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176 M. Papi and E. Fiscarelli
Fig. 19 Hydroxyurea ulcer in the supra-malleolar area. Typical linear hyperpigmentation of the
nail
Atypical Wounds and Wounds Resulting from Infection 177
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Drug-Related Cutis Embolism (Nicolau’s Disease)
Drug related cutaneous embolism (DICE) called also “ Nicolau livedoid dermatitis”
is an adverse reaction to drugs that arises in the seat of intra vascular injection of
various drugs whose pathogenesis is uncertain.
It has been reported as being caused by penicillin injection, ant-inflammatory
non steroidal drugs, local anaesthetics, antihistamines, steroids and vitamin B
complex. Less frequently, it has been observed after administration of pyradolon,
chlorpromazine, interferon alfa and beta, vaccines and anodynes (Sarifakioglu
2007).
Clinically, it is characterized by sharp pain that arises immediately after intramuscular injection with quick appearance of paleness due to local vasospasm. In the
following 24 h a livedoid reticulum appears that, in some patients, can present with
a haemorrhagic aspect with cutaneous and subcutaneous necrosis that might involve
muscles and develop deep ulcers difficult to heal (Fig. 20).
It has been reported more frequently on the glutei but other localizations, such as
shoulder, thigh and knee have been reported.
Generally, there is not supra-infection; if the glutei are involved, livedoid dermatitis can be associated to rectal haemorrhage up to the transitory or permanent
ischemia of the homolateral limb.
Neurological disorders, such as hypoesthesia and paraplegia, are possible; an
increase of hepatic enzymes and creatine-phosphokinase can occur.
Fig. 20 Drug-related cutis embolism (Nicolau’ s disease) Initial necrotic-livedoid lesion soon after
a penicillin injection. A severe-chronic ulcer developed after 2 weeks
178 M. Papi and E. Fiscarelli
It involves mainly adult patients, although some cases have been reported also at
paediatric age.
Presumably, MCE pathogenesis is of vascular origin, as proven by the histological aspects characterized in some cases by thrombotic phenomena in the
medium and small size vessels at the reticular dermis level: a periarterial or
perivenous injection causes the stimulation of the sympathetic nerve endings, thus
causing sharp pain, vasospasm with consequent ischemia and cutaneous necrosis.
Diagnosis: intramuscular injection, glutei most common area, pain.
Warfarin-Induced Skin Necrosis
Warfarin-induced skin necrosis (WISN) is a rare but well-known complication of
warfarin treatment with literature estimating WISN to cause complications in
between 0.01 and 0.1% of patients on warfarin (Murad et al. 2014). WISN is
thought to be caused by the paradoxical prothrombotic state that arises from warfarin therapy as a result of an initial relative decrease in vitamin K-dependent
clotting factors (e.g. protein C). This imbalance can cause microthrombi which
interrupt blood flow to the skin and cause necrosis. Protein C, S and antithrombin
III deficiencies are, in fact, considered risk factors for WISN.
Drug Abuse
Chronic skin ulcers are rare among healthy young adults. Local injection of cocain e
and heroin has been identified as a cause of chronic skin ulcers in young adults
abusing intravenous drugs (Sönmez Ergün et al. 2012).
Chronic skin ulcers in young adults should be an indication of intravenous drug
abuse and should be considered in the differential diagnosis of nonhealing AW
(Fig. 21). Abscesses are common in those who use heroin because the substance is
not sterile and is often mixed with citric acid. Citric acid can also cause acid burns in
the vessels or subcutaneous tissues, leading to necrosis. When an user cannot find a
good site (skin popping), the drug can build up under the skin and be absorbed into
subcutaneous tissues and result in clinically atypical skin ulcers (Onesti et al. 2014).
Ulcer Resulting from Arterial Hypertension (Martorell
Hypertensive Ischemic Ulcer)
Martorell hypertensive ischemic leg ulcer (HYTILU) is an uncommon but probably
underestimated lower extremity wound characterized by progressive, painful
unique or multiple necrotic ulceration. “Necrotic angiodermitis” is the descriptive
term used in French literature but it is also indicated with the term “ulcer with
cyanotic and purpuric edges”.
