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3 Anatomical Base forDiagnosis
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23
can present red dots consisting of capillaries. A
single plaque or segmentary plaque may be
present.
Hyperpigmentation and telangiectasias are
often found around clinically asymptomatic
lesions. It is not a specic nding of venous
insufciency because it can also be detected in
other vascular disorders [10]. It may be a prognostic factor because its severity is associated
with poor wound healing [11].
Stasis Dermatitis
Stasis dermatitis is a chronic eczema forming on
the skin where venous stasis is present. Initially,
it is more localized and subsequently extends. It
is characterized by the presence of yellow serum
crusts. Becoming chronic, it may have a
lichenied appearance. Dermatitis around the
lesion can also be aggravated by sensitization to
topical drugs [9].
Pigmented Purpuric Dermatosis
Pigmented purpuric dermatoses are a group of
dermatoses that may have different causes. Some
triggers can be autoimmune pathologies such as
dermatomyositis and rheumatoid arthritis, infectious pathologies such as infections with HBV
and HCV, and neoplasias such as Hodgkin’s lymphoma. There are also idiopathic forms such as
Schamberg’s pigmentary purple, Majocchi’s telangiectasic purple, Doucas and Kapetanakis’
eczematid-like purple, and Gougerot and Blum’s
lichenoid dermatitis. There is then a form that can
develop in the context of venous insufciency of
the lower limbs and is called chronic pigmentary
Favre-Chaix purple. It is characterized by purple
and hyperpigmentation associated with other
signs of venous insufciency such as edema and
cyanosis.
The hyperpigmentation is determined by hemosiderosis or chronic hemoglobin deposition.
3.2.2 Arterial Leg Ulcers
Arterial ulcers usually develop in patients with
peripheral arterial disease, represented in most
cases by atherosclerosis. On physical examination, arterial ulcers have well-demarcated borders, and they seem to be “punched out” [7].
They are mainly located on bone prominences or
pressure sites and particularly on the front of the
legs, the toes, the forefoot, the malleolar region,
and the heel, where vascularization is less effective. Wounds are often painful. At the base of the
wound, there is no granulation tissue but necrosis. The skin around the lesion is often pale or
cyanotic, cold, and atrophic. Alterations of the
skin adnexa can be present. In severe peripheral
arterial disease, the peripheral pulse may be
absent and tissue necrosis may develop, which
can lead to gangrene. However, this condition is
present in just 20% of peripheral ulcers [12].
3.2.3 Diabetic Ulcers
Diabetic ulcers usually develop in patients with
uncontrolled diabetes mellitus for a long time.
Diabetes causes damage to both peripheral nerves
and arterial vessels. Diabetic ulcers may be associated with peripheral neuropathy with reduced
tactile, vibratory, and pain sensitivity.
Hyperkeratosis or callous can be present in areas
under pressure and is a sign of risk for the formation of this kind of ulcer. Diabetic ulcers are often
located on the soles of the feet and the ngers.
Diabetic ulcers can be deep to the bone. Softtissue infections and osteomyelitis should always
be excluded as they increase the consequences
and often the diagnosis is delayed. If osteomyelitis is suspected, it is necessary to carry out laboratory and imaging tests to exclude it.
Exudate
High ambulatory intravenous pressure can produce exudate. The quality of the exudate and its
composition may be useful for diagnosing an
underlying infection.
3.2.4 Uncommon Type ofUlcers
Besides the main groups of ulcers represented by
venous, arterial, and diabetic ones, there are some
others. In these cases, the patient’s history is fun-
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I. Zalaudek and M. Pauluzzi
damental for the diagnosis. However, they have
some clinical features that can lead to the correct
diagnosis.
3.2.4.1 Hematological Ulcers
Hematological ulcers develop in patients with
beta-thalassemia or sickle cell anemia. There is
an increased blood viscosity that leads to blood
stasis and insufcient oxygen intake to the tissues, developing ulcers. The main features of
these ulcers are dull pain and slow healing [13].
