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56
Autolysis
Osmosis
Enzymes
Hydro
Ultra
Surgery
90 days
60 days
45 days
35 days
25 days
10 days
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Table 6.5 Environmental and behavioral factors of the patient
EBF: environmental and behavioral factors of the patient
Score
FAC Indicators Yes=1/no=0
1° Intake of corticosteroid drugs 1
2° Taking anti-cancer drugs 1
3° Taking anticoagulant drugs 1
4° The patient has no assistance 1
5° The patient lives in an unhealthy environment 1
6° The patient lives alone 1
7° The patient does not exercise any physical activity 1
8° The patient smokes 1
9° The patient drinks excess alcohol 1
10° The patient has no scholarship 1
Max 10
Table 6.6 TIMEH protocol
C. Ligresti
T
I
M
E
25 days
Physiological
Solution
Ringer
55 days
Hydrocolloids
Hydrogel
55 days
Hydrocolloids
Hydrogel
Collagen
Hyaluronic
acid
20 days
Local
antiseptics
40 days
Collagen
Hyaluronic
acid
45 days
Growth
Factors
Carboxy
therapy
Larvae
15 days
Antiseptic
Silver
Dressings
35 days
Alginates
35 days
VAC
Oxidized
Regenerated
Cellulose
therapy
1 day
Antiseptic
Silver
Dressings
VAC
21 days
Hydrofibers
28 days
Allo-Skin
Graft
Dermal
substitutes
sound
1 day
Antiseptic
Silver
Dressings
VAC
Antibiotic
15 days
Poly
urethane
21 days
VAC
Growth
factors
Dermal
substitutes
1 day
Surgery
VAC
12 days
VAC
15 days
Skin
graft
Flaps
Surgery
Antiseptic
Silver
Dressings
VAC
Antibiotic
7 days
Surgery
10 days
non-healing. Because of poor perfusion, metabolic gas exchange at the level of tissues becomes
inefcacious.
It has been shown that the healing of a wound
following surgery is compromised by dehydra-
tion and by a low body temperature of the patient,
factors that are associated with reduced perfusion
tissue and poor oxygenation (Table6.6).
Physical factors, such as diabetes mellitus,
obesity, malnutrition, advanced age [over 60],
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57
decreased perfusion, peripheral vascular disease,
cancers, organ failure, sepsis, and even restrictions on mobility, can affect the healing process.
Marston etal. have found that improved glycemic control has a positive inuence on the outcome of diabetic foot wounds, particularly when
dermal substitutes are used.
Terms of immunodeciency, use of immunosuppressive drugs [corticosteroids, azathioprine,
or methotrexate], and the presence of diseases
[such as diabetes mellitus] known to affect the
immuno-inammatory response are all circumstances that may inuence negatively healing and
increase the risk of wound sepsis It was also
found that psychosocial factors such as social
isolation, gender, smoking, the economic conditions, and the experience of pain could inuence
wound healing.
Stress and depression have been linked to
changes in immune function and may therefore
adversely inuence a wide range of physiological
processes, including wound healing. In a human
experimental model, it was found that stress and
depression had a possible role in the modulation
of matrix metalloproteinases [MMPs] and
expression of tissue inhibitors of metalloproteinases [TIMP].
According to some studies, also the ability to
cope with stress is a factor that can inuence
healing times. Salaman etal. studied a group of
45 hospital patients with venous ulcers, 16 [36%]
of who do not make satisfactory progress. Only
half of these 16 patients said they had received
any explanation about the cause of the ulcer and
the treatment method used.
This study raises important questions about
the impact on wound healing of the patient’s
beliefs and their condence in treatment. Blunting
is the case of patients who are indifferent to the
processing and not very interested in the progress
of the wound toward the healing. Although the
feeling of helplessness is experienced by some
patients, many of them make every effort to
ensure that the care they receive meets their
needs. Some patients become experts in their
own condition, often using the Internet to gather
information on it.
When a wound is located on a pressurebearing surface or a mobile area such as around a
joint, the choice of the material of the dressing
and the method of attachment is of extreme
importance.
However, Chipchase et al. observed that,
while the overall healing rates of foot ulcers were
similar, lesions located in the heel tended to heal
more slowly. The authors concluded that the outcome was generally favorable, with 65.6% of
heel ulcers healed in a median time of 200days.
Harding has the potential effect of broblast
senescence on chronic wound healing.
There was a correlation between the ratio of
senescent broblasts/non-senescent broblasts
and healing outcomes: An accumulation of more
than 15% senescent broblasts is considered the
threshold beyond which wounds will have trouble healing.
Moreover, the response to treatment can be an
indicator of tissue viability and healing potential.
For example, it was suggested that a reduction in
wound area of around 15% within 1–2weeks of
topical negative pressure therapy is a positive
indicator of the likely evolution of the wound and
that this observation can be the decision to continue therapy.
As seen above, many attempts and proposals
tend to quantify the time required for wound
healing. On the basis of previous attempts, our
aim is to propose an algorithm not only to accurate the quantication of healing time, but also a
precise protocol of treatment to be associated
with any situation and any type of wound. It is
therefore clear, as the challenge of healing a skin
lesion cannot be achieved by a single specialist.
It is fundamental collaboration between various
specialists. It is obvious that the planning therapy
must be organized by a team leader to coordinate
the rest of the medical staff [various specialists
including plastic surgeon, vascular surgeon, the
internist, the nutritionist, the endocrinologist, the
dermatologist, etc.] and not by hospital nurses or
domiciles medical gures. Only with careful collaboration and clearly careful training, you can
pursue the goal in the shortest time possible and
with the greatest patient comfort.
58
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C. Ligresti
This protocol sets itself as a general guideline for the ulcer treatment for all types of professionals involved in the management of the
patient but is particularly useful for those who
approach the world of vulnology [wound treatment], but who do not yet have detailed knowledge about it. It appears a useful tool, and since
for the rst time, it offers a mathematical model
in which a score is calculated and according to
the same applies a type of therapy.
In conclusion, the algorithm that we propose
is a useful tool for staging the severity of injuries and provides a simple means to adjust therapy. It describes how the therapy used should
change signicantly according to the type and
severity of the wound that we are facing and
how this in turn can affect signicantly the healing time estimated.
It is clear that, not always, the mathematical
calculations are an exact prediction, but allow,
however, to have a prediction of the initial situation. There are margins of error, especially when
it takes over factors that complicate the wound
management.
It is highly appreciated that, to predict the outcome of recovery in individual patients, it will be
necessary to use not a single marker, but the data
resulting from a combination of several markers,
as we proposed. Many authors have stressed the
importance of training the nursing staff, designed
to provide the knowledge and skills necessary to
establish appropriate treatment and process protocols and forms relating to wound care [25].
However, we can conclude by saying that
we do not presume to have created a perfect
model for the treatment of skin lesions, and we
only want to provide a useful tool to the caregiver based on current knowledge and on current therapeutic strategies. We are still waiting
for new knowledge that can lead us to an even
higher level in the treatment of this complex
disease [26].
References
1. Chase SK, Melloni M, Savage A.A forever healing:
the lived experience of venous ulcer disease. J Vasc
Nurs. 1997;15(2):73–8.
2. Kramer JD, Kearney M. Patient, wound, and
treatment characteristics associated with healing in pressure ulcers. Adv Skin Wound Care.
2000;13(1):17–24.
3. Franks PJ, Moffatt CJ.Do clinical and social factors
predict quality of life in leg ulceration? Int J Low
Extrem Wounds. 2006;5(4):236–43.
4. Moor AN, Tummel E, Prather JL, Jung M, Lopez JJ,
etal. Consequences of age on ischemic wound healing in rats: altered antioxidant activity and delayed
wound closure. Age (Dordr). 2014;36(2):733–48.
5. Margolis DJ, Berlin JA, Strom BL.Risk factors associated with the failure of a venous leg ulcer to heal.
Arch Dermatol. 1999;135(8):920–6.
6. McGinnis E, Greenwood DC, Nelson EA, Nixon
J. A prospective cohort study of prognostic factors
for the healing of heel pressure ulcers. Age Ageing.
2014;43(2):267–71.
7. Little MO.Nutrition and skin ulcers. Curr Opin Clin
Nutr Metab Care. 2013;16(1):39–49.
8. Leymarie F, Richard JL, Malgrange D.Factors associated with diabetic patients at high risk for foot ulceration. Diabetes Metab. 2005;31(6):603–5.
9. Kiguchi MM, Hager ES, Winger DG, Hirsch SA,
Chaer RA, et al. Factors that inuence perforator
thrombosis and predict healing with perforator sclerotherapy for venous ulceration without axial reux. J
Vasc Surg. 2014;59(5):1368–76.
10. Guo S, Dipietro LA.Factors affecting wound healing.
J Dent Res. 2010;89(3):219–29.
11. Costa A, Cunha M.Prevalence of pressure ulcers in
person victim of trauma: predisposing factors. Servir.
2013;58(1–2):60–77.
12. Abbade LP, Lastória S, Rollo Hde A.Venous ulcer:
clinical characteristics and risk factors. Int J Dermatol.
2011;50(4):405–11.
13. Ahmad W, Khan IA, Ghaffar S, Al-Swailmi FK, Khan
I.Risk factors for diabetic foot ulcer. J Ayub Med Coll
Abbottabad. 2013;25(1–2):16–8.
14. Baba M, Davis WA, Davis TM. A longitudinal study of foot ulceration and its risk factors in
community- based patients with type 2 diabetes: the
Fremantle diabetes study. Diabetes Res Clin Pract.
2014;106(1):42–9.
15. Astudillo B, Cruz M, del Prado L, Domenack R, Nasi
E, etal. Prole of patients admitted with infected skin
ulcers at Bella Vista Hospital Mayagüez. Bol Asoc
Med P R. 2013;105(3):29–35.
16. Haji Zaine N, Burns J, Vicaretti M, Fletcher JP,
Begg L, etal. Characteristics of diabetic foot ulcers
in Western Sydney, Australia. J Foot Ankle Res.
2014;7(1):39.
17. Huliev D. Obstacles in wound healing. Acta Med
Croatica. 2013;67(Suppl 1):5–10.
18. Raju D, Su X, Patrician PA, Loan LA, McCarthy
MS. Exploring factors associated with pressure
ulcers: a data mining approach. Int J Nurs Stud.
2014;52(1):102–11.
19. Peghetti A, Mantovani M, Canova G, Ferri L. Le
medicazioni avanzate per il trattamento delle ferite
6 The TIMEH Protocol
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59
acute e croniche. Dalle evidenze della letteratura
alla pratica quotidiana. Commissione Regionale
Dispositivi Medici Reg Emilia Romagna, 2012:
1–126.
20. Bailey MA, Mc Pherson SJ, Troxler MA, Peach
AH, Patel JV, et al. Ischemic skin ulceration complicating glue embolization of type II endoleak after
endovascular aneurysm repair. J Vasc Interv Radiol.
2011;22(2):163–7.
21. AISLeC.Prolassi delle lesioni da decubito e cambio
posturale: ricerca multicentrica. AISLeC; 1995.
22. Bateman S.Principles of preventative foot care. Br J
Community Nurs Suppl. 2014;S30(S32–4):S36–8.
23. Gantwerker EA, Hom DB.Skin: histology and physiology of wound healing. Facial Plast Surg Clin North
Am. 2011;19(3):441–53.
24. Registered Nurses Association of Ontario Risk
Assessment and Management of Pressure Ulcers;
2011.
25. Hien NT, Prawer SE, Katz HI. Facilitated wound
healing using transparent lm dressing following Mohs micrographic surgery. Arch Dermatol.
1988;124(6):903–6.
26. Ligresti C, Bo F. Wound bed preparation of difcult wound: an evolution of principles of TIME.Int
Wound J. 2007;4(1):21–9.
Part II
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Dressing and Bandages
Ulcer Debridement
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TedeschiPasquale andMicheleMaruccia
7
7.1 Debridement Overview
Wound management is a crucial aspect of health
care, particularly for patients who have experienced chronic wounds or non-healing ulcers [1].
Wound bed preparation is a fundamental aspect
of this process, which involves creating an optimal environment for the wound to heal.
Achieving a clean, moist, warm, and granular
wound bed is essential for promoting healing
and protecting the periwound and intact skin.
Debridement, bacterial control, and exudate
management are all critical components of
wound bed preparation [2].
At its core, debridement is the process of
removing necrotic tissue, foreign material, and
debris from the wound bed. This procedure is
vital for wound management and serves several
purposes:
• Decreasing bacterial concentration.
• Increasing the effectiveness of topical
treatments.
• Improving leukocyte activity.
• Shortening the inammatory phase.
T. Pasquale (*) · M. Maruccia
Division of Plastic and Reconstructive Surgery,
Department of Precision and Regenerative Medicine
and Ionian Area (DiMePRe-J), University of Bari
Aldo Moro, Bari, Italy
• Freeing up energy for wound healing.
• Removing barriers for healing.
• Decreasing wound odor.
Debridement is essential in cases where
necrotic tissues, foreign materials, or debris are
present within the wound bed [3]. Large blisters
and calluses should also be debrided to promote
optimal healing. However, it is important to note
that not all wounds are suitable for debridement.
Three primary contraindications exist for this
procedure. Firstly, red granular wounds should
not be debrided, as this tissue is essential for
healing. Secondly, non-infected ischemic wounds
are contraindicated for debridement, as they lack
the necessary blood supply for optimal healing.
Lastly, current guidelines suggest that stable heel
ulcers with dry eschar should only be debrided if
they have edema, erythema, uctuance, or drainage [4, 5].
There are six primary types of debridement:
autolytic, enzymatic, biological, mechanical,
sharp, and surgical debridements. Autolytic
debridement involves the use of a moist wound
dressing to encourage the body’s natural enzymes
to break down necrotic tissue. Enzymatic debridement utilizes topical enzymes to break down
necrotic tissue, while biological debridement
involves using maggots to remove necrotic tissue. Mechanical debridement uses physical force
to remove debris and necrotic tissue, while sharp
debridement involves using surgical tools to
© 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_7
63
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T. Pasquale and M. Maruccia
remove necrotic tissue. Lastly, surgical debridement involves removing necrotic tissue through
surgical intervention [6, 7].
When deciding on the most appropriate
debridement method, clinicians should consider
the patient’s clinical condition, the type of wound,
the location of the wound, and the amount of
necrotic tissue present. Additionally, patients’
pain levels, comorbidities, and cognitive status
should also be considered when selecting the
most appropriate debridement method [8].
7.2 Autolytic Debridement
Autolytic debridement is a type of wound debridement that uses the body’s own natural enzymes to
break down and remove necrotic tissue from a
wound. This process occurs when a moistureretentive dressing is applied to the wound, which
keeps the wound bed moist and allows the body’s
enzymes to work more effectively.
In more detail, the moist environment created
by the dressing helps to activate enzymes called
proteases that are naturally present in the wound
bed. These proteases break down the proteins that
make up necrotic tissue, making it easier for the
body to remove it through the normal healing process [9].
One example of a dressing that is commonly
used for autolytic debridement is a hydrocolloid
dressing, which is designed to absorb excess
moisture from the wound and create a moist environment. Other types of moisture-retentive dressings, such as hydrogels and foams, may also be
used depending on the specic needs of the
wound [10].
Eschar (hardened or dead tissue) should be
crosshatched; this will aid in promoting the circulation of uids and enzymes during autolytic
debridement. The moisture-retentive dressing
should be applied to the wound and should extend
at least 2cm beyond the edges of the wound to
ensure a proper seal. The periwound area should
also be protected to prevent damage to the surrounding healthy tissue. Finally, signs and symptoms of infection should be carefully monitored
to ensure that the wound is healing properly.
Autolytic debridement is considered to be the
most conservative, least invasive, and least painful method of debridement. It is also easy to teach
to patients and caregivers, and it may reduce the
long-term cost of treatment. However, it is important to note that autolytic debridement requires
time for the body to naturally debride tissue, and
it does not allow frequent visualization of the
wound bed.
Autolytic debridement is indicated for noninfected wounds with necrotic tissue, patients
who cannot tolerate other forms of debridement,
and home or long-term care settings. It is not
appropriate for infected or deep cavity wounds
and wounds that require sharp or surgical debridement. If necrotic tissue fails to decrease in the
expected amount of time, other types of debridement should be considered.
In conclusion, autolytic debridement is a natural and effective way to remove necrotic tissue
from wounds. By creating a moist environment
that supports the body’s natural healing processes, autolytic debridement can help promote
healthy tissue growth and speed up the healing
process. With proper patient selection and wound
care, autolytic debridement can be a valuable tool
for managing non-infected wounds with necrotic
tissue.
7.3 Enzymatic Debridement
Enzymatic or chemical debridement refers to the
use of a topical enzyme to remove devitalized tissue. It is a form of selective debridement that utilizes the body’s natural enzymes or articial
enzyme preparations to digest necrotic tissue.
The three main types of enzymes used for enzymatic debridement are proteolytics, brinolytics,
and collagenases [11].
Proteolytic enzymes such as papain and bromelain break down proteins in the necrotic tissue,
while brinolytic enzymes such as streptokinase
and urokinase dissolve brin clots in the wound
bed. Collagenase, on the other hand, is used to
break down collagen in the wound bed, which
helps to loosen and remove necrotic tissue
(Fig.7.1) [12, 13].
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a
b
c
Fig. 7.1 Enzymatic debridement using bromelain-based
ointment on a deep burn wound. (a) Pre-debridement: A
photograph of the deep burn wound of thorax and abdomen before enzymatic debridement. (b) Application of
enzymatic ointment: The enzymatic ointment is applied to
the burn wound. The ointment contains proteolytic
enzymes that selectively target and break down necrotic
tissue, facilitating the removal of nonviable material. (c)
Post- debridement: Following enzymatic debridement, the
burn wound shows signicant improvement. Necrotic tissue has been effectively removed, revealing a clean wound
bed. The wound appears more viable and is better prepared for subsequent wound management and healing
interventions
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T. Pasquale and M. Maruccia
Collagenase-impregnated gauze or ointment
is applied directly to the wound bed and covered
with a secondary dressing to maintain a moist
environment. The dressing must be kept moist to
maximize the enzymatic activity and therefore
may require frequent dressing changes [11].
Enzymatic debridement is considered less
invasive and less painful than other methods of
debridement, except for autolytic debridement,
which also uses the body’s endogenous enzymes
to remove necrotic tissue. It requires less
advanced technique than sharp or surgical
debridement and is easy to instruct patients and
caregivers to perform. However, enzymatic
debridement can be expensive and may require
dressing changes up to three times a day.
This kind of debridement is appropriate for
those who cannot tolerate sharp debridement,
home or long-term care settings, and infected and
uninfected wounds with necrotic tissue. It is
especially useful for wounds that are difcult to
access, such as deep cavities or wounds in the
feet. Enzymatic debridement may also be used as
a precursor to sharp debridement to reduce the
amount of necrotic tissue in the wound bed and
make it easier to perform the procedure.
Enzymatic debridement is not appropriate for
facial wounds, calluses (since enzymes cannot
debride calluses), wounds free of necrotic tissue,
and wounds with exposed deep tissues including
tendons, blood vessels, and ligaments. If necrotic
tissue fails to decrease in the expected amount of
time, other types of debridements should be
considered.
7.4 Biological Debridement
Biological debridement is a unique form of
debridement that involves the use of live medical
devices, specically maggots. These tiny larvae
have been used for centuries to treat wounds and,
more recently, have been recognized as a legitimate medical treatment.
The process involves placing maggots onto
the wound bed, where they produce and release
enzymes that break down the necrotic tissue.
What is remarkable is that they do this without
harming the surrounding viable tissue.
Additionally, they ingest the dead tissue and bacteria, further assisting in the debridement
process.
Studies have shown that maggots are more
effective at debriding wounds than some other
debridement methods, making them a viable
option for wound care. However, it is important
to note that biological debridement may not be
suitable for all patients, particularly those with a
weak immune system or those with an allergy to
maggots [14].
While the thought of using maggots for wound
care may seem unorthodox, it is worth considering given its effectiveness and relative affordability. It is important to discuss the benets and risks
with a healthcare professional before making any
decisions regarding wound care.
7.5 Mechanical Debridement
Mechanical debridement is a process of removing devitalized tissue, foreign materials, and
debris from a wound bed through the application
of physical force. This form of debridement is
usually performed using simple techniques that
are easy to learn and perform, and it can be used
in a wide range of wound care settings. However,
it is important to note that mechanical debridement is nonselective and can potentially damage
healthy tissue, which makes it unsuitable for
some types of wounds [15].
There are several methods of mechanical
debridement, including wet-to-dry dressing,
hydrophobic dressing, and scrubbing.
Wet-to-dry dressings are commonly used for
the debridement of necrotic wounds. This
involves applying saline-moistened gauze to the
wound bed, which is allowed to dry. The dressing is then removed, along with any necrotic tissue that adheres to it. However, this method has
several disadvantages. Viable tissue can adhere
to the gauze and be traumatized on removal. The
wet-to-dry procedure can also cause wound bed
desiccation and periwound maceration, making
it unsuitable for wounds with granular tissue
[16, 17].
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Hydrophobic dressings are another type of
mechanical debridement that can be effective in
removing bacteria from infected wounds. These
dressings are coated with a fatty acid derivative
that makes them highly hydrophobic. Bacteria
are attracted to the dressing in the moist environment of the wound and become irreversibly
bound to it. When the dressing is removed, the
captured bacteria are also removed, preventing
them from multiplying or escaping while in contact with the dressing [18].
Scrubbing is a nonselective form of mechanical debridement that involves using a sponge,
brush, or gauze with water saline to clean the
wound bed. This method can be effective in
removing debris and necrotic tissue, but it can
also potentially traumatize healthy tissue within
the wound bed. As a result, scrubbing may be
contraindicated for granulating wounds.
Mechanical debridement is a useful tool for
wound care providers, particularly in settings
where access to more advanced debridement techniques is limited. However, it is important to use
mechanical debridement carefully and only in
appropriate cases to prevent further damage to the
wound bed. This is particularly important in the
case of wounds with granulation tissue, where
mechanical debridement may be too harsh and
cause further damage. In such cases, more selective methods of debridement, such as enzymatic or
surgical debridement, may be more appropriate.
7.5.1 Wound Irrigation
Wound irrigation is a procedure that uses saline
or another prescribed liquid in a syringe to wash
out excessive discharge, debris, and bacteria from
an open wound. The pressure applied should be
sufcient to reach the desired area, typically
applied manually. The type of solution to be used,
the desired strength, and correct temperature
should be selected carefully. Wound irrigation
facilitates debridement, assists with maintaining
a moist wound environment, and enhances wound
healing. The procedure is simple, quick, inexpen-
sive, and effective. Irrigation can be easily performed on any location on the body and in any
treatment setting. Disadvantages of wound irrigation include the potential for irrigant runoff to
soil linens or clothing. Wound irrigation is an
acceptable intervention for all types of wounds,
especially for healing granular wounds, but is not
indicated for active, profusely bleeding wounds
[19, 20].
7.5.2 Pulsed Lavage
Pulsed lavage (pulsatile lavage) is the delivery of
a wound irrigant under pressure by an electrically
powered device to assist in debridement of
necrotic and infected tissues [21]. It enhances
granulation tissue formation, epithelialization,
and local tissue perfusion. The goal is to remove
unwanted tissue without disturbing healthy tissue. Pulsed lavage involves regular, automatic
interruption of uid ow with a handheld device
to regulate irrigation pressure. Normal saline is
the most commonly used irrigating solution, and
antibiotics can be added to the irrigation uid to
help reduce the wound’s bioburden. A pressure of
4–15 psi is considered [22]. Pulsed lavage has
several advantages, including portability, shorter
treatment times, lower cost, less risk of crosscontamination, and less patient stress. However,
it is not appropriate for extensive wounds. Pulsed
lavage is indicated for cleansing or debriding a
variety of wounds, including venous, pressure,
and neuropathic ulcers. Pulsed lavage is also
appropriate for tunneling or undermining
wounds. No absolute contraindications exist
when a psi of 15 or less is used. However, pulsed
lavage should not be used in body cavities, on
facial wounds, on recent grafts, or on actively
bleeding wounds. It should be used with caution
on patients taking anticoagulants, insensate
patients, and deep tunneling wounds. Irrigation
with greater than 15psi is contraindicated. When
pulsed lavage is performed, both the patient and
clinician should wear appropriate barrier devices
due to aerosolization [23].
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