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Arterial Leg Ulcers
JosefAschwanden, JurgHafner,
VincenzoJacomella, andSeverinLäuchli
48
48.1 Introduction
Leg ulcers are not a diagnosis but a symptom of
many different diseases. In this chapter, we will
describe leg ulcers caused by arterial disease.
However, many other causes should be considered in refractory ulceration on the lower extremity such as venous disease, neuropathy, and
miscellaneous causes like vasculitis, malignancy,
and autoimmune disease and even rare causes
like pyoderma gangrenosum [1], thromboangiitis
obliterans, or arterial-venous malformation.
Martorell hypertensive ischemic leg ulcers [2] as
part of the arterial causes are not discussed here
as they are described in another chapter. Very
often, the ulcers of the lower leg result from a
combination of factors [3]. Therefore, it is important to rule out arterial insufciency even when
other causes or clinical signs are present. For
example, about 15% of all leg ulcers are of a
mixed arterial-venous origin [4–6]. We postulate
that every patient with ulceration on the lower leg
should receive an arterial workup, not only
because a concomitant arterial disease may delay
healing but also because of the underlying systemic process (arteriosclerosis) for which the
J. Aschwanden · J. Hafner · S. Läuchli (*)
Department of Dermatology, University Hospital
Zürich, Zurich, Switzerland
e-mail: Severin.laeuchli@usz.ch
V. Jacomella
Department of Angiology, University Hospital
Zürich, Zurich, Switzerland
patient might prot from an appropriate systemic
therapy [7, 8].
48.2 Epidemiology
andClassication
Chronic ulceration of the lower leg can result
from several underlying factors as mentioned
above. The most common cause is venous insufciency in about 75%, followed by ulcers of
mixed venous and arterial (15%) and those of primarily arterial (4%) origin [4, 5]. Arterial leg
ulcers are caused by an oxygen decit in the tissue resulting from reduced tissue blood perfusion
due to occlusion of the arterial lumen. The most
common cause for this occlusion is peripheral
arterial occlusive disease (PAOD) due to an arteriosclerotic process. Generalized arteriosclerosis
is therefore the most common cause not only of
cardiovascular and cerebrovascular disease but
also of peripheral vascular disease. The prevalence of PAOD in the general population varies
between 7% and 21% [9]. It is related to age, gender, and denition of PAOD (by the cutoff value
of the ankle-brachial index (ABI) and/or the presence of symptoms). The Fontaine stages classify
the clinical appearance of PAOD (Table 48.1).
Before progressing to a clinically symptomatic
stage such as intermittent claudication or even
critical limb ischemia, PAOD is typically asymptomatic for several years. Approximately 23% of
all patients are asymptomatic, and this is proba-
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_48
305
306
J. Aschwanden et al.
Table 48.1 Fontaine classication for PAOD
Stage I Asymptomatic
Stage II Intermittent claudication
Walking distance:
IIA >200m, with no disablement
IIB <200m with disablement
Stage III Resting pain
Stage IV Peripheral necrosis/gangrene
bly one reason that PAOD stage I seems to be
underestimated [8]. Sometimes, symptoms can
also be masked by reduced walking distance due
to other reasons or by polyneuropathy secondary
to diabetes. In stage II with intermittent claudication as the main symptom, rest pain is normally
missing. Stage III ischemic rest pain is typically
a nocturnal pain. Approximately 15–20% of
patients with intermittent claudication will
progress to critical ischemia. The distinction
between arterial insufciency and critical ischemia is not clearly outlined in the literature, and
critical limb ischemia occurs only in a minority
of patients with PAOD [10]. In 1996, the Second
European Consensus [11] outlined criteria for the
diagnosis of chronic critical limb ischemia: recalcitrant rest pain or distal necrosis of more than
2weeks’ duration in the presence of (A) a systolic ankle pressure (AP) 50mmHg or less, (B) a
systolic toe pressure of 30mmHg or less, or (C)
a transcutaneous oxygen pressure (tcPO2) of
10mmHg or less. In the last few years, the threshold for critical ischemia has been raised several
times. Necrotic ulceration occurs in stage IV,
usually on the toes or the back of the feet, but can
also occur in stage II after trauma or in combination with chronic venous disease and is then generally considered a “complicated” stage IIB. In
fact, the majority of arterial ulcers occur in “complicated” stage IIB on the lateral lower leg and do
not match the criteria for critical ischemia. The
angiosome concept is one possible explanation
for the occurrence of nonhealing ulcers above the
threshold of critical ischemia. It was rst
described by reconstructive plastic surgeons in
1987 [12]. They divided the tissue into specic
three-dimensional sectors of the body supplied
by specic arteries and veins, named angiosomes.
