New Advances in the Understanding of the Pathophysiology of Chronic Venous Insufficiency

Angiology ◽  
2001 ◽  
Vol 52 (1_suppl) ◽  
pp. S27-S34 ◽  
Author(s):  
Geert W. Schmid-Schönbein ◽  
Shinya Takase ◽  
John J. Bergan

Chronic venous insufficiency (CVI) is inseparably linked to elevated venous pressure and is accompanied by vascular, dermal, and subcutaneous tissue damage and restructuring. Abundant evidence exists both in humans and in experimental models to suggest that the tissue damage may be initiated by generation of an inflammatory reaction. inflammatory indi cators include elevation of endothelial permeability; attachment of circulating leukocytes to the endothelium; infiltration of monocytes, lymphocytes, and mast cells into the connective tissue; and development of fibrotic tissue infiltrates and several molecular markers, such as growth factor or membrane adhesion molecule generation. Indicators of an inflammatory reaction are already detectable at early stages of CVI and may be involved in the development of primary venous valve dysfunction. One of the important questions is to identify trigger mechanisms for the inflammatory reaction in CVI. Current evidence suggests that, among several possible mechanisms (hypoxia, humoral stimulation), a shift in fluid shear stress from normal physio logical levels and endothelial distension under the influence of elevated venous pressure may serve as trigger mechanisms for inflammation.

2017 ◽  
Vol 12 (2) ◽  
pp. 28-32
Author(s):  
Marilena SPIRIDON ◽  
◽  
Dana CORDUNEANU ◽  

Chronic venous insufficiency (CVI), frequent cause of lower limb edema, represents a severe consequence of the dysfunction of the venous valve, which results from the venous hypertension together with the degenerative processes at this level. CVI defines only the severe stages of the chronic venous disease (CVD), accompanied by morphological and functional damage, with significant alteration in quality of life. The treatment of CVI involves, depending on the severity of the case, a combination of general nonpharmacologic, pharmacologic, and surgical measures. Non-pharmacologic measures involve the use of a continuous and controlled external pressure represented by compression stockings which can significantly improve the venous return and lead to a major symptoms improvement. Pharmacologic treatment aims on one hand to alleviate hemodinamics by lowering blood viscosity, decreasing venous pressure and preventing intravascular thrombus formation and, on the other hand, restoring thevascular glycocalyx/endothelium, reducing parietal inflammation and increasing the venous wall tone. Within this pathology, sulodexide represents an innovative biological product with polypharmacological actions targeting more sites involved in the pathogenesis of CVD/CVI that alleviate hemodynamics and restore vascular structure which lead to a significant symptoms improvement and a slow disease progression. Surgery remains the procedure of choice in patients initially treated conservatively in whom symptoms persist or worsen, but also in case of those who already come to doctor in a severe stage of the disease.


Angiology ◽  
2001 ◽  
Vol 52 (1_suppl) ◽  
pp. S43-S47 ◽  
Author(s):  
John J. Bergan ◽  
Geert W. Schmid-Schönbein ◽  
Shinya Takase

