Lower Extremity Soft Tissue & Cutaneous Plastic Surgery, 2e

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essential to get the calf muscle pump to assist in eliminating fluid
retention.
For patients with arterial ulcers, the reduction of risk factors respon­
sible for the development of arteriosclerosis is crucial. In addition to
age, sex, and race, the major controllable risk factors that should be
closely managed include hyperlipidemia, hypertension, diabetes mel­
litus, and smoking.
Diabetics should avoid going barefoot, indoors or out. They should
inspect their feet daily, and pay attention to the interdigital space,
using mirrors to facilitate examination. The feet should be washed
daily, after testing water temperature with the hand or elbow. Dryness
of the skin, and especially the feet, should not go untreated. Women
should avoid garters or elastics to hold up stockings and panty girdles
that are tight around the legs. The feet should not be exposed to
extremes such as very hot sand, water that is very hot, heating pads or
hot water bottles, and heaters (including car heaters for long trips).
Foot care should be carried out by a professional. Patients should
avoid cutting calluses or using physical or chemical agents to reduce
them. A podiatrist or other physician should inspect the foot twice a
year. Sudden onset of a blister, sore, or puncture should be evaluated
immediately by a physician.
For patients not requiring an orthotic or other shoe device to
manage deformities and post-surgical care, only comfortable, well-
fitting shoes should be used at all times. They should always be worn
with socks, and ideally shoes should be changed several times a day.
These shoes should have leather uppers that can mold to the shape
of the feet. To ensure optimal comfort, new shoes should be bought
late in the day. Shoes tried on early in the morning may feel too tight
as the day goes by. Sandals and open-toe shoes should be avoided. To
ensure integrity of the shoe, shoes should be inspected before wearing,
and patients should be encouraged to bring in new shoes for inspec­
tion before they begin to wear them. Socks should be 100% cotton
or blends of cotton. Wool can be worn, but not by those who get
ulcers. The physical findings of basal cell carcinomas arising from
venous ulcers include exuberant granulation tissue rolling onto the
wound edges.53
Prevention
Although general good health is helpful in preventing leg ulcers, many
common-sense issues should be considered. Good nutrition with a
high protein intake and vitamin supplementation has been helpful
in prevention as well as setting the stage for proper healing. Allman
et al.54 demonstrated that pressure ulcer patients whose protein intake
was >590 mmol/day were significantly more likely to improve or to
completely heal. Taylor et al.55 have shown that oral vitamin C at
1000 mg daily plays a role in the healing of pressure ulcers. Proper
hygiene and control of urinary incontinence can improve the setting
to prevent skin breakdown and avoid the onset of pressure ulcers. Use
of pressure-relieving devices can help lighten the weight-bearing effect
on points over a bony prominence, the site of pressure ulcers. Control
of infection is essential to avoid cutaneous damage that can extend
ulcers or prevent their healing.
The best prevention for patients with recurrent venous ulcers is the
wearing of a compression garment, which will prevent accumulation
of fluid within the lower extremities.56 Optimal compression is
achieved by garments providing 30–40 mmHg. This serves to slow
fluid accumulation, which plays such an important role in the patho­
genesis of venous ulcers and in the sense of fatigue so frequently
expressed by these patients. Measures to increase adherence to the use
of compression garments include careful measuring and fitting of the
compression stockings, and specific instructions with regard to stock­
ing application. Additionally, patients with comorbidities such as
obesity and arthritis, or aged patients may benefit from aids to assist
with stocking application.57 Proper fitting shoes that allow normal
heel to toe walking can assist in comfortable walking, which is so
Figure 31.8  A diagrammatic representation illustrating important elements in obtaining and interpreting the ankle–brachial index (ABI). DP, dorsalis
pedis; PT, posterior tibial.
Obtaining the index
Right arm systolic pressure
Right ankle
systolic pressure
Left ankle
systolic pressure
DP
PT
Left arm systolic pressure
Right ABI
Higher right ankle pressure
Higher arm pressure
Left ABI
Higher left ankle pressure
Higher arm pressure
Interpretation
>1.30
Noncompressible
0.01–1.30
Normal
0.41–0.90
Mild-to-moderate peripheral
arterial disease
0.00–0.40
Severe peripheral arterial
disease
DP
PT

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
recurrence.56 Specific instructions on the use of compression stockings
may help to increase patient compliance. Additionally, aids to assist
in the application of compression stocking have been developed.
These devices greatly assist elderly, arthritic, or obese patients who can
have difficulty in putting on stockings.
Pharmacologic therapy for venous ulcers
A number of medications have been studied for their role in increasing
healing rates of venous ulcers. Aspirin has been associated with
improved healing speed for venous ulcers. It is believed that aspirin’s
main mechanism of action here is through its anti-inflammatory
action and its action on hemostatic mechanisms.65 In one study, 20
subjects with chronic venous leg ulcers were randomized to daily
enteric-coated aspirin (300 mg) or placebo, with standardized com­
pression bandaging for both groups.66 After 4 months of treatment,
38% of the patients receiving aspirin demonstrated healing compared
with 0% of those receiving placebo (p<0.007). Additionally, 52% of
the aspirin-treated group showed a significant reduction in ulcer size
compared with 26% of placebo recipients (p<0.007); and reduction
in ulcer surface area was significantly better in the aspirin-treated
group at 2 (p<0.01) and 4 months (p<0.002) compared with that in
the placebo group. Although these findings are promising, a larger
sample size must be studied to make definitive conclusions.
Pentoxifylline, a methylxanthine derivative, has also been studied
as a pharmacologic adjunct in the treatment of venous ulcers. Its
mechanism of action may be due in part to its fibrinolytic properties,
its ability to reduce leukocyte adhesion to the endothelium, and its
antithrombotic effects.67,68 The Cochrane Collaboration performed
a systematic review on the use of pentoxifylline to treat venous leg
ulcers and concluded that pentoxifylline (800 mg three times a day)
irritation from it. Socks should be free of wear and tear or holes, and
should be changed daily.
It is a natural expectation that proper glucose control, proper nutri­
tional diet, and avoidance of smoking are three major essential meas­
ures all diabetics must observe.
TECHNIQUES
Compression therapy
Graduated compression therapy is the standard first-line therapy of
patients with venous leg ulcers. Patients who comply with compres­
sion therapy have improved healing rates, and continued compression
after healing prevents recurrence.58 Although most patients tolerate
compression without adverse effects, care must be taken in patients
with chronic heart failure because compression of the lower extremi­
ties can lead to an increase in preload volume and exacerbate their
condition.
The exact pressure needed to overcome venous hypertension is not
completely known, but an external pressure of 35–40 mmHg at the
ankle is required to prevent capillary exudation in legs affected by
venous disease.59 Two types of compression bandages are commonly
employed: inelastic and elastic bandages. The prototype rigid bandage
is the Unna Boot, a moist zinc oxide impregnated paste bandage that
hardens to inelasticity.60 These, rigid, inelastic bandages provide
limited pressure at rest, but high pressure with muscle contraction
during ambulation. The principal disadvantage of this compression
method is that the Unna Boot does not accommodate changes in the
volume of the leg subsequent to compression and associated edema
reduction; furthermore, it has limited absorptive capacity for highly
exudative wounds, leading to potential periwound maceration. Thus,
Unna Boots require frequent reapplication. Rigid bandages such as
the Unna Boot may be useful to reduce the initial edematous phase
commonly associated with venous ulcers.61
Alternatively, elastic compression bandages provide continual pres­
sures and conform to the leg, subsequent to changes in leg volume.
These elastic compression wraps supply high pressures both during
ambulation and at rest. Their major disadvantage is that they require
some degree of training for optimal application.62 Elastic compression
bandages are available as single or multilayer systems. A review of the
literature with meta-analysis demonstrated that multilayer compres­
sion bandages seem to be superior to single-layer bandage systems.59
A number of multilayer compression systems have been developed
and are presently the mainstay of treatment for venous leg ulcers
(Table 31.5).
The overall standard composition of multilayer compression band­
ages is as follows: a wool or cotton layer for absorption of exudate
and padding; one or two elastic wraps, and a self-adherent wrap to
hold all of the layers in place and to maintain the proper position of
the bandage on the leg.63 Multilayer compression systems can be tai­
lored to fit a wide range of ankle circumferences, providing consistent
pressures of 40–45 mmHg at the ankle and approximately 17 mmHg
below the knee. Although three- or four-layer elastic compression
bandages are initially more costly than single-layer bandages, they are
cost-effective because they promote faster healing rates.64 Compres­
sion therapy must be used judiciously in patients with concomitant
cardiac failure as well as in patients with arterial insufficiency because
both these conditions can potentially be exacerbated by lower extrem­
ity compression.
Treatment of venous ulcers with compression therapy should con­
tinue until the ulcers are healed. Subsequent to complete healing,
patients should use graded compression stockings to prevent ulcer
Table 31.5  Compression systems for leg ulcers
Compression
system
Brand name
Manufacturer
Unna Boots
(inelastic
bandages)
Gelocast
Beiersdorf (Wilton, CT)
Unna Flex
ConvaTec (Princeton, NJ)
Viscopaste PB7
Smith & Nephew (Largo,
FL)
Primer Flexible
Unna
Glenwood Inc (Tenafly, NJ)
Unna Boot
Bandage
Dynarex Corp (Brewster,
NY)
Tenderwrap
Kendall (Mansfield, MA)
Elastic bandages
SurePress
ConvaTec (Princeton, NJ)
SetoPress
Seton Healthcare Group plc
(Oldham, UK)
Multilayer
bandages
Profore
(four-layer)
Smith & Nephew (Largo,
FL)
Dynaflex
(three-layer)
Johnson & Johnson (New
Brunswick, NJ)
Tubular bandages
and compression
stockings
Jobst Stockings
Beiersdorf (Wilton, CT)
TubiGrip
ConvaTec (Princeton, NJ)

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strengthen the validity of wound culturing as a predictor for wound
infection.
Many factors predispose wounds to infection and influence the
manner in which colonized wounds respond, such as advancing
patient age, diabetes, compromised immune status, obesity, impaired
circulation, malnutrition, and remote infection.80–88 Acute wounds are
more predisposed to infection than chronic wounds. Additionally,
wounds that have not been debrided of necrotic tissue or eschar are
more susceptible to infection, thereby emphasizing the importance of
wound debridement and thorough wound cleansing.89
Antibiotics and antiseptics
The use of topical antibiotics in leg ulcers is controversial because
antibiotic-related increased healing rates remain unproven; the poten­
tial emergence of resistant organisms with their unnecessary use
is a concern.90,91 Additionally, topical antiseptics have demonstrated
cellular toxicities that surpass their bactericidal effects and have
been shown to impair wound epithelialization.92 Of note, however,
studies have shown cadexomer iodine preparations are safe and effec­
tive as topical applications with antimicrobial properties for wound
debridement, stimulation of granulation tissue, and overall wound
healing.93
Systemic antibiotics used to treat active leg ulcer infections can be
divided into five main groups: penicillins, cephalosporins, aminogly­
cosides, fluoroquinolones, and sulfonamides.79 Other antibiotics less
commonly used in this setting include clindamycin, metronidazole,
and trimethoprim.
Many important factors come into play when considering systemic
antibiotic therapy for a patient with a leg ulcer. First, the practitioner
must fully evaluate the patient to determine the presence of a wound
infection. Clinical signs of leg ulcer infection and the overall physical
status of the patient, as previously described, must be assessed. The
spectrum of coverage provided by the antibiotic should also be con­
sidered. Patient-specific factors must be assessed, such as known drug
allergies and metabolic impairments, as well as antibiotic-specific
parameters, such as the capacity for tissue penetration and the means
by which the drug is metabolized. Lastly, antibiotic resistance must be
taken into consideration when implementing antibiotic therapy.
Methicillin-resistant Staphylococcus aureus (MRSA), penicillin-resistant
Streptococcus pneumoniae, vancomycin-resistant Enterococcus, and
multidrug-resistant Gram-negative bacilli are the commonly encoun­
tered organisms of concern. Therefore, one must be attentive to signs
of antibiotic resistance, with particular consideration to the results of
laboratory tests, such as wound culture and sensitivity.
Dressings for leg ulcers – moist wound healing
Occlusion refers to the ability of a dressing to reduce the transmission
of vapor from the wound surface to the atmosphere.94 Dressings that
achieve this goal have commonly been described as ‘occlusive’ dress­
ings. Studies have demonstrated that a moist wound environment
induces acute wounds to re-epithelialize up to 40% faster than air
exposed wounds.95 The beneficial physiologic action extends to the
dermis, resulting in a modified inflammatory infiltrate compared with
the dermis of air-exposed wounds.96 The physiological benefit of
moist wound healing in chronic wounds is less well understood, but
it is believed that these dressings can provide pain relief, decreased
pain on wound debridement, and the development of a healthy
appearing granulation ulcer bed.97 Additionally, decreased frequency
of changes commonly employed with these dressings maximizes
effectiveness.98
Conventional wound dressings, such as gauze dressings, do not
preserve wound moisture unless they are covered with an
seems to be an effective adjuvant to compression therapy.69 The most
commonly reported side-effects include indigestion, nausea, and
diarrhea.
In terms of topical therapies for venous ulcers, a number of growth
factors have been studied and have demonstrated preliminary efficacy.
Keratinocyte growth factor-2 (KGF-2), a member of the fibroblast
growth factor family in the skin, stimulates normal keratinocyte pro­
liferation. In animal models its topical application has demonstrated
increased re-epithelialization and enhanced granulation tissue forma­
tion on chronic wounds.70 Phase IIb trials are presently being con­
ducted to determine the efficacy and safety of KGF-2 in promoting
wound healing in humans, and preliminary results from recently
completed phase IIa trials are encouraging.71 Many studies have shown
that topical and perilesional injection of granulocyte macrophage-
colony stimulating factor (GM-CSF) promotes healing of leg ulcers
and is safe.72,73 Lastly, a randomized trial has reported efficacy with
calcitonin gene-related peptide in combination with vasoactive intes­
tinal peptide for the treatment of venous ulcers.74
Topically applied high-potency corticosteroids are commonly
employed for the treatment of associated venous dermatitis, which is
characterized by eczematous changes with redness, scaling, and pru­
ritus. However, one must proceed with caution when treating these
symptoms because this eczematous dermatitis is often caused or
aggravated by sensitization to the application of topical medications.
Furthermore, the prolonged use of high-potency topical steroids
should be avoided.41
Antimicrobials and the bacterial
balance of leg ulcers
Background
The role of microorganisms in leg ulcers and the effects of these
microorganisms on the healing process are not completely under­
stood. In an acute wound, which follows the normal phases of healing,
the risk of infection is greatest during the first 48–72 h after injury.
Hence, microorganisms detected during this time-frame should be
considered clinically significant until proven otherwise. Alternatively,
chronic leg wounds are commonly at lower risk for infection, except
for those in patients with diabetes or compromised immunity. The
detection of microorganisms from these wounds typically represents
colonization rather than infection.
Diagnosis
The distinction between a wound resulting from injury and one result­
ing from invasive infection is often not completely clear because
both physiologic processes can acutely manifest as inflammation.
Additionally, colonizing microorganisms may be identified in wounds
resulting from injury. However, simple isolation of colonizing micro­
organisms from leg ulcers is not always associated with reduced
healing rates.75 In an infected wound the microorganisms invade
the healthy tissue and a polymorphonuclear leukocyte response
can be demonstrated histologically.76 Although tissue levels of >105
organisms/g of tissue have been correlated with clinical infection in
acute wounds, the specificity and predictive value of this quantifica­
tion are poor.77,78
Both microbiologic studies, such as a swab culture or tissue biopsy
for culture, as well as the patient’s clinical signs of infection, including
edema, erythema, pain, purulent exudate, lymphadenitis, or systemic
signs (fever or leukocytosis), must be present to make the diagnosis
of active infection. Identifying microorganisms in the culture samples
from leg ulcers is not sufficient evidence to demonstrate an active
infection that may retard healing.79 Further research is necessary to

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
tissue may have deleterious effects on wound healing by stimulating
chronic inflammation, delaying both granulation tissue formation
and epithelialization.100 Wound debridement can be accomplished
through several methods including surgical, mechanical, autolytic,
enzymatic, and biosurgical.
impermeable secondary dressing. Primary dressings are those that are
in direct contact with the wound bed. Secondary dressings cover the
primary dressing and help to maintain it in place. Table 31.6 describes
some of the wound dressings used for leg ulcers.
SURGICAL TECHNIQUES
Wound bed preparation and debridement
The approach to the treatment of chronic wounds has historically
been relatively simple, consisting primarily of measures for infection
control and the use of gauze dressings for coverage and protection.
Wound care has evolved significantly in the past few years, chiefly
because of the advent of a number of new technologies for the treat­
ment of chronic wounds. Innovations, such as topically applied
growth factors and bioengineered skin products, have brought the
concept of advanced wound bed preparation to the forefront. The
ability to achieve maximal results from today’s advanced wound care
products is, however, contingent upon an appropriately prepared
wound bed, which is characterized by optimally vascularized granula­
tion tissue with minimal to no wound exudate.99 Additionally, critical
to the successful healing of chronic wounds is the treatment of factors
that may impede the wound repair process, such as necrotic and
desiccated tissues, impaired vascularization preventing oxygenation,
decreased cytokine levels, and the presence of senescent or non-
migratory cells. One active therapeutic intervention for treating all
these factors is wound debridement (Fig. 31.9).
Debridement is commonly defined as the process of removing
necrotic, devitalized tissue and foreign matter from a wound. Necrotic
Table 31.6  Wound dressings used for leg ulcers
Type (examples)
Advantages
Disadvantages
Indications
Hydrogels
  IntraSite Gel (Smith & Nephew, Largo, FL)
Semi-transparent, soothing,
do not adhere to wounds,
absorbent
Require secondary
dressing and frequent
dressing changes,
expensive
Painful, laser, and partial-
thickness wounds; after
dermabrasion or chemical
peel
  Nu-Gel (Johnson & Johnson, New Brunswick, NJ)
  Vigilon (Bard Medical, Covington, GA)
Alginates
  AlgiDerm (Bard Medical, Covington, GA)
Absorbent, hemostatic, do
not adhere to wounds,
fewer dressing changes
Require secondary
dressing, gel has foul
smell
Highly exudative wounds,
partial- or full-thickness
wounds; after surgery
  Kaltostat (ConvaTec, Princeton, NJ)
  Sorbsan (Bertek Pharmaceuticals, Morgantown, WV)
Hydrocolloids
  Comfeel (Coloplast, Marietta, GA)
Fibrinolytic, enhance
angiogenesis, absorbent,
create bacterial and
physical barrier
Opaque, gel has foul
smell, expensive
Partial- or full-thickness
wounds, stages 1–4
pressure ulcers
  DuoDerm (ConvaTec, Princeton, NJ)
  Restore (Hollister, Libertyville, IL)
Foams
  Allevyn (Smith & Nephew, Largo, FL)
Absorbent, conform to
body contours
Opaque, require
secondary dressing,
may adhere to
wounds, expensive
Partial-thickness exudative
wounds, for pressure relief
  Curafoam (Kendall, Mansfield, MA)
  Lyofoam (Seton Healthcare Group, Oldham UK)
Films
  OpSite (Smith & Nephew, Largo, FL)
Transparent, create bacterial
barrier, adhesive without
secondary dressing
May adhere to
wounds, can cause
fluid collection
Donor sites, superficial
burns, partial-thickness
wounds with minimal
exudate
  Polyskin II (Kendall, Mansfield, MA)
  Tegaderm (3M, St Paul, MN)
Figure 31.9  A venous leg ulcer with a yellow fibrinous base before
surgical debridement.

Chapter
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Wound bed debridement helps to remove senescent fibroblasts,
thereby allowing for the growth of younger and more viable cells,
which will potentially stimulate healing.
Effects of stimulation of growth factors
Studies have demonstrated that chronic wounds may be deficient in,
or have reduced accessibility to, critical growth factors, such as: fibrob­
last growth factor (FGF); platelet-derived growth factor (PDGF); epi­
dermal growth factor (EGF), and TGF-β.112 Although growth factors
may be present, their availability and efficacy may be hindered as a
result of abnormal binding to matrix proteins, such as the metallo­
proteinases.113 Growth factors present in normal amounts may be
ineffective if they are not exposed to properly functioning cells with
the proper receptors. Thus, in chronic wounds, dead or necrotic tissue
can act as a physical barrier to communication between growth factors
and their receptors.113 Debridement may help to speed the wound
healing process by exposing the viable receptors for proper growth
factor–receptor interaction. Debridement often results in bleeding of
the wound bed tissue, thereby stimulating the chemoattractant and
mitogenic effects of blood-borne growth factors, the most important
of which are the platelet associated growth factors, including PDGF,
TGF-β, and fibronectin.114 Debridement often precedes the topical
application of growth factors in clinical practice. Although not com­
pletely proven, debridement in this setting may help to optimize the
wound bed for growth factor activity. In fact, a clinical trial demon­
strated that patients heal a greater percentage of the time when recom­
binant human PDGF (rhPDGF) is applied subsequent to surgical
debridement in diabetic foot ulcers compared with the application of
rhPDGF alone.107
REMOVAL OF NON-MIGRATORY TISSUE
Chronic wounds often develop a non-migratory, hyperproliferative
edge. This edge, although thickened and hyperproliferative, does not
confer any healing properties to the wound because epithelial prolif­
eration and migration are two distinct biologic phenomena.115 In fact,
a hyperproliferative epithelium can often hinder the healing process.
Types of debridement
Several methods for wound debridement have been described. Numer­
ous factors are important when choosing which approach is best for
a particular wound. Although some forms of debridement, such as the
surgical approach, may act to quickly remove all unwanted necrotic
debris in a non-specific fashion, a more conservative and selective
approach may often be desired, such as autolytic or enzymatic
debridement.
Surgical/sharp debridement
Surgical debridement is the removal of necrotic or devitalized tissue
from the wound bed using a sharp instrument. Most commonly, a
scalpel, scissors, curette, or forceps is used (Fig. 31.10). Additionally,
sharp debridement with lasers has been described in chronic burn
wounds.116 Large wounds, with a great amount of necrotic debris are
particularly good candidates for surgical debridement. Additionally,
in cases of fulminant infection, such as sepsis or cellulitis secondary
to infected necrotic tissue, surgical debridement is the treatment of
choice. Although surgical debridement is rapid, it is also non-selective.
Viable tissue lying adjacent to the necrotic tissue may often be excised
as well.117 Controlling patient pain during the procedure is important,
Removal of bacteria
Necrotic tissue within a chronic wound bed supports the growth of
bacterial microorganisms. Although the presence of microbial organ­
isms in a chronic wound is unavoidable and is not necessarily detri­
mental to the healing process, studies have suggested that significant
numbers of bacteria within a wound may impede healing.101 It is well
known that most chronic wounds that heal do so in a polymicrobial
environment. However, when bacteria are present in increased
numbers or have assumed phenotypes of increased pathogenicity,
wound healing may be delayed. The exact number of bacteria required
for delayed wound healing is an issue of great controversy, and con­
ventionally, >105 colonies/g of tissue has been associated with reduced
healing rates when compared with wounds with fewer bacteria.102
However, it is unknown whether the bacterial number within wounds
is a cause or consequence of impaired healing.
Chronic wounds heavily colonized by bacteria have friable and
hemorrhagic granulation tissue with associated decreased tensile
strength.101 In addition to the sheer number of bacteria, the type of
bacteria present may also play an important role in delaying healing.
Particular bacterial species such as beta-hemolytic streptococci, or
certain combinations of species, can be detrimental to the wound
healing process, regardless of number.103 Additionally, recent studies
have described the potential role of bacterial biofilms in delaying the
wound healing process. Biofilms are aggregates of bacteria and other
organisms that are embedded within an exopolysaccharide matrix.104
Microorganisms within these structures undergo phenotypic changes
allowing for increased adherence to the wound bed, increased resist­
ance to antimicrobial agents, and resistance to the host’s immune
system defense mechanisms.105 Debridement is performed with the
detachment and removal of biofilms from the wound bed.
Many distinct mechanisms have been recognized for the delay of
the wound healing process by bacteria. The presence of bacteria within
chronic wounds for extended periods of time can lead to a prolonged
inflammatory response. Consequently, the release of free oxygen radi­
cals and various lytic enzymes can result in tissue damage.106 Tissue
hypoxia may also occur during the inflammatory response, which may
further support bacterial growth. The bacteria may also act directly to
impair the healing process by releasing proteases that inactivate
growth factors and other cytokines important to the healing process.107
Lastly, the presence of excessive exudate secondary to increased bacte­
rial burden may impair healing by the degradation of growth factors
and matrix proteins, which results in a reduction of cell prolifera­
tion.108 In summary, wound bed debridement can have major effects
in the treatment of chronic wounds by effectively decreasing bacterial
burden and thereby reducing a number of critical elements that
impede the healing process.
Removal of senescent cells
Chronic wounds are populated by senescent (or aged) cells that have
significantly decreased proliferation and protein production. Studies
have demonstrated that wounds present for a prolonged period of
time are characterized by fibroblasts that are less responsive to growth
factor stimulation compared with acute or healing wounds. In an
in-vitro study conducted on the fibroblasts from the edge of non-
healing venous ulcers, the authors concluded that this population of
cells is unresponsive to the action of TGF-β, and that this blunted
response may cause faulty deposition of the extracellular matrix
needed for re-epithelialization and wound healing.22 Additionally,
senescent fibroblasts have been identified in many different chronic
wound models.109,110 These findings correlate well with studies that
have demonstrated that wounds present for an extended period of
time are more difficult to heal with standard of care interventions.111

