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Revista mexicana de angiología

versión On-line ISSN 2696-130Xversión impresa ISSN 0377-4740

Rev. mex. angiol. vol.49 no.2 Ciudad de México abr./jun. 2021  Epub 23-Ago-2021 

Articulos de revisión

Chronic venous insufficiency symptoms and its potential causes: Are we doing it right?

Síntomas de la insuficiencia venosa crónica y sus posibles causas. ¿Lo estamos haciendo bien?

Enrique Santillán-Aguayo1  * 

José de J. Rivera Sánchez2 

Verónica Carbajal-Robles1 

Javier Duarte-Acuña1 

Felipe A. Piña-Avilés1 

Miriam V. Ramírez-Berumen1 

1Angiology and Vascular Surgery Service. Hospital General de México, Mexico City, Mexico

2Research Department. Hospital General de México, Mexico City, Mexico



Chronic venous insufficiency has symptomatology associated with venous hypertension; until now they have never been approached for the purpose of describing a characteristic pattern presentation allowing a clinical differential diagnosis. The largest study addressing this topic is the Vein Restoration Study (VRS) that included 38,750 patients demonstrating discrepancy between signs and symptoms among age groups studied, coupled with the fact that in our own medical practice as a vascular specialist we may face patients with advanced degrees of venous hypertension but completely asymptomatic. Symptoms have been reported as subjective and potentially confoundable with other comorbidities such as neuropathies, as there is a close anatomic relationship between veins and nerves.


Electronic literature searches were performed from 1947 to 2021 by the first author using PubMed and the Cochrane Central Register of Controlled Trials.


We found 1200 articles using those related to venous symptoms noting any of them focused on the pattern presentation with evident discrepancies between signs and symptoms.


Venous symptoms must be considered subjective, and potentially caused by an underlying and undefined condition or comorbity. Until now, no author has demonstrated that these are caused directly by venous disease.

Key words Venous symptoms; Chronic venous insufficiency; Venous hypertension



La insuficiencia venosa tiene síntomas relacionados con hipertensión venosa, pero hasta ahora éstos no se han enfocado con el propósito de describir un patrón de presentación característico que permita establecer de forma clínica un diagnóstico diferencial. El estudio más grande Vein Restoration Study (VRS) que incluyó a 38,750 pacientes demostró una discrepancia de los síntomas y signos entre dos grupos etarios estudiados; en la práctica de los autores como especialistas vasculares es posible atender a un paciente con grados avanzados de hipertensión venosa pero asintomáticos. Los síntomas se han notificado como subjetivos y tal vez confundibles con los de otras anomalías comórbidas como las neuropatías, dado que existe una estrecha relación anatómica con los nervios.


Búsqueda electrónica de artículos en relación con síntomas venosos entre los años 1947 y 2021, por investigador principal, a través de PUBMED y Cochrane.


Se encontraron 1200 artículos y se utilizaron aquéllos vinculados con síntomas venosos, sin identificar alguno enfocado en el patrón de presentación esperado y con evidentes discrepancias entre signos y síntomas.


Los síntomas venosos deben considerarse como subjetivos, y pueden ser causados por una comorbilidad subyacente y no identificada. Hasta ahora ningún autor ha demostrado que estos sean causados de forma directa por la enfermedad venosa.

Palabras clave Síntomas venosos; Enfermedad venosa crónica; Hipertensión venosa


A book regarding the description and clinical characterization of the symptoms provoked by chronic venous insufficiency (CVI) was first published in 19641. It is no surprise that anatomy and the initial comprehension of venous physiology but above all, its physiopathology was not concentrated by a vascular specialist (vascular surgeon, angiologist, or vascular medicine specialist) because the first workgroup created and identified in the world with medical and no surgical purposes was in 19912 in Europe, emitting first recommendations for the specialty in 19933. Arnoldi1, a recognized physician focused on the treatment of diverse orthopedic pathologies, was first in writing a 75 page and 15 chapter's book titled "The venous return from the lower leg in Health and CVI: A Synthesis" based on its own experience and observations on dynamic phlebography, collaboration among with Bauer, Barcroft, Burch, and Sodeman as well of the anatomic studies previously reported by Askar, Cockett, Dodd, Eger, and many other authors; 35 bibliographic references, published in different scientific medical journals.