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Fig. 21 Drug abuser atypical leg ulcer
It is included in the group of organic microangiopathies due to its characteristic
clinic-histological aspects. It prevalently affects females. The local micro trauma
can be a triggering factor. It is characterized by purplish plaques with central
necrosis that tend to extend to the periphery with livedoid-inflamed edges that
progressively necrotize (Fig. 22). During its evolution we can observe one or
180 M. Papi and E. Fiscarelli
Fig. 22 Hypertensive ulcer in a 71 years old male with arterial hypertension. Livedoid and
inflamed aspects of the periulcerative area
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multiple necrotic, blackish plaques that, although superficial, are strongly attached
to the deep dermis, are very painful with surrounding erythematosus and/or purpuric skin. It is a less rare pathology than thought and generally associated to badly
controlled arterial hypertension (90% of cases). The most frequent location is on the
legs and the lesions are often multiple or bilateral. It tends to relaps (Alavi et al.
2012; Lima Pinto et al. 2015
). The necrosis that is observed at the beginning can be
removed quite easily and, when it is superficial, the ulcer may rapidly heal. The
histological picture is characterized by arteriosclerosis of the deep dermis arteries
associated with sub-endothelial non-specific hyalinosis, intima thickening, concentric hyperplasia of the muscle smooth media muscle fibres and substantial
reduction of the vessel lumen. Such alterations sometimes are also present on areas
althy skin of the same patient.
of he
The distal wrists are palpable and the exams confirm the absence of occlusive
arteriopathies of the larger vessels and in anomalies in the venous circulation.
These ulcers are typical of young people with severe hypertension, according to
Martorell’s initial description. The functional and structural alterations on hypertensive basis firstly involve the cutaneous arterioles narrowing and might be
responsible for an increased “vascular resistance” and a reduced “perfusion pressure”.
The thera py must first aim at reducing the hypertension and mitigating the pain.
Early surgical management is the most valuable definitive treatment for Martorell HYTILU. Ulcers > 3 cm in diameter benefit from surgical debridement of
necrotic tissue followed by split-thickness grafting (Conde Montero et al. 2018)
Prostanoids, pentoxifylline, and other vasodilators have been used with variable
results.
Diagnosis: arterial hypertension out of control, presence of peripheral arterial
pulses, pain.
Atypical Ulcers Associated to Infections
Chronic wounds are always contaminated by microorganisms originating from the
surrounding skin. The initial bacterial burden, virulence and capacity of invading
pathogens to grow within biofilms, together with the ability of the host to create
protective immune responses may cause the development of an ulcer infection.
Chronic wounds can also occur as a result of a primary infection with microorganisms. Some of woun ds may be clinically unusual and do not respond to standard
care treatments.
Mycobacterial-Induced Ulcers
Tuberculosis (TB) is still prevalent in many developing countries and can pose a
new potential threat to global health due to international migration. In 2020, the 30
high TB burden countries accounted for 86% of new TB cases. Eight countries
182 M. Papi and E. Fiscarelli
account for two thirds of the total, with India leading the count, followed by China,
Indonesia, the Philippines, Pakistan, Nigeria, Bangladesh and South Africa (data
from World Health Organization 2021).
As an uncommon form of extrapulm
onary TB, cutaneous TB is complicated in
its clinical manifestation, pathogenesis, and classification (Kaul et al. 2022a, b).
Cutaneous TB can be divided into two major categories, true cutaneous TB and
tuberculid, depending on the source of infection, the route of transmission, the
amount of bacteria, and the immune state of the host. Clinical manifestations may
include patches and plaques (lupus vulgaris, TB verruc osa cutis), macules and
papules (acute miliary TB, papulonecrotid tuberculid, lichen scrofulosorum), nodules, and abscesses (erythema induratum of Bazin, tuberculous gumma), erosions,
and ulcers (tuberculous chancre, orificial TB (Fig. 23), scrofuloderma), mimicking
diverse skin diseases.
Cutaneous mycobacterial infections may cause a wide range of clinical manifestations, which are divided into four main disease categories: (i) cutaneous
manifestations of Mycobacterium tuberculosis infection, (ii) Buruli ulcer caused by
Mycobacterium ulcerans and other related slowly growing mycobacteria,
(iii) leprosy caused by Mycobacterium leprae and Mycobacterium lepromatosis,
and (iv) cutaneous infections caused by rapidly growing mycobacteria. Clinically,
cutaneous mycobacterial infections present with widely different clinical presentations, including cellulitis, nonhealing ulcers, subacute or chronic nodular lesions,
abscesses, superficial lymphadenitis, verrucous lesions, and other types of findings.
