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252 ASSESSMENT OF LEG ULCERATION
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TABLE5.4 The 6Ps ofperipheral arterial disease (PAD).
Pain
Pallor
Poikilothermia
Pulselessness
Paraesthesia
Paralysis or power loss
FIGURE5.9 Skin tone tool.
Source: Wounds UK (2021). Reproduced withpermission.
WOUND ASSESSMENT
The holistic assessment of a wound is essential to identify causative
and contributory factors, support diagnosis and determine factors
that may contribute to delayed wound healing. Wound assessment
should include assessment of the wound bed, care and intervention
planning, evaluation of treatment and interventions and continual
reassessment. Accurate and timely wound assessment underpins
eective clinical decision- making, appropriate patient- centred goals,
and reduced morbidity and costs associated with the burden of
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wound care (Posnett and Franks2008).
It is important that clinicians understand the factors that inuence wound healing as part of the holistic assessment (Table5.5).
On the rst presentation build up a picture of the origin of the
ulcer. This presentation will help to identify the patient’s specic
Assessment of Leg Ulceration 253
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TABLE5.5 Intrinsic andextrinsic factors that aect wound healing.
Intrinsic
Oxygenation: oxygen is essential for cell metabolism and energy
production. Hypoxic wounds are at increased risk of infection, reduced
angiogenesis (the development of new blood vessels), reduced
epithelialisation, broblast (connective tissue cell) proliferation, collagen
synthesis and wound contraction (Guo and DiPietro2010).
Infection: once the skin is injured, micro- organisms that are normally on
the skin surface access underlying tissue. Infected wounds become ‘stuck’
in the inammatory phase. The pathogenic microbes compete with the
broblasts for nutrients and other resources (Guo and DiPietro2010).
Venous insuciency: increased venous pressure over time leads to a
chronic inammatory response, which can cause the breakdown of tissue
resulting in venous leg ulceration (Wounds UK2016).
Diabetes: prolonged wound hypoxia, dysfunction in broblasts and
epidermal cells, impaired angiogenesis and neovascularisation (natural
formation of new blood vessels) decrease host immune resistance and
neuropathy (Guo and DiPietro2010).
Peripheral arterial disease: decreased blood ow to the lower extremities
and wound, reducing the amount of oxygen and nutrients to the wound bed.
Temperature: the cooler the wound, the longer it will take to heal. Higher
temperatures promote vascular dilation.
Necrotic tissue or foreign bodies: both prolong the inammatory
response and increase the risk of infection.
Oedema: aects the permeability of vascular membranes, inammation or
tissue trauma. Also, uid can leak into the surrounding tissue.
Dehydration: uids are required for oxygen profusion, hydration of the
wound bed, transportation of nutrients, as a solvent for vitamins,
minerals, glucose, amino acids and to transport waste away from cells.
Extrinsic
Age: skin loses its elasticity with ageing. Collagen is reduced and blood
ow can be restricted due to other chronic conditions. Other factors that
delay wound healing in older people are altered inammatory response,
delayed Treduced macrophage phagocytic capacity.
Sex: oestrogen helps to regulate a variety of genes associated with
regeneration. Older males and post- menopausal women are at a higher
risk of chronic wounds (Oh and Phillips2006).
Co- morbidities: conditions such as diabetes, chronic venous insuciency,
peripheral arterial disease and immune deciency disorders are known
to delay the wound healing process. Additional screening for these
co- morbidities in patients with wounds is recommended.
cell inltration and alterations in chemokine production, and
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(Continued)
254 ASSESSMENT OF LEG ULCERATION
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TABLE5.5 (Continued)
In diabetes narrowed blood vessels lead to decreased blood ow and
oxygen to a wound. Elevated blood sugars decrease red blood cells, which
carry nutrients to the tissue, and lower the ecacy of white blood cells
(neutrophils and monocytes) in ghting infection.
Obesity: reduces the availability of oxygen to the wound. Skin folds can
harbour bacteria and damage can be caused by skinincrease the risk of pressure ulcer development (Mitchell2018). Obesity
can also be connected to stress, anxiety and depression.