Arnoldi, based on 307 patients to whom he made phlebography's, characterized five symptoms described in table 1. Arnoldi focused predominantly on bursting diffuse pain but considered all symptoms as subjective. He associated bursting pain mostly to anomalies of the deep venous system, and almost exclusively to extent deep valvular incompetence, either post-thrombotic syndrome (PTS) or as he referred idiopathically. About 17.9% (n = 55) of the cohort studied without symptoms and as high as 42% (n = 21) in Group Ia (only varicosities, normal venous pump, and no thrombosis) and 22% in Group IIa (impaired but functional venous pump with incompetent perforating veins compensating at some point with the superficial system) reporting themselves as asymptomatic, even though by severity, Group II had the higher venous hypertension with 50% of ulcers in IIa and 80% in Group IIb1.

Table 1 Symptoms and signs reported by Arnoldi in its book, 19641 

Records the subjective symptoms noted on the day of admittance in the various phlebographic groups, together with the number of leg ulcers
Symptoms Group Ia (n = 48) Group Ib (n = 12) Group IIa (n = 130) Group IIb (n = 49) Group III (n = 68) Total (n = 307)
Without 21 (42%) 3 (25%) 28 (22%) 2 (4%) 1 (1.5%) 55 (17.9%)
Heaviness and tiredness 24 (48%) 8 (67%) 57 (43%) 34 (70%) 37 (54%) 160 (52.1%)
Slight pain 12 (24%) 5 (42%) 43 (33%) 18 (38%) 22 (32%) 100 (32.5%)
Bursting pain 0 1 (8%) 18 (14%) 13 (27%) 31 (46%) 63 (20.5%)
Restless legs and nightly cramps 1 (2%) 3 (25%) 18 (14% 6 (13%) 13 (29%) 41 (13.3%)
Leg ulcers 7 (14%) 4 (33%) 69 (50%) 50 (81%) 9 (12%) 139 (45.2%)

All the authors as mentioned above have described different surgical techniques, some of them surprising attempts to achieve clinical improvement to patients with severe venous pathology as Bauer's reported technique resecting popliteal vein, treating what we know as PTS, and first-ever lineal venoplasty4, forerunner to mayor stripping studies realized by Boyd5. All of them had surgical training, and their contributions to our recent experience were a cornerstone. In America, a pioneer in understanding venous function was Seligman in 19566 and its contribution to surgical technique in 19637. Trying to understand physiology, physiopathology, and a way to surgically treat venous disease, all of them described in their studies edema, color ochre discoloration, and sclerosis of the skin (described as induration) with the consequent development of stasis ulcer. The skin's sclerosis was subsequently considered a dermoepidermitis, identifying since 1969 eczema as a characteristic sign in these patients8. All of them considered nosologically signs, many of which were described, as well as new strategies for surgical treatment, reported based on experiences in areas as phlebology, allergology, topic dermatotherapy, and dermatosurgery9. Never characterized symptoms nor efforts were focused on determining potential comorbidities explaining such symptoms.

Materials and methods

Electronic literature searches were performed from 1947 to 2021 by the first author using PubMed and the Cochrane Central Register of Controlled Trials. The search strategy included "CVI" AND "symptoms" NOT "treatment;" "CVI" AND "symptoms;" "CVI" AND "symptoms pattern presentation," then, we manually search relevant articles missed by electronic searches, language limitation to English and Spanish. After identifying relevant titles, abstracts were revised by the author trying to select those related to venous symptoms and pattern presentation not finding a single one, thereby deciding to revise and concentrate those symptoms in a way allowing us to identify the expected pattern presentation, opening a previously closed subject on to understand venous symptoms better.


There were found 1200 articles. Approximately between 1960 and 1990, all literature reported regarding signs and symptoms is not available online, only historical record; nonetheless, titles focus almost solely on signs provoked by venous stasis, along with different surgical approaches8-17. In most recent studies, few of them exclusively concentrate on symptoms, and as shown in table 21,18-21, none of them report pattern presentation22-24.