3.2.4.2 Martorell’s Ulcer
Martorell’s ulcer is an ischemic ulcer of the lower
extremities in patients with hypertension. They
present clinically with disproportionate pain to
the size of the ulcer itself and a specic color. It
is located at the middle third of the leg. Often, a
cyanotic area can be seen, formed as a result of
trauma. They expand quickly, having a bottom
not very deep, clean margins, and a red center.
3.2.4.3 Lymphatic Ulcers
Lymphatic ulcers originate in tissues with chronic
edema due to the accumulation of lymph.
Cynically, there are often blistered lesions leaving erosions after their rupture. The bottom of the
lesions is rosy, and cutaneous dystrophies around
the ulcer can be found.
3.3 Dierential Diagnosis Based
onClinical Features
3.3.1 Localization
They are located at the right and left legs indifferently. The 21% of cases are bilateral. Venous
ulcers can also involve the lateral malleoli, and
one in 20 patients, the dorsum or lateral aspects
of the feet [15].
Arterial ulcers are usually located on the anterior leg, distal dorsal foot, or toes and typically
show additional signs of cyanosis and pain [4].
Neuropathic ulcers are usually deep. They are
localized to the areas of highest body pressure
such as plantar regions. Sometimes, they are
associated with calluses, a sign of repeated
trauma and pressure exerted.
Pressure ulcers are usually localized at the
level of the coccyx, heels, and hips, typically
above the bone prominences.
3.3.2 Size ofUlcers
Evaluating a patient with ulcers, another aspect
to consider during the physical examination is the
size of the ulcer. Venous ulcers are dimensionally
larger than those of different etiology.
Furthermore, venous ulcers are irregular, supercial, with well-dened margins, and often localized on bone prominences. The recurrence of an
ulcer in the same area is highly suggestive of a
venous etiology [16].
The slow healing of arterial ulcers implies the
presence of poor granulation tissue with sometimes exposition of tendons. Arterial ulcers can
also be associated with the absence of peripheral
pulse, cold extremities, and longtime venous lling [7].
The initial assessment of an ulcer must rst consider its localization.
Venous ulcers are more frequently located on
the legs, while those on the foot are more frequently arterial or neuropathic ulcers [4].
Venous ulcers, also called varicose or stasis
ulcers, [14] can occur anywhere on the leg.
Specically, they are more often found near the
medial malleolus. This anatomical region is
called the “gaiter area” because it corresponds
with the location of certain styles of boots of
British soldiers.
3.3.3 Symptoms
Another important clinical aspect of diagnosis is
the presence of symptoms. Venous ulcers are
typically dened as asymptomatic. In patients
with pain, a different etiology should be considered, for example, arterial insufciency
(Table3.1). However, 3/4 of patients report pain
even with venous ulcers. Despite the symptoms,
venous ulcers are extremely impacting on the life
quality of the patients.
3 Anatomical Base forDiagnosis
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Table 3.1 Differential diagnosis between venous, arteriale and neuropathic extremity ulcers
Lower extremity ulcers—differential diagnosis
Ulcer type Pathophysiology Location Morphology Symptoms
Venous Venous
insufciency
Arterial Tissue ischemia Anterior leg, distal
Neuropathic Pressure trauma Foot below the ankle,
Gaiter area on medial
malleolus
dorsal foot, anterior leg
Pressure sites
Supercial
Varicose veins
Edema
Atrophie blanche
Lipodermatosclerosis
Well-demarcated
borders
Pale
Necrosis
Hyperkeratosis or
callous
Evening pain
Feeling of weight relieved
by elevation of leg
Painful
Peripheral neuropathy
25
Arterial ulcers are extremely painful. Pain
may be absent when associated with diabetic
neuropathy.
Diabetic ulcers present the symptoms of
peripheral neuropathy with tactile, painful, and
vibratory sensory decits.