Medications: steroids, non-
chemotherapy– many medicines interfere with clot formation or platelet
function, inammatory responses and cell proliferation.
Nutrition: nutrition is required to provide adequate support for the
increased energy demands during the healing process. Inadequate
protein leads to skin fragility, decreased immune function and poor
wound healing. The body requires 30–35Kcal daily to heal a wound and
40Kcal if the patient is underweight.
Lifestyle factors: smoking causes vasoconstriction, which leads to
hypoxia. Neutrophil and monocyte (cells that help prevent infection)
activity is reduced and broblast proliferation and migration are reduced.
Collagen is reduced in smokers, which means less tensile wound
strength. Alcoholism diminishes host resistance, making the body more
at risk of infection. Alcohol decreases phagocytic function (phagocytosis
is a threemacrophages engulf and destroy microand cell debris). Release of cytokines (small secreted proteins released by
cells that have a specic eect on the interactions and communications
between cells) is suppressed and angiogenesis is reduced.
Immunocompromised conditions: cancer, radiotherapy, AIDS.
Chemotherapy and radiation can slow wound healing. Processes such as
cellular replication, inammatory reactions and tissue repair are
compromised. Radiation therapy can cause permanent tissue damage.
Stress and anxiety: stress delays wound healing by altering the multiple
physiological pathways required in the repair processes (Gouin and
Kiecolt- Glaser2011). Stressors can lead to negative emotional states, for
example anxiety and depression, which have an impact on physiological
processes and behavioural patterns that inuence health outcomes (Guo
and DiPietro2010).
Pain: ineective wound pain management can delay wound healing and
contribute to lack of concordance with treatment (Frescos2011).
stage process in which neutrophils, monocytes and
steroidal anti- inammatory drugs,
organisms, other foreign antigens
to- skin friction and
Source: Adapted from Mitchell (2020), with permission of the British Journal
of Nursing.
本书版权归John Wiley & Sons Inc.所有
Assessment of Leg Ulceration 255
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treatment pathway. Many wounds start as the result of a trauma and
some wounds appear spontaneously or for no obvious reason. Ask
the patient some specic questions:
When and how did the wound occur?
Where is the wound located?
Is this the rst episode of a wound?
Have you been diagnosed with a leg ulcer before?
What was the time taken to heal the previous ulcer?
How long have you not had an ulcer for?
What were the past treatments (successful and unsuccessful)?
TIMES (Tissue viability, Inammation or Infection, Moisture
balance, Edge of wound, Surrounding skin or peri- wound area) is a
framework used to focus on specic wound bed parameters to aid
management and guide treatment. It should be used as part of a
holistic assessment (Atkin2019) (Table5.6).
During the initial assessment, clues with respect to the location
of the ulcer and basic clinical descriptors may point to the likely
cause and diagnosis (Chapter1). Leg ulcers do not always t into two
distinct categories. Observations in clinical practice indicate that
there is a belief that three types of ulceration exist: venous, arterial
and mixed aetiology. In reality there are many other, perhaps less
commonly observed types of ulceration, which are examined in
Chapter 3. Basic clinical descriptors of unusual aetiologies may
include the following:
Atypical site for the suspected aetiology. Be wary if the ulcer is in
an unusual location and develops spontaneously.
Atypical tissue type. Observe for wounds that bleed easily: appear
to scab over quickly and or break down recurrently; look healthy
but fail to show normal signs of healing.
Atypical history. Did it occur very quickly or spontaneously? Is it
not progressing as expected? Observe for clusters of small ulcers,
blistering and ulcers that rapidly increase in size.
Atypical shape or depth.
Atypical edges. Observe for any raised or rolled edges or
discoloured wound margins.
本书版权归John Wiley & Sons Inc.所有
TABLE5.6 TIMES wound assessment.
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T– Tissue viability ( Figure5.10).Repair
and regeneration or non- viable tissue?
FIGURE5.10 Repair and regeneration.
Is the wound showing signs of regeneration and repair, such as granulation tissue or
epithelial cells, or is the wound bed displaying non- viable tissue, for example slough,
necrosis or eschar? Consider if the amount of devitalised or non- viable tissue is
inuencing wound healing or facilitating infection (Atkin2019).
