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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
have been placed equidistance along the incision and directly oppo
site each other, the remaining incision is then closed with multiple
simple interrupted sutures.
In complex cases, or in cases with high vascularity, it is prudent
to place a vacuum drain deep within the wound to suction the imme
diate fluid that forms to prevent a postoperative seroma or hematoma
formation (Fig. 28.42). The drain should be placed into the deeper
tissues, or areas of excessive oozing, and should exit through normal
skin adjacent to the incision rather than through the incision itself.
This way, the drain can be removed at any time without disruption of
the incision. The drain is typically removed in 24–36 h following
surgery, or sooner if no drainage is noted after the first 12 h. Drains
may be used for any lower extremity surgery where intraoperative
bleeding is persistent or expected to continue even after closure or in
areas of large dead space formation.
Once the procedure is performed and the incision is closed, the next
step usually involves applying an appropriate dressing, which depends
somewhat on the nature of the surgery. For small uncomplicated
procedures, a light bandage is all that may be needed. For more
complex cases, it may be appropriate to apply mild-to-moderate com
pression bandage or splint to control postoperative swelling. Once the
basic sterile dressings are applied, the mild compression bandage is
applied with alternating layers of cotton cast padding and cohesive
D
E
F
A
B
C
Figure 28.28 Excision of widespread scar. (A) Initial appearance of unusual shaped scar with underlying traumatic neuroma. (B) Outline of scar
margins to plan excision. (C) Fusiform incision around scar. (D) Edges are undermined and neuroma identified. (E) Traumatic neuroma exposed and
removed. (F) Postoperative scar at 2 months.
Once the entire incision is closed and finished with Steri-Strips a few
may be placed across the ends to prevent suture slippage or excessive
pulling from occurring (Fig. 28.38). Excessive tension should be
avoided when applying the Steri-Strips to prevent traction blister for
mation postoperatively.
If the incision has the potential for motion, tension, swelling or
other forms of stress that might jeopardize the healing of the incision,
it may require multiple forms of sutures for optimal closure (Fig.
28.39). There is a distinct advantage to using a combination of simple
interrupted sutures with an occasional retention vertical or horizontal
mattress suture. The tension on the incision can be reduced by
thoughtful placement of each suture. This approach also allows the
staging of suture removal to better manage the incision healing. The
placement of sutures can also be a problem for wound healing if they
are placed too close to the skin edges at the incision line, have too
much tension or are too tightly tied (Fig. 28.40).
If the wound was previously infected or if a revisional procedure
has been performed on a problem scar it may be necessary to allow
for additional protection of the incision with buttress sutures. These
buttress sutures are performed in the same manner as horizontal mat
tress sutures with the addition of small tubes of plastic or rubber (Fig.
28.41). Cutting small equal sections of pediatric IV tubing or a small
French catheter tube creates these tubes. Once the buttress sutures
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compression wrap (Fig. 28.43). This bandage is light and easy for the
patient to deal with. It is quickly changed when necessary and pro
vides enough general compression to prevent normal postoperative
edema.
The moderate compression Jones splint, on the other hand, begins
with a layer of stockinette over the sterile dressings, which is placed
from the toes to just below the knee. A layer consisting of three or
four rolls of cotton cast padding is then applied and covered with a
4- or 6-inch elastic Ace bandage. The next layer is composed of more
rolls of cotton cast padding to cover the Ace bandage. A posterior
splint of 5 × 30-inch plaster, five to 10 strips thick, is applied and
formed to the arch, heel and posterior calf and another set of five to
Figure 28.29 Planned design for excision of widespread scar that will
result in an atypical incision appearance. The irregular shaped incision
should provide reduced problems with contracture and be relatively well
accepted cosmetically.
Figure 28.30 A single non-stop perpendicular skin incision creates less
tissue damage than several short cutting incisions with jagged edges.
Figure 28.31 Skin markings. (A) The incision is marked with a skin
marker and crosshatches are drawn across the incision before the
procedure starts. (B) The crosshatches are lined up during the suture
process for accurate closure of the incision.
A
B
10 strips of plaster splints is used to make stirrups along the sides of
the ankle and leg. The plaster is then covered with a layer of cotton
cast padding and the final wrap is with another elastic Ace bandage
(Fig. 28.44). This compression dressing allows very little edema
without the constriction as would be seen with a below-knee cast. It
can also be unwrapped in layers or cut if necessary and it is easily
removed without the need for special tools.
At the time of the first visit, it may be too soon to remove all of the
sutures, but the Steri-Strips, or a few of the retention sutures, may be
removed without disruption of the normal healing of the incision
(Fig. 28.45). It is frequently beneficial to stage the removal of sutures
thus allowing certain sutures to remain reinforcing the incision closure
until the wound is completely healed (Fig. 28.46). During this post
operative time it is also important to refrain from removing the dried
blood and dark areas around the incision (Fig. 28.47). This darkened
tissue will frequently act as an additional barrier to contamination
while the normal healing is occurring underneath. Early removal may
disrupt the incision and increase postoperative infection and scarring.
There is, nevertheless, an ideal time to remove the sutures and that is
when the wound can maintain closure without gapping or dehiscence.
If the sutures are left in place for an extended amount of time the
consequences may be suture tracks (see Fig. 28.4).
If the final skin closure was inadequate, or at the time of suture
removal the incision opens, it is necessary to be relatively aggressive
404
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
Figure 28.35 Steri-Strip closure. (A) The ends of the subcuticular sutures or the incision are taped first. (B) Additional Steri-Strips are applied across the
incision from the low side to the high side. If both sides are equal then the Steri-Strips are applied to both sides at the same time.
A
B
Figure 28.34 Proper suture technique. When closing the deep layers
or subcuticular layer it is beneficial to decrease tissue handling with
forceps and learn to place the suture needle through the tissues in
a smooth fashion.
Figure 28.33 Proper suture technique. When closing the incision with
external sutures it is beneficial to start the needle at its sharpest point
with the tip at 90° to the skin edge. This decreases pullout from sutures
placed at a biased angle.
Figure 28.32 Minimizing skin damage. (A) Using skin hooks or small retractors to lift the skin instead of tissue forceps. (B) Using sutures in flaps
instead of holding the tips with forceps causes less potential damage to the skin edges during surgery.
A
B
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Figure 28.36 Steri-Strip closure. The Steri-Strips may be applied using
atraumatic forceps to prevent them from sticking to the surgical gloves.
Figure 28.37 Steri-Strip closure. The curved incision has individually
placed Steri-Strips running perpendicular to the incision line.
Figure 28.38 Steri-Strip closure. The ends of all of the Steri-Strips may
be held in place by anchoring strips to prevent slippage or excessive
pulling from occurring.
Figure 28.39 Multiple sutures. Multiple simple interrupted sutures
combined with vertical and horizontal mattress sutures provide exacting
closure of wounds that may have increased risks of motion or stress.
They may also be removed in stages during healing.
