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112 ATYPICAL CAUSES OF LEG ULCERATION
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Intervention
The management of PG is often challenging due to a lack of
recognised clinical guidelines and is usually based on disease severity
and the extent of PG (George etal.2019; Fletcher etal.2019). Early
identication of PG is essential to ensure that prompt referral to an
appropriate speciality such as dermatology is undertaken, and that
treatment with systemic therapies is instigated in a timely manner
(George etal.2019). Treatment options must be patient centred and
consider patient preferences, location and size of the wound,
underlying systemic disease and possible side eects of interventions
(Fletcher etal.2019). Delays in appropriate interventions may result
in delayed healing and have a signicant impact on an individual’s
quality of life, which may include pain, low self- esteem and scarring.
Treatment for PG is described in the following sections.
Reducing Systematic Inflammation
Local topical therapy with potent corticosteroids or tacrolimus
ointment to the wound and aected surrounding skin can be
instigated as an adjunct to systemic treatment. Topical therapy alone
is not usually sucient to manage PG (George etal.2019).
The rst line of systemic treatment is oral corticosteroids. These
can be used on their own or in conjunction with immunosuppressants
such as cyclosporine. More recently there has been growing evidence
to support the use of biologics such as iniximab to improve healing
and remission rates (George etal.2019). Biologics assist in promoting
a pro- inammatory environment and act as a chemoattractant for
neutrophils, and have been useful for patients who have been
unresponsive to corticosteroids and immunosuppressant therapies
(Maronese et al.2022). Due to the many possible side eects and
contraindications, systemic therapies are usually commenced and
monitored by a dermatologist throughout the treatment.
Optimising theLocal Wound Environment
Local wound management goals should address the outcomes of the
wound assessment using the TIMES framework and the principles of
moist wound healing. Dressings selected should manage exudate
appropriately while allowing atraumatic removal. Mechanical or
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surgical debridement to devitalised tissue within the wound bed
would only be considered if the PG was responding to systemic
treatment and should be carried out by a trained HCP due to the risk
of wound enlargement (Isoherranen et al. 2019). Less traumatic
methods of debridement can be considered, such as utilising
dressings that support autolytic debridement or larvae therapy
(Isoherranen et al.2019). Wound bed preparation and methods of
debridement are discussed fully in Chapter5.
Corticosteroids and immunosuppressant agents are known to
suppress the activity of the immune system, which results in an
increased risk of developing an infection for patients who have these
prescribed to manage their PG (Youse etal.2016). Wound infection
is discussed in Chapter5. HCPs should familiarise themselves with
the signs and symptoms of infection and be particularly vigilant in
this patient group. If infection is suspected, antimicrobials should be
initiated accordingly (International Institute of Wound Infection
2022). For example, topical antimicrobials should be commenced if
local wound infection is suspected. Systemic antibiotics should be
prescribed if spreading infection/sepsis or systemic infection is
present. Prescribing of any antimicrobial must follow local prescribing
policy and guidance (see Chapter5).
Compression therapy is advocated if oedema is present to support adjunctive therapies and the wound healing environment
(Fletcher et al. 2019). The importance of compression therapy to
aid healing in PG is undecided, but expert opinion is that compression therapy is benecial for all patients with lower extremity
wounds (Isoherranen etal. 2019). Compression to counteract the
impact ofgravity remains a cornerstone of treatment (Partsch and
Mortimer2015).
Compression can be instigated safely after an assessment of
vascular status (see Chapter 5). Due to the pain experienced in
patients with PG, it may not be possible to instigate full compression
at 40
mmHg and therefore it may be more acceptable for the patient
to start at a lower compression of 20 mmHg (Isoherranen etal.2019).
Wrap systems and hosiery are available in reduced compression
formats, bandage systems can also be adapted to provide reduced
compression and familiarity with compression products is an
important part of treating and managing any patient with leg
ulceration. Types of compression therapy are discussed in full
inChapter8.
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Appropriate Management ofPain
Patients with PG often present with high levels of uncontrolled pain.