Coexisting comorbidities may also help during the diagnosis process. With concomitant
rheumatologic diseases, (10–15% of patients
with ulcers) arterial damage can be hypothesized.
Diabetes mellitus more frequently deals with
neuropathic or arterial ulcers.
References
1. Nelzen O, Bergquist D, Lindhagen A. Venous and
non-venous leg ulcers: clinical history and appearance
in a population study. Br J Surg. 1994;81:182–7.
2. Callam MJ, Harper DR, Dale JJ, Ruckley CV.Chronic
ulcer of the leg: clinical history. Br Med J (Clin
Res Ed). 1987;294(6584):1389–91. https://doi.
org/10.1136/bmj.294.6584.1389.
3. Spear M. Venous ulcers-an evidence-based update.
Plast Surg Nurs. 2012;32(4):185–8. https://doi.
org/10.1097/PSN.0b013e31827781b8.
4. Valencia IC, Falabella A, Kirsner RS, Eaglstein
WH. Chronic venous insufciency and venous leg
ulceration. J Am Acad Dermatol. 2001;44(3):401–24.
https://doi.org/10.1067/mjd.2001.111633.
5. Alguire PC, Mathes BM. Chronic venous insufciency and venous ulceration. J Gen Intern Med.
1997;12:374–83.
6. Hampton S. An introduction to various types of
leg ulcers and their management. Br J Nurs. (Mark
Allen Publishing). 2006; https://doi.org/10.12968/
bjon.2006.15.sup2.21235.
7. Millan SB, Gan R, Townsend PE. Venous ulcers:
diagnosis and treatment. Am Fam Physician.
2019;100(5):298–305.
8. Wright N, Fitridge R.Varicose veins: natural history,
assessment and management. Aust Fam Physician.
2013;42(6):380–4.
9. Falanga V.Venous ulceration. J Dermatol Surg Oncol.
1993;19(8):764–71. https://doi.org/10.1111/j.1524-
4725.1993.tb00422.x.
10. Cooper DL. Atrophie blanche in a patient with
gamma-heavy-chain disease. Arch Dermatol.
1991;127(2):272b–273. https://doi.org/10.1001/
archderm.127.2.272b.
11. Greenberg AS, Hasan A, Montalvo BM, Falabella
A, Falanga V. Acute lipodermatosclerosis is associated with venous insufciency. J Am Acad
Dermatol. 1996;35(4):566–8. https://doi.org/10.1016/
S0190- 9622(96)90681- 7.
12. Collins TC, Suarez-Almazor M, Petersen NJ. An
absent pulse is not sensitive for the early detection of peripheral arterial disease. Fam Med.
2006;38(1):38–42.
13. Van Gent WB, Hop WC, van Praag MC, Mackaay AJ,
de Boer EM, Wittens CH.Conservative versus surgical
treatment of venous leg ulcers: a prospective, randomized, multicenter trial. J Vasc Surg. 2006;44(3):563–
71. https://doi.org/10.1016/j.jvs.2006.04.053.
14. Chamanga ET.Understanding venous leg ulcers. Br
J Community Nurs. 2018;23:S6–S15. https://doi.
org/10.12968/bjcn.2018.23.Sup9.S6.
15. Schneider C, Stratman S, Kirsner RS. Lower
extremity ulcers. Med Clin N Am. 2021; https://doi.
org/10.1016/j.mcna.2021.04.006.
16. Collins L, Seraj S.Diagnosis and treatment of venous
ulcers. Am Fam Physician. 2010;81(8):989–96.
Wound Hygiene: FromTraditional
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toMicroenvironment inCleansing
ArturoCaniglia
4
Since the birth of modern wound care according
to the principles of healing in a moist environment [1] and, certainly, for the last two decades,
the focus of wound care professionals has mainly
been the assessment, needs, and evolutionary
state of the wound [2]. Despite the need to contemplate a holistic vision [3] of the patient with
skin ulcers being formalized in 2019, the importance of hygiene, as a “set of behaviors aimed at
good health,” has never been of such crucial
importance as it has today.