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
covering the wound with a saline-moistened dressing and allowing it
to completely dry. The dressing is subsequently removed, thereby
removing the adherent necrotic tissue. This method of debridement
is nonselective and can produce considerable patient discomfort
because it also lifts away viable tissue within the wound. Wet-to-dry
debridement may be the most commonly used technique, but this
method of debridement is outdated and should only be used as a last
resort. Both high-pressure irrigation and whirlpool baths effectively
debride wounds using water; however, over-zealous debridement with
these methods can lead to periwound maceration. Additionally, there
are theoretical concerns that water-borne pathogens could contami­
nate the wound bed.
Autolytic debridement
Autolytic debridement takes advantage of the body’s own enzymes to
break down necrotic tissue within the wound. Occlusive and semioc­
clusive dressings may be used to promote a moist environment to
accelerate the autolytic process and allow enhanced contact between
the necrotic debris and lysosomal enzymes in the wound.120 Several
moist interactive dressings are available for autolytic debridement
including hydrocolloids, hydrogels, alginates, and transparent films.
Autolytic debridement has many advantages because it is selective,
thereby only removing the necrotic debris, and it causes little or no
pain. However, this method of debridement may be slow.
Biosurgical debridement
Biosurgical debridement involves the application of maggots to the
wound bed to disinfect and remove necrotic tissue. Wounds best
suited for biosurgical debridement include chronic wounds with a
great amount of necrotic tissue that have been refractory to other
forms of chemical debridement, particularly insensate wounds such
as diabetic foot and pressure ulcers.121 Maggot therapy has also been
used before surgical closure or as an alternative to surgical debride­
ment in patients who cannot or choose not to undergo surgery. Sterile
maggots are applied directly to the wound and covered with a dressing
for approximately 1–3 days. The maggots act to liquefy and ingest the
necrotic tissue.122 Additionally, maggots have the ability to consume
bacteria, including antibiotic-resistant strains, which may decrease the
patient’s risk of developing an infection.123 Maggots secrete a sub­
stance described as a ‘healing secretion’.124 These larval secretions
promote the growth of human fibroblasts in vitro, and may augment
the effects of debridement for stimulating granulation tissue.125 Any
discomfort experienced by patients from maggot therapy can be
treated with analgesics. Furthermore, patients must be comfortable
with the notion of applying a living organism to the wound bed.
(Presently, maggots can be purchased through a variety of European
manufacturers, and in the USA from the laboratory of Ronald A.
Sherman of the Maggot Therapy Project at:
com/pathology/sherman/home_pg.htm). Biosurgery with maggot
therapy appears to be an effective non-surgical option for debriding
chronic wounds.
Enzymatic and chemical debridement
The enzymatic debridement approach works faster than autolytic deb­
ridement, and is more conservative and specific than surgical methods.
Several different enzymatic preparations, each with their own unique
set of chemical properties, are readily available. The two most com­
monly used today are the topical preparations of collagenase (such
as Collagenase Santyl Ointment; Smith & Nephew, Largo, FL), and
papain–urea (such as Accuzyme; Healthpoint, Fort Worth, TX). The
collagenase preparation is composed of a partially purified form
of collagenase derived from bacteria. It has the ability to degrade
and is most commonly managed with topical anesthesia such as
lidocaine 2% jelly applied to the wound bed. Postprocedure pain is
most commonly managed with analgesics. Only excellent atraumatic
surgical technique should be used to avoid damaging the healthy
tissue within the wound, so surgical debridement should only be
performed by a trained individual.118 Surgical debridement may be
performed either at the bedside or in the operating room, depending
on the scale of debridement required. For extensive cases, the use of
an operating room may be prudent to limit the risk of secondary
infection.
Mechanical debridement
Mechanical debridement can be performed by various methods,
including the application of wet-to-dry dressings, whirlpool baths
(Fig. 31.11), and high-pressure irrigation.119 Wet-to-dry debridement
is widely used by many wound care practitioners. It is performed by
Figure 31.10  Surgical debridement for the removal of periwound
non-migratory tissue using a pair of scissors and forceps.
Figure 31.11  Whirlpool bath for the mechanical debridement of
leg ulcers.

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epidermis and all of the dermis as well as variable amounts of subcu­
taneous tissue. Thin grafts, such as split-thickness skin grafts require
little revascularization during the healing process and therefore have
a greater chance of graft survival than full-thickness grafts. Alterna­
tively, full-thickness grafts are likely to retain the color and texture of
the donor skin. Thus, split-thickness skin grafts are more applicable
when the desired therapeutic goal is the restoration of function,
whereas full-thickness grafts may be more suitable when cosmetic
outcome is a central concern.
Split-thickness skin grafts can be divided into three different
categories depending on their thickness: thin (0.005–0.012 inch);
medium thickness (0.013–0.018 inch), or thick (0.019–0.028 inch).
Medium split-thickness grafts provide both optimal graft survival and
durability.
Preoperative preparation
Skin grafting of lower extremity ulcers can be performed as either an
outpatient or ideally as an inpatient procedure – success rates vary
between both approaches among centers.130 By admitting the patient
to the hospital for the procedure the potential for graft take can be
optimized by controlling for extraneous factors such as patient ambu­
lation and infection surveillance. Patients are treated preoperatively
with strict bed rest, leg elevation, debridement of the wound bed, and
antibiotics. With these measures in place, the ulcer bed is commonly
ready for grafting by the third treatment day. The combination of
antibiotic treatment79 and leg elevation is important for reducing the
bacterial load within the wound bed, thereby optimizing the chance
for graft survival.
Patient comfort throughout the procedure can be optimized with
the proper premedication regimen. An intramuscular injection of
meperidine hydrochloride and hydroxyzine hydrochloride in combi­
nation with an oral dose of diazepam 1 h before the procedure allows
for the comfortable administration of the local anesthetic, while also
taking advantage of the amnestic effect of the diazepam.
The thigh is usually used as the donor site and is carefully prepared
before the procedure. First, it is precisely measured and marked. Both
the donor area and the ulcer to be grafted are then thoroughly cleansed
with povidone–iodine (Betadine) and rinsed with normal saline. The
donor site is subsequently anesthetized with the injection of a local
anesthetic. If necessary, surgical debridement of the recipient ulcer bed
can then be performed. A curette can be used to obtain a bleeding
ulcer base, which is then covered with saline-soaked gauze. The ulcer
bed is now ready for grafting.
Techniques
One method is performed freehand and is commonly referred to as
‘pinch grafting’ (Fig. 31.13). This method, in which small pieces of
skin were pinched between the thumb and forefinger and subse­
quently shaved from the donor site, was first described in 1869.129 This
method has since been modified with the use of various instruments
including forceps,131 skin hooks,132 and the tip of a needle133 or
suction134 to grasp the skin with increased precision. The skin is then
shaved with either a scalpel or a double-edged razor blade.135 This
method can also be altered with the use of a punch biopsy instrument
for harvesting the tissue. The method, described by Kirsner and
Falanga,136 uses a 4 mm punch biopsy blade to create a uniform size
graft. A thin horizontal slice of tissue is then shaved for transplanta­
tion onto the ulcer bed. Much of the ulcer area is covered with mul­
tiple grafts; with several millimeters of space maintained between each
graft to allow exudate to drain from the wound. Pinch grafting has
many advantages – it is a simple to perform office procedure requiring
collagen as well as other substrates within the wound bed, with an
optimal activity in a pH range of 6–8.126 Additionally, in-vitro studies
have demonstrated its efficacy in degrading elastin, heat denatured
porcine skin, and fibrin.127 The papain-based product is composed of
papain, a proteolytic enzyme purified from the papaya fruit, mixed
with the chemical agent urea, which acts as an humectant and renders
the non-viable proteins within the necrotic tissue more susceptible to
the proteolytic action of papain.
Studies have demonstrated the efficacy of the papain–urea combi­
nation in heat-denatured degrading porcine skin, with considerable
effectiveness against fibrin, which is a common component of necrotic
eschar. Both collagenase and papain–urea are considerably more
effective against denatured proteins as opposed to proteins in their
native state, thereby limiting their adverse effects on the healthy sur­
rounding tissue.
Clinical studies have also been performed to study the relative
efficacy of these two products. In a prospective, randomized, parallel
group, tricenter, and open-label clinical trial with an evaluation period
of 4 weeks’ duration, 28 patients were randomly assigned to ulcer
treatment with either collagenase ointment (n = 12) or papain–urea
ointment (n = 14). The papain–urea debriding ointment was signifi­
cantly more effective (p<0.0167) than the collagenase ointment in
reducing the amount of necrotic tissue. Additionally, the development
of granulation tissue in wounds treated with papain–urea was signifi­
cantly enhanced compared with wounds treated with collagenase.
Although epithelialization generally correlated with the development
of a granulating wound bed, as determined by visual assessment, the
general increase in the amount of epithelial tissue associated with the
papain–urea-treated wounds did not predict a significantly different
rate of reduction in the actual wound area between groups. These
findings seem to suggest that the papain–urea-based combination is
more effective, but a larger study is required to make any significant
conclusions. Of note, neither debriding ointment was associated with
any adverse events. Additionally, in the authors’ experience, it appears
that both papain–urea and collagenase may be slightly more effective
when the substrate is solid eschar as opposed to unbound fibrin
slough (Fig. 31.12).128
SKIN GRAFTING
Skin grafting has three major applications in wound care:
1. To hasten the wound healing process
2. To improve cosmetic appearance
3. To improve the function of healed wounds.
Skin grafting for the treatment of wounds has been employed for
centuries,129 and although there are no particular indications specify­
ing when skin grafting should be employed, large or nonhealing
wounds are cases in which grafting can be considered. In normal
individuals, without any underlying pathophysiologic defect, large
lower extremity ulcers may require a prolonged period of time to
heal. Consequently, it may be impractical to wait for healing by
second intention in these wounds and skin grafting may help to
accelerate the healing process. Additionally, skin grafting can play
an important role in the treatment of all types of hard-to-heal ulcers,
such as ulcers secondary to venous insufficiency, diabetes mellitus,
and vasculitides.
Split- and full-thickness skin grafts
A split-thickness skin graft, also known as a partial-thickness skin
graft, is a portion of skin that contains both epidermis and varying
portions of the dermis. A full-thickness skin graft is composed of the

462
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
Meshing is the process of expanding the graft by passing the
skin through an electric or manual mesher that creates precisely
placed cuts through the graft allowing the solid sheet of tissue to be
converted to a net, which covers a far larger area. The combination
of using an adjustable dermatome and meshing the skin provides
for reliable control of graft thickness, the ability to cover large
ulcer areas with speed and efficiency, and the capacity to allow
blood and exudate to drain from the wound bed without com­
promising graft survival (Fig. 31.14). Pinch grafts are usually immo­
bilized by the dressing whereas large split grafts are usually stapled
in place.
no specialized instruments or complex training. Conversely, pinch
grafting is also associated with many drawbacks such as inconsistent
graft sizes, relatively poor cosmetic outcome of the donor site, and the
need for a lengthy procedure for grafting large ulcers.
Another method for harvesting tissue for split-thickness skin grafts
employs the use of a specialized cutting instrument – a dermatome.
This instrument is available in both an electrical form or as a manually
operated freehand unit. The main advantage of the dermatome is
that it can be set at predetermined depths, thereby allowing for
consistent thickness between grafts. One additional step that may
be implemented in harvesting skin grafts is ‘meshing’ of the tissue.
Figure 31.12  Clinical effectiveness of chemical debridement with papain–urea based preparations in three different ulcers. (A,B) At day 0 and week 1.
(C,D) At week 1 and week 2. (E,F) At day 0 and week 1.
A
B
C
D
E
F

Chapter
Leg ulcer management
463
| 31 |
maintain a moist environment, while concomitantly absorbing excess
exudate and helping to maintain the proper position of the graft. In
venous ulcers, inelastic compression can also be added. The donor
site can be treated with the same type of dressing as the graft site;
alternatively, a polyurethane occlusive dressing can be applied. Bed
rest and leg elevation should be implemented for the first 3 days
following grafting. Infection control is accomplished with the main­
tenance of postoperative systemic antibiotics. Additionally, pain
medications are given as needed. The initial dressing change is per­
formed after 2–3 days postoperatively, and daily thereafter. Once the
staples are removed on the fifth postoperative day, the patient may
begin to ambulate, with continued leg elevation. Ideally, the patient’s
postoperative care should also be managed as an inpatient, but all
these procedures can be easily performed in the outpatient setting
as well.
Pitfalls and their management
The most common cause of graft failure is infection of the ulcer
bed. Pre- and perioperative antibiotics and leg elevation are two
key preventative measures. Excessive exudate can also lead to graft
failure as a result of separation of the graft from the wound bed.
This problem can be controlled by a meticulous approach to post­
operative dressing changes, as described above. The postoperative
use of occlusive dressings on the graft site has been associated
with graft failure because of excessive accumulation of exudate.136
Alternatively, the use of occlusive dressings at the donor site
appears to limit the likelihood of infection. Using very thin split
thickness skin grafts can also play an important role in optimizing
graft take.
Bullae, of unknown etiology, have been noted to occur at the
recipient sites of split-thickness skin grafts.137 Although the etiology
of these bullae is unknown, findings suggest a disease process
confined to the skin graft recipient site with ultrastructural and anti­
genic features, identical to those described with recessive dystrophic
or immunofluorescence-negative acquired epidermolysis bullosa
(Box 31.1).138
A
B
Figure 31.13  (A) The harvesting of pinch grafts from the thigh of a
patient using the scalpel technique for the treatment of a chronic ulcer
secondary to arterial insufficiency. (B) The appearance of the ulcer bed
after pinch grafting. (C) Re-epithelialization of the ulcer approximately
2 months after pinch grafting.
(With permission from J Dermatol Surg Oncol 1992; 18(4): 272–283. Blackwell
Publishing Ltd.)
C
Figure 31.14  The appearance of a meshed split-thickness skin graft on
a chronic ulcer. The fenestrations created by the mesher allow fluid to
escape from the underlying ulcer bed.
(With permission from J Dermatol Surg Oncol 1992; 18(4): 272–283. Blackwell
Publishing Ltd.)
Optimizing outcomes
Presently, no formal method for postoperative care of the grafted
site has been established. The wound bed can be covered with
petroleum-impregnated gauze, super sponges, and gauze bandages, to

464
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
understood, but Graftskin is thought to stimulate healing from the
wound margins or appendage structures. In a study using polymerase
chain reaction analysis to determine the longevity of the allogeneic
fibroblasts and keratinocytes of Graftskin in venous leg ulcers, inves­
tigators found that allogeneic DNA was present in two of eight speci­
mens at 1 month after initial grafting, whereas neither of the two
patients showed persistence of the allogeneic DNA at 2 months after
initial grafting.143 Additionally, an acute neonatal epidermolysis
bullosa wound failed to show evidence of viable allogeneic DNA
beyond a period of 4 months.144 These results suggest that allogeneic
cells from Graftskin do not survive permanently after grafting and
other mechanisms of action are most likely responsible for the efficacy
of Graftskin, including cytokine release, and matrix-induced cell
migration and activation.
In a prospective, controlled, randomized, multicenter study, signifi­
cantly more patients achieved complete wound closure of venous
ulcers when treated with Graftskin plus compression therapy com­
pared with compression therapy alone (ulcer healing rate of 63% vs
49%). Additionally, patients treated with Graftskin healed more
rapidly (61 days vs 185 days).145 These positive findings were again
demonstrated in another prospective randomized study by Sabolinski
and colleagues,146 which also evaluated the efficacy of Graftskin in
healing venous ulcers. In this study, the tissue-engineered product was
Bioengineered skin equivalents
Since the 1980s, the discipline commonly referred to as tissue engi­
neering or the use of tissue-engineered skin for wound healing has
greatly advanced. The concept of cultivating tissues to replace or to
stimulate the regeneration of human skin was once merely theoretical,
and the only methods for skin regeneration in chronic and acute
wounds of diverse etiologies were split- or full-thickness skin grafts as
described above, or other surgical interventions such as free tissue
transfers, or tissue flaps. Presently, there is a wide range of tissue engi­
neered products approved for use by the US Food and Drug Admin­
istration (FDA) and several others currently undergoing testing
through well-developed clinical trials.
The advantages to using tissue-engineered products, as opposed to
autologous skin grafting are numerous and include the ability to
provide tissue therapy without using a donor site and the potential
for faster healing with improved cosmetic results.139 The concept of
tissue engineering was first defined in 1987 by the National Science
Foundation bioengineering panel as ‘the application of the principles
and methods of engineering and the life sciences toward the develop­
ment of biological substitutes to restore, maintain, or improve func­
tion’. Although the exact mechanism by which tissue engineered skin
products aid in healing acute and chronic wounds is not completely
understood, they appear to function by providing the needed matrix
materials, cells or cell products, such as growth factors, to stimulate
the healing process.140 Additional clinical studies focusing on genetic
modifications of transplanted cells and novel systemic gene product
delivery mechanisms are broadening the field of tissue engineering.141
A complete review of the bioengineered skin equivalents is beyond
the scope of this chapter. A brief description of the role of the living
allogeneic bilayered skin equivalent known as Graftskin (Apligraf,
Organogenesis Inc, Canton, MA) in wound healing is given below,
and Table 31.7 provides an overview of the numerous products
created from cells, extracellular matrix materials, or a combination
thereof.
Graftskin as a bioengineered
skin equivalent
Graftskin is a living human skin equivalent derived by combining a
gel type I bovine collagen with living neonatal allogeneic fibroblasts,
along with an overlying cornified epidermal layer of neonatal alloge­
neic keratinocytes. Graftskin closely resembles human skin histologi­
cally and is currently the most sophisticated commercially available
tissue engineered product. In vivo, Graftskin makes matrix proteins
and growth factors; if wounded, Graftskin has the capacity to heal
itself.142 The exact mechanism for Graftskin’s efficacy is not completely
Table 31.7  Bioengineered skin equivalents
Graft type
Type of tissue
engineering
Uses
Epidermal grafts
Cultured
epidermal
autografts
(Epicel, Genzyme
Tissue Repair,
Cambridge, MA)
Living autologous
keratinocyte sheets
Burns, leg ulcers,
vitiligo, congenital
nevi, epidermolysis
bullosa, chronic
otorrhea,
hypospadias, corneal
replacement
Cultured
epidermal
allografts
Living allogeneic
keratinocyte sheets
Leg ulcers,
epidermolysis bullosa,
burns, dermabrasion,
wounds
Dermal
replacements
Alloderm (Life
Cell Co,
Woodlands, TX)
Nonliving allogeneic
acellular extracellular
matrix bullosa
Surgical wounds,
epidermolysis
Integra (Integra
Life Science
Corporation,
Plainsboro, NJ)
Nonliving extracellular
matrix of chondroitin-6-
sulfate and silicone
backing
Burns
Dermagraft
(Smith and
Nephew, Largo,
FL)
Living allogeneic dermal
fibroblasts grown on a
degradable scaffold
Diabetic foot ulcers
Composite grafts
Apligraf
(Organogenesis,
Canton, MA)
Living allogeneic
bilayered construct
containing keratinocytes,
fibroblasts, and bovine
type I collagen
Venous ulcers,
epidermolysis bullosa,
donor sites,
excisional wounds,
diabetic foot ulcers
Box 31.1  Pitfalls and their management
• Chronic wounds can develop malignancies, which will not be
diagnosed if not suspected and biopsied
• It is vital to differentiate between venous, arterial, diabetic,
pressure, and immune-modulated inflammatory ulcers to avoid
incorrect and ineffective treatments
• Surgical debridement must be performed by a skilled well-trained
operator, otherwise it can result in unnecessary destruction of
healthy tissue
• Thorough pre- and postoperative planning are important to avoid
skin graft failure.