Appropriate pain management is therefore an important part of the
patient’s treatment pathway and should be guided by the type, duration
and severity of the pain, as identied within the patient’s pain
assessment. The type of pain experienced may be a signicant inuence
in the choice of analgesia (Brown2015). For example, neuropathic
pain, which is usually associated with nerve damage, is often described
by the patient as tingling, shooting pain, burning, stabbing or pins and
needles (Brown2015). Conversely, nociceptive pain is associated with
damaged tissue and can be described as aching or throbbing
(Brown2015). Various resources are available to guide decision- making
around analgesia prescribing, as outlined in Chapter 6. Should
neuropathic pain be present, certain neuropathic medications may be
helpful such as antidepressants or anticonvulsants, including
amitriptyline or gabapentin (Anekar and Cascella2023). As with any
analgesia, the eectiveness should be monitored and reassessed at each
dressing change using a personalised approach; see Chapter6 for more
exploration.
Vasculitis
Cutaneous vasculitis is an inammatory event that causes inammation and damage to the walls of the blood vessels (Rayner etal.2009).
The condition can aect any blood vessel or any organ and is usually
classied by the size of the vessels that are involved. Large vessel vasculitis aects the large and medium- sized arteries, while small vessel
vasculitis aects the small arteries, arterioles, capillaries and small
veins (Isoherranen etal.2019). The resulting ischaemia due to vessel
damage often leads to skin necrosis and ulceration (Isoherranen
et al. 2019). Cutaneous vasculitis has several manifestations
(Table3.3). The severity of symptoms and whether there is organ
involvement dictate treatment choice (Micheletti 2022). Vasculitis
can be triggered by reactants such as infection, malignancy, medications and connective tissue diseases (Weinstien etal.2012).
History
The patient may have a history of general malaise, joint pain, fever
and raised inammatory markers. Vasculitis may also be associated
with autoimmune disorders such as RA, scleroderma or lupus
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TABLE3.3
Examples of
cutaneous vasculitis
Takayasu arteritis
Giant cell arteritis
Polyarteritis nodosa
cutanea (cutaneous
arteritis)
Microscopic polyarteritis
Granulomatosis with
polyarteritis
Leucocytoclastic
vasculitis
Churg Strauss syndrome
Cutaneous
immunoglobulin
(Ig)M/IgG
Vasculitis associated
with systemic disease
(e.g. rheumatoid
vasculitis)
Some common forms ofvasculitis.
Vessels
involved Clinical features
Large vessel
vasculitis
Medium vessel Often localised to the lower leg
Small vessel Palpable round and
Small vessel
disease
Usually aect large arteries
such as aorta
Skin manifestations are rare
Occasionally necrosis is
observed if the
extracutaneous arteries that
feed the skin are aected
May be associated with
infection (e.g. hepatitis B,
hepatitis C or Streptococci),
but can also be drug induced
Palpable subcutaneous
nodules are often seen
Deep ulceration may occur
inammatory purpura
Livedo (a network-
of reddish-
discoloration)
Haemorrhagic nodules
Palpable round
inammatory purpura
Livedo
Haemorrhagic necrosis
like pattern
blue skin
Source: Adapted from Isoherranen etal. (2019) and Micheletti (2022).
( Todhunter2019). Other factors that can contribute to vasculitis are
infection and some medications, for example anticoagulants, penicillin and sulphonamides (Rayner etal.2009).
Examination
The appearance of vasculitis diers according to the size of the blood
vessel that is aected (Weinstien etal.2012). Vasculitis aecting the
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FIGURE3.3 Typical presentation of vasculitis.
Source: Used with permission from Cardi & Vale University Health Board.
small vessels, such as leucocytoclastic vasculitis, often presents with
regular lesions and ulcers on the skin, while large or medium vessel
vasculitis, such as polyarteritis nodosa, may present with irregular
widespread purpura, necrosis and ulceration (see Table 3.3)
(Falanga2007; Weinstien etal.2012).
The typical clinical presentation of vasculitis includes
(Figure3.3):
Rash
Purpura
Necrosis
Painful wounds
Investigations
The most common investigation to conrm the diagnosis of vasculitis
is a tissue biopsy for histological examination (Isoherranen etal.2019).
Tissue biopsies are only helpful if performed as early as possible after
the presentation of symptoms. Biopsies performed later in the disease
process may not be able to adequately detect the inammatory cells
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and their by- products that are usually present in vasculitis lesions
(Weinstien etal.2012). Biopsies may reveal inammation within the
blood vessels and can be used to assist in diagnosis. Blood tests such
as erythrocyte sedimentation rate (ESR) or C- reactive protein can
reveal the presence of inammation, or antineutrophil cytoplastic
antibody (ANCA) is a blood test used to identify specic proteins that
are associated with vasculitis (Isoherranen etal.2019).