Until very few years ago, in fact, if practices
such as debridement, control of the bacterial
load, or management of the exudate were potentially led by codied and shared procedures, with
cleansing we relied on the assessment and discretion of the operator assuming, erroneously, that it
could be taken for granted and that it was not supported by well-dened scientic principles, other
than those of common sense.
The methods of coarse removal of evident
debris—such as the practice of “cleansing”
was defined—were commonly performed only
when blatantly necessary, mainly by means of
irrigation with saline solution, Ringer lactate,
or antiseptic solutions and, eminently, only on
the wound bed and on the surrounding skin,
A. Caniglia (*)
ASST Centro Specialistico Ortopedico
Traumatologico Gaetano Pini-CTO, Milan, Italy
understood as a radius of about 5cm around
the lesion [4].
With the exception of any patient allergies of
the patient to specic components, the only recommendation was not to use histo-/cytodamaging solutions or products expressly
contraindicated for use on damaged skin.
Cleansing is the rst physical action of topical
cleansing, both on the wound bed and peri-wound
skin, to remove debris; it must be a constant act in
standard care and is a process that promotes tissue regeneration and promotes healing.
It is important to constantly perform cleansing
to reduce the bacterial load and remove devitalized tissue, waste, and debris of various origins,
thus enabling assessment of the wound background and promoting optimal conditions for the
repair process.
Wound cleansing algorithm is displayed in
Fig.4.1.
A number of factors must be taken into
account to perform proper cleansing:
• The right solution that must not be cytotoxic
and must not procure sensitivity reactions, but
must be biocompatible, and must reduce the
number of pathogenic microorganisms from
the bottom of the lesion.
• The right temperature should be body tem-
perature. Cold solutions should be avoided
because they slow down cell repair and cause
vasoconstriction, and by blocking mitotic
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. Maruccia et al. (eds.), Pearls and Pitfalls in Skin Ulcer Management,
https://doi.org/10.1007/978-3-031-45453-0_4
27
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A. Caniglia
Wound Assessment
Clean
Epithelializing
Wound
Irrigate with < 7 PSI
pressure, or pour
solution over the
wound bed.
Use at least 100cc’s
of solution, at room
or body temperature.
Cleanse the
periwound skin of
debris, exudates.
No antimicrobial
solutions.
Clean Granulating
Wound, Decreasing in
Surface Area 20-30%
in 3-4 Weeks*
Irrigate with < 7 PSI
pressure, or pour
solution over the
wound bed.
Use at least 100cc’s
of solution, at room
or body temperature.
No antimicrobial
solutions.
Clean Granulating
Wound NOR
Decreasing in Size
20-30% in 3-4
Irrigate with 7-15 PSI
pressure.
Use at least 150cc’s
of solution, at room
or body temperature.
Cleanse the
periwound skin of
debris, exudates.
*Granulationg wounds
not decreasing in size
may have a localized
infection.
Necrotic Healable
Wound
(Debridement is
Appropriate)
Irrigate with 7-15 PSI
pressure.
Use at least 150cc’s
of solution, at room
or body temperature.
Cleanse the
periwound skin of
debris, exudates.
Necrotic Non-
Healable Wound
(Debridement is NOT
Appropriate)
Do not irrigate or
cleanse the wound
itself (the intent is to
allow the necrotic
tissue to dry out and
stabilize).
If there is exudate
present on the
periwound skin,
gently cleanse it and
pat dry.
Topical application of
proviodine-ipdine
solution or
Chlorhexadine to the
wound surface is
appropriate, i.e.
paint with
Proviodine.
Fig. 4.1 Wound cleansing algorithm
activity for ¾hours, macrophages are inhibited, leukocyte activity is nullied, and this
can result in the increased incidence of sepsis
and cause discomfort and pain sensation to the
patient.
• The right hydraulic force, i.e., an irrigation
pressure, is 8psi.