Each angiosome therefore consists of a topographically specic arteriosome and corresponding venosome supply, which build block systems
of perfusion. Neighboring angiosomes are linked
by numerous communicating vessels, so-called
choke vessels. In ischemic conditions, these
interconnections between adjacent angiosomes
create a very effective compensatory system in
non-atherosclerotic and nondiabetic limbs [13].
In atherosclerotic or other changes of the large
collateral vessels, such as those typically accompanying diabetic arterial disease below the knee
and end-stage renal disease (ESRD), this natural
“rescue system” between adjacent angiosomes
may be jeopardized.
48.3 Clinical Findings
The typical localization for arterial leg ulcers is
the lateral malleolar region for PAOD stage IIB
(Fig. 48.1), whereas distal arterial necrosis
(PAOD stage IV) is usually localized in the foot
and toe region (Fig. 48.2). Arterial leg ulcers
often have irregular edges and/or a “punchedout” appearance. The ulcer base is usually poorly
developed with a grayish granulation tissue.
Signs of chronic venous disease are missing
except in mixed ulcers. Painful and necrotic
areas are the typical appearance for all ischemic
ulcers.
48 Arterial Leg Ulcers
Fig. 48.1 Typical arterial leg ulcer on the lateral malleolar aspect of the lower leg (PAOD complicated stage IIB)
Fig. 48.2 Distal arterial necrosis due to PAOD stage IV
48.4 Diagnosis
The rst test to rule out arterial insufciency
should be the palpation of the pedal pulses. It
should be mentioned that the dorsalis pedis pulse
307
Table 48.2 Doppler ankle-brachial ratio [15]
0.91–1.4 Normal, if under exercise no ABI loss
0.5–0.85 PAOD, claudication (mild to moderate
disease); a wound can heal
<0.5 Severe PAOD, threat of tissue and limb loss
>1.4 May be due to diabetes, Mönckeberg disease,
renal disease
is missing in about 10% of individuals and the
palpation of the posterior tibial pulse may be difcult due to swelling or presence of ulceration
caused by a concomitant chronic venous insufciency. If a pulse is palpable, we can assume that
the ankle pressure is >100mmHg [14] and wound
healing should be possible. If no pulses can be
detected, noninvasive vascular testing should
always be performed.
As a fast and simple test, the ankle-brachial
index (ABI) can be measured very easily with a
cheap and simple continuous-wave (CW)
Doppler probe (8–10mMHz). The ABI is dened
as the systolic ankle pressure divided by the systolic arm pressure and is considered an accurate
and reliable marker of symptomatic and asymptomatic PAOD (Table48.2). Signicant arteriopathy is normally dened as an ABI <0.91 and an
ABI <0.5 as severe arterial insufciency [16].
The ABI measurement can therefore identify
patients at risk of any systemic atherothrombotic
events even in an asymptomatic stage.
Identication of asymptomatic PAOD also leads
to intensied targeted prophylactic antiatherothrombotic treatment that can reduce morbidity and mortality as mentioned above [8].
To recognize critical ischemia, the measurement of ankle systolic pressure is the most accurate test. If the pressure is below the level of
critical limb ischemia as dened with an ankle
systolic pressure <50mmHg [11], leg ulcers will
only heal in 20% of cases, and aggressive revascularization therapy should be performed [17]. In
