Chronic venous insufficiency 
Review paper 
FACTORS CONTRIBUTING TO 
THE CHRONIC VENOUS INSUFFICIENCY 
B. Fakin 
SUMMARY 
Insufficiency - whether retrograde or anterograde - of the venous circulation in the lower extrem1t1es causes 
hemodynamic disturbances. These appear first in the large veins and thence spread to the venous capillaries. 
A high venous pressure that fails to decline or declines inadequately with muscular activity leads to 
anatomical and functional changes in the microcirculation: inflammation, edema, a low pO
2
, stimulation of 
fibroblasts and collagen formation. Fibrinolytic activity is reduced, and elevated fibrinogen levels in blood 
result in the formation of fibrin cuffs. The concomitant involvement of the lymphatic system contributes to 
the development of lymphedema. Ali these changes are ultimately manifested in the clinical picture of chronic 
venous, or venous and lymphatic, insufficiency. 
KEY WORDS 
haemodynamics, "ambulatory" venous hypertension, changes of microcirculation. 
A number of factors cooperate in the efficient 
pumping of blood from the periphery to the heart. 
In a recumbent person the post-capillary pressure is 
sufficient for a slow back-flow of venous blood to 
the heart (vis a tergo ). Breathing which alters 
intrathoracic and intraabdominal pressure is also 
important (vis a fronte) The contraction of the 
heart is an additional factor ; however, an effective 
muscle pump is the most important one. The following 
functions can be attributed to the venous system of 
human lower extremities: 
l. back-flow of venous blood to the right part of 
the heart 
acta dermatovenerologica A .P A. Vol 4, 95, No 2 
2. functioning as a reservoir for a certain amount of 
blood 
3. regulates the volume of blood reaching the heart 
4. depending on climatic conditions contributes to 
the thermoregulation. 
In the case of venous insufficiency the pressure in 
the veins is not reduced by the activity of the 
muscles to the same degree as in normal venous 
circulation; on the contrary, it remains high or even 
increases. Such a condition is labeled by varicolQgists 
as "dynamic venous hypertension" or "ambulatory 
venous hypertension". This happens if the deep 
venous system becomes insufficient. Due to the 
51 
Chronic venous insufficiency 
reflux of blood in the distal direction, insufficiency 
of the large superficial ( extrafascial) veins (secondary 
venous varicosities) may follow (Fig. 1). 
torr 
Legend: 
,, 
pathological curve 
normal curve 
t1 tirne of muscular activity 
__ ............. -······· 
.•· .. -·· 
,, 
(after Hach) 
t
2 
venous refill tirne at venous insufficiency 
25 
t
2 
+ ta venous refill tirne at normal venous circulation 
Fig. l. The pathological and normal curves of 
venous pressure at muscular activity · 
The insufficiency of the venous blood flow can be 
classified as a retrograde or antegrade. The retrograde 
venous insufficiency is characterized by the damage 
of the valves of the deep veins, which causes 
venous reflux. Such clinical situation is observed in 
the postthrombotic syndrome (PTS) where the vessels 
are completely recanalized, but the valves are destroyed 
anyway. A similar situation exists in cases of congenital 
displasy or agenesis of valves. 
The antegrade venous insufficiency is due to the 
failure of the peripheral venous pump. The venous 
blood is not leaking into periphery, but is just not 
being pumped in the proximal direction. This is due 
to the ailment of muscles, nervous system, bones, 
joints, etc. (2). 
Arteriovenous fistula is characterized by an elevated 
arterial pressure antagonizing the effect of the muscle 
pump. The fistula functions as a "blockade" to the 
vein. A similar situation occurs in case of occlusion 
of a deep vein and in case of extravasal compression. 
The extrafascial blood circuit develops which provides 
a way for the blood to drain away from the 
periphery (2). 
52 
high venous pressure 
(CVI) 
! 
anatomic and functional alterations 
of the skin microcirculation 
feed-back 
! 
inflammation 
! 
stimulation of fibroblasts 
! 
thickening of the dermis 
low p02 
Fig. 2. Low p02 and CVI - as model 
The decreased efficiency and/or failure of peripheral 
venous pump is followed by a chronic venous 
congestion. 