Table 2 Symptoms of venous hypertension reported by some authors in literature 

Prevalence of symptoms
Author/year Author/year
Arnoldi1, 1964 (307) Symptoms Total Marston19, 2010, two sub-analysis Symptoms Total
55 Without 17.9% National venous screening program27 (2234) Pain 77%
160 Heaviness and tiredness 52.1% Mild
Moderate 29%
100 Slight pain 32.5% Severe 19%
63 Bursting pain 20.5% The San Diego Study20 (2211) Cramps 10-15%
41 Restless legs and cramps 13.3% Heaviness 10-15%
Swelling 10-15%
139 Ulcer 45.2% Pain <10%
Duque18, 2005 (100) Symptoms Total Vein Restoration Study21, 2018 (38,750) Symptoms Total
A <65a 27,536 B >65a 11,214 A <65a B >65a
66 Itch 66% 4717 1485 Aching 17.1% 13.2%
44 Pain in itching area 44% 6718 2803 Cramping 24.3% 24.9%
63 Leg fatigue 63% 7348 2736 Fatigue 26.6% 24.3%
62 Leg pain 62% 8315 3005 Heaviness 30.1% 26.7%
48 Muscle aches 48% 2843 1097 Restless legs 10.3% 9.7%
47 Heaviness 47% 16,907 6159 Pain 61.3% 54.9%
53 Cramps 53% 6284 3300 Swelling 22.8% 29.4%
74 Burning sensation 47% 2063 624 Burning 7.4% 5.5%
1950 542 Itching 7% 4.8%

The symptoms that patients with venous hypertension present have varied little over the years (Table 2)18,19,25,26. There are no reports in the literature regarding asymptomatic patients, regardless of the severity of the disease, including chronic ulceration. Some papers report generic symptoms like pain in different degrees. Others focus on heaviness, tiredness, pain, and swelling indistinct to edema. Some are more precise at describing symptoms and signs, establishing a clear difference between swelling and edema but none of them focusing or even mentioning a symptom pattern presentation and differential diagnosis.

It should be noted from table 2, in the study reported by Duque, itching was the predominantly sign and focus of the study; 66 patients referred itching and 62% had presented it in the past 6 months, 95% mostly during late-afternoon and night, 50% of whom even had sleeping troubles, 40% woke up during the night because of it, and 15% requiring sleep meds to achieve it. About 62% of patients said that itch was in the pretibial region, 45% posterior calf region, and 40% in the thigh with a symmetrical pattern in both legs in 64%. By last, 44% of patients referred pain and 74% burning sensation in the same spot of itching, all of them characteristic neuropathy symptoms, with no correlation between symptoms and severity of the disease, authors concluding according to observations that symptoms despite no correlation with severity, it does with chronic venous disease18.

In a revision published by Marston19 from a sub analysis of "National venous screening program" (NVSP)27 and "San Diego Population Study" (SDPS)20, the results contrast regarding pain, reported as high as 77% in NVSP and 10-15% in SDPS; author concluded that although pain is the most predominantly symptom, none of the symptoms referred are specific for the disease, and multiple other diseases may be confused with venous insufficiency. Noting that neither of the two studies described symptoms in the text nor presented frequency, only signs or QoL questionnaires. In "Vein Restoration Study" (VRS)21, one of the largest, included prospective and retrospectively 38,750 patients in two main groups, those aged more than 65 years and those aged < 65 years with a significant statistical difference between groups in symptoms and signs. Those aged < 65 years had more frequent pain (61.3% vs. 54.9%), fatigue (26.6% vs. 23.4%), heaviness (30.1% vs. 23.7%), and aching (17.2% vs. 13.2%) p < 0.0001 (Tables 2 and 3), but higher rates of signs in those aged more than 65 years such as swelling (29% vs. 23%), skin changes (12% vs. 6%), hyperpigmentation (8% vs. 4%), edema (55% vs. 43%), and ulcer (5% vs. 2%) p < 0.0001 (Table 3), with no significant difference between cramping (25% vs. 24%) and restless legs (10% vs. 10%). Thus, it is necessary to do further studies explaining why, even though patients aged more than 65 years old presented more signs, they had fewer symptoms with strong statistical significance.

