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12 Wound Care andTreatment ofScars
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Fig. 12.29 Some
examples of enzymatic
debridement agents. At
the top of the picture, a
barrier lm spray can be
seen that is used to
protect intact or
damaged peri-wound
skin (Cavilon, 3M
Fig. 12.30 Alginate
(left) and hydrober
(right)
®
)
223
– T for tissue: nonviable or decient
– I for infection/inammation
– M for moisture imbalance
– E for edge of wound, nonadvancing or
undermined
Therefore, according to TIME acronym, rstly it
is necessary to remove all damaged or necrotic tissue and foreign bodies on the surface of the wound.
Debridement is the quickest and most efcient
method of removing these materials. The second
point refers to control infection and management of
inappropriate inammation unrelated to infection.
Infection should be prevented or, in case it is present, treated. The best way to avoid infection is
wound cleansing and shielding the wound from
bacterial invasion. Thirdly, the wound should not be
desiccate, neither can have excess of exudate. The
relevance of moisture balance has led to the development and use of a wide range of dressings [7]. A
draining wound requires a dressing with the ability
to absorb moisture and protect the surrounding
wound from maceration, such as hydrobers, alginates (Figs. 12.30 and 12.31), or foam dressings
(Fig.12.32). A nondraining wound requires a dressing that provides moisture or prevents evaporative
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Fig. 12.31 Alginate
(left) and hydrober
(right) after absorbing
exudates
Fig. 12.32 Different
foam dressings
M. Estiragues et al.
uid loss, such as hydrogels or hydrocolloids
(Fig. 12.33). Even in highly exuding wounds,
negative- pressure wound therapy can be applied.
NPWT provides a closed moist wound healing
environment and regulates the quantity of exudate.
Finally, it is advisable to use creams or dressings
that facilitate the process of healing and epithelialization, but also that protect the surrounding skin.
Dressings should be adapted to the wound bed, and
the progress of the wound changes over time.
During the phase of epithelialization, wounds
require a dressing that will protect from trauma and
promote a moist environment, for example lms of
polyurethane (Fig.12.34).
Fig. 12.33 Hydrocolloid (left) and hydrogel (right)
12 Wound Care andTreatment ofScars
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Fig. 12.34 Dressings
recommended in the
epithelialization phase.
From left to right:
hydrocolloid, parafn
gauze, non-perforated
lm, and perforated lm
225
Many studies have veried the fact that a
moisturized environment promotes wound healing better than a dry one. A moist wound environment facilitates all three phases of wound healing
by trapping endogenously produced enzymes to
facilitate autolytic debridement, preserve endogenously produced growth factors, and reduce
patient pain complaints. Furthermore, a moist
wound usually results in a more cosmetically
appealing scar.
Principles at second healing:
• T (tissue) → Early excision of nonviable
tissue
• I (infection) → Microbial control
• M (moisture) → Control exudate/avoid
desiccation
• E (edge of wound) → Advanced wound
healing techniques
There are no xed principles in choosing the
dressing material. Dressings should be selected
based on the information obtained from the
wound examination, preferences of the patient or
medical team, economic impact, frequency of
dressing changes, location, etc [55]. Some char-
acteristics of the ideal wound dressing would be
the following:
– Provide a barrier to microorganisms.
– Create a moist wound environment.
– Manage quantity of exudate.
– Provide adequate gas exchange.
– Provide thermal insulation.
– Protect exposed nerves (decrease pain).
– Eliminate dead space.
– Remove debris, necrotic tissue, and foreign
material.
– Allow dressing changes painlessly and
atraumatically.
– Protect peri-wound skin.
12.6.2 Treatment ofDehiscence
Treatment should be based on the debridement of
wound edges, and the debridement of s damaged
or necrotic tissue from wound bed if it is present,
and healing by rst or second intention. As in
skin necrosis, the chosen technique in this kind of
acute wounds after surgery is usually sharp or
surgical debridement and primary closure with
sutures, although it depends on the preferences of
the patient and the medical team. If the area of
dehiscence is reduced, second healing (following
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M. Estiragues et al.
the same principles as seen above) is also a good
option.
12.6.3 Treatment ofInfection
Skin is naturally colonized by many microorganisms, which are named skin microbiota. Most are
nonpathogenic microorganisms; some of them
are commensal (meaning they coexist without
harming their host) and some are mutualistic
(meaning they coexist and also offer a benet to
their host). They are found principally in the
supercial layers of the epidermis and the upper
parts of hair follicles.
Attention
Contamination (microorganisms are present, but
do not result in signs or symptoms) and infection
(there are signs or symptoms) are not the same.
When there is a wound, skin integrity is lost
and microorganisms are allowed to enter the
human body, where they can proliferate and grow
at the expense of damaged or necrotic tissue.
Risk factors for developing a surgical
wound infection are the following:
– Patient factors: smoking, aging, obesity,
diabetes, weakened immune system,
chronic steroid use, malnutrition, …
– Local factors: necrotic tissue, bad perfu-
sion, foreign bodies, hematomas, dead
space, …
– Surgery factors: emergency surgeries,
long period of surgery (>2h), …
The basic treatment for surgical wound infection can be summarized in a three-step process
[55, 58].
1. Irrigation: It is important for diminishing the
bacterial load and removing loose material.
Open wounds should be irrigated on initial
examination and with each dressing change.
The most frequently used irrigation solution is
normal saline. However, it has been proved
that potable tap is as safe as sterile water or
saline. Nonetheless, tap water must be used
with caution in immunosuppressed patients,
particularly if the water might be non-potable.
Other cytotoxic antiseptic irrigation solutions
(dilute iodine, chlorhexidine, hydrogen peroxide, …) are also frequently used, although the
evidence of benets for their use is weak and
may have negative inuence on tissue regeneration due to toxicity to host cells.
2. Debridement: All damaged and died tissues
should be removed, as well as purulent collections. Debridement plays a vital role in
the management of wound infections.
Debridement of necrotic tissue and exudate
helps to reduce wound bioburden and may
also increase the effectiveness of topical
antimicrobials.
3. Topical antimicrobial treatment: The term
antimicrobial is used broadly to describe disinfectants, antiseptics, and antibiotics. It can
be applied in the form of impregnated dressings or irrigants. Most frequently used antimicrobials are silver, iodine, and
polyhexamethylene biguanide, while some
antibiotics often used in infected surgical
wounds are silver sulfadiazine, nitrofurazone, or mupirocin. Infected wounds should
not be occluded and should be rebandaged at
least once a day. Antimicrobial therapy is not
indicated for all wounds and should be
reserved for the following:
– Prevention of infection in patients who
are considered to be at an increased risk
– Treatment of localized wound with clini-
cal signs of infection
– Local treatment of wound infection in
cases of local spreading or systemic
wound infection, in conjunction with systemic antibiotics
Systemic antimicrobial treatment would only
be needed if there are systemic symptoms, for
example fever.
12 Wound Care andTreatment ofScars
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227
Tip
Infection signs are similar to the cardinal signs of
inammation (redness, heat, swelling, and pain),
but these signs are typically excessive or disproportionate to the size and extent of the wound.
Some other signs of infection are delayed healing, presence of pus, or foul smell.
12.7 Conclusion
Management of scars is a therapeutic challenge.
The progressive knowledge of the wound healing
process and the physiological events that take
place in each type of scar have allowed the development of new treatments for hypertrophic scars
and keloids, as well as the development of multiple techniques for minimizing scar formation
and correcting unaesthetic scars. Nevertheless,
there is still much to know and to advance in this
eld of research, and we hope that the dream of
being able to erase the scars will become true in
the future.
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Striae Gravidarum andIts
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Treatments
E.Moreno-Artero andL.Aguado
13
Take-Home Points
• Striae distensae are atrophic linear scars that
generally develop in the connective tissue due
to various physiological states, such as
pregnancy.
• Striae gravidarum are a subtype of striae dis-
tensae that develop in pregnant women.
Mechanical stress, pregnancy hormonal environment, younger maternal age, primigravidas, higher maternal body mass index, and
higher weight gain in pregnancy have been
described as risk factors.
• Striae gravidarum are initially seen as dark-
pink or bright-red atrophic linear scars. This
initial stage is known as striae rubra. Later on,
they become paler or lightly brown, being
renamed as striae alba.
• Treatment is difcult. Topical tretinoin and
pulsed dye laser may improve the clinical
aspect of striae rubra, while the fractional
ablative lasers (CO
when treating striae alba.
E. Moreno-Artero (*)
University Clinic of Navarra, Madrid, Spain
e-mail: emartero@unav.es
L. Aguado
University Clinic of Navarra, Pamplona, Spain
e-mail: laguado@unav.es
and Er:YAG) are superior
2
13.1 Introduction
Striae distensae (SD) are atrophic linear scars
that generally develop in the connective tissue
due to various physiological states, such as pregnancy and growth spurt during puberty, or rapid
changes in body mass, such as in weightlifters,
obese, or weight loss. Striae gravidarum (SG) are
a subtype of SD, which develop in pregnant
women [1, 2].
13.2 Epidemiological andClinical
Aspects
SG usually develop between the end of the second trimester or the beginning of the third trimester of pregnancy. The prevalence is estimated to
be around 55–90% of pregnant women. SG affect
mostly the abdomen and breasts, but they can
also affect the hips, thigh, groins, and armpits [2].
Clinically, SG are initially seen as dark-pink
or bright-red atrophic linear scars. This initial
stage is known as striae rubra (SR; Fig.13.1).
Later, SR become paler or lightly brown, being
renamed as striae alba (SA; Fig.13.2). SA are
less perceptible, but they never have spontaneous
resolution, and treatment remains, especially in
this chronic phase, difcult [3, 4].
© Springer Nature Switzerland AG 2023
M. Gomes-Ferreira, J. Olivas-Menayo (eds.), Post-maternity Body Changes,
https://doi.org/10.1007/978-3-030-43840-1_13
231
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Fig. 13.1 Red or pinkish atrophic linear scars in the
abdomen of a pregnant woman. This initial stage is known
as striae rubra
E. Moreno-Artero and L. Aguado
13.3 Etiopathogenesis
The etiopathogenesis is multifactorial. The extracellular matrix of the dermis is a framework of
different structural proteins such as brillin, elastin, bronectin, and collagen. In the pathogenesis
of SD, there is a rigid cross-linked collagen network, low expression of collagen and bronectin
genes, and elastolysis. Thus, genetic predisposition is critical, but there are other factors that may
be involved [3].
Among maternal risk factors, mechanical
stress, pregnancy hormonal environment,
younger maternal age, primigravidas, higher
maternal body mass index (BMI), and higher
weight gain in pregnancy, as well as a history of
striae in the mother and/or sister, have been
described [1, 2]. Fitzpatrick V–VI skin types and
ethnicities have also been documented as risk
factors; in fact, Chinese women seem to have a
lower risk than Indian or Malay [1]. Additionally,
it seems that the absence of social security
increases the risk two times, probably by affecting the nutritional state of pregnant women [2].
Interestingly, it seems that a sleep duration of 9h
and more rises the risk of developing SG by
approximately two times when compared with
pregnant women who sleep 7–8 h a day [2].
However, there are some inconsistences between
different studies; in fact, a recent study has shown
that younger age and parity have no association
with the prevalence of SD [1]. In parallel, higher
birth weight has also been related to SD
(Table13.1) [1].
Fig. 13.2 Chronic atrophic white linear scars in the
abdomen. SG in this chronic phase are known as striae
alba (SA)
! Attention
“Higher maternal body mass index (BMI) and
higher weight gain in pregnancy have been
described as risk factors of SG.”
13 Striae Gravidarum andIts Treatments
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233
Table 13.1
Maternal risk factors
Younger maternal age High birth
Primigravids Pregnancy hormonal
Higher maternal BMI and higher
weight gain in pregnancy
Familial history of striae
Fitzpatrick V and VI
13.4 Histology
Risk factors of SD
Fetal risk
factors
weight
Risk factors associated with
pregnancy
Mechanical stress Absence of social security
environment
Group’s Trials Register and included all the randomized or quasi-randomized controlled trials
In the normal skin, the epidermis shows quite
regular projections toward the dermis, called rete
ridges. The papillary dermis is composed of a
mix of collagen bundles and elastin bers, randomly arranged. In the reticular dermis, collagen,
which is organized in thick dermal bundles, predominates [3].
In the initial stage of SR, the epidermis is
almost normal; dermis is edematous with a perivascular lymphocytic inammatory inltrate,
and there is an increase of the dermal microvasculature, contributing to its red color. Normal
elastin bers predominate in the papillary dermis, while collagen bundles become small and
thin [3].
In the chronic phase, an atrophic epidermis
with loss of rete ridges and absence of skin
appendages characterizes SA. In the papillary
dermis, elastic bers are scant, and collagen
bers, densely packed, are disposed in parallel to
the epidermis [3].
comparing different topical preparations, comparing topical preparations with placebo or topical preparations with no treatment. Six trials with
800 women were included, with no statistically
signicant differences in the development and
severity of SG when comparing the different topical preparations with active ingredients. In the
same way, there were no statistically signicant
differences in the development and severity of
SG when comparing the application of topical
preparations with placebo or no treatment.
Topical preparations with active ingredients
included Alphastria, Trofolastin, Verum, olive
oil, and cocoa butter, all of them containing vitamin E; Alphastria and Verum also contain hyaluronic acid (HA) [6].
In 2015, Korvagkar etal. supported the anterior hypothesis by afrming that there is limited
evidence that Centella asiatica, cocoa butter,
olive oil, and HA, and massage with bitter almond
oil, may prevent SG and/or reduce their severity,
due to the lack of strong evidence from rigorous,
well-designed, randomized controlled trials with
13.5 Prevention
a sufcient number of subjects [7].
Two small randomized controlled trials have
SG can affect women, as they may be a cause of
stress during pregnancy or become an aesthetic
or cosmetic problem later. In this sense, prevention is the rst concern, and many women use
diverse commercially available products for preventing their development during pregnancy [5].
There is not a consensus and high-quality evidence to support their use. In 2012, Brennan etal.
searched the Cochrane Pregnancy and Childbirth
demonstrated the efcacy of HA in the prevention of SD [8, 9], but some limitations were the
lack of follow-up and a subjective measure of the
clinical improvement [3]. Another trial showed a
mild improvement when compared with the topical application of HA by massage with no massage or no application; however, limitations were
poor randomization and lack of placebo control
[7, 10]. When evaluating the efcacy of HA, the
Socioeconomic and lifestyle
risk factors
Sleep duration of 9h and
more
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