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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_782_Библиотеки_им_академика_М_И_Перельмана
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12 Aetiology
Super
v
Inf
Right atr
Ao
Pu
Right v
Hepatic por
Sy
capillar
g
Ve
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= Oxygenated blood
= Deoxygenated blood
Systemic capillaries of
head, neck and upper limbs
rta
Left pulmonary artery
lmonary trunk
ior
ena cava
ium
entricle
erior vena cava
tal vein
stemic
ies of
astrointestinal tract
nules
Pulmonary capillaries of
left lung
Left pulmonary veins
Left atrium
Left ventricle
Arterioles
FIGURE1.1 Transportation of blood around the body. Peate (2021) / John
wiley & Sons.
Aetiology 13
t
y
To heart
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From hear
Arteriole
Capillary
Capillar
bed
Venule
FIGURE1.2 Blood ow from capillaries to venules. Peate (2021) / John
wiley & Sons.
Venules unite to form veins. They contain three layers from the
inside out:
Tunica interna
Tunica media
Tunica externa
The walls of veins are thinner compared to arteries and contain
less elastic, collagenous tissue and smooth muscle. Veins have a
14 Aetiology
As the muscles move and contract, the blood is pushed towards the heart
Skeletal striated muscles
Muscles contract and expand
The muscles relax
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The upper valves open
The lower valves closed
FIGURE1.3 One- way bicuspid valves.
larger lumen compared to arteries. Some veins, most commonly in
the lower extremities, contain one- way paired semilunar bicuspid
valves. Their function is to prevent any backward reux of blood
towards the capillaries– allowing blood only to ow back towards
the heart (Figure1.3).
The supercial venous system includes the great and lesser
saphenous veins as well as the anterior, posterior and supercial
accessory saphenous veins. Supercial leg veins run between the dermis and muscle fascia. The deep venous systems are located below
the muscle facia and contain the femoral vein, the common femoral
vein, the deep femoral vein and the popliteal vein, as well as the anterior and posterior tibial veins and the bular veins. The two systems
are linked by perforating veins that pass through the muscle fascia.
The upper valves closed
The lower valves open
Aetiology 15
Arteries and Veins of the Leg
ein
Dorsalis Pedis Artery
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Veins in the leg are classied into three main categories:
The deep vein (can withstand high pressures during muscle
contraction).
The supercial veins (not designed to withstand prolonged high
pressures).
The perforator veins.
Lying deep in the muscles of each leg is a deep vein that runs the
length of the leg. In the calf this is also known as the anterior tibial
vein, in the knee the popliteal vein and in the thigh the femoral vein.
These are all sections of the deep vein. In the groin, the deep vein
joins the common iliac vein, which leads to the vena cava and eventually the heart (Figure1.4).
Femoral Artery
Popliteal Artery
Tibil Artery
Peroneal Artery
Plantar Arch
FIGURE1.4 The venous system of the leg.
External Iliac Vein
Femoral Vein
Perforating Veins
Great Saphenous Vein
Small Saphenous V
Dorsal Venous Arch
16 Aetiology
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There are numerous supercial veins that lie outside the muscle
just below the skin. They comprise:
Long saphenous veins – originate from the medial malleolus
(inner ankle) and empty into the femoral vein.
Short saphenous veins– run from the lateral malleolus (outer
ankle) and empty into the popliteal vein.
There are also tributaries of these veins.
The perforator veins pass through the muscles, transporting
blood from the supercial system into the deep vein. These are
located at regular intervals along the leg and are particularly abundant in the ankle.
VEINS INACTION
The veins have an important job forcing blood upwards towards the
heart against gravity. Table1.1 depicts all the mechanisms of action
that facilitate this.