Mycobacterial infections of the skin and subcutaneous tissue are associated with
Fig. 23 TBC ulcerative lesion in periorificial area
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severe stigma, deformity, and disability. Geography-based environmental exposures influence the epidemiology of cutaneous mycobacterial infections. Cutaneou s
tuberculosis exhibits different clinical phenotypes acquired through different routes,
including via extrinsic inoculation of the tuberculous bacilli and dissemination to
the skin from other sites, or represents hypersensitivity reactions to M. tuberculosis
infection.
Buruli Ulcer
Buruli ulcer is a chronic skin wound due to the infection of Micobacterium ulcerans
(Clancey 1964; Kumar et al. 2015). It is the third most common mycobacterial
disease worldwide, The identification of a microdeletion on chromosome 8 in a
familial form of severe Buruli ulcer suggested a monogenic basis of susceptibility
(Manry 2020) It prevalently occurs in tropical developing countries. It has been
reported in several countries in Africa, the Americas, Asia and the Western Paci fic.
Most cases occur in tropical and subtropical regions (Guarner 2018). The higher
concentration of cases has been reported West Africa. Buruli ulcer has been widely
described also in Australia (Johnson and Roltgen 2019).
The mycobacteria produce mycolactones that cause tissue necrosis. The disease
presents as a painless skin nodule that ulcerates as necrosis expands (Fig. 24).
Finding acid-fast bacilli in smears or histopathology, culturing the mycobacteria,
and performing M. ulcerans PCR in presumed cases confirm the diagnosis.
The skin and the bone are the favourite target organs. The chronicity of the
lesion may lead to disfigurement and disability. M. ulcerans is environmental but
the exact mechanism of transmission is still unclear. Rifampicin (10 mg/kg once
daily) and clarithromycin (7.5 mg/kg twice daily) for 8 weeks is now the first-line
treatment (Yotsu et al. 2018).
Lehismania
The protozoan parasite Lehismania (L) is another major cause of primary infectious
ulcers. Cutaneous Leishmaniasis (CL) is endemic in 88 countries.
Ninety percent of cases present as CL, but the infection may also affect internal
organs (visceral leishmaniasis). Nodular lesions on exposed skin with a tendency to
ulcerate over time in combination with a travel history should therefore do a prompt
workup for leishmaniasis (Fig. 25). The diagnosis is made through histology,
parasite culture, and PCR using biopsy material (Handler et al. 2015).
It is caused by the protozoa of the genus L. The disease is transmitted by
phlebotomes: Phlebotomus (P) sp. in the Old World and Lutzomyia in the New
World. The carriers are represented by dogs, mice, rats, wild rodents and, more
rarely, by humans. In the Mediterranean basin, CL is commonly observed: L
infantum, transmitted by P. Perniciosus and P. Perfiliewi, is responsible for most
cases. On the clinical side, the leishmaniasis of the Mediterranean basin is
184 M. Papi and E. Fiscarelli
Fig. 24 Buruli’s ulcer in a 32 years-old male from Sudan
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Fig. 25 Ulcerated cutaneous leishmaniasis in 18 years old Italian boy
characterized by a single polymorphic lesion, localized to the uncovered areas,
especially the face, followed by the upper limbs (Fig. 24).
Atypical lesions may include the following
forms: erythematous volcanic ulcer,
lupoid, eczematous, erysipeloid, verrucous, dry, zosteriform, paronychial,
sporotrichoid, chancriform and annular (Meireles et al. 2017).
In recent years, various cases of cutaneous L caused by tropical and sub-tropical
species of leishmaniasis, such as L. tropica, L. mexicana, L. panamensis and L.
brasiliensis, have been observed in the Western world, especially in tourists
returning from trips to exotic countries: the latter may cause ulcers localized on the
wrist and back of the hands, often atypical and very painful.
Deep Fungal Infection-Related Atypical Wounds
Sporothricosis
Cutaneous sporotrichosis is the most common form of this fungal infection. It
usually occurs on a person’s hand or the arm after touching contaminated plant
matter. Sporotrichosis is caused by scratches or bites from animals, above all cats.
Sporothrix scenckii is the fungus saprophyte which causes the subcutaneous
mycoses. It tends to involve lymphatics and develops lymphangitis. The common
clinical aspect is multiple inflammatory nodules that are connected by lymphangitic
linear inflamed lesions. Single nodules can evolve into a chronic ulcer (Roldan-Mari
et al. 2009). A biopsy is mandatory (often not specific), but the diagnosis is usually
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