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Subfascial endoscopic perforator
surgery (SEPS)
Developments in the surgical management of patients with chronic
venous insufficiency (CVI) and venous leg ulcers have recently
emerged. Linton and Dodd first described the surgical approach for
the ligation of incompetent lower extremity veins in the mid-1940s.149
This technique, known as the Linton procedure, employed an incision
spanning the entire length of the leg to ligate incompetent lower
extremity perforator veins. The main disadvantage of this technique
was a high incidence of postoperative wound healing complications,
which often resulted in prolonged hospital stays and increased costs
for caring for patients with CVI.150 Although abundant evidence was
compiled in support of the role of incompetent perforator veins in
symptomatic CVI, and many modifications of the open technique
were performed, postsurgical patient morbidity limited the acceptance
of perforator ligation.151
More recently, the techniques for perforator vein ligation have been
expanded. The development of an endoscopic approach to subfascial
surgery was first described in Germany during the 1980s.152 In the
1990s, these endoscopic techniques were applied to the treatment of
CVI. The technique, known as subfascial endoscopic perforator surgery
(SEPS), is considerably less invasive than the open Linton technique
and decreases the risk of wound healing complications. The goal of
the SEPS procedure is to bypass the faulty one-way valves in the per­
forator veins of the lower extremities in patients with CVI. Access to
the lower calf is obtained by placing small incisions in the upper calf,
thereby avoiding trauma to lower calf tissue, which may be compro­
mised by lipodermatosclerotic tissue. This tissue in particular demon­
strated the greatest postoperative wound healing complications when
the Linton procedure was performed.
A clinical classification system for reporting venous disease was
developed by a subcommittee of the Society for Vascular Surgery and
the International Society for Cardiovascular Surgery in the late
1990s.153 It describes venous ulcers based on their Clinical picture,
Etiology, Anatomic distribution, and Pathophysiology and is known
as the CEAP classification system. This classification system is based
on objective clinical signs of CVI (Table 31.8). Patients who fulfill the
criteria described in classes 4–6 are considered candidates for SEPS.
The goal of the procedure is to heal existing ulcers or reverse skin
changes consistent with lipodermatosclerosis, decrease hemosiderin
staining, and to prevent recurrence of venous ulcers secondary to
perforator vein incompetence.
three times more effective than compression therapy alone in achiev­
ing complete wound closure at 8 weeks.140
Graftskin has also been studied as treatment for acute wounds. A
prospective, multicenter, open study of 107 patients with acute,
partial-, or full-thickness excisional wounds mostly resulting from
excision of skin cancer, suggested that Graftskin is safe, useful, and
well tolerated.147 The study found no evidence of clinical or laboratory
rejection. Graftskin has also been used successfully in the treatment
of the acute and chronic wounds of epidermolysis bullosa.144,148 Graft­
skin has garnered approval by the FDA for the treatment of venous
(Fig. 31.15) and diabetic ulcers, and is commercially available. It is
shipped in a ready-to-use format and has a shelf-life of 5 days. Graft­
skin has many advantages in that it is easy to use and can be applied
in the outpatient setting. Its major disadvantages include its relative
cost and short shelf-life (5 days).
Figure 31.15  Venous leg ulcer (A) before and (B) after treatment with
Apligraf bioengineered skin equivalent.
A
B
Table 31.8  Objective clinical signs of the CEAP
classification system
Clinical stages
Clinical picture
Class 0
No visible signs of venous disease
Class 1
Presence of telangiectasias
Class 2
Visible varicose veins
Class 3
Presence of edema
Class 4
Skin changes, including thickening
and increased pigmentation
Class 5
Includes skin changes as in class
4 as well as healed ulcers
Class 6
Active ulceration

466
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
superficial to the fascia in a horizontal approach. As layers of skin are
removed, the pattern and amount of bleeding are carefully assessed
within the indurated area. In the same surgical procedure, meshed
split-thickness skin grafts are placed to cover the wound area. Shave
therapy can also be combined with saphenectomy or with dissection
and ligation of insufficient perforator veins.
One study reported both short-term and long-term results for
patients following shave therapy.159 At 3 months following shave
therapy skin grafting, a healing rate of 79% was reported. Additionally,
of patients treated in this study, a 1-year, long-term, healing rate of
88% was reported. Only minor adverse events to the procedure were
reported at the onset of the trial, and included transient postoperative
increases in body temperatures and the need for postoperative blood
transfusion in four patients.
In summary, shave therapy seems to be a safe and effective surgical
treatment option for patients with recalcitrant venous ulcers and sig­
nificant lipodermatosclerosis. Although larger trials are still needed to
confirm efficacy, short and long-term results are favorable thus far.
SUMMARY
Leg ulcers are debilitating, are usually caused by venous insufficiency,
and are seen most often in the elderly. They are therefore a major
health issue in an aging population. Recent developments in the
understanding of wound healing have helped to explain why leg
ulcers can become chronic and have assisted in developments in
therapy. Compression remains the mainstay of therapy, often with
aspirin or pentoxifylline as adjuncts to speed healing. However,
chronic wounds may require more intervention. Surgical debridement
may be needed, particularly when using advanced wound care prod­
ucts that require debridement as a preparatory step. Skin grafting,
SEPS, and shave therapy may be employed. Finally, the use of topical
antibiotics remains controversial and antibiotic therapy is often not
necessary in the healing of ulcers colonized by bacteria.
We can expect to see future therapeutic developments in leg ulcer
therapy in response to improved understanding of the inflammatory
processes and wound healing.
The utilization of SEPS in the prevention of venous leg ulcer recur­
rence has demonstrated some promising results. In a recent study,
Murray et al. demonstrated an 85% healing rate for patients with
CEAP classification class 6 venous disease, within an 8-week period
after surgery, in 67 patients.154 The patients were followed-up for a
total of 55 months and ulcer healing was demonstrated in 89% of
class 6 limbs, while four of 38 ulcerated limbs failed to heal within
3 months. Ulcer recurrence of 23% was demonstrated in 24 months,
most commonly in patients with a history of deep venous
thrombosis.
SHAVE THERAPY FOR VENOUS ULCERS
Ulcers secondary to chronic venous insufficiency are typically sur­
rounded by indurated and hyperpigmented skin in the form of acute
or chronic lipodermatosclerosis. Histologically, this area of skin is
characterized by clusters of small vessels with prominent endothelial
cells and thickened walls, surrounded by several basement mem­
branes, fibrinogen, laminin, and type IV collagen,155 with the presence
of microthrombi. Studies examining the microcirculation by Doppler
have demonstrated increased venous blood flow along with decreased
transcutaneous and intracutaneous oxygen tension in these diseased
areas.155,156 Additionally, the extent of morphologic and functional
abnormalities has been found to correlate with the amount of lipo­
dermatosclerosis.157 The underlying mechanisms leading from lipo­
dermatosclerosis to venous ulceration have not been completely
elucidated, but lipodermatosclerosis has been reported as a poor prog­
nostic factor for healing.158 Therefore, studies have identified this area
of diseased skin as a potential site for therapeutic intervention for
patients with chronic venous leg ulcers.
Because extirpation of circumscribed areas of lipodermatosclerosis,
as well as the venous ulceration has proven beneficial in the treatment
of refractory venous ulcers, a surgical procedure known as shave
therapy has been employed for the treatment of patients with exten­
sive lipodermatosclerosis and nonhealing ulcers. Briefly, the proce­
dure uses a dermatome to surgically remove all indurated areas beside
and underneath the ulcer. The technique excises cutaneous layers
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CHAPTER CONTENTS
Dressings
471
Introduction
471
Historical perspective
472
Functions of dressings
472
Acute wounds vs chronic wounds
472
Acute wounds
472
Chronic wounds
472
Types of dressings
473
Non-adherent fabrics
473
Absorptive dressings
473
Occlusive/moisture-retentive
473
Non-biologic occlusive dressings
473
Foams
473
Films
474
Hydrocolloids
475
Hydrogels
476
Alginates
476
Hydrofibers
477
Collagen dressings
477
Hyaluronic acid dressings
477
Biologic/biosynthetic dressings
477
Grafts
477
Skin substitutes
477
Cultured epidermal grafts
478
Postoperative care and wound care
481
Acute wounds
481
Post-excision wounds healing by primary intention
481
Post-excision wounds healing by second intention
481
Uncomplicated partial-thickness and full-thickness
wounds
481
Chronic wounds
482
Venous ulcers
482
Compression stockings
482
Compression bandages
482
Unna Boot
482
Four-layer bandage
483
Orthotic device
483
Pneumatic compression
483
Wound dressings
483
Arterial ulcers
483
Diabetic foot ulcers
483
Pressure ulcers
484
Pitfalls and their management
484
Optimizing outcomes
484
Ways to optimize results in wound care
484
Pitfalls in postoperative care and the use of dressings and
their management
484
Practical applications
485
Cost vs cost-effectiveness
486
Summary
486
DRESSINGS
Introduction
A dressing is defined as a covering applied to a lesion. This simple
definition belies the importance of dressings in wound healing and
the complexities of choosing the correct dressing for a particular
lesion. At present, there is a myriad of categories, subcategories, and
©2012 Elsevier Ltd.
Dressings and postoperative carea
May Leveriza-Oh, Tania J. Phillips
Chapter
32 
aThis article was published in Surgery of the Skin, Procedural Dermatology, May
Leveriza-Oh and Tania J Phillips, Dressings and Postoperative Care, 117–135,
Copyright Elsevier (2005).

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
dressings in maintaining a moist environment is critical in facilitating
healing. In fact, acute wounds have been shown to heal 40% faster in
a moist environment than when air-exposed.7 The specific effects of a
moist environment and occlusion on wound healing are well-
established in this wound type.
Enhancement of epithelial migration
Rovee established that in moist wound healing of acute wounds,
wound resurfacing occurs more rapidly because keratinocytes begin
to migrate sooner, and not because of a higher rate of mitosis.8
Stimulation of angiogenesis
Moist wound healing promotes a greater rate of vascularization. The
accumulation of angiogenesis-stimulating factors, such as tumor
necrosis factor and heparin, under the dressing, partly accounts for
this.3 In addition, because hypoxia often stimulates angiogenesis, the
dressing establishes a steep oxygen gradient, which stimulates capil­
lary growth toward the more hypoxic center.9
Retention of growth factors
Acute wound fluid beneath occlusive dressings has been shown to
stimulate proliferation of fibroblasts, keratinocytes, and endothelial
cells.10 The growth factors involved in this were: platelet-derived
growth factor (PDGF); basic fibroblast growth factor (bFGF); trans­
forming growth factor (TGF)-β; epidermal growth factor (EGF), and
interleukin (IL)-1.3 PDGF is a powerful mitogenic, chemotactic, and
angiogenic factor. EGF is an important player in epidermal cell growth,
survival, and differentiation. TGFβ induces angiogenesis, fibrosis, dif­
ferentiation, and proliferation.11
Facilitation of autolytic debridement
Retained water and proteolytic enzymes interact and achieve painless
wound debridement of necrotic tissue.
Protection against exogenous organisms
Although the bacterial count is higher in occlusive dressings than
non-occlusive dressings, this does not predispose to infection.12
Overall infection rate is 2.6% for occlusive dressings vs 7.1% for non-
occlusive dressings.13 As well as acting as a physical barrier, occlusive
dressings allow neutrophils to infiltrate easily and function more
actively. Occlusion is also associated with the presence of higher levels
of lysozymes and globulins.3 Lastly, occlusion maintains a mildly
acidic pH, which is inhibitory to the growth of some bacteria, espe­
cially Pseudomonas and Staphylococcus spp.14
Maintenance of voltage gradients
Moist wound healing helps in the maintenance of an electric field,
which is essential in keratinocyte migration. Also, an increase in the
synthesis of growth factors by human fibroblasts has been demon­
strated during in-vitro electrical stimulation.7
Chronic wounds
Chronic wounds are wounds in which the normal process of healing
has been disrupted at one or more points in the phases of hemostasis,
inflammation, proliferation, and remodeling.6 In this wound type,
there is usually an underlying pathology, which produces a delay in
the healing process.15 The effect of occlusion in these wound types is
not as well established because there is a dearth of randomized con­
trolled trial data for chronic wounds.
In contrast to acute wound fluid, chronic wound fluid was found
to be inhibitory to epithelialization, and to contain degradation pro­
ducts of vitronectin and fibronectin, which inhibit keratinocyte
types of dressings with different functions, structural compositions,
and physical and chemical characteristics, some common and some
very unique.
Historical perspective
Even during ancient times, the Egyptians had a keen interest in wound
healing. They formulated homemade concoctions of lint, grease, and
honey as topical therapy for wounds, or would soak strips of bandage
material in oils and resins and use them as dressings. They even rec­
ommended the use of raw, fresh meat to cover wounds during the first
day of healing.1
In 1867, the first antiseptic dressings were introduced by Lister who
soaked lint and gauze in phenol and then applied them to wounds.
In general, before the twentieth century, it was believed that wounds
healed best when left open (to allow them to breathe) and dry (to
keep them ‘germ-free’) as advocated by Pasteur.2 This view began to
change in 1958 when Odland observed that a blister healed faster
when left unbroken.3 This was further supported by Winter’s landmark
study on swine in 1962, which showed that superficial wounds kept
moist by covering them with a film healed twice as fast as those
exposed to the air.4 Hinman and Maibach5 repeated Winter’s study
using humans, and found a similar increase in epithelialization rate
for occluded wounds.
These studies revolutionized the approach to wound care by dem­
onstrating the importance of moist wound healing. Since then, a
multitude of more sophisticated occlusive dressings made of newer
materials and agents have been formulated, studied, and become
commercially available.
FUNCTIONS OF DRESSINGS
Dressings serve several basic functions (see Table 32.1).
Acute wounds vs chronic wounds
Acute wounds
Acute wounds are wounds with no underlying healing defect that
proceed to heal in an orderly and timely fashion, passing through
well-defined phases of an inflammatory response, granulation tissue
formation, and remodeling.6 In acute wounds, the function of
Table 32.1  Basic functions of wound dressings
Function
Benefit
Cover wound
Protection from trauma and contamination
from bacteria and foreign materials
Minimize fluid and heat loss
Absorb wound
drainage
Keep wound moist, but not wet
Minimize maceration
Compression
Increase hemostasis
Minimize edema and hematoma formation
Prevent dehiscence
Provide moist
environment
Facilitate healing of acute wounds
Reduce pain in chronic wounds

Chapter
Dressings and postoperative care
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| 32 |
Mansfield, MA), Xeroform (The Kendall Company), and Telfa (The
Kendall Co). In contrast, the hydrophilic dressings are less occlusive,
but have the ability to readily facilitate the drainage of fluids and
exudates into overlying dressings. Examples are: Xeroflo (The Kendall
Company); Mepitel (Molnlycke Health Care, Gotenberg, Sweden);
Adaptic (Johnson & Johnson Medical, Arlington, TX), and N-Terface
(Winfield Laboratories, Dallas, TX).
Absorptive dressings
Gauze is one of the most commonly used absorptive dressings. It is
excellent at drawing fluids and exudates away from the wound surface,
but loses its efficacy when saturated. It is usually used to cover non-
occlusive, non-adhering fabric dressing materials and absorbs dis­
charges, which drain through them. It may also be used, however, over
occlusive dressings as a secondary dressing to keep them in place.
Wide mesh gauze is usually not placed in direct contact with wounds
because it adheres to the surface of the wound, resulting in pain on
removal. The only occasions this is done on purpose, is when mechan­
ical debridement is desired.21
Foam dressings and alginates are classified as both absorptive and
occlusive/moisture-retentive dressings.
Occlusive/moisture-retentive
A moist wound environment is provided by a dressing that transmits
moisture vapor at a rate lower than that at which a wound loses
moisture. This is measured as moisture vapor transmission rate
(MVTR) through the dressing when it is left in place for 24 h. MVTR
of intact normal skin is about 200 g/m2 per day, while that of wounded
skin is 40 times higher. Dressings with an MVTR of <35 g/m2 per h
are defined as occlusive or moisture-retentive.22
Non-biologic occlusive dressings
Traditional occlusive dressings are classified into five basic categories
(Table 32.2).
Foams
Foam dressings are composed of hydrophobic, polyurethane foam
sheets and are characteristically soft, highly absorbent, and opaque
(Fig. 32.1). They are available in varying forms and may be adhesive
or non-adhesive, and thick or thin. They have the unique ability of
being able to expand to conform to the size and shape of the wound
to be dressed.
Some commercially available foam dressings are Allevyn (Smith &
Nephew United, Largo, FL); Biopatch (Johnson & Johnson Medical);
Curafoam (The Kendall Company); Flexzan (Dow B. Hickam, Inc,
Sugarland, TX); Hydrasorb (Tyco Health Care/The Kendall Company);
Lyofoam (ConvaTec, Princeton, NJ); Mepilex (Molnlycke Health
Care); Polymen (Ferris Corp, Burr Ridge, IL), and Vigifoam (Bard,
Murray Hill, NJ).
The primary advantages of foam dressings are that they can be used
on wounds with unusual configurations and are highly absorptive.
Other advantages are that they do not stick to the wound surface and
can thus be easily removed for cleaning, and that they may be utilized
for pressure relief, such as in cushioning bony prominences.23
Because they are opaque, foam dressings allow limited inspection.
Their high absorptive properties may also be a disadvantage in that
they may dry up the wound bed. Foams often require a secondary
dressing.
Foams are used on moderately to heavily exudative wounds, as well
as infected wounds. Foams themselves may be used as secondary
migration.16 Furthermore, when chronic wound fluid is added to cul­
tures of keratinocytes, fibroblasts, or endothelial cells, it fails to stimu­
late DNA synthesis directly, contrasting the DNA-synthesizing ability
of acute wound fluid.17,18 Another important biochemical difference
in chronic wounds is that they exhibit considerably higher protease
activity than acute wounds.19
A study on occluded vs non-occluded venous ulcers showed that
the difference in the number of wounds healed at the end of 12 weeks,
was not statistically significant; however, the rate of healing was more
rapid in the occlusive dressing group.20 For patients with chronic
wounds, moisture-retentive dressings do offer the advantages of pain
relief, painless wound debridement, containment of wound exudates,
reduction in the incidence of complications, and improved quality
of life.3
TYPES OF DRESSINGS
Dressings may be classified based on their clinical functions as well
as their physical appearance and composition (Box 32.1).
Non-adherent fabrics
Non-adherent fabrics are derived from a combination of fine mesh
gauze and tulle gras, commonly impregnated with chemicals to poten­
tiate the dressing’s occlusive or non-adherent characteristics, its ability
to facilitate healing, or its antimicrobial properties.21 They may be
subdivided into hydrophobic and hydrophilic types. Hydrophobic
fabrics have greater occlusive capability, but hinder fluid drainage
through them. These include Vaseline gauze (The Kendall Co,
Box 32.1  Types of dressings
• Non-adherent fabrics
• Absorptive
• Gauze
• Foams
• Alginates
• Occlusive/moisture-retentive dressings
• Non-biologic – traditional
• Foams
• Films
• Hydrocolloids
• Hydrogels
• Alginates
• Non-biologic – new
• Hydrofiber dressings
• Collagen dressings
• Hyaluronic acid dressings
• Biologic – grafts
• Split-thickness skin grafts (STSGs)
• Full-thickness skin grafts (FTSGs)
• Composite grafts
• Biologic/biosynthetic – skin substitutes
• Cultured epidermal grafts
• Dermal replacements
• Composite skin substitutes
• Antimicrobial dressings

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
dressings when additional absorption is needed. Because of their
dehydrating capabilities, they are not to be used on dry wounds.
Technique
During application, a 2 cm margin is left around the wound edges.
The non-adhesive foam is kept in place with tape or gauze rolled
around it. Foam dressings are relatively easy to remove. If the dressing
has dried up, it has to be soaked first with saline solution before
removal, to prevent damage to the epithelium.23
Films
Films are generally made of clear polyurethane membranes with
acrylic adhesive on one side for adherence. They are thin, transparent
sheets that are permeable to oxygen, carbon dioxide, and water, and
impermeable to fluids and bacteria. The specific type of product deter­
mines the degree of permeability. Examples are Tegaderm (3M Health­
care, St Paul, MN); Bioclusive (Johnson & Johnson Medical); Blisterfilm
(The Kendall Company); Omniderm (Omikron Scientific Ltd,
Renovot, Israel); Polyskin II (Kendall Healthcare); Proclude (Con­
vaTec); Mefilm (Molnlycke Health Care); Carrafilm (Carrington Lab,
Irving, TX), and Transeal (DeRoyal, Powell, TN).
Table 32.2  Types and characteristics of occlusive/moisture-retentive wound dressings
Type
Advantages
Disadvantages
Indications
Examples
Foams
Absorbent, conform to
body contours
Opaque, require
secondary dressing
Partial-thickness wounds,
moderately to heavily exudative
wounds, pressure relief
Allevyn
Flexzan
Hydrasorb
Lyofoam
Vigifoam
Films
Transparent, create
bacterial barrier, adhesive
without secondary
dressing
May adhere to
wounds, can cause
fluid collection
Donor sites, superficial burns
and ulcers, partial-thickness
wounds with minimal exudates
Tegaderm
Bioclusive
Blisterfilm
Omniderm
Transeal
Hydrocolloids(+)
Autolytic debridement,
enhance angiogenesis,
absorbent, create
bacterial and physical
barrier
Opaque, gel has
unpleasant smell,
expensive
Partial- or full-thickness wounds,
mildly to moderately exudative
wounds, pressure ulcers, venous
ulcers, donor sites, acute
surgical wounds
Duoderm
NuDerm
Comfeel
Cutinova
Replicare
Hydrogels
Semitransparent,
soothing, do not adhere
to wounds, hydrating
Require secondary
dressing, frequent
dressing changes
Painful wounds, partial-thickness
wounds, wounds after laser,
dermabrasion, or chemical peel,
donor sites
Vigilon
Tegagel
Curagel
ClearSite
Curafil
Elasto-Gel
SoloSite wound gel
2nd Skin
Alginates
Highly absorbent,
hemostatic, do not
adhere to wounds, fewer
dressing changes
Require secondary
dressing, gel has
unpleasant smell
Highly exudative wounds,
partial- or full-thickness wounds,
after surgery
Algiderm
AlgiSite
Algisorb
Kaltostat
Curasorb
Polymen
SeaSorb
Sorbsan
Figure 32.1  A foam dressing on a lesion medial aspect of the lower leg.

Chapter
Dressings and postoperative care
475
| 32 |
of fluid within the dressing signals that it is time for a dressing
change.23
Hydrocolloids
Hydrocolloid dressings are a family of dressings containing a hydro­
colloid matrix consisting of materials such as gelatin, pectin, and
carboxymethylcellulose (Fig. 32.3). They are opaque, absorbent, adhe­
sive waterproof wafers that contain hydrophilic colloidal particles in
a hydrophobic polymer. Upon contact with wound exudates, the
hydrophilic particles absorb water, swell, and liquefy to form a gel
over the wound, which enhances autolytic debridement. Hydrocol­
loids are impermeable to water vapor, oxygen, and carbon dioxide.
They come in preparations of varying thickness and are even available
as powders and pastes.
Examples of hydrocolloid dressings are Duoderm (ConvaTec);
NuDerm (Johnson & Johnson Medical); Comfeel (Coloplast Sween,
Inc, Marietta, GA); Hydrocol (Dow Hickman, Sugar Land, TX); Cuti­
nova (Smith & Nephew); Tegasorb (3M, New York, NY); Replicare
(Smith & Nephew United), and Restore (Hollister, Libertyville, IL).
The advantage of using hydrocolloids is that the autolytic debride­
ment enhances angiogenesis, granulation tissue formation, and
healing.23 Hydrocolloid dressings are slightly bulkier than other dress­
ings such as films, providing more physical protection for the wound.
In practical terms, their impermeability to water allows patients to
bathe and swim freely.
One of the disadvantages of hydrocolloids is that due to their deb­
riding abilities, they may initially cause the size of the wound to
increase. Occasionally, the skin surrounding the wound macerates.24
Hydrocolloids are also associated with the formation of a yellow gel,
which has a characteristic unpleasant odor and can be easily confused
with infection of the wound.
Indications for the use of hydrocolloids are: abrasions, postopera­
tive wounds, pressure and venous ulcers, burn wounds, and donor
sites. They are not to be used in 3rd-degree burns or actively infected
ulcers.
Because this type of dressing is relatively transparent, it has the
distinct advantage of permitting easy visualization of the underlying
wound for observation and monitoring purposes (Fig. 32.2). In addi­
tion, because they are thin and self-adhesive, they generally do not
require a secondary dressing, minimizing their interference with the
patient’s normal function. This type of dressing can also stay in place
for several days and decrease pain.
The biggest disadvantage of film dressings is that, because they
are non-absorptive, there is a tendency for fluid to collect under
them and eventually leak out. This breaks the antibacterial seal
created by the dressing’s adhesive, and necessitates frequent dressing
changes.21 It also requires intact periwound skin for dressing adher­
ence because there is the possibility that it could adhere to the wound
itself, and thereby strip away newly formed epidermis on removal.
Minor disadvantages of films are their tendency to wrinkle easily,
making them hard to handle, and occasional contact dermatitis from
adhesives.
Film dressings are ideally used for mildly exuding wounds, includ­
ing lacerations, superficial surgical and burn wounds, donor sites,
superficial ulcers, and arterial and venous catheter sites. They may
also be used as secondary dressings over alginates, foams, and hydro­
gels. They are not to be used as primary dressings of moderately to
heavily exuding or infected wounds, sinus tracts, or cavities. They are
also not recommended for patients with fragile skin, such as the
elderly.
Technique
The area surrounding the wound should be clean and dry. The recom­
mended margin is 3–4 cm around the wound.23 The best way to apply
the film is to gradually peel off the backing, while simultaneously
pressing the dressing onto the skin. The uninitiated should be fore­
warned that the film sticks to latex gloves and to itself very easily.
During removal, film dressings should be peeled off with care.
Stretching the film with light pressure disrupts the continuity of the
adhesive and makes it easier to remove. The accumulation of a pocket
Figure 32.2  A film dressing covering an ulcer on the medial malleolus.
Figure 32.3  A hydrocolloid dressing covering a lesion on the anterior
aspect of the ankle.