TABLE1.1
Heart The heart exerts a mild ‘pull’ on the veins due to
Veins Dilate and contract
Respirator pump Plays a limited role in venous return. During
Mechanisms ofaction.
the pressure gradient between the right atrium
(pressure is around 0
system. This is sucient to produce some blood
ow back to the heart when the person is
horizontal, but insucient in aiding venous
return when upright
inspiration the diaphragm pushes against the
abdomen, causing a rise in pressure in the
intra-
abdominal veins. At the same time, the
pressure in the thorax falls (pressure also falls in
the intra- thoracic veins and right atrium) and
blood is drawn from the abdominal cavity into
the thorax. The deeper the inspiration, the
greater the venous return
mmHg) and the venous
Aetiology 17
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TABLE1.1 (Continued)
Calf muscle and
foot pumps
Source: Adapted from Moatt etal. (2007).
These are the most important mechanisms for
aiding venous return. The foot pump (contraction
of the plantar muscles during movement)
squeezes and empties veins in the foot. During
exercise, the calf muscle contracts, compressing
the deep vein and forcing the displacement of
blood. The one- way valves prevent blood from
reuxing, forcing the ow upwards against
gravity. When the muscles relax the deep vein
expands, which causes pressure to drop below
that of the supercial veins. The resulting
pressure gradient draws blood via the perforator
veins from the supercial veins into the deep
vein. As exercise continues, muscle contraction
squeezes the relled vein, forcing blood towards
the heart. This is a continuous cycle
It is important to note that the eectiveness of the calf muscle
and foot pumps depends on healthy one- way valves and good ankle
function/movement. Valve incompetence and limited ankle movement are major contributors to the development of venous disease
and non-
healing leg ulceration (see Chapter4).
BLOOD PRESSURE INVEINS ANDCAPILLARIES
Blood pressure in the capillary network is around 5–15 mmHg.
Blood pressure in veins uctuates according to position and level
of activity for each individual.
When a person is standing, venous pressure is equal to the weight
of the volume of blood from the foot to the right side of the heart,
which is about 80–100 mmHg. This falls to 10–20 mmHg when
the calf muscle and foot pumps empty the veins during exercise.
The values in the perforating veins that connect the supercial
veins to the deep veins prevent reux. Pressure in the supercial
veins remains low (Grey and Patel2022).
Venous blood pressure is reduced when the person lies horizontally.
18 Aetiology
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VENOUS DISEASE
Venous disorders are thought to be a major cause of morbidity and
decreased health- related quality of life (White and Ryjewski2005).
Venous leg ulcers (VLUs) are typically long- lasting, and there is a
high risk of recurrence that can have a negative impact on a patient’s
quality of life (Green etal. 2014). VLUs arise from chronic venous
insuciency (CVI) in the lower limb. The prevalence of VLUs in
adults over 18 years rose to 1 per 100individuals in 2017/2018 (Guest
etal.2020). In the United Kingdom, complex wounds such as VLUs
are mostly treated by community nursing teams (Urwin etal.2022).
The estimated national cost of treating a VLU in the United Kingdom
is £102 million, with a per- person annual cost of £4787.70 (Urwin
etal. 2022). The average cost per person of treating a VLU is estimated at £166.39 (Urwin et al. 2022). The cost of managing an
unhealed VLU is thought to be 4.5 times more than managing a
healed VLU (£3000 per healed VLU and £135 000 per unhealed VLU)
(Guest etal.2018). Subsequent studies have identied a decrease in
healing rates for VLUs in 2020 and 2021 by 16% and 42%, respectively,
following the COVID- 19 pandemic (Guest and Fuller2023). The pandemic appears to have had a deleterious impact on the health of
patients with VLU (Guest and Fuller2023).
Venous disease occurs when the calf muscle pump and foot muscle pumps are unable to eectively empty veins. This results in
venous hypertension (increased pressure in the veins). This is often
due to valve incompetence allowing blood to ow backwards (‘reux’)
towards capillaries as well as forwards towards the heart. Valve
incompetence in the deep vein causes increased pressure on the valve
below and the corresponding perforator vein valve. As a result, these
valves also become incompetent, causing the supercial veins to varicose and leading to disease progression (Figure1.5). The same eect
happens whether the primary incompetence occurs in the perforator
or supercial veins.