contrast, a systolic pressure over 70mmHg can
nearly exclude arterial insufciency as a cause
for the ulcers. If the arteries are not compressible,
i.e., the ABI is higher than 1.4 or the difference of
the measured pressure between ankle and arm
exceeds 75 mmHg, calcication of the arteries
should be considered. In these cases, a toe sys-
308
J. Aschwanden et al.
Table 48.3 Use of noninvasive vascular tests to predict
the presence of underlying severe arteriopathy [18]
Noninvasive
avascular testing Findings
Pedal pulses Present Unlikely
Absent Possible
Ankle systolic
pressure
With ulcer <50–70mmHg Possible
Without ulcer, with
rest pain
Toe systolic pressure >50mmHg Unlikely
tcPO
2
a
Proceed with further, noninvasive vascular tests to conrm or rule out severe arteriopathy especially if clinical
evolution is poor
>70mmHg Unlikely
<30–50 Likely
<50mmHg Likely
>30mmHg Unlikely
<30mmHg Likely
Severe
arteriopathy
a
a
tolic pressure or a tcPO2 measurement should be
performed. In cases of Mönckeberg mediacalcinosis, the pole test technique can also give further
information concerning the critical ischemia of
the lower limbs. A toe systolic pressure lower
than 50mmHg or a tcPO2 lower than 30mmHg is
diagnostic for critical ischemia (Table 48.3). If
the tcPO2 is over 30mmHG, a wound can heal.
Ultrasonic duplex scanning or arteriography can
localize the arterial lesion but cannot make any
statement about the severity of the arterial disease. In contrast, it is a very good surveillance
tool after an invasive intervention or as rst-step
screening in order to evaluate an invasive procedure. The gold standard to investigate PAOD is
still angiography, especially when an intervention is planned. Recently, magnetic resonance
angiography has emerged as a noninvasive imaging modality without the risks associated with
conventional angiography (e.g., arterial puncture,
plaque embolization, and contrast-induced
nephropathy).
48.5 Treatment
The arteriosclerotic process as a systemic problem needs an interdisciplinary approach. The
common arteriosclerotic risk factors should be
treated aggressively (Table48.4). Whenever possible, revascularization should be attempted by
Table 48.4 Risk factors for arteriosclerosis and PAOD
Hypertension
Diabetes
Elevated cholesterol, especially low-density lipoprotein
Smoking
angioplasty or vascular surgery. This is the only
effective therapeutic option to allow wound healing when ischemic necrosis is present.
Furthermore, it often provides the most efcient
pain relief. If revascularization by interventional
or surgical means is not possible, intravenous
application of iloprost can ameliorate the situation, but this is often limited by side effects (e.g.,
hypotension, headaches). Exercise also plays an
important role in improving the maximal walking
distance and thus increasing the blood perfusion.
Adjuvant medical treatment with antithrombotic
or rheological agents can improve the outcome
[19].
For the local therapy, the common principles
of modern wound care should be applied. Sharp
surgical debridement is of foremost importance
to remove the bioburden, which can delay wound
healing. However, as arterial ulcers often reach to
deeper structures, it should be performed by surgeons or wound care experts with adequate training. Enzymatic debridement and biosurgery with
maggots can be viable alternatives. Local wound
infection can be treated with wound antiseptics or
silver dressings; if signs of systemic infection are
present, systemic antibiotics have to be utilized.
The choice of wound dressing must take into
consideration the amount of exudation and necrosis and the phase of wound healing. Generally,
occlusive dressings should be avoided, as their
main mode of action, a local increase of CO2 tension, is not desirable for ischemic ulcers and the
detection of wound infection could be delayed.
Semiocclusive dressings can be utilized with caution, if granulation tissue exceeds necrotic areas
and there are no signs of wound infection. The
type of wound dressing does not signicantly
inuence healing times [20, 21]. Therefore, the
choice of wound dressing should be guided by
patient-centered concerns such as exudate management and pain control [22]. Wound pain is
one of the main concerns of patients [23].
48 Arterial Leg Ulcers
309
Dressings that avoid desiccation of the wound
and which do not traumatize the wound when the
dressing is changed are therefore ideal.
Arterial leg ulcers can show a very protracted
healing time, especially if surgical or interventional revascularization is not possible. In these
cases, advanced methods often have to be utilized, such as acellular matrices, keratinocyte
cultures, or growth factors. In many instances,
split-thickness skin grafts can improve the wound
pain immediately and accelerate healing, even if
the wound bed does not show sufcient granulation for a full graft take.
