ABC of wound healing: Wound assessment
Most
wounds, of whatever aetiology, heal without difficulty. Some
wounds, however, are subject to factors that impede healing,
although these do not prevent healing if the wounds are managed
appropriately. A minority of wounds will become chronic and non-healing.
In these cases the ultimate goal is to control the symptoms and
prevent complications, rather than healing the wound.
Causes of ulceration
- Vascular
(venous, arterial, lymphatic, vasculitis)
- Neuropathic
(for example, diabetes, spina bifida, leprosy)
- Metabolic
(for example, diabetes, gout)
- Connective
tissue disease (for example, rheumatoid arthritis, scleroderma,
systemic lupus erythematosus)
- Pyoderma
gangrenosum (often reflection of systemic disorder)
- Haematological
disease (red blood cell disorders (for example, sickle cell
disease); white blood cell disorders (for example, leukaemia);
platelet disorders (for example, thrombocytosis)
- Dysproteinaemias
(for example, cryoglobulinaemia, amyloidosis)
- Immunodeficiency
(for example, HIV, immunosuppressive therapy)
- Neoplastic
(for example, basal cell carcinoma, squamous cell carcinoma,
metastatic disease)
- Infectious
(bacterial, fungal, viral)
- Panniculitis
(for example, necrobiosis lipoidica)
- Traumatic
(for example, pressure ulcer, radiation damage)
- Iatrogenic
(for example, drugs)
- Factitious
(self harm, “dermatitis artefacta”)
- Others (for
example, sarcoidosis)
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Local and systemic factors that impede wound
healing
|
| Local factors |
Systemic factors |
- Inadequate blood supply
- Increased skin tension
- Poor surgical apposition
- Wound dehiscence
- Poor venous drainage
- Presence of foreign body and foreign body reactions
- Continued presence of micro-organisms
- Infection
- Excess local mobility, such as over a joint
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- Advancing
age and general immobility
- Obesity
- Smoking
- Malnutrition
- Deficiency
of vitamins and trace elements
- Systemic
malignancy and terminal illness
- Shock
of any cause
- Chemotherapy
and radiotherapy
- Immunosuppressant
drugs, corticosteroids, anticoagulants
- Inherited neutrophil disorders, such as leucocyte adhesion deficiency
- Impaired
macrophage activity (malacoplakia)
|
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Some complications of chronic wounds
|
- Sinus
formation
- Fistula
- Unrecognised
malignancy
- Malignant
transformation in the ulcer bed (Marjolin’s ulcer)
- Osteomyelitis
- Contractures
and deformity in surrounding joints
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- Systemic amyloidosis
- Heterotopic
calcification
- Colonisation
by multiple drug resistant pathogens, leading to antibiotic
resistance
- Anaemia
- Septicaemia
|
It is important that the normal
processes of developing a diagnostic hypothesis are followed before
trying to treat the wound.
A detailed clinical history should include
information on the duration of ulcer, previous ulceration, history
of trauma, family history of ulceration, ulcer characteristics
(site, pain, odour, and exudate or discharge), limb temperature,
underlying medical conditions (for example, diabetes mellitus,
peripheral vascular disease, ischaemic heart disease,
cerebrovascular accident, neuropathy, connective tissue diseases
(such as rheumatoid arthritis), varicose veins, deep venous
thrombosis), previous venous or arterial surgery, smoking,
medications, and allergies to drugs and dressings. Appropriate
investigations should be carried out.
Assessing wounds
Size of wound
The size of the wound should be assessed at
first presentation and regularly thereafter. The outline of the
wound margin should be traced onto transparent acetate sheets and
the surface area estimated: in wounds that are approximately
circular, multiply the longest diameter in one plane by the longest
diameter in the plane at right angles; in irregularly shaped
wounds, add up the number of squares contained within the margin of
the outline of the wound from an acetate grid tracing.