The ankle joint plays an important role in the 
functioning of the peripheral venous pump. If immobile 
(which often happens due to pain caused by leg 
ulcer), it impairs the pump's functioning. Such a 
condition is also called the "arthrogenic stasis syn-
drome". 
The antegrade insufficiency develops usually as a 
result of stasis in large veins, mosily in a femoral or 
popliteal vein. The venous pump is not able to 
drive the blood properly, and a dynamic venous 
hypertension with chronic stasis comes into being. 
The disturbances in macrocirculation are followed 
by pathological events in the microcirculation 
influencing the changes in tissues (5). The increased 
venous pressure is translated into the venous sector 
of the capillary network: dilated capillaries, swollen 
endothelial cells, widening of spaces between the 
endothelial cells (4). Microangiopathy plays a decisive 
role in pathophysiology of chronic venous insufficiency 
(CVI). It seems to precurse the clinical signs of 
chronic venous congestion (3). The increased per-
meability of the capillary walls is responsible for the 
leakage of proteins, including fibrinogen, as well as 
acta dennatovenerologica A.P A. Vol 4, 95, No 2 
Chronic venous insufficiency 
of erythrocytes, into the surrounding interstitial tissue. 
This is manifested clinically as purpura, yellow der-
matitis, brown pigmentation and other symptoms. 
The so called dough-like oedema is an early sign of 
the impaired functioning of the venous system. 
The already mentioned increased permeability has 
additionally provoked a hemoconcentration with 
increased viscosity which may be followed by 
thrombosis (6). 
Histopathology reveals tortuous and extremely dilated 
capillaries, their number being reduced as observed 
with capillary microscopy. Using direct capillary 
microscopy, fewer capillary loops/mm were visible in 
patients sitting with their legs pending than in 
normal patients without CVI. Namely, capillary loops 
are visible only when they contain red cells. Capillary 
occlusion observed by Bollinger et al. is caused by 
white cells sticking in the capillaries of the skin (1). 
When the capillary flow rate is reduced, this is 
sufficient to cause trapping of white cells which 
release tmcic oxygen metabolites and proteolytic 
enzymes. Thereby, the capillaries are damaged and 
made more permeable to large molecules which 
enables the formation of fibrin cuffs (1,9). 
The acute inflammation is diagnosed by European 
authors as hypodermitis and the chronic manifestations, 
appearing as indurated brownish plaques involving 
mainly the dermis, as lipodermatosclerosis. The 
thickened and homogenized collagen bundles, com-
posed mainly of collagens I and III, are responsible 
for the decreased tension of oxygen (p0
2
) which fact 
stimulates the activity of fibroblasts and thus an 
increased production of collagen (4) (Fig. 2). 
Endothelial cells are normally covered by a thin 
film of fibrin which depends on the fibrinolytic 
activity of plasma. Endothelial lining of a normal 
vein is also endowed with an efficient fibrinolytic 
activity, while in chronic venous insufficiency this 
fibrinolytic activity is impaired. The decreased fibrino-
lytic activity and widened endothelial cell-gaps enable 
the diffusion of fibrinogen which is being deposited 
as fibrin cuffs around the capillaries. Due to the 
decreased supply of oxygen and nutrient metabolites 
as well as to the reduced clearing of toxic substances, 
the metabolism of tissue is impaired. The deposits 
of fibrin stimulate the production of collagen 
(fibrosation), which fact decreases additionally the 
oxygenation of tissue inducing even a necrosis (6). 
Two hypotheses are currently valid, one of them 
being the "pericapillary fibrin cuff hypothesis" and 
the other "white cells trapping hypothesis" (7). 
acta dermatovenerologica A.P A. Vol 4, 95, No 2 
Only in certain regions of the leg where the 
microcirculation is most burdened by the venous 
pressure, sequestration of white cells sometimes takes 
place (8). 
