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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_781_Библиотеки_им_академика_М_И_Перельмана
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TABLE5.2 (Continued)
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Category Description
C4a Hyperpigmentation.
A red/brown discoloration of the
skin (this is a deep brown in
darker skin) caused by leakage
and breakdown of red blood cells
from the capillary network into
the skin. Presentation can be
small, localised patches or extend
over the gaiter region.
C4a Varicose eczema, an inammatory
condition caused by the irritation
of blood products that have
leaked into the skin and present
as red, itchy, scaly or aky skin
that may have blisters and crusts
(NICE2022).
This can be quite a distressing symptom to the patient as it can look like dirty
marks on the skin (Figure5.3). A note of caution is that although this is a sign
of venous disease, it does not disappear when the ulcer is healed and as the
patient ages may still be present with arterial disease (Lymphoedema
Framework2006).
Varicose eczema (Figure5.4) can present as wet or dry and can be localised or may
involve the whole gaiter region. Occasionally, if the patient scratches the eczema
this can lead to a much more widespread manifestation. It can often be confused
with contact dermatitis and irritant eczema. Both of these are also commonly
found in combination with varicose eczema and leg ulceration.
FIGURE5.4 Varicose eczema.
C4b Atrophie blanche (AB; white
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atrophy), angular scars on the
lower leg or foot.
AB is mainly located on the lower leg. This is a condition whereby white, ‘lacy’
areas of vascular tissue are interspersed with visibly engorged capillaries, which
are seen as tiny red dots below the surface of the skin and are often surrounded
by regions of skin hyperpigmentation (Figure5.5) (McVittie and Holloway2015). AB is caused by low blood ow as a result of brin plugs causing
occlusion to the vessels, increasing the propensity to ulcerate (McVittie and
Holloway2015). These patches can be small or extensive, arising on areas of the
skin that have never ulcerated or areas where there was a previous ulceration.
AB results in localised hypoxic areas that can lead to ulceration. It can be
classied as idiopathic (the absence of related diseases) or secondary (as a
consequence of other systemic conditions, most commonly CVI). Patients
describe excruciating neuropathic stabbing or shooting pain. This is likely to be
caused by a combination of localised ischaemia and inammation of the
capillary walls and can make the introduction of compression intolerable. (For
pain associated with AB, see Chapter6.) The patient can experience painful,
purpuric lesions that progress to punched- out ulcers. These will heal with
white, stellate scars (Harper and Crane2022).
porcelain-
(Continued)
TABLE5.2 (Continued)
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Category Description
FIGURE5.5 Atrophie blanche.
Lidodermatosclerosis (LDS),
chronic inammation and
hardening (brosis) of the dermis
and subcutaneous tissue of the
lower limb (NICE2022).
LDS is often present in venous disease and is thought to be caused by leakage and
laying down of the brin from the capillary network, fat necrosis, inammation
and scarring. Progressive brosis leads to increased skin fragility and atrophic
skin surface, with loss of sweat glands and hair follicles. The presentation is a
hard, woody layer just below the surface of the skin, often beginning around the
ankle region and gradually extending up to the mid-
This process can give rise to an ‘inverted champagne bottle’–shaped leg whereby
soft swelling accumulates in the calf, distorting the leg shape as a result of
brinous tissue replacing the fatty layer and oedema being trapped above,
usually in the knee and thigh (Figure5.6).
calf region over the years.
The skin around the ankle becomes too tight to stretch. Acute stages of LDS are
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often misdiagnosed as cellulitis and phlebitis (Miteva etal.2010). Unlike
cellulitis, its borders do not change quickly, and the patient will not be pyrexic.
LDS can be acute or chronic. In the acute phase it can be very painful. Chronic
pain with LDS tends to be more of a dull ache (Miteva etal.2010). Unless
treated with compression, the leg will continue to become increasingly inamed
and break down. Compression may need to be introduced gradually with
analgesia if AB is present. Generally, acute LDS progresses to a chronic state. It
is important to note that chronic LDS does not always begin with an acute
episode. This presents as areas of pale to dark brown leathery skin that is too
tight to pinch up (it may be harder to spot in dark skin tones).
FIGURE5.6 Lipodermatosclerosis and venous staining.
Courtesy ofAccelerate.
(Continued)
TABLE5.2 (Continued)
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Category Description
C4c Corona phlebectatica (ankle are)
is a distended myriad of tiny
varicose veins caused by
perforator vein incompetence,
which causes the blood to pool
and stretch the blood vessels.
FIGURE5.7 Signs of ankle are.
Look for a fan-
located around the medial or lateral aspects of the ankle and foot (Figure5.7)
(Collares and Faintuch2017).
C5 Healed. A person’s leg will always be at risk of reoccurrence of ulceration and so they must
be transitioned into the correct dose and type of compression hosiery stockings
once healed to prevent reoccurrence. This is discussed further in Chapter9. If
venous leg ulcers have not healed within 12 weeks of treatment, the patient
should be referred to appropriate specialist services (Wounds UK2022).
shaped pattern of several small intradermal veins commonly
C6 Venous leg ulcer.
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A leg ulcer is dened as a break in
the skin that has failed to heal in
two weeks (NICE2021).
C6r Recurrent active venous ulcer. When a venous leg ulcer has healed, prevention of recurrence is vital. Regular
Source: Adapted from Lurie etal. (2020).
These typically occur in the medial or gaiter region. They are the most common
type of leg ulcer and in the United Kingdom 420 000leg ulcer patients are
managed by the NHS (Guest etal.2018).
review and reassessment are essential, together with educating the patient to
keep vigilant for any signs of changes to the lower limb (Wounds UK2022).