Early manifestations of chronic venous insufficiency (CVI) are edema, hyperpigmentation, and lipodermatosclerosis. Late complications are cutaneous ulceration and delayed healing. The specific hallmarks of this inflammation include CD68-positive infiltration into the dermal tissue, monocytes, and lymphocytes and enhanced endothelial permeability. This may lead to "fibrin cuff" formation. In addition, membrane adhesion molecules are present and cytokine expression is seen. In one experimental model of mesenteric venous hypertension, the inflammatory process was detected in its earliest stages. This was evident in the form of neutrophilic leukocyte adhesion to venular endothelium as well as migration of cells across the endothelium and basement membrane into the interstitial space. Simultaneously, parenchymal cell death was detected. This suggests that the mechanism that triggers the inflammatory reaction is venous hypertension. This may cause venous distension and a shift in fluid shear stress. Our obser vations suggest that patients with venous insufficiency demonstrate circulatory humoral stim ulators for leukocyte activation. Otherwise, there is evidence that the inflammatory reaction is limited to the region of the venous ulceration or at least to the skin areas with severe microangiopathy. It may be that activated leukocytes traverse perivascular cuffs and release active transforming growth factor-β1 (TGF-β1) which has been found to be elevated exclu sively in areas of clinically active CVI. Surgical intervention markedly decreases the number of dysfunctional vein segments and allows pharmacologic agents to protect normal structures from continuing damage. Daflon® 500 mg, the purified micronized flavonoid fraction containing 90% diosmin and 10% hesperidin, acts favorably in venous ulcer treatment by inhibiting the synthesis of prostaglandins and free radicals. It decreases bradykinin-induced microvascular leakage and may act favorably to inhibit leukocyte activation, trapping, and migration. Clinically, edema is reduced, ulcer healing is accelerated, and leukocyte trapping diminished. The action of micronized purified flavonoid fraction is beginning to be better understood, and as further knowledge is gained, better pharmacologic control of CVI is a tantalizing promise.


1986 ◽  
Vol 1 (3) ◽  
pp. 159-169 ◽  
Author(s):  
P. Haselbach ◽  
U. Vollenweider ◽  
G. Moneta ◽  
A. Bollinger

Fluorescence video microscopy after intravenous injection of Na-fluorescein was used to study capillary morphology, pericapillary halo diameters, microvascular flow distribution and transcapillary diffusion of the dye in 15 healthy controls and 15 patients with severe chronic venous insufficiency (CVI). The recordings were made in the medial ankle region. Transcapillary diffusion was monitored within a densitometer window encompassing 3.2 mm2 of skin surface. Microangiopathy known from previous studies was documented in the patients with severe CVI. The number of skin capillaries within the field of observation was not reduced. In some cases inhomogeneous microvascular flow distribution and probable microthrombosis were detected. Mean halo size averaged 81 — 15 μm in the controls and 146 ± 47 μm in the patients (P < 0.001). Unexpectedly, transcapillary diffusion of Na-fluorescein was not significantly increased in the field of measurement. Possible explanations include asynchronous inflow of the dye, the presence of thrombosed and therefore not perfused capillaries, a pericapillary fibrin layer limiting diffusion and redistribution of flow in favour of the subcutaneous tissue.


Angiology ◽  
2005 ◽  
Vol 56 (6_suppl) ◽  
pp. S21-S24 ◽  
Author(s):  
John J. Bergan

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.


1988 ◽  
Vol 3 (3) ◽  
pp. 147-154 ◽  
Author(s):  
A.J.M. Brakkee ◽  
J.P. Kuiper

The influence of an elastic stocking upon the venous muscle pump function in a healthy subject and in a patient with chronic venous insufficiency is discussed. Taking into account the alinear relationship between venous pressure and limb volume the experiences concerning the effects of tissue compression, some of which seem to be contradictory, are clarified.


Phlebologie ◽  
2011 ◽  
Vol 40 (05) ◽  
pp. 245-250 ◽  
Author(s):  
O. Wolff ◽  
T. D. Wentel ◽  
S. W. I. Reeder ◽  
H. A. M. Neumann

SummaryIncreased ambulatory venous pressure is the key feature of chronic venous insufficiency, and causes capillary leakage and venous edema. This capillary leakage can be measured with plethysmography and is called the capillary filtration rate (CFR).Reduction of the CFR leads to less edema formation and improves the healing of venous ulcers. Aim: To show that the use of compression ulcer stockings reduces the CFR. Methods: The capillary filtration rate of both legs of 17 patients, 6 with chronic venous insufficiency and 11 healthy subjects was measured with both (day and night) stockings, only the night stocking and without stockings. Results: The reduction of the CFR was significant (p <0.0001) for the total population in the group wearing 2 stockings versus 1 stocking (CFR=0.019 vs. 0.084 ml/100 ml/min), 1 stocking versus no stocking (CFR=0.149 vs. 0.084 ml/100 ml/min) and 2 stockings versus no stockings (CFR=0.019 vs. 0.149 ml/100 ml/ min). Conclusion: Compression ulcer stockings are highly effective in reducing CFR and thus reducing edema formation, which leads to improved healing of venous ulcers.