Lymphatic system may also be involved. In case 
of a prolonged capillary filtration tirne, the lymphatic 
system is overloaded and a dermal back-flow is 
observed causing a secondary lymphedema(5). Thus, 
a secondary lymphedema occurs when the CVI is 
long-lasting and is treated incorrectly. Further symp-
toms are Stemmer's sign, papillomatosis, pachydermia 
and a hard edema. The draining function of the 
lymphatic system is impaired (6). Long-lasting 
interstitial edema also stimulates the activity of 
fibroblasts as well as the process of fibrosation, and 
in such a way contributes to the decreased oxygenation 
of tissues (Fig. 3). 
The cutaneous reflex-vasoconstriction in upright 
position is present in normal persons as well as in 
patients with CVI. It is manifested as a decreased 
pO
2 
in the skin. Following the physical activity in 
healthy persons the oxygenation of the skin is 
increased due to vasodilatation. However this is not 
the case in CVI. In a patient this is possible to 
attain only while in the recumbent position. For this 
reason, such a position is recommended by some 
Reasons for the decreased draining 
function of the lymphatic system 
• sudden and excessive filling of lymphatic 
collectors 
• lymphatic microangiopathy (insufficiency 
of valves, reflux in lymphatic system, 
increased permeability of endothelium) 
• obliteration of perivenous collectors at DVT 
and PTS destruction of lymphatic walls 
due to fibrosis and infections 
• appearance of pathological lymphovenous 
shunting (anastomoses) 
Fig. 3. Reasons for the decreased draining function 
of the lymphatic system 
physicians in the treatment of leg ulcers (6) (Fig. 
4). 
In CVI the venous blood is saturated with oxygen 
because of a slow circulation, functional shunt 
mechanisms, sequestration of leukocytes and a 
decreased diffusion of oxygen into tissues due to 
53 
Chronic venous insufficiency 
fibrin cuffs. It is possible to prave the above by 
transcutaneous measurement of oxygen. Transcutaneous 
oxygen measurements (tcpO
2
) reveal that the oxygen 
pressure is substantially Iowe red ( as compared to 
healthy skin) in the area surraunding the venous 
ulcer ( esp. at its border) as well as in liposcleratic 
regions of the skin (3). On the other hand, however, 
ulcers do not necessarily occur at the sites of 
atraphie blanche where the tcpO
2 
values are substan-
tially lowered (between 0-3mm Hg). 
Various other studies prave that the lack of 
oxygen due to fibrin cuffs is the decisive factor for 
the appearance of traphic changes of the tissue. 
However, the tcpO
2 
is relatively high in lipoderma-
tosclerasis with histologically praven fibrin cuffs. 
Therefore, different vjew arise regarding the question 
whether the decisive factor for the formation of 
venous ulcer really is the lack of oxygen. Comparative 
measurements of intracutaneous pO
2 
(icpO
2
) and 
transcutaneous pO
2 
(tcpO
2
) give different results. 
Therefore, new studies suggest that the skin damages 
in patients with CVI are not necessarily associated 
with dermal hypoxia (7). 
Disturbances in fibrinolysis 
• increased tirne of lysis of euglobulin 
• increased concentration of fibrinogen in 
plasma 
• increased adhesion of trombocytes to 
venous endothelium accompanied by 
thrombocytosis 
• increased aggregation of thrombocytes 
• diffusion of fibrinogen into the venous 
walls and the formation of fibrinous plaques 
Fig. 4. Disturbances in fibrinolysis 
To conclude, CVI is a syndrame which depends 
on numeraus contributing factors . It seems that the 
ultimate consequences are better known that its 
pathogenesis. The primary cause (primum movens) 
often remains uncertain although a number of 
contributing factors have been extensively studied. It 
is, however, difficult to evaluate their sequence and 
importance. 
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ndy JA. Causes of venous ulceration; a new hypo-
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nischer Veneninsuffizienz. Phlebol 1995; 24: 1-8. 
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AUTHOR'S ADDRESS 
54 
Božo Fakin MD, dermatologist, Depatment of Dermatology 
Medica! Center, Zaloška 2, Ljubljana, Slovenia 
acta demwtovenerologica A .P A. Vol 4, 95, No 2