Table 3 Signs and symptoms reported in "Vein Restoration Study"21 

2015 2016 Total
< 65 years 11,252 16,284 27,356
> 65 years 4409 6805 11,214
Women 12,204 17,980 30,184
Men 3450 5100 8550
Presenting symptoms <65 years No. (%) >65 years No. (%) p value
Aching 4714 (17) 1485 (13) < 0.0001
Bleeding 417 (2) 210 (2) < 0.01
Cramping 6718 (24) 2803 (25) < 0.21
Fatigue 7348 (27) 2736 (24) < 0.0001
Heaviness 8315 (30) 3005 (27) < 0.0001
Pain 16,907 (61) 6159 (55) < 0.0001
Restless legs 2843 (10) 1097 (10) < 0.11
Skin changes 1539 (6) 1290 (12) < 0.0001
Spider veins 4625 (17) 1367 (12) < 0.0001
Swelling 6284 (23) 3300 (29) < 0.0001
Thrombosis 1189 (4) 304 (3) < 0.0001
Ulcer 576 (2) 542 (5) < 0.0001
Varicosities 1607 (6) 567 (5) < 0.02
Associated symptoms
Burning 2063 (7) 624 (6) < 0.0001
Dermatitis 171 (1) 137 (1) < 0.0001
Edema or swelling 11,872 (43) 6155 (55) < 0.0001
Hyperpigmentation 1159 (4) 925 (8) < 0.0001
Itching 1950 (7) 542 (5) < 0.0001
Pelvic symptoms 199 (1) 22 (0) < 0.0001
Skin ulceration 332 (1) 130 (1) < 0.718
Superficial thrombophlebitis 206 (1) 84 (1) > 0.99
Tingling 1027 (4) 316 (3) < 0.0001


Today, we understand that venous pathology, either primary or secondary, has important mechanical implications as, in the first place, the unidirectional valve function, which works as cardiac valves, through dynamic gradient pressure. Veins, unlike cardiac valves, are considered capacitance vessels, meaning their distensibility is high. They work along with muscles function in the calf against hydrostatic pressure. Unlike the myocardium, veins are not autonomic. They depend directly proportional to muscular trophic and tropism, physical activities, and movements in the hip, knee but mostly ankle, even mobility in metatarsophalangeal joints, so any pathologic condition targeting those previously mentioned may provoke muscular venous pump dysfunction, venous stasis, and its consequences.

Signs of venous disease are secondary to venous hypertension and are fully elucidated and include dilation of capacitance vessels until the formation of varix of different degrees, paths, and thickness, the presence of skin discoloration such as blanche atrophy and ochre color and induration now known as dermatoliposclerosis, edema, eczema, and as maximal consequence ulceration, which frequently is chronic and relapsing, mostly in perimalleolar territory, but atypical locations too as calf, toes, or sole. On the contrary, venous symptoms had been transcribed article by article, book by the book based on the observational results in 307 patients, and as the same Arnoldi mentioned, totally subjective. Those symptoms, even nowadays, are subjective in the validated quality of life (QoL) questionnaires, such as SF-36 and Euro-QoL DF and specific for the disease like CIVIQ-2. They are validated on precisely these subjective symptoms (mostly pain). CIVIQ-2 was presented in 1996 and translated into many languages and includes pain in the past weeks (without any specification), physical, social, and psychological repercussions in daily activities. Many authors use these questionnaires based on subjective symptoms as a guide to evaluating surgical, therapeutic compression, and pharmacological outcomes28-30.

Returning to previous stipulated conceptions by Arnoldi, where symptoms referred by patients were subjective and by Marston assuming multiple etiologies can produce similar symptoms, open, diverse investigation questions to answer to comprehend symptoms better.