Figure 28.40 Suture technique variables. This incision was partially
closed by the surgeon and partially closed by a trainee. It is obvious that
there is a difference in the skin edge apposition, approximation, tension
and tissue damage present (see also Fig. 28.15).
and reclose the incision immediately rather than allowing it to heal
in by secondary intention healing (Fig. 28.48). In many of these cases,
the wound edges are damaged from previous suture material, impro
per instrument handling of the edges, or only partial healing takes
place. This irregular skin edge usually needs to be excised to make
fresh skin edges for the reclosure with new suture. Frequently, the
author recommends using a different suture material than was used
on the first closure. Additionally, this incision should then be kept as
immobile as possible after surgery and the sutures will be left in a
little bit longer to assure that the wound is healed completely. In this
scenario, it is better to get a few suture tracks than to have the wound
open for a second time. If longer than 24 h has passed since the
wound opened, it is considered contaminated and it may not be advis
able to close primarily.
406
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
Figure 28.42 Vacuum suction of wound. A large vascularized heel flap
was transferred over a defect and a vacuum drain was applied to prevent
excessive fluid buildup under the graft. The drain is typically removed in
24–36 h.
(Courtesy of Dr Jeffrey Christensen.)
Figure 28.43 Mild compression splint. This type of dressing is usually
applied after procedures that have little postoperative edema or drainage.
It is composed of the normal sterile dressings followed by gauze wraps
alternating with elastic cohesive bandaging. Two or three layers may be
applied as needed.
Figure 28.41 Buttress sutures. (A) The tubing used in this case was a small pediatric IV tubing. The incision is also closed with multiple interrupted
sutures. (B) The tubing in this case was the softer tubing from a small French catheter. The buttress suture provides additional compression of the skin
edges and reduces the individual tension of each suture.
A
B
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Figure 28.44 Moderate compression Jones splint. This dressing is used in
cases where moderate to severe edema or drainage is possible.
Figure 28.45 The Steri-Strip may be removed when it appears that the
incision is healed sufficiently.
Figure 28.46 Stage suture removal. Key sutures may be left in place
until a future visit, especially when the incision does not appear to be
healed sufficiently to remove all of the sutures.
Figure 28.47 Superficial dried blood or darkened tissues at the incision
site should not be removed prematurely since this may actually open the
incision leading to dehiscence or early increased scarring.
CONCLUSION
Although prevention of excessive scar formation is the ultimate goal
of surgery, scars are unpredictable and in some cases the excessive scar
is inevitable. There are several forms of treatment available to help
reduce or eliminate unsightly, restrictive, or symptomatic scars on the
lower extremities. Understanding the nature of the different types
of scars is beneficial in providing a successful treatment program.
The scar treatment with the least amount of secondary risk to the
patient is preferred. Silicone gel sheeting appears to be a product
that fulfills many of the needs in the treatment of scars, whether as a
first-line treatment or following other treatments, such as surgery to
remove scars.
408
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
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CHAPTER CONTENTS
Introduction
411
Historical aspects
411
Mechanism of action
412
Vacuum therapy system anatomy
412
Animal studies and foundation of NPWT
413
Clinical studies
414
General considerations
415
Acute vs chronic wounds
415
Infected wounds
416
Exposed tendon, fascia and joint capsule
416
Exposed bone or orthopedic hardware
416
Diabetic wounds
421
Venous stasis ulcerations
422
Compartment syndrome
422
Split-thickness skin grafts
422
Degloving injuries
423
Completion of therapy
423
Vacuum holiday or therapeutic pause
425
Advanced techniques
425
Contraindications
428
Complications of negative pressure wound therapy
429
Conclusion
431
INTRODUCTION
Negative pressure wound therapy (NPWT) has become a recognized
standard used to promote normal wound healing through rapid gran
ulation tissue formation. It involves applying a topical subatmos
pheric pressure (50–200 mmHg below ambient) across a wound
surface creating a favorable environment for healing by removing
excess edema, decreasing bacterial colonization and increasing
vascularity.
Negative pressure wound therapy has been cleared for marketing by
the United States Food and Drug Administration since 1995, for assist
ance in closure of both complex and chronic wounds. Since then, this
unique therapy has become commonplace in medical practice and is
used to treat a multitude of wounds (Box 29.1). In the lower limb, it
is especially useful in treating acute and chronic wounds, dehisced
wounds, open fractures with soft tissue loss and for diabetic limb
salvage.
HISTORICAL ASPECTS
The concept for negative pressure wound therapy was developed and
pioneered at Bowman Gray Medical School in North Carolina by
the collaboration of Argenta and Morykwas, a plastic surgeon and a
researcher, respectively.1,2 Concurrently in Europe and independent of
the work of Argenta and Morykwas, Fleischmann also experimented
with the effects of vacuum therapy.3,4 Several terms are used interna
tionally to describe negative pressure wound therapy, including:
Vacuum Assisted Closure®, topical negative pressure therapy, negative
pressure dressing, foam suction dressing, sealed surface wound
suction, subatmospheric pressure therapy, subatmospheric pressure
dressing and vacuum sealing technique.1–11 However, the most
©2012 Elsevier Ltd.
Negative pressure wound therapy in lower
extremity reconstructiona
Neal M. Blitzb, John S. Steinbergc
Chapter
29
cThis author is not employed by Kinetic Concepts, Inc or Smith & Nephew, Inc. The
author did not receive payments or other benefits or a commitment or agreement
to provide such benefits from Kinetic Concepts, Inc or any of its subsidiaries or
affiliations. No commercial entity paid, or directed or agreed to pay or direct, any
benefits to any research fund, foundation, educational institution or other charitable
or non-profit organization with which this author is affiliated or associated.
bThis author is not employed by Kinetic Concepts, Inc or Smith & Nephew, Inc. The
author did not receive payments or other benefits or a commitment or agreement
to provide such benefits from Kinetic Concepts, Inc or any of its subsidiaries or
affiliations. No commercial entity paid, or directed or agreed to pay or direct, any
benefits to any research fund, foundation, educational institution or other charitable
or non-profit organization with which this author is affiliated or associated.
aThis chapter supports general wound-healing indications and it may also support
indications that have not been cleared by the United States Food and Drug
Administration. Consult a physician or product labeling for proper indications,
contraindications and precautions for negative pressure wound therapy.
412
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
VACUUM THERAPY SYSTEM ANATOMY
The components necessary to apply negative pressure include the fol
lowing: (1) vacuum base system; (2) effluent collection canister;
(3) open celled foam; (4) egress tubing and (5) occlusive drapes.2
Basic application involves cutting the foam to mirror the shape of the
wound and secure with the plastic occlusive drape. The egress tubing
is placed into the foam and connected to a collection canister inside
of the vacuum base station (Fig. 29.1). This system creates a closed
airtight seal in order for the therapy to function properly. The pump
base station is programmed to produce the interval of suction (con
tinuous vs intermittent), as well as the level of subatmospheric therapy
(−50 to −200 mmHg). Two companies have negative pressure therapy
systems, they are Kinetic Concepts, Inc (V.A.C.® Systems) and Smith
& Nephew, Inc (Renasys™ Systems). Both companies provide base
system models (Fig. 29.2) that are selected based on the wound type
and size, treatment location (inpatient vs outpatient) and ambulatory
status (Table 29.1).22
Three types of foam are available from Kinetic Concepts, Inc for use
with the V.A.C.® Systems. They are open celled structures that are
selected based on the wound characteristics (Fig. 29.3). It is the open
celled nature of the foam that imparts the subatmospheric pressure
uniformly across the wound. The black polyurethane foam (Granu
Foam™) is most commonly used about the lower limb. Its major
advantage is its ability to promote robust granulation tissue forma
tion. The hydrophobic quality of the black foam also promotes
recognized term is Vacuum Assisted Closure®, or its acronym
V.A.C.®, which are trademarked by KCI (Kinetic Concepts, Inc,
San Antonio, TX).
