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62
M. Nou Howaldt
to endothelial cell activation, migration, and
leukocyte adhesion. The accumulation of oxidized LDL leads to the agglomeration of foam
cells between intima and media and the proliferation and migration of smooth muscle cells.
Gradually, a lipid core forms, creating a
plaque that is covered by a brous cap of muscle cells. In the event of plaque rupture or
bleeding, arterial thrombosis may occur,
obstructing the vessel lumen (Fig. 7.1).
Arterial obstruction generates ischemia and
tissue hypoxia, leading to skin necrosis [2–4].
• Mixed ulcers are associated with venous
insufciency
Ninety percent of venous return is provided
by the deep veins and 10% by the supercial
veins (saphenous veins and their tributaries).
The two networks communicate via perforat-
ing veins (Dodd, Hunter, Boyd, and Cockett),
saphenous junctions, and Giacomini’s vein,
which provides an anastomosis between the
saphenous veins. The veins are equipped
with valves that prevent the blood from ow-
ing back downwards in an orthostatic posi-
tion. Pressure in the veins is determined by
two components: hydrostatic pressure
(weight of the blood column) and hemody-
namics resulting from muscle contraction. In
a static position, venous pressure is around
90 mmHg at the ankles. On initiation of
walking, this pressure gradually decreases to
an average of 30mmHg, thanks to the con-
traction of the calf muscles (muscular pump)
and the crushing of the plantar sole, which
Fig. 7.1 From top to bottom: Atherothrombotic plaque formation in an artery
7 Arterial andMixed Leg Ulcer
Fig. 7.2 Evolution of
venous pressure in the
lower limbs when
walking. Hyperpressure
in subjects with varicose
veins or post-thrombotic
syndrome
Ambulatory pressure on walking
100
mmHg
90
80
70
60
50
40
30
20
10
0
WALK7 STEPS 10 STEPS IMMOBILISATION
63
Hyper pressure
Normal
Varicose vein
Post thrombotic
syndrome
behaves like a veritable blood-lled sponge
(Fig.7.2). The valvular system ensures segment-by-segment return of the blood column,
and the abdominodiaphragmatic system acts
on hydrostatic pressure [5, 6].
Chronic venous insufciency is linked to
poor venous return, which generates venous
and veno-capillary hyperpressure. The result
is capillary and venous dilatation, increased
endothelial cell permeability, and leukocyte
inltration, leading to toxin accumulation
and cellular hypoxia, which in turn leads to
the production of inammatory mediators.
Ultimately, this leads to skin remodeling,
culminating in the appearance of skin ulceration [5, 6].
7.4 Clinical Diagnosis
• Arterial ulcer
Arterial ulcers are painful trophic disorders.
Most often of recent onset (a few days to a few
weeks), it is located on both the leg and the
foot. The patient has cardiovascular risk factors (hypertension, diabetes, smoking, dyslipidemia, etc.). The characteristics of arterial
ulcers are as follows: rounded, clean edges,
possible exposure of underlying structures
(tendon, bone), low exudation, and presence
of necrosis (Fig.7.3) [1].
Skin involvement is accompanied by signs of
arterial insufciency: intermittent claudica-
tion of the lower limbs (i.e., pain in the lower
limbs when walking), pain at rest, coldness,
paleness of the limb with declivity erythrocya-
nosis, coldness of the foot, disorders of the
Phanera (thin skin; thick, brittle nails; depila-
tion; dry skin, etc.), and sometimes
amyotrophy when the PAD has been evolving
for a long time [3].
• Mixed ulcer
Mixed ulcers combine signs of arterial ulcer-
ation with signs of chronic venous insuf-
ciency. Signs of venous stasis include edema,
phlebalgia (pain along the veins), and corona
radiata phlebectatica. Skin changes such as
ochre dermatitis (brown pigmentation of the
leg due to hemosiderin deposition), lipoderma-
tosclerosis, inammatory hypodermatitis, and
Milian’s white atrophy may also be present [1].
The mixed ulcer is exudative and can be pain-
ful, and the peri-ulcer skin is pathological
(erythema, maceration, hyperkeratosis,
64
Fig. 7.3 Arterial ulcer
Fig. 7.4 Mixed ulcer predominantly venous
Fig. 7.5 Mixed ulcer predominantly arterial with exposed
tendon
eczema). The difculty lies in assessing the
predominant vascular component, as this will
determine the choice of treatment (Figs. 7.4
and 7.5).