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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
granulation tissue. The gel form is irrigated with saline to facilitate
removal.
Alginates
Alginate dressings consist of the soft non-woven fibers of a cellulose-
like polysaccharide derived from the calcium salts of seaweed.26 They
are biodegradable, hydrophilic, non-adherent, and highly absorbent.
When the insoluble calcium alginate of this type of dressing comes
into contact with wound exudate, a soluble sodium salt is produced,
and a hydrophilic gel is formed as a byproduct in the process. Algi­
nates are commercially available as pads (Fig. 32.5), ropes, or ribbons.
Examples are: Algiderm (Bard); Algisite (Smith & Nephew); Algisorb
(Calgon-Vestal, St Louis, MO); Algosteril (Johnson & Johnson
Medical); Kaltostat (ConvaTec); Curasorb (The Kendall Company);
Carasorb (Carrington Lab); Dermacea (Sherwood Medical Co, St
Louis, MO); Melgisorb (Molnlycke Health Care); SeaSorb (Coloplast,
Holtedam, Denmark); Kalginate (DeRoyal), and Sorbsan (Dow B.
Hickam, Inc).
Because of their exceptional absorptive qualities, alginates are pri­
marily used for heavily exuding wounds.21 They can also be utilized
for deep wounds, sinuses, and cavities. The rope and ribbon forms
Technique
The periwound area is cleansed and dried for maximum adherence.
Ideally, the dressing is cut extending 2 cm beyond the wound margins.
Using scissors to round the corners will minimize rolling up of the
hydrocolloid dressing. The backing is peeled off carefully while press­
ing the pad gently on the skin. The warmth of the hand can be used
to help seal the dressing. At the start of treatment, the dressing usually
needs to be changed frequently, sometimes daily. However, as the
amount of material draining from the wound decreases, the frequency
of changing the dressing is likewise decreased, eventually becoming
every 3–7 days. Zinc oxide applied to the wound margins can be used
to minimize the maceration, irritation, or inflammatory responses of
the periwound area.23
For removal, hydrocolloids are peeled off the overlying skin with
minimal trauma. Remnants of the hydrocolloid left sticking on the
intact skin are removed easily using mineral oil. The wound bed is
subsequently cleaned with saline to make sure there is no hydrocol­
loid left on the bed. Patients and caregivers should be advised that
removing the dressing prematurely can injure newly formed
epidermis.
Hydrogels
Hydrogel dressings consist of a hydrophilic polymer, usually a starch
polymer such as polyethylene oxide, and up to 80% water.21 They are
available as gels, sheets, or impregnated gauze, which are absorbent,
non-adherent, semitransparent, and semipermeable to water vapor
and gases. Their high water content gives them the ability to rehydrate
dry wounds, giving them a soothing and cooling effect.25 Hydrogels
also act on necrotic tissue by autolytic debridement, thereby facilitat­
ing granulation tissue formation.23
Trade names are: Vigilon (Bard); Nu-gel (Johnson & Johnson
Medical); Tegagel (3M); FlexiGel (Smith & Nephew); Curagel (The
Kendall Company); Flexderm (Dow B. Hickam, Inc), ClearSite
(Conmed Corp, Utica, NY); Curafil (The Kendall Company); Curasol
(The Kendall Company); Carrasyn (Carrington Lab); Elasto-Gel (SW
Technologies, North Kansas City, MO); Hypergel (Scott Health Care,
Philadelphia, PA); Normgel (SCA Hygiene Products, Eddy Stone, PA);
SoloSite wound gel (Smith & Nephew); 2nd Skin (Spenco Medical,
Ltd, Waco, TX), and Transigel (Smith & Nephew).
Because they are semi-transparent, hydrogels allow some degree of
wound inspection. Refrigeration augments their cooling and soothing
effects on the wound. As hydrogels are non-adherent, they require a
secondary dressing or tape to hold them in place. They also have very
little absorptive ability.
Wounds that respond best to hydrogels are dry and mildly exuding
wounds, after-procedures such as dermabrasion and chemical peeling
wounds, superficial burns, and blisters and ulcers with a necrotic bed.
Heavily exuding wounds should not be dressed with hydrogels.
Technique
The hydrogel sheet must first be cut to the appropriate size in relation
to the size and configuration of the wound. These sheets are manu­
factured with a protective covering on both sides. The covering on one
side of the sheet is removed to expose the hydrogel (Fig. 32.4), and
the exposed side is then placed on the wound. Tape is then used to
secure it. The gel form of this type of dressing can be squeezed into
the wound cavity. A secondary dressing such as film, foam, or hydro­
colloid is used as a protective cover.
To prevent the hydrogel from adhering to the wound bed, the sheets
should not be allowed to dry out. They are usually changed every 3
days for necrotic wounds, and every 7 days on granulating wounds.23
They must be removed very gently to avoid damage to the forming
Figure 32.4  A hydrogel dressing being peeled carefully from its backing.
Figure 32.5  An alginate dressing on a lesion on the medial malleolus.

Chapter
Dressings and postoperative care
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| 32 |
Technique
Hydrofibers are applied to the wound site and reinforced with a sec­
ondary dressing. In removing the dressing, it may be necessary to
irrigate the wound with saline solution to remove the gel and prevent
stripping of the granulating tissue.
Collagen dressings
Collagen dressings are derived from cowhide and consist of type
1 bovine collagen. They are available as particles, sheets, or gels,
and are used for moderately exudative wounds and recalcitrant
ulcers.23 They act by providing a collagen matrix for cellular migration.
Examples are: Fibracol (Johnson & Johnson, Skillman, NJ); Medifil
(Biocore Medical Technologies, Inc, Silver Spring, MD), and Nugel
collagen wound gel (Johnson & Johnson Medical). They have been
known to occasionally cause irritation or increased drainage on
initial use.
Technique
First clean the wound, then apply the collagen dressing directly,
followed by a secondary dressing. To remove, carefully remove the
secondary dressing, then moisten with saline solution.
Hyaluronic acid dressings
Hyaluronic acid dressings are biodegradable, absorbent biopolymers
that form a hydrophilic gel with the serum or exudates of the wound.
Topical application accelerates granulation tissue formation and
re-epithelialization. An example is: Hyalofil (ConvaTec).
Biologic/biosynthetic dressings
Grafts
Grafts are pieces of skin that have been separated completely from
their local blood supply and transferred to other locations so that they
are wholly dependent on the development of a new blood supply
from the recipient bed.28 They may be classified according to the
source of donor tissue. A xenograft is a graft transplanted between
different species. In humans, the most common xenografts used are
derived from pig skin.21 They are temporary dressings in the sense that
they are eventually rejected and replaced by host epithelium.29
Autografts are grafts taken from the patient, meaning skin in one
area of a patient harvested and transplanted to another area. Allografts
are taken from donors of the same species. This could mean cadaveric
skin or skin from other living humans. Technological advances have
resulted in cultured dermal and epidermal components in vitro, which
have been used individually or combined as biologic wound dress­
ings, commonly referred to as skin substitutes.
Skin grafts can be categorized based on their thickness or composi­
tion. Partial or split-thickness skin grafts (STSGs) contain epidermis
and a portion of the dermis while full-thickness skin grafts (FTSG)
contain the entire thickness of the epidermis, dermis, and various
amounts of subcutaneous tissue.30 Table 32.3 compares STSGs and
FTSGs. Composite grafts are composed of at least two different types
of tissues, most frequently skin and cartilage.
Skin substitutes
The quest for developing a widely available product with structural
and functional properties as close as possible to those of natural skin
continues. Currently, a variety of skin substitutes are available for
clinical use and many more are undergoing testing or are pending
FDA approval.
can be used for packing narrow wounds and sinuses. They are to be
avoided in dry or mildly exuding wounds because they may dry out
these types of wounds. Their use in deep narrow sinuses is also con­
traindicated because removal may be difficult.27
As well as their absorptive ability, alginates also have hemostatic
properties. This sometimes lessens the number of dressing changes
needed. Their disadvantages are that the gel formed may be foul-
smelling or misleadingly appear purulent, and because they are non-
adherent, a secondary dressing is needed.
Technique
Before the application of an alginate dressing, the wound is cleaned
with saline and left wet while the surrounding skin is dried. The algi­
nate is applied in a dry condition to the wound surface, with a margin
of at least 2 mm around the wound edges.23 When ribbons or ropes
are to be used, they are rolled in a loose spiral fashion into the wound,
doubling back on themselves until the entire wound is covered. A
secondary dressing is placed over the dressing.
For removal, the gel formed by the alginate is simply lifted carefully
from the wound surface. Irrigation with saline solution and the use
of forceps after moistening may remove any components of the dress­
ing left behind after lifting.
Hydrofibers
Hydrofiber dressings are composed of soft, absorbent carboxymethyl
cellulose fibers that interact with wound exudates to form a soft gel.
They are available as non-woven pads or ribbons under the trade
name Aquacel.
They are especially useful for moderately to heavily exuding wounds
(Fig. 32.6) and wounds that are prone to bleeding because they are
almost three times more absorbent than alginates.23 They are indicated
for abrasions, lacerations, after excision wounds, pressure or leg ulcers,
burns, and donor sites. Hydrofiber ribbons may also be used for
packing wound cavities.
Figure 32.6  A hydrofiber dressing on a moderately exudative lesion on
the lateral malleolus.

478
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
fragile keratinocyte sheets, the lack of a dermal component, and the
short-term stability of the graft.
Cultured epidermal allografts
For cultured epidermal allografts, the skin is obtained from allogeneic
tissue, such as newborn foreskin. Cadaver skin was first used as
the source of cultured allografts; however, because of the many prob­
lems associated with their use, such as the potential for transmitting
disease, limited supply, and variable quality, its use as donor tissue
has been reduced.35–37 Neonatal skin is now the tissue source
of choice for cultured epidermal allografts owing to its increased
sensitivity and responsiveness to incorporated mitogens, and its
own release of growth-stimulating factors and mediators, such as
epidermal-derived thymocyte activating factor, interleukins, fibronec­
tin, and TGFβ.38
Cultured allografts were originally thought to act directly as a skin
replacement. However, recent studies have shown that allografts are
progressively replaced by the patient’s own skin. Some investigators
suggest that cultured epidermal allografts function by stimulating
migration and multiplication of the recipient’s keratinocytes,39 prob­
ably by way of growth factors rather than by permanent take of the
allograft itself.40 Others theorize that allografts provide a potent stimu­
lus for wound healing simply by the production of a biologic dressing
that prevents dehydration.41 Although they do not survive perma­
nently on the wound bed, cultured allografts provide efficient pain
relief within hours after grafting in addition to their protective
functions.
Cultured epidermal allografts have been used to treat donor sites,
partial-thickness burns, chronic leg ulcers, epidermolysis bullosa, and
wounds resulting from tattoo removal.28 Many investigators have
reported the acceleration of healing of STSG donor sites and partial-
thickness burns, resulting in re-epithelialization in 4–7 days.42
Skin substitutes act as a scaffold for tissue regeneration in vivo, or
as tissue replacement, providing matrix material and cells when grown
in vitro. They can be temporary or permanent; synthetic, biosynthetic,
or biologic.
Based on their components, skin substitutes can be classified into
three categories: epidermal grafts, dermal replacements, or composite
grafts consisting of both epidermal and dermal components.
Cultured epidermal grafts
Cultured epidermal autografts
Cultured epidermal autografts are grown from the patient’s own skin.
The technique currently in use for the culturing of epidermal grafts
was designed in 1975 by Rheinwald and Green.31 By serial subculture
of human keratinocytes, they were able to grow large epidermal sheets
from a small sample in vitro.
Ideally, epidermal cultured autografts need to be sutured or stapled
onto the recipient’s tissues to prevent separation from the wound bed.
At least two other layers of dressings are needed to protect the autograft.
A secondary dressing, usually a mesh gauze, is used to cover the graft
and is left in place for 7–10 days. Another more outer dressing is then
placed over the secondary dressing.32 This functions to absorb wound
exudates, and is changed every or every other day depending on the
amount of drainage from the wound.
Cultured keratinocyte autografts were initially used in the 1980s to
treat severely burned patients.33 At present, they are utilized for burns,
chronic leg ulcers, epidermolysis bullosa wounds, scar revision,
wounds resulting from excision of giant congenital nevi, and
vitiligo.34
One of the major disadvantages of cultured autografts is that they
require a 2–3-week period for growth of an adequate amount of epi­
thelial sheets. Other disadvantages include the difficulty of handling
Table 32.3  Split-thickness vs full-thickness skin grafts
STSG
FTSG
Composition
Epidermis plus part of the dermis
Epidermis plus dermis plus various amounts of fat
Survival
Greater, because requires less revascularization after transfer
Less chance of survival
Resistance to
trauma
Less resistant
More resistant
Cosmetic
appearance
Poor cosmetic appearance owing to poor color and texture
match; does not prevent contraction
Superior cosmetic appearance; it is thicker, preventing wound
contraction or distortion.
Indications
Temporarily or permanently after removal of skin cancer with
a high chance of recurrence.
If a flap is not viable, in areas with limited vascular supply
When esthetic outcome is essential (e.g. facial defects)
Common uses
Chronic lower leg ulcers (e.g. venous, irradiated tissues;
exposed periosteum, cartilage, or tendon)
Surgically induced large defects (e.g. for birthmarks, nevi)
Facial defects – nasal tip, dorsum, ala or sidewall, lower
eyelid, ear
Donor site tissue
Anteromedial thigh
Others – buttock, abdomen, inner or outer aspect of arm,
inner forearm
Nearby site, with similar color or texture to skin surrounding the
defect (e.g. preauricular and postauricular, supraclavicular,
clavicular, neck, nasolabial folds, inner arms)
Disadvantages
Poor cosmetic appearance (e.g. color and texture mismatch,
greater chance of distortion or contraction)
Greater risk of failure
If not closed primarily, the donor wound site has a prolonged
healing time and a greater risk of distortion and hypertrophic
scar formation
Adapted from Valencia, I.C., Falabella, A.F., Eaglestein, W.H., 2000. Skin grafting. Dermatol Clin 18 521–532.

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layer is removed and covered with an autograft. This allows for har­
vesting of thinner epidermal autografts compared to conventional
autografts. Thinner autografts enable donor sites to heal faster, allow­
ing earlier reharvesting and less hypertrophic scarring of the donor
site.34 The FDA requires clinicians to complete a company-sponsored
training program before using Integra. Its application procedure is
complex, and there is an increased susceptibility to infection in com­
parison to autografts.34
Refinements of the matrix concept led to the development of Tran­
sCyte (formerly known as Dermagraft-TC). This is a live, metabolically
dynamic, immunologically inert human dermis made up of a matrix
synthesized by the proliferation of allogeneic human neonatal fibrob­
lasts on a nylon bioabsorbable mesh and an outer silicone polymer
layer. The fibroblasts are capable of undergoing cell division and
secreting growth factors. TransCyte provides a temporary covering that
helps protect the wound from desiccation and contamination. It has
been successfully used for temporary wound coverage of partial-
thickness burns. It was shown to be superior to silver sulfadiazine in
achieving faster re-epithelialization in partial-thickness burns.45
Dermagraft evolved as a modified version of TransCyte. It consists
of neonatal fibroblasts seeded on a three-dimensional polyglactin
bioabsorbable mesh with no outer silicone membrane, so allowing
for a single-step procedure (Figs 32.7, 32.8). This skin substitute stim­
ulates the formation of granulation tissue, re-epithelialization, and
angiogenesis.34 The fibroblasts produce fibronectin, glycosaminogly­
cans, collagens, and growth factors. Dermagraft was designed as a skin
substitute for full-thickness wounds. It has the advantages of avoid­
ance of non-human tissue, ready availability, less chance of wound
contracture and scarring, and mesh absorption in 60–90 days.
In the treatment of chronic diabetic ulcers, Dermagraft was shown
to be of significant clinical benefit in achieving wound closure within
12 weeks compared with conventional therapy alone (30 vs 18.3%,
p = 0.023).46 It has also been shown to be more cost-effective,47 and
currently has FDA approval for this indication. Clinical trials are
underway to assess its efficacy in the treatment of venous ulcers.
Cultured epidermal allografts have the significant advantage of
avoiding the creation of a donor wound site. In addition, they are
readily available, and do not require the 2–3 week growth interval of
cultured epidermal autografts.
Cultured epidermal allografts are not commercially available in the
USA. They are available in only some centers, are expensive, and
require a tissue culture facility.
Dermal replacements
A variety of products are available as dermal replacements. These are
synthetic, biosynthetic, or biological materials with functional or
structural similarities to the dermis. The dermis is composed of cel­
lular (fibroblasts) and extracellular components (collagen, matrix
proteins) and plays a vital role in the healing of skin by influencing
epithelial migration and differentiation, dermoepidermal junction
formation, wound contraction, and scar formation.
Skin substitutes functioning as dermal replacements include: cadav­
eric allograft skin, BioBrane (Dow B. Hickam, Inc); EZ Derm (Brennen
Medical Inc, St Paul, MN); Oasis (Cook Inc, Bloomington, IN); Tran­
scyte (Smith & Nephew), and Dermagraft (Advanced Tissue Sciences
Inc, La Joya, CA).
In cadaveric dermal replacements, human cadaver skin is chemically
treated to remove its antigenic components, which are usually found
as cellular elements. This results in an immunologically inert complex
made up of an acellular collagen dermal matrix and an intact base­
ment membrane. This can be used alone or in combination with other
grafts or skin substitutes. AlloDerm (Life Cell Co, Woodlands, TX), a
human cryopreserved, acellular cadaveric de-epidermalized dermis
has been successfully used in combination with STSGs to treat burn
wounds and dermal defects, and for periodontal, plastic, and recon­
structive surgery.34
Biosynthetic dressings were initially introduced for the coverage of
burns and donor sites. Biobrane consists of a bilaminate biosynthetic
material made up of silicone film and nylon fabric containing porcine
collagen peptides as the biological component.34 When used on donor
sites, Biobrane proved superior to Scarlet Red (The Kendall Company)
in pain relief, healing time, and absorption of exudates.43
Another biosynthetic porcine-derived dermal substitute is EZ Derm
in which the porcine collagen is chemically cross-linked using an
aldehyde. There are perforated and non-perforated types and it comes
attached to a gauze liner, which is detached before grafting. It is used
for temporary coverage of partial-thickness skin loss injuries, includ­
ing burns and ulcers. It has the advantages of immediate availability,
a long shelf-life, and the absence of human communicable disease.33
Limited clinical studies have been carried out.
Oasis is a biologic dressing derived from porcine small intestinal
submucosa that has been processed to exclude the serosa, smooth
muscle, and mucosa layers, producing a collagenous, acellular matrix
rich in cytokines and cell adhesion molecules. Because it is packaged
dry and then rehydrated, Oasis has the advantage of a longer shelf life
than other porcine heterografts. It is also relatively easy to apply and
reapply.34 One of its primary disadvantages is that because it is very
thin, it is easily traumatized, so requiring a secondary dressing for
additional protection and to prevent it from drying up.
Integra (Integra LifeSciences Corp, Plainsboro, NJ) is a biosynthetic,
temporary, bilaminated skin substitute consisting of a matrix of
bovine collagen and chondroitin-6-sulfate covered by a synthetic sili­
cone elastomer (Silastic). It is FDA-approved for the treatment of
burns. In a 2-year study, Integra was successfully used in the recon­
struction of burn scars of the upper extremities, and was shown to be
a good alternative for patients with severe burns in whom there is
insufficient available skin for a full-thickness skin graft.44 The dermal
component is designed to be slowly biodegradable while the silicone
Figure 32.7  Preparation for applying Dermagraft. The configuration of
the ulcer is traced on the transparent protective covering of the
Dermagraft.