These methods are the simplest, but it should
be recognised that they are not precise. However, they do provide a
means by which progress over time to wound closure can be
identified. Patient positioning, body curvature, or tapering
of the limbs will affect the accuracy of these techniques.
Edge of wound
Although not diagnostic, examination of the
edge of the wound may help to identify its aetiology in the context
of the history of the wound. For example, venous leg ulcers
generally have gently sloping edges, arterial ulcers often appear
well demarcated and “punched out,” and rolled or
everted edges should raise the suspicion of malignancy. A biopsy
should be taken of any suspicious wound.
Site of wound
The site of the wound may aid diagnosis;
diabetic foot ulcers often arise in areas of abnormal pressure
distribution arising from disordered foot architecture. Venous
ulceration occurs mostly in the gaiter area of the leg (see next
article in this series). Non-healing ulcers, sometimes in unusual
sites, should prompt consideration of malignancy.
Wound bed
Healthy granulation tissue is pink in colour
and is an indicator of healing. Unhealthy granulation is dark red
in colour, often bleeds on contact, and may indicate the presence
of wound infection. Such wounds should be cultured and treated in
the light of microbiological results. Excess granulation or
overgranulation may also be associated with infection or
non-healing wounds. These often respond to simple cautery with
silver nitrate or with topically applied steroid preparations.
Chronic wounds may be covered by white or yellow shiny fibrinous
tissue (see next article in this series). This tissue is avascular,
and healing will proceed only when it is removed. This can be done
with a scalpel at the bedside.
The type of tissue at the base of the wound
will provide useful information relating to expectation of total
healing time and the risk of complications—for example, bone
at the base may suggest osteomyelitis and delayed or non-healing.
Necrotic tissue, slough, and eschar
The wound bed may be covered with necrotic
tissue (non-viable tissue due to reduced blood supply), slough
(dead tissue, usually cream or yellow in colour), or eschar (dry,
black hard necrotic tissue). Such tissue impedes healing. Necrotic
tissue and slough may be quantified as excessive (+++), moderate
(++), minimal (+) or absent (-).
Since necrotic tissue can also harbour
pathogenic organisms, removal of such tissue helps to prevent wound
infection. Necrotic tissue and slough should be debrided with a
scalpel so that the wound bed can be accurately assessed and
facilitate healing. Eschar may be adherent to the wound bed, making
debridement with a scalpel difficult. Further debridement, as part
of wound management, may be required using other techniques.
Accurate methods for measuring wound depth are
not practical or available in routine clinical practice. However,
approximate measurements of greatest depth should be taken to
assess wound progress.
Undermining of the edge of the wound must be
identified by digital examination or use of a probe. The depth and
extent of sinuses and fistulas should be identified. Undermining
areas and sinuses should be packed with an appropriate dressing to
facilitate healing.
Undermining wounds and sinuses with narrow
necks that are difficult to dress may be amenable to be laid open
at the bedside to facilitate drainage and dressing. Wounds
associated with multiple sinuses or fistulas should be referred for
specialist surgical intervention.
Surrounding skin
Cellulitis associated with wounds should be
treated with systemic antibiotics. Eczematous changes may need
treatment with potent topical steroid preparations. Maceration of
the surrounding skin is often a sign of inability of the dressing
to control the wound exudate, which may respond to more frequent
dressing changes or change in dressing type. Callus surrounding and
sometime covering neuropathic foot ulcers (for example, in diabetic
patients) must be debrided to (a) visualise the wound, (b) eliminate potential source of infection, and (c) remove areas
close to the wound subject to abnormal pressure that would
otherwise cause enlargement of the wound. This can be done at the
bedside.
Infection
All open wounds are colonised. Bacteriological
culture is indicated only if clinical signs of infection are
present or if infection control issues (such as methicillin
resistant staphylococcus aureus (MRSA)) need to be considered. The
classic signs of infection are heat, redness, swelling, and pain.
Additional signs of wound infection include increased exudate,
delayed healing, contact bleeding, odour, and abnormal granulation
tissue. Treatment with antimicrobials should be guided by
microbiological results and local resistance patterns.