M. Nou Howaldt
7.5 Vascular Explorations
• Ankle-Brachial Pressure Index (ABI) and
Toe-Brachial Index (TBI)
Measurement of ABI is recommended, as it
offers good sensitivity and specicity in the
detection of PAD (Fig. 7.6).It is the ratio of
ankle systolic pressure to humeral systolic
pressure. In the event of a result <0.91 or >1.4,
it is necessary to search for PAD by means of
additional examinations [2–4, 7].
However, PAD is less accurate in the case of
wounds, particularly if there is Mönckeberg
mediacalcosis (calcium deposits in the arte-
rial wall responsible for parietal stiffness).
The guidelines recommend measuring toe
systolic pressure and calculating the TBI,
which is the ratio of toe systolic pressure to
humeral systolic pressure, in patients with
diabetes and kidney failure and the very
elderly (Fig. 7.7). The pathological threshold
is a ratio <0.7 [2, 3, 7].
• Arterial Doppler Ultrasound of the Lower
Limbs
Arterial Doppler ultrasound is a noninvasive,
rst-line examination for leg ulcers. It is thus
possible to visualize hemodynamically signif-
icant arterial lesions (stenoses or occlusions)
that may explain the ischemic picture [7].
In the case of mixed ulcers, arterial assess-
ment must be complemented by an analysis of
the venous network, in order to identify the
cause of supercial venous insufciency (var-
icose veins) or deep venous insufciency
(post-thrombotic syndrome). In the case of
varicose veins, there is venous reux, and in
the case of post-thrombotic syndrome, there
may be obstructive sequelae or valvular
incompetence [8].
• Venous Doppler Ultrasound of the Lower
Limbs
This exploration is indicated in case of
venous insufciency signs in order to detect
varicosis or to research a post-thrombotic
syndrome. This test can be used to detect
venous reux.
7 Arterial andMixed Leg Ulcer
Figs. 7.6 and
7.7 Measurement of
ankle-brachial pressure
index (ABI) and
toe-brachial index (TBI)
65
• TcPO
2
This is a subcutaneous oxygen pressure measurement. Using polarographic sensors (Clark
electrodes) positioned close to the trophic disorder, an automaton will record an 02 pressure
value expressed in mmHg. The cutoff value
for healing is 30mmHg. Below this value, the
prognosis for healing is very poor, and impossible if <10mmHg [7].
• Vascular Imaging
Vascular imaging (CT angiography, MRI
angiography, or arteriography of the lower
limbs) is essential if revascularization is to
be performed. These examinations enable a
more detailed analysis of the lesions
detected by echo-Doppler. Arteriography is
used in cases where the sub-popliteal arterial axes of the leg are affected, as it is more
effective than MRI or CT angiography in
exploring the leg axes, especially if there is
mediacalcosis.
7.6 Treatment
Arterial ulcer treatment aims to correct arterial
ischemia. Revascularization may be proposed
either by surgery or by transluminal angioplasty.
Medical treatment of PAD combining lipidlowering therapy, antiplatelet therapy, and a converting enzyme inhibitor is systematically
associated with the control of cardiovascular risk
factors and a healthy lifestyle including daily
walking [2–4, 7].
There are no recommendations to guide the
therapeutic management of mixed ulcers, and the
role of compression therapy for patients with ABI
<0.8 is controversial as there is thought to be a
greater risk of iatrogenic skin damage with the
use of compression therapy in the presence of
arterial disease. However, it has been demonstrated that modied compression therapy, using
short stretch or inelastic material with a pressure
<40mmHg, is very effective in obtaining healing
of a mixed ulcer, provided that the absolute value
of the ankle pressure is >60mmHg, the toe pressure >30 mmHg, and the ABI >0.6 [8–11]. In
addition, curative treatment of supercial venous
insufciency would be effective in treating mixed
ulcers [8–10]. In case of post-thrombotic
syndrome, for patients with iliac vein outow
obstruction and severe symptoms/signs, endovascular treatment should be considered [8].
Revascularization may nevertheless be necessary if compression is no longer tolerated and the
wound no longer progresses, or if it worsens
under compression.