480
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
181 days; p = 0.003).50 In a multicenter study of 208 patients with
diabetic foot ulcers comparing Apligraf treatment with saline-
moistened gauze (both with standard adjunctive therapy including
debridement and foot off-loading), Apligraf resulted in complete
wound closure in 56% of patients vs 38% in the control group
(p = 0.0042) at the end of 12 weeks. Median closure time was also
shorter (65 vs 90 days; p = 0.0026).51
Apligraf was a suitable and clinically effective treatment for excised
burn wounds when applied over meshed autografts. Furthermore,
cosmetic and functional advantages were demonstrated over standard
therapy.52
Bilayered cellular matrix (BCM) or OrCel (Ortec International Inc,
New York, NY) consists of a porous collagen sponge containing cul­
tured keratinocytes and fibroblasts derived from allogeneic cells har­
vested from neonatal foreskins. This has been FDA approved for use
in treatment of split-thickness donor sites of burn patients and
patients with recessive dystrophic epidermolysis bullosa. Clinical
trials for its use in the treatment of burns, diabetic ulcers, and venous
ulcers are underway.
Antimicrobial dressings
Silver-impregnated dressings are becoming popular antimicrobial
dressings. They are bactericidal without antibiotics while maintaining
a moist environment to facilitate wound healing.53 Silver has broad-
spectrum action on bacteria, including against vancomycin-resistant
enterococci and methicillin-resistant Staphylococcus aureus. It acts on
bacterial cell wall synthesis, ribosome activity, and transcription. It
also exhibits activity against fungi and yeast. Commercially available
examples of silver-containing dressings include: Aquacel Ag (Con­
vaTec); Contreet (Coloplast Sween, Inc); Arglaes (Medline Industries,
Mundeline, IL); Acticoat (Smith & Nephew); Silveron (Silveron Con­
sumer Products, Mundeline, IL), and AcryDerm Silver (AcryMed Inc,
Portland, OR). In a matched-pair randomized study on burns, silver-
coated Acticoat dressings resulted in less pain and decreased sepsis
compared with the application of silver nitrate.54
Cadexomer iodine, a slow-release formulation of iodine, is com­
posed of starch microspheres cross-linked with ether bridges and
iodine. It slowly absorbs moisture, while releasing iodine in low con­
centrations, which are antibacterial yet not cytotoxic.3 Cadexomer
iodine provides broad-spectrum antibiotic coverage, and can signifi­
cantly decrease the bacterial load on the wound surface. It resulted in
a significant reduction in S. aureus (p < 0.001), β-hemolytic strepto­
cocci, proteus, and klebsiella in a randomized control trial on venous
ulcers.55 Iodosorb, a cadexomer iodine ointment, is antibacterial and
an effective debriding agent in pressure, venous, and diabetic ulcers.56
Composite skin substitutes
Composite skin substitutes contain both epidermal and dermal com­
ponents. The first true composite skin equivalent consisting of both
epidermal and dermal elements, each with living cells, approved for
use by the FDA is Apligraf (Organogenesis, Canton, MA; also known
as Graftskin). This is a biosynthetic, bilayered living construct made
up of cultured human neonatal foreskin keratinocytes overlying
fibroblasts cultured on a dermal matrix of bovine type I collagen (Figs
32.9, 32.10). It is metabolically, morphologically, and biochemically
similar to human skin,28 but lacks appendages, nerves, and blood
vessels, and is immunologically inert. Because it lacks macrophages,
lymphocytes, and Langerhans cells,21 there appears to be no host
antibody or cell-mediated response or clinical rejection.
Apligraf is a useful adjuvant to standard ulcer therapy for patients
with venous leg ulcers or neuropathic diabetic foot ulcers that do not
respond to conventional ulcer therapy,48,49 and is FDA approved for
these indications. In a multicenter study of 293 patients with non-
healing venous ulcers, treatment with Apligraf in conjunction with
standard compression was shown to be more effective than compres­
sion therapy alone in achieving wound closure within 6 months (63
vs 49%; p = 0.02), and to be superior in healing larger (>1000 mm2,
p = 0.02) and deeper ulcers (p = 0.003), and ulcers of more than 6
months’ duration (p = 0.001). Median time to complete wound closure
was also significantly shortened in the Apligraf-treated group (61 vs
Figure 32.8  Dermagraft being applied to an ulcer.
Figure 32.9  The meshed-type Apligraf before application.
Figure 32.10  A close-up of the meshed-type Apligraf overlying an ulcer.

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Dressings and postoperative care
481
| 32 |
tissue. An absorptive layer consisting of gauze pads can be used for
draining wounds.
The last layer is the binding or securing layer, which keeps the dress­
ing in place and may also function in compression and immobiliza­
tion, if needed. Adhesive tape is most commonly used; however,
tubular gauze, elastic bandages, and gauze rolls may be added. To
increase the holding property of tape, especially when working on a
mobile or sebaceous region, the area can be degreased with acetone
or alcohol and prepped with liquid adhesive (Mastisol–Ferndale
Labs, Ferndale, MI).62 Hairy areas on which tape is to be applied
should be shaved.
The dressing is to be left undisturbed for 48–72 h after surgery,
mainly to reduce the risk of incidental trauma and contamination to
the fresh wound.59 This also allows the patient physical and psycho­
logical relief at the time the wounds are most likely to cause pain and
discomfort. However, if the dressing becomes soaked with blood or
wound exudate before then, a change of dressing is necessary.
At home, gentle cleansing is carried out once or twice a day using
soap and water, saline solution, or half-strength hydrogen peroxide.
There is some controversy about the use of hydrogen peroxide because
it has been shown to have an inhibitory effect on fibroblasts and the
microcirculation,63 and might therefore actually retard healing.
However, its effervescence is excellent in removing dried-up debris and
crusts on wounds, and the few minutes of contact with it has been
deemed more helpful than harmful.59 Saline is the most commonly
used irrigation solution for the removal of inflammatory contents
from the wound surface.56
In removing the initial dressing, the patient is instructed to wash or
wet the dressing first to reduce pain and prevent damage to the granu­
lating wound bed. Cleansing the wounds with normal saline delivered
at 8 lb/in2 (35-mL syringe and 19-gauge angiocatheter) is usually
enough to dislodge debris from the wound bed.23 A sterile cotton-
tipped applicator may also be used to carefully remove debris from
more superficial wounds. For deeper wounds, the cleansing solution
can be poured over the surface then blotted with sterile gauze. The
layered dressing is then reapplied. This is continued until complete
re-epithelialization has occurred (several weeks or more for open
wounds). Usually, if no complications occur, changes of dressing
become less frequent as the wound site gradually re-epithelializes and
exudes less fluid.
Another alternative for post-excision wounds is the use of occlusive
dressings with or without a secondary dressing. This gives adequate
protection from trauma, desiccation, contaminants, and bacteria,
while providing a moist environment, which facilitates wound
re-epithelialization.21 For the more superficial wounds with minimal
exudation, films may be used. For the deeper wounds, hydrogels or
hydrocolloids may be used. If the wound is highly exudative, foams
and alginates are preferred. There are no hard-and-fast rules about
how long this type of dressing should stay on the wound, but it is
recommended that the dressing is changed before leakage occurs.
For superficial wounds on the legs, one of the more practical options
is to simply apply an antibacterial ointment. Its main advantage is
that it is a one-step procedure, and interferes minimally with function
and appearance.21 Its main disadvantage is that the ointment can be
easily wiped off unintentionally, so providing limited protection and
absorption.
Uncomplicated partial-thickness and
full-thickness wounds
An approach applicable for both partial- and full-thickness wounds is
the use of the moisture-retentive occlusive dressings. The moist envi­
ronment provides the optimal conditions to facilitate healing and
POSTOPERATIVE CARE AND WOUND CARE
Acute wounds
Postoperative wound management involves caring for patients from
the conclusion of their surgical procedure (which may take hours)
through the early remodeling phase of the surgical site (which may
take weeks to months).53 The importance of postoperative manage­
ment in obtaining satisfactory results cannot be overemphasized.
The desired end-result is the most cosmetically acceptable healed
wound in the least amount of time.52 This involves the absence of
scarring, infection, and contact dermatitis from topical medications
used; and can be achieved by good postoperative care techniques
including the proper choice of dressings.
Excisional surgery is one of the most common procedures carried
out by lower extremity surgeons. After excision, wounds may heal by
primary or second intention. In primary intention closure, there is
direct apposition of wound edges by suturing. In contrast, in second
intention healing, the wound is left open after the surgery and allowed
to epithelialize from its edges.28
Post-excision wounds healing by primary intention
Wounds sutured closed after excisional surgery, in most instances, do
not require special dressings because normal immunity from phago­
cytes ingesting and killing bacteria is often sufficient to prevent infec­
tion.57 A simple low- or non-adherent gauze dressing secured with
tape, or a semipermeable film will usually suffice. For post-excision
sites that are still actively bleeding, a thicker more absorbent dressing
is needed. Despite the low infection rate, some clinicians still opt to
include an antibiotic or aquaphor ointment in the contact layer, if
only to make the patient more comfortable.
Wounds healing by primary intention rarely require cleansing.58 In
fact, disturbance of the dressing should be minimized to prevent
bacterial contamination as well as removal of re-forming epithelium.
When needed, cleansing is usually done with care using saline.
Changes of dressing are likewise carried out as needed.
It takes approximately 1 week for sutured wounds to re-epithelialize.
The correct time for suture removal depends on several factors, and
therefore the practitioner can only follow general guidelines: 4–6 days
for the head and neck; 7 days for the upper limbs; 10 days for the
trunk and abdomen, and 14 days for the lower limbs.58 Some prob­
lems that may be encountered in sutured wounds are dehiscence,
hematoma formation, and suture reactions.59
Post-excision wounds healing by second intention
’Shave’ or tangential removal of skin is usually performed by derma­
tologists for biopsy, transverse excision of lesions such as moles, or
for Mohs surgery layers.53 It results in an open wound, which is left
to heal by second intention and will generally take longer to heal than
a sutured wound.
The traditional approach to this type of wound is to apply an oint­
ment followed by two or more layers of dressing. Many dermatologists
prefer Polysporin (Pfizer, Inc, New York, NY) or Bacitracin (Fougera
and Co, Melville, NY) ointments, and avoid neomycin-containing
ointments because of their well-established increased potential for
causing contact dermatitis.60 However, randomized controlled trials
have shown that white petrolatum is as safe and effective as Bacitracin
with less risk for inducing allergy.61
After the ointment layer, the contact layer, which directly touches
the wound, is applied. It is usually composed of non-adherent pads
such as Telfa and Adaptic, which do not disturb forming granulation

482
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
ulcers of the leg is 30–40 mmHg.67 The most effective way of deliver­
ing compression remains controversial. The advantages and disadvan­
tages of different compression systems are shown in Table 32.4.
Compression stockings
Some patients find it difficult to put on compression stockings, espe­
cially those who are elderly and have arthritis. Some types have silk
liners, which allow them to slide onto the leg more easily, while others
have a zipper to make them easier to put on and remove.
Compression bandages
Elastic bandages
Various types of elastic bandages are available. One of the more famil­
iar ones is the ACE type, which has the advantage of being reusable.
Its primary disadvantage is that because it is not self-adherent, it often
unravels. Also if improperly applied by the patient, it does not achieve
the correct level of compression.
Compression bandages
Compression bandages should be applied evenly from right above the
toes to just below the knee. A useful guide for instructing caregivers
about how to apply the appropriate tension to elastic compression
bandages is to use a bandage with a rectangle drawn on it – Setopress
or Surepress (ConvaTec). This rectangle turns into a square when the
bandage is stretched to the correct tension. It should be applied in a
spiral with 50% overlap between turns to produce a double-layer
bandaging effect and provide sustained pressures.67
Unna Boot
The Unna Boot is a semirigid paste bandage that is applied by a physi­
cian or nurse with the foot at a 90° angle (Fig. 32.11). It should be
relieve pain. The choice of dressing depends on the type of wound
and its characteristics.
Options for the treatment of partial- and full-thickness burns are
biologic and biosynthetic skin grafts and skin substitutes such as
STSGs, FTSGs, cultured epidermal autografts,33 Alloderm,34 Integra,44
Transcyte,45 and Apligraf.52
Chronic wounds
For chronic wounds, it is essential to define and treat the underlying
cause. The most common causes such as venous insufficiency, arterial
insufficiency, diabetic neuropathy, and pressure necrosis are consid­
ered first.53 When these are ruled out or unlikely, less common causes
such as vasculitis, pyoderma gangrenosum, malignancy, and infection
are to be taken into account. Determining the etiology of the wound
is a key component in deciding how to approach treatment of the
wound as well as the underlying condition. Treatment of the most
common types of chronic wounds is briefly discussed below.
Venous ulcers
Venous ulcers are the most common form of leg ulcers.58 The corner­
stone of treatment comprises compression, edema reduction, and
improvement of venous return. This can be achieved by bed rest, leg
elevation, and the use of compression devices, such as elastic support
stockings, elastic bandages, nonelastic bandages such as Unna’s Boots,
and pneumatic compression pumps.
To improve abnormal venous return, patients are advised to elevate
the affected leg 18 cm above the level of the heart or ‘toes higher than
the nose’ for 2–4 h during the day, as well as the night.67 Before com­
pression is applied to the limb, occlusive arterial disease should be
ruled out, and the ulcer base should be clean and uninfected. Com­
pression should be applied on arising from bed and removed at
bedtime. The recommended ankle pressure in patients with venous
Table 32.4  Types of compression therapy
Type
Advantages
Disadvantages
Elastic wrap
Inexpensive, can be reused
Often applied incorrectly by the patient, tends to
unravel, does not maintain sustained
compression, loses elasticity after washing
Self-adherent
wraps
Self-adherent, maintains compression
Expensive, cannot be reused
Unna Boot
Comfortable, protects against trauma, full maintenance of ambulatory
outpatient status, minimal interference with regular activities, substitute for
a failing pump
Pressure changes over time, needs to be applied
by trained physician or nurse, does not
accommodate highly exudative wounds
Four-layer
bandage
Comfortable, can be left in place for 7 days, protects against trauma,
maintains a constant pressure for 7 days due to the overlap and elasticity
of the bandages, used for highly exudative wounds
Needs to be applied by well-trained physician or
nurse
Graduated
compression
stocking
Reduces the ambulatory venous pressure, increases the venous refilling
time, improves calf pump function, different types of stocking
accommodate different types of leg, dressings underneath can be changed
frequently
Often cannot monitor patient compliance,
difficult to put on
Orthotic device
Adjustable compression, sustained pressure, easily put on and removed,
comfortable
Expensive, bulky appearance
Compression
pump
Augments venous return, improves hemodynamics and microvascular
functions, enhances fibrinolytic activity, prevents postoperative
thromboembolic complications in high-risk patients
Expensive, requires immobility for a few hours/
day
Adapted with permission from Blackwell Publishing Ltd, from Phillips, T.J., 2001. Current approaches to venous ulcers and compression. Dermatol Surg 27, 611–621.

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compression therapy alone.20 However, these dressings are beneficial
in that they relieve pain, reduce the infection rate, and enhance auto­
lytic debridement and granulation tissue formation.68
Larger venous ulcers may require the use of skin grafts or skin sub­
stitutes. Meshing of STSGs is helpful for venous ulcers because it
allows drainage of wound fluid without disturbing the adherence of
the graft to the wound bed. Another treatment option for persistent
venous ulcers is shave therapy. This involves the excision of ulcers with
the surrounding lipodermatosclerotic tissue and covering the wounds
with meshed split skin grafts. Healing rates of 79% of 59 patients after
3 months, and 88% of 18 patients after an average of 2 years after
shave therapy were observed.69
Apligraf is FDA-approved for the treatment of venous ulcers, and in
combination with compression therapy has been shown to be signifi­
cantly better at healing ulcers secondary to venous insufficiency com­
pared with compression alone. It is especially helpful in treating
venous ulcers of >6 months duration.49
Arterial ulcers
Management of arterial ulcers requires surgical re-establishment of an
adequate vascular supply whenever possible. Diabetes mellitus, ciga­
rette smoking, hypertension, and hyperlipidemia should be control­
led. Moderate exercise may promote development of collateral
circulation, and elevation of the head of the bed 10–15 cm (4–6 in)
improves gravity-dependent arterial flow.70 Limbs should be kept
warm. Patients should observe good foot care. General principles for
proper wound care as well as choice of dressings are observed for
arterial ulcers.
Diabetic foot ulcers
Good diabetic foot ulcer care starts with a thorough assessment of
the ulcer, including determining whether neuropathy or peripheral
vascular disease is present. The principles of good wound care include
use of proper footwear and the correct antibiotics when needed,
avoidance of weight-bearing, pressure-relieving aids, debridement as
necessary, aggressive revascularization, and control of the serum
glucose levels.71
There is a remarkable lack of consensus over dressing choice for the
diabetic foot ulcer.72 The principle of moist healing does still apply,
but it has been questioned whether this philosophy applies to all
diabetic wounds.73 The ideal dressing should protect the wound space
replaced weekly, or more frequently if heavy drainage is present. Some
physicians theorize that the rigid compression is beneficial in that it
makes the calf muscles press against the rigid bandage when the
patient walks, ensuring the pumping effect of the calf muscles. Other
physicians feel that the rigidity is disadvantageous in that the bandage
fails to accommodate changing leg volume during fluctuations in
edema. The Unna Boot can also cause an unpleasant odor, which
develops from the wound exudates and has the potential for causing
contact dermatitis.
Four-layer bandage
The four-layer compression bandage has been proposed to be the
optimal device for achieving compression. It is more flexible and
absorbent than the Unna Boot, and is capable of maintaining evenly
distributed pressure throughout the affected limb for long periods of
time. From innermost to outermost, its four layers consist of an ortho­
pedic wool layer, a crepe layer, an elastic layer applied in a figure of
eight pattern, and an elastic layer applied in a spiral pattern.
Orthotic device
A legging orthosis with Velcro tape is an adjustable device that can
be loosened and tightened as needed to adjust to changes in leg cir­
cumference (Fig. 32.12). It is useful in patients who cannot tolerate
other compression modalities or who require frequent dressing
changes.
Pneumatic compression
For patients who are unresponsive to conventional compression
bandages or stockings, home compression pumps may be used. They
were developed for the prophylaxis of deep venous thrombosis, and
should be considered when a venous ulcer does not respond to stand­
ard compression therapy. They can be rented or bought for outpatient
use. They are contraindicated in patients with uncontrolled congestive
heart failure, during episodes of inflammatory phlebitis, or when
increased venous or lymphatic return is undesirable.
Wound dressings
Moisture retentive dressings combined with compression therapy may
produce more rapid healing rates initially, but long-term follow-up
has failed to demonstrate any statistically significant advantage over
Figure 32.11  Unna Boot application. The boot is applied with the foot
at a 90° angle, starting just above the toes, in a figure-of-8 manner
around the ankle, and up to the knee in a spiral fashion with 50%
overlap. A layer of self-adherent elastic bandage is frequently wrapped
around it.
Figure 32.12  A legging orthosis using Velcro tape.

484
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
proper dressing (e.g. alginates and foams for heavily exuding
wounds)
•
Control pain: avoid trauma to site; use moisture-retentive
dressings (especially hydrogels); oral analgesics (e.g.
acetaminophen); apply EMLA (Astra-Zeneca Pharmaceuticals,
Wilmington, DE) for 30–45 min before debridement
•
Prevent maceration: apply zinc oxide paste on the periwound
area (Fig. 32.14); do not leave dressings on for prolonged
periods of time
•
Minimize odor: apply Metrogel (Galderma Laboratories, Inc, Fort
Worth, TX); use odor-absorbing dressings, e.g. Actisorb Plus
(Johnson & Johnson Medical); Lyofoam C (ConvaTec);
Carboflex (ConvaTec)
•
Remove necrotic tissue: perform debridement, mechanical (Fig.
32.15), autolytic, enzymatic, or biologic; irrigate under pressure
during cleansing
•
Ensure patient compliance: instruct the patient and caregiver
thoroughly with regular follow-up visits
•
Check intrinsic factors: address any underlying systemic
conditions (e.g. venous or arterial disease, hypertension,
psychological stress, debility, immunocompromised state);
ensure proper nutrition (especially protein)
•
Keep wound moist, but not wet: use dressings of appropriate
absorbency (e.g. alginates for highly exuding wounds).
It is always easier to avoid complications than to treat them.
Pitfalls in postoperative care and the use of dressings
and their management
•
Infection: use topical and systemic antibiotics as needed;
practice clean or aseptic techniques for dressing wounds;
from secondary contamination, maintain a moist environment,
remove exudates, be able to be removed without trauma to the wound,
and resist the stresses of standing and walking.
Topical antibiotics keep the surface bacterial colony count low while
providing a moist environment in which healing may occur. Saline-
moistened gauze also provides a moist wound environment. Occlu­
sive dressings such as hydrogels, hydrocolloids, and polymers play a
big role in the treatment of diabetic ulcers.71 In addition to the tradi­
tional occlusive dressings, the latest state-of-the-art biosynthetic dress­
ings Dermagraft46 and Apligraf49 have likewise been shown to be
effective in the treatment of these ulcers, and have been approved for
this use by the FDA. Bilayered cellular matrix (BCM; Ortec Interna­
tional Inc) has also shown promise in the treatment of diabetic ulcers,
but is not yet FDA approved for this indication.74
The total contact cast is commonly used in the USA, but requires
skilled application and close follow-up.72
Pressure ulcers
The most important aspect of treatment of pressure ulcers is tissue
load management.75 This refers to specific interventions designed to
decrease the magnitude of pressure, friction, and shear on the tissue.
The goal is to create an environment that enhances soft tissue viability
and promotes healing of the pressure ulcers, and can be met through
vigilant use of proper positioning techniques and support surfaces,
whether the individual is in bed or sitting on a chair.75
Management also involves addressing factors such as nutrition,
immobility, and comorbid disease, and protection from fecal or urine
soiling.76 Nutrition is very important in preventing and healing pres­
sure ulcers, especially an adequate protein content in the diet. Incon­
tinence contributes significantly to the development of pressure sores
because constant exposure of skin to urine and stool leads to macera­
tion, weakening of the tissue, and eventual breakdown. Containment
devices and skin-protective barriers are useful in counteracting mois­
ture from incontinence.
Wound care of the pressure ulcer involves debridement of devital­
ized tissue, wound cleansing, application of dressings, and possible
adjunctive therapy with electrical stimulation for Stage III and IV
unresponsive ulcers. These are full-thickness ulcers that may extend to
the subcutaneous tissue (Stage III) or to muscle and bone (Stage IV).75
Normal saline is the preferred cleansing agent. In the selection of
dressings, the cardinal rule is to choose a dressing that will keep the
ulcer tissue moist and the surrounding intact skin dry.75 Studies com­
paring different types of moist wound dressings showed no differences
in pressure ulcer healing outcomes;75 however, sequential dressing
therapy using alginates followed by hydrocolloids showed signifi­
cantly faster healing (p<0.001) in Stage III and IV ulcers compared
with hydrocolloid alone.77 Foams or wound fillers may be adjunctively
used to eliminate dead space in deep ulcers.76 Dressings applied on
the plantar foot should be given special attention because they are
difficult to keep intact. Picture-framing or taping the edges of the
dressing may reduce this problem.75
PITFALLS AND THEIR MANAGEMENT
Optimizing outcomes
Ways to optimize results in wound care
•
Avoid leakage: provide adequate margins of dressing around
wound edges (Fig. 32.13); vary frequency of dressing changes
as needed; increase thickness of absorptive layer; select
Figure 32.13  Leakage through a foam dressing applied on the ankle
occurs because of an inadequate inferior margin.

Chapter
Dressings and postoperative care
485
| 32 |
irrigate under pressure or debride to remove necrotic tissue
(Fig. 32.16)
•
Contact dermatitis (Fig. 32.17): switch to another type of
dressing, adhesive, or topical ointment or antibiotic; apply zinc
oxide or other lubricating protectants to periwound area; apply
low-potency topical corticosteroids
•
Seroma formation: aspirate with a large-bore needle; puncture
with a lancet
•
Excessive pressure from dressing: loosen dressing
•
Excessive granulation tissue: apply pressure; change dressing type;
pare with curette; cautery with silver nitrate
•
Pigmentary alteration: may be left alone (improves with time)
•
Milia or suture granuloma: usually resolve spontaneously, may be
left alone.
PRACTICAL APPLICATIONS
In general, once the underlying cause of a wound has been addressed
along with any conditions that may impair healing, wounds have rela­
tively straightforward requirements. Specific needs may be determined
by the physical characteristics of the wound, including its size, shape,
location, depth, phase of healing, tissue type and quantity, condition
of the skin surrounding it, and bacterial and exudate levels. Dressing
functions to be considered are absorptive capacity, hydrating capacity,
adhesive quality, debriding capabilities, conformability, and odor
control ability (Table 32.5).78
No single dressing can provide all things to all wounds, especially
because most wounds have a variety of needs. This leaves clinicians
Figure 32.14  Zinc oxide paste is applied on the periwound area to
function as a protectant and minimize maceration.
Figure 32.15  Surgical debridement using a curette to remove necrotic
tissue and debris from the ulcer bed.
Figure 32.16  Necrotic tissue such as eschar is an optimal substrate for
microbial growth which may lead to local and systemic infection.
Figure 32.17  Typical appearance of contact dermatitis on the periwound
area. Note the erythema.

