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132 ATYPICAL CAUSES OF LEG ULCERATION
(a)
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ulceration are the medial and lateral malleolus, the foot and the
Achilles’ tendon (Figure 3.7). The clinical appearance is similar to
ischaemic ulceration with wounds being heavily colonised, presenting
with slough and necrosis. The presence of biolms with episodes of
wound infection is common. The severe pain of the ulceration
isunrelated to size and is against a background of sickle cell pain
from the disease process itself (see Chapter 6) and other organ
complications. Ulceration may be slow and dicult to heal, with
management often being challenging and complex because of the
disease pathology and progression, the site of the ulcer(s) and the
management challenges of SCD. Wound infection and associated
pain may precipitate a sickle cell crisis that in turn has adverse
impacts on wound healing.
(b)
FIGURE3.7 (a, b) Sickle cell ulceration.
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Commonly observed biomechanical changes in those with lower
limb sickle cell ulceration include leg length discrepancy, calf muscle
atrophy, loss of ankle range of motion and the foot xed into a
position of pronation or supination. Hip necrosis may oer further
complications in terms of pain and biomechanical changes (see
Chapter4). Reduced ankle function is common in those with SCD
ulceration due to the pain experienced; pain causes the person to
adapt their gait and walk on the ball of their foot to reduce the pain
and any pull of dressings (Farrelly 2018). While biomechanical
changes are common in those suering from leg ulceration, Farrelly
(2018) states that those with SCD present these changes in the
extreme. Thus, obtaining biomechanical advice is essential for this
cohort. All these factors add to the complexity of management
andhealing outcomes; healing of ulceration may be up to 16 times
slower compared to purely venous disease ulceration (Trent and
Kirsner2004).
Management
Sickle cell management is complex and presents with various care
challenges. The underlying pathology needs to be determined and
medically managed by haematology. Medical management is ongoing
and relates to medication and care of sickle cell crisis episodes, which
will often involve acute admissions. Regular blood transfusions are
appropriate and helpful for some but not all sickle cell patients. Due
to the diverse range of symptoms and the dierent areas of the body
that are aected, care is multidisciplinary and will involve both acute
and community nursing. Besides haematology, it is common for
people to be supported by vascular and specialist SCD teams, tissue
viability, pain teams, social care agencies and more. Cohesive
communication between the dierent professions is foundational to
delivering eective and therapeutic care.
Management will draw on the principles of good leg ulcer
management:
Wound management and regular debridement. See Chapter8 on
clinical management.
Compression therapy remains a cornerstone of clinical
management due to the presence of venous disease or ineective
134 ATYPICAL CAUSES OF LEG ULCERATION
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calf muscle pump resulting from reduced ankle range of
movement. It is critical to recognise that ulceration over the
forefoot or behind the malleolus in the presence of rigid ankles
will reduce the ecacy of a standard compression regime. Nonhealing will exacerbate pain and referral will be required to a
specialist practitioner who may need to provide a more bespoke
compression regime that will optimise compression at the
ulcer bed.
Prevention of recurrence can be supported with hosiery, often
at- knit, and supportive or corrective footwear. See Chapter4 on
biomechanical assessment and Chapter 9 on lifelong
management.
Principles of management for the SCD leg or foot ulcer will be
similar to other leg ulcers.
Together with standard clinical management, it is critical to
provide validation of the person’s pain, their likely struggles working
with a less than perfect healthcare system and, because they are often
of working age, their need to manage all these conicting priorities
alongside their day job. Personalised care (see Chapter7) alongside a
deep understanding of pain management and the patient’s own
triggers is vital for people with sickle cell ulceration.
METABOLIC DISORDERS
Necrobiosis Lipoidica
Necrobiosis lipoidica (NL) is a rare non- infectious inammatory
condition of the skin, predominantly aecting the subcutaneous
tissue (Isoherranen etal.2019; Mistry etal.2017). Although NL- like
lesions can be found alongside conditions such as thyroid disease,
RA, sarcoidosis, inammatory bowel disease and even in otherwise
healthy patients (Murray and Miller1997; Reid etal.2013), it is most
associated with diabetes mellitus (DM). For this reason, it is also
often referred to as necrobiosis lipoidica diabeticorum. Approximately
50–80% of patients with NL will have diabetes or go on to develop it,
although NL only aects about 0.7% of the diabetic population (Feily
and Mehraban2015; Rayner etal.2009).
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The underlying aetiology of NL is largely unknown, but is
thought to relate to reduced blood ow in the microcirculation linked
to diabetes, combined with an immune system/inammatory
response and abnormal collagen degradation (Bonura et al. 2014;
Rayner etal.2009).
History
NL is three times more common in females than males, and onset
usually occurs in young to middle age (Reid etal.2013). Patients will
normally present with a history of DM, although if this is not the
casethen close monitoring for the onset of DM should take place, as
it has been documented as a precursor to the disease (Paron and
Lambert2000).