1990 ◽  
Vol 5 (2) ◽  
pp. 85-94 ◽  
Author(s):  
G.M. McMullin ◽  
H.J. Scott ◽  
P.D. Coleridge Smith ◽  
J.H. Scurr

Ambulatory venous hypertension is closely associated with the signs and symptoms of venous disease. It has been shown that reverse flow of blood in the superficial and deep veins is responsible. The pressure derangement caused by incompetence of perforating veins has not been established. The present study documents the pressure disturbances caused by incompetence in each of the three compartments of the venous system, the deep, the superficial and the perforating veins. In total 90 limbs of 49 patients with chronic venous insufficiency were examined and classified by duplex scanning and ascending venography. Ambulatory venous pressure measurements were performed on all 90 limbs and a venous sufficiency index (VSI) for each limb calculated from the percentage drop in pressure and refilling time. VSI was lowest in the group with deep vein incompetence (median 0.9, range 0–36.9), intermediate in the groups with superficial vein incompetence (median 7.6, range 0.4–59) and with incompetent perforating veins (median 14.6, range 0.4–35.7) and highest in the group with normal veins (median 41.7, range 3.5–87.5). The association of symptoms and VSI was also examined. The lower the VSI the more severe were the clinical symptoms and all ulcerated limbs had a VSI < 20. However a number of clinically normal limbs were also found to have low values of VSI.


1984 ◽  
Vol 148 (2) ◽  
pp. 203-209 ◽  
Author(s):  
Gurinder K. Randhawa ◽  
Jatinder S. Dhillon ◽  
Robert L. Kistner ◽  
Eugene B. Ferris

2011 ◽  
Vol 26 (5) ◽  
pp. 197-202 ◽  
Author(s):  
J T Christenson ◽  
C Prins ◽  
G Gemayel

Objective Increased intramuscular and subcutaneous tissue pressures are often found in patients with severe chronic venous insufficiency venous ulcer disease. Additional subcutaneous para-tibial fasciotomy promotes early ulcer healing. This study evaluates the mid-term effect of eradication of superficial reflux with additional fasciotomy in patients with increased tissue pressures. Method Between January 2006 and June 2009, 58 patients underwent fasciotomy. Tissue pressures (intramuscular and subcutaneous) were measured. Sixty-nine limbs with 91 venous ulcers were treated. Mean duration of the venous ulcer was 3.4 years. Underlying disease was post-thrombotic syndrome (PT) in 19 patients (33%, 24 limbs, 27 ulcers) and non-post-thrombotic (non-PT) severe chronic venous insufficiency in 39 (67%, 45 limbs, 64 ulcers). All patients were C6 at the time of surgery. Preoperative tissue pressures were 23.5 ± 6.1 mmHg (intramuscularly) and 9.8 ± 3.2 mmHg (subcutaneously). Results Ninety ulcers (99%) healed postoperatively (42 with and 48 without skin grafting). Tissue pressures significantly decreased following surgery and remained low at three months postoperatively. Ten ulcers in six patients recurred six to 20 months postoperatively (11%), resulting in 86.4 actuarial freedom from venous ulcer recurrence at three years following surgery. Four patients (1 non-PT and 3 PT) had re-fasciotomy; all healed initially but two ulcers (2 patients, PT) recurred at 11 and 12 months. Those patients underwent re-fasciotomy, one healed and one recurred six months later. Conclusion Eradication of superficial reflux with additional subcutaneous fasciotomy for chronic and recurrent venous ulcer improves ulcer healing or success of skin grafting. Mid-term results are excellent particularly in patients with non-PT disease. Recurrence is more frequently seen in patients with PT syndrome. In patients with ulcer recurrence and high tissue pressures, re-fasciotomy can be helpful to promote healing, particularly in patients with primary venous disease.


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