486
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
SUMMARY
This chapter presents an extensive discussion of the different types of
dressings currently available, including their advantages, disadvan­
tages, and indications. From simple gauze dressings, advances in tech­
nology have led to the development of complex biosynthetic dressings,
which closely approximate the structure and function of natural skin.
From the belief that wounds heal best when kept dry and exposed to
air, it has been established that acute wounds undoubtedly heal best
in a moist environment.
This chapter also reviews the technical aspects for applying some
types of dressings as well as specific dressings for venous ulcers. The
importance of postoperative care cannot be stressed enough. It may
make the difference between patient and doctor satisfaction and dis­
satisfaction. Once the surgical procedure is completed, a careful selec­
tion of dressings, close monitoring of the phases of healing, and
prompt and correct management of complications all come into play.
It is useful to remember that postoperative complications are always
easier to prevent than to treat.
Table 32.5  Dressing materials and relative performance
Dressing
material
Absorption
ability
Adhesive
quality
Conformability
level
Hydration/
debridement
Odor control
ability
Clinical
applications
Film
None
Fully adhesive
Conformable to
surface anatomy
Will hydrate
slowly
None
Superficial, lightly
exuding wounds, as
a secondary dressing
Hydrogel
Low
Non-adhesive or
adhesive borders
Conformable to
surface anatomy
Will hydrate
moderately
None
Superficial, light to
moderately exuding
wounds, painful
wounds
Hydrocolloid
Low to
moderate
Fully adhesive
surface
Conformable to
surface anatomy
Will hydrate
moderately to
quickly
depending on
water content
May exacerbate
odor (without
ill-effect)
Superficial light to
moderately exuding
wounds
Foam
High
Non-adhesive,
fully adhesive
surface, adhesive
borders
Some versions
conformable to
cavities
Not hydrating
Slight, due to
absorption only,
some versions
contain charcoal for
active control
Superficial to deep,
moderately to heavily
exuding wounds
Alginate
High
Non-adhesive
Conformable to
cavities
Not hydrating
Anecdotal evidence
for minor effect,
charcoal version
exists
Superficial to deep,
moderately to highly
exuding wounds
Contact layer
None
Non-adhesive
Conformable to
surface anatomy
Slightly
hydrating,
depending on
cover dressing
None
Superficial wounds
of any exudate level
Adapted from Ovington, L.G., 2001. Wound dressings: their evolution and use. In: Falanga, V. (Ed.), Cutaneous wound healing. Martin Dunitz Ltd, London.
to weigh the pros and cons of possible dressing choices, and to make
the decision about which they think is the most appropriate. As the
patient’s wound progresses, several different categories of dressing
may be necessary during the wound-healing process to address the
changing wound parameters.
Cost vs cost-effectiveness
A prevalent misconception is that the use of occlusive dressings is too
costly in comparison with traditional materials like gauze. However,
the cost of wound care is not simply the cost of the dressing material,
but the labor cost (especially if a healthcare professional is required),
the indirect costs of ancillary supplies (e.g. gloves, biohazardous waste
disposal), and the duration of care.78 Some studies have shown that a
more expensive dressing that requires less frequent changes is actually
less expensive to use than a cheaper dressing that requires more fre­
quent changes.78 Not only do occlusive dressings require fewer
changes, they also shorten the healing time and provide superior
protection, so shortening the total duration of treatment and reducing
expenses from possible complications such as infection.
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Index
Note: page numbers followed by ‘f’ indicate
figures.
A
A–T closure, 119–121, 121f–122f
Abductor digiti minimi (ADM) muscle flap,
275, 275f, 278f–279f
Abductor hallucis brevis (AHB) muscle flap,
276, 279f–282f
Achilles tendon
exposed, vacuum therapy, 416, 418f
reconstruction, 258f
Acrylate tissue adhesives, 71, 83–85
Activated partial thromboplastin time (APTT),
70
Acute wounds, 415
bioengineered skin grafts, 465
functions of dressings, 472
negative pressure wound therapy, 414–415,
416t
postoperative care, 56, 481
Adductovarus deformity of toes, 322–323,
325f
skin wedge procedure, 329, 329f
Adhesive tape strips, 81–82, 81f–82f
see also Steri-Strips
Adipocytes, 9
Adipose tissue, subcutaneous, 9–10
Adnexa, epidermal, 8
Adrenaline see Epinephrine
Adson tissue forceps, 32
Advancement flaps, 144, 177–189
double, 179–180, 180f
pantographic expansion, 179, 179f
single, 177–179, 178f–179f
types, 177
Alcohol injections, 358, 358f
fibromas, 363, 364f
hypertrophic and keloid scars, 394–395,
397f
Alcohol solutions
hand scrubbing, 60
surgical site preparation, 62, 129
Alginate dressings, 383, 383t, 474t, 476–477,
476f
leg ulcers, 458t
relative performance, 486t
Allergic reactions
history taking, 2–3
leg ulcers, 453
local anesthetics, 46
topical antibiotics, 440
vacuum therapy, 431
AlloDerm®, 228b, 479
Allografts
cultured epidermal, 227, 478–479
defined, 207, 225
skin, 226–227, 477
storage, 220
Aluminium chloride hexahydrate, 72–73,
72f
Alvarado bowtie closure, 121–123, 123f–124f
Alvarado combined-V closure, 123, 124f–125f
Alvarado double-S see S-plasty
Amputations, partial-foot, 231–242
comorbidities, 233, 233b
principles of closure, 232–234, 234f
skin grafts, 213f, 216f, 221f
soft tissue reconstruction, 232–242
treatment of infection, 233
vascular assessment, 233
without tourniquets, 71
see also Toe amputations; specific amputations
Anaphylaxis, 444
Anatomy
cutaneous, 7–10, 208–209, 208f
vascular see Vascular anatomy
Anemia, 103, 233–234
Anesthesia, 45–51
Angiogenesis, 101–102, 452, 472
see also Revascularization
Angioleioma, digital, 310–311, 310f
Angiosomes, 10, 13–16, 14t, 144–147,
270–271
anastomoses between, 17, 19f, 147, 271
anterior tibial artery, 14t, 15–16, 145–147,
146f, 270
compromised blood supply, 17–18
evaluation of source artery flow, 18
flap design, 147–148, 148f
incision planning, 18, 19f
partial-foot amputations, 232
peroneal artery, 14t, 16, 145, 146f, 147
posterior tibial artery, 14–15, 14f, 14t,
145–146, 145f
489
Index
Angiotome, 144–145
Ankle-brachial index (ABI), 211, 453, 455f
Ankle tourniquets, 70–71
Anterior medial malleolar artery, 14
Anterior perforating peroneal angiosome, 14t,
16, 147
Anterior tibial artery, 15, 270
angiosomes, 14t, 15–16, 145–147, 146f, 270
Anterolateral thigh (ALT) flap, 256–257
Antibiotics (antimicrobials)
inhibition of wound healing, 104
leg ulcers, 457–458
postoperative infections, 441–443
prophylactic, 53, 442
resistance, 457
topical, surgical site, 382, 481
Anticoagulants
impaired wound healing, 104
microsurgical free flaps, 253
monitoring of therapy, 70
perioperative discontinuation, 436
Antifungal therapy, preemptive, 128
Antimicrobial dressings, 480
Antimicrobials see Antibiotics
Antiphospholipid syndrome, 451
Antisepsis, defined, 54
Antiseptics
leg ulcers, 457
surgical hand scrubbing, 59–60
surgical site preparation, 62
surgical wounds, 382–383
Antithrombotic agents, 436
Apical sutures, 91, 95f
Apligraf® see Graftskin
Apocrine glands, 8, 209
Appendages, epidermal, 8
Arterial ulcers, 449–450, 450f
clinical features, 452–453, 454t
diagnostic assessment, 453, 454f
management, 484
prevention, 455
see also Peripheral vascular disease
Arterial–arterial connections, 17, 19f, 147,
271
Artery forceps, 36, 37f
Arthrodesis, flexor tendon transfer with, 330
Arthroplasty, digital, 330, 332f–333f
flexor tendon transfer with, 330, 334f

490
Index
Blisters (bullae)
fracture and postoperative, 440, 441f
skin graft recipient sites, 463
Blood vessels
anatomy see Vascular anatomy
damage during microsurgery, 252–253, 252f
injury, hemostasis, 69, 436
ligation, 70
Bolster dressings, 384, 386f
negative pressure wound therapy, 422–423
Bone
exposed, vacuum therapy, 416–421,
420f–422f
fixation, 265
Bone-cutting forceps, 38
Bone flaps, vascularized, 259–262
Bone forceps, rongeur, 38, 39f
Bone grafts, negative pressure wound therapy,
417, 423f
Bone rasps, 38, 39f
Bone wax, 71, 71f
Bouché distal wedge resection, 297, 299f
Bovine collagen microfibrillar hemostat, 73–74
Bowtie closure (Alvarado), 121–123,
123f–124f
Braided polyester sutures, 79t
Bridging technique, negative pressure wound
therapy, 425–428, 426f–430f
Brown–Adson tissue forceps, 32, 33f
Bullae see Blisters
Bunnell stitch, modified, 93f
Bupivacaine, 45–46, 46t
Burns, wound care, 483
Bürow’s triangles (or wedges), 92, 97f
advancement flap, 177–178, 178f–179f
rotational flap, 181, 182f
Bursa, 359, 359f–361f
Buttress sutures, 402, 406f
C
Cadexomer iodine, 480
Calcaneal fractures, extensile lateral approach,
18, 19f
Calcaneal wounds, negative pressure therapy,
419–421, 422f–424f
Calcanectomy, partial, 240–242, 242f–245f
Calluses see Helomata
Cameras, digital, 106–108
accessories, 108, 108f
focal length, 106, 107f
image collection and transfer, 107, 108f
lighting sources, 108, 109f
macro capability, 106, 109
optical and digital zoom, 107
resolution, 107–108, 107b
Campbell de Morgan spots, 313–314, 317f
Capillarity, suture materials, 78
Caps, surgical, 57, 58f
Cardiac arrest, 444
Cardiovascular disease, partial-foot
amputations, 233
Catanzariti–Wehman rotation flap, 181–183,
182f
CEAP classification, venous disease, 465, 465t
Cefazolin, 442
Cellulose, oxidized, 73, 73f
Asepsis, 53–65
defined, 53–54
postoperative incision management, 56
preoperative preparation, 59–65
techniques, 58–65
Aspiration, fluid-filled lesions, 358, 358f
Aspirin, 436, 456
Atrophie blanche, 451
Autoclaves, 57
Autografts, 477
cultured epidermal, 227, 478
defined, 220, 225
skin, 225–226, 226f
storage, 220
Autonomic nerves, dermal, 9
Autonomic neuropathy, 233
Avitene, 73–74
Axial pattern flap, 143, 144f
B
Bacteria
leg ulcers, 457–459
negative pressure wound therapy, 412,
414
under occlusive dressings, 381
postoperative wound infections, 442
skin graft recipient bed, 212–213, 220
see also Microorganisms; Wound (or
incision) contamination
Bandage scissors, 33, 35f
Bard–Parker scalpel handles, 30, 30f
Basal cell layer, 7
Basement membrane, 9
Beak plasty (lazy-S Z-plasty), 167–170,
169f–170f
Beaver scalpel mini-handle, 31f
Benign soft tissue masses, 357–380
Bier block, 50
Bilayer matrix wound dressing, 227–229, 228f,
480
Biobrane, 383t, 479
Bioengineered skin equivalents see Skin
substitutes
Biofilms, 459
Biomechanics
skin flaps, 195
skin grafting, 211, 220
BiopBlade™, 130–132, 131f
Biopsy, 127–140
indications, 128
leg ulcers, 128, 453
local anesthesia, 129, 129f
nail and periungual, 291–296, 292f–296f
pathology, 127–128, 138–140
patient preparation, 128–129
selection of technique, 129–130
techniques, 130–138
see also Excisional biopsy; Incisional biopsy;
specific techniques
Bipedicle random flap, 143
Bleeding, 436–437
control of see Hemostasis
negative pressure dressing changes,
429–430
see also Hematomas, postoperative
Bleeding time, 70
Central facilitation, 49
Central ray resections, 236, 238f–239f
Charcot neuroarthropathy, 233, 450
Chemotherapy, cancer, 435
Cherry hemangiomas, 313–314, 317f
Chlorhexidine, 60, 62, 129
Chloroprocaine, 45
Choke vessels, 17, 144–145
flap design, 147–148, 148f
Chopart’s disarticulation, 240, 241f
Chronic venous insufficiency (CVI), 449, 453
subfascial endoscopic perforator surgery,
465–466
see also Venous ulcers
Chronic wounds, 415, 448
debridement, 458–461, 458f
functions of dressings, 472–473
management, 483–486
negative pressure therapy, 414–415, 416t
see also Ulcers, leg
Clawtoe deformity, 322, 324f–325f
Clindamycin, 442
Clothing, operating room, 57–58, 57f
Clotting see Coagulation
Clubbing deformity, distal
after nail avulsion, 290, 291f
skin plasty for, 297, 298f–299f
Coagulation
cascade, 69, 70f
disorders, 436–437
testing, 69–70
Cocaine, 45
Collagen, 9
dressings, 477
wound healing, 78, 102, 452
Collagenase, topical, 460–461
Combined-V closure (Alvarado), 123,
124f–125f
Common peroneal nerve block, 46, 47f
Communication, using hand signals, 39,
41f–43f
Compartment syndrome, negative pressure
wound therapy, 422
Complications, surgical, 435–444
life-threatening, 443–444
principles of managing, 444, 444f
risk factors, 435
see also specific complications
Composite grafts, 477
Composite skin substitutes, 227–229, 480
Composite tissue allo-transplantation (CTA),
265–266
Compression bandages, 456, 483, 483t
Compression pumps, pneumatic, 483t,
482–483
Compression stockings, graduated, 455–456,
456t, 482, 482t
Compression therapy, venous ulcers, 450f,
456, 482–483
Compressive dressings, 71
materials, 384, 384f–386f
scar prevention, 400, 406f–407f
Computed tomography (CT), 109, 357–358
Connective-tissue diseases, 103
Consent, informed, 2
Consent form, 3f–4f
Contact dermatitis, 440, 454t, 485, 485f

491
Index
Contamination
routes of, 54
strike through, 65
wound (or incision) see Wound
contamination
Continuous horizontal sutures, 91–92, 96f
Continuous subcuticular sutures, 91–92, 96f
Continuous sutures, microsurgery, 253
Contour lines, skin, 23
Contraction, skin grafts, 210–211
Contractures
V–Y plasty, 151–152, 153f–154f
Z-plasty, 163, 164f–165f, 165, 329, 332f
Corns see Helomata
Corticosteroid injections, 358, 358f
fibromas, 362–363
mucoid cysts, 314–315, 318f
scars, 394, 396f, 397
Corticosteroids, topical, venous dermatitis,
457
Cosmetic suturing techniques, 91–93
Creep, 195
Crescentic ellipse, 118–119, 120f
Crile artery forceps, 36, 37f
Cross-over second toe, 323, 326f
Crucial stitch, Z-plasty, 166, 167f
Cryotherapy, scars, 397
Cultured epidermal grafts, 227, 464t, 478–480
allogeneic, 227, 478–479
autologous, 227, 478
Cutaneous circulation, 9, 10f, 13, 16–17, 18f,
145f
Cutaneous horn, 311, 311f
D
Dead space, 78
Debridement
autolytic, 460, 472
biosurgical, 460
enzymatic and chemical, 460–461, 462f
free flap recipient bed, 265
leg ulcers, 458–461, 458f
mechanical, 460, 460f
negative pressure wound therapy, 415
partial-foot amputations, 232–233
postoperative, 484
rationale, 459
skin graft recipient bed, 213, 213f–214f
surgical/sharp, 459–460, 460f, 485f
types, 459–461
Decubitus ulcers see Pressure ulcers
Deep buried knot sutures, 89, 93f–94f
Deep buried vertical sutures, 89
Deep fascia
blood circulation, 13, 16–17
suture retention techniques, 89–91
Deep over-and-over suture, modified, 89, 94f
Deep peroneal nerve block, 47, 47f
Degloving injuries, negative pressure wound
therapy, 416t, 423
Dehiscence, wound, 438–440, 438f
incision reclosure after, 403–405, 408f
negative pressure wound therapy, 416t
Delay phenomenon/procedure, 147–148
local muscle flaps, 271
Depilatories, 54
DermaClose® RC continuous tissue expander,
86, 86f–89f
Dermagraft®, 228b, 479, 479f–480f
Dermal neuroma, 311, 311f–312f
Dermal replacements, 227, 228b, 464t, 479
Dermalon sutures, 79t
Dermatitides, biopsy, 128–130
Dermatofibroma, 311–312, 312f
Dermatomes, skin graft harvesting, 212–214,
212f
Dermatopathology, 128, 140
Dermatophyte test medium (DTM), 291
Dermatophytosis, biopsy, 129–130
Dermis, 9, 208–209
Desiccation, wound, 103
Desyndactylization, digital, 339–344
fusiform graft, 219f, 344, 347f–349f
rectangular flap, 340–344, 344f–345f
Z-flap, 344, 346f
Dexon® (polyglycolic acid), 78, 79t
Diabetes mellitus
comorbidities, 233–234, 233b
flexor hallucis longus transfer, 234, 235f
local muscle flaps, 278f, 286f
microsurgical free flaps, 255, 260f–261f
negative pressure wound therapy, 414–415,
417f–419f, 421–422, 425f, 430f
partial-foot amputations, 231–232
risk of complications, 435
skin grafts, 211
vascular assessment, 233
wound healing, 103
Diabetic foot ulcers, 450, 450f
clinical features, 454t
management, 484
prevention, 455–456
Digital arteries, 289–290
Digital photography see Photography, digital
Digits see Toe(s)
Digitus abductus, 323, 326f
Digitus adductus see Adductovarus deformity
of toes
Disinfectants, chemical, 57
Disinfection
instrument, 57
skin, 62
Dissecting scissors, 33, 34f
Distal digital amputation see Terminal Syme
operation
Distant flaps, 144
Dog-ear deformity
deep to superficial, oblique half-buried
stitch, 91, 95f
repair methods, 92–93, 96f–98f
W-plasty, 174, 174f
Doppler sonography, 18, 147
free flaps, 265
local muscle flap dissection, 280–285
Dorsal foot, free flaps, 256–257, 257f,
263f–264f
Dorsalis pedis angiosome, 14t, 15–16, 17f,
146–147
Dorsalis pedis artery, 15, 270–271
Double advancement flap, 179–180, 180f
Double elliptical excision see Crescentic ellipse
Double-lobed rotation flap, 183–189,
189f–192f
Double opposing semicircular flap, 172,
172f–173f
Double opposing Z-plasty, 171–172, 172f
Double rhomboid transpositional flap, 200,
201f
Double-Z rhomboid flap, 173, 173f
Drains, wound, 103, 402, 406f, 437f
Drapes, sterile, 5, 55, 63–65, 67f
Drawings, preoperative, 2, 5f
Dressings, 381–386, 471–472
absorbent layer, 383, 384f, 473
acute surgical wounds, 481
antimicrobial, 480
biologic/biosynthetic, 477–480
compressive see Compressive dressings
cost vs cost-effectiveness, 486
functions, 472–473, 472t
handling/changing, 55, 65
historical perspective, 472
leakage through, 484, 484f
leg ulcers, 457–458, 458t
negative pressure see Negative pressure
wound therapy
non-adherent, 381–383, 382f, 473
occlusive see Occlusive dressings
pitfalls and their management, 484
practical applications, 485, 486t
pressure ulcers, 484
scar prevention, 400
skin graft donor sites, 218–220
skin grafts, 216–218, 218f, 384, 385f, 463
traditional, 382–384
types, 473–480, 473b
venous ulcers, 473, 484
Dufourmentel flap, 199, 201f
DuVries plasty, hypertrophied nail lip, 297,
297f
E
Eccrine glands, 8, 209
Edema, postoperative, 440, 440f
prevention, 400, 406f–407f, 440
treatment, 440
Elastic compression bandages, 456, 456t, 482,
482t
Elastic fibers, 9
Elasticity
suture materials, 78
tissue, 189
Electrical stimulator, regional nerve blocks, 49,
50f
Electrocautery, 71–72, 72f
Electrocoagulation, 71–72, 72f
Electrosection, 71–72
Elevators, tissue and periosteal, 38, 39f
Elliptical excisions see Crescentic ellipse;
Fusiform ellipse
Emla, 46
End-to-end technique, microvascular
anastomosis, 253, 254f
End-to-side technique, microvascular
anastomosis, 253
Epidermal–dermal junction, 9
Epidermal grafts, cultured see Cultured
epidermal grafts
Epidermal growth factor (EGF), 459, 472