MECHANISM OF ACTION
The therapeutic effects of negative pressure wound therapy are result
ant from local tissue responses of the wound to the mechanical force
and suction.12 The exact mechanism of action of subatmospheric pres
sure is believed to be a multifactorial process involving the removal
of excess interstitial fluid, increasing local tissue vascularity and
decreasing bacterial colonization.1,2,13 In 1911, Thoma14 first postu
lated that mechanical stress induces angiogenesis and tissue growth.
Ilizarov15,16 also noted that mechanical distraction induces bone and
soft tissue growth. These mechanical forces are believed to increase
the rate of cellular mitosis, which is responsible for the tissue expan
sion and regeneration.1,2
Removal of excess wound exudate is believed to enhance wound
healing through several processes. The active removal of the third
space fluid reduces local edema, which dilates the local blood vessels
and improves oxygenation to tissues.13 Increased blood supply also
brings nutrients and acute inflammatory cells to the wound bed. The
wound exudate that is actively removed by the vacuum contains
chronic proteinases that are known to inhibit wound healing. A pro
teinase imbalance is suspected to play an important role in the patho
physiology of chronic wounds.17
Increased tissue oxygenation is necessary for the oxygen-dependent
killing properties of the polymorphonucleocyte, fibroblast function,
and the inhibition of anaerobic bacterial activity.18 Active suction of
the wound bed may simply prevent infection by decreasing the
number of microbes available to proliferate and mount an attack
against the host.1,2 An infected wound is believed to have an extended
inflammatory phase of wound healing.19–21 Negative pressure wound
therapy has been shown to decrease the bacterial load from 107 per
gram of tissue to 102–103 per gram of tissue by treatment day 5.1,2
Box 29.1 Clinical uses for negative pressure
wound therapy
• Acute and chronic wounds
• Traumatic wounds
• Infected wounds
• Pressure ulcers
• Diabetic foot ulcers
• Leg ulcers – various etiologies
• Exposed tendon, capsule or bone
• Exposed orthopedic hardware
• Skin graft recipient site fixation
• Skin graft donor sites
• Flap salvage
• Fasciotomy wounds
• Degloving injuries
• Burns (partial-thickness)
• Wound dehiscence
• Sternal wound breakdown
• Abdominal dehiscence
• Hidradenitis suppurativa
• Spider bites
Figure 29.1 Illustration demonstrating foam sponge on wound with
vacuum suction.
(Courtesy of KCI, San Antonio, TX.)
Table 29.1 KCI Vacuum Assisted Closure® (V.A.C.) models
Model
Mobile
Effluent
Wound
number
V.A.C.®
No
Moderate/heavy
Multiple
V.A.C.® ATS
No
Moderate/heavy
Multiple
MiniV.A.C.®
Yes
Minimal (>15 cc/day)
Single
V.A.C.® Freedom
Yes
Moderate/heavy
Multiple
(Modified from KCI V.A.C.® Therapy Clinical Guidelines 2003.)
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Negative pressure wound therapy in lower extremity reconstruction
413
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over this area, allowing for quick and easy application. Additionally,
the T.R.A.C.® Pad technology allows for pressure monitoring at the
wound site.
ANIMAL STUDIES AND
FOUNDATION OF NPWT
Argenta and Morykwas originally performed a series of pig model
experiments to identify and better understand the therapeutic effects
of vacuum therapy.2 These studies provided the evidence that deter
mined the guidelines for treatment protocols in humans. Five groups
of five pigs were used to research blood flow, granulation tissue
formation, bacterial clearance and random pattern flap survival.
The blood flow studies measured laser Doppler signals in the sub
cutaneous tissue and muscle directly adjacent to experimentally
created wounds undergoing pressure therapy. Continuous measure
ments were recorded as the subatmospheric pressure increased every
15 min by 25 mmHg increments (range, 0–400 mmHg). This was
studied for both continuous and intermittent therapy with intermit
tent therapy cycled on for 1–10 min and off for 1–5 min. Results
demonstrated peak flow of four times baseline during the 125 mmHg
pressure and depressed blood flow baseline at pressures greater than
400 mmHg. These increases in blood flow declined back to baseline
after several minutes of the continuous therapy. Because the intermit
tent mode cycles pressure on and off, the local increases of blood
supply could be reproduced intermittently throughout therapy.
The most favorable intermittent cycle was determined to be 5 min on
and 2 min off.
Granulation tissue formation was studied with both continuous
and intermittent therapy. Three experimentally created wounds were
compared; one wound was treated with saline gauze dressings to serve
as a control group. Vacuum therapy at 125 mmHg was applied to the
other two wounds – continuous vs intermittent (5 min on/2 min
off cycle). Wound volume was measured by fluid displacement and
alginate impressions. Results demonstrated statistically significant
mean increases in the rate of granulation tissue formation
(63.3 ± 26.1% and 103.4 ± 35.3% for the continuous and intermit
tent cycles, respectively).
A
Figure 29.2 Negative wound pressure therapy systems. (A) V.A.C.®
System models. (Courtesy of KCI, San Antonio, TX.) (B) Renasys™ system
models. Left: Renasys™ GO; Right: Renasys™ EZ.
(Courtesy of Smith & Nephew, St Petersburg, FL.)
B
Figure 29.3 Close-up image comparing the structure of the black
GranuFoam™ dressing (foreground) vs the white VeraFoam™ dressing
(background).
increased effluent removal. The GranuFoam Silver® is polyurethane
foam that has been microbonded with metallic silver, acting as a
barrier to bacterial penetration. The other type of foam available is
the VersaFoam™, which is made of polyvinyl alcohol and is white in
color. It is a denser structure that is inherently hydrophilic and is
packaged pre-moistened with sterile water. As such, higher vacuum
pressures may be needed to achieve adequate pressure therapy. Its
non-adherent qualities make it useful in situations where the underly
ing structures need protection (i.e. exposed nerve and/or tendon). Two
types of dressing kits are available from Smith & Nephew, Inc for use
with the Renasys™ Systems. A foam dressing kit (Renasys™-F Foam
Dressing Kit) and a gauze dressing kit is available (Renasys™-G Gauze
Dressing Kit).
The occlusive drape may be applied in one sheet or applied in
overlapping strips. Smaller strips are easier to handle and adjust for
the underlying contoured anatomy.23 Once the drape is placed, a 1 cm
slit or window is created over the foam and the T.R.A.C.® Pad is placed
414
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
vacuum in decreasing the size and depth of a wound; however, these
patients were not followed until wound closure.
In another negative pressure, wound therapy was compared with
Iodosorb® (Healthpoint Ltd, Fortworth, TX) and/or Panafil® (Health
point Ltd) treated pressure ulcers in a prospective randomized control
led trial of 22 patients (35 wounds).25 A 51.8% mean volume reduction
was seen in the NPWT group compared to 42.1% with controls.