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Dormandy JA.The nature and importance of changes
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16. Norgren L, Hiatt WR, Dormandy JA, Nehler MR,
Harris KA, Fowkes FG.Inter-society consensus for
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UV.Management of leg ulcers. Curr Probl Dermatol.
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Prevention ofSkin Necrosis
inCosmetic Medicine
HuguesCartier, LeonieSchelke, andPeterVelthuis
49
49.1 Introduction
Aesthetic medicine is a constantly evolving eld,
which includes minimally invasive treatments,
i.e., considered as nonsurgical.
Nevertheless, the current evolution makes
some procedures more intrusive.
Most of the patients treated are healthy people
looking for an aesthetic improvement, so the
treatments performed must be as safe as
possible.
This treatment cannot be done without a medical diagnosis, a precise history, informed information, and a choice of treatment options to be
weighed against a benet-risk ratio.
49.1.1 Aesthetic Procedures
49.1.2 Filling Products
Filling products play a signicant role in aesthetic medicine. The rheology of the products has
not stopped evolving over the last 20 years.
Fortunately, nonabsorbable products such as sili-
H. Cartier (*)
Saint-Jean Dermatologic Center, Arras, France
L. Schelke · P. Velthuis
Dermatology Department, Erasmus University
Medical Center, Rotterdam, Netherlands
e-mail: leonie.schelke@cutaneous.org; p.velthuis@
erasmusmc.nl
cone, Gore-Tex, and acrylamides have been
banned in Europe.
At present, four types of products that integrate well into the cutaneous and subcutaneous
tissue and that are slowly resorbable can be identied: hyaluronic acid, calcium hydroxyapatite,
polycaprolactone, and polylactic acid, which is in
the form of powder to be diluted in sterile water.
Of these four lling or collagen stimulation
products, only hyaluronic acid can be dissolved
rapidly with hyaluronidase in case of complications (such as bad placement, accumulation of
product, associated infection, sterile inammatory reaction, or vascular occlusion).
The major complication is vascular occlusion
or compression. At best, they cause cutaneous
and subcutaneous suffering that is resolved
thanks to the contiguous arterial network. At
worst, they cause extensive and deep necrosis in
the vascularized area. Cases of occlusion of the
central retinal artery with loss of ocular function
due to migration of the product in the bloodstream are fortunately rare compared to the number of injections performed every day in the
world but nevertheless regularly reported and
published.
Vascular complication can occur at any time,
especially since needles or ne cannulas are used
that can easily perforate an artery. The reason for
this is simple: even though all doctors who perform injections of lling products must know the
facial anatomy, injections are done blindly. We
do have the blood aspiration test technique, but it
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_49
311
312
H. Cartier et al.
is far from reliable. To date, only ultrasound
imaging, a dynamic, noninvasive examination to
be used prior to injection, can supply an answer,
but it requires training, a certain amount of dexterity, and adequate equipment. The world of aesthetics is discovering this technique, which
cannot guarantee to ban this complication but
contributes to reducing this risk [1].
Venous embolisms rarely cause skin suffering
at rst because they are diluted in the general vascular system. However, there have been reports
of cavernous sinus thrombosis in facial injections
and pulmonary embolism in genital or gluteal
injections with massive quantities of ller.
The cutaneous signs of arterial vascular complications are with important variations:
– Immediate pain like a cramp
– Immediate or delayed blanching extending as
a livedoid pattern
– Progressive cyanosis of the skin that may look
like bruises but may not be declining but
ascending
– Pustules, inammation that may resemble the
false vesicular eruptions of herpes or shingles
– Cyanotic suffering with extensive tissue
necrosis depending on the vascular territory
49.1.3 Lifting Eect or Collagen
Stimulation by Threads
A distinction is made between absorbable and
nonabsorbable threads. In themselves, the threads
only cause a conned inammation around them.
Depending on their characteristics, the threads
can also pull the skin to give this tensor effect.
Intrinsically, they do not cause skin necrosis,
but a cutaneous or subcutaneous injury. This tearing of the tissues during their introduction under
the skin by needles of varying lengths induces
microtrauma, even more so since they are armed
with small spines allowing for better xation and
maintenance over time. Avoid combination with
radiofrequency to stimulate neocollagenesis
because it induces more exaggerated inammatory responses such as development of nodular
panniculitis and adipocyte necrosis [2].