• The right volume to ensure adequate cleansing
over the entire lesion bed may vary depending
on the size, but is usually quantied between
100 and 150ml.
The right technique is choosing between
swabbing, soaking, or irrigation, the one that is
most appropriate in a given context and that can
guarantee the effectiveness of the cleansing
process.
Cleansing should be done at every approach to
the wound and at every dressing change, before
and after the use of antiseptics, and before and
after debridement procedures.
Commonly used simple isotonic cleansers
include:
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29
• Physiologic Solution—Which is an isotonic
solution, biocompatible, does not alter pH,
maintains chemical balance at the bottom of
the wound, and has no antimicrobial action.
• Drinking Water—Not a very popular method
although recommended by some authors in
the literature.
• Ringer’s Lactate Solution—Contains lactic
acid, calcium chloride, sodium chloride, and
potassium chloride that is credited with promoting skin trophism.
Recent generation cleansers, on the other
hand, are:
• Surfactant enriched with surface-active action
such as the combination of polyhexanide
(Phmb), which is an antimicrobial substance
that inhibits the growth of microorganisms,
and betaine (surfactant), which acts on biolm
by promoting its detachment and inhibiting
bacterial growth.
• Superoxidized solutions with chlorine that
reduce the microbial load and help create a
favorable environment for the healing
process.
In June 2020, supported by numerous studies
[5–8], biolm was formally identied as the primary cause of delayed wound healing [9], effectively redening, on the basis of the characteristics
of this community of pathogens, a skin ulcer
management approach according to an operating
procedure in four consequential phases (cleansing, debridement, reactivation of the edges, and
medication), published in an International
Consensus document called, not surprisingly,
Wound Hygiene [10].
Here, it is unequivocal how much the very
purposes of cleansing must inevitably change,
hand in hand with the evolution of our knowledge
about the causes of delayed healing, moving
toward a methodical application of cleansing procedures, made up of consequential steps,
extended to a large area of healthy skin (at least a
10–20 cm radius around the lesion, given the
migratory capacity of mature biolm colonies
[11, 12]), and with specic solutions and
methods.
Hygiene and, more precisely, the cleansing
procedure of healthy skin, as well as that affected
by the lesion, become a direct tool to contrast the
chronicity status of the lesion, acquiring an
essential importance and a new denition, which
includes, in addition to the removal of visible
dirt, even that of what is invisible, i.e., antisepsis
[10–12].
According to current evidence [11, 12], simple irrigation with solutions, albeit antiseptic, is
not effective for the disintegration of the biolm
EPS matrix and, therefore, for the elimination of
pathogens and elements favoring their engraftment and proliferation.
A correct cleansing procedure involves three
consecutive acts [13, 14] necessarily united by a
mechanical action of variable intensity, depending on the etiology of the lesion [10, 15], one’s
own skills15, and the evolutionary state of the tissues [15]:
1. Transition with surfactant solutions or non-
foaming soaps at physiological pH [16].
Surfactants, especially if left in a compress,
have the ability to reduce surface tension and
consequently facilitate the removal of debris
and of the EPS matrix (consisting mainly of
polysaccharides)12, which protects the bacterial colonies of the biolm from the action of
antimicrobials. Furthermore, it appears that
they can help reduce the perception of procedural pain in the patient [17]. Respecting the
pH of the skin also helps to preserve its functional characteristics and to create an environment hostile to bacterial engraftment.
2. Passage with antiseptic solutions.
Antimicrobials, if used subsequently or concomitantly to the mechanical action, allow
effective bacterial killing and inhibition of the
sessile aggregation of pathogens [9, 11–13].
When choosing the active ingredient, solutions with high cytotoxic power, for example,
based on hydrogen peroxide or povidone–
iodine, are not recommended [13, 18].
3. Rinse with saline or Ringer lactate. The inten-
sive and repeated use of surfactant and antiseptic solutions could lead to impairment of
skin integrity, as well as induced irritation or
sensitization phenomena [19–21]. The good
30
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A. Caniglia
health of the wound bed, peri-wound skin,
and healthy skin are essential for a rapid healing process.
