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L. Téot et al.
Bruschi S. Surgical debridement with Versajet: an
analysis of bacteria load of the wound bed pre- and
post-treatment and skin graft taken. A preliminary
pilot study. Int Wound J. 2011;8(2):155–61.
5. Sainsbury DC. Evaluation of the quality and costeffectiveness of Versajet hydrosurgery. Int Wound J.
2009;6(1):24–9. Review.
6. Téot L, Boissiere F, Fluieraru S. Novel foam dressing using negative pressure wound therapy with
instillation to remove thick exudate. Int Wound J.
2017;14(5):842–8. https://doi.org/10.1111/iwj.12719.
Epub 2017 Feb 28.
7. Rohrich RJ. The “soft-tissue wound management:
current applications of negative-pressure wound
therapy with instillation” supplement. Plast Reconstr
Surg. 2021;147(1S-1):1S–2S. https://doi.org/10.1097/
PRS.0000000000007629.
8. Stratmann B, Costea TC, Nolte C, Hiller J, Schmidt
J, Reindel J, Masur K, Motz W, Timm J, Kerner W,
Tschoepe D.Effect of cold atmospheric plasma therapy vs standard therapy placebo on wound healing in
patients with diabetic foot ulcers: a randomized clinical
trial. JAMA Netw Open. 2020;3(7):e2010411. https://
doi.org/10.1001/jamanetworkopen.2020.10411.
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.
Part VIII
Skin Necrosis in Children
Introduction toSkin Necrosis
Treatment inYoung Age
LucTéot
64
Skin in young age differs from adults, due to the
physiological evolution from the immature skin
present in the neonate to a highly inammatory
reactive skin, varying during the different stages
of the child growth.
Neonatal skin acclimates rapidly to dry, aerobic conditions at birth, and skin function gradually matures throughout infancy. Three
mechanisms are different from adults: oxygen
tension-regulating angiogenesis and revascularization; transforming growth factor-β (TGF-β)
kinetics controlling collagen deposition; and
mechanical stretch stimulating cellular mitosis
and extracellular matrix remodeling.
There is an increased systemic absorption of
topics due to the skin fragility, and the tolerance
of adhesives is limited in neonates and infants.
Wound types are more acute, like surgical
wounds (extravasation and thermal injuries;
chemical burns; pressure ulcers, iatrogenic intravascular injections) [1, 2] and wounds secondary
to congenital conditions. Wound infection can
lead to skin necrosis in highly contaminated situation like bite wounds which require special
attention.
Radiations at high doses as well as drug injections may lead to severe skin lesions, including
necrosis of the involved area [3, 4].
L. Téot (*)
Department of Plastic Surgery, Burns and Wound
Healing, Montpellier University Hospital, Hôpital La
Colombière, CICAT Occitanie, Montpellier, France
e-mail: l-teot@chu-montpellier.fr
Deep wounds with suspected damage to
nerves, tendons, and bones need general anesthetic to explore and assess the lesions. For
instance, children and neonates very often receive
intravenous therapy. There is a lack of systematic
data on the incidence of extravasation injuries in
children and neonates. Individual studies involving neonates receiving intravenous therapy on
intensive care units report incidence rates of
18–46%. Serious complications, such as necrosis
and ulceration, develop in 2.4–4% of cases,
which in the long term can lead to contractures,
deformities, and loss of limb function secondary
to unfavorable scar formation [5]. There are no
guidelines available to date on the management
of pediatric extravasation injuries.
During childhood, hypertrophic scarring risk
is increased, especially in persistent inammatory periods like burns, or after surgical reconstruction of necrotic areas using skin grafting or
aps and have to be managed properly in proportion of the high risk of esthetic and psychological
sequelae.
References
1. Koklu E, Ariguloglu AE, Koklu S.Foot Skin Ischemic
Necrosis following Heel Prick in a Newborn.
Case Rep Pediatr. 2013;2013:912876. https://doi.
org/10.1155/2013/912876. Epub 2013 Oct 28.
2. Bakal Ü, Abeş M, Sarac M. Necrosis of the ventral
penile skin ap: a complication of hypospadias surgery
© The Author(s) 2024
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L. Té ot
in children. Adv Urol. 2015;2015:452870. https://doi.
org/10.1155/2015/452870. Epub 2015 Apr 1.
3. Ravi M, Ridpath A, Audino AN, Guinipero T,
Chung C.Fernandez faith E high-dose methotrexateinduced epidermal necrosis in two pediatric patients.
Pediatr Dermatol. 2021;38(3):659–63. https://doi.
org/10.1111/pde.14591. Epub 2021 Apr 7.
4. Brook I.Late side effects of radiation treatment for head
and neck cancer. Radiat Oncol J. 2020;38(2):84–92.
https://doi.org/10.3857/roj.2020.00213. Epub 2020
Jun 25.
5. Kostogloudis N, Demiri E, Tsimponis A, Dionyssiou
D, Ioannidis S, Chatziioannidis I, Nikolaidis N.Severe
extravasation injuries in neonates: a report of 34 cases.
Pediatr Dermatol. 2015;32(6):830–5. https://doi.
org/10.1111/pde.12664.
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.
Skin Necrosis inChildren: Physical
andInfectious Causes
GuidoCiprandi
65
65.1 Introduction
When we talk about skin necrosis and the underlying soft tissues, we mean the death of a large
number of cells, on the order of billions of cells,
with consequent reworking of the tissues that can
dehydrate and undergo decay. The nal result is
that of a brown, hard eschar, not removable, or a
yellow, soft and sometimes soft eschar, with margins indistinguishable from surrounding healthy
tissue. In both cases, the visible change on the
surface represents only the tip of the iceberg,
since the damage is rst warped deeply, in the
heart of the soft tissues, until it then reaches the
size of a full-thickness damage that subsequently
reaches the skin on the surface [1, 2].
In some situations, necrosis occurs secondary
to the initial presence of bullous lesions (blistering early effect), and the child only after 48–72h
begins to manifest an ecchymotic and/or edematous skin area that is tinged more and more
darkly. As a result, the necrosis proceeds and is
much more evidenciating because of the last step
of a direct substance-dependent damage or of an
indirect damage following an arteriolar-capillary
occlusion.
In the pediatric age, necrosis is very fast and
whatever the cause that determines the blockage
G. Ciprandi (*)
Division of Plastic and Maxillofacial Surgery,
Bambino Gesu’ Children’s Hospital, Research
Institute, Rome, Italy
of arterial blood ow, locoregional hypooxygenation, or secondary damage to lymphaticvenous engorgement, a very rapid outcome in
necrosis can be observed [3, 4].
This rapidity is noted for several reasons: on
the one hand, the necrosis is due to the insufcient number of newly formed capillary beds and
to an immaturity of growth and differentiation of
the various layers of the skin. In this way, a small
insult can already be very serious due to the poverty of the capillary networks and therefore cause
serious damage with severe tissue loss.
From another perspective, the rapidity of
necrosis can be attributed to the physiological
edema observed in the neonatal period: the imbibition of the lining tissues, much richer in water
than in later ages (85–90% in neonatal age and in
infants 55–60% in senile ages), reduces the speed
with which oxygen diffuses into the skin mantle.
Normally, in fact, the oxygen comes out as ultraltered from the capillary bed of the dermis until
it soaks the tissues of the dermoepidermal layer.
From the pathophysiological point of view,
the occlusion pressure of the dermal capillaries,
normally equal to 36–38mmHg in adults, is very
low in pediatric age and is equal to about
22–24mmHg. Therefore, a much lower pressure
is enough to occlude the dermal capillaries and
this status is responsible, especially in patients
with reduced mobility, for an early damage, often
unexpected, with third degree necrotic pressure
lesions that appear in less than 24h. All the more
reason, the reduction in thickness of the dermo-
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_65
415
416
G. Ciprandi
epidermal complex which is observed from 0 to
36months fails to adequately defend the host’s
tissues from the pressures exerted by the hospital
materials.
Even the immaturity of the immune system of
the youngest patients contributes to the rapid
onset of a necrosis of the skin mantle, this time
mostly on a septic basis. Poor immaturity is not
only systemic in pediatric patients but also
locoregional: especially the skin of the extremely
preterm infant (LBW—Low Birth Weight,
VLBW—Very Low Birth Weight) is structurally
and functionally immature at birth [5].
Although there is rapid postnatal maturation,
transient hypothermia, and reduced oxygen supply, manifesting ssures and skin breakdowns,
with an increase in permeability toward toxins,
pathogenic germs, are both responsible for
inammation and infection, rst locoregional,
and then systemic (Table65.1).
Necrosis is the side effect, sometimes late
effect of these crucial events.
Other than vascular occlusive disease, additional pediatric causes of necrosis include intrauterine epidermal necrosis, SSFTN, toxic epidermal
necrolysis, severe and septic vasculitis (Neisseria
meningitidis), drugs and injection extravasation
Table 65.1 Immature skin in different pediatric categories and topical impairment in host defense
Immature skin in different pediatric categories
Premature/preterm Born before 37 wg
Late preterm Born between 34 and 36 wg
Moderate premature
Very premature Born before 32 wg
Micropreemie Born at or before 26 wg
A micropreemie is a baby born weighing less than
800g or before 26weeks gestation
Topical impairment in host defense
1. Increased susceptibility to bacterial infections
2. 30% immature neutrophils (vs. 5–15% in
childhood)
3. 30% storage pool (vs. 60% in childhood)
4. Severe reduction of myeloid progenitor stem cells
5. Severe impairment in adhesion of GN
6. Severely immature pseudopodal activities and
phagocitosis
Born between 32 and 34 wg
(Arginine, Warfarin, Cysplatinum), necrosis resulting from bang bite and bike accidents or mainly due
to inborn error of metabolism. But now let’s go into
the specics of some single pathologies capable of
inducing skin necrosis in neonatal and pediatric age
and let’s focus on these [6–10].
65.2 SSFTN (Skin
andSubcutaneous Fat
Necrosis oftheNewborn:
“Adiponecrosis Subcutanea
Neonatorum”)
65.2.1 General Aspects
This is a rare benign inammatory condition
which occurs in strictly neonatal age with rm and
tense, well-circumscribed subcutaneous nodules
(1–5 cm of largest diameter). Usually, the preferred sites of neonatal brown fat predominance
(i.e., cheeks, neck, upper back or sacrococcygeal
site, upper arm, thigh, buttocks) are much more
affected by these injuries. The skin overlying these
nodules looks like red purple induration plaque
(sometimes very evident, sometimes quite invisible at the beginning) over the bone prominences,
with which subsequently not infrequently undergoes necrosis with extensive ulceration and more
often tends to a spontaneous resolution [11, 12].
The age at diagnosis is more often between 4
and 25days, with a peak of incidence between 6
and 12days. In most cases, the gestational age is
normal, at term, the newborn weight is ageconcordant but a severe perinatal hypoxia it’s
almost always part of the medical history: the
fetal distress is reported in almost all cases and
consequently an emergency cesarean section is
required with a primary resuscitation needed,
usually during the rst 24–72h of birth. In some
cases, the hypoxic-ischemic encephalopathy
could intervene [13]. This condition is mainly
considered as a form of panniculitis, less severe
than sclerema neonatorum, another condition
causing hardened skin and limited necrosis during the neonatal period.
65 Skin Necrosis inChildren: Physical andInfectious Causes
417
65.2.2 Predisposing Factors
There’s neither a prevalent race nor a prevalent
gender. However, some maternal predisposing
factors have been studied and believed to be elements that may play a role in pathogenesis: preeclampsia, gestational type I diabetes, cocaine
abuse, and use of calcium channel blockers during pregnancy have been all investigated and considered as predisposing to SSFTN.
On the other hand, they are believed to be specic neonatal factors in the development of neonatal adiponecrosis such as hypoxemia,
hypothermia, rhesus incompatibility, birth
asphyxia, meconium aspiration syndrome, hypoglycemia, and obstetric trauma (perinatal
asphyxia, therapeutic hypothermia). The complex and often coincident set of these stressors
results in reduced tissue perfusion, and the nal
hypoxemia leads to crystallization of free fatty
acids in the subcutaneous fat tissue followed by
tissue necrosis. Both the ischemia and the drastic
inammatory reaction that is activated consequently lead to an intense hyperemia and then to
necrosis of the overlying skin, with local infection and often stulization or conuence of skin
areas of necrosis in the most serious and fortunately rare cases.
guided ne-needle aspiration aspirates a thick
liponecrotic liquid, otherwise drums of brownish
yellow tissue are sent for histopathological examination. The histological pattern is as follows:
some nodules are rm; others could become uctuant as abscesses. Usually the ne-needle aspiration cytology revealed a dirty background with
necrotic fat-containing characteristic, radially
oriented, refractile, needle-shaped crystals [14,
15]. A tissue pattern-based approach to diagnosis
shows clusters of adipocytes, histiocytes, broblasts, scanty lymphocytes, and numerous foreign body giant cells, granulomatous fat necrosis,
and some calcication areas (Fig. 65.1). In a
completely different way, sclerema neonatorum
(SN) is characterized by hardening of the skin
along with edema; histology shows a severe
inammatory inltrate and edema in skin as well
as in subcutaneous tissues. SN has a high case
fatality rate, whereas SSFTN is a self-limiting
condition and lesions resolve within a few weeks
to months, when a skin necrosis is not part of the
clinical pool of signs.
65.2.3 Laboratory Examinations
Serum albumin levels are usually normal, and
serum calcium levels may be complicated by
increased Ca++ or reduced Ca++ (manifesting
with hypotonia and poor suking reex). Whereas,
vitamin D levels are normal and PTH is normal
or slightly elevated. PLT–platelets showed a
marked increase, low Mg and K blood levels.
65.2.4 Diagnosis
The anamnesis allows to highlight a previous
fetal distress, associated with impaired calcium
blood levels, subcutaneous nodules at various
sites (clinical examination), and clearly evident
during sonographic examinations: sometimes, if
a colliquation has occurred, the ultrasound-
Fig. 65.1 Neonatal adiponecrosis in a 22-day-old patient:
areas of skin necrosis overlying a large nodule of subcutaneous necrosis on the back. Other nodules without subcutaneous necrosis are present in the neck and right armpit
418
Table 65.2 Team of consultants and aetiopathogenetic
steps
Team of consultants
Neonatologist
Neurologist
Cardiologist
Nephrologist
Dermatologist
Plastic surgeon
Aetiopathogenetic steps
1. Thrombocytosis
2. Lower blood perfusion
3. Hypoxia
4. Hypothermia
5. NSAdiponecrosis (transient panniculitis)
65.2.5 Course andOutcome
Diarrhea and vomiting are the most evident signs
associated with the clinical picture, in a sort of
self-limited course, with a spontaneous resolution occurring in the following 2 or 3weeks up to
3 months. Specic therapies are not yet established and if something is required, this is limited
to precise complications. In very few cases, low
dose prednisone has been administered by mouth.
Among the systemic complication, we must
mention hypercalcemia, hypocalcemia, hyperuricemia, hypoglycemia, hypertriglyceridemia,
thrombocytopenia, resulting in morbidity and
mortality, if not early detected and promptly cared.
Local complications are reported such as
necrotic epidermal atrophy, ulceration, scarring,
and/or local infection. At a discharge breast feeding is clearly advocate, and an oral Vit D supplementation (1.200UI, each day) is introduced for
at least 2–4weeks [5] (Table65.2).
65.3 Extravasation Injuries
Necrosis
65.3.1 Introduction andDenition
Extravasation is the accidental release of one
drug or a mixture of them from the veins used for
the delivery of solutes and medicaments, into surrounding peri and paravascular connective tissue
sheats. This phenomenon has an incidence ranging from 1 to 6%; however, the severity and type
G. Ciprandi
Fig. 65.2 Yellow necrosis due to extravasation of the
saphenous right external to the malleolus in a 12-day-old
infant. The necrosis area also affects the subcutaneous tissue and is due to extravasation of antibiotics
of treatment vary according to the type of extravasated uid [16]. The outcomes of extravasation
are related to the characteristics of the patient, his
age, the state of the venous circulation, nutritional aspects, and various comorbidities.
Pediatric patients most at risk are represented by
premature (LBW, VLBW, micropreemies) and
newborn for the characteristics of the fragile skin
and because of a narrow and underdeveloped
venous heritage. In rst ages of life, the risk of
extravasation and a subsequent necrosis are
increased as well as the major late outcomes. The
consequences can be of different severity: from
local redness to deep tissue necrosis, which can
involve tendons and ligaments, causing severe
tissue damage and severe functional sequelae and
disabilities including contractures, deformities,
and loss of function of the limbs secondary to the
formation of retracting and/or keloid scars [17,
18] (Figs. 65.2 and 65.3). Some studies con-
ducted in infants admitted to intensive and subintensive care units report incidence rates of
18–46%. In 2.4–4% of these cases, serious complications develop and necrosis is the most unfa-
65 Skin Necrosis inChildren: Physical andInfectious Causes
419
a
Fig. 65.3 (a, b) Brown eschar affecting the dorsum of
the foot due to extravasation of hyperosmolar electrolytic
agents after cannulation of the dorsal vein of the left foot.
vorable one, leading to permanent damages if not
promptly surgically cared [19].
65.3.2 Actions andInjuries
Based on the potential tissue damage, various
agents are recognized and then categorized on the
basis of their ability to create the most evident
necrotic effects with different mechanisms of
action:
1. Transformations from rapid tissue necrosis
are due to substances that produce immediate
deep damage and, by binding to DNA, remain
in the tissues for a long time causing progressive and worsening injuries, with severe
necrotic ulcers or full-thickness necrosis
which more often appear as real plaque of
rigid, black or dark brown tissue, shaped on
the anatomical site of the lesion. In these
small patients, the plastic surgeon intervention is rapidly advocated. Severe pain and
functional outcomes are always present if a
surgical treatment is not instituted and sometimes even in an emergency regime.
2. Blistering substances that can cause deep tis-
sue damage, as they are rapidly metabolized
and cause severe or prolonged pain, they represent the second category of agents responsible for tissue necrosis, more often
circumscribed and limited to small islands of
b
A large surface of about 5cm is involved, as can be seen
from the completely removed eschar, which also traces
the convexity of the neck and back of the entire foot
skin that undergoes progressive and not
immediate disintegration and exfoliation.
The mechanisms that determine necrosis
resulting from extravasations are different:
– Some drugs bind to nucleic acids in DNA and
are initially absorbed locally causing cell
death. After endocytosis, the death of surrounding cells occurs through the release of
the drug from dead cells. The repetitive nature
of this process strongly delays the healing processes and can lead to progressive and chronic
tissue damage, with deep scars.
– Other drugs do not bind to DNA but are
metabolized, limiting the degree of tissue
damage, and therefore are easier to pharmacologically neutralize.
65.3.3 Epidemiology
The incidence of extravasations in pediatric age
ranges from 0.1 to 6.5% of children undergoing
chemotherapy, in other estimates 11–28% in children admitted to a pediatric intensive care setting.
A not recent UK-based survey of regional neonatal intensive care units published in 2004, estimated the incidence of extravasation injuries
resulting in skin necrosis to be 38 per 1000
babies. Seventy percent of the cases occurred in
preterm infants born before 27weeks’ gestation;
420
G. Ciprandi
4% of infants leave the TIN with signicant
functional scars or lesions resulting from extravasation lesions [20, 21].
65.3.4 Distribution by Body Area
andCare Setting
The incidence of necrotic injuries due to extravasation or drug inltration and the deepness of tissue damage are related to various factors,
including the infused agent, its concentration and
volume, the duration of inltration, the timing of
diagnosis, the body site, and gestational age of
the patient.
In the pediatric age, especially in the neonatal
age, the areas chosen for nding venous accesses
are the back of the hand, the forearm, the cubital
fossa, the back of the foot, and the epicranial area.
These areas are represented by a subcutis that
allows easy retrieval of the vessels visible in
transparency but, at the same time, they are more
delicate and fragile. In situations perceived as
more difcult, the positioning of the venous line
is always ultrasound-guided, thus reducing possible risk for necrosis. No area of the body is exempt
from the risk of extravasation. This is especially
true for newborns and for those born preterm or
low birth weight (LBW, VLBW, ELBW).
65.3.5 Care
65.3.6 Physiology of Extravasation
In the human body, vascular lesions, oxidative
stress, and inammation are closely related.
Inltration and extravasation are both conditions responsible for vascular damage. When a
vascular injury occurs, the release of free radicals is stimulated and the cells’ ability to produce energy becomes dysfunctional due to
damage to the mitochondria. This leads to limited energy production, and the balance between
nitric oxide and superoxide is disrupted, increasing the damage. There is a continuous cycle of
free radical production and endothelial apoptosis leading to damage to membranes and cell
vessels.
Symptoms of this process include redness,
swelling, and visible tissue lesions. The interaction of the biological response to chemical and
non-chemical risk factors, when exposed to the
extravasated drug, directly affects the healthy
endothelium, leading to vascular lesions, starting
from the vessel intima. Inltration or extravasation can be caused by displacement of the intravenous catheter, puncture of the vein during
insertion or handling of patients. The tolerance of
the vein to an infusion is inuenced by the osmolarity and pH of the blistering substance, the
duration of exposure, and the irritation of the
endothelial cells. An additional factor in causing
the vein to rupture and leak is the pressure of the
drug being infused.
When the rst signs or symptoms of extravasation or inltration occur, including, for example,
redness or edema, the current infusion must be
stopped immediately and the team involved.
After stopping the infusion, the necessary antidote is administered through the same device
within 1 h and then the device with the entire
infusion line is removed. If the device was
removed before administering the antidote,
administer the antidote by subcutaneous injections in the area affected by the extravasation.
The limb is then placed in unloading for at least
48h to allow normal absorption and drainage of
liquids. To facilitate the management of extravasation in “rst aid,” the Team has an antidote kit
with the various procedures to be performed.
65.3.7 Factors Aecting
thePathophysiology of
Extravasation
• The volume of the drug infused; since, as is
known, during extravasation there is a loss of
uids in the subcutis which impart pressure to
the venous reticulum and then to the arterial
one, present at the site of the extravasation,
thus reducing the blood supply to others;
therefore, depending on the volume of the
extravasated drug, there will be more or less
severe ischemic damage.
• The local toxicity of the drug, due to the chem-
ical nature of the substance itself.