Wound biopsies were obtained before and after 6 weeks of treatment.
Interestingly, the mean number of polymorphonucleocytes and lym
phocytes decreased in the NPWT treated wounds, whereas an increase
was noted in the Iodosorb®/Panafil® group. Also, the NPTW treated
wounds demonstrated a mean increase in capillaries. This study
further supports the ability of the vacuum to promote granulation
tissue formation compared with other methods of wound care.
McCallon and colleagues26 evaluated NPWT on 10 diabetic foot
wounds in a randomized controlled study. These patients were
followed until wound healing, defined as secondary intention or a
surgical procedure that resulted in wound closure (i.e. STSG, flap or
delayed primary closure). Vacuum-treated wounds reached an end
point almost twice as rapidly as saline-dressing-treated wounds; 22.8
(±17.4) days vs 42.8 (±32.5) days, respectively. Statistical analysis was
not performed in this study.
Conversely, the healing endpoint of negative pressure therapy vs
saline dressings in forming granulation tissue was found to be similar
in a randomized controlled prospective study by Wanner and col
leagues.27 They treated pelvic region pressure sores in 11 patients. The
treatment endpoint was defined as a decrease in the initial volume by
50%, because all wounds were subsequently closed with a flap. The
mean time until the endpoint was 27 days for the NPWT group com
pared to 28 days for the control group.
Armstrong and colleagues28 retrospectively reviewed their experi
ence with the negative pressure therapy in 31 patients with diabetic
foot wounds. Approximately 51% of the wounds occurred on the
digits or ray, 26% transmetatarsal or midfoot level, and 23% were
located on the heel. The mean surface area was rather large, measuring
27.9 ± 19.5 cm2 and almost half of the wounds demonstrated exposed
bone or an open joint. After surgical debridement, vacuum therapy
was applied until the wound beds were completely granular. Interest
ingly, 90% of patients did not require a further level of amputation,
suggesting that the vacuum therapy was effective in granulating over
bone, as 50% of the wounds had exposed bone prior to the vacuum.
Due to the retrospective nature of this study, it is not clear if the
success at preventing further amputation is truly due to the vacuum
therapy, the initial debridement, control of infection, vascular compe
tency, glucose control and/or other potential variables.
Another retrospective study on negative pressure in the treatment
of non-healing diabetic and dysvascular wounds involving the lower
extremity was performed by Clare and colleagues.29 They reported
82% successful healing in 17 patients, 14 of whom had diabetes
and eight of whom had severe peripheral vascular disease. Vacuum
therapy was maintained for an average of 8.2 weeks and discontinued
when closure with STSG or growth factors, or simple dressing changes
were initiated. Most wounds were located at or below the ankle;
however, no mention was made with regard to wound size, volume
or depth.
Mullner and colleagues30 performed a prospective study evaluating
the vacuum sealing technique on 45 patients with acute and chronic
wounds. Three types of wounds were studied: 17 sacral ulcers, 12 acute
soft tissue defects and 16 infected soft tissue defects with exposed
bone or hardware after lower extremity fracture and open reduction
internal fixation. Twelve of the 17 patients with sacral ulcers responded
to vacuum therapy. All patients in the acute soft tissue defect group
were brought to definitive closure in a mean healing time of 16 days
and 14 of the 16 infected fractures formed granulation tissue over
The bacterial clearance experiments involved the introduction of an
infectious concentration of Staphylococcus aureus and epidermidis (108
organisms) to experimentally created wounds. Vacuum therapy was
applied and full-thickness punch biopsies were obtained for culture
every 24 h during a 2-week period. Results were compared to a control
wound that was not treated with pressure therapy. A slight decrease
in the gross number of organisms was seen in all wounds during the
first four post-inoculation days. At post-inoculation day 5, the vacuum-
treated wounds demonstrated a subinfectious level of bacteria (<105
organisms) and remained subinfectious for the remainder of therapy.
Interestingly, the control group demonstrated an opposite effect at
post-inoculation day 5 as the number of organisms peaked and finally
dropped below 105 organisms at a mean of 11 days.
The flap-survival experiments evaluated the effects of continuous
vacuum (125 mmHg) on random-pattern flaps in four scenarios:
(1) pre- and post-surgical vacuum; (2) pre-surgical only; (3) post-
surgical only and (4) no exposure of vacuum therapy (control group).
The pre-surgical vacuum was applied for 4 days. The post-surgical
vacuum was immediately placed and removed at 72 hours, followed
by 48-hour intervals until any necrosis ceased to expand or healing
occurred. The greatest percentage survival occurred in the pre- and
post-surgical vacuum treated flaps, 72.2 ± 10% and 67.8 ± 4.0%,
respectively. The vacuum therapy before and after random flap surgery
demonstrated a statistically significant (p<0.01) increase in percentage
survival when compared to the control group.
A separate but related animal and human study also demonstrated
increased rates of re-epithelialization of skin graft donor sites.13
The pig donor sites that were treated with subatmospheric pressure
were grossly healed at postoperative day 4 compared to the controls
that healed by postoperative day 7. Although split-thickness skin
graft (STSG) donor sites differ from acute and chronic wounds in
pathophysiology and underlying anatomy, this study demonstrates
the ability of the vacuum to promote epithelialization. Moreover,
biopsy of a vacuum-treated pig-donor site demonstrated a mature
epidermis with stratum corneum and rete ridges, while the control
group did not.
CLINICAL STUDIES
Several clinical studies have investigated the effectiveness of subatmos
pheric therapy. The first series of human wounds treated with NPWT
was presented by Argenta and Morykwas in 1997.1 A total of 300
wounds of various etiologies were treated until a defined healed end
point (complete healing, wound progression to a salvageable state for
delayed closure, patient refusal or patient expiration). The categories
of wounds treated included: 175 chronic wounds (pressure ulcers,
venous stasis ulcers and other vasculitic ulcers); 94 subacute wounds
(dehisced wounds, open wounds with exposed orthopedic hardware
and/or bone, and miscellaneous wounds open for less than 7 days)
and 31 acute wounds (contaminated wounds, hematomas, abscesses,
degloving injuries). This text mainly reviews the authors’ clinical expe
rience with the vacuum and establishes many of the treatment proto
cols used today, but it does not reveal quantitative wound volume and
wound area responses to treatment, healing rates, or statistical analy
ses that verify its therapeutic effect.
Joseph and colleagues24 performed a randomized controlled study
comparing the vacuum vs saline dressings in 36 chronic wounds over
a 6-week period. Results demonstrated a significant positive effect, as
vacuum-treated wounds underwent a 78% change in volume vs 30%
seen with the control group. Additionally, a statistically significant
change in wound depth was observed: 66% with NPTW and 20% with
saline treatments. This study demonstrates the effectiveness of the
Chapter
Negative pressure wound therapy in lower extremity reconstruction
415
| 29 |
bone or hardware; two of which were closed by secondary intention
and the remaining patients were closed by STSG.