Moreover, the number of threads accumulated
under the skin can cause vascular breaches and
poor tissue integration. We have seen cutaneous
suffering and even necrosis, particularly on the
nose.
49.1.4 Laser andEBD
In general, the effect of lasers and EBD treatment
is mediated by controlled damage to tissue. After
this, regeneration occurs that should lead to an
improved appearance [3].
49.1.4.1 Ablative Lasers
Ablative lasers are represented by the CO2 laser
and the erbium-YAG laser.
They cause vaporization of the epidermis and
middle dermis in resurfacing mode. In fractionated mode, ablative lasers cause micro-wells that
perforate the skin to a depth of up to 3.5 mm.
This is a focused necrosis that forms just around
the well due to the brutal heating of the skin tissue. This is normally a controlled burn if the
energy delivered and the density of the points that
are juxtaposed are not too high. The higher these
two parameters are, the greater the thermal
trauma. The burn is then uncontrollable, leading
to skin necrosis and consequently to vicious,
anged, and hypochromic scars.
The skin structure plays a key role because the
tissue regeneration is induced by this skin vaporization and the thermal effect. Thus, the healing
process is very variable depending on the type of
the skin, its age, and density in pilosebaceous
appendages and in vascular network that contributes to it. Outside the face, the risk of burning is
increased since densities of these structures are
much less.
49.1.4.2 Non-ablative Thermal Lasers
Non-ablative lasers induce a thermal effect that is
supposed to regenerate the dermis. There are
numerous devices, fractionated or not. If too much
heat is accumulated, the effect of the laser radiation can cause skin suffering up to the point of skin
necrosis. This is nevertheless rare and related to a
bad use or an error of parameterization.
49 Prevention ofSkin Necrosis inCosmetic Medicine
313
49.1.4.3 Vascular Lasers
We distinguish the KTP laser, the pulsed dye
laser, the vascular diode, the yellow laser, the
pulsed lights with vascular lter, and the longpulse Nd-YAG laser.
Vascular lasers are characterized by wavelengths that are preferentially absorbed by the
redness of the skin. It is important to distinguish
skin redness from inammation, which is rarely a
good indication for vascular lasers.
In fact, all vascular lasers cause inammation
that should not be added to an already existing
inammation.
This inammation causes an edema that will
vary according to the type of laser and its photon
energy setting, the size of the vascular target to be
destroyed, and the intrinsic drainage of the skin
in each case or according to the site treated.
In addition, depending on the type of laser and
the adjustment of emission time and energy, a
purpura can be seen in the presence of purple
spots that will fade in 5–10 days.
The burn is the consequence of an excessive
accumulation of energy with a dispersion of the
heat that is not well done. We can therefore have
a surface epidermolysis, which is to say a blowout or a real cutaneous necrosis which will leave
a hypochromic scar.
On tanned or self-tanning skin or for a phototype above III on the Fitzpatrick scale, there is an
increased risk of burning and reactive
hyperpigmentation.
Special mention should be made of the longpulse Nd-YAG laser, which delivers very high
light energy and should be used with caution, as
it induces the most dermal necrosis with systematic scarring.
49.1.4.4 Pigment Lasers
A distinction is made between hair removal lasers
and those used to erase sunspots or tattoos. The
wavelengths are identical, but it is the emission
time of the laser beam that will change.
For tattoos, we can only use picosecond or
nanosecond lasers. The energy delivered must be
high enough to burst the tattoo pigment and dissolve it progressively. Other pigment lasers
deliver their photonic energy in milliseconds. If
these are used for tattoos, they will systematically cause skin necrosis by deep burning. Indeed,
the instantaneous accumulation of dermal pigment in tattoos is so important and brutal that the
skin does not have time to disperse the heat.
For laser hair removal, the laser radiation follows the hair like an electric current follows a
conducting wire. The heat accumulation causes
its destruction, but if the skin is tanned, covered
with self-tanner or on phototype beyond IV on
the Fitzpatrick scale, then the photons will also
be absorbed by the skin surface which by itself
becomes a target and causes a surface burn, from
epidermolysis to dermolysis. And thus, at best a
hypochromia and at worst a burn will occur
which will be deep enough to leave denitive
hypochromic scars. In these cases, Nd-YAG
long-pulse lasers or hair removal diodes are recommended, unlike alexandrite and pulsed light
lasers.
