Exercise Training as an Adjunctive Therapy for Chronic Venous Insufficiency Patients: Evidence from Research to Practice

2021 ◽  
pp. 153473462110601
Author(s):  
Sothida Nantakool ◽  
Busaba Chuatrakoon ◽  
Maurits van der Veen ◽  
Amaraporn Rerkasem ◽  
Kittipan Rerkasem
Keyword(s):  
Exercise Training ◽  
Chronic Venous Insufficiency ◽  
Adjunctive Therapy ◽  
Venous Insufficiency ◽  
Healing Process ◽  
Compression Therapy ◽  
Venous Hypertension ◽  
Leg Ulcers ◽  
Calf Muscle Pump ◽  
Compression Treatment

Chronic venous insufficiency, which is defined as a condition relevant to persistent ambulatory venous hypertension, is a common cause of venous leg ulcers. Compression therapy is commonly used to relieve ambulatory venous hypertension and heal leg ulcers. Exercise is considered as adjunctive therapy, targeting calf muscle pump function, to additionally favor the compression treatment for facilitating the healing process. Different exercise training regimens for promoting wound healing and its relevant outcomes are reviewed and discussed in this study.

scholarly journals Venous ulcer treatment requires inelastic compression

Phlebologie ◽  
2018 ◽  
Vol 47 (01) ◽  
pp. 7-12 ◽  
Author(s):  
G. Mosti
Keyword(s):  
Healing Rate ◽  
Healing Process ◽  
Compression Therapy ◽  
Venous Hypertension ◽  
Leg Ulcers ◽  
Skin Damage ◽  
Foam Sclerotherapy ◽  
Compression Pressure ◽  
Inelastic Material ◽  
Hemodynamic Impairment

SummaryLeg ulcers have a venous pathophysiology in the vast majority of cases (1–4). Superficial or deep venous insufficiency and deep vein obstruction produce ambulatory venous hypertension due to venous reflux and venous pumping function impairment. The impaired venous hemodynamics is the key pathophysiologic mechanism leading to skin damage through several intermediate steps. Fibrin cuff formation around the microvessels, impairing gases (O2, CO2) exchange (5), white cells entrapment (6) causing skin necrosis, growth factors inhibition (7) producing a stagnation of the healing process have been considered involved in ulcer onset and maintenance. The treatment of venous leg ulcers (VLU) must be based on the correction of the hemodynamic impairment which can be achieved conservatively by means of compression therapy, walking and leg elevation or by means of invasive procedures (open surgery, endovascular procedures as endovenous Laser ablation, radiofrequency, foam sclerotherapy, conservative hemodynamic treatment). Compression therapy is frequently considered the first treatment option and it is the only therapeutical procedure which achieved the grade 1A in most recent guidelines or consensus documents (8–10). The crucial point is choosing the most effective compression modality. There are clear evidences that inelastic is more effective than elastic material in counteracting the venous hemodynamic impairment (11–14) that should „ensure” a superior effectiveness in promoting a higher healing rate of VLU, which are due to venous hemodynamic impairment. When looking at evidences we have some data showing that the higher the compression pressure the higher the healing rate (9, 15–17) and this is clearly in favors of inelastic bandages which exert a much higher pressure that elastic materials. On the other side we have many papers claiming a greater effectiveness of elastic stockings or elastic bandaged compared with inelastic material (18–30). Nevertheless studies comparing elastic and inelastic devices have so many flaws that their conclusions are hard to trust (31). Aim of this work is providing updated information about compression therapy effects on venous hemodynamic and the most effective compression modality to achieve the best outcome in VLU treatment.

scholarly journals Why Venous Leg Ulcers Have Difficulty Healing: Overview on Pathophysiology, Clinical Consequences, and Treatment

2020 ◽  
Vol 10 (1) ◽  
pp. 29
Author(s):  
Joseph D. Raffetto ◽  
Daniela Ligi ◽  
Rosanna Maniscalco ◽  
Raouf A. Khalil ◽  
Ferdinando Mannello
Keyword(s):  
Endothelial Cell ◽  
Reactive Oxygen ◽  
Compression Therapy ◽  
Venous Hypertension ◽  
Chronic Venous Disease ◽  
Venous Disease ◽  
Leg Ulcers ◽  
Nitrogen Species ◽  
Venous Leg Ulcers ◽  
Tissue Metabolites