In summary, the previous studies and case reports clearly identify
an overall general trend towards improved and faster healing rates
with the V.A.C.® System. However, the studies are severely lacking in
sample size, thus underscoring the need for further multicenter rand
omized controlled studies to establish the V.A.C.® System’s effective
ness when compared with conventional methods of wound care.31
Additionally, comparing new granulation tissue formation between
studies is difficult, as some investigators measured healing in regards
to wound size, while others measured wound volume. Measuring
wound volume may be more practical as it accounts for areas of
undermining that will not be identified with simple wound measure
ments alone. A standardized method of evaluating wound healing is
needed to better compare studies.
GENERAL CONSIDERATIONS
A patient’s general medical status must be thoroughly evaluated and
those medical conditions that are known to inhibit wound healing
treated concomitantly. For example, a patient’s age, nutritional status
and glucose control should be considered and evaluated prior to the
initiation of therapy. Poor control of blood glucose is known to inter
fere with wound healing. Neuropathic diabetic wounds often occur
on weight-bearing surfaces and these wounds must be appropriately
offloaded. Similarly, neuropathic wounds in non-ambulatory patients
with paraplegia and spina bifida must be protected from pressure.
Autoimmune diseases may impair wound healing, as well as some of
the medications used to treat such diseases. Steroids should be dis
continued or tapered if patients can tolerate their absence. Smoking
is a well-known inhibitor by producing decreased tissue oxygenation
as well as constricting the microcirculation. Patients with peripheral
vascular disease may benefit from vascular consultation and possible
intervention to restore adequate perfusion.
Although NPWT actively treats the wound, it is merely an adjunct
to wound care and the basic principles of wound care apply regardless
of vacuum therapy. All wounds must be thoroughly assessed prior to
initiating subatmospheric negative pressure. The wound size, dura
tion, location and depth are all considered to determine an appropri
ate treatment protocol. Routine measurements and photographs are
important to evaluate the response of a wound to treatment.
The wound must be appropriately prepared prior to initiating
vacuum therapy. Acute wounds should be immediately debrided and
foreign material removed. Grossly infected wounds may require serial
debridements until a stable clean wound is obtained. All wounds
should be devoid of necrotic non-viable tissue. The remaining tissue
should appear healthy and vascular. The wound margins may need to
be refreshed, especially in long-standing wounds. An epithelial layer
located centrally in the wound may need to be removed to allow for
uniform healing across the wound bed. Finally, the wound should be
thoroughly cleansed to remove topical contaminants. The hair located
on the periphery of the wound is shaved to enhance adherence of the
occlusive drape.
In general, NPWT guidelines involve an initial continuous cycle for
the first 48 h followed by subsequent intermittent cycles (5 min
on/2 min off) for the remainder of the therapy. The pressure is typi
cally set to 125 mmHg for the black foam, but may need to be
decreased if adverse effects are experienced. The therapeutic response
of the V.A.C.® System is typically rapid as granulation tissue often
forms by the second foam dressing change. Existing granulation tissue
is transformed into exuberant healthier appearing granulation tissue
(Fig. 29.4). Dressings are changed every 48 h for most wounds, and
Figure 29.4 (A) Dehisced wound after first ray amputation. (B) After
second vacuum dressing change – note healthier granulation tissue
formation when compared with pre-vacuum treatment. In this clinical
situation, the vacuum was used as an intermediate procedure as a
transmetatarsal amputation was subsequently performed for osteomyelitis
of the second metatarsal.
A
B
every 12–24 h in the presence of infection. The pressure and cycle
settings for different clinical scenarios are illustrated in Table 29.2.
ACUTE VS CHRONIC WOUNDS
All wounds are not created equal; however, all wounds must progress
through the three stages of wound healing inflammatory, proliferative
and remodeling.17 A wound that is arrested in one of the phases of
wound healing is considered a chronic wound, whereas an acute
wound is defined as a newly formed/created wound that has just
begun to progress through the stages of wound healing.20,21 The patho
physiology and milieu between an acute and chronic wound are quite
different and should be considered throughout treatment. An acute
or traumatic wound is generally free of bacteria unless it was contami
nated during the time of injury, whereas a chronic wound is often
colonized with multiple microorganisms. A chronic wound may be
converted to an acute wound through debridement; which may then
enable the wound to progress normally through the stages of wound
healing.20,21
416
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
The plantar fascia is a thick ligamentous structure that will form
granulation tissue with subatmospheric pressure (Fig. 29.5). Negative
pressure wound therapy is extremely useful with plantar foot wounds
since healing by secondary intention is often the treatment of choice
due to the nature of the volar skin. STSG of the plantar surface is less
desirable because the grafted skin is not as durable as the native
plantar skin and often results in breakdown. Negative pressure wound
therapy may also be useful to treat exposed Achilles tendon, but
should be considered on a case-by-case basis (Fig. 29.6). Heugel and
colleagues33 used vacuum therapy to successfully heal an exposed
Achilles tendon secondary to a burn injury. A STSG was placed 12 days
after the initial V.A.C.® placement.
Vacuum therapy has been shown to be extremely useful in treating
exposed joint capsule or bone in acute and chronic situations. Before
initiating NPWT, osteomyelitis must be considered and treated accord
ingly. Antibiotic therapy is necessary in the presence of exposed bone
and in many situations continued for 6–8 weeks. Patients with
exposed joint capsule are suspicious for underlying osteomyelitis and
serial radiographs should be obtained to monitor for bone changes
(Fig. 29.7). Capsular tissue that does not form granulation tissue
within 2 weeks of treatment may benefit from nuclear imaging or
magnetic resonance to rule out osteomyelitis.
EXPOSED BONE OR
ORTHOPEDIC HARDWARE
Wounds with exposed bone, tendon or orthopedic hardware are often
a treatment challenge, especially on the foot and ankle region because
of the limited availability of local musculocutaneous or fasciocutane
ous flaps.32,34,35 The advantage of NPWT is the ability to rapidly form
granulation tissue and convert an open wound into a controlled,
closed wound. This is extremely useful for the treatment of acute
wounds and open fractures where soft tissue coverage is compromised
from swelling and/or frank tissue loss. Negative pressure wound
therapy may be placed sterilely in the operating room before infection
has occurred, which is usually best accomplished within 72 h after
injury.36 Once swelling has subsided, NPWT may be discontinued and
the wound can be closed primarily. Granular tissue beds are often
treated with a STSG to facilitate rapid wound closure (Fig. 29.8).
Exposed hardware is often a precarious situation in both acute and
chronic situations. Several surgeons have noted the ability of NPWT
INFECTED WOUNDS
Acutely infected wounds must undergo an incision and drainage in
the operating room, especially where gross purulence and necrotic
tissue are present. The wounds are packed open with saline dressing
changes and inspected daily. Negative pressure wound therapy is
applied once the infection is controlled and the wound is stable
without gross purulence or necrotic tissue. Additionally, cellulitis
should be resolving and patients are concomitantly treated with
appropriate antibiosis. Negative pressure wound therapy dressing
changes are performed every 12–24 h with infection and the device
is programmed to continuous suction. Use of silver impregnated foam
is considered for use with infection. Although silver’s antimicrobial
properties have been known for years, only recently has it been com
bined with negative pressure therapy.