492
Index
Epidermal inclusion cyst, 359–361, 361f
direction incisional technique, 359–361,
362f
fusiform excision, 361, 362f–364f
Epidermis, 7–8, 208
Epidural block, 49
Epinephrine
biopsy procedures, 129
hemostatic properties, 73, 436–437
local anesthesia, 45–46, 46t
local toe blocks, 296
Equipment
digital photography, 106–108
microsurgery, 249–252
sterilization, 57
Eschar, 381, 382f, 485f
Ethibond sutures, 79t
Ethilon sutures, 79t
Etidocaine, 45
Excisional biopsy, 127
elliptical incisions, 136, 138f–139f
M-plasty, 116
patient preparation, 129
potentially malignant lesions, 128, 130
punch biopsy, 133
Excisions, 113–123
benign soft tissue masses, 358–375
crescentic ellipse, 118–119, 120f
M-plasty, 116–118, 117f–118f
postoperative care, 481
reciprocal approaches and variations,
119–123
S-plasty (Alvarado), 118, 118f–120f
simple (fusiform ellipse), 113–116, 114f
Exostosis
interphalangeal joint, 318, 323f
subungual see Subungual exostosis
Expectations, patient, 5
Extensile lateral approach, calcaneal fractures,
18, 19f
Extensor digitorum brevis (EDB) muscle flap,
279–280, 286f–287f
Extensor digitorum longus and peroneus
tertius muscle flap, 272f, 274
Extensor digitorum longus tendon
lengthening, 324–325, 328f
Extensor digitorum longus tenotomy, 323,
326f
Extensor hallucis longus muscle flap, 272f,
275
Eye protection, surgical staff, 58, 58f
EZ Derm, 479
F
Facemasks, surgical staff, 57–58, 58f–59f
Factor VII, activated (FVIIa), 69
Factor X, activated (FXa), 69
Fascia
deep see Deep fascia
exposed, negative pressure therapy, 416
Fasciocutaneous flaps, 144
free transfer, 256–257
revision, 265
Fasciotomy, negative pressure wound therapy,
416t, 422
Fat, subcutaneous, 9–10
Fibrin, 436
Fibrin sealant and glues, 74
Fibroblast growth factor (FGF), 101, 451f, 459,
472
Fibroblasts, 9
chronic wounds, 459
composite grafts, 227
cultured autologous, 227
wound healing, 77–78, 101–102
Fibrokeratoma, acquired digital, 309, 310f
Fibromas, 362–364, 364f
injection therapy, 362–363, 364f
surgical excision, 363–364, 365f–368f
Fibronectin, 101–102, 452
Fibula flaps, vascularized, 259–262
Fifth ray resections, 236–238, 240f
Figure-of-eight suture, 89, 94f
Filaggrin, 7–8
Fillet flaps, toe, 234–235, 236f
Film dressings, 383t, 474–475, 474t, 475f
leg ulcers, 458t
relative performance, 486t
First ray resections, 235–236, 237f
Fitzpatrick dimple sign, 311–312
Flail toe, 339, 340f
Flaps, 143–149
assessing viability, 148–149
biomechanical aspects, 195
classification, 143–144, 151
design, 147–148
failure and survival factors, 148–149
grafts vs, 143, 225
medicinal leeches, 74
necrosis, 438–439, 439f
negative pressure wound therapy, 414
use of tourniquets, 71
vascular anatomy, 144
see also specific types
Flexor digiti minimi muscle flap, 277–278
Flexor digitorum brevis muscle flap, 277,
282f–285f
Flexor digitorum longus muscle flap, 272f
Flexor digitorum longus tenotomy, 323,
327f
Flexor tendon transfers, 327, 328f
arthroplasty or arthrodesis with, 330,
334f
contracted great toe, 234, 235f
FloSeal, 74
Fluid-filled lesions, aspiration, 358, 358f
5-Fluorouracil, intralesional injections, 396
Foam dressings, 383t, 473–474, 474f, 474t
leg ulcers, 458t
negative pressure wound therapy, 412–413,
413f
relative performance, 486t
technique of use, 474
Foot covers, surgical staff, 58, 59f
Forceps
artery, 36, 37f
bone-cutting, 38
microsurgery, 250–251, 250f
rongeur bone, 38, 39f
tissue-handling, 32, 32f–33f
Four-layer compression bandage, 456, 456t,
483
Four-point corner stitch, 91, 95f
FRAIL concept, 452
Frazier skin hook, 35–36
Free flaps, microsurgical, 143–144, 144f
basic science concepts, 252–253, 252f
failure, 256
future trends, 265–266
histological changes after surgery, 262–263,
264f
history, 252
microscope and microinstrumentation,
249–252, 250f
patient factors, 255–256
postoperative regimen, 265
revising, 265
selection, 144, 256–263
technical factors, 253–255, 254f
vascular, orthopedic and podiatric surgery
and, 263–265
Freer skin hook, 35–36
Frost partial matrixectomy, 298, 301f
Full-thickness skin grafts (FTSG), 207,
217–220, 219f, 225, 461, 477
anatomical basis, 208–209, 208f
contraction, 210–211
donor site healing, 218–220
donor site locations, 218
dressing, 218
harvesting, 218
healing, 209–210
postoperative care, 218
split-thickness skin grafts vs, 211, 478t
Fusiform ellipse, 113–116, 114f
closure techniques, 115–116, 117f
excisional biopsy, 136, 138f–139f
incision technique, 114–115, 115f–116f
incisional biopsy, 136–138, 139f
scar excision, 398–399, 399f
specimen removal, 115, 117f
G
Ganglion cyst, 364–370, 368f–372f
Gauze dressings, 473
Gelatin sponges, absorbable, 73, 73f
Gelfoam, 73
Geometric broken-line closure (GBLC), 174,
175f, 398–399, 401f
Giant cell tumor of tendon, 374–375,
376f–379f
Girdlestone toe tendon procedure, 327
Glomus tumors, 312, 313f
Gloves, surgical, 60
removing, 61, 62f
without handwashing, 60, 61f
Gloving, sterile, 60–61, 66f
Glucocorticoids, wound healing effects,
103–104
Glycolic acid and trimethylene carbonate
(Maxon®) sutures, 78–79, 79t
Gowning, surgical, 60, 65f
Gracilis muscle flap, 257–259, 260f–261f
Grafts, 225, 477
composite, 227–229, 228f, 477
see also Skin grafts
Graftskin (Apligraf®), 228b, 464, 464t, 480
venous ulcers, 464–465, 465f, 483
GranuFoam™, 412–413, 413f

493
Index
Granulation tissue, 452
excessive, management, 486
exposed bone or orthopedic hardware,
416–417
vacuum therapy, 413–415, 415f
Granulocyte macrophage colony-stimulating
factor (GM-CSF), 457
Great toe see Hallux
Ground substance, 9
Growth factors
acute wounds, 472
chronic wounds, 448, 459
topical therapy, 457
wound healing, 101–102, 451f
H
H-plasty (double advancement flap), 179–180,
180f
Hair follicles, 8
Hair removal, preoperative, 54, 62
Hallux (great toe)
amputations, 234, 353f–355f
innervation, 290
tip ulcers, 234
ungual tuft amputation, 234, 235f
vascular supply, 15, 16f, 147f
webbing procedures, 339, 343f
see also First ray resections
Hallux varus or valgus, 323, 326f
Halsted mosquito hemostat, 36, 37f
Hammertoe deformity, 322, 324f–325f
arthroplasty, 330, 332f–333f
surgical syndactylization, 339, 341f
Hand drying, surgical, 60, 64f
Hand scrubbing, surgical, 59–60, 60f, 62f–64f
Hand signals, 39, 41f–43f
Hansen’s disease, 452–453
Hartman mosquito hemostat, 36
Head cover, surgical staff, 57, 58f
Healing see Wound healing
Heel
amputation, 240–242, 242f–245f
local muscle flaps, 276, 276f–278f, 283f
negative pressure wound therapy, 419–421,
422f–424f
Helomata (corns), 312–313, 313f–314f
surgical syndactylization, 339, 340f
surgical treatment, 314f–317f
Hemangiomas, 313–314, 317f
Hematomas, postoperative, 103, 437, 437f
prevention, 71, 400, 437, 437f
skin grafts, 209, 220
treatment, 437
Hemi-soleus muscle flap, 272
Hemophilia, 436–437
Hemostasis, 69–74
chemical methods, 72–74
laboratory testing, 69–70
mechanical methods, 70–71
physiology, 69, 436
thermal methods, 71–72
Hemostats, mosquito, 36, 37f
Heparin, 70, 104, 253
Herbal medications, 436, 453
Hirudin, 74
History taking, preoperative, 2–3
Hooks, skin, 35–36, 36f
Horizontal mattress suture, 86, 92f
Horizontal nail biopsy, 293–294, 294f
Hyaluronic acid dressings, 477
Hyaluronidase, 296, 362–363
Hydrocolloid dressings, 383, 383t, 474t,
475–476, 475f
leg ulcers, 458t
relative performance, 486t
technique of use, 476
Hydrofiber dressings, 477, 477f
Hydrogel dressings, 383t, 474t, 476, 476f
leg ulcers, 458t
relative performance, 486t
Hydrogen peroxide, 72–73, 213, 481
Hyperbaric oxygen therapy, 425
Hyperpigmented scars, 393, 393f
Hypertrophic scars, 391–392, 391f–392f, 439,
439f
combined treatment, 397
intralesional injections, 394–396,
396f–397f
laser therapy, 398
pressure therapy, 394
silicone gel sheeting therapy, 397–398,
398f–399f, 439, 439f
surgical therapy, 398–399, 398f–399f
Hyponychium, 289
Hypopigmented scars, 393–394, 394f
Hypoxia
improving flap survivability, 148
wound healing and, 77–78, 103
I
Iatrogenic disorders, 54
Iida double transposition flap, 201–202, 202f
Images, digital
from 35-mm slides, 109
collection and transfer, 107, 108f
editing software, 110
medical presentations, 106, 110
publishing, 110
from radiological images, 109
storage formats, 107–108
see also Photography, digital
Imbibition phase, skin grafts, 209, 225
Immunocompromised patients, 103, 435
Immunotolerance, 227
Incision(s)
benign soft tissue masses, 358–359
biased or skived, 26f, 27
classification, 56, 56b
contamination see Wound contamination
digital skin, 308–309, 308f–310f
healing see Wound healing
infections see Surgical site infections
making, 25–27
marking skin see Skin marking
placement, 25–26, 26f, 78
postoperative management, 481
scar prevention, 400, 403f
techniques, 26–27, 26f, 31, 32f, 86, 90f
undermining edges, 86, 90f
Incision planning, 24–25, 78
relaxed skin tension lines, 24, 24f
vascular perspective, 18, 19f
Incisional biopsy, 127, 136–138, 139f
potentially malignant lesions, 128
Infections
leg ulcers, 453, 457
partial-foot amputations, 233
postoperative, 440–443, 441f
skin graft failure, 220
see also Bacteria; Microorganisms; Surgical
infections; Surgical site infections; Wound
(or incision) contamination
Infiltration, local anesthetic, 46–48
Inflammatory conditions
biopsy, 128–130
incisional biopsy, 136–138
Inflammatory phase, 78, 101, 451, 451f
Inflammatory response, postoperative edema,
440
Inflammatory ulcers, 450–451
Informed consent, 2, 3f–4f
Ingrown toenail (onychocryptosis), 290, 291f
partial and total nail avulsions, 297–298
partial matrixectomy, 298, 301f
total matrixectomy, 298
Inosculation, 209–210, 225–226
Instrument stand, 30, 30f
Instruments, surgical, 30–39
aseptic handling techniques, 65
disinfection, 57
microsurgery, 249–252, 250f–251f
sterilization, 57
Integra®, 228b, 479
Interferon-gamma, intralesional scar injection,
395–396
Intermittent claudication, 449–450, 453
Interpolation flaps, 143–144, 204–205, 205f
Interrupted sutures, microsurgery, 253
Intradermal sutures, 91–92, 96f
Intralipid, 46
Intraoperative care
aseptic technique, 65
prevention of infection, 54
Intravenous regional anesthesia, 50
Intravenous sedation, 48
Iodosorb, 480
Ischemia, complicating vacuum therapy, 431,
431f
Island flaps, 143–144, 144f
oblique sigmoid, 161, 161f
see also V–Y island flap
Isograft, 207, 225
Isopropyl alcohol, 129
Isoxsuprine, 148
J
Jamison scissors, 41f
Jewelry, 60
Joint capsule, exposed, negative pressure
therapy, 416, 419f
Jones splint, 403, 407f
JPEG files, 107–108
K
Kelly artery forceps, 36, 37f
Keloids, 392–393, 392f–393f, 439–440, 439f
combined treatment, 397
intralesional injections, 394–396

494
Index
laser therapy, 398
pressure therapy, 394
silicone gel sheeting therapy, 397–398
surgical therapy, 400
Keratinization, 7
Keratinocyte growth factor-2 (KGF-2), 457
Keratinocytes, 7–8
cultured, 227, 478–480
wound healing, 102, 452
Keratohyalin, 7–8
Kessler stitch, modified, 93f
Kinetic Concepts, Inc, 412–413
Krackow stitch, multistrand, 93f
Kuwada–Dockery correction of elongated toes,
331–333, 334f–335f
Kuwada–Dockery flexor tendon transfer, 327,
328f
L
Langerhans’ cells, 8
Langer’s lines, 24
Laser therapy, scars, 398
Lateral arm flap, 256, 258f
Lateral calcaneal angiosome, 14t, 16, 17f,
147
Lateral nail biopsy, 293–294, 293f–294f
Lateral plantar angiosome, 14t, 15, 16f,
146
Lateral plantar artery, 15, 271, 275
Latissimus dorsi flap, 257
Lazy-S Z-plasty, 167–170, 169f–170f
Leashing the dog ear technique, 93, 98f
Leeches, medicinal, 74, 74f
Leg, vascular anatomy, 270–271
Leg ulcers see Ulcers, leg
Leiomyomas, digital, 310–311, 311f
Leprosy, 452–453
Lidocaine, 45–46, 46t
Bier block, 50
Life-threatening complications, 443–444
Ligaments, suture techniques, 89–91
Lighting, digital photography, 108, 109f
Limberg rhomboid flap, 196–199, 197f–200f
Lines of maximal extensibility (LME), 23, 24f,
113
Limberg rhomboid flap, 197–198
Lines of minimal movement (LMM), 24
Linton procedure, 465
Lipodermatosclerosis, 449, 449f, 453
shave therapy, 466
Lipomas, 370–374, 373f–375f
digital, 314, 318f
Liposuction, 257f, 265, 373–374
Lisfranc disarticulation, 239–240, 240f–241f
Lister bandage scissors, 33, 35f
Loading, skin graft, 209
Local anesthesia, 46–48
biopsies, 129, 129f
nail procedures, 296–297, 296f
negative pressure wound therapy, 426f,
429–430
Local anesthetics, 45–46
nerve blocks and infiltration, 46–48
regional nerve blocks, 49–50
topical, 46
toxic doses, 46, 46t
Local flaps, 144
Local muscle flaps, 269–288
classification, 269–270, 270f
distal one-third of leg, 271, 272f–273f
Doppler for muscle dissection, 280–285
Longitudinal nail biopsy, 292–293, 293f
Longitudinal wedge nail biopsy, 294,
294f–295f
Longitudinal wedge nail matrix biopsy,
295–296, 296f
Lossy/Lossless formats, 108
Lunula, 289, 290f
Lupus anticoagulant syndrome, 451
Lymphatic drainage, 18–19
Lysozyme, 7
M
M-plasty, 116–118, 117f
dog-ear repair, 92, 97f, 174, 174f
modified, 117–118, 118f
Webster flap with, 199–200, 201f
Macerated wound edges
negative pressure therapy, 429, 431f
prevention, 485, 485f
Macro photography, 106, 109
Macrophages, 9, 101
Maggots, 443, 443f, 460
Magnetic resonance imaging (MRI)
photographing images, 109
soft tissue masses, 357–358, 375, 376f
Magnification loupes, 250, 250f
Malignant lesions
benign lesions vs, 357
excision, 113–114
potentially, excisional biopsy, 128, 130
ulcerated, 453
Mallet-toe deformity, 322, 325f
skin wedge procedure, 329, 330f
tendon transfers, 325–327
Masses, soft tissue
benign, 357–380
biopsy, 128
diagnostic options, 357–358
history and physical examination, 357
malignant vs benign, 357
postoperative considerations, 314
treatment options, 358–375
see also Malignant lesions; specific types
Mast cells, 9
Matrixectomy
partial, 298, 300f–301f
total, 298–300, 302f–303f
Maxon® sutures, 78–79, 79t
Mayo scissors, 33, 34f
Mayo stand, 30, 30f
Mayo–Hegar needle holder, 37–38, 38f
MCA automatic coupling device, 253–255,
255f
Mechanics see Biomechanics
Medial calcaneal angiosome, 14, 14t, 15f,
145–146
Medial calcaneal artery, 14, 271
Medial plantar angiosome, 14–15, 14t, 15f,
145–146, 147f
Medial plantar artery, 14–15, 271
Megapixels, 107, 107b
Meissner’s corpuscles, 209
Melanocytes, 8
Melanocytic nevi, compound, 317, 321f
Melanoma, malignant, 128, 130, 426f
Mepivacaine, 45, 46t
Mercedes Benz closure, 119, 121f
Mersilene sutures, 79t
Meshed skin grafts
leg ulcers, 462, 463f
negative pressure wound therapy, 416t
Meshing, 215–216, 215f–216f
Metzenbaum scissors, 33, 34f
Micro-instrumentation, 249–252, 250f–251f
Microorganisms
causing postoperative infections, 54
leg ulcers, 457–459
negative pressure wound therapy, 412, 414
resident skin flora, 54, 61–62
routes of transmission, 54
see also Bacteria; Wound (or incision)
contamination
Microscope, operating, 249–252, 250f
Microsurgery
basic science concepts, 252–253, 252f
history of, 252
techniques, 253–255
see also Free flaps, microsurgical
Microsutures, 251
Microvascular clamps, 251, 251f
Milia, suture line, 484
Moist wound environment, 381, 457–458,
473, 484
Moisture vapor transmission rate (MVTR),
473
Monocryl® (poliglecaprone 25), 79, 79t
Monsel’s solution, 72–73
Mooring ligaments, 232, 232f
Mosquito hemostats, 36, 37f
Mucoid cysts, 314–315, 318f–320f
Muscle flaps, 144
classification, 269–270, 270f
free transfer, 257–259, 260f–262f
local, 269–288
revision, 265
Musculocutaneous blood vessels, 144
Myiasis, cutaneous, 443, 443f
Myocardial infarction, 444
Myofibroblasts, 210
N
N-terface dressings, 383t
Nail(s), 289–306
anatomy, 289–290, 290f
biopsy, 291–296, 293f–296f
diagnostic techniques, 291–296
ingrown see Ingrown toenail
malaligned, soft tissue correction, 297, 297f
pathological anatomy, 290
postoperative care, 300
punch biopsy, 293, 293f
surgical procedures, 296–300
trauma, 290
see also Periungual tissues
Nail avulsion, 297–298
deformities complicating, 290, 291f
total and partial, 297–298, 299f–300f

495
Index
Nail bed, 289, 290f
biopsy, 292–294, 293f–295f
Nail folds, 289, 290f
hypertrophied, DuVries plasty, 297, 297f
Nail grooves, 289, 290f
Nail matrix, 289–290, 290f
biopsy, 294–296, 296f
resection see Matrixectomy
Nail plate, 289, 290f
biopsy, 292–294, 293f–295f
Nail spicule, 290, 291f
Necrosis, wound, 438–440, 439f
Necrotic tissue, removal see Debridement
Needle holders/drivers, 37–38, 37f–38f
Needles, surgical, 80–81, 80f
coding system, 81
microsurgery, 251
Negative pressure wound therapy (NPWT),
384–386, 411–433
advanced techniques, 425–428, 429f–430f
clinical studies, 414–415
clinical uses, 412b, 415–423
completion, 423–425
complications, 422f, 429–431, 431f
contraindications, 428
evaluation and preparation for, 415
experimental studies, 413–414
historical aspects, 411–412
as intermediate procedure, 421, 424f
mechanism of action, 412
pressure and cycle settings, 415, 416t
skin grafts, 217, 218f, 384–386, 414,
422–423
systems available, 412–413, 412f–413f, 412t
vacuum holiday/therapeutic pause, 425
Neoplasms
biopsy, 128, 130
see also Malignant lesions; Masses, soft
tissue
Neovascularization, skin grafts, 209–210
Nerve blocks, 46–48
Nerve damage, tourniquets, 71
Nerve fibers
dermal, 9
epidermal, 8, 9f
see also Reinnervation
Neuroma, dermal, 311, 311f–312f
Neuropathic ulcers, 450, 454t
Neurorrhaphy, 262, 263f–264f
Neutrophils, 101
Nevi, 317, 321f
Nonsteroidal antiinflammatory drugs
(NSAIDs), 436
Nosocomial infections, 54
Novafil sutures, 79t
Nurolon sutures, 79t
Nutrition, pressure ulcers and, 454, 484
Nutritional disorders, wound healing, 103
Nylon sutures, 79–80, 79t
O
O–H flap (double advancement flap),
179–180, 180f
O–T closure, 119–121, 121f
O–Z closures, 119, 121f
OASIS® Wound Matrix, 228b, 479
Oblique sigmoid island flap, 161, 161f
Occlusive dressings, 381–382, 473
categories, 383t, 473–477, 474t
cost-effectiveness, 486
leg ulcers, 457, 473
post-excision wounds, 481
Odland bodies, 8
Odor, 453, 485
Older patients
leg ulcer management, 452
microsurgical free flaps, 255
wound healing, 103
Olsen–Hegar needle holder, 37–38
Omental flaps, 259–262
One-half buried horizontal mattress suture, 91,
95f
One-half buried vertical suture, 93f
Onychocryptosis see Ingrown toenail
Operating room, 29
attire, 57–58, 57f
digital photography, 109
Opponens digiti minimi muscle flap,
277–278, 285f
OpSite™ dressing, 382, 383t
OrCel™, 228b, 480
Organization phase, skin graft healing, 210
Orthopedic hardware
exposed, vacuum therapy, 416–421,
420f–421f
removal, 419–421
Orthopedic surgeons, working with, 263–265
Orthotic compression device, 482t, 484,
484f
Osteochondroma, 317–318, 321f
Osteomyelitis, 233
heel amputations, 240, 242f
leg ulcers, 453
local muscle flaps, 273f–274f, 277f–278f,
283f–284f
negative pressure wound therapy, 416, 419f,
423f
omental flaps, 259–262
ray resections, 236, 237f
toe fillet flaps, 234
webbing procedures, 339, 341f
Osteophyte see Exostosis
Over-and-over sutures, 89, 94f
Oxycel, 73
Oxygen tension, optimal, for wound healing,
381
P
Pacinian corpuscles, 209
Padgett-Hood® drum dermatome, 212
Pain
leg ulcers, 452
negative pressure wound therapy, 429–430
sensation, 45
skin grafts, 210
wound care and, 484
Palliative care, leg ulcers, 452
Pantographic expansion flap, 179, 179f
Papain–urea preparations, 460–461, 462f
Parascapular flap, 256, 257f
Partial-foot amputations see Amputations,
partial-foot
Pathology, biopsy specimens, 127–128,
138–140
Pediatric patients, 1
microsurgical free flaps, 255
Pedicle flap, 144
Pedicle random flap, 143
Peninsular axial pattern flap, 143, 144f
Pentoxifylline, 456–457
Perforator arteries, 17, 18f, 144, 270
Periodic-acid Schiff (PAS) reaction, 291–292
Periosteal elevators, 38, 39f
Peripheral vascular disease (PVD), 17–18,
449–450
diagnostic assessment, 453, 453f
negative pressure wound therapy, 414, 431,
431f
partial-foot amputations, 232–233
poor wound healing, 103
skin grafts, 211, 220
see also Arterial ulcers
Periungual tissues, 289–306
anatomy, 289–290, 290f
biopsy, 291–296, 292f
correction of malaligned toenail, 297, 297f
diagnostic techniques, 291–296
distal skin plasty for clubbing, 297,
298f–299f
lateral wedge resection, 297, 297f
surgical procedures, 297
see also Nail(s)
Peroneal artery, 16, 270–271
angiosomes, 14t, 16, 145, 146f, 147
perforators, 270
Peroneus brevis muscle flap, 272–273, 272f
Photography, digital, 105–110
equipment, 106–108
guidelines, 108–110
image editing software, 110
medical uses, 106
preoperative, 2
see also Cameras, digital; Images, digital
Physical examination, 3–4
Pie-crusting, 216, 216f, 218
Pigmentation changes
around wounds, 486
scars, 393–394, 393f–394f
skin grafts, 210–211
Pigmented lesions, biopsy, 128, 130, 136,
138
Pigmented villonodular synovitis, 374–375,
376f–379f
Pigmented villonodular tenosynovitis see Giant
cell tumor of tendon
Pincer nail, 290, 292f
Pinch grafting, 218, 219f
leg ulcers, 461–462, 463f
Pinch test, relaxed skin tension lines, 24, 25f,
113, 114f
Plantar foot
biopsy, 130
free flaps, 257, 260f
incision planning, 25
negative pressure wound therapy, 416,
417f–418f, 426f, 428, 430f
soft tissue reconstruction, 232, 232f
Plasticity, suture materials, 78
Platelet count, 69–70