For sunspots, all these lasers can be used, and
it is only a question of setting and wavelength.
The spots will turn into small supercial scabs
that will disintegrate in a few days without leaving any trace. A deeper burn is in most cases secondary to a bad use of the device.
49.1.4.5 Radiofrequency
Radiofrequency is an electric current that disperses heat according to its operating mode.
Contact with a handpiece that is swept over the
skin surface accumulates local heat and causes
tissue remodeling. Fractional radiofrequency
aims to place contact microelectrodes on the surface of the skin to induce dermal-epidermal
micro-bulges and nally radiofrequency with
microneedles. The microneedles penetrate the
skin up to 4mm deep; they are protected up to the
tip or not, depending on the device.
The electrical effect causes skin coagulation,
tissue, and vascular damage, which is supposed
to regenerate the skin. Too long an emission time,
too much energy, and repetition of passages can
cause tissue damage. From the spike scar to the
loss of skin substance by dermal-epidermal burn,
everything is possible but rare.
314
H. Cartier et al.
49.1.5 EBD
49.1.5.1 LEDs
The diodes juxtaposed on a panel are athermal.
The mode of operation therefore does not cause
skin necrosis unless they are used to activate a
photosensitizing substance. In this case, they
contribute to cause it. LEDs emit in the visible
spectrum and therefore do not contain UV
radiation.
49.1.5.2 High-Intensity Focused Ultrasound (HIFU)
Focused ultrasound concentrates its energy on a
focal point at 1.5mm, 3mm, 4.5mm, 6mm, or
more. The sudden rise in temperature causes
coagulation and punctual necrosis in the form of
aligned micro-points. Paresis due to nerve damage has been seen.
Used to obtain a rming and tensing effect on
the oval of the face, it is necessary to multiply the
lines of points to obtain a result. The closer the
lines of stitches are to each other, the more skin
suffering is induced.
Skin burns are rare unless the handpiece is not
applied correctly to the skin.
49.1.5.3 Cryolipolysis
Cryolipolysis is based on the freezing of a volume of skin and fat caught in a vacuum chamber. The combination of cold, up to −12°C, and
suction to x the volume to be melted by
destroying the adipocytes has proved its medical interest with numerous publications to support it. Nevertheless, many devices have
appeared on the world market of aesthetic medicine and aesthetic centers of nondoctors.
Medical ability is necessary to avoid complications such as thermal burns caused by the cold.
Cases of surface burns and even skin necrosis
of the bedsore type have even been reported.
They are much more frequent when the temperature descent is not progressive, when the
skin contact interface has been forgotten or is
not conrmed for this use, or when the duration
of the cold and the suction force is not adapted
to the volume of the fat mass.
49.1.6 Peelings
49.1.6.1 Epidermal Peel
The leader in epidermal peels is glycolic acid. All
its exfoliating agents can give epidermolysis,
rarely deeper burns.
49.1.6.2 Medium andDeep Dermal
Peels
They are essentially represented by trichloroacetic acid and phenol associated with croton oil.
These peels are of varying concentrations and
pH. They aim at provoking a dermal-epidermal
regeneration. Incorrect use, i.e., too many applications and too high a concentration, can cause
serious burns with permanent scarring. Learning
to use them is essential to set limits to their use.
It should be remembered that healthy skin
serves as a natural protection, if one causes skin
breaches.
49.1.7 Other Injectable Active
Ingredients
Mesotherapy with unsuitable products can cause
skin necrosis at the injection site, as can deoxycholate, a chemical agent designed to destroy
localized fatty areas.
49.2 Complications
Complications are multiple but essentially
inammatory, scarring, and infectious.
49.2.1 Inammation
andPigmentation
The inammation caused by all the techniques
mentioned above is a normal phenomenon that is
the consequence of any trauma. This normal process is gradually reduced, but if it persists, it can
cause a resurgence of pigment on the surface,
hypersensitivity, or sensitive skin. It is mainly
embarrassing but does not lead to tissue destruction but can give way to brosis.