EXPOSED TENDON, FASCIA
AND JOINT CAPSULE
Although tendon is often described as a relatively avascular tissue,
subatmospheric pressure may facilitate closure through direct granular
tissue formation and wound contraction. Tendons with intact para
tenon are theoretically protected and may form granulation tissue
easier than simply exposed tendon. Nonetheless, secondary intention
healing over exposed tendon may take several months of treatment.32
Greer and colleagues11 used NPWT successfully for exposed wrist flexor
tendons after donor site breakdown of radial forearm free flap in two
patients.
Depending on the involved tendon, location and amount of
exposed tendon, NPWT is often used as an adjunct to prevent tendon
desiccation until another more definitive procedure may be per
formed, such as local or free flaps. A non-adherent dressing (i.e.
Adaptic®, Johnson and Johnson Medical, Inc, New Brunswick, NJ)
must be placed between the black foam and exposed tendon. The
VersaFoam™ Dressing may be placed directly on the tendon. It is
important to debride any necrotic tendon prior to initiating therapy.11
In some situations, the vacuum may be used until full wound closure;
however, adhesions may occur between the tendon and newly
formed skin.11
Table 29.2 Vacuum Assisted Closure® (V.A.C.) recommendations
Wound type
Initial cycle
Subsequent cycle
Pressure (mmHg)a
Duration
Acute or traumatic
Continuous
Intermittent
125
q 48 h
Infected
Continuous
Continuous
125
q 24 h
Dehiscence
Continuous
Intermittent
125
q 48 h
Meshed graft
Continuous
n/a
50–125
d/c @ 4–5 days
Degloving injury
Continuous
n/a
50–125
d/c @ 4–5 days
Fasciotomy
Continuous
Intermittent
125
q 48 h
Chronic
Continuous
Continuous
50–125
q 48 h
Pressure ulcers
Continuous
Intermittent
125
q 48 h
(Modified from KCI V.A.C.® Therapy Clinical Guidelines 2007.)
aPressure settings for black polyurethane foam.
Chapter
Negative pressure wound therapy in lower extremity reconstruction
417
| 29 |
A
B
C
Figure 29.5 (A) Diabetic with necrotizing plantar medial foot infection. Note the large area of necrotic skin. (B) Significant tissue loss after
debridement and exposed plantar fascia. (C) Exuberant granulation tissue over plantar fascia with vacuum therapy.
to help promote granulation tissue over hardware. Argenta and
Morykwas first reported successful closure in 37 patients with exposed
hardware.1 Mullner and colleagues30 demonstrated successful granula
tion formation in 14 of 16 open tibial fractures with exposed hard
ware and bone. It has also been used to cover spinal wounds with
exposed hardware.37
DeFranzo and Argenta achieved successful closure in 71 of 75
patients in a variety of lower extremity wounds, 52 of which were
below the knee.36 Some 65% of wounds were the result of trauma,
most secondary to a motor-vehicle accident or gunshot. Of the non-
traumatic wounds, 13 were secondary to dehiscence or infected ortho
pedic wounds. Twelve patients had exposed orthopedic hardware at
the time of vacuum placement. Negative pressure wound therapy was
placed immediately after the initial operating room debridement in
approximately half of the cases. Closure with STSG was performed in
more than half of the cases, delayed primary closure in 12 wounds
and flap closure in five wounds. This report illustrates the utility of
NPWT when treating exposed bone and/or hardware.
Exposed bone must be debrided until healthy, bleeding and stable
bone is encountered.20,21 The foam sponges may be placed directly
over the bone. Depending on the clinical situation and specific bone
involved, the initial dressing changes may be initiated in the operating
room and then performed at the bedside as granular tissue has formed
directly on the bone (Fig. 29.9). NPWT may be performed over bone
graft as well (Fig. 29.10). It is important to note that complete healing
may occur over infected bone, and a sequestrectomy may need to be
performed at a later date. DeFranzo and Argenta reported two of 12
patients requiring hardware removal and sequestrectomy.36
418
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
Figure 29.6 (A) Exposed tendon after Achilles surgery treated with the NPWT. Granulation tissue formation directly on tendon. (B) Vacuum therapy on
Achilles tendon. A non-adherent interface is placed between the tendon and black foam (not shown).
A
B
D
E
F
(D) V.A.C.® System in place. Ideally, bridge technique should be used to keep the egress tubing off of the plantar aspect of
the foot. (E) Interval picture demonstrating wound contracture and robust granulation tissue. (F) Complete healing by secondary intention with wound
NPWT. (Courtesy of Graham Hamilton, DPM.)
Figure 29.5, Continued
Chapter
Negative pressure wound therapy in lower extremity reconstruction
419
| 29 |
Figure 29.7 (A) Diabetic with lateral foot wound after debridement for necrotizing infection resulting in significant tissue loss. (B) Wound V.A.C.®
system in place. (C) A granular bed was created; however, the vacuum was unable to promote granulation over the fifth metatarsophalangeal joint
capsule – suggestive of underlying infection. Also, note macerated wound edges secondary to foam contact with normal skin during therapy.
(D) Status post-metatarsal head resection for osteomyelitis and fillet toe amputation with primary closure. (E) Healed and stable 1 year after index
operation.
A
B
C
D
E
The decision to remove orthopedic hardware depends on the indi
cation for the index operation. Exposed hardware may be removed if
the underlying osseous structures have healed and the hardware is no
longer needed. If the hardware is required for bone healing, NPWT
may be used to heal the soft tissue over the hardware. Hardware stabil
ity is the best predictor for fracture/bone healing and should only be
removed if absolutely necessary.36 Grossly infected implants require
removal. Depending on the location and size of the wound, the
hardware may need to be removed and an external fixator applied to
stabilize the bone segments during healing. Mullner and colleagues30
removed three of 11 lower extremity implants due to septic loosening
in subacutely infected wounds, but this was performed after subat
mospheric therapy had already healed the wounds after incision and
drainage. Attinger and Cooper38 have advocated the use of NPWT for
calcaneal soft tissue reconstruction for dehisced wounds after open
reduction internal fixation. Calcaneal wounds of <2 cm may be treated
420
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
A
B
C
D
E
Figure 29.8 (A,B) Open lateral ankle dislocation after fall from a ladder resulting in large wound. Monolateral external fixator is used to stabilize the
ankle. (C) Wound appearance after serial debridements. (D,E) Negative pressure wound therapy is used to promote a stable granular wound ready for
skin grafting.
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Negative pressure wound therapy in lower extremity reconstruction
421
| 29 |
F
G
(F) Skin graft is harvested from the posterior calf and placed on the wound. (G) Complete healing.
Figure 29.8, Continued
with subatmospheric therapy and STSG. Attinger and Cooper38 also
recommend larger calcaneal wounds with exposed bone or hardware
be treated with a local or free tissue flap.
Exposed tendon, bone and/or orthopedic hardware should be
covered with a healthy granular soft tissue bed as soon as possible to
prevent infection and allow for rapid patient mobilization. In many
situations, NPWT may be used as an intermediate procedure until a
more definitive closure may be performed (Fig. 29.11). Of course,
treatment is dependent on wound etiology, patient’s health status,
wound location and involved underlying structures.