Pain
Pain is a characteristic feature of many
healing and non-healing wounds. Pain can be caused by both
nociceptive and neuropathic stimuli. Intermittent pain is often
related to dressing removal or recent application of new dressings
and may necessitate the use of analgesia before the dressing is
changed. Constant pain may arise as a result of the underlying
condition, such as ischaemia, neuropathy, tissue oedema, chronic
tissue damage (for example, lipodermatosclerosis), infection, or
scarring (for example, atrophie blanche). The nature and type of
pain should be identified and treated appropriately. Pain
assessment tools can help to assess the nature and severity of
pain. With recalcitrant pain or pain that is difficult to control,
consider referral to a local pain team.
Non-healing wounds
Non-healing wounds have traditionally been
defined as those that fail to progress through an orderly sequence
of repair in a timely fashion. Such wounds are sometimes thought of
as being caused by neglect, incompetence, misdiagnosis, or
inappropriate treatment strategies. However, some wounds are
resistant to all efforts of treatment aimed at healing, and
alternative end points should be considered; measures aimed at
improving the quality of life will be paramount in these instances.
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Laboratory investigations before treating a
wound
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| Investigation |
Rationale |
|
Haemoglobin
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Anaemia may delay healing
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White cell count
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Infection
|
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Platelet count
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Thrombocytopenia
|
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Erythrocyte sedimentation rate; C reactive protein
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Non-specific markers of infection and inflammation; useful in diagnosis and
monitoring treatment of infectious or inflammatory ulceration
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Urea and creatinine
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High urea impairs wound healing. Renal function important when using
antibiotics
|
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Albumin
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Protein loss delays healing
|
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Glucose, haemoglobin A1C
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Diabetes mellitus
|
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Markers of autoimmune disease (such as
rheumatoid factor, antinuclear antibodies, anticardiolipin
antibodies, lupus anticoagulant)
|
Indicative of rheumatoid disease, SLE and
other connective tissue disorders
|
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Cryoglobulins, cryofibrinogens, prothrombin
time, partial thromboplastin time
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Haematological disease
|
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Deficiency or defect of antithrombin III,
protein C, protein S, factor V Leiden
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Vascular thrombosis
|
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Haemoglobinopathy screen
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Sickle cell anaemia, thalassaemia
|
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HIV status
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Kaposi’s sarcoma
|
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Serum protein electrophoresis; Bence-Jones
proteins
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Myeloma |
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Urine analysis
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Useful in connective tissue disease
|
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Wound swab
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Not routine; all ulcers colonised (not the
same as infection); swab only when clinical signs of infection
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Overgranulation may be a sign of
infection or non-healing |
Tracing a wound for measurement and
measuring a wound
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Wound edge characteristics
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|
Edges Type of ulcer
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Type of ulcer
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Sloping
Punched out
Rolled
Everted
Undermining
Purple
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Venous ulcer
Arterial or vasculitic ulcer
Basal cell carcinoma
Squamous cell carcinoma
Tuberculosis, syphilis
Vasculitic (such as pyoderma
gangrenosum) |
| Site of wound and type of ulcer |
| Site |
Type of ulcer |
| Gaiter area of the leg |
Venous ulcer |
|
Sacrum, greater trochanter, heel
|
Pressure ulcer |
| Dorsum of the foot |
Arterial or vasculitic
ulcer |
| Shin |
Necrobiosis lipoidica |
| Lateral malleolus |
Venous, arterial, or pressure ulcer or hydroxyurea induced ulceration |
|
Plantar and lateral aspect
|
Diabetic ulcer of foot and toes |
| Sun exposed areas |
Basal cell carcinoma; squamous cell carcinoma |
| |
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Wound exudate
Wound exudate may be serous, serosanguinous,
or sanguinous
The quantity of exudate is usually classified
as heavy (+++ (dressing soaked)) medium (++ (dressing wet)), or
minimal (+ (dressing dry))
Excessive exudate may be due to wound
infection or gross oedema in the wound area and may complicate
wound healing
The exudate should be controlled with the use
of dressings appropriate for the level of exudate and any infection
treated
Barrier films applied to the surrounding skin
help to prevent further maceration (see the ninth article in the
series)
The oedematous leg should be raised when the
patient is seated
Quality of life
Several studies have shown that patients with
non-healing wounds have a decreased quality of life. Reasons for
this include the frequency and regularity of dressing changes,
which affect daily routine; a feeling of continued fatigue due to
lack of sleep; restricted mobility; pain; odour; wound infection;
and the physical and psychological effects of polypharmacy.