7.7 Conclusion
Since 80–90% of leg ulcers have a vascular cause,
a vascular assessment using ABI, TBI, and arterial and/or venous Doppler ultrasound should be
66
M. Nou Howaldt
carried out systematically in the case of chronic
leg or foot wounds. Arterial ulceration is a serious pathology resulting from arterial insufciency and responsible for ischemia. The
appearance of necrosis is often a clinical element
that guides the diagnosis, and revascularization is
the only curative treatment. In the case of mixed
ulcer, management will depend on the degree of
severity of the PAD, which can be quantied and
assessed using the various vascular function tests.
Venous insufciency must not be neglected, as
this may delay healing. Appropriate venous compression is often necessary in the case of mixed
ulcers and warrants monitoring of treatment tolerance and efcacy.
References
1. Nou Howaldt M, et al. Vascular assessment for
chronic wounds of the lower limbs. La Lettre du
Médecin Vascul. 2022.
2. Franck U, et al. Guideline on peripheral arterial
disease. Vasa. 2019;48(Suppl 102). https://doi.
org/10.1026/a000002.
3. Task Force Members. 2017 ESC guideline on the diagnosis and treatment of peripheral arterial diseases, in
collaboration with the European Society for Vascular
Surgery (ESVS). Eur Heart J. 2018;39:763–816.
https://doi.org/10.1093/eurheartj/ehx095.
4. Criqui MH, et al. Lower extremity peripheral artery
disease: contemporary epidemiology, management
gaps and future directions: a scientic statement
from the American Heart Association. Circulation.
2021;144:e171–91.
5. Nou Howaldt M, Quéré I, Godin SM, Henneton P,
Tapon M, Laroche JP.Venous chronic insufciency.
In: Guillevin L, Mouthon L, Lêvesque H, editors.
Traîté de médecine. 5th ed. Paris: Tdm Edition; 2018.
p.1–8.
6. Youn YJ, Lee J. Chronic venous insufciency and
varicose veins of the lower extremities. Kor J Intern
Med. 2019;34:269–83.
7. Mahé G, etal. Disparities between international guidelines (AHA/ESC/ESVS/ESVM/SVS) concerning
lower extremity peripheral arterial disease. Consensus
of the French Society of Vascular Medicine (SFMV)
and the French Society for Vascular and Endovascular
Surgery (SCVE). Ann Vasc Surg. 2020;72:1–56.
8. De Maeseneer MG, et al. European Society for
Vascular Surgery (ESVS) 2022 clinical practice
guidelines on the management of chronic venous
disease of the lower limbs. Eur J Vasc Endovasc
Surg. 2022;63:184–267. https://doi.org/10.1016/j.
ejvs.2021.12.024.
9. Mosti G, etal. Compression therapy in mixed ulcers
increases venous output and arterial perfusion. J Vasc
Surg. 2012;55:122–8.
10. Mosti G, et al. Recalcitrant venous leg ulcers may
heal by outpatient treatment of venous disease even in
the presence of concomitant arterial occlusive disease.
Eur J Vasc Endovasc Surg. 2016;52:385–91.
11. Lim SLX, et al. Modied compression therapy in
mixed arterial–venous leg ulcers: an integrative
review. Int Wound J. 2021;18:822–42.
7 Arterial andMixed Leg Ulcer
Open Access This chapter is licensed under the terms of the Creative Commons Attribution-NonCommercialNoDerivatives 4.0 International License (http://creativecommons.org/licenses/by- nc- nd/4.0/), which permits any noncommercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit
to the original author(s) and the source, provide a link to the Creative Commons license and indicate if you modied the
licensed material. You do not have permission under this license to share adapted material derived from this chapter or
parts of it.
The images or other third party material in this chapter are included in the chapter's Creative Commons license,
unless indicated otherwise in a credit line to the material. If material is not included in the chapter's Creative Commons
license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to
obtain permission directly from the copyright holder.
67
Part II
Dierent Clinical Context of Skin Necrosis
Physical Injuries
Introduction toPhysical Injuries
inSkin Necrosis
SebastianProbst
8
Skin necrosis, a distressing condition characterized by the death of skin cells and tissues, is a
medical concern with a range of underlying
causes [1]. Physical injuries leading to skin
necrosis are one of the most common triggers for
this condition, posing serious challenges to
patients and healthcare professionals alike.