DIABETIC WOUNDS
Diabetic foot wounds occur in a variety of locations and often lead to
partial-foot amputation or below-knee amputation. These wounds are
often complicated by peripheral neuropathy, peripheral vascular
disease, infection, Charcot arthropathy and non-compliance. Several
investigators have demonstrated the ability of NPWT to successfully
treat diabetic wounds, as described earlier in this chapter (Fig.
29.12).28,29 In a small series of patients, negative-pressure salvaged
422
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
VENOUS STASIS ULCERATIONS
Venous stasis ulcerations of the lower extremity are caused by incom
petent perforators and typically occur about the medial malleolus.
Argenta and Morykwas treated 31 venous stasis or vasculitic ulcera
tions with NPWT.1 Once granular, closure was obtained with STSG or
bioengineered grafts. These wounds often require a lower initial pres
sure cycle due to pain, which is then increased accordingly. The dif
ficulty in treating these wounds is maintenance of long-term closure
because the wound will recur if patients are not compliant with com
pression therapy.
COMPARTMENT SYNDROME
Negative pressure wound therapy has also been used to manage
extremity wounds after fasciotomy for compartment syndrome. Fleis
chmann and colleagues4 reported successful closure in 25 lower
extremity fasciotomy sites in an average of 12.7 days. Some 20 wounds
were closed primarily, while the remaining wounds were closed with
skin grafting. Other case reports have also elucidated the utility of
NPWT after fasciotomy.41,42 Based on an animal study, it has been
hypothesized that vacuum therapy may help reduce the incidence of
myoglobin-induced renal failure associated with compartment syn
drome as a decrease in serum myoglobin was identified in rabbit thigh
fasciotomies treated with subatmospheric pressure.43
SPLIT-THICKNESS SKIN GRAFTS
Enhanced on-lay STSG incorporation rates have been noted with sub
atmospheric negative pressure bolster dressings (Figs 29.13–29.15).
The skin graft is secured to the wound in a standard fashion and a
non-adherent non-occlusive type interface dressing (Adaptic®, Johnson
and Johnson Medical, Inc, New Brunswick, NJ; Mepite®, Mölnlycke
Health Care, Norcross, GA) is placed between the foam and the graft
to prevent shearing. The active removal of fluid helps prevent seroma
or hematoma formation, a leading cause of graft failure.44 Addition
ally, the ability of the foam to conform to the wound and irregular
surfaces is thought to prevent graft mobilization, another common
cause for graft failure.44 Other factors that are attributed to better STSG
healing with the vacuum include enhanced neovascularization and
the active removal of degradation products and bacteria.
The treatment guidelines for STSG NPWT bolster dressings dramati
cally differ from other therapy recommendations. The initial dressing
and foam remains untouched until postoperative day 3 or 5; unless a
graft complication or infection is suspected.1,44,45 A good indicator of
graft incorporation is a decrease in effluent output after the first 24 h.45
The vacuum cycle remains on continuously for the duration of therapy,
at a pressure of 75–125 mmHg with the black foam. The white
VersaFoam™ dressing may be placed directly on the graft and set at
an initial pressure of 125 mmHg.
The bolster use of NPWT has been advocated by several surgeons.
Argenta and Morykwas mention the bolster use in their landmark
paper.1 Blackburn and colleagues also discussed their successful clini
cal experience with NPWT bolster dressing and reported a small case
series of three patients.45 They noted a 95% successful graft incorpora
tion and reduction of the bolstering period to 3 days, decreased from
the typical 5–7 days.
A retrospective study of 61 patients comparing the classic bolster
dressing vs NPWT bolster dressing was performed by Scherer and
A
B
Figure 29.9 (A) Posterior heel wound with exposed bone in diabetic
patient status post partial calcanectomy for osteomyelitis. Image with
vacuum therapy in place. (B) Poor application technique as tubing is
placed along suture line and directly on skin. A pressure indentation of
the skin is seen superior to the incision line. (C) Healed wound over
calcaneus.
C
wounds resulted in a decreased hospital stay and overall cost when
compared with below-knee amputation.39 Because these wounds are
often associated with infection and partial-foot amputation, resultant
extremity function is considered throughout treatment. This patient
population often utilizes negative pressure wound therapy until
full wound closure because of medical co-morbidities, which may
preclude closure by other methods. Bioengineered tissue may be used
with negative pressure to facilitate closure.40
Chapter
Negative pressure wound therapy in lower extremity reconstruction
423
| 29 |
colleagues.46 Their indications for STSG included wounds secondary
to burns, soft tissue loss and fasciotomy. They concluded that NPWT
offers improved STSG survival because the NPWT treated patients
required less repeat same site skin grafting (3% vs 19%).
DEGLOVING INJURIES
Several case reports have demonstrated successful use of NPWT bolster
dressing in treating degloving injuries.47–50 The avulsed skin is imme
diately defatted and replaced as a full-thickness skin graft; however,
failure is frequently due to seroma/hematoma formation and is espe
cially prevalent in highly contoured areas, such as the hands and feet.
Negative pressure wound therapy is believed to improve graft adher
ence because of its ability to provide even pressure across the graft and
contoured areas. In addition, the active removal of fluid prevents
seroma and hematoma formation. In the lower leg, an average
91% graft adherence was reported in 42 patients treated with these
measures.51 Three separate reports of vacuum treated degloving
Figure 29.10 (A) Vasculopathic patient with osteomyelitic sequestra of posterolateral heel that was treated with debridement and placement of
antibiotic beads. Negative pressure wound therapy was used to form granulation tissue over the monofilament wire with antibiotic beads. (B) After
infection is eradicated, the beads are removed and Papineau bone graft technique is performed with autologous iliac crest. Negative pressure wound
therapy was used directly on this onlay bone graft. (C) Nearly healed wound. Bone graft incorporated (X-ray not shown). No recurrence was seen at
most recent follow-up several years after index operation.
A
B
C
injuries involving the foot demonstrated graft takes of 60%, 95% and
100%.47–50 The foam may be rapidly placed on the foot by partially
splitting the foam to create a clamshell, which is placed onto the foot
like a slipper.51 Negative pressure wound therapy settings for degloving
injuries are similar for other grafts and should be placed on continu
ous cycle at 125 mmHg. The initial dressing remains undisturbed for
4–5 days. Difficult or complex wounds may require a longer duration
of therapy.49
COMPLETION OF THERAPY
The goals of treatment should be defined before initiating NPWT, and
therapy discontinued when the objectives are achieved. The average
length of vacuum treatment is approximately 4–6 weeks, however,
definitive wound closure should be performed in a timely, medically
appropriate and cost-effective manner. Wounds that have a granular
bed should be considered for an STSG. Surgically dehisced wounds
may be closed primarily once the tissue contraction has occurred.
424
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
Figure 29.11 (A) Non-healing heel decubitus (Stage IV) of 2 years duration in bed bound paraplegic. (B) Incision and drainage and partial
calcanectomy performed. (C) Negative pressure wound therapy is used as an intermediary before delayed primary closure. In this case, silver
impregnated foam was used. (D) Delayed primary closure is performed after the acute infection is under control and the patient is on appropriate
antibiotics based on intraoperative cultures. (E) Healed after approximately 3 weeks.