Chronic venous hypertension causes an above- normal rise in
pressure within the capillaries (which are not capable of withstanding high pressure). Although capillaries are very porous, their pores
are normally too small to allow for larger molecules and blood cells
to pass into the surrounding tissue. If there is a rise in pressure the
Aetiology 19
Nor
ow
med
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Abnormal
blood fl
Val ve
mal
blood
flow
(a) Normal vein (b) Varicose vein
Dilated
vein
Defor
valve
Skin
bulging
Thin wall
of vein
FIGURE1.5 (a, b) Varicose veins.
capillaries swell, stretching their delicate walls, which increases the
size of the pores and allows blood products to leak into the surrounding tissue.
PATHOPHYSIOLOGY OFCHRONIC VENOUS DISEASE
Evidence suggests that chronic venous disease (CVD) is primarily a
blood pressure–driven inammatory disease. The sequence of events
is not fully understood and may be dierent for each patient depending on the risk factors involved (Figures1.6 and1.7) (Mansilha and
Sousa2018).
20 Aetiology
Risk factors: obesity, prolonged standing, multiparity, previous history of DVT,
Water filtration
Protein filtration
Erythrocyte filtration
Lipodermatosclerosis
Leucocyte filtration
Changes in capillary
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increasing age (Table 1.4)
Elevated venous pressure, venous valve
dysfunction, reflux, obstruction
Vessel wall inflammation (low shear stress leads to an increase in
pro-inflammatory messages)
Endothelial glycocalyx shredding
Pro-inflammatory changes in the endothelial cells, T-lymphocytes
Inflammatory cells infiltrate: macrophages, mast cells, T-lymphocytes
Wall/valve/tissue cell
structural functional
changes, MMPs
MMPs lead to venous dilation/remodelling, skin changes, leg ulcers
FIGURE1.6 DVT, deep vein thrombosis; MMP, matrix metalloproteinase.
Changes in fluid shear stress
(force of blood flowing at the
endothelial surface of the vein)
Genetic factors
FIGURE1.7 Consequences of glycocalyx and endothelium changes in
flow
venules and capillaries. MMP, matrix metalloproteinase.
Oedema
Hard oedema
Skin pigmentation
Inflammation
MMPs
Venous leg ulcer
Aetiology 21
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THEORIES OFTISSUE DAMAGE
The progression from venous hypertension to leg ulceration is not
fully understood. Several theories exist as to how this happens:
Fibrin cu theory (Browse and Burnard1982; Herrick etal.1992).
White cell trapping theory (Coleridge- Smith etal.1988).
Mechanical theory (Chant1988).
‘Trap’ growth factor theory (Higley etal.1995).
Fibrin Cuff Theory
Venous hypertension causes capillary distension that results in
endothelial pore dilation, allowing brinogen to leak through. Layers
of brin are laid down as cus along the capillary wall. This causes a
diusion barrier inhibiting oxygen and nutrient transfer, leading to
atrophic skin, tissue hypoxia, induration, liperdermatosclerosis and
ulceration (Figure1.8). In addition, chronic inammation occurs
due to extracellular proteins and leucocytes.
White Blood Cell Theory
White cells adhere to (are trapped by) the endothelium of the capillaries as a result of venous hypertension. The accumulation and activation of trapped white blood cells in patients with venous
hypertension release toxic metabolites, tumour necrosis factor (TNF,
a pro- inammatory cytokine) and proteolytic enzymes that cause
vascular destruction and lead to increased vascular permeability.
Leucocytes become trapped in the capillaries in static blood and
obstruct the ow. Monocytes become active, causing skin damage by
the release of cytokines. Increased permeability leads to brin cu
formation, as in the brin cu theory.
Mechanical Theory
High pressure in the capillary bed leads to oedema, which increases
tissue pressure and stretches the skin. It is thought that ulceration
arises from tissue ischaemia. Tissue ischaemia is a restriction on the
blood supply of tissues. This causes a shortage of oxygen and glucose
required for cellular metabolism.
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