GUIDELINES

Facial Vascular Events and

ABSTRACT
The Complications in Medical Aesthetics
Collaborative (CMAC) is a nonprofit
organization established to promote best
patient outcomes through educating
clinicians in the prevention, diagnosis, and
Tissue Ischemia: A Guide
to Understanding and
Optimizing Wound Care
by ASTRA FARMER, RN, NMP; GILLIAN MURRAY, MPharm, PG Clin Pharm INP;
BRITTONY CROASDELL, NP, ARPN, CANS; EMMA DAVIES, RN, INP;
CORMAC CONVERY, MB CHB, MSC; and LEE WALKER, BDS, MFDS, RCS
Ms. Farmer is with Devon and Cornwall Aesthetics Academy in Exmouth, England. Ms. Murray is with the Clinical Academic Kings College,
London in London, England. Ms. Croasdell is Clinical Director at The Fitz® in Chicago, Illinois, United States. Ms. Davies is Clinical Director
of Save Face UK in Bath, England. Dr. Convery is with the Ever Clinic Glasgow in Glasgow, Scotland. Dr. Walker is with B City Clinic in
Liverpool, England. All authors are founding board members of the Complications in Medical Aesthetics Collaborative (CMAC).
J Clin Aesthet Dermatol. 2021;14(12 Suppl 1):S39–S48

management of complications that can arise
following nonsurgical cosmetic procedures.
The organization is a global community
sharing information, learning, experience,
and data to promote best practices. This
article explores how dermal filler vascular
events can cause tissue ischaemia leading to
a facial wound. Ideally, vascular events will
be diagnosed early and amenable to reversal
with hyaluronidase if caused by a cross-linked
hyaluronic acid. If there is significant and
extensive hypoxia to the area, there is delayed
diagnosis, or the injected product cannot be
reversed, the management should center
around optimizing wound care. Both simple
and complex wounds will benefit from good
care. Patients seek aesthetic treatments to
improve how they look and can be vulnerable
to poor outcomes. Wounds, if not treated
appropriately, can result in permanent
scarring or other sequalae, such as post-
inflammatory hyperpigmentation. There are
many publications addressing vascular events
in aesthetic practice, but providing optimal
care for facial wounds is not addressed.
KEYWORDS: Vascular occlusion,
vascular ischaemia, vascular event, facial
ischaemia, facial wound, wound, dermal filler,
hyaluronic acid, aesthetic complication
I
Injection of dermal filler for soft tissue
augmentation is a rapidly expanding practice.
According to Belezney et al,1 the number of
soft tissue augmentation procedures in the
United States increased 300 percent from the
year 2000 to the year 2017.1 The indications for
treatment with dermal fillers include correction
of acne scars, volume replacement following
traumatic injuries, human immunodeficiency
virus (HIV)-related lipodystrophy, age-
related volume loss, and body contouring.2 In
addition to their increased frequency, tissue
augmentation procedures are becoming more
complex, with greater volumes being injected as
product indications and outcome goals evolve.
The contribution of these factors will inevitably
result in more vascular events causing facial
ischemia.
Common products used for soft tissue
augmentation include fat, calcium
hydroxyapatite, polymethylmethacrylate
microspheres, poly-L-lactic-acid, and cross-
linked hyaluronic acid.2 While hyaluronic acid-
based fillers (HA) can be readily dissolved by the
enzyme hyaluronidase, it can be challenging to
remove permanent products. As such, the use of
non-HA products pose higher risk for ischemic
complications, which typically require wound
care.3
When considering the incidence of vascular
events, a study by Alam et al surveyed 370
dermatologists,2 the results of which indicated
an incidence of "vascular occlusion" correlating
to one in 6,410 if a needle was used and one
in 40,882 with a cannula. However, statistics
in relation to these events vary from study to
study. One study found that the relative risk of
a vascular occlusion was twice as high among
practitioners during their first five years of
practicing compared to those in practice longer,
indicating clinician experience is a factor in
vascular occlusion occurrence.2
The purpose of this guideline is to outline
the stages of a vascular event; provide guidance
on assessing ischemia, identifying necrosis,
and managing these conditions; and describe
the wound healing process to assist clinicians
in effectively supporting wound healing and
optimizing patient outcomes.
STAGES OF A VASCULAR
OCCLUSION
In the event of vascular compromise
following injection with a dermal filler, skin
color and gradual deterioration are important
markers of issue ischemia severity and how
much time has passed since the event. If
the vascular flow is disrupted, there are

FUNDING: No funding was provided for the preparation of this article.

DISCLOSURES: The authors have no conflicts of interest relevant to the content of this article.
CORRESPONDENCE: Gillian Murray, MPharm, PG Clin Pharm, INP; Email: gillianmurray@cmacworld

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TABLE 1. Stages describing the severity of ischemic insult and likelihood of a requirement for ongoing wound care The authors found that Stages 4 and 5 can be
(amended from CMAC "Guideline for the Management of Hyaluronic Acid Filler- induced Vascular Occlusion") further complicated depending on which artery
STAGES OF has been affected, its anatomical variations/
TYPICAL ONSET
VASCULAR PATHOPHYSIOLOGY
OCCLUSION
AND DURATION anastomotic connections, and/or formation of
sufficient collaterals. Anatomical variations are
• Immediate blockage of the artery or spasm leading to an Instant, lasting a few
Stage 1—Pallor
abrupt interruption in blood flow and tissue perfusion seconds, or may persist
commonly discussed in the literature.5 Therefore,
Stage 2—Livedo • Build-up of deoxygenated blood within the surrounding Can occur rapidly and
injury may be limited to the dermis, or it may also
reticularis venous network last 24–36 hours progress through deeper tissue structures, such
• Reduction in pH and sweat production Approximately 72 hours
as fat and muscle. Severe ischemic injuries may
Stage 3—Pustules • Metabolic changes allowing Staphylococcus aureus to over (beginning of necrosis) require escalation to secondary care for surgical
grow as a facultative aerobe management.
• Tissue blackens due to worsening hypoxia, cell lysis, and Occurs over a number An ischemic wound might be covered in
outpouring of blood into the tissues. of days necrotic nonviable tissue, which can occur as
Stage 4—Coagulation*
• Tissue is firm with retained architecture as a function of the slough (usually yellow or green) or eschar (dry,
coagulative necrotic process. hard black tissue).6 Necrosis is usually visible
• Destruction of the tissues and a build-up of denatured Occurs over a number if reperfusion does not occur and the tissue is
Stage 5—Devitalized
tissue
structural proteins (collagen, fibrin, elastin) and of days unable to gain oxygen via sufficient collateral
hemoglobin occurs. formation. This is usually evident in Stages 3 to
Stage 5A—Slough
• Slough is moist and creamy/yellow or green. 5 if perfusion of the area isn’t sufficient. In a case
Stage 5B—Eschar
• Eschar is black (dark) and dry. series of ischemic injuries, Hong et al7 reported
* Coagulation may occur before Stage 3, at the same time, or pustular overgrowth may mask tissue damage below. This that treating ischemic injuries within the first
stage indicates necrotic changes. three days is best for optimal intervention and
healing the wound without scarring.7 Khalil et al8
observed that whether an ischemic area develops
to Stage 3 or beyond depends on individual
variation, extent of blockage, vascular anatomic
connections, extent of spasm in adjacent arteries,
and development of prompt and adequate
collateral vessels.8 Less severe superficial
sequelae following an ischemic insult may heal
uneventfully, even after Day 3, and wound care
should only be deployed if required.
In the event of a vascular occlusion, the
goals are to establish reperfusion if possible
(reverse a cross-linked hyaluronic acid and
support the wound healing. It is important to
note that tissue damage does not stop at the
ischemic insult. If significant ischemia persists
for days, the wound will start to break down
once the vascular supply is re-established
following dissolving the hyaluronic acid filler
FIGURE 1. Layers of cells in the epidermis by formation of collateral flow. Oxygen carried
by the blood prompts enzymatic reactions
progressive changes and, if caught early, a It is important to highlight that pallor and a that produce harmful mediators including
wound can be averted. Although efficient and reticulated appearance (described as Stage 1 or superoxide, hydrogen peroxide, and hydroxyl
swift management is important, there is time to 2) does not necessarily indicate that necrosis will free radicals. These free radicals cause damage
escalate and seek collaborative management if occur.4 If the vascular obstruction is removed at to the endothelial cells, reduce nitric oxide (NO)
required.3 this point, and flow is restored, it is likely that levels, and impair neutrophil-mediated killing of
In the CMAC Guideline for the Management the tissue will resolve to baseline uneventfully. bacteria. They further induce production of more
of Hyaluronic Acid Filler-induced Vascular If the vascular occlusion progresses to Stage 3 or inflammatory mediators, causing a localized
Occlusion, stages of vascular occlusion were beyond, supportive wound care may be required. increase in neutrophils. Intervention is therefore
described to help aid in the understanding of A current limitation to the vascular occlusion time sensitive, with prolonged ischemia resulting
ischemic severity and the likelihood of requiring staging system identified in the CMAC guideline in a more significant reperfusion injury. When
ongoing wound care (Table 1).3 is that depth of ischemic injury is not addressed. necrosis occurs, there will already be a wound on

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 GUIDELINES
presentation, and reperfusion may accelerate the
breakdown of the tissues. While optimal time to
reperfusion is well understood in other organs
(e.g., cardiac tissue), it remains unclearly defined
in skin, underscoring the importance of promptly
managing ischemic injury.3 Further research is
needed to better understand optimal time to
reperfusion of ischemic tissue in the skin.
PHYSIOLOGY AND ANATOMY OF
THE SKIN
Epidermis. The epidermis, or outer layer,
of the skin contains multiple layers of cells,
including the stratum corneum, stratum lucidum,
stratum granulosum, stratum spinosum, and
stratum basale.10 Figure 1 illustrates the layers of
cells in the epidermis. The stratum basale is the
deepest layer of the epidermis, and, in healthy
uncompromised skin, this layer continually
produces keratinocytes, which gradually migrate
to the top via all the strata layers. By the time
these cells reach the stratum corneum, they
have evolved into flat dead skin cells, which
are worn away through natural shedding. The
stratum basale also contains melanocytes,
which produce and contain melanin.10 If
there is an over production of melanin due to
ultraviolet (UV) damage, hyperpigmentation
occurs. Inflammation can also stimulate the
over-production of melanin, leading to post-
inflammatory hyperpigmentation (PIH), which
can occur in all skin types, but more frequently
affects individuals with skin of color, including
African Americans, Hispanics/Latinos, Asians,
Native Americans, Pacific Islanders, and those of
Middle Eastern decent.11 PIH can be minimized if
good wound care protocol is facilitated, including
moist wound healing principles.11
Dermis. The second layer of the skin, the
dermis, is composed of connective tissues,
collagen, elastin, blood vessels, lymph vessels,
nerve endings, sweat, sebaceous glands, and hair
follicles (Figure 2). Collagen is a fundamental
protein in regard to wound healing by providing
structural stability.10 Elastin is intrinsic to giving
the skin elasticity and resilience.
INTRODUCTION TO ISCHEMIC
WOUNDS
There is a lack of research into the breakdown
of tissues and formation of wounds following
vascular events of the face, and management of
these wounds has not been directly addressed
in the literature. Ischemic tissue resulting from
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FIGURE 2. Layers of cells in the dermis
a dermal filler vascular event can break down
quickly (Table 1) and can be painful for the
patient. Healing will be delayed if perfusion is
not restored. Potential additional trauma to the
tissue, due to the following, should also be taken
into consideration:
• The initial injecting of the dermal filler
• The hyaluronidase injections, including the
quantity and treatment duration
• The firm massage used to try to reperfuse the
tissues after hyaluronidase administration
• Any thermal injury that may have occurred
through application of heat.
Following a dermal filler-induced vascular
event, the longer the ischemia is present with
insufficient collateral flow, the more the tissue
will be compromised with a risk to deeper
structures. Any treatment delay or inability to
dissolve the problematic filler may consequently
lead to necrosed tissue and a wound. It is
paramount to the patient’s recovery that the
treating clinician be equipped with a basic
knowledge of wound healing.
For optimum patient recovery, administration
of hyaluronidase and prescribing of drug-based
adjuvants (e.g., antibiotics, steroids, nitrate
preparation or phosphodiesterase inhibitors) is
often recommended19 However, consideration is
not often given to the presence of a wound. Drug
adjuvants alone are not sufficient for optimal
wound healing.12 The wound should not be
allowed to become dry, as this will increase the
risk of secondary complications and scarring.17
For the patient to make a full psychological and
physical recovery, the tissue must be treated with
the correct topical agents for the best possible
outcome. Topical agents and dressings that
facilitate the restoration of collagen, elastin, and
support the extracellular matrix are essential to
good wound healing.12 For example, moist wound
healing, the benefits of which have been well-
documented over the last 40 years,13-18 has been
shown to increase the rate of healing and reduce
the risk of infection and scarring.
STAGES OF WOUND HEALING (WHS)
AND OPTIMAL MANAGEMENT
A wound is a disruption to the epidermis or
both the epidermis and the dermis. If an aesthetic
clinician is faced with a wound, it is important to
understand the stages of wound healing and to
identify and assess what, if any, management is
required.20 If there is no skin breakdown, there is
no wound.
The stages of wound healing, once being
described as three stages and evolving to four,
differ in their description within the literature.
However, the series of events that culminate
into the healing of a wound, as we understand
them now, are represented the various models
described. The classification model chosen to
represent wound healing in the context of an
ischemic wound does not refer to the hemostasis
phase, a phase (or stage) that is commonly
included in other wound healing classification
models. This is because wounds encountered
after dermal filler ischemic events are not
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 GUIDELINES
TABLE 2. Typical facial wounds caused by vascular compromise
TYPICAL WOUND ASSESSMENT
Sterile pustules
1. There is no breakdown of the epidermis.
2. Sterile pustules are present due to
hypoxia.
3. No slough/eschar wound bed is present.
1. The wound is in the inflammatory
stage.
2. Erythema is present, which is common
in a wound in this stage.
3. Small pustules and larger areas of
Slough slough as present. The two are very
similar in appearance but pustules
will usually be reabsorbed by the body
whereas slough needs to be removed
via debriding methods. The production
of slough is the body’s natural response
to trauma. It is a collection of white
blood cells, fibrin, cellular debris, and
devitalized tissue, as observed in this
image.
4. If the slough appears encrusted and
dried, it is vital to create a moist healing
environment to facilitate healthy
granulation tissue formation.
1. This wound is in the inflammation
Exudative stage and is showing clinical signs of
infection.
2. The surrounding tissue has visible signs
of erythema combined with edema,
visible exudate. Due to how long this
wound has been present, these signs
indicate infection is highly probable.
3. Important to treat the localized
infection, manage the exudate levels,
protect the surrounding healthy skin.
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SUGGESTED WOUND CARE PLAN REVIEW
On administration of hyaluronidase and re- The area should be observed the next day
establishment for blood flow, it is likely that the to monitor for any skin breakdown. If the
sterile pustules will resorb, or be disrupted by skin breaks down, follow management as
mechanical massage. per wound status.
1. This dressing regimen should be
1. Soak gauze in a wound irrigation solution and repeated every 5 days to ensure
lay over the wound for 5 minutes to moisten the treatment effectiveness for healing.
area, then, using circular motions, gently cleanse 2. Monitor exudate levels closely. Contact
the area. This will reduce the bioburden and the patient daily to confirm the
manually debride some of the slough. secondary dressing is managing the
2. Apply an antimicrobial alginate gel to the wound exudate levels.
prevent infection and moisten slough to facilitate 3. At dressing changes, the clinician
autolytic debridement. should assess erythema for changes.
3. Apply a bordered gel dressing as a secondary If ierythema isn't decreasing and the
dressing to protect the wound, keep the surrounding skin becomes hot to touch
antimicrobial gel in place, and facilitate moist or edematous, this may indicate a
wound healing. This will prompt the wound to localized infection, in which case the
enter the proliferation/reconstruction stage and treatment plan should be adjusted
form granulation tissue. accordingly.
1. Soak gauze in a wound irrigation solution and
lay over the wound for 5 minutes to moisten
the area, then, using circular motions, gently
cleanse the area. This will reduce the bioburden
and manually debride some of the slough and
suspected superficial necrosis, as well as help 1. This wound should be reassessed
remove the exudate to enable the clinician to in 3 days to ensure infection is not
assess the wound and skin integrity. worsening, exudate levels are being
2. Apply barrier film foam to the periwound and managed adequately, and surrounding
skin directly surrounding the wound bed to skin is not becoming macerated.
protect from maceration and to stop the healthy 2. If, at the second dressing change,
skin from deteriorating. exudate levels and slough are reduced,
3. Apply a low-adherent, antimicrobial silver barrier the next dressing change can occur in
dressing designed for management of partial- 5 days.
and full-thickness wounds to the wound bed. 3. After the infection has been treated, if
Low adherent silver dressings combat bacteria further debridement to the necrosed
and pathogens and prevent tissue trauma at area is needed, a hydrocolloid dressing
dressing changes. can be applied.
4. Apply a multilayered hydrocellular foam dressing
to manage high exudate levels by drawing and
locking exudate away from the wound bed. A
silicone-based adhesive border can help prevent
tissue trauma and pain at dressing changes.
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 GUIDELINES

TABLE 2. Typical facial wounds caused by vascular compromise, continued

TYPICAL WOUND ASSESSMENT SUGGESTED WOUND CARE PLAN REVIEW

1. oak gauze in a wound irrigation solution and lay

Superficial necrosis
1. Presence of eschar indicates the wound
has been in the inflammatory stage
some time.
2. If erythema is minimal, infection
may not be present, but infection
can develop the wound is not treated
accordingly.
3. If moist wound healing protocol is
delayed, scarring may also develop.
Immediate moist wound care can
prevent the formation of eschar
and other complications, such as
postinflammatory hyperpigmentation,
as well as aide autolytic debridement.
over the wound for 5 minutes to moisten the
area, then, using circular motions, gently cleanse
the area. This will reduce the bioburden and
remove the probable biofilm that has formed on
the eschar due to the duration of time the wound
has been present without correct wound care.
2. Apply barrier film foam to the periwound and 1. Monitor the secondary dressing for
skin directly surrounding the wound bed to exudate levels, but these dressings
protect from maceration and to stop the healthy should stay in situ for 7 days to
skin from deteriorating due to the use of medical hydrate the eschar and create a
honey in Step 3. moist wound healing environment,
3. Apply 100% medical grade Manuka honey, which encouraging the start of autolytical
provides antimicrobial cover and hydrates the debridement.
eschar, facilitating autolytic debridement so the 2. When the eschar has been debrided,
wound can move into the next stage of healing, only then can the depth and severity
proliferation. of future complications, such as
4. Apply a highly absorbent, hydrocapillary scarring and PIH, be accurately
adhesive dressing as a secondary dressing to assessed.
absorb any exudate. This foam silicone dressing is
highly conformable to the wound bed and draws
exudate caused by the honey away from the
wound bed into a vertical layer then distributes
the exudate into a horizontal secondary layer. It
is also highly waterproof, allowing the patient to
bathe and shower.

Necrosis requiring 1. The depth of the eschar into the

specialist support for underlying structures indicates the
debridement wound has been in the inflammatory
stage for some time.
2. The eschar requires debridement to
assess the depth and condition of the
wound bed for optimal management.
3. It is unlikely topical medications and
dressings will debride this wound—
surgical input is required.
• This wound requires input from tissue viability
specialists and plastic surgeons.
• Sharp or surgical debridement of the necrosis as
Refer to specialists for input
well as vacuum-assisted dressings to promote
granulation and reduce the severity of scarring
will likely be required.

inflicted by trauma and present mainly at the
inflammation stage of the wound process.21 Thus,
in the context of this article, the four stages of
wound healing are denoted as inflammation,
proliferation, epithelialization, and remodeling.20
A wound that is likely to present acutely after
a vascular event, or if the wound has not been
managed correctly, will be stuck in Phase 1—the
inflammatory stage—and will not progress into
healing.12,13
Wound Healing Stage (WHS) 1:
Inflammation. The inflammatory stage is
the first stage that occurs when the skin integrity
is compromised due to the epithelial cells being
disturbed. This will occur during Stages 3 to 5 of a
vascular occlusion.
Edema, pain and erythema. Cells require
oxygen to maintain aerobic metabolism and
retain cellular function. As cells become hypoxic,
oxidative phosphorylation ceases. Adenosine
triphosphate (ATP) stores are depleted, and
energy-dependent functions stop. Ion transport
is affected, with loss of intracellular k+ and
increased intracellular Na+. Glycolysis is initially
accelerated, and cells produce large quantities
of lactic acid. These variations in ion balance
and lactic acid production contribute to cellular
edema.23 On assessment, the inflammatory
stage will also present as erythematous, painful,
and edematous. Pain, in response to skin
injury, is referred to as cutaneous neurogenic
inflammation. Skin damage activates receptor
Types TPRV1 and TPRA1, which are present on
primary sensory neurones, keratinocytes, mast
cells, dendrites, and endothelial cells. Activation
of these receptors stimulates a nociceptive

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TABLE 3. Common topical wound therapies

DRESSING DESCRIPTION RECOMMENDATIONS

• Used for moderately to heavily exuding wounds

• Used as a primary or secondary dressing
• Protect wounds from further injury and infection and promote moist wound healing environment
Absorbent Biatain® Super, adhesive
• Commonly have an adhesive border
dressings (Coloplast)
• Most modern absorbent dressings absorb exudate into secondary contact layer away from wound bed
• Polymer and viscose commonly used materials in bonded pads
• Tend to be water resistant to allow patient bathing/showering
• Used for moderately to heavily exuding wounds
• Some can be used for bleeding wounds due to hemostatic properties
• Not suitable for dry, necrotic wounds, such as wounds with eschar
• Derived from brown seaweed
Flaminal Hydro® and Flaminal
• Commonly used as primary dressings
Forte®(Flen Health) are topical
Alginates • Absorbent and biodegradable
alginate gels that contain
• Can vary in composition and arrangement of fibers (commonly nonwoven or fibrous)
antimicrobial enzymes.
• Available in sheet or rope forms (suitable for packing wound cavities)
• More recently available as topical gels
• Polymers of alginic acid found in seaweed provide mannuronic and glucuronic acids, which form a gel when wound exudate is
absorbed into the dressing, preventing trauma to tissue when removing

• For infected wounds/biofilms Acticoat Flex 3 (Smith & Nephew)

• Treat wide range of pathogens, including Staphylococcus aureus; reduce wound bioburden is a highly conformable polyester
Antimicrobials
• Use in place of oral antibiotics to treat localized infections; oral antibiotics only used in cases of systemic infection dressing impregnated with silver,
• Topical forms include povidone-iodine, polyhexamethylene biguanide dihydrochloride, hypochlorous acid, and silver which combats localized infection.

• For moderately to heavily exuding wounds

Allevyn lifeTM (Smith & Nephew)
• Forms include polyurtethane, polyvinyl alcohol, or silicone, due to ease of application and atraumatic removal
is for heavily exuding wounds;
• Available in a variety of depths to manage all exudate levels
dressing can stay in situ for up to 7
Foams • Silicone-based dressings can often be removed and reapplied with minimal disturbance to wound (to observe healing
days; Mepilex Border® (Molnlycke)
progress)
is for minimally to moderately
• Transmit water vapor via outer surface to prevent maceration of periwound while maintaining optimum moist wound healing
exuding wounds.
environment

• Autolytic debrider; not suitable if periwound is compromised or macerated, due to its exudate-increasing properties; not
suitable in patients with poorly controlled diabtes
Activon Manuka Honey® tube
Medical-grade • Antibacterial and anti-inflammatory properties
(Advancis Medical); Medihoney®
honey • Deodorizes wound and stimulates formation of granulation tissue
(Mckesson, US)
• Available as impregnated tulle or topical gel
• Periwound should be protected with barrier film to prevent maceration, due to potent debriding properties

• Ideal for noninfected dry wounds (where eschar is present) and low-exuding granulating wounds
• For minimally to moderately exuding wounds
• Highly conformable; create optimum moist wound healing environment
Hydrocolloids DuoDERM® Dressings (ConvaTec)
• Aid in debridement of devitalized tissue
• Offer semipermeable, highly occlusive barrier
• Available in sheet, paste, and powder forms

• For dry wounds

• Gentler alternative to medical honey
• No antimicrobial properties but good choice for wounds with eschar to aid autolytic debridement
Hydrogels • Available in topical gels or sheets ActiForm cool® (Activa Healthcare)
• Provide a moist wound healing environment, promoting debridement and granulation.
• Usually require a secondary dressing to ensure the agent stays in situ
• Synthetic hydrogels very biocompatible so suitable for sensitive skin types

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TABLE 3. Common topical wound therapies, continued

DRESSING DESCRIPTION RECOMMENDATIONS

• Prevent hypertrophic or keloid scarring

• Applied once wound has healed through primary intention
Silicone gels or • Hydrates stratum corneum, aiding in the redaction of disorganized collagen formation
Mepiform® (MonInIycke)
sheeting • Used daily for 2–6 months after wound bed has healed
• Aids in the regulation and expression of growth factors, having a net effect of increasing collagenases, which break
down excess collagen
• When using any wound dressings, particularly where autolytic debridement will take place, with dressings such as
honey or hydrogels, it is imperative to protect the periwound and surrounding healthy skin to prevent maceration and • For wound cleansing—
excoriation burns. Octenilin® (Schülke & Mayr
• There are a range of barrier film products that create protective barriers, available as foam applicator sticks, ideal for GmbH); Prontosan® solution
Skin protection,
periwounds protection. (B. Braun Medical Inc.)
irrigation, and
• It is important to cleanse any wound prior to application of a wound dressing. Historically, normal saline (NaCL 0.9%) • For wound irrigation and
cleansing
was used to irrigate and cleanse wounds, but more recently, better products, such as Octenilin® wound irrigation periwound protection—
solution (Schülke & Mayr GmbH) and Prontosan® solution (B. Braun Medical Inc.) have emerged. Both products are Cavilon™ 1ml barrier foam
antiseptic and can eradicate gram positive and negative bacteria while removing biofilms and aiding in the removal of applicator sticks (3M)
devitalized tissue.

response by cascading the production of
substance P and calcitonin gene-related peptide.
These neuropeptides have three main targets:
smooth muscle of blood vessels (increasing
blood flow and causing vasodilation); vascular
endothelium (causing an increase in vascular
permeability, edema, and recruitment of
inflammatory leukocytes); and stimulation
of mast cell degranulation (with release of
histamine, serotonin, proteases, and other
mediators). This cascade of events promote
microvascular permeability of blood vessels
surrounding the wound (redness and heat) and
cause an influx of inflammatory mediators into
the area, causing swelling.20,23,24 The blood vessel
dilation and series of events also allow essential
cells—antibodies, white blood cells, platelets,
growth factors, enzymes, and nutrients—to
reach the wounded area, which assists in fighting
any bacteria present and formation of a platelets
plug to protect the wound. This is the body’s
natural response to tissue trauma.20
Pustules. In many vascular occlusions, visible
white pustules form during the inflammatory
phase. This is commonly seen on Day 3 of
a vascular occlusion if collateral supply is
insufficient or individual anatomy has not
presented anastomotic connections with other
arteries. The pustule formation around Day 3 is
not fully understood, as it only seems to occur on
the face. During ischemia, anaerobic metabolism
in the tissue is dominant and there is dysfunction
of the sweat glands and a reduction of sweat
production, increasing the pH and reducing
the amount of salt on the skin.3 These factors,
combined with the breakdown of normal cellular
architecture, allow bacteria to overgrow. Resident
bacterial flora penetrate deeper into the dermis,
which provides a warm, moist, oxygen-deficient,
and nutrient-rich environment where they can
thrive.25 Staphylococcus, a normal skin pathogen
that is usually harmless if the skin barrier in
intact, is facultative, can thrive in oxygen-reduced
environments, and is the immediate cause of
bacterial overgrowth. The authors consider that
the density of pilosebaceous units on the face
may explain this phenomenon.3 Pilosebaceous
units, in addition to being colonized by
Staphylococcus aureus (S. aureus), also contain
Cutibacterium acnes (C. acnes), which is a gram-
positive anaerobic organism. More research is
needed to fully understand the pathology that
occurs as part of dermal filler ischemic events.26 If
the artery remains compromised, this is when the
tissue will begin breaking down further.
Exudate. Exudate is a generic term to describe
the liquid produced from a wound. Exudate is
generated as part of the inflammatory response
and is essential to healing. It is usual to see a
small amount of exudation on the apposed
edges of the skin, providing a seal to bacteria and
debris. A narrow border of erythema around the
edge of a wound and some dry surface exudate
are normal findings in a wound that is healing
well. Exudate is high in protein and nutrients,
providing a moist environment in the absence of a
protective epidermis. It also contains electrolytes
and a number of inflammatory components and
supports the ingress of white blood cells.20,27,28
A wound starts producing exudate in the
inflammatory stage. The level of exudate
produced will depend on the depth and size of the
wound and may change over the different stages
of the wound. Exudate can differ in composition
and characteristics, and can indicate to the
status of the wound (i.e., if infection is present).
Moderately to highly exuding wounds can affect
the periwound (the area surrounding the wound).
The periwound can become compromised and
macerated, which will impair the healing process.
It is important that exudate is managed to create
an optimum wound healing environment without
disturbing the periwound integrity (Table 2).27
Slough and eschar. Astute observation and
prompt action will allow an HA filler occlusion
to be reversed, but, in the event of a permanent
filler product, slough and/or eschar may be a
possibility. Wounds in WHS 1 may remain in this
stage of constant inflammation if not properly
debrided.28
Slough is a form of nonviable tissue.28 The
presence of nonviable tissue is a barrier to
effective healing, and removing it reduces the risk
of bacterial attachment and biofilm formation.
Slough may be recurrent in a wound, so removal
may be repeatedly needed. Slough is typically
light in color and can be yellow/green if the
wound is infected. Slough is loosely attached and
contains white blood cells mixed with exudate.
It has viscoelastic properties, similar to gel or
slime.28
Eschar is necrotic tissue that is dark brown or
black in color. It is firmly attached to the wound
bed and is dry, housing no exudate or white
cells.28 Eschar is a barrier to effective wound

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39-48_CMAC .indd 45 12/15/21 11:59 AM

 GUIDELINES
healing and can cause infection. If the wound
is covered in this leathery substance, topical
agents that promote a moist wound healing
environment should be used to encourage
autolytic debridement. Severe or neglected cases
of ischemic injury may require surgical or sharp
debridement.28
Use of antibiotics. The inflammation stage of
wound healing may be confused with infection,
spurring the clinician to commence antibiotic
treatment prematurely. However, antibiotic
treatment will not heal the damaged tissue,
and oral antibiotics should only be initiated if
the patient is systemically indicating signs of
infection, such as a pyrexia. Many published
studies and clinical papers provide evidence that
antibiotics should not be a first line treatment for
wounds. After analyzing randomized, controlled
trials of patients with non-bite wounds, a study
by Cummings and Del Beccaro found no evidence
to suggest prophylactic antibiotic treatment
prevents localized wound infections.29
Use of topical treatments. During WHS 1, it is
vital that the correct topical management of the
wound and surrounding tissue is commenced
as soon as possible to avoid delayed healing.
Failure to initiate the appropriate topical
management during WHS 1 may result in
complications, including biofilm formation,
infection, PIH, and scarring.20,22,24 Primary
dressings, which include topical creams, gels
and ointments, and nonadhesive impregnated
dressings, are applied directly onto a wound.
They are frequently used underneath adhesive
secondary dressings, which are used to hold the
primary dressing in place, absorb exudate, and/
or protect the wound from further damage.
Secondary dressings are adhered to the healthy
skin surrounding the damaged area. Silicone
adhesive dressings are very versatile, and are
suggested if a secondary dressing is required.
Silicone dressings are soft and can be removed
without causing tissue trauma. This allows the
clinician to continually assess the tissue under
the dressing in the earlier stages of healing
without causing damage to the wound bed.30
WHS 2: proliferation. As the wound
begins to heal, angiogenesis takes place and
granulation tissue begins to form. The granulation
stage typically lasts 2 to 4 weeks depending
on the size and depth of the wound bed. For
the wound to enter this stage, it must have
been treated correctly during the inflammation
stage with topical agents that promote a moist
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39-48_CMAC .indd 46
wound healing environment, as well as be
free of devitalized, necrosed tissue, eschar, and
infection.20 If eschar is present on the wound
bed and autolytic debridement has failed or the
wound is not responding to the topical use of
dressings, it is important to refer the patient to
a wound care specialist for input. Granulation
tissue will always form from the base of the
wound upwards, and healthy granulation tissue
will always appear pink in color. If the wound
is bleeding, dark red, or friable, it indicates
an abnormality and can be an indication of
infection or that the wound has been disturbed
by overcleansing or dressing. When healthy
granulation tissue has formed, new capillaries can
start to grow. Capillaries are extremely fragile,
and it is important to ensure dressing changes are
as atraumatic to the tissue as possible to prevent
further damage. The wound should only be
redressed according to the exudate levels.24
To aid in granulation tissue formulation, a
high protein diet and good oral hydration for the
patient are needed. Poor water intake leads to
less elasticity in the skin. The body continually
deposits protein into new cells to enable them to
repair and grow. During the proliferation stage,
protein deficiency can delay the wound from
progressing from the inflammatory phase to the
remodeling stage, and fibroblast activity may be
reduced.31 The patient should also be educated on
the risks of smoking. Nicotine is a vasoconstrictor
and reduces nutritional blood flow to the skin and
tissues. It also increases platelet adhesiveness and
the longevity of tissue ischemia.32
WHS 3: Epithelialization. Once
healthy granulation tissue has reached the
height of the wound, collagenesis will occur
and elastin will form, which will enable
the skin to start meeting at the edges. A
moist environment is essential for this stage
to occur quickly. If the wound is treated
optimally during the inflammation and
proliferation stages, epithelial cells will form
more quickly, which will lead to a better
long-term outcome for the patient regarding
scar tissue formation.12,13,20,22 Winter, who
was the first to understand the benefit of
moist wound healing, published his initial
findings in 1962. The study demonstrated that
healing rates were slower if wounds were left
uncovered compared to wounds that were
occluded with a polymer dressing to promote
a moist environment.14,15 These findings
broadened our understanding of an optimal
healing environment to increase the rate of
reepithelialization.
WHS 4: Remodeling. This is the final
stage of the wound healing process in which
collagen fibers are synthesized. Elastin formation
begins to take place, and the extracellular
matrix is restored. The remodeling phase can
begin as soon as 21 days after the initial injury
or it can be delayed for years depending on the
degree of trauma to the tissue and the level and
duration of ischemia. There is no consensus as
to the timeframe that defines when a wound
becomes chronic; chronic wounds, however, fail
to proceed through the normal phases of wound
healing in a timely manner.20,22 Such wounds
are challenging to heal and are at risk of re-
occurring infections and biofilm formation. It is
important that correct treatment is commenced
as early as possible to ensure optimum healing.
There is less vascularity during the maturation
stage. To ensure collagen synthesis continues,
epithelial cells need to be protected and the
skin barrier needs to be strengthened by using
a good-quality, medical-grade, humectant-
based moisturizer and a broad-spectrum
sunscreen.12,13,33,34,35
Unless there is considerable tissue loss at
the point of presentation, aesthetic ischemic
wounds should heal quickly. When presented
with an actual or potential wound, clinicians
should review the patient's medical history and
identify risk factors that may impair healing.
FACTORS THAT AFFECT WOUND
HEALING
Nutrition. Wound healing requires
vitamins, minerals, fatty acids, proteins,
and carbohydrates to effectively regenerate.
Malnutrition impairs the progress through
the stages of wound healing. This may be an
issue if the patient has an eating disorder or is
otherwise malnourished.12,33
Infection. When the skin barrier is breached,
there is the possibility of bacterial infection, which
can delay wound healing. S. aureus, S. Spp. and P.
aeruginosa are the primary bacteria responsible
for wound infections.33 Though inflammation is
part of the initial response to a wound, continued
inflammation caused by infection can result in
leukocyte migration and cytokine release. The
leukocytes, being phagocytic, release endotoxins
upon engulfing the bacteria, which can result in
local necrosis and chronic inflammation. Chronic
inflammation affects epithelialization, delays
12/15/21 11:59 AM
 GUIDELINES
wound retraction, and affect the skin's ability to
mature and remodel.33,34
Age. Age is a major risk linked to impaired
healing.34 As we age, the epidermal layer
becomes thinner and the inflammatory response
decreases. An inadequate inflammatory
response results in delayed leukocyte activity,
reduced phagocytosis, and decreased growth
factor and cytokine release, resulting in delayed
angiogenesis, epithelialization, and remodeling.34
Chronic disease. Many chronic
diseases can impact wound healing, but
diabetes mellitus (DM) is the most problematic
given its multifactorial nature. DM impairs
leukocyte migration and induces the release
of proinflammatory cytokines, which results
in chronic inflammation. DM also impacts the
microenvironment of the wound, reducing
oxygen tissue concentrations and decreasing
angiogenesis. It impacts the development of
keratinocytes and fibroblasts, which delays
epithelialization and wound remodeling.33,34
Obesity is another chronic issue, though less
problematic in a face wound. However, obesity
leads to reduced microperfusion of the skin,
increased release of pro-inflammatory cytokines,
and decreased immune response to the area.34
Medication. Drugs that typically interfere
with wound healing include those that affect
coagulation, have an impact on inflammatory
mechanisms, and those that impact on cell
proliferation.32 Corticosteroids are of concern if
there is a wound; not only do they modulate the
immune response, but the anti-inflammatory
effect of steroids also decrease in the release
of growth factors and cytokines (which
modulate other mechanisms of healing) and
decrease fibroblast activity.11 Disease modifying
antirheumatic drugs and biologic agents may
also have a negative effect on wound healing.
Chemotherapeutic drugs decrease cellular
metabolism and proliferation in cells with a
high turnover, specifically the skin. Clinicians
should use significant caution when considering
dermal filler treatment in patients undergoing
chemotherapy.33
Smoking. It is well known that smoking
impairs wound healing. Tissue hypoxia is a
particular issue. It decreases the proliferation
of erythrocytes, oxygenation, blood flow, and
angiogenesis in the wound tissue.33,36 Smoking
also increases platelet aggregation and
adhesiveness, increasing blood viscosity, which
results in higher risk of thrombosis. Further,
NP+PA Perspectives in Dermatology—A Supplement Series for NP and PA Healthcare Professionals in Dermatology S47
39-48_CMAC .indd 47
cigarette compounds are involved in decreased
fibroblast migration, proliferation, and collagen
remodeling. Smoking also augments the immune
system by decreasing neutrophils, macrophage,
and lymphocyte activity, resulting in a higher risk
of infection.32
Genetic predisposition. Cutaneous
would healing can be impacted by genetic
factors. Keloid scarring, for example, has a strong
occurrence in patients with African, Asian, or
Hispanic ancestry, with a minor occurrence
in the Caucasian population. Ehlers-Danlos
syndrome is a cluster of several disorders that
affect connective tissue and collagen synthesis,
characterized by skin fragility, hyperflexibility,
joint hypermobility, and impaired wound healing.
PIH is an issue that can manifest due to trauma. It
results from the overproduction of melanin or an
irregular placement of pigment after cutaneous
inflammation. Aesthetic clinicians should take
a careful history of all patients prior to initiating
cosmetic procedures to determine if a patient is
at high risk of complications should an ischemic
event or other procedure-related complication
occurs that results in a wound. Clinicians should
also be equipped to address any PIH that may
result.11
KEY STEPS TO WOUND ASSESSMENT
AND MANAGEMENT
Recognizing factors that might impact wound
healing can allow the clinician to foresee possible
complications in their patients, as well as explain
why healing might be delayed, which may assist
clinicians in augmenting the wound management
plan accordingly. When ischemic injuries are
situated on the face, quality wound care is vital
to limit scarring and permanent damage to the
tissues. Patients seeking aesthetic treatment are
looking for an improvement compared to baseline
and may be more sensitive to poor outcome that
leave them looking "worse." To safeguard against
potential litigation, thorough contemporaneous
notes and standardized photographic images
should be taken during each assessment. There
should be regular patient follow up with clear
communication and instructions. Professionalism
should always be maintained. Consider the
following recommendations:
• Assess and document the wound bed using the
wound assessment tool.
• All wounds should be cleansed using a topical
antimicrobial cleansing agent to breakdown
the bioburden.
• All wounds should be photographed at each
dressing change. Any changes should be
documented.
• Consult Tables 2 and 3 to aid in selection of
appropriate dressings.
TYPICAL WOUNDS SEEN POST-
DERMAL FILLER ISCHEMIC
EVENT AND RECOMMENDED
MANAGEMENT
The authors have put together a list of typical
wounds that have been caused by both reversible
and nonreversible dermal fillers. Table 2 gives
suggested wound management following the
principle of moist wound healing. The choice
of dressings and topical agents are available in
the UK market, with Table 3 detailing generic
information about the dressings and topicals
that are available. This should help guide choice
in other respective countries. CMAC can guide on
appropriateness of dressings and agents.
COMMON TOPICAL AND WOUND
DRESSINGS
Table 3 outlines common topicals and
dressings that may be helpful in treating an
ischemic wound. The table details the rationale
behind the use and how they may be beneficial.
OXYGEN THERAPY
Oxygen is required by all cells. A
microenvironment of hypoxia is important for
angiogenesis, epithelialization, and synthesis of
growth factors. However, it leads to the synthesis
of reactive oxygen species and pro-inflammatory
cytokines that can impair healing. The correct
oxygen concentration is needed to create balance,
prevent wound infection, improve angiogenic
response, increase fibroblast and keratinocyte
production, and ensure proliferation and
migration of the skin cells.33
The evidence base for use of hyperbaric oxygen
therapy (HBOT) in acute filler complications is
weak. It has been effective in treating idiopathic
cilioretinal artery (CLRA) and central retinal vein
occlusion,36 and provided some benefit in treating
visual impairment linked to extraocular muscle
ischemia following calcium hydroxyapatite filler
injection.37 HBOT appeared particularly efficacious
in treating visual impairment due to anterior
segment ischemia following HA injections, and,
when included in therapy, two cases of skin
necrosis.38,39 Zhang40 further reported inclusion of
HBOT in treating three patients with visual loss
12/15/21 11:59 AM
 GUIDELINES
and skin necrosis; all showed improvements in
skin healing but not in terms of sight recovery.
HBOT is often included as part of a treatment
strategy, but there is a lack of head-to-head
research focused on this intervention. As a result,
it is still unknown whether the use of additional
HBOT is beneficial or at which stage its use would