If presenting with existing ulceration/lesion, patients will
normally have experienced initial signs of demarcated reddened
papules and non- scaly plaques to the skin of the lower leg, most
commonly to the pretibial area (Du etal. 2015). NL can occur in
other areas of the body, such as the hands, face and abdomen, but
this is more unusual (Reid et al. 2013). Patients may report the
presence of plaques for many months or years before lesions develop
(Dissemond etal.2018), with ulceration of the inammatory plaques
aecting approximately 35% of patients (Nelzen et al. 1994).
Ulceration can arise spontaneously, but often occurs following
localised trauma.
Examination
On examination, NL may present in dierent phases of the condition.
In the initial stages, papules or nodules are normally present with
raised, reddened and sometimes hardened, brous edges that can
then slowly coalesce into large, reddened plaques (Figure3.8). The
centre of the lesions usually begins as red/brown colour evolving into
a yellow/brown discoloration that can take on a waxy appearance
(Reid etal.2013). The skin here is often atrophied– shiny, thin and
fragile– with visible ne blood vessels. Lesions should be closely
examined for signs of ulceration or potential breakdown; these
should be monitored on initial examination and on followsigns of malignant changes as the evolution of squamous cell
up for any
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FIGURE3.8 Reddened plaques to the pretibial region associated with
necrobiosis lipoidica.
Source: Used with permission from Cardi & Vale University Health Board.
carcinoma (SCC) has been identied in long- standing lesions
(Santos- Juanes etal.2004).
NL lesions are normally present as multiple, painless lesions
aecting both lower limbs. The lesions can become very painful if an
ulcer develops (Figure3.9) (Lacroix etal.2008).
Investigations
Clinical presentation and patient history are the key components to
making a diagnosis of NL, although skin biopsies can be taken to
conrm the diagnosis. Blood tests for diabetes may be taken where
NL is suspected in patients who are not known to be diabetic (British
Association of Dermatologists2019).
A vascular assessment is recommended due to the increased risk
of PAD present in diabetic patients (Jecoate et al.2006). This can
help to guide appropriate vascular interventions and compression
therapy following diagnosis if required.
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FIGURE3.9 Ulcerated necrobiosis lipoidica.
Source: Dissemond etal. (2018) / John Wiley & Sons. Reproduced with
permission.
Diagnosis
Clinical diagnosis is usually made based on the identiable skin
changes seen on examination and on the evolution of these skin
changes as described by the patient. If a skin biopsy has been taken
to conrm a diagnosis, the histological examination would indicate
granulomas and inammatory reaction around destroyed collagen,
and thickening of blood vessel walls (Oakley2021). This aligns with
the disease processes thought to cause the development of NL as
described earlier, namely reduced blood ow, immune response and
abnormal collagen degradation.
Intervention
Treatment for NL can be challenging and inconsistent due to a lack
of substantial evidence to support various treatment options. If
associated with diabetes, improved diabetes management and
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glycaemic control can contribute to the improvement and eventual
healing of any ulcerations, although this is not always the case
(Mistry etal.2017). The condition can be self- limiting, spontaneously
resolving in up to 17% of cases (British Association of
Dermatologists2019).
The mainstay of treatment for NL is often topical or intralesional
steroid therapy, with the occasional need for oral steroids (Du
etal.2015). Topical steroids should be applied to the active borders of
lesions, avoiding the thin and fragile atrophic areas in the centre
(Reid etal.2013). Other topical treatments and systemic medications,
such as tacrolimus, pentoxifylline and phototherapy, have been used
with varying results (Feily and Mehraban2015; Reid etal.2013) and
would only be commenced following specialist dermatology advice.
Identifying and managing infection can be challenging but
important with diabetic patients. The disease process of diabetes
leads to an altered local and systemic inammatory and immune
response, meaning that the incidence and severity of infection are
increased in diabetic patients and innate defence is poor (Edmonds
and Sumpio 2019). A diminished systemic response and other
complications of diabetes, such as neuropathy and reduced blood
supply to the lower limb, can lead to classic signs and symptoms of
infection being lesser or absent, thus diagnosis can be delayed and
progression more rapid than normal (Edmonds and Sumpio2019).
Poorly controlled diabetes is also associated with an increased risk of
wound infection (IWII2022). This, along with the altered response to
infection with diabetes, leads to wounds being classed as at high risk
of infection and so judicious prophylactic use of topical antimicrobials
may be appropriate in these cases (IWII2022).