Identify the site of the wound, which may give an indication of whether an ulcer is venous,
arterial or mixed aetiology. Classically venous ulcers present in the gaiter area of the leg,
but be mindful that there are always exceptions to these rules.
Measure the wound size. This should be documented in the patient’s notes and updated on
dressing changes. If taking photographs, adhere to any local guidelines and seek
permission from the patient (Ousey and Cook2012).
Identify the wound depth, if necessary take a measurement using a sterile probe. This
procedure should only be carried out by qualied practitioners who are familiar with
anatomical structures in close proximity to the wound. Also look for tracking, cavities or
stulae from the wound bed.
Consider debridement. The type of debridement needs to be determined by the clinical
presentation, the patient’s preferences and circumstances, and variations in clinical skills
(Atkin2019).
Assess the extent of tissue involvement. Does the wound involve the epidermis, dermis, fat,
fascia? Review if there is exposed muscle and/or bone.
Document any wound odour. A slight odour may be associated with an occlusive dressing
type. Fungating and necrotic wounds are often malodorous. If a wound is heavily
colonised this can cause malodour (Edward-
Jones2018).
Consider using an odour assessment tool when documenting odour:
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Strong odour– evident when entering the room, dressing is intact.
Moderate odour– evident when entering the room, dressing removed.
Slight odour– evident during dressing change.
No odour– no odour during dressing change (Haughton and Young1995).
Hypergranulation, also known as overgranulation, can exercise clinicians; healthy granula-
tion is often misdiagnosed as hypergranulation in lower leg wounds.
Granulation develops in the proliferation stage and is a critical stage in wound healing. Hypergran-
ulation is when the granulation tissue ‘over grows beyond the wound surface’ (Mitchell and
Llumigusin2021) and can inhibit healing, often due to adverse conditions at the wound bed.
Healthy granulation tissue: very vascular, pink and moist. Usually at the level of the sur-
rounding skin except when oedematous or simply very active tissue, responding well to the
treatment regime.
Unhealthy granulation tissue: darker tissue bed, can be very at or raised and is friable,
bleeding easily when touched. Raised or hypergranulating wound beds also are protruding,
not just a raised mound, and these protrusions are jelly- like when pushed and bleed
readily. The wound healing gets stuck and the energy appears to go to growing upwards
rather than into the maturation phase. This may be exacerbated by infection or biolm.
The clinician will be seeing a wound that is not reducing in width.
When is a raised granulating wound bed healthy and not a concern? The raised granulation
tissue remains pink and healthy, even globular in nature, but on weekly review the clinician
will nd that the width of the wound continues to contract and exudate is controlled.
Despite the raised tissue, the edges are still attening and contracting. Healing is continuing. This is therefore not true adverse hypergranulation tissue that needs clinical attention;
carry on with standard wound management. Adopt a wait- and- see approach (Vuolo2010).
It is important to note that true hypergranulation is more common in surgical wounds and
uncommon in leg ulceration. Non- healing hypergranulation may also be suspicious; see
Chapter4 on unusual aetiologies.
(Continued)
TABLE5.6 (Continued)
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I– Infection or Inammation
(Figure5.11).
FIGURE5.11 Infection and inammation
of the tissue.
Inammation (or the inammatory response) is a normal stage of wound healing. If the
wound is red, hot, swollen or painful within the rst 1–7 days of injury occurring, then this
is a normal inammatory response and unless the wound is physically dirty it is not likely
to be infected.
Chronic inammation, however, is problematic and is often caused through a high bacterial
burden in the wound bed. This is frequently related to the presence of biolm.
Biolms are made up of micro- organisms that gather in islands across the wound bed and
attach themselves to the wound surface. They are protected within a polysaccharide matrix
that is impervious to antimicrobials; this can delay wound healing and cause chronic
inammation (Steven etal.2012) as the normal inammatory response of phagocytosis,
often referred to as the ‘clearing- up phase’, is unable to occur as the micro- organisms are
protected by the matrix, and so the wound bed itself is attacked. This causes a state of
ongoing inammation that impedes wound healing.