The loss of independence associated with
functional decline can lead to changes, sometimes subtle, in
overall health and wellbeing. These changes include altered eating
habits, depression, social isolation, and a gradual reduction in
activity levels.
Many patients with non-healing wounds complain
of difficulties with emotions, finances, physical health, daily
activities, friendships, and leisure pursuits.
Healthy granulation tissue in a hidradenitis suppurativa excision.
wound.
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Unhealthy granulation tissue in a venous leg ulcer
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Necrotic tissue (black areas) in a
pressure ulcer.
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Slough at the base of a pressure ulcer.
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Eschar covering a heel pressure ulcer
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Digital examination of a wound.
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Examining a wound with a probe
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Fistula in a diabetic foot ulcer
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Maceration of the skin surrounding a diabetic foot ulcer
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Clinical features of non-healing wounds
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- Absence
of healthy granulation tissue
- Presence
of necrotic and unhealthy tissue in the wound bed
- Excess exudate and slough
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- Lack of
adequate blood supply
- Failure
of re-epithelialisation
- Cyclical
or persistent pain
- Recurrent
breakdown of wound
- Clinical or subclinical infection
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Further reading
Lazarus GS, Cooper DM, Knighton DR, Margolis
DJ, Pecoraro RE, Rodeheaver G, et al. Definitions and guidelines
for assessment of wounds and evaluation of healing. Arch Dermatol 1994;130:
489-93.
Izadi K, Ganchi P. Chronic wounds. Clin Plast Surg 2005;32:
209-22.
Falanga V, Phillips TJ, Harding KG, Moy RL,
Peerson LJ, eds. Text atlas of wound
management. London: Martin Dunitz,
2000.
Stuart Enoch is research fellow of the Royal
College of Surgeons of England and is based at the Wound Healing
Research Unit, Cardiff University.
The ABC of wound healing is edited by Joseph E
Grey (joseph.grey@cardiffandvale.wales.nhs.uk), consultant
physician, University Hospital of Wales, Cardiff and Vale NHS
Trust, Cardiff, and honorary consultant in wound healing at the
Wound Healing Research Unit, Cardiff University, and by Keith
G Harding, director of the Wound Healing Research Unit, Cardiff
University, and professor of rehabilitation medicine (wound
healing) at Cardiff and Vale NHS Trust. The series will be
published as a book in summer 2006.
Competing interests: KGH’s unit receives
income from many commercial companies for research and education,
and for advice. It does not support one company’s products
over another.
Quality of life is not always related to
healing of the wound. It may be clear from the outset that wounds
in some patients will be unlikely to heal. In such patients control
of symptoms and signs outlined above — particularly odour, exudate, and pain — may improve the individual’s quality
of life.
Additionally, optimal chronic wound management
will lead to a reduction in the frequency of dressing changes,
further enhancing quality of life. In a minority of instances,
seemingly drastic measures - such as amputation in a person with chronic leg
ulceration - may need to be considered when the quality of life is
severely affected by the non-healing wound and its complications.
The drawing is adapted from one provided by
Wendy Tyrrell, School of Health and Social Sciences, University of
Wales Institute, Cardiff.
studentBMJ 2006;14:89 - 132 March ISSN 0966-6494