be optimal. The authors have seen patients with
wounds after a vascular occlusion where HBOT
has been prioritized, and the wound has been
left uncovered to dry out. This is not optimal
management.
If concentrated oxygen therapy is deployed,
clinicians may have the option to use a continuous
oxygen therapy (COT) device that is provided with
a dressing. Water-based topicals can be applied
underneath to stop the wound from drying.
Devices are available in the US and UK and may
be a practical treatment option if the clinician
deems oxygen therapy appropriate. In the US,
the company, EO2 Concepts® (San Antonio, Texas),
allows the clinician to prescribe an inexpensive
COT device that can be shipped to the patient and
worn continually until the wound has healed.
CONCLUSION
Wounds that occur due to a dermal filler
ischemic injury are not addressed in the literature
or managed optimally in practice. This guideline
serves to provide a basic guide to wound healing,
create awareness of basic wound management
principles, and recommend management
approaches to typical wound presentations
following a vascular ischemic event. For further
support please contact CMAC for specialist advice.
REFERENCES
1. Belezney K, Carruthers J, Humphrey S, et al. Update on
avoiding and treating blindness from fillers: a recent
review of the world literature. Aesthet Surg J. 2019; 39
(6): 662-674.
2. Alam M, Kakar R, Dover JS et al. Rates of vascular
occlusion associated with using needles vs cannula for
filler injection. JAMA Dermatol. 2021;157(2):174-180.
3. Murray G, Convery C, Davies E, Walker L. Guideline
for the management of hyaluronic acid filler-
induced vascular occlusion. J Clin Aesthet Dermatol.
2021;14(5):E61-69.
4. Urdiales-Gálvez F, Delgado NE, Figueiredo V, et al.
Treatment of soft tissue filler complications: expert
consensus recommendations. Aesthetic Plast Surg.
2018;42(2):498–510.
S48 The Journal of Clinical and Aesthetic Dermatology • December 2021 • Volume 14 • Number 12 • Supplement 1
39-48_CMAC .indd 48
5. Pierrefeu A, Brosset S, Lahon M, et al. Transverse facial
artery perforators: anatomical, two- and three-
simensional radiographic study. Plast Reconstr Surg.
2019;143(4):820e-828e.
6. Kalogeris T, Baines G, Krenz M, Korthuis R. Cell biology
of ischaemia/reperusion injury. Int Rev Mol Biol.
2012;298:229-317.
7. Hong JY, Seok J, Ahn GR, et al. Impending skin necrosis
after dermal filler injection: A ‘golden time’ for first-aid
intervention’. Dermatol Ther. 2017;30:e12440.
8. Khalil H, Cullen M, Chamnbers H, et al. Elements
affecting wound healing time: an evidence-based
analysis. Wound Rep and Reg. 2015;23:550-556.
9. McGarr G, Hodges G, Mallette M, Cheung S. Ischaemia-
reperfusion injury alters skin microvascular responses
to local healing of index finger. Microvascular research.
2018;(118):12-19.
10. Yousef H, Alhajj M, Sharma S. Anatomy, Skin
(Integument), Epidermis.[updated 2021 Jul26].
In:StatPearls [Internet]. Treasure Island (FL): StatPearls
Publishing; 2021 Jan.
11. Davis EC, Callender VD. Postinflammatory
hyperpigmentation: a review of the epidemiology,
clinical features, and treatment options in skin of color.
J Clin Aesthet Dermatol. 2010;3(7):20-31.
12. Benbow M. Exploring the concept of moist wound
healing and its application in practice. Br J Nurs.
2008;17(15).
13. Flanagan M. Wound Healing and Skin integrity.
Philadelphia, PA: John Wiley and Sons;2013.
14. Winter G. Effect of air exposure and occlusion
on experimental human skin wounds. Nature.
1963;200:378-379.
15. Winter G. Formation of the scab and rate of
epithelialisation of superficial wounds in the skin of
the young domestic pig. Nature;193(4812): 293-294.
16. Dyson M, Young S, Pendle CL, et al. Comparison of the
effects of moist and dry conditions on dermal repair. J
Invest Dermatol. 1988;91(5):434-439.
17. Chen WY, Rogers AA, Lydon MJ. Characterization of
biologic properties of wound fluid collected during
early stages of wound healing. J Invest Dermatol.
1992;99(5):559-564.
18. Kunugiza Y, Tomita T, Moritomo H, Yoshikawa H. A
hydrocellular foam dressing versus gauze: effects on
the healing of rat excisional wounds. J Wound Care.
2010;19(1)10-14.
19. Garvier MH, Bass LM, Fitzgerald R, et al.
Differentiating non permanent injectable fillers:
prevention and treatment of filler complications. Aesth
Surg J. 2018;38(1):S29-40.
20. Cañedo-Dorantes L, Cañedo-Ayala M. Skin acute
wound healing: a comprehensive review. Int J Inflam.
2019;2019:3706315.
21. Dealey C. The Care of Wounds: A Guide for Nurses, 4th
ed. Hoboken, NJ: John Wiley and Sons Ltd.;2012.
22. Lawrence JC. Moist wound healing: critique I. J Wound
Care. 1995;4(8):368-370.
23. Farber JL, Chien KR, Mittnacht Jr. Myocardial
ischaemia:the pathogenesis of irreversible cell injury
in ischaemia. Am J Pathol. 1981;102(2):271.
24. Kamolz LP, Wild T. Wound bed preparation: the impact
of debridement and wound cleansing. Wound Med.
2013;1:44-50.
25. Patel GK. How to diagnose and treat a hemorrhagic
skin necrosis. Wounds UK. 2007;34.
26. Makrantonaki E, Ganceviviene R, Zouboulis C.
An update on the role of the sebaceous gland in
pathogenesis of acne. Dermato-Endocrinology.
2011;3(1):41-49.
27. Cutting KF. Wound exudate: composition and
functions. Br J Community Nurs. 2003;8(9 Suppl):4-9.
28. Percival SL, Suleman L. Slough and biofilm: removal
of barriers to wound healing by desloughing. J Wound
Care. 2015;24(11):498-510.
29. Cummings P, Del Beccaro MA. Antibiotics to prevent
infection of simple wounds: a meta-analysis of
randomized studies. Am J Emerg Med. 1995;13(4):396-
400.
30. Meuleneire, Rüknagel . Soft silicone dressings made
easy . Wounds International. 2013.
31. Barchitatta M, Maugeri A, Favara G, et al. Nutrition
and wound healing: an overview focusing on the
beneficial effects of curcumin.Int J Mol Sci. 2019;20:
1119
32. Ellis P. The impact of smoking on wound healing: the
role of the nurse. Br J Nurs. 2018;27(6):S10-S14.
33. Gushiken LFS, Beserra FP, Bastos JK, Pellizson
CH. Cutaneous wound healing: an update from
physiopathology to current therapies. Life.
2021;11;665-684.
34. Khalil H, Cullen M, Chambers H, et al. Elements
affecting wound healing time: an evidence-base
analysis. Wound Rep and Reg. 2015;23:550-556.
35. Bryan J. Moist wound healing: a concept that changed
our practice. J Wound Care. 2004;13(6):227-228.
36. Celebi AR, Kilavuzoglu AE, Altiparmak UE, et al.
Hyperbaric oxygen for the treatment of the rare
combination of central retinal vein occlusion and
cilioretinal artery occlusion. Diving Hyperb Med.
2016;46(1):50-53.36)
37. Sung WI, Tsai S, Chen LJ. Ocular complications
following cosmetic filler injection. JAMA Ophthalmol.
2018;136(5):e180716.
38. Worley N, Lupo M, Holcomb K et al. Hyperbaric oxygen
treatment of keratitis following Facial hyaluronic acid
injection. Ochsner J. 2020;20(2):193–196.
39. Darling MD, Peterson JD, Fabi SG. Impending necrosis
after injection of hyaluronic acid and calcium
hydroxylapatite fillers: report of 2 cases treated
with hyperbaric oxygen therapy. Dermatol Surg.
2014;40:1049–1052.
40. Zhang L, Pan L, Xu H et al. Clinical observations
and the anatomical basis of blindness after facial
hyaluronic acid injection. Aesthetic Plast Surg.
2019;43(4):1054-1060. NPPA
12/15/21 11:59 AM