Diagnosis
Diagnosis of vasculitis will primarily be based on the observable
criteria seen on examination, such as palpable purpura and necrosis,
although it can mimic other disorders. Test investigations that may
assist in diagnosing vasculitis are a raised ESR or C- reactive protein,
a positive ANCA result, along with a biopsy that may indicate
inammation within the blood vessels.
Intervention
The main objective in managing patients with vasculitis is to establish
and treat the causative factor (Falanga2007), Treatment will also be
guided by the severity of the disease and whether there is internal
organ involvement (Micheletti 2022). A multidisciplinary approach
may be required to assist in management due to the lack of robust
evidence to indicate the most eective treatment and the complexities
that may accompany the disease (Micheletti 2022). Reduction of
inammation is usually a priority for treatment and drugs that can
reduce inammation and are commonly used. Firstare corticosteroids, dapsone or colochine (Micheletti 2022). Topical
steroids can be used if the surrounding skin becomes itchy and oral
non- steroidal anti- inammatory drugs (NSAIDs) can be helpful to
reduce inammation locally (Micheletti2022). For systemic or severe
vasculitis, immunosuppressants may be considered (e.g. methotrexate,
azathioprine). For vasculitides that are unresponsive, treatment with
biologics may be considered (Micheletti 2022). Due to the lack of
robust clinical studies into the treatment of vasculitis and the fact that
management is often variable and based on expert opinion, further
studies in this area are needed to support implementation practice
(Micheletti2022).
line considerations
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Local wound management should follow the principles of
TIMES as outlined in Chapter5. If oedema is present, elevation of
the limb can be helpful to reduce swelling (Micheletti2022).
Rheumatoid Arthritis
RA is a chronic systemic inammatory disease that is thought to
aect about 1% of the population (NICE 2020). Leg ulceration
develops in approximately 10% of patients with RA (Chakrabarty and
Phillips2003). These wounds often have poor outcomes, such as nonhealing, and have been linked to an increased risk of amputation and
a higher incidence of mortality (Jebakumar etal.2014). Table3.4 lists
the co- morbidities and risk factors that are associated with leg ulcers
in RA, highlighting the multifactorial nature of ulcer development
that can be attributed to several dierent aetiologies.
RA is also a well- documented co- morbidity in patients who
develop PG and vasculitic ulceration, therefore assessment of the
underlying cause is important, as the disease may occur concurrently
and require additional treatment approaches.
The treatment for RA can make clinical management of any
associated leg ulceration challenging due to the inammatory nature
of the disease process, which needs to be brought under control. RA is
often treated with steroid therapy and immunosuppressive treatments,
such as disease- modifying anti- rheumatic drugs (DMARDs) and
tumour necrosis factor (TNF) inhibitors (e.g. iniximab), which have
TABLE3.4
rheumatoid arthritis (RA).
Severity and duration of RA Venous disease
Age Arterial disease
Medication to treat RA (e.g.
oral
immunosuppressant agents)
Diabetes and/or neuropathy Venous thromboembolism
Cardiovascular disease Limited ankle movement and reduced calf
Pressure damage Vasculitis
Source: Adapted from Isoherranen etal. (2019); Jebakumar etal. (2014); NICE (2020).
Co- morbidities andrisk factors forleg ulceration in
corticosteroids and
Mixed vessel disease
muscle pump function
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a known link with delayed wound healing (Bootan 2013).
Immunosuppressive treatments reduce the production and/or
proliferation of the inammatory mediator cells that are required to
regulate the normal wound healing process (Bootan2013). Anti- TNF
treatment can have an adverse eect on the immune system overall,
and as a consequence patients can be more susceptible to wound
infection (Firth and Critchley2011). Corticosteroids can also adversely
aect the inammatory, proliferative and maturation stages of wound
healing, preventing normal cell division, which leads to delayed
epithelialisation and fragile, thinned skin, and causing vasoconstriction,
which reduces blood supply to the tissues (Firth2005).
