nueva página del texto (beta)
Inglés (pdf)
Artículo en XML
Referencias del artículo
Traducción automática
Enviar artículo por email
Citado por SciELO 
Similares en
SciELO 
Permalink
Introduction
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.
Results
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 | |
|---|---|---|---|
| Age | |||
| < 65 years | 11,252 | 16,284 | 27,356 |
| > 65 years | 4409 | 6805 | 11,214 |
| Gender | |||
| 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 |
Discussion
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
EDEMA
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 |
| Infectious | |
| 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 |
| MayThurner 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 |
| Tuberculosis | |
| 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 |
| Fasciitis |
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 Yes No Yes Yes |
Yes No No Yes No No |
Yes Yes Yes No |
No |
| 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 |
Always Yes Yes, may not improve |
No | No No No Yes |
| 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 |
Schbinger: 1 No edema or mild 2 Mild edema or absent, constant 3 Moderate edema, constant 4 Cardiac failure pattern, constant |
May Yes Yes Yes |
Yes No No No |
No | No Yes Yes Yes |
| 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 |
Yes Yes Yes |
Yes Mild No |
No | No Yes Yes |
| 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.
Conclusion
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.