Symptomatic differential diagnosis


First of all, it would be essential to establish a pattern presentation of symptoms associated with venous insufficiency; based on our physiological and physiopathological knowledge, whose we comprehended better than Arnoldi, Bauer, and Barcroft31,32. The venous pump has a 65% ejection fraction approximately, calculated by indirect means (plethysmography), to favor venous return against the column of hydrostatic pressure from ankles to the right atrium, going around 100 mmHg in the erect position and < 30 mmHg after 12 dorsiflexions of ankle's foot33-38. We also know in supine position hydrostatic pressure in every point measured turns equal; thus, we assume that venous edema (or symptoms) must never be present at rest while favoring gravitational potential energy, and not only improve but also disappear after some minutes of leg elevation, and above all in early disease stages.

Edema is studied since the eighties and caused by many diseases, initially by Andrew Dale15 in a text of 66 pages. It laid the foundations for actual etiological classification (Table 4), which required modifications based on physiopathologic mechanisms better defined. Including increased hydrostatic pressure, increased capillary permeability, lymphatic obstruction, hypoalbuminemia, hypercoagulability, refeeding edema (fasting, sodium retaining), and drug induced39, thus modifying Dale's table based on physiopathologic mechanisms to our current knowledge would be as table 540,41.

Table 4 Etiology of edema of the leg by Dale in 197315 

General Lymphatic
Hepatic cirrhosis Primary lymphedema
Heart failure Congenital
Nephrosis Praecox
Hypoproteinemia Tarda
Allergic disorders Acquired secondary edema
Idiopathic cyclic edema Infection
Venous Filaria
Thrombosis acute Lymphogranuloma venereum
Chronic post-phlebitic syndrome Tuberculosis
Extrinsic pressure Syphilis
Tumor Tumor
Retroperitoneal fibrosis Post-radiation
Pressure of overlying iliac artery Post-operative
Interruption Toxic
Trauma Snakebite
Surgical Insect bite
Arteriovenous fistula Miscellaneous
Inflammation after vascular repair

Table 5 Etiologic classification of edema of leg by Dale modified by our current concepts15,39-42 

Increased hydrostatic pressure Lymphatic, primary
Hepatic cirrhosis Primary
Cardiac failure Congenital
Acute and chronic renal disease Praecox
Venous insufficiency Tarda
Arteriovenous fistula Musculoskeletal
Arterial and venous anomalies Ruptured Baker's cyst
Arteriovenous malformations Ruptured medial head of gastrocnemius
May–Thurner syndrome, pelvic congestion Compartment syndrome, muscular infarct
Acute venous thrombosis Neurogenic, reflex sympathetic dystrophy
Post-thrombotic syndrome Lymphatic, secondary
Lymphatic extrinsic compression Infection sequelae
Tumor Filaria
Retroperitoneal fibrosis Lymphogranuloma venereum
Hypoalbuminemia Syphilis
Protein-losing enteropathy Post-radiation
Malnutrition Post-operative
Liver disease, nephrotic syndrome, preeclampsia Drug induced
Increased capillary permeability Opioids
Acute and chronic bacterial infections Antihypertensives (+ channel calcium blockers)
After vascular repair NSAID
Snakebite Hormones: corticosteroids, estrogen, testosterone
Insect bite Pioglitazone, rosiglitazone
Chronic venous edema, mix Monoamine oxidase inhibitors
Allergic reactions, myxedema Other
Post-traumatic Sickle cell crisis
Rheumatic Idiopathic
Inflammatory myopathy, myositis Refeeding edema, obesity

This comprehension leads us to affirm that venous edema is caused firstly, by increased hydrostatic pressure in acute illness, plus to the increased capillary permeability in its chronic form, and finally by the potential neurogenic role reported by Napier42. In patients with joint movement limitation by any reason, either neurogenic or even without neuropathy secondary to inappropriate muscular contractions, which may be caused by multiple reasons not necessarily neuropathic, rarely studied. However, without considering this last precept, acute venous edema must have a characteristic pattern presentation caused by increased hydrostatic pressure, different from the causes presented in table 5.

Given the fact that it is caused mostly by standing postures and less intense during sitting positions43, not abolished by the effects of gravitational potential energy during walking, exerted mechanically (but not exclusively) by venous valves44, absent in patients with valvular dysfunction. Therefore, edema must disappear during leg elevation for some minutes and mainly during absolute rest, exacerbated during walking directly proportional to activity, repeating this pattern day after day, never present at mornings in early stages (Table 6).

