicose veins also express pain, clinicians find it difficult to accurately assess pain in varicose veins. First, venous pain can manifest itself in association with other unpleasant sensations that are multifaceted and are often difficult to explain. Second, the pain intensity of venous disease varies from patient to patient, and varies even in a patient over time. Third, clinically and experimentally, the causal relationship between venous disease and pain remains difficult to explain (
To measure venous pain, various types of stimulation were applied to the veins of the back of the hands of participants through the human venous pain model, and the intensity of pain was evaluated (
To date, the prevailing hypothesis for the mechanism of venous disease pain is local inflammation associated with venous stasis. Local hypoxia associated with capillary stasis is believed to cause pain in venous diseases. Interestingly, these mechanisms appear to be involved in the structural changes of the venous wall and in the varicose remodeling process over a long period of time (
Interestingly, no correlation was found between venous disease and pain intensity based on the CEAP classification. In a cohort study of 132 patients with varicose veins, the visual analog scale (VAS) scores were 2.8 for C2, 4.5 for C3, 0.5 for C4, and 0 for C5 or higher. The reason for the lack of correlation is that in the CEAP classification, C2 can include all types of varicose veins, and C3 includes edema without distinguishing the cause, which can cause bias in the CEAP scale itself. Another hypothesis is that ischemia caused by microangiopathy may result in the loss of sensory axons and an elevated sensory threshold in the late stage of CVD (
In a study on postmenopausal women, no correlation was found between pain and the CEAP classification. However, pain showed a significant correlation with the osteoarthritis index and venous refill time. Associations with factors related to calf muscle dysfunction suggest that impairment of movement may affect pain (
Cold temperatures are believed to be much kinder to the veins. Cold temperatures cause the swollen veins to shrink. Contrastingly, the pain worsens in warm weather because the blood vessels dilate. However, there is an interesting study on temperature-related beliefs. This study compared cytokine expression between the autumn and spring groups. They found that eotaxin, interleukin-8, monocyte chemo-attractant protein-1, tumor necrosis factor-a, and vascular endothelial growth factor levels increased in autumn, but significantly reduced in spring. Interestingly, cytokine levels were significantly higher in autumn and downregulated in spring. Researchers speculate that these results may be correlated with the action of vitamin D (
Venous pain was not correlated with the CEAP classi-fication, reflux, or inflammatory markers. If hypoxia is an important factor in inducing pain, lower extremity pain may be experienced in various hypoxia-related situations, such as long standing or sitting for a long time, difficulty in walking at the end of the day or at certain times during the menstrual cycles, osteoarthritis, etc. As observed during the Edinburgh study, patients with no varicose veins on clinical examination and no reflux on Doppler may complain of symptoms, such as leg pain or heaviness. Pain occurs as a short-term consequence of venous hypoxia, while varicose dilatation occurs in the later stages of venous disease. The fact that pain does not correlate closely with varicose dilatation suggests that the site of primary activation of venous pain receptors may be absent in relatively large veins. Instead, the hypothesis of hypoxia-induced pain receptor activation in the microvasculature is more plausible, and methods to study pain receptors in microcirculation need to be developed. A previous study reported that transient blood reflux was cured and QOL increased when MPFF was prescribed for 3 months in C1 patients (
This paper was presented at the 41st Conference of the Korean Society for Phlebology on Nov 07, 2021.
The author declares no potential conflict of interest.