Whether the result of trauma, extremes of temperature, radiation exposure, or electric shock,
skin necrosis can have devastating consequences,
impacting the affected individuals’ quality of life
and often requiring complex medical interventions. This chapter aims to explore the various
forms of physical injuries that can lead to skin
necrosis, their underlying mechanisms, and the
potential treatment strategies employed to manage and alleviate the distressing effects of this
condition. Understanding the complexities of
skin necrosis due to physical injuries is crucial
for early detection, prompt intervention, and,
ultimately, improvement of patient outcomes.
Through enhanced awareness and comprehensive research, health care professionals can strive
to prevent and mitigate the burden of skin necrosis in those vulnerable to its development.
Reference
1. Hakkarainen TW, Kopari NM, Pham TN, Evans
HL.Necrotizing soft tissue infections: review and current concepts in treatment, systems of care, and outcomes. Curr Probl Surg. 2014;51(8):344–62. https://
doi.org/10.1067/j.cpsurg.2014.06.001.
S. Probst (*)
HES-SO University of Applied Sciences and Arts
Western Switzerland, Geneva, Switzerland
e-mail: sebastian.probst@hesge.ch
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_8
71
72
Open Access This chapter is licensed under the terms of the Creative Commons Attribution-NonCommercialNoDerivatives 4.0 International License (http://creativecommons.org/licenses/by- nc- nd/4.0/), which permits any noncommercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit
to the original author(s) and the source, provide a link to the Creative Commons license and indicate if you modied the
licensed material. You do not have permission under this license to share adapted material derived from this chapter or
parts of it.
The images or other third party material in this chapter are included in the chapter's Creative Commons license,
unless indicated otherwise in a credit line to the material. If material is not included in the chapter's Creative Commons
license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to
obtain permission directly from the copyright holder.
S. Probst
Skin Mechanobiology: FromBasic
Science toClinical Applications
AlekseiOrlov andAmitGefen
9
9.1 Introduction
The skin forms the physical interface between the
human body and the environment, and its mechanical properties are therefore important in both
health and disease. Among other functions, this
largest organ of the human body constantly counteracts external and internal mechanical forces
during all daily activities. For tolerating these
forces, the human skin has evolved to have remarkable biomechanical properties that are uniquely
suited to its function, both locally and overall.
While it is relevant to know how skin tissue
deforms and fails from a basic science aspect, it is
even more important, from an applied medicalclinical perspective, to understand how mechanical forces act on skin tissue to maintain normal
tissue physiology and to regulate inherent biologi-
A. Orlov
Department of Biomedical Engineering, Faculty of
Engineering, Tel Aviv University, Tel Aviv, Israel
e-mail: alexeyorlov@mail.tau.ac.il
A. Gefen (*)
Department of Biomedical Engineering, Faculty of
Engineering, Tel Aviv University, Tel Aviv, Israel
Skin Integrity Research Group (SKINT), University
Centre for Nursing and Midwifery, Department of
Public Health and Primary Care, Ghent University,
Ghent, Belgium
Department of Mathematics and Statistics, Faculty of
Sciences, Hasselt University, Hasselt, Belgium
e-mail: gefen@tauex.tau.ac.il
cal processes such as wound healing. In addition
to its protective mechanical function and ability to
conform to the changing body structure, the skin
maintains water equilibrium in the body, reduces
heat and water loss, and contains nerve bers for
sensation and immune-responsive cells [1, 2].
The external layer of the skin, called the epidermis, varies in thickness depending on its anatomical location and function. This layer consists
of a stratied squamous epithelium of keratinocytes, delimited by the basal membrane and containing melanocytes, Langerhans cells, and
Merkel cells [3, 4]. The internal skin layer,
termed the dermis, is a connective tissue that represents most of the skin substance and structure.
The dermis is composed of broblasts and extracellular matrix (ECM) enriched in collagen and
elastin bers and can be divided into two sublayers: the upper papillary and the thicker lower
reticular dermis. The skin mechanical properties
at a certain anatomical site, such as the stiffness
and strength, are mostly due to the local composition, organization, and directional preference of
the ECM microarchitecture in the dermis [5].
Lastly, beneath the dermis is the hypodermis
which is composed primarily of adipocyte cells
that store lipids and triglycerides; this is often not
regarded as an integral part of the skin organ.
Healthy skin tissue is normally “pre-stretched”
over the body surfaces, that is, has inherent residual tension internally (known as residual tension
stresses), but upon even a small incisional wound,
the skin relaxes as cell-cell and cell-matrix forces
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_9
73