Table 6 Pattern presentation of edema caused by increased hydrostatic pressure 

Disease Contributing factors Edema pattern Increase during walking Improve during leg elevation Improve with diuretic Swelling
Hepatic cirrhosis Hypoproteinemia Right cardiac failure Portal hypertension Total blood volumen Pulmonary hydrostatic pressure Supine Mild: Absent in mornings Moderate: Mildly present in mornings Severe: During all day
Bimalleolar/All foot Mild: Absent in mornings Moderate: Mildly present in mornings Severe: During all day, including at waking up
Yes Yes
Cardiac failure Total blood volumen Vascular tone Pulmonary hydrostatic pressure
Renal insufficiency Total blood volume
Chronic venous disease Valvular disfunction Increased local blood volume
Increased permeability
Mild: Absent in supine and in morning, it appears hours after walking, it is bimalleolar including anterior foot and toes
Moderate: Same characteristics, from middle third leg to the foot including anterior foot and malleolus, usually associated to mild skin changes
Severe: All leg, from calf and down, with swelling, usually associated to severe skin changes, atrophy blanche or eczema
Yes / Afternoon
Yes / Morning or Late morning
Yes / May be present in morning
Yes, may not improve
No No
Venous malformation
Posthrombotic syndrome Valvular disfunction
Increased local blood volumen Return obstruction
Arteriovenous fistula Arteriovenous malformations Increased arterial flow Vascular tone
Increased permeability
Increased local blood volume
Valvular disfunction
Increased arterial flow
Vascular tone
Increased local blood volume
1 No edema or mild
2 Mild edema or absent, constant
3 Moderate edema, constant
4 Cardiac failure pattern, constant
No No
Arterial malformations
May-Thurner syndrome, pelvic congestion Return obstruction Valvular disfunction Mild: Absent in supine and absent in mornings, few patients
Moderate: May be present in mornings, swelling may be present in mornings too or initiate during walking
Severe: Present in mornings with swelling all day
No No
Acute venous thrombosis Return obstruction Increased local blood volume

In all cases, to a greater or lesser degree, contribute increased hydrostatic pressure (46) and all of improve with compression; venous etiology tends to improve significantly with compression.

In the context of chronic venous disease, when venous hypertension is constant, and the valve extent damage is vast and involves numerous valves, plus the increased hydrostatic pressure and intrinsic relationship with that column of blood with capillaries, factors are added that contribute to the increase of vascular permeability. Leukocyte trapping (adhesion and migration of macrophage's, T lymphocytes, and mast cells), pro-inflammatory cytokines (select in, ICAM-1, ELAM-1, VCAM-1, VEGF, and TGF-β1), and the role of pressure and shear stress when inverted promoting inflammation and reactive free radical formation had been identified as contributing factors45-47. Under this condition, edema may, accordingly to severity, be present in the morning, less in patients with thin skin trophic changes (or without it) and more in patients with profound skin sclerosis and atrophy blanche, but above all in those with eczema and ulcer; not excluding foot, fingers, or only be present in ankle or shin.

We should avoid confounding edema with venous swelling, which depends directly on venous volume in muscular veins such as soleus and gastrocnemius plexuses in the calf, considered the venous bellows in the leg; when present, there will not be Godette sign during digit pressure because the excess of volume will be in the intravascular compartment but not in the interstitial compartment. Nonetheless, they are frequently confused. Along Godette's sign absence, we will observe venous dilation, increased in leg perimetry, and muscular tension, which we most differentiate from muscular contracture.

Pruritus and burning pain

Itching is a symptom present in multiple potential etiologies, since dermatologic as inflammatory, infectious dermatoses, autoimmune, genodermatoses, dermatoses of pregnancy, and cutaneous neoplasms. Systemic diseases are associated with endocrine, metabolic, infectious, hematological and lymphoproliferative diseases, visceral neoplasms, pregnancy and drug-induced pruritus, and even associated with neurologic and psychiatric disorders such as neurogenic (without nerve damage), neuropathic (nerve damage), psychosomatic disorders, mixed, and even idiopathic48. All of them are poorly studied and understood, with some authors reporting contradictory results49. It is important to note that the paper from the International Forum for the Study of Itch does not mention to venous disease as a cause, although many authors in literature does. We may think that it is included and grouped among inflammatory groups. On the contrary, a complete table for those associated with neurogenic or neuropathic etiology. We must not forget itching is considered as a minimal pain expression.

Trying to associate itching with venous disease, remembering the current role of mast cell degranulation secondary to leukocyte entrapment45, may explain why in advance disease with eczema and ulcer patients frequently, although not all of them, refer it. A study by Paul50 found a correlation between disease severity and itching of 0.26 p = 0.025, not strictly linear because itch increased with the skin changes (CEAP 4 and 5) (n = 33, 44.5%), but not necessary with the presence of an ulcer (n = 5, 6.8%). A study by Paul49 found a correlation between disease severity and itching of 0.26 p = 0.025, not strictly linear because itch increased with the skin changes (CEAP 4 and 5) (n = 33, 44.5%), but not necessarily with the presence of an ulcer (n = 5, 6.8%), coupled with the fact that up to 54.7% of patients had an itch in many parts of their bodies, 45.9% of them specifically in legs. Some of them associate itch to a burning sensation in the same spot as Duque described18 both characteristic symptoms of neuropathies.

Tiredness, heaviness, and pain

These three symptoms are dominant in chronic venous disease symptoms, as proven in VRS21. As far as now, there is no author capable of explaining physiopathological mechanisms on those symptoms. We could assume that heaviness and tiredness are associated with increased venous volume, thus as edema present during standing position and exacerbated during walking hours, relieving leg elevation within the 1st min, and never being present at waking up or early in mornings. Because no author concentrates on pattern presentation of these symptoms in venous disease, we must still consider them as subjective. Arnoldi1 stated that intense (bursting) pain, which was intense enough for some of them to consider amputation, were exclusively present in those with important deep vein damage, associated with the practically constant high pressure in the deep veins of the leg, emphasizing it was never met in patients with simple varicose veins. It is important to remember again that in Arnoldi's study existed an asymptomatic group (n = 55, 19.7%) with no other author or study group considering it as a study variable and the many potential causes explaining leg pain such as musculoskeletal or soft-tissue diseases.

Cramps and restless legs

Cramps and lack of strength are commonly associated with musculoskeletal diseases. There is no physiopathological mechanism explaining the presence of cramps and restless legs in CVI. Thus again, resorting to conjectures, assuming that because of venous congestion (swelling), muscles in calf in an attempt to counteract increased hydrostatic pressure provoke involuntary contractions, nonetheless, those contractions must not be severe or incapacitating or derive in residual muscular contractures, and never be present during night rest. On the other hand, restless legs should not be present during night rest as well considering venous hypertension is absent, thus, until now it is still necessary to make more studies focused in understanding exactly why these patients refer specific types of symptoms.


We may have taken the wrong direction in understanding venous disease symptoms because there is no symptomatic correlation, even though it exists for signs21. New studies are necessary considering the potential role of the anatomic relationship between veins and nerves, described by many authors in other medical areas, trying to rule out causality, but never casualty51-55. Comorbid pathologies to consider are peripheral neuropathy (26-54%)56-57 and underdiagnosed low back pain associated with radiculopathy58,59, as herniation incidence has been reported similar between low back pain and radiculopathy60-62, with a higher prevalence in younger patients59,63.

There may be other contributing factors to consider such as leg shortness64, history of trauma, and even microtraumas associated with daily life activities, against we know spinal hygiene. We must not forget that nerves are known as "the great simulators of the body" because they can simulate when damaged syndromes65,66 or minor symptoms such as itching or cough67.


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FundingThis research has not received any specific grant from agencies in the public, commercial, or non-profit sectors.

Ethical disclosures

Protection of people and animals. The authors declare that no experiments were performed on humans or animals for this research.

Confidentiality of the data. The authors declare that no patient data appear in this article.

Right to privacy and informed consent. The authors declare that no patient data appear in this article.

Received: December 03, 2020; Accepted: February 24, 2021

* Correspondence: Enrique Santillán-Aguayo E-mail:

Conflicts of interest

The authors declare no conflicts of interest.

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