A
B
C
D
E
Chapter
Negative pressure wound therapy in lower extremity reconstruction
425
| 29 |
Figure 29.12 (A) Plantar lateral foot wound treated with vacuum
therapy in diabetic patient. (B) Healed wound after split-thickness graft.
A
B
Figure 29.13 (A) Guillotine amputation through Chopart’s joint. (B)
Complete adherence of split-thickness skin graft treated with vacuum
bolster dressing at first dressing change.
A
B
Open fractures with soft tissue loss or chronic wounds may benefit
from NPWT until a definitive soft tissue flap may be performed. Some
patients may not be surgical candidates for surgical wound closure
and subatmospheric therapy may be used until full wound closure is
achieved by secondary intention.
VACUUM HOLIDAY OR THERAPEUTIC PAUSE
Wounds that fail to make progress in a timely fashion or expand
during treatment should be re-evaluated and in some situations,
vacuum therapy is temporarily discontinued – also known as a
vacuum holiday or therapeutic pause. Although there is not a standard
duration for a vacuum holiday, the manufacturer recommends a 1–2-
day pause before reinitiating therapy. During this period, other modal
ities of wound care are employed; such as saline dressing changes,
enzymatic topicals and/or growth factors. In some situations, topical
wound care agents may be used in conjunction with subatmospheric
pressure. Hyperbaric oxygen therapy also may be used concomitantly
with NPWT and the foam dressing changes are coordinated with the
oxygen treatment (Fig. 29.16).52
Long-standing wounds unresponsive to treatment are suspicious for
malignancy and should undergo biopsy. The patient’s current medica
tions should be reviewed and new medications checked for inhibitory
wound-healing properties. Underlying osteomyelitis should be con
sidered and excluded if the wound is overlying an osseous structure.
The wound may become infected and require antibiotics. A culture
should be obtained to identify the infecting pathogens as well any
resistant patterns. The presence of necrotic tissue requires debride
ment and irrigation. An expanding painful ulcer with a violaceous
purple undermining border is suggestive of pyoderma gangrenosum,
and treatment that is medically based on debridement is
contraindicated.53
ADVANCED TECHNIQUES
Multiple wounds may be treated with a single negative pressure device.
Classically, the use of ‘Y’ connectors allows the suction to be shared
among wounds at separate locations. Wounds in close proximity may
also share a single negative pressure device by utilizing the bridging
technique. It involves connecting the wounds together with a piece of
426
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
Figure 29.14 Elderly patient with malignant melanoma of plantar arch. (A) Appropriate resection margins are determined by the biopsy. (B) Wide
resection is performed deep to plantar fascia. A large soft tissue defect remains that will be treated with negative pressure wound therapy. Methylene
blue remains from sentinal lymph node biopsy performed at the same operative session. Fortunately for this patient, the resultant defect avoids the
weightbearing portion of the foot. (C) Injecting an anesthetic into foam at dressing change may lessen patient discomfort that is associated with the
dressing change. Note the bridging technique is used to keep the egress tube away from the plantar foot. (D) Granulation tissue forms within the
wound. Coverage of the plantar fascia takes longer than coverage of the adipose tissue. (E) With negative pressure wound therapy, the wound is
100% granular and ready for skin grafting for definitive coverage.
A
B
C
D
E
Chapter
Negative pressure wound therapy in lower extremity reconstruction
427
| 29 |
A
B
C
D
E
F
Figure 29.15 (A) The wound is measured for allowing for appropriate size graft to be harvested. (B) Split thickness skin graft was harvested from
patient’s thigh, meshed, and secured to the wound bed. (C) Occlusive drape if placed circumferentially around the grafted wound to avoid periwound
maceration. (D) Non-adherent dressing placed directly on the skin graft to avoid foam adherence to the graft. (E,F) Negative pressure wound therapy
placed with bridge technique.
foam that overlies normal skin directly between the wound. The
bridged normal skin is covered directly with an occlusive drape that
provides protection from the vacuum forces (Fig. 29.17). Also, the
tubing is placed between the two wounds to prevent cross-wound
contamination and the wounds must be of similar pathophysiologies
for vacuum treatment settings.
Small wounds may be treated with NPWT by utilizing the draping
or framing technique. An occlusive drape is placed on the skin directly
surrounding the wound. Foam larger than the wound can then be
used as long as the surrounding skin is protected. At some point, the
wound becomes too small and the patient is better served by other
wound-care methods.
428
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
be evaluated. If the wound is stable, the same foam is replaced in its
previous position and a new occlusive drape is applied covering the
incised area to recreate an airtight seal.
CONTRAINDICATIONS
Absolute contraindications for NPWT include untreated osteomyelitis,
malignancy within the wound bed or surrounding tissue, exposed
blood vessels or organs, necrotic tissue with eschar present and unex
plored and non-enteric fistulas. Relative contraindications where
negative pressure therapy must be used cautiously include active
bleeding or in anticoagulated patients and difficult wound hemosta
sis. Additional precautions and safety tips along with product litera
ture should be consulted prior to negative pressure placement.
Undermined wounds may be united if the wound surfaces are
not fully interposed with the foam. The vacuum is programmed on
continuous suction, which will collapse the wound surfaces onto
themselves. A similar technique is used to collapse tunnels, often
seen in plantar deep space wounds. Plantar foot wounds represent a
therapeutic challenge for NPWT because of their weight-bearing loca
tion. Typically, patients with plantar wounds are kept non-weight-
bearing; however, non-compliant patients often bear weight and may
interrupt the vacuum seal if the tubing foam interface is located
plantarly. The bridging technique may be used to place the tube inter
face dorsally. In addition, negative pressure therapy may be used in
conjunction with external skin closure devices to aid wound contrac
ture (Fig. 29.18).
Wound inspection between dressing changes may be accomplished
by incising the occlusive drape at the foam wound margin interface.
The foam may be raised in a fish mouth fashion and the wound can
(G) Skin graft appearance at first dressing change 5 days from the index operation. Complete incorporation of the graft is
noted. (H) Completely healed wound.
G
H
Figure 29.15, Continued
Chapter
Negative pressure wound therapy in lower extremity reconstruction
429
| 29 |
A
B
Figure 29.16 (A) Multiple foot wounds in a patient with peripheral
vascular disease prior to debridement, vacuum therapy and hyperbaric
oxygen treatments. (B) Vacuum sponge covering multiple wounds
utilizing the bridging technique. (C) Healed wounds after split-thickness
skin graft dorsally and secondary intention plantarly.
C
Figure 29.17 Advanced techniques. (A) ‘Y’ technique. Allows multiple
wounds of similar pathophysiologies at different locations to be treated
concomitantly with a single vacuum unit. (B) Bridging technique allows
for wounds in close proximity to be treated with single vacuum unit and
single tubing.
A
B
COMPLICATIONS OF NEGATIVE PRESSURE
WOUND THERAPY
There are very few complications of NPWT and they are typically due
to improper application of the technique. Proper training and instruc
tion of NPWT therapy placement is necessary to maximize treatment.
The most common occurrence is loss of vacuum suction due to an
inadequate seal. Vacuum failure may occur at the foam tube interface
and it may be reinforced with an additional occlusive drape, such as
Tegaderm™ (3M, St Paul, MN), or Ioban™ (3M, St Paul, MN). