MOC-CME

Evidence-Based Medicine: Wound Management

Christine M. Jones, M.D.
Alexis T. Rothermel, M.D.
Donald R. Mackay, M.D.
Hershey, Pa.
Learning Objectives: After reading this article, the participant should be able
to: 1. Describe the basic science of chronic wounds. 2. Discuss the general and
local factors that should be considered in any patient with a chronic wound. 3.
Discuss the rationale of converting a chronic wound into an acute wound. 4.
Describe techniques used to prepare chronic wounds. 5. Discuss the appropri-
ate use of different dressings presented in this article. 6. Discuss the pros and
cons of the adjuncts to wound healing discussed in this article.
Summary: This is the second Maintenance of Certification article on wound
healing. In the first, Buchanan, Kung, and Cederna dealt with the mechanism
and reconstructive techniques for closing wounds. In this article, the authors
have concentrated on the chronic wound. The authors present a summary of
the basic science of chronic wounds and the general and local clinical factors
important in assessing any chronic wound. The evidence for interventions of
these conditions is presented. The surgical and nonsurgical methods of wound
preparation and the evidence supporting the use of the popular wound dress-
ings are presented. The authors then present the evidence for some of the
popular adjuncts for wound healing, including hyperbaric oxygen, electro-
therapy, and ultrasound. A number of excellent articles on negative-pressure
wound therapy have been written, and are not covered in this article.  (Plast.
Reconstr. Surg. 140: 201e, 2017.)

R
oughly 1 percent of the population will
develop a chronic wound in their lifetime.1,2
An estimated 6.5 million Americans have
chronic wounds.3 Wound care is a massive industry
that accounts for 2 to 4 percent of all health care
spending in developed countries.1 An estimated
$10 to $25 billion is spent annually to manage
chronic wounds in the United States.4,5 Hundreds
of products are available, but the evidence to sup-
port use of many of them is weak.
CHRONIC WOUNDS
Basic Science of Chronic Wounds
Wound repair is a complicated, highly regu-
lated process, divided into three phases: inflam-
mation, proliferation, and remodeling.6,7 Initial
wound healing, mediated by activation of the
immune system, leads to a cascade of proinflam-
matory events. Platelet degranulation facilitates
hemostasis and releases cytokines that signal
an influx of inflammatory cells, beginning with
From the Division of Plastic Surgery, Penn State Hershey
Medical Center.
Received for publication July 17, 2016; accepted November
21, 2016.
Copyright © 2017 by the American Society of Plastic Surgeons
DOI: 10.1097/PRS.0000000000003486
neutrophils. The major role of neutrophils in
wound healing is host defense and killing infec-
tious agents. Paradoxically, neutrophil activa-
tion negatively affects wound repair through the
production of oxygen free radicals, which causes
oxidative stress. Neutrophil-derived matrix metal-
loproteinases degrade extracellular matrix com-
ponents, and elastase destroys vital growth factors,
including platelet-derived growth factor and
transforming growth factor-beta. These enzymes
are increased in chronic wounds.8 Normally, neu-
trophil influx is limited to several days. In chronic
wounds, neutrophil infiltration persists. Dysfunc-
tional macrophages with reduced rates of effero-
cytosis are characteristic of diabetic ulcers, leading
to an increased burden of apoptotic neutrophils
Disclosure: The authors have no financial interest
to declare in relation to the content of this article.
Supplemental digital content is available for
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 Plastic and Reconstructive Surgery • July 2017

at the wound site.9 The increased level of pro-

teolytic enzymes in chronic wounds causes direct
tissue damage and decreases growth factors neces-
sary for healing.
Monocytes enter the wound with the neu-
trophils and differentiate into macrophages.
Activated macrophages promote inflammation
through the production of proinflammatory
cytokines. Increased levels of these cytokines
such as tumor necrosis factor-alpha, interleukin-
1-alpha, and interleukin-6 are found in venous
stasis ulcers.10 Additional phenotypes of macro-
phages become activated to transition into the
proliferative phase and serve an antiinflamma-
tory function.11 These cells remove neutrophils
and promote cell proliferation and angiogenesis.
Nonhealing, chronic wounds do not progress past
a persistent state of inflammation. In chronic isch-
emic wounds, classically activated macrophages
are present in increased numbers, resulting in an Fig. 1. Distribution of wound types. (Adapted with permission
imbalance between proinflammatory mediators from Fife CE, Carter MJ. Wound care outcomes and associated
and tissue synthesis.12 cost among patients treated in US outpatient wound centers:
During the inflammatory phase, increased Data from the US wound registry. Wounds 2012;24:10–17.)
vascular permeability contributes to the forma-
tion of exudate, a serous fluid that contains many wound care
factors that support healing, including macro-
phages, matrix metalloproteinases, and growth Assessment of the Chronic Wound
factors.13 In chronic inflammation, the exudate An important principle in treating chronic
volume increases, and its composition changes wounds is to identify and correct the pathologic
to include proinflammatory factors and degrad- condition that has prevented the progression of
ing enzymes that cause further tissue damage and wound healing beyond the inflammatory phase.
inhibit healing. A useful way to assess the patient is to consider
The proliferative phase includes reepithelial- general and local conditions that might impede
ization, where keratinocytes from wound edges normal healing (Table 1).
and dermal appendages create a barrier against
bacterial infiltration and fluid loss. Reepithelial- GENERAL CONDITIONS
ization is mediated by epidermal growth factor,
fibroblast growth factor, and transforming growth Nutrition
factor-beta. Fibroblast migration into the wound Protein-energy and protein-calorie malnutri-
and collagen production occurs during the prolif- tion are well recognized as problems.15 Malnutri-
erative phase and continues into the remodeling tion doubles the risk of developing pressure ulcers16
phase. Tissue synthesis is reliant on oxygen supply, and increases mortality in patients in nursing
which is required for hydroxylation of proline and homes.17,18 Dietary protein supplements improve
lysine in collagen synthesis. chronic wound healing in healthy volunteers and
malnourished geriatric patients.19–21 Serum albu-
Common Chronic Wounds min has a half-life is 18 to 21 days, making it a poor
Pressure ulcers, diabetic foot ulcers, venous indicator for assessing acute changes in wound
stasis wounds, and ischemic wounds of arterial healing capacity. Prealbumin and transferrin, with
or postirradiation cause are the most common half-lives of 3 to 5 days and 7 to 10 days, respec-
chronic wounds (Fig.  1). Chronic wounds have tively, are better acute markers and are checked
a unique pathophysiology in their mechanism of weekly in patients receiving nutritional support.21
healing impairment, but common mechanisms Screening patients for recent unintended weight
include cellular and systemic changes of aging, loss reliably assesses the effect of nutritional sta-
repeated ischemia-reperfusion injury, and bacte- tus on wound healing.15–17,21,22 Elective reconstruc-
rial colonization.14 tive surgery should be postponed until a positive

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 Volume 140, Number 1 • Wound Management
Table 1.  General and Local Conditions Affecting
Chronic Wounds
General factors
  Nutrition
  Cardiopulmonary disease
  Medical treatment (chemotherapy)
  Diabetes
  Smoking
  Autoimmune disease
Local factors
  Peripheral vascular disease
  Venous stasis
  Peripheral neuropathy (diabetes)
  Radiation therapy
  Pressure
  Infection
  Edema
protein balance is observed. Protein deficiencies
marked by low albumin levels have been found to
be strong predictors of wound healing complica-
tions and higher mortality rates.23
In vitro evidence suggests that glutamine and
arginine have beneficial effects on wound heal-
ing.24–26 As the most abundant amino acid in the
body, glutamine serves as a nitrogen donor, is a
precursor for nucleic acid synthesis in fibroblasts,
aids in gluconeogenesis, and has immunomodu-
lating effects.27–30 Arginine aids in maintaining a
positive nitrogen balance, enhancing collagen
deposition, and stimulating T lymphocytes.24,31
However, most in vivo studies, including a 2014
Cochrane review, have shown no clear benefit
from supplemental glutamine or arginine.32–36
Micronutrients, including zinc and magne-
sium, play important roles in normal wound
healing, acting as cofactors in many biological
reactions. Zinc deficiency is known to impair
wound healing.37 An early trial suggested that
oral zinc supplements helped heal wounds more
quickly.38 Ever since, zinc supplements have been
used in many protocols. A recent meta-analysis
evaluated six trials of zinc supplementation for
patients with venous or arterial ulcers, and found
no effect on ulcer healing.39 Magnesium acts as a
cofactor for enzymes involved in protein and col-
lagen synthesis, but supplements have not shown
any benefit for healing chronic wounds.6,18,21,32,40
Cardiopulmonary Disease
Ischemic heart disease decreases tissue per-
fusion. In heart failure, a reduction in cutane-
ous microcirculation parallels the decline in
ejection fraction.41–43 Pulmonary and hemato-
logic diseases decrease oxygen-carrying capacity.
Chronic obstructive pulmonary disease is a dem-
onstrated predictor of complications in healing
Copyright © 2017 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
acute wounds,44–47 but its specific role in chronic
wounds has not been studied. Optimizing these
disease states is a vital step in any patient with a
chronic wound.
Medical Therapy
Chemotherapy drugs would be expected to
impede wound healing. However, outcome studies
on their effects have shown mixed results. Several
large studies have shown higher rates of wound
dehiscence,48 infection,49–51 and tissue expander
explantation,52 although others have found no
such effect.53–58 Regardless, wound healing seems
to return to normal 1 year after chemotherapy.59
Corticosteroids are well known to impair
wound healing. Steroids decrease the inflamma-
tory infiltrate and fibroblast replication, decreas-
ing collagen production.60,61 Daily administration
of 25,000 IU of vitamin A mitigates these negative
effects.62–64
Smoking
Cigarette smoking impairs wound healing.65
Nicotine is a potent vasoconstrictor66; one ciga-
rette reduces subcutaneous tissue oxygen tension
by 30 percent for nearly 1 hour.67 Nicotine also
increases platelet adhesiveness, raising the risk
of microvascular thrombi and local tissue isch-
emia.68 Carbon monoxide constitutes 4 percent of
cigarette smoke and reduces the oxygen-carrying
capacity of erythrocytes by irreversibly binding to
hemoglobin.6,23,69 Hydrogen cyanide inhibits the
enzymes of oxidative metabolism and cellular oxy-
gen transport.23,68 Recent level I evidence showed
that a 4-week abstinence period is significantly
better compared with shorter intervals, but that
longer cessation further reduces wound healing
complications.70
Diabetes
Diabetes has profound systemic and local
effects, both causing chronic wounds and impair-
ing healing. Hyperglycemia affects protein and
enzyme function by a nonenzymatic glycosylation
of proteins including collagen. The glycosyl-
ation end products perpetuate the inflammatory
response.23,71,72 There is good evidence showing
that tight perioperative glucose control reduces
infections and wound healing complications.23,73–79
The cellular processes of wound healing are nega-
tively affected by hyperglycemia,80,81 but limited
evidence exists to guide the regimen of glucose
control when treating chronic wounds.82 Hemo-
globin A1c seems to be the best predictor of wound
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healing problems.78 Studies demonstrate reduced
healing rates with each 1 percent increase in A1c
above 7 percent,83 and that an A1c value greater
than 9.4 percent is predictive of lower extremity
amputation.84 A meta-analysis found a lower all-
cause amputation rate in diabetics who followed a
regimen of intensive glucose control.85
Patient education is very important. In the
absence of protective sensation, patients should
be educated in pressure relief. Diabetics with
peripheral neuropathy need a meticulous foot
care regimen.86
LOCAL CONDITIONS
Peripheral Vascular Disease
Peripheral vascular disease results in impaired
healing because of decreased oxygen delivery to
tissue. Optimizing perfusion with effective arte-
rial reconstruction improves healing in chronic
wounds of the lower extremity. The understand-
ing of angiosomes, a concept introduced to plas-
tic surgery by Ian Taylor, which explains how a
single vessel supplies a composite anatomical unit
including an area of skin and the block of tis-
sue deep to it, has refined how revascularization
is performed.87 Targeting revascularization to a
specific angiosome that includes a chronic ulcer
improves wound healing.88,89
Venous Stasis
Venous stasis ulcers occur when incompetent
valves transmit high pressure from the venous
Fig. 2. (Left) Extensive venous ulceration with necrotic tissue. (Right) The same patient after sharp
débridement and dressing wet-to-dry saline gauze dressing changes. The wound has a healthy
granulating base and is now ready for a skin graft.
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Copyright © 2017 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
Plastic and Reconstructive Surgery • July 2017
column directly to the subcutaneous tissue, caus-
ing edema, scarring, decreased perfusion and
oxygenation, and ulceration (Fig.  2). Compres-
sion therapy with stockings and bandages has
been conclusively shown to improve healing but
must be used continuously or recurrence is high.90
Compliance with treatment is a problem for many
patients. A combination of vein stripping and
compression reduces the rate of recurrence,91
but may not be suitable for patients with multiple
comorbidities. Although there is no high-level
evidence, endovascular vein ablation appears to
improve ulcer healing when combined with com-
pression treatment.92–94
Pressure
Pressure ulcers arise from localized ischemia
in patients who either have peripheral neuropa-
thy and cannot feel any pain or are unable to
move after loss of consciousness or heavy sedation
(Fig. 3). Pressure relief is obviously important in
preventing and healing these wounds. Risk strati-
fication and programs that educate patients and
health care providers effectively reduce the rate
of hospital-acquired ulcers.95,96 There is no high-
level evidence that wound teams have an impact
on reducing rates, but institutions with poorly
organized systems have a higher rate of hospital-
acquired pressure sores.97
Infection
Bacteria will contaminate all open wounds.
In time, wounds become colonized as bacteria
 Volume 140, Number 1 • Wound Management
Fig. 3. Paraplegic patient with full-thickness sacral pressure sore
before surgical débridement.
replicate (Fig. 4). When this replication proceeds
to a point where the colonization interferes with
healing, the wound has become critically contami-
nated. Critical contamination can be thought of
as a subclinical infection. The wound becomes
infected when the bacterial replication causes a
local inflammatory response, with heat, pain, and
swelling. Untreated wound infection can lead to
fever, an elevated white blood cell count, and sep-
sis.98 A bacterial count of 105 bacteria per gram
of tissue is associated with wound infection and
impaired healing.99 Systemic antibiotics essential
for treating sepsis cannot penetrate a biofilm,
whereas appropriate topical antibiotics have
been shown to be effective in reducing bacterial
bioburden.99
Fig. 4. Infected scalp pressure sore that will require débride-
ment of the necrotic tissue. Antibiotics will be needed only if the
cellulitis does not resolve.
Copyright © 2017 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
Antiseptics such as hydrogen peroxide,
sodium hypochlorite (Dakin solution), acetic
acid, povidone-iodine, or chlorhexidine are use-
ful bactericidal adjuncts to débridement but
should not be used in clean wounds. Their effect
is nonselective and they destroy local healthy tis-
sue and bacteria.100 Antiseptics are also often inef-
fective in clearing bacteria because they bind to
organic material.101 Quarter-percent acetic acid is
effective for treating wounds contaminated with
Pseudomonas.102
Radiation Damage
Radiation negatively affects fibroblasts, growth
factors, and mesenchymal stem cells. Microvascu-
lar endarteritis and microvascular thrombosis are
commonly seen. Epithelialization is slower, infec-
tion rates are higher, and dehiscence is seen more
commonly in irradiated wounds103,104 (Fig. 5).
Malignancy
Chronic wounds that have been present for more
than several months or ones that do not respond
to treatment in the expected manner should be
approached with a high index of suspicion. Marjo-
lin ulcers can develop within chronic wounds from
a longstanding cycle of irritation,105 coupled with an
elevated level of proto-oncogene expression,106,107 tis-
sue that is more susceptible to carcinogens,105,108 and
scar that prevents normal immune surveillance.108,109
Malignant transformation most commonly produces
an aggressive form of squamous cell carcinoma with
a higher propensity for metastasis, although basal
cell carcinoma and malignant melanoma have also
been described.110,111 Approximately 75 percent
of Marjolin ulcers arise from burn scars.105,108 Early
biopsy and resection with 2- to 4-cm margins are the
mainstays of therapy.112,113
Foreign Body
Nonhealing wounds should be examined
carefully for exogenous material. Foreign bodies
can produce an inflammatory response that pre-
cludes normal wound healing. Retained gauze,
permanent suture, or environmental debris are
common examples.
Direct Local Wound Care
To stimulate healing of chronic wounds, prep-
aration should focus on addressing three primary
components: bacterial imbalance, necrotic bur-
den, and excess wound exudate.114 These compo-
nents can be addressed through débridement and
selection of the appropriate dressing.
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Fig. 5. (Left) Radiation wound of right upper anterior thorax with exposed mesh. (Center) Wound after extensive débridement.
(Right) Covered with a pedicled cutaneous flap.
DÉBRIDEMENT
Débridement is the mainstay of dealing with
any chronic wound. Effective débridement removes
devitalized tissue that may serve as a nidus for infec-
tion and impair wound healing. The aim is to con-
vert a chronic wound to an acute one.98,115 (See
Video, Supplemental Digital Content 1, which dem-
onstrates wound débridement of chronic wounds.
This video is available in the “Related Videos” sec-
tion of the full-text article on PRSJournal.com or,
for Ovid users, at http://links.lww.com/PRS/C229.)
Surgical Débridement
Sharp débridement is the gold standard for
removing devitalized tissue, biofilm, and gan-
grene.116 Tissue can be removed with scalpels, scis-
sors, rongeurs, or curettes; this treatment is simple
and cost-effective. A no. 15 blade scalpel works well
for removing soft tissue around bone, and a no. 10
or 20 blade efficiently removes soft tissue alone.
Video 1. Supplemental Digital Content 1, which demonstrates
wound débridement of chronic wounds, is available in the
“Related Videos” section of the full-text article on PRSJournal.
com or, for Ovid users, at http://links.lww.com/PRS/C229.
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Plastic and Reconstructive Surgery • July 2017
Curettes are effective for débriding large areas of
chronic granulation tissue or deep cavities.98
After débridement, tissue should be irrigated
thoroughly. Pulsed-lavage systems reduce the
bacterial burden and the débrided tissue,117 and
contribute to better healing of pressure ulcers.118
Some evidence suggests that continuous irrigation
reduces bacterial contamination as well or better
than pulsed lavage, offering an economical solu-
tion.119–121 Caution using pulsed lavage has been
advocated because of the possibility of micro-
trauma122 and propagation of bacteria through
medullary bone and to a lesser extent through
soft tissue. The clinical effects are unclear.123–125
Alternative tangential hydrodissection systems
(Versajet; Smith & Nephew, Cambridge, England)
can precisely débride tissue passing through a
high-pressure water stream on a handpiece tip.
This method is useful for débriding thin layers
of soft, friable tissue. The reduction in operating
room time can make hydrodissection cost neutral
or cost saving, despite the expense of the unit and
disposable handpiece.126,127 Methodologic flaws
and the potential for bias necessitate further well-
designed studies.128
Enzymatic Débridement
Several products containing exogenous
enzymes have become popular alternatives to
sharp débridement. The most commonly used
are collagenase, papain/urea, and fibrinolysin/
DNAse (Table  2). These products have a role in
Table 2.  Products Containing Exogenous Enzymes
for Wound Débridement
Enzyme Product Manufacturer
Fibrinolysin/DNase Elase Jouveinal
Collagenase Santyl Smith & Nephew, Inc.
Papain/urea Accuzyme Healthpoint, Ltd.
 Volume 140, Number 1 • Wound Management

removing slough and eschar in the rare instances
when surgical débridement is not an option.
Some studies showed that collagenase removed
necrotic tissue more rapidly than placebo;129–131
however, a recent meta-analysis found no such
benefit.132 A number of studies reported its cost-
effectiveness; however, these are often industry-
sponsored and subject to potential bias.133,134
Papain, a nonspecific cysteine protease, is typi-
cally combined with urea, a natural protein denatur-
ant.135 A papain-urea preparation was more effective
than collagenase in a small randomized prospective
study on pressure sores.136 A fibrinolysin/DNAse
product showed no benefit compared to a placebo
and is no longer commercially available.137
WOUND DRESSINGS
Until the late twentieth century, drying wounds
to prevent bacterial infection was common prac-
tice (Table  3).137–141 Numerous studies have now
established the principle of maintaining a moist
environment to optimize healing.115,135,142–147 It is
important for practitioners to realize the big dif-
ference in the regulatory requirements between
drugs, which require proof of efficacy for licen-
sure, and dressing materials, which do not. Clini-
cians have the responsibility to critically evaluate
the literature to understand whether a dressing is
efficacious and cost effective or not and also to
fully understand the influence that industry has
on our decision-making in this area.
Gauze
The simplest form of basic contact dressings,
gauze is made of woven cotton fibers. The fibers
can be formed into sheets, ribbons, or rolls with a
variety of applications. Some gauze dressings are
impregnated with petroleum jelly to reduce adher-
ence, iodine to improve antimicrobial properties,
or other substances for specific indications. To
retain the proper level of moisture, gauze dress-
ings must be changed frequently, typically twice
daily. These dressings can be used to pack wound
cavities. Removal of adherent dry gauze from a
wound is one method of débridement. Gauze
dressings have the advantages of being inexpensive
and readily available; however, because of the fre-
quency with which they need to be changed, some
authors have questioned their cost-effectiveness.135
Low-Adherent Dressings
Several dressing types are available that have
reduced tissue adherence and a low absorbency
profile (Table  4). Low-adherent dressings are
designed to allow wound exudate to pass through
the dressing and retain a desirable level of wound
moisture. These dressings are inexpensive and
readily available, and are best used on flat, shal-
low wounds.147

Table 3.  Overview of Wound Dressings, in Increasing Order of Absorbency

Type Characteristics Advantages Disadvantages Form Frequency
Gauze Woven cotton or synthetic Inexpensive; widely Painful removal; Sheets, Once or twice
fibers available; simplicity limited absorbency; ribbons daily
nonselective
débridement;
evaporative
moisture loss
Low-adherent Open weave, coated gauze Transparent; can Low absorbency Tulles or Every 1–7 days
dressings or synthetic material observe wound; textiles
inexpensive; widely
available; less
painful removal
Films Semipermeable Transparent Low absorbency Sheets Every 1–7 days
Hydrogel Donate moisture to May predispose to Sheet or Every 1–7 days
wound; cooling maceration,139 amorphous
effect, pain relief yeast140 gel
Hydrocolloid Polycarboxymethylcellulose, Low-moderate May macerate Sheets, Every 7 days
gelatin, pectin, elastomer absorbency periwound skin or pastes, or
bound to film adhere to hydrofibers
wound,137, 138
brown, malodorous
exudate141
Foam Polyurethane or silicone Moderate absorbency; May adhere to wound Sheets or Every 1–7 days
foam cushioning; or need secondary pouches
thermal insulation dressing
Alginate Derived from brown sea- Highly absorbent; Foreign-body Sheet or Daily
weed inherently reaction fibers
hemostatic

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 Plastic and Reconstructive Surgery • July 2017

Table 4.  Examples of Low-Adherent Dressings
Material Brand Name Characteristics
Tulles Bactigras, Jelonet, Open-weave gauze
Paranet, Paratulle, material coated with
Unitulle, Urgotul paraffin plus
medication
Textiles Mepitel, NA Dressing, Synthetic materials
NA Ultra, Tegapore, creating transparent,
Tricotex nonadherent dressing
Films
Films are transparent polyurethane dress-
ings that adhere to periwound skin but not to
the wound itself, as the acrylic adhesive is inac-
tivated by moisture. The semipermeable barrier
allows transmission of air and water vapor, but
not fluid or bacteria, making them best suited to
wounds with little exudate.135,138,147 Wounds can
be observed through the dressing, allowing the
dressing to be changed only as often as necessary.
They may be useful for securing nonadherent
dressings, covering intravenous sites, and dressing
wounds over joints (Table 5).146
Hydrogel Dressings
Hydrogels are insoluble, cross-linked, glycerin- or
water-based polymers capable of hydrating wounds
because of their high water content (Table 6).146,147
They are semipermeable dressings used to main-
tain a moist environment in wounds with minimal
amounts of exudate.135,146 Because they can hydrate
necrotic tissue and eschar, they are thought to pro-
mote autolytic debridement148; however, this phe-
nomenon has only been studied in vitro.149
Two recent Cochrane reviews compared
the efficacy of hydrogels with alternative wound
dressings for diabetic foot ulcers and pressure
ulcers.150,151 Meta-analysis of three studies152–154
showed that hydrogels are better than basic
contact dressings at healing diabetic foot ulcers.150
No difference was found between hydrogels and
basic contact dressings, foams, and hydrocolloids
when treating pressure ulcers.151
Hydrocolloid Dressings
Hydrocolloids are semiocclusive, absorbent
dressings made up of sodium carboxymethylcellu-
lose, gelatin, pectin, elastomers, and adhesives on
a carrier film or foam sheet (Table 7).146,147 Hydro-
colloids are capable of absorbing a low to moder-
ate amount of wound exudate. They can be used
to prevent skin shearing that can lead to pressure
ulcer development,155 and can be worn for up to
7 days. Proper selection is important, as the adhe-
sive is inactivated by moisture138: use on too dry
a wound can allow the dressing to adhere to the
wound, and use on too moist a wound can cause
maceration of the surrounding skin.155,156
A recent Cochrane review comparing hydro-
colloid dressings to basic contact dressings, foams,
and alginates in diabetic foot ulcers did not demon-
strate improved outcomes.157 Hydrocolloids used
in pressure ulcers showed substantially improved
healing compared with gauze dressing.132
Foam Dressings
Polyurethane or silicone foam dressings are
manufactured in sheets or small chips in a poly-
urethane bag that is packed into wound cavities
(Table 8). They are moderately absorbent and are
indicated in wounds with moderate exudate. They
can help cushion bony prominences and prevent
skin shearing.155
Two recent metadata studies compared foams to
basic contact dressings, hydrocolloids, and alginates
Table 7.  Examples of Hydrocolloid Dressings
Form Brand Names

Table 5.  Examples of Film Products Sheets Allevyn, Alione, CombiDERM, Comfeel
Plus, Cutinova Thin, DuoDERM, Invac-
Brand Name Supplier are Hydrocolloid, Tegaderm Hydrocol-
loid, Versiva
OpSite Smith & Nephew Gels, ointments DuoDERM Hydroactive
Tegaderm 3M Company Hydrofibers Aquacel
Bioclusive Johnson & Johnson
BlisterFilm Kendall

Table 8.  Examples of Foam Dressings

Table 6.  Examples of Hydrogels Form Brand Names

Form Brand Names Adhesive sheets Allevyn, Biatain Adhesive, Hydrocell

Foam, Kendall Foam, Mepilex,
Adhesive sheets Curagel, Kendall Hydrogel, XCell Versiva, 3M Adhesive Foam
Cellulose Nonadhesive sheets Lyofoam Max
Amorphous gels Carrasyn Hydrogel, Intrasite, Restore Foam chips in Allevyn Plus Cavity
Hydrogel, SĀF-Gel nonadherent film

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 Volume 140, Number 1 • Wound Management
for treating venous leg ulcers and diabetic foot
ulcers, respectively. Both studies found similar rates
of healing and comparable adverse events.158,159
Alginate Dressings
Alginates are highly absorbent dressings
derived from seaweed (Table  9).147,160 The dress-
ings rely on alginic acid, which gives them the
capacity to absorb wound exudate 15 to 20 times
their weight.147,160 With hydration, alginates con-
taining more mannuronate (Kaltostat) form soft,
amorphous gels that completely dissolve, whereas
those predominant in guluronate (Sorbsan) form
firmer gels that retain their basic shape.135,161 The
products are dehydrated and formed into porous
sheets for topical dressings or woven, flexible
fibers for wound packing.
Recent large meta-analyses comparing alginate
dressings to basic contact dressings for diabetic
foot ulcers, venous stasis wounds, and pressure
ulcers found no evidence to support improved
healing times or reduced adverse effects.162,163 In
addition to cost, a drawback of alginate dressings
is their ability to cause a foreign-body reaction
within wounds when the dressing is not fully bro-
ken down and resorbed, such as when it is used on
too dry a wound.164
Silver-Impregnated Dressings
Silver has wide-reaching antimicrobial prop-
erties against bacteria, fungi, and viruses, includ-
ing methicillin-resistant Staphylococcus aureus. The
highly reactive, negatively charged silver ion binds
to DNA and RNA, preventing cellular replica-
tion.165,166 Silver sulfadiazine and silver nitrate have
long been used to reduce infection in burns. More
recently, products containing silver nanoparticles
have become popular for treating open wounds
and chronic ulcers. Recent Cochrane reviews
have failed to demonstrate high-level evidence of
benefit from silver-containing dressings in either
preventing or treating infected wounds.167,168 Pres-
sure ulcers treated with silver-based dressings have
demonstrated a faster reduction in area.132 There
is little evidence to support the use of silver dress-
ings in diabetic foot ulcers.169
Table 9.  Examples of Alginate Dressings
Brand Name Description
Algosteril, Comfeel Alginate, Calcium alginate
Kaltostat, Sorbsan; ActivHeal,
Algisite, Curasorb, Melgisorb,
SeaSorb, Suprasorb A,
Tegagel, Urgosorb
Copyright © 2017 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
Adjuncts to Wound Healing
Hyperbaric Oxygen
Hyperbaric oxygen therapy subjects the
body to 100 percent oxygen at increased atmo-
spheric pressure, increasing oxygen tension
in wounds with the aim of improved healing
(Figs. 3 and 6 and Table 10).156–158,170–174 Hyper-
baric oxygen therapy is widely used as a panacea
for chronic wounds despite limited evidence of
benefit for many patients. There is good evi-
dence to support hyperbaric oxygen therapy
for diabetic foot ulcers and late radiation tis-
sue injury.175,176 Goldman found that hyperbaric
oxygen therapy improved wound healing and
reduced the incidence of amputation in dia-
betic foot wounds.175 A cautionary note comes
from a similar study by the Cochrane Wounds
Group showing that the benefit for both dia-
betic foot ulcers and venous stasis wounds was
limited to the first 6 weeks after therapy; there-
after, healing and amputation rates approached
that of controls.139
Electrical Stimulation
Electrical stimulation has been used both to
treat wounds and to prevent pressure ulcers in
spinal cord injuries. Moderate-strength evidence
suggests that using high-voltage pulsed current
electrical stimulation helps speed the process of
healing pressure ulcers.140 Electrical stimulation
used to prevent pressure sores using either per-
cutaneous electrodes or electrodes embedded
in muscles appears to hold promise. More high-
level evidence is needed before the treatment
become mainstream.141
Electromagnetic Therapy
The application of electromagnetic fields
has some enthusiastic supporters as an adjunct
in treating chronic wounds. Two recent
Cochrane reviews, however, failed to show
improved healing in either pressure ulcers or
venous stasis wounds treated with electromag-
netic therapy.171,172
Therapeutic Ultrasound
Ultrasound has been proposed to favor
wound healing by a thermal effect, increasing
blood flow and promoting collagen remodel-
ing.173,174 The stimulation of inflammatory cells,
protein synthesis, cell proliferation, collagen
deposition, and angiogenesis have never been
observed in vivo.177 The best available evidence
currently shows no benefit from therapeutic
ultrasound in healing pressure ulcers or venous
leg ulcers.132,178,179
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 Plastic and Reconstructive Surgery • July 2017

Fig. 6. Therapeutic mechanisms of hyperbaric oxygen. (Adapted from Marrocco CJ, Atkins MD, Bohannon WT, Warren TR, Buck-
ley CJ, Bush RL. Endovenous ablation for the treatment of chronic venous insufficiency and venous ulcerations. World J Surg.
2010;34:2299–2304; Ohura N, Ichioka S, Nakatsuka T, Shibata M. Evaluating dressing materials for the prevention of shear force
in the treatment of pressure ulcers. J Wound Care 2005;14:401–404; and Baker KG, Robertson VJ, Duck FA. A review of therapeutic
ultrasound: Biophysical effects. Phys Ther. 2001;81:1351–1358.)

Burn wound management
General Principles
Initial burn management begins with an
assessment of the location, depth, and extent of
the burn. The American Burn Association has
established guidelines for referral to a burn cen-
ter. Any patient being transferred to a regional
burn center should have a simple dry dressing
to keep the site warm and clean, avoid delaying
transport, and avoid obscuring burn depth evalu-
ation at the receiving institution.180
Superficial burns involve the epidermis only.
These wounds heal within 3 to 4 days without
scarring. Superficial partial-thickness burns show
damage to the superficial layer of the dermis, spar-
ing enough adnexal structures deeper in the der-
mis to allow spontaneous healing in 10 to 14 days.
The mainstay of therapy for these wounds is topi-
cal wound care. Superficial débridement of bullae
can be performed at the bedside with a basic set
of instruments.
Deep partial-thickness burns are those that
extend into the reticular dermis. In the absence
of infection, they typically require 3 to 8 weeks
to heal, with significant scarring.181 Full-thickness
burns extend into the subcutaneous tissue; dam-
age to the adnexal structures prevents spontane-
ous healing. Deep partial- or full-thickness burn
should undergo early excision and grafting to
reduce hypertrophic scarring (Fig. 4). In mixed-
depth burns, a 5- to 7-day course of topical ther-
apy will allow enough time for any spontaneous
healing to occur.180
Débridement is performed at the fascial
level or tangentially. Fascial débridement loses

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Copyright © 2017 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
 Volume 140, Number 1 • Wound Management

Table 10.  Indications and Evidence-Based Practice less blood, is faster to perform, and leaves a well-
for Hyperbaric Oxygen Therapy vascularized fascial bed that easily accepts a skin
Demonstrated
graft. It is best used in large burns but sacrifices
Indication Benefit Level of Evidence some healthy tissue and leaves an unaesthetic
Diabetic foot Yes Level I156, 158
contour181 (Fig.  7). Tangential excision removes
ulcers only the damaged tissue. Tangential excision is
Pressure ulcers Unclear Data is lacking158, 171; typically performed with a Weck or Goulian blade
level IV benefit172 for small or irregularly contoured areas, and a
Venous stasis Short-term Level I158
wounds to 6 wk Watson blade for larger areas. (See Video, Sup-
Postirradiation Yes Level I156, 157 plemental Digital Content 2, which demonstrates
ischemia three different types of burn wounds. This video
Osteomyelitis Unclear Level III no effect173;
level IV benefit174 is available in the “Related Videos” section of the
full-text article on PRSJournal.com or, for Ovid
users, at http://links.lww.com/PRS/C230.)
Systemic antibiotics do not reduce the inci-
dence of burn wound infection or all-cause
mortality.182 Targeted prophylaxis with trime-
thoprim-sulfamethoxazole may play a role in
helping prevent pneumonia, based on results of
a small trial.183 Increasing antibiotic resistance is
of paramount concern when administering a sys-
temic prophylactic antibiotic.

Burn Wound Dressings

Silver sulfadiazine was considered a mainstay
treatment for many years; however, two recent
Cochrane reviews showed an increased rate of burn
wound infection, poorer healing outcomes, and
longer hospital stay when compared with biosyn-
thetic, silicone-coated, and silver dressings or skin
substitutes.182,184 Mafenide acetate is bactericidal
and has the added advantage of better penetration
of burn eschar98,185; it is particularly useful in treat-
ing burns over auricular or nasal cartilage. Burns
treated with hydrogels showed a trend toward
healing more quickly than with other dressings.184

Video 2. Supplemental Digital Content 2, which demonstrates

Fig. 7. (Above) Full-thickness burn with painless leathery eschar. three different types of burn wounds, is available in the “Related
(Center) Healthy well-vascularized wound base following wound Videos” section of the full-text article on PRSJournal.com or, for
débridement. (Below) After application of a full-thickness skin graft. Ovid users, at http://links.lww.com/PRS/C230.

211e
Copyright © 2017 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.

A review of studies of topical treatments for facial
burns showed that skin substitutes such as human
cadaver allograft healed faster and with less pain
compared with bacitracin or silver sulfadiazine.186,187
Conclusions
Application of the advances in basic science
to chronic wound care has led to advances in
the commonly used wound dressings. Although
anecdotal evidence abounds, well-designed, ade-
quately powered clinical trials free from industry
bias are scarce. As leaders of the wound care team,
plastic surgeons should equip themselves with the
knowledge to select an appropriate dressing with
sound reasoning. Further large-scale clinical trials
are needed to define this segment of the health
care supply industry.
Donald R. Mackay, M.D.
Division of Plastic Surgery
Penn State Hershey Medical Center
500 University Drive
Mail Code H071
Hershey, Pa. 17033
dmackay@hmc.psu.edu
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