496
Index
Platelet-derived growth factor (PDGF), 451f,
459, 472
Platelets
dysfunction/reduced numbers, 70, 436
hemostatic function, 69, 436
thrombus formation, 252–253
wound healing, 451
Podiatric surgeons, working with, 263–265
Poliglecaprone 25 (Monocryl®), 79, 79t
Polybutester sutures, 79t, 80
Polydioxanone (PDS) sutures, 78–79, 79t
Polyglactin 910 (Vicryl®), 78, 79t
Polyglycolic acid (Dexon®), 78, 79t
Polypropylene sutures, 79–80, 79t
Popliteal block, 49, 49f–50f
Porcine xenografts, 228b
clinical use, 213, 226–227, 227f
fusiform desyndactylization, 344, 347f
storage, 220
Posterior medial malleolar artery, 14, 271
Posterior tibial artery, 14, 270–271
angiosomes, 14–15, 14f, 14t, 145–146, 145f
perforators, 270
Posterior tibial nerve block, 47–48, 48f
Postoperative care, 481–485
excision wounds, 481
laser resurfacing, 481–482, 482t
pitfalls and their management, 485–486,
485f
prevention of infection, 55, 65
wound management, 56, 481–482
Potassium hydroxide (KOH), 291
Povidone-iodine solutions, 60, 62, 129
skin grafting, 213–214
Preoperative patient evaluation, 1–5
history, 2–3
informed consent, 2
patient expectations, 5
physical examination, 3–4
second opinion, 1–2
Preoperative preparation, 59–65
biopsy procedures, 129–130
patient/surgical site, 4–5, 54, 61–65
surgeon, 59–61
Presentations, medical, 106, 110
Pressure therapy, scars, 394
Pressure ulcers, 450, 450f
management, 484–485
negative pressure wound therapy, 414, 416t,
424f
prevention, 455
Prewounding, 209, 213
Prilocaine, 45, 46t
Primary intention, wounds healing by, 481
Procaine, 45, 46t
Prolene sutures, 79t
Proliferative phase, 78, 101–102, 452
Prostaglandins, 101
Prothrombin time, 70
Proxiderm™ external tissue expander, 85–86
Punch biopsy, 133–136
indications, 129–130, 133
instruments (punches), 38, 38f, 133–134,
134f
nail, 293, 293f
nail matrix, 294–295, 296f
technique, 134–135, 135f–138f
Purse-string suture closure, 119
Pyoderma gangrenosum, 425, 452–453, 453f
Pyogenic granuloma, 318–322, 324f
R
Radial forearm flap, 256, 259f, 263f–264f
Radiation therapy, free flap transfer after,
256
Radiographs, photographing, 109
Ragnell tissue retractor, 36, 36f
Random cutaneous flap, 143, 144f
Rapid intraoperative tissue expansion (RITE),
85
Rapid slide method, wound bed evaluation,
212–213
‘Reading Man’ transposition flap, 203–204,
204f
Rectus abdominus muscle flap, 257–259, 260f,
264f
Reese® drum dermatome, 212
Regional nerve blocks, 49–50
Reinnervation
free flaps, 262, 263f–264f
skin grafts, 210
Relaxed skin tension lines (RSTLs), 24,
24f–25f
crescentic ellipse, 118–119
digital skin incisions, 308, 308f
fusiform ellipse, 113
Limberg rhomboid flap, 197–198
pinch test, 24, 25f, 113, 114f
Remodeling phase, 102, 452
Renasys™ Systems, 412–413, 413f
Retractors, tissue, 29, 34–36, 35f
hand-held, 34–35, 36f
self-retaining, 34–36, 37f, 41f
small malleable, 38, 39f
Revascularization
skin grafts, 209–210
surgery, 232, 265
Rhombic transpositional flap, 196, 196f
Rhomboid transpositional flaps
comparative procedures, 204, 204f
double, 200, 201f
Dufourmentel, 199, 201f
Limberg, 196–199, 197f–200f
with multiple Z-plasty, 202–203, 203f
triple, 200–201, 201f–202f
Rigid rake retractor, 36, 36f
Rongeur bone forceps, 38, 39f
Rotational flaps, 143–144, 180–189
Catanzariti–Wehman, 181–183, 182f
classic, 181, 181f–182f
double-lobed, 183–189, 189f–192f
Satterfield–Jolly, 181, 182f
single-lobed, 183, 183f–188f
transpositional flaps vs, 204, 204f
Running buried stitch, 89, 94f
S
S-plasty (Alvarado double-S), 118, 118f–119f
modified, 118, 120f
Saline dressings, 383
Saphenous nerve block, 48, 49f
Satterfield–Jolly rotation flap, 181, 182f
Saucerization biopsy, 130–133
blade types, 130–132, 131f
indications, 130
technique, 132–133, 132f
Scalpel blades, 30–31, 31f
angle to skin, 86, 90f
selection, 26, 86
Scalpels, 30–31
disposable plastic, 30–31, 31f
handles, 30–31, 30f–31f
position for holding, 30, 31f
Scar(s), 389–407, 439–440
definitions, 389–394
depressed, 393, 393f
digital skin incisions, 308, 308f
formation, 102, 452
hyperpigmented, 393, 393f
hypertrophic see Hypertrophic scars
hypopigmented, 393–394, 394f
intralesional injections, 394–398, 396f
irregular, 394, 394f
keloid see Keloids
laser therapy, 398
normal, 389, 390f
plantar surface of foot, 232
pressure therapy, 394
prevention, 400–405, 403f–408f
silicone gel sheeting, 397–398, 397f–399f
surgical therapy see Scar revision
suture track, 390, 391f
treatment, 394–400, 395f
widespread, 389–390, 390f, 399–400,
402f–403f
Scar revision, 398–400
fusiform excision, 398–399, 399f, 402f
geometric broken-line closure, 174, 175f,
398–399, 401f
short wavy incision method (SWIM),
398–399, 400f
W-plasty, 174, 398–399
Z-plasty, 163, 165
Scarlet red ointment dressing, 382, 383f
Schrudde type-1 flap, 183, 183f–185f,
187f–188f
Schrudde type-2 flap, 183, 183f–186f
Schrudde type-3 flap, 183, 183f
Schuberth flexor tendon transfer, 327, 328f
Sciatic nerve block, 49
low, 49, 49f–50f
Scissor biopsy, 133, 134f
Scissors, 32–33, 33f–35f, 41f
microsurgical, 250–251, 250f
Scrub suits, surgical, 57, 57f
Sebaceous glands, 8, 209
skin grafts, 210
Second opinion, 1–2
Second toe, transverse plane deformities, 323,
326f
Secondary intention, wounds healing by, 481
Sedation, intravenous, 48
Segmental blood vessels, 144
Seizures, 443–444
Senile angiomas, 313–314, 317f
Senn tissue retractor, 36, 36f
Sensation
dermal receptors, 9
epidermal receptors, 8, 9f

497
Index
free flaps, 262–263, 263f–264f
skin grafts, 209–210
Seromas, postoperative, 103, 437, 438f
management, 486
prevention, 402
skin grafts, 209, 220
Serratus anterior flap, 257–259, 261f
Sgarlato toe tendon transfer, 327, 328f
Shave biopsy, 130–133
equipment, 130–132
indications, 130, 132
periungual soft tissue, 292, 292f
technique, 132–133, 133f
Shave therapy, venous ulcers, 466, 483
Shaving, preoperative, 54, 62
Shoe covers, surgical staff, 58, 59f
Shoes, ulcer prevention, 455–456
Short wavy incision method (SWIM),
398–399, 400f
Silicone gel sheeting, 397–398, 397f–399f,
439, 439f
Silk sutures, 79
Silver-impregnated dressings, 480
Silver sulfadiazine, 213
Single-lobed rotation flap, 183, 183f–188f
Skin
anatomy, 7–10, 208–209, 208f
artificial acellular, 227–229
biomechanical properties, 195
blood circulation, 13, 16–17, 18f
contour lines, 23
healing see Wound healing
properties, 23–24
Skin-cutting scissors, 33, 34f
Skin equivalents, bioengineered see Skin
substitutes
Skin flaps see Flaps
Skin graft recipient bed
factors causing graft failure, 220
intraoperative preparation, 213, 213f–214f
preoperative preparation, 212–213
prewounding, 209, 213
Skin grafts, 207–224, 221f, 477
anatomy, 208–209, 208f
autologous, allogeneic and xenogeneic, 207,
225–229
classification, 207, 225, 461
complications, 220
composite, 227–229, 228f, 477
contraction, 210–211
desyndactylization, 219f, 344, 347f–349f
dressings, 216–218, 218f, 384, 385f, 463
flaps vs, 143, 225
historical background, 207–208
indications, 211
leg ulcers, 461–466
loading, 209
necrosis, 439
negative pressure wound therapy, 217, 218f,
384–386, 422–423
physiology, 209–210
storage, 220
take, 209
venous ulcers, 483
see also Full-thickness skin grafts; Skin
substitutes; Split-thickness skin grafts
Skin hooks, 35–36, 36f
Skin marking, 26, 26f
excisional biopsy, 129, 136, 138f–139f
fusiform ellipse, 114, 114f
scar prevention, 401, 403f
Skin preparation, 5, 54, 61–62
biopsy, 129
skin graft donor site, 213–214
Skin staplers, 38, 39f–40f, 82–83, 83f
Skin staples, 82–83
application technique, 40f, 83, 83f–84f
configuration, 82
indications, 83
removal, 40f, 83, 84f
Skin substitutes, 227, 228b, 464t, 477–480
composite, 227–229, 480
leg ulcers, 464–465, 465f, 483
Skin wedges, toe alignment, 329, 329f–331f
Sleeve technique, microsurgery, 253, 254f
Slides, photographic, digitizing, 109
Smith & Nephew, Inc, 412–413
Smoking, tobacco, 103, 256, 435
Soft tissue masses see Masses, soft tissue
Sole of foot see Plantar foot
Soleus muscle flap, 272, 272f, 274f
Spencer stitch scissors, 33, 35f
Spinal block, 49–50
Split-thickness skin grafts (STSG), 207,
211–217, 225, 461, 477
anatomical basis, 208–209, 208f
application, 216, 217f
categories of thickness, 207, 461
contraction, 210–211
donor site locations, 211–212, 212f
dressing, 216–217
full-thickness skin grafts vs, 211, 478t
harvesting technique, 213–214, 215f
healing, 209–210
instruments for harvesting, 212, 212f
leg ulcers, 462, 463f
meshing and pie-crusting, 215–216,
215f–216f
negative pressure wound therapy, 422–423,
425f–428f
postoperative care, 217
Stainless steel wire sutures, 79, 79t
Stand, instrument, 30, 30f
Staphylococcus infections, 442, 442f
Staples
microvascular anastomoses, 253–255
skin see Skin staples
Steri-Strips, 81f–82f, 82
removal, 403, 407f
scar prevention, 401, 404f–405f
Sterility, 54
Sterilization, 57
Steroid injections see Corticosteroid injections
Stitches see Suture(s)
Strain, 195
Stratum basalis (stratum germinativum), 7, 8f
Stratum corneum, 8, 8f
Stratum granulosum, 7–8, 8f
Stratum Malpighii, 7–8
Stratum spinosum, 7, 8f
Streptococcus infections, 442, 442f
Stress, 195
Stress relaxation, 195
Strike-through contamination, 65
Subcutaneous layer, 9–10
Subfascial endoscopic perforator surgery
(SEPS), 465–466
Subungual exostosis, 318, 322f
ingrown or pincer nails, 290, 291f–292f
surgical excision, 318, 322f
Superficial fascia, blood circulation, 13, 16–17,
18f
Superficial peroneal nerve block, 46–47, 47f
Sural artery, 270–271
Sural artery flaps, 241–242, 243f–245f
Sural nerve block, 48, 48f
Sure-Closure Skin Stretching Device, 85
Surgical infections, 54, 440–443
diagnosis, 442–443
etiology, 442, 442f
poor wound healing, 103
prevention, 54–55, 58–65, 442, 486, 485f
risk factors, 55–56, 56b
sources of microorganisms, 54
treatment, 443, 443f
types, 55b
see also Surgical site infections
Surgical instruments, 30–39
Surgical principles, 23–27
Surgical site
draping, 63–65, 67f
preparation, 5, 54, 61–62
Surgical site infections (SSI), 54, 55b,
440–443, 441f
deep incision, 55b
diagnosis, 442–443
etiology, 442, 442f
negative pressure wound therapy, 416, 416t,
417f–419f
organ/space, 55b
prevention, 54–55, 58–65, 442
risk factors, 55–56, 56b
superficial incision, 55b
treatment, 443, 443f
Surgicel, 73, 73f
Surgifoam, 73f
Surgilene sutures, 79t
Surgimate® staples, 82
Suture(s), 78–80
absorbable, 78–79, 79t
alternatives to, 81–83
buried, 89, 93f–94f
classification, 80
complications, 438
intradermal, 91–92, 96f
materials, characteristics, 78
memory, 78
microsurgery, 251
needles, 80–81, 80f
non-absorbable, 79–80, 79t
retention, 86, 92f
timing of removal, 91, 403, 407f, 481
see also specific sutures
Suture (stitch) abscess, 54, 55b, 438
Suture granuloma, 485
Suture scissors, 33, 35f
Suture tracks, 390, 391f
Suturing techniques, 86, 91f
cosmetic, 91–93
deep suture retention, 89–91, 93f–94f
internal, 89

498
Index
microsurgical free flaps, 253, 254f
rule of halves, 116, 117f, 120f
scar minimization, 401–402, 404f
special, 88–89, 93f
Sweat glands, 8
skin grafts, 209–210
Swing-slide plasty (Schrudde type-1 flap), 183,
183f
Syndactylization, digital, 334–339
full-length, 338, 339f–342f
fusiform, 337, 338f, 341f–343f
mini, 337, 337f, 340f, 343f
modified, 338–339, 339f, 343f
partial, 337, 338f, 341f
Syndactyly, 339–344
camouflage, 344, 349f
surgical correction see Desyndactylization,
digital
T
Table, operating, 29
Tape strips, adhesive, 81–82, 81f–82f
see also Steri-Strips
Tegaderm™ dressing, 382, 383f, 383t
Tendon
exposed, negative pressure therapy, 416,
418f
lengthening procedures, 324–325, 328f
sutures, 88–89, 93f
Tendon transfers, toe, 325–329, 328f
arthroplasty or arthrodesis with, 330
see also Flexor tendon transfers
Tenotomies, toe deformities, 323, 326f–327f
Tension
excessive, surgical techniques, 439
during incision placement, 26, 26f
orientation of incision and, 24
wound healing and, 86
Tension assisted wound closure (TAWC),
85–86
Terminal Syme operation, 349–350, 350f
nail conditions, 298–300, 303f
Tetracaine, 45
Thigh tourniquets, 70–71
Three-point corner stitch, 91, 95f
3M™ staplers, 83, 83f
Thrombin, 69
topical, 74, 74f
Thrombin time, 70
Thrombocytopenia, 70, 436
Thrombosis, microsurgical free flaps, 252–253
Tibial nerve block, 47–48, 48f
Tibialis anterior muscle flap, 273f, 275
Tisseal, 74
Tissue adhesives (TA), 71, 83–85
Tissue-cutting scissors, 33, 34f
Tissue elasticity, 189
Tissue elevators, 38
Tissue expansion, 85–86
continuous external, 85–86
rapid intraoperative (RITE), 85
Tissue factor (TF), 69
Tissue handling, 29, 400, 404f
Tissue-handling forceps, 32, 32f–33f
Tissue movability, 189
Tissue reactivity, suture materials, 78
Tissue remodeling phase, 102, 452
Tissue retractors see Retractors, tissue
Tobacco smoking, 103, 256, 435
Toe(s)
arthroplasty, 330
elongated, correction, 331–333, 334f–335f
etiology of conditions, 308
fillet flaps, 234–235, 236f
great see Hallux
skin and soft tissue lesions, 309–322
skin incisions, 308–309, 308f–310f
soft tissue angular correction, 322–329
surgical procedures, 307–352
Toe amputations, 234, 344–352
distal see Terminal Syme operation
incisions, 347, 350f
partial, 350, 351f
total, 352, 352f–355f
Toe blocks, 296–297, 296f
Toe deformities
osseous correction, 329–334
planes of deformity, 322–323
skin procedures, 329
skin wedges, 329, 329f–331f
skin Z-plasty, 329, 332f
soft tissue correction, 322–329
staged-combined procedures, 333–334,
336f
tendon lengthening, 324–325, 328f
tendon transfers, 325–329, 328f
tenotomy, 323, 326f–327f
V–Y plasty, 151–152, 153f–154f
Toenails see Nail(s)
Topical anesthesia, 46
Tourniquets, 70–71
Bier block, 50
complications, 71
Towel clips, 29, 63–65
Towels, hand drying, 60, 64f
Toxic-shock syndrome, 431
T.R.A.C.® Pad, 413
TransCyte®, 228b, 479
Transforming growth factor-β (TGF-β), 451f,
459, 472
Transmetatarsal amputations (TMA), 238–239,
240f
Transpositional flaps, 143–144, 195–204
comparative procedures, 204–205, 204f
complex, 196–204
simple or classic, 196, 196f
Transverse fusiform nail matrix biopsy, 295,
296f
Trapdoor defects, 195
Trauma
microvascular anastomotic failure, 252–253
nail, 290
Triple rhomboid transpositional flap, 200–201,
201f–202f
Tulle dressing, 382–383, 382f
24-hour hammertoe operation, 330, 333f
Tyrell skin hook, 35–36, 36f
U
Ulcers, leg, 447–466
antimicrobials and bacterial balance,
457–458
biopsy, 128, 453–454
causes, 448t, 449–451
clinical features, 452–453, 454t
compression therapy, 456
diagnostic assessment, 453–454, 454t
dressings, 457–458, 458t
FRAIL concept, 452
management techniques, 456–458
preoperative preparation, 452–456
prevention, 455–456
skin grafting, 461–466
subfascial endoscopic perforator surgery,
465–466
surgical techniques, 458–466
types, 448t
wound bed preparation and debridement,
458–461
see also specific types
Undermining, tissue, 86, 90f
Ungual tuft amputation, 234, 235f
Unilobe flap see Single-lobed rotation flap
United States Pharmacopeia (USP), suture
classification, 80
Unna Boot, 456, 456t, 483, 483f, 482t
V
V–Y island flap
double, 160f, 161
extended, 160–161, 160f
single, 157–160, 157f–159f
V–Y plasty (V–Y advancement flap), 143,
151–152, 152f
contracted toes, 151–152, 153f
technique, 151–152, 154f–156f
Wilson, 151, 153f
V–Y–S-plasty, 152, 157f
Vacuum Assisted Closure® (VAC®), 411–412
skin grafts, 217, 218f
systems, 412–413, 412t, 413f
see also Negative pressure wound therapy
Vacuum drains, 402, 406f, 437f
Valgus toe deformities, 322–323
Vancomycin, 442
Varus toe deformities, 322–323, 326f
Vascular anastomoses see Arterial–arterial
connections; Microsurgery
Vascular anatomy, 13–21
angiosomes see Angiosomes
cutaneous, 9, 10f, 13, 16–17, 18f, 145f
incision planning, 18, 19f
leg, 270–271
skin flaps, 144
skin grafts, 209
surgical implications, 10, 13–21
Vascular assessment
microsurgical free flaps, 265
partial-foot amputations, 233
Vascular disease, 17–18
partial-foot amputations, 233
see also Peripheral vascular disease
Vascular surgeons, working with, 263–265
Vasculitis ulcers, 450–451
Vasospasm, 252–253
Vein grafts, free flaps, 256
Venosomes, 18, 144–145
Venous drainage, 18–19

499
Index
Venous ulcers, 449–451, 449f
bioengineered skin grafts, 464–465, 465f,
480, 483
CEAP classification, 465, 465t
as chronic wounds, 448
clinical features, 452–453, 454t
compression therapy, 450f, 456, 482–483
diagnostic assessment, 454t
dressings, 473, 484
local muscle flaps, 274f
negative pressure wound therapy, 422
pharmacologic therapy, 456–457
prevention, 455
shave therapy, 466, 483
subfascial endoscopic perforator surgery
(SEPS), 465–466
wound care, 482–484
see also Lipodermatosclerosis
Verapamil hydrochloride, intralesional keloid
injection, 396
Verrucas, 322, 324f
VersaFoam™, 412–413, 413f
Vertical mattress suture, 86, 92f
Vicryl® (polyglactin 910), 78, 79t
Video photography, 108
Vitamin deficiencies, 103
Vitamin supplements, 436
Von Willebrand disease, 436–437
W
W-plasty, 174, 174f
postoperative care, 174–175
scar excision, 174, 398–399
Warfarin, 70, 104, 436
Warts, 322, 324f
Web space infections, chronic, 339, 342f
Webbing procedures see Syndactylization,
digital
Webster flap, 199–200, 201f
Weight-bearing surfaces, skin grafting, 211, 220
Weitlaner tissue retractor, 37f
Wet-to-dry debridement, 460
Whirlpool baths, 460, 460f
Wiener skin hook, 35–36, 36f
Wilson V–Y plasty, 151, 153f
Wind up, 49
Winograd partial matrixectomy, 298,
300f–301f
Wound(s)
debridement see Debridement
moist environment, 381, 457–458, 473, 486
see also Acute wounds; Chronic wounds
Wound bed preparation
free flaps, 265
leg ulcers, 458–461
skin grafts, 212–213, 213f–214f
Wound care, 481–485
chronic wounds, 482–485
partial-thickness and full-thickness burns,
481
pitfalls and their management, 485–486,
485f
postoperative, 481–482
Wound closure, 77–93
after negative pressure wound therapy,
423–425
alternatives to sutures, 81–83
cosmetic, 91–93
decision tree, 211
materials, 78–83
partial-foot amputations, 232–242, 234f
repeat, 403–405, 408f
scar minimization, 401–402, 404f–405f
tension assisted (TAWC), 85–86
see also Skin grafts; Suture(s); Suturing
techniques
Wound (or incision) contamination
classification, 56, 56b
prevention, 54–55
risk factors, 55–56, 56b
routes, 54
skin graft recipient bed, 212–213, 220
see also Microorganisms; Surgical site
infections
Wound healing, 10, 101–104, 451–452
around sutures, 78
cells involved, 102f
factors compromising, 102–104
minimizing tension, 86
moist environment, 381, 457–458
negative pressure therapy, 414–415
optimal environment, 381
phases, 101–102, 451–452, 451f
physiological factors, 77–78
by primary intention, 481
by secondary intention, 481
skin grafts, 209–210
Wound infections see Surgical infections;
Surgical site infections
X
X-rays, photographing, 109
X stitch, 89, 93f
Xenografts, 226–227, 228b, 477
clinical use, 213, 226–227, 227f
defined, 207, 225
storage, 220
see also Porcine xenografts
Y
Y–V-plasty, 152, 156f–157f
Z
Z-plasty, 163–176
asymmetrical, 167, 168f
curved-arm, 167, 169f
dog-ear repair, 174, 174f
double opposing (five-flap), 171–172, 172f
double-Z rhomboid flap, 173, 173f
extended planimetric, 170, 171f
extension of limbs or central arm, 167,
168f
four-flap, 173, 173f
lazy-S, 167–170, 169f–170f
long central-arm, 167, 169f
multiple, 171, 171f–172f
oblique continuous planimetric, 170–171,
171f
planimetric, 170, 170f
planning, 165, 165f
postoperative care, 174–175, 175f
principles, 163–165, 164f–165f
rhomboid flap with multiple, 202–203,
203f
single, 163–165
standard, 163, 164f
technique, 165–166, 166f–167f
toe alignment, 329, 332f
variations, 167–173
Zadik total matrixectomy, 298, 302f
Zimmer® dermatome, 212, 212f
Zinc, 103
Zone of injury, 256, 271