While there is no conclusive evidence on the benets of
compression therapy with NL, particularly as a rstanecdotal evidence and expert opinion have recommended it for
treatment and prevention if there are no other contraindications, due
to the clinical benets associated with reduced oedema and
inammatory cytokines and improved microcirculation that are
achieved with compression therapy (Erfurt- Berge et al. 2015;
Isoherranen etal.2019; Zhang and McMullin2022). Padding of the
lesions using simple gauze pads, absorbent pads or soft cotton
wadding is also recommended to reduce the risk of injury and
ulceration. These can be applied directly over the area of ulceration
line treatment,
Atypical Causes of Leg Ulceration 139
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to provide protection of fragile skin and plaques, or in the case of soft
cotton wadding used underneath compression therapy, applied to the
lower leg as recommended by the manufacturer of the specic
compression system used.
Martorell’s Ulcers
Martorell’s ulcers, sometimes referred to as Martorell hypertensive
ischaemic leg ulcers (HYTILU) or due to ischaemic arteriolosclerosis, are a rare condition that can occur in patients with prolonged,
severe or sub- optimally controlled hypertension (Graves etal.2001;
Mansour and Alavi2019). The eect of prolonged hypertension is to
cause localised tissue ischaemia and skin infarction due to the
increased resistance in blood vessels and narrowing of the arterioles
(Isoherranen etal.2019).
History
Martorell’s ulcers were originally more common in females than
males, particularly between the ages of 55 and 65 years, although in
more recent studies males and females can be equally aected
(Hafner etal.2010; Mansour and Alavi2019). Approximately 60% of
patients will also have type 2 DM and 50% will have PAD (Hafner
etal.2010).
Examination
Martorell’s ulcers often manifest as lower leg ulcers above or around
the ankle, to the outer posterior region or over the Achilles’ tendon
that gradually worsen, contain dry, necrotic tissue and are
disproportionally painful to the size of the wound (Figure 3.10).
Initially Martorell’s ulcers can present as dusky, painful plaques with
a mottled appearance to the surrounding skin.
Investigations
Alongside assessment of the clinical presentation, a tissue biopsy is a
key investigation if there is a suspicion of arteriolosclerosis linked to
hypertension being the underlying cause of the ulceration. Biopsy
140 ATYPICAL CAUSES OF LEG ULCERATION
(a) (b)
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FIGURE3.10 (a) Martorell’s ulceration to the lower limb with typical dry
necrotic tissue and (b) progressing to an ulcer with a livid edge and
satellite lesions.
Source: King etal. (2017) / John Wiley & Sons. Reproduced with
permission.
ndings would show thickening of the small–medium arterial walls
and narrowing of the vessels.
A vascular assessment is also recommended due to the high incidence of PAD with Martorell’s ulcers to determine the need for vascular intervention, such as angioplasty (Isoherranen etal.2019).
Diagnosis
The diagnosis of Martorell’s ulcers must primarily be dierentiated
from calciphylaxis and PG. Martorell’s ulcers are most misdiagnosed
for these conditions, which can adversely aect outcomes. Treatments
for each condition are signicantly dierent, and if incorrect
treatments are given wounds can be exacerbated rather than
Atypical Causes of Leg Ulceration 141
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improved. Thus, it is important to identify the correct aetiology before
treatment plans are formulated. Once other typical causes of
ulceration have been excluded and the histopathology results of the
biopsy are supportive (usually indicated by the thickening of some
layers of the arterial walls), a diagnosis of Martorell’s can be made.
Intervention
A key area of the treatment plan for this aetiology to promote wound
healing involves a multidisciplinary approach to optimise antihypertensive medication and pain control, and to assess the need for
early surgical intervention. A multidisciplinary approach to engaging
with the patient will also be important if there are lifestyle issues, such
as poor diet and smoking, and other co- morbidities, particularly poorly
controlled diabetes, that are contributing to the challenge of controlling
hypertension and increasing cardiovascular risk.
Early surgical intervention has been suggested to give the best
outcomes, particularly for larger areas of ulceration, and may take
the form of surgical debridement, application of negative- pressure
wound therapy and, in some cases, use of split- thickness skin grafting
(Dagregario and Guillet 2006; Hafner et al. 2010). While pain
reduction is usually experienced quite quickly following surgical
treatment, appropriate analgesia will be required up to this point and
beyond as clinically indicated.
Electrostimulation, achieved through commercially available
medical devices that deliver a lowdressing electrode on intact skin, has also been shown to have some
success in those patients unsuitable for surgical intervention (Leloup
et al. 2015). Electrostimulation is thought to encourage wound
healing by promoting new blood vessels within the wound, wound
debridement and increasing granulation tissue by restoring the skin’s
natural electrical eld. It has also been found to be benecial for
wound pain in some cases (Leloup etal.2015).
voltage electrical current via a
Calciphylaxis
Calciphylaxis is a rare and complex condition that is mostly
associated with end- stage renal failure (ESRF) in patients usually
receiving haemodialysis (Nigwekar et al.2018). It occurs due to
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