To be effective, each of these steps should be
performed with the application of mechanical
energy, with due exceptions for all those lesions
whose etiology determines an explicit contraindication (e.g., neoplastic, autoimmune, and ischemic lesions [10, 15]).
Furthermore, the intensity of action should
respect the progressive state of the tissues and
modulate accordingly, reducing the intensity as
the positive results of the entire treatment are
conrmed and as epithelialization approaches
[15]:
• Necrotic Tissue: Vigorous action, compatible
with the patient’s procedural pain, to ensure
adequate reclamation of the environment.
• Slough: Vigorous action, compatible with the
patient’s procedural pain, to ensure adequate
reclamation of the environment.
• Unhealthy Granulation: Vigorous action,
compatible with the patient’s procedural pain,
to ensure adequate reclamation of the
environment.
• Healthy Granulation: Moderate action, so as
not to cause traumatism.
• Epithelialization: Delicate action, in order not
to damage the newly formed tissues, but to
ensure the reclamation of the environment in
the most critical phase of scarring.
The appropriate tools for the transmission of
mechanical energy can vary, depending on the
materials available, from pre-soaked sponges, to
pads and common gauzes, in which case frequent
replacement is suggested.
In addition, particular attention should be paid
to the removal of hyperkeratotic plaques or skin
scales, often home to biolm colonies with the
ability to cross-migrate between the wound bed
and surrounding areas of healthy skin.
Compliance with the correct execution is
essential in contributing to the disintegration of
the biolm, in the inhibition of its reformation, in
creating an environment hostile to the contamina-
tion and proliferation of pathogens and, therefore, in accelerating the natural healing process
of the lesions.
References
1. Winter GD. Formation of the scab and the rate of
epithelization of supercial wounds in the skin of the
young domestic pig. Nature. 1962;193:293.
2. Schultz GS, Gary Sibbald R, Falanga V, Ayello EA,
Dowsett C, Harding K, Romanelli M, Stacey MC,
Teot L, Vanscheidt W.Wound bed preparation: a systematic approach to wound management.
3. International consensus document. Implementing
TIMERS: the race against hard-to-heal wounds. Part 3
February 2020. Br J Health Care Manag 14(2):80-83.
https://doi.org/10.12968/bjhc.2020.14.2.80.
4. LeBlanc K, Beeckman D, Campbell K, et al. Best
practice recommendations for prevention and management of periwound skin complications. Wounds
International; 2021.
5. Høiby etal, 2015; Wolcott etal, 2016; Wolcott, 2017.
6. Bjarnsholt T, Eberlein T, Malone M, etal. Management
of biolm. Wounds International. 2017;8:2.
7. Schultz G, Bjarnsholt T, James GA, etal. Consensus
guidelines for the identication and treatment of biolms in chronic nonhealing wounds. Wound Repair
Regen.
8. Haesler E, Swanson T, Ousey K, etal. Clinical indicators of wound infection and biolm: reaching international consensus. J Wound Care. 2019;28:s4–12.
https://doi.org/10.12968/jowc.2019.28.Sup3b.S4.
9. International Wound Infection Institute (IWII).
Wound infection in clinical practice: international
consensus update 2016. Wounds International; 2016.
10. Murphy C, Atkin L, Swanson T, Tachi M, Tan YK,
Vega de Ceniga M, Weir D, Wolcott R.International
consensus document. Defying hard-to-heal wounds
with an early antibiolm intervention strategy: wound
hygiene. J Wound Care. 2020;29(Suppl 3b):S1–28.
11. Stewart PS. Biophysics of biolm infection. Pathog Dis. 2014;70:212–8. https://doi.
org/10.1111/2049-632X.12118.
12. Malone M, Swanson T. Biolm-based wound care:
the importance of debridement in biolm treatment
strategies. Br J Community Nurs. 2017;22:S20–5.
https://doi.org/10.12968/bjcn.2017.22.Sup6.S20.
13. Wolcott R, Fletcher J. The role of wound cleansing in the management of wounds. Wounds Int.
2014;1(1):25–30.
14. Kamolz L-P, Wild T. Wound bed preparation: the
impact of debridement and wound cleansing. Wound
Med. 2013;1:44–50.
15. Murphy C, Atkin L, Vega de Ceniga M, Weir D,
Swanson T. International consensus document.
Embedding Wound Hygiene into a proactive wound
healing strategy. J Wound Care. 2022;31:S1–S24.
4 Wound Hygiene: FromTraditional toMicroenvironment inCleansing
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16. Percival SL, Chen R, Mayer D, et al. Mode of action
of poloxamer-based surfactants in wound care and
efcacy on biolms. Int Wound J. 2018;15:749–55.
https://doi.org/10.1111/iwj.1292216.
17. Tyldesley HC, Salisbury A, Chen R, etal. Surfactants
and their role in biolm management in chronic
wounds. Wounds Int. 2019;10(1):20–4.
18. Sibbald RG, Leaper DJ, Queen D.Iodine made easy.
Wounds Int. 2011;2:2.
19. Antisepsi e disinfezione in ambito sanitario e sociosanitario Regione Emilia Romagna aprile 2011.
20. Roberts CD, Leaper D, Assadian O.The role of topical antiseptic agents within antimicrobial stewardship
strategies for prevention and treatment of surgical site
and chronic open wound infection. Adv Wound Care.
2017;6(2):63–71.
21. Alves PJ, etal. Update on the role of antiseptics in the
management of chronic wounds with critical colonization and\or biolm. Int Wound J. 2020:1–17.
Principles ofAntiseptic Treatments
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ElisabettaIacopi , FrancescoGiangreco,
andAlbertoPiaggesi
5
5.1 Denition ofAntisepsis
Antisepsis is a term that derives from the Greek
words “αντι,” which stands for “against” and
“σῆψις” meaning “putrefaction.” It consists in
the complete abolition of bacterial load, both
pathogenic and not from a naturally or articially
sterilized substrate [1]. Antisepsis procedures
aim to get an ideal state in which it has been
achieved the complete absence of pathogenetic
organisms and transient ora: the asepsis.
Antisepsis can be considered as the collection of
preventative methods to promote asepsis [2].
Antisepsis in this sense must be distinct from
“disinfection,” which is related to the elimination
of only pathogenic species, and from “sterilization,” which consists in the process of full
removal of all bacteria, viruses, and fungi from a
solid, aerial, or liquid medium [3].
5.2 History ofAntisepsis
The great physicians of ancient ages knew infection as pathological entity and were aware of its
importance in determining death for many
patients. They were still completely clueless
regarding possible causes of infection, and there-
E. Iacopi (*) · F. Giangreco · A. Piaggesi
Diabetic Foot Section, Pisa University Hospital,
Pisa, Italy
fore, no concept regarding antisepsis or disinfection was developed [4].
The rst proof of some attempts to treat skin
wounds to achieve healing dates back to Ancient
Egypt where many papyri report suggestions
regarding ulcer treatment. Egyptian doctors had
understood the importance of cleaning ulcers:
They used honey and donkey feces that are rich
in trypsin, an amino acid subsequently proven to
be involved in healing processes. They furthermore suggested to clean wounds with boiled
water or wine [5].
About one thousand years later, other reports
of wound treatment were reported in
Mesopotamia, under the age of Sumeri. They
produced more than 19 different types of beer
using some of them also for medical purposes, in
particular, applying it on chronic wounds. They
also used a mixture of different herbs, among
which Aloe Barbadensis, to avoid worsening the
wound’s conditions [6].
Going forward also regarding wound
approach, as for many other medicinal elds, the
Greeks were forerunners and visionaries. The
most important intuitions were attributable to
Galen, a philosopher and doctor from Pergamum
who worked in Greece and Rome and who, in
occasion of an epidemic, suggested to isolate
affected patients and to keep people away from
the city; Hippocrates, instead, for rst described
the best behavior in case of wounds. He started to
clean the wound with vinegar or wine and to
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M. Maruccia et al. (eds.), Pearls and Pitfalls in Skin Ulcer Management,
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cover it with clean towels. They were aware that
there was something deeper to be understood but
still far from achieving full comprehension [7].
Contemporarily, in Asia, both Ayurvedic
Indian medicine and traditional Chinese one
developed some theories focused on the search
for useful substances to heal wounds. Indian
medicine foresaw the complete cleansing of the
wound and then the application of copper or silver powder and of turmeric paste that contains
curcumin, a powerful anti-inammatory active
principle still in use nowadays, and also able to
control pain symptoms [8]. In China, instead, the
use of herbs was spreading to control inammation, and their application on chronic wounds
was considered particularly important.
In the Middle Ages, Europe underwent a long
period of obscurantism and scientic censorship
in which superstition and religion prevented,
with their limitations, the evolution of medical
knowledge in general. Therefore, also the awareness and knowledge in terms of wound infection
and wound healing were limited [9]. In this
period, the only ndings were attributable to
Hieronymus Fracastorius and Francois Parè. The
former postulated that the cause of infectious diseases was invisible living seeds. In his work, “De
contagione” published in 1546, he described
three modalities of disease spreading: direct contact with infected persons, indirect contact with
fomites, and airborne transmission. Parè, considered one of the fathers of modern surgery, similarly believed infection was introduced from the
environment and highlighted the importance of a
sterile environment in the prevention of disease
transmission [10].
In the Modern Ages, with the evolution of
medical knowledge and the development of surgical techniques, great relevance was given to the
huge frequency of post-surgery infection. It was
related to dramatic hygiene conditions of hospitals, surgical elds, and instruments [11]. First,
Ignac Semmelweiss, in the nineteenth century, a
Hungarian surgeon who led the rst division of
the maternity hospital at Vienna General Hospital,
forced doctors, nurses, and midwives to clean
their hands with a solution of calcium chloride
before visiting women in labor. The result was a
sudden collapse of puerperal fever and subsequent deaths [12].
The modern concept of infection was born in
1861 by the father of microbiology: Louis
Pasteur. With the famous chicken broth experiment, he refuted the theory of spontaneous generation according to which bacteria, protozoa,
and other microscopic beings could arise directly
from matter [13]. In the same period in Germany,
an arch-competitor of Pasteur, Robert Koch,
demonstrated the direct microbe’s responsibility
in the development of infectious diseases. The
German physician and scientist, through his studies on tuberculosis and cholera, created the socalled Koch Postulates, which earned him the
Nobel Prize in 1905. In these rules, he stated that
the pathogenetic microorganism must be present
in affected patients, isolable and cultivable, and
when inoculated in a healthy subject must determine the initial disease [14].
Eventually, Joseph Lister, a Professor of
Surgery at Glasgow, in the 60s of the nineteenth
century applied Pasteur discoveries in clinical
surgical practice, and he observed that cases of
infection were much more numerous in overcrowded hospitals in English cities than in the
countryside, where the patient was usually treated
in farmhouses. Based on these assumptions, he
understood that infection and gangrene were
associated with transmission of microorganisms
among patients. He therefore decided to apply on
an exposed fracture, a recently synthesized compound used as a disinfectant for sewers: phenol,
at the time called carbolic acid. With this method,
he managed to avoid the death of the patient. He
continued to use this substance in a series of
patients and described his experience in a paper
published on Lancet in 1867, entitled “Antiseptic
Principle of the Practice of Surgery” where the
term “antisepsis” [15] appeared for the rst time.
5.3 Denition ofAntiseptic
Agent
Antiseptic is dened as an agent able to inhibit
the growth and development of microorganisms.
Antiseptics are chemical products with antimi-
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