Biolms are almost impossible to see with the naked eye. However, if a wound is static with
no signs of overt infection, it is highly likely that a biolm will have been formed (Stoodley
etal.2002).
The clinical indications of a biolm may present as:
No response to antimicrobial treatment.
Delayed healing beyond expectations.
Friable granulation tissue that bleeds easily on contact.
Low- level inammation and erythema.
Increase in wound exudate.
Wound breakdown following completion of antibiotics.
Signs of secondary infection (IWII2016).
The opposite of a biolm infection is a spreading infection. This is when the microbial
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burden in the wound increases and the person is at risk of becoming unwell as infection
spreads and there is a risk of systemic infection.
Assess for signs of infection, which may be indicated by swelling, localised heat or pain,
erythema, purulent discharge (white, yellow or brown and might be slightly thick in
texture), increased exudate, malodour and pyrexia (Wilson2012).
Measure the patient’s core temperature. Laboratory investigations for inammation markers
such as C- reactive protein (CRP) may be indicated.
Assess the wound for any foreign bodies present in the wound bed, which may be a source of
infection.
The wound infection continuum guides the clinician to the signs and symptoms of wound
infection to support accurate diagnosis and to enable the appropriate use of antimicrobial
wound dressings and antibiotics for systemic infection.
The diagnosis of wound infection should be made using a combination of clinical presenta-
tion and clinical judgement. Routine swabbing is not indicated in leg ulcer management.
However, if it is decided that a swab is rationalised, then use the Levine technique to
collect cultures.
Do not delay the commencement of antibiotics for spreading infection while waiting for a
swab result, but keep in mind that antibiotics do not promote wound healing in a leg ulcer
that is not clinically infected (NICE2020).
(Continued)
TABLE5.6 (Continued)
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M– Moisture balance.
Is there too much or too little exudate?
A moist wound bed has been shown to improve healing and reduce pain, discomfort and
infection (Winter1962). Whereas contact with wound uid is benecial to the healing
process in acute wounds, it contains substances detrimental to cell proliferation and can
inhibit healing of hard- to- heal wounds (Cutting and White2002). Large amounts of
exudate can be indicative of infection or unmanaged oedema.
Exudate usually occurs as a result of vasodilation in the inammatory phase. Exudate is
mainly water, but also contains electrolytes, nutrients, proteins, inammatory mediators,
digesting enzymes such as matrix metalloproteinases (MMPs), growth factors,
proteinneutrophils, macrophages, platelets and waste cells (Cutting2004).
Assessment of exudate is an essential part of wound management and should include type,
colour, amount, odour (if any) and viscosity at each dressing change. Table5.7 describes
the exudate and its signicance.
If the wound is too dry, this will inhibit the epithelial cell’s ability to migrate across the
wound bed, thus an overly dry wound bed is also detrimental to wound healing.
E– wound Edge (Figure5.12).Epithelial
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edges or non- viable edges?
Wound margins tend to change in appearance as the wound heals or deteriorates
(Wilson2012).
Classically the edges of an arterial ulcer will be ‘punched out’ in shape and the wound will be
deep from the edges. This is sometimes termed ‘cli edges’.
Typically in venous ulceration a less conforming edge that slopes gradually is noted.
It is unlikely that epithelial advancement will occur if high levels of exudate, underlying
pathology, biolm or infection have not been addressed (Atkin2019).
The edge of the wound should be attened and advancing across the granulation tissue. If
rolled edges are present (hyperbole), this is a sign of a long- standing wound where
epithelial advancement has been hindered due to an overly dry or high bacterial burden in
the wound bed over a continued period of time.
FIGURE5.12 Epithelial wound edges.
S– Surrounding skin Assess the peri- wound skin for moisture damage or compromise. Peri- wound moisture-
associated dermatitis may indicate that more absorbent dressings or frequent dressing
changes are required or that the dose of compression therapy is subRegular washing, cleansing and moisturising of the surrounding skin are an integral part of
lower limb management. See Chapter8 for more.
Source: Adapted from Mitchell (2020) with permission of the British Journal of Nursing.
optimal.
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