History
Patients will present with a history of RA that is often long- standing,
as the risk of ulceration increases with the duration of the disease
(Rayner etal.2009). Patients will also often have a concurrent history
of venous and/or arterial disease, with suggestions that peripheral
arterial disease (PAD) occurs concurrently with RA in approximately
a third of patients, and venous insuciency in approximately half of
patients (Hafner etal.2010; Seitz etal.2010). Rates of macrovascular
disease are higher than expected in patients with RA due to a
proposed link between the pathology of RA, endothelial cell
dysfunction and the formation of atheroma (Firth2005). Immobility
and reduced ankle movement due to xed ankle joints can lead to
calf muscle pump failure, contributing to reduced venous return
(Jebakumar etal.2014); an increased risk of venous thromboembolism
has also been identied in association with RA (Conforti etal.2021).
In addition, patients may experience peripheral neuropathy as a
result of nerve damage from joint deformity (Firth2005).
There can be evidence of foot deformities and rheumatoid
nodules. Nodules usually occur over bony prominences, such as the
elbows, ankles and heels, and can vary in size. Prominent nodules
can mean that there is increased pressure and friction on the skin
from external factors, such as footwear and mobilising, which can
lead to skin breakdown and ulceration (Firth2005). Joint destruction
and joint displacement aecting the muscles in the foot from RA
cause various foot deformities, such as claw and hammer toes, hallux
valgus (bunion), attening of the arch of the foot and valgus heel
120 ATYPICAL CAUSES OF LEG ULCERATION
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deformities (Firth2005). All these issues also contribute to increased
pressure, friction and potential for trauma to the skin of the foot and
ankle, which can result in ulceration (Figure 3.4), particularly if
associated with a loss of protective sensation due to neuropathy.
Due to the multifactorial causes of leg ulcers in patients with RA,
there can be confusion or inconsistencies around what to classify as
the ulcer aetiology– as pressure is a frequent contributing factor in
ulcer development, it can be dicult to decide if the ulcer is a
pressure ulcer or a rheumatoid ulcer. The same debate has raised its
head for many years around the classication of diabetic foot ulcers
and pressure ulcers, particularly to the heel (Greenwood2021; Ousey
etal.2011). There is some suggestion that if the ulcer occurs on a
bony prominence, such as the posterior aspect of the heel, in an
immobile or bedbound patient, then the most likely cause is pressure;
if it occurs in an area of the foot or ankle aected by ill- tting
footwear, for example, in a mobile patient, then the underlying
disease could be considered the primary cause (Greenwood2021).
Ultimately, regardless of the label given to the wound, the common
denominator is the reduction of pressure where this is deemed to be
FIGURE3.4 Punched- out ulceration to the foot with visible foot deformity
due to rheumatoid arthritis.
Source: Used with permission from Cardi & Vale University Health Board.
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a contributory factor, and also holistic assessment and management
of the patient (Ousey et al.2011). Consideration should always be
given to the eect that the underlying disease, in this case RA, is
having on the potential for delayed wound healing and increased risk
of wound complications to ensure that an appropriate management
plan is devised that covers all aspects that are contributing to the
wound development and progression.
Examination
Leg ulceration related to RA will typically present on the lower gaiter,
ankle and foot and can be associated with high levels of pain. Lesions
may include nodules, purple non- blanching papules, plaques,
bruising and signs of ischaemic involvement to the lower limb, such
as pale or discoloured, hairless, shiny skin and pain on elevation
(Chakrabarty and Phillips2003). Wound beds are often sloughy with
clear demarcation of the wound edge, often appearing punched out
in the same way as arterial ulceration (Figure3.4).
Mobility status should be assessed during the examination to
decide if immobility, footwear or other potential sources of pressure
are contributing to the ulcer.
Investigations
A vascular assessment is recommended due to the known link with
venous and arterial disease. Testing for neuropathy is useful to
determine if loss of protective sensation is a potential causative factor
for the development of the ulcer and should be considered as part of
the management plan.
A skin biopsy can help to determine any cosuch as vasculitis or PG, and to rule out other causes, such as
malignancy and atypical infections.
Diagnosis
A diagnosis of rheumatoid ulceration is made in the rst instance
based on the patient’s history and examination, namely a diagnosis
of RA and signs of disease progression, such as foot and joint
deformity, rheumatoid nodules and neuropathy. The diagnosis is
often multifactorial and considered in relation to signs and symptoms
existing pathology,
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