Venous leg ulcers (VLUs) are one of the most common ulcers of the lower extremity. VLU affects many individuals worldwide, could pose a significant socioeconomic burden to the healthcare system, and has major psychological and physical impacts on the affected individual. VLU often occurs in association with post-thrombotic syndrome, advanced chronic venous disease, varicose veins, and venous hypertension. Several demographic, genetic, and environmental factors could trigger chronic venous disease with venous dilation, incompetent valves, venous reflux, and venous hypertension. Endothelial cell injury and changes in the glycocalyx, venous shear-stress, and adhesion molecules could be initiating events in VLU. Increased endothelial cell permeability and leukocyte infiltration, and increases in inflammatory cytokines, matrix metalloproteinases (MMPs), reactive oxygen and nitrogen species, iron deposition, and tissue metabolites also contribute to the pathogenesis of VLU. Treatment of VLU includes compression therapy and endovenous ablation to occlude the axial reflux. Other interventional approaches such as subfascial endoscopic perforator surgery and iliac venous stent have shown mixed results. With good wound care and compression therapy, VLU usually heals within 6 months. VLU healing involves orchestrated processes including hemostasis, inflammation, proliferation, and remodeling and the contribution of different cells including leukocytes, platelets, fibroblasts, vascular smooth muscle cells, endothelial cells, and keratinocytes as well as the release of various biomolecules including transforming growth factor-β, cytokines, chemokines, MMPs, tissue inhibitors of MMPs (TIMPs), elastase, urokinase plasminogen activator, fibrin, collagen, and albumin. Alterations in any of these physiological wound closure processes could delay VLU healing. Also, these histological and soluble biomarkers can be used for VLU diagnosis and assessment of its progression, responsiveness to healing, and prognosis. If not treated adequately, VLU could progress to non-healed or granulating VLU, causing physical immobility, reduced quality of life, cellulitis, severe infections, osteomyelitis, and neoplastic transformation. Recalcitrant VLU shows prolonged healing time with advanced age, obesity, nutritional deficiencies, colder temperature, preexisting venous disease, deep venous thrombosis, and larger wound area. VLU also has a high, 50–70% recurrence rate, likely due to noncompliance with compression therapy, failure of surgical procedures, incorrect ulcer diagnosis, progression of venous disease, and poorly understood pathophysiology. Understanding the molecular pathways underlying VLU has led to new lines of therapy with significant promise including biologics such as bilayer living skin construct, fibroblast derivatives, and extracellular matrices and non-biologic products such as poly-N-acetyl glucosamine, human placental membranes amnion/chorion allografts, ACT1 peptide inhibitor of connexin 43, sulodexide, growth factors, silver dressings, MMP inhibitors, and modulators of reactive oxygen and nitrogen species, the immune response and tissue metabolites. Preventive measures including compression therapy and venotonics could also reduce the risk of progression to chronic venous insufficiency and VLU in susceptible individuals.

Contact allergy in patients with chronic venous leg ulcers - possible role of chronic venous insufficiency

2006 ◽  
Vol 54 (2) ◽  
pp. 100-105 ◽  
Author(s):  
Maria Zmudzinska ◽  
Magdalena Czarnecka-Operacz ◽  
Wojciech Silny ◽  
Lucyna Kramer
Keyword(s):  
Chronic Venous Insufficiency ◽  
Venous Insufficiency ◽  
Contact Allergy ◽  
Leg Ulcers ◽  
Venous Leg Ulcers

Changes in Microcirculation in Venous Ulcers with Essaven Gel

Angiology ◽  
2001 ◽  
Vol 52 (3_suppl) ◽  
pp. S23-S27 ◽  
Author(s):  
L. Incandela ◽  
G. Belcaro ◽  
M.R. Cesarone ◽  
M.T. De Sanctis ◽  
M. Griffin
Keyword(s):  
Placebo Group ◽  
Treatment Group ◽  
Chronic Venous Insufficiency ◽  
Venous Insufficiency ◽  
Local Treatment ◽  
Venous Hypertension ◽  
Controlled Study ◽  
Single Application ◽  
Venous Ulcers

Microcirculatory changes in chronic venous insufficiency (CVI) due to venous hypertension produce venous hypertensive microangiopathy (VHM) and lead to ulceration. VHM is charac terized by enlarged, convoluted capillaries; increase in flux, permeability, and edema; and altered microlymphatics. PO2 is decreased and CO2 increased. Capillary exchanges are altered and nutritional alterations in association with microtrauma may cause venous ulcers. The aim of this pilot, cross-over, randomized, placebo-controlled study was to evaluate the effect of local treatment with Essaven gel (EG) (single acute application) in 10 subjects with VHM and venous ulcers. The study was structured over 3 days: day 1 was used for the control evalua tion for all patients. One group was randomized for the sequence placebo (day 2) and EG the following day; the second group with the sequence EG (day 2) and placebo (day 3). Indepen dently from the sequence, measurements of flux and PO2 in standard conditions showed positive changes (significant decrease of the abnormally increased flux, PO2 increase) in the EG treatment group. Changes in the placebo group were limited and associated with skin manip ulation. In conclusion, EG acutely improves microcirculation in limbs with VHM and ulceration even with a single application.

Chronic Venous Insufficiency and the Therapeutic Effects of Daflon 500 mg

Angiology ◽  
2005 ◽  
Vol 56 (6_suppl) ◽  
pp. S21-S24 ◽  
Author(s):  
John J. Bergan
Keyword(s):  
Shear Stress ◽  
Chronic Venous Insufficiency ◽  
Venous Insufficiency ◽  
Venous Pressure ◽  
Vena Cava ◽  
Venous Hypertension ◽  
Therapeutic Effects ◽  
Inflammatory Cascade ◽  
Perforating Veins ◽  
Days Of Therapy

Chronic venous insufficiency is linked to venous hypertension and forces of shear stress on the endothelium. Venous hypertension depends upon two forces: the weight of a column of blood from the right atrium transmitted through the valveless vena cava and iliac veins to the femoral vein, and pressure generated by contracting skeletal muscles of the leg transmitted through failed perforating veins. When valve failure occurs in superficial axial veins and perforating veins, the venous pressure in the veins and venules of the skin and subcutaneous tissue is raised. The skin changes in chronic venous insufficiency are directly related to the severity of the venous hypertension. Also, pathologic changes in the valves are linked to venous hypertension and leukocyte infiltration and activation. It is hypothesized that acute venous pressure elevations cause a shift in the venous hemodynamics with changes in wall shear stress. This initiates the inflammatory cascade. Daflon 500 mg ameliorates the effects of chronic inflammation. In randomized trials, 60 days of therapy with Daflon at a dosage of 500 mg 2 tablets daily was effective, in addition to elastic compression, in accelerating venous ulcer healing. Because venous insufficiency is linked to venous hypertension and an inflammatory reaction, it appears that Daflon 500 mg 2 tablets daily shows a great potential for accomplishing blockade of the inflammatory cascade.

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