248 ASSESSMENT OF LEG ULCERATION
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ARTERIAL DISEASE
While venous leg ulceration is reportedly the most commonly
occurring type of ulceration, healthcare practitioners need to develop
competence in recognising clinical symptoms of PAD, ischaemic
changes and arterial pain (Figure5.8). These are discussed further in
Table5.3 and the 6Ps of PAD are listed in Table5.4.
A simple way for healthcare practitioners to be cognisant of this
variety of clinical presentations related to PAD is the 6 Ps of PAD,
described in Table5.4. See Chapter8 for a discussion of clinical management in the presence of PAD.
Eective wound treatment and preventative care depend on
accurate and thorough assessment, leading to a diagnosis that triggers action and is tailored to the individual patient, their skin and
their wound. Assessment should involve a thorough inspection of
the skin, and this should include nding out about the patient’s
baseline skin tone. This is vital so that any changes to patients’
skin, for example signs of inammation and haemosiderin, are
observed and monitored in the same way. Skin inspection and
awareness of skin tone should be carried out as part of a holistic
assessment. The use of a validated skin tone classication tool is a
simple way of assessing skin tone across healthcare settings
(Figure5.9).
FIGURE5.8 Arterial ulceration. Courtesy of Accelerate.
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TABLE5.3 Identifying arterial disease inthe lower limb.
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Ischaemic limb
changes– acute
limb ischaemia is a
sudden decrease in
limb perfusion
threatening the
viability of the limb
due to artery
occlusion, vascular
bypass graft or
stent(Cai and
Forsyth2022).
Cold limbs– note if
the limbs are cold in
a warm environment and feel the
dierence between
the two limbs.
In the presence of arterial disease, the limb may range from very pale to mottled
blue due to the lack of oxygenated blood. Limbs may have a deep red/purple hue
in pale skin tones. Dependent rubor (when the limb is in a dependent position)
is caused by the dilation of dermal arterioles and capillaries in the presence of
increased hydrostatic pressure (Mintz etal.2013) in the foot, as an attempt to
adequately oxygenate the limb. This results in the pooling of arterial blood. N.B.
It can often be mistaken for cellulitis or a well- perfused limb. In darker skin
tones these colour changes are important to note and to compare with another
limb; dependent rubor will present as darker than other areas and paler if the
person is hypoxic.
Buerger’s test (Buerger1924) identies the position of the rubor (in a healthy limb
this should stay the same whether elevated or dependent). To assess dependent
rubor ask the patient to lie at on their back and gently elevate their limb to
above the heart at a 90° angle (hold this for approx. 30 seconds). Lower the limb
noting any changes in colour. If dependent rubor is the cause for colour change,
the limb will become pale on elevation; redness or a darkening of the skin in
darker skin tones will gradually return once the limb is lowered (Eder
etal.2019).
Although this remains a very benecial test when vascular assessment equipment
may not be available, it has been replaced in part by the pole test (1994),
whereby a handheld Doppler is used when the limb is elevated to a height of
77 cm. If Doppler sounds can still be heard, this is a good indication that there is
adequate arterial ow to the foot (Eder etal.2019).
(Continued)
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TABLE5.3 (Continued)
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Loss of sensation, hair
loss, atrophic skin
changes with white
skin tones turning
paler, trophic
changes to nails and
muscle wastage
resulting in
weakness in the
legs. Non- healing
foot or leg ulcer.
Lower limb oedema. Dependent oedema–
Absent pedal pulses. Feel for pedal pulses
Assess for any lower
limb changes.
check the limb for
dependent oedema.
and note any
absence.
These are all symptoms of peripheral arterial disease (PAD). The arteries become
Patients with arterial disease may still have signicant limb oedema (Nickles
Refer to the section on ankle brachial pressure index assessment. The palpation of
hardened when plaque attaches to the artery walls and blood ow to the lower
limb is restricted.
etal.2023). This can result in the patient being unable to sleep at night with
their legs elevated because of ischaemic night pain. For most patients relief is
found by spending the night in a chair with their legs down, although this may
then cause an increase in oedema from limb dependency and further reduce the
arterial blood ow (Woelk2012). There is some evidence to suggest that patients
with lower limb oedema and peripheral arterial disease may benet from some
compression therapy (Nickles etal.2023), but caution should be exercised and
this should only be instigated through specialist experts within tissue viability or
under vascular guidance.
pedal pulses on its own is insucient to detect the presence or absence of
arterial disease.
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Ischaemic pain. Pain is associated with
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the lack of oxygen
to the lower limb.
Assess the patient’s
experiences of pain.
This can present in several ways depending on severity.
There can be intermittent claudication. The muscles of the lower limb require
increased blood ow when walking and exercising. Patients with PAD have a
decreased blood supply to the lower limb when this is maximised, and no
further perfusion can be supplied to the lower extremity muscles. The supply
and demand mismatch causes temporary ischaemia of the muscles that presents
as pain, cramping and fatigue (Zemaitis etal.2022). The pain disappears at rest
when the oxygen demand is reduced. Record how far the patient can walk
before the onset of pain.
Night pain occurs when legs are elevated at night. Blood pressure drops during
sleep. In patients with PAD this reduced blood pressure is not sucient to
maintain perfusion in the lower limb. Relief can be gained by hanging the legs
over the edge of the bed.
Rest pain occurs even when sitting. It often involves the foot and indicates a severe
reduction in arterial blood ow required for normal tissue metabolism (see
Chapter6 for pain assessment and management).
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