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156 M. Papi and E. Fiscarelli
Sacchelli and co-workers recently examined 866 consecutive patients with
chronic non-healing leg ulcers who underwent skin biopsy of the wound. They
found 7% of neoplasms, more commonly basal and squamous cell carcinomas in
elderly patients (Sacchelli et al. 2018).
Chronic leg ulcers can be misdiagnosed as chronic venous ulcers and mas-
querade a malignant complication (Gil et al. 2015). The neoplastic lesions can
become chronically ulcerated, as the well-known Marjolin ulcer, or present as
ulceration from their early appearance (Khan et al. 2016; Pranteda et al. 2014).
Marjolin ulcer occurs in burned, constantly injured or chronically inflamed skin. It
is mainly a squamous cell carcinoma (Figs. 2 and 3) but it may be histologically
defined by many other pathological types of neoplasms.
Malignant transform
of a chronic ulcer is preferentially toward a
ation
well-differentiated form of squamous cell carcinoma. The clinical verrucous aspect
creates difficulties in histologically distinguishing from a benign pseudoepithe-
liomatous hyperplasia (Pranteda et al. 2014; Senet et al. 2012) (Fig. 4). The clinical
suspicion of a skin cancer may rise from: the development of an exophytic mass,
irregularities of the ulcer bed or thickening, abnormal and extensive granulation,
unusual pain and abnormal bleeding (Figs. 5 and 6).
Fig. 2 Marjolin ulcer. A vegetating squamous cell carcinoma developed in a osteomyelitis sinus
tract
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Fig. 3 Marjolin ulcer. Squamous cell carcinoma complicating a chronic skin ulcer
Fig. 4 Basal cell carcinoma. Hyperplastic nodules are difficult to differentiate from benign
pseudoepithelioumatous hyperplasia
158 M. Papi and E. Fiscarelli
Fig. 5 Chronic ulcers caused by a squamous cell carcinomas
Fig. 6 Basal cell carcinoma recurrently bleeding
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The risk of a tumoral nature of a chronic ulcer increases over time. The necessity
of a skin biopsy is commonly delayed in clinical decision. The opportunity to
obtain multiple samples from a suspected chronic wound, may be encouraged by
the rapid healing of the wound bed edge after punch biopsy (Panuncialman et al.
2010).
Haematologic Ulcers
Haemoglobinopathies-Associated Ulcers
Major haemoglobinopathies complicated by chronic ulcers are sickle cell syndromes and thalassemia disorders.
Leg ulcers are the most common cutaneous complication of sickle cell disease
(SCD). They may be disabling and are often misdiagnosed (Alavi and Kirsner
2015).
They may be caused by various and concurrent pathogenetic processes:
mechanical obstruction due to dense sickle red cells, venous incompetence, bacterial infections, abnormal autonomic control with excessive vasocon striction when
in the dependent position, in situ thrombosis, anaemia with decreased oxygen
carrying capacity, and decreased nitric oxide bioavailab ility leading to impaired
endothelial function. In brief, the increased susceptibility to leg ulcers in people
with SCD is due to a chronic ischaemia and defective immunity. Chronic ischaemia
may be explained by a blood hypercoagulability, venous incompetence, or postural
vasoconstriction, with these mechanisms conditioned by a low nitric oxide that may
itself be genetically influenced.
Skin wounds are prevalent in areas with low subcutaneous fat and which are
frequently traumatized. Medial malleolus of the leg is the preferential site (Fig. 7).
The role of hydroxyurea in the treatment of SCD’s ulcers is still unclear, though
it is the first drug to be approved in the treatment of SCD (Lanzkron et al. 2008).
Pentoxifylline has been administered with success in the vessel-occlusive phases
of the disease. It may be useful in healing ulcers and preventing their recurrence
(Monfort and Senet 2019).
However, allogeneic bone marrow transplantation or peripheral blood stem cell
transplantation are presently considered the best curative therapies for patients with
sickle cell disease (Connor et al. 2017). An updated Cochrane Review of interventions for treating leg ulcers in people with sickle SCD provided a limited
evidence of very low quality that a systemic pharmaceutical interventions (arginine
butyrate) may reduce ulcer size in treated participants compared to controls (MartíCarvajal et al. 2021).
Diagnosis: blood count, detection of haemoglobin anomalies, exclusion of primary venous refluxes.
Leg ulcers are less often seen in b thalassemia in comparison to SCD.
160 M. Papi and E. Fiscarelli
Fig. 7 Chronic bilateral ulcer in a young man (31) with sickle cell anaemia
Polycythaemia Vera and Leg Ulcers
Polycythaemia vera is characterized by an abnormal proliferation of bone marrow
elements, erythrocytes, leukocytes, and platelets. Arterial thrombosis, superficial
thrombophlebitis, leg ulcers, and livedo reticularis may be a complication of the
disorder. Skin ulcers are extremely painful and prevalently located in the acral areas
of the lower limbs and feet (Figs. 8 and 9). They may be improved with the
decrease of the number of platelets or with the treatment with modern biological
molecules (e.g. Jak-1 and 2 inhibitors) (Wirth et al. 1998; Tremblay et al. 2021;
Shanmugam et al. 2013).
Diagnosis: blood count, skin biopsy, arterial circulation assessment, coagulation
screening.
Metabolic Anomalies
Calcific Uremic Arteriolopathy (Calciphylaxis)
Calcific uremic arteriolopathy (CUA) also known as calciphylaxis is the term which
indicates a tissue deposit of calcium frequently secondary to chronic renal insufficiency (CRI). However, the frontier between uremic calciphylaxis and non-uremic
calciphylaxis is difficult to define. CUA seems to be the result of multiple
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Fig. 8 Polycythaemia vera. Acral necrotizing and ulcerative lesions in a 35 years-old male
Fig. 9 Polycythaemia vera. Chronic painful ulcer of the foot and blue toe (40 years old male)
162 M. Papi and E. Fiscarelli
conditions (obesity, bone mineral disease abnormalities, uraemia, inflammation)
with a broad spectrum of variations (Gaisne et al. 2020).
It is clinically characterized by distal cutaneous
following calcium deposition in the media and intimal hyperplasia of the
sub-cutaneous arterioles or by acral gangrene due to extensive calcification of the
media and thickening of the arterial intima of hands and feet. Hafner et co-worker s
debated the pathogenetic role of the secondary hyperparathyroidism noticed in the
course of CRI and in dialyzed patients (Hafner et al. 1995).
In CUA skin ulcers are severe, often multiple, painful and prevalently localized
in the lower limbs (Fig. 10).
On the dorsum of the hands the ulcers can be multiple, symmetrical and present
a typically crater-like aspect (Fig. 11). Hands Rx shows complex thin arteriolar
calcifications.
Therapeutic guidelines and evidence-based recommendations for CUA are only
partially defined (Kodumudi et al. 2020). Calcium-based phosphate binders, Vitamin D and calcium supplements should be avoided. For patients with secondary
hyperparathyroidism and hyperphosphatemia, cinacalcet may be used to correct the
excess of phospho-calcic products. In several cases, parathyroidectomy has allowed
a quick resolution of the pain and the ulcerative lesions by correcting the condition
of secondary hyper-parathyroidism. Treatment of pain is central in this condition.
Diagnosis: kidney function screening (including glomerular filtration rate), calcium phosphate products detection, parathyroid function anomaly, Rx examination
of the lower limbs and hands showing calcium deposit in the arterioles.
necrosis induced by ischemia
Inflammatory and Immune Disorders-Correlated
Vasculitis
Cutaneous vasculitis (CV) is a spectrum of conditions characterized by an angiocentric inflammation diffusely involving the vessels of the skin (Shavit et al. 2018
are caused by the deposition of circulating immunocomplexes in the vessel
They
wall. A smaller group of CV is caused by anti-neutrophils antibodies: they include
mainly cutaneous-systemic vasculitis. The inflammatory infiltration and the severe
vessel damage commonly result in purpuric palpable lesions of the lower half of the
legs. The type, location and calibre of the involved vessel district influence the
localization and severity of the clinical features which may cause cutaneous ulcers.
The vasculitic etiology of a chronic skin ulcer can be usually only suspected. We
often can’t see the early clinical aspects (palpable purpura) of the CV which
commonly tend to heal after some days or weeks (Papi and Papi
histological confirmation of the diagnosis is mandatory for a vasculitic ulcer. Tissue
culture is useful if a suspicion exists of an infective etiology (Papi and Didona
1999).
2016).
The
).
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Fig. 10 Calciphylaxis of the lower limb. Severe necrotic-ulcerative lesions in an elderly female
patient
164 M. Papi and E. Fiscarelli
Fig. 11 Calciphylaxis. Multiple painful non-healing crateriform ulcers of the hand. 71 years old
men under dialytic treatment
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Table 1 Investigation protocol in case of suspected cutaneous ulcerative vasculitis
First level investigation
Confirm Histological examination
Assessment of extracutaneous involvement
- Direct immunofluorescence
- Haemochrome, ESR, PCR, fibrinogen
- Proteic electrophoresis
- Creatinine, blood urea
- GOT, GPT, alkaline phosphatases, cGT
- PT, PPT
-C
3,C4
- Antinuclear antibody (ANA)
- Extractable nuclear antigens antibodies (anti-ENA)
- Antineutrophil cytoplasmic antibodies (c, p-ANCA)
- Cryoglobulins
- Rheuma-test
- Antibodies anti Hepatitis B virus (anti-HBV), antibodies anti Hepatitis C (anti-HCV)
- Urine test
Second level investigation
- Tumour markers
- Virological research (cytomegalovirus, Epstein-Barr, Chlamydia)
- Rx thorax
- Tuberculosis tests
- Electromyography, muscular biopsy
- Selective angiographic tests
Theoretically, any type of CV can cause skin ulcerations due to a focal ischemia
which develops in a small cutaneous area as result of vessel-function loss or a
severe decrease in microvascular blood flow (Papi 2008).
CV are idiopathic in 50% of cases and associated with drug intake, infections,
connective tissue diseases or malignancies in other cases. A laboratory investigation
protocol is necessary to identify skin-limited forms from extracutaneous visceral
involvement (Table 1). Kidney, lung, and gut are the most commonly affected
internal organs.
Panarteritis nodosa, cryoglobulinemic vasculitis and granulomatosis with
polyangiitis (Wegener disease) are commonly associated with cutaneous necrotizing lesions and possibly chronic atypical ulcers (Figs. 12 and 13).
Corticosteroids and other immunosuppressant drugs (most commonly
cyclophosphamide and methotrexate) can be useful in non-healing vasculitic ulcers
caused by cutaneous-systemic vasculitis. In recent years, rituximab has been used
with very good results in many systemic vasculitis (Terrier and Durel 2020).
Topical lidocaine and prilocaine lidocaine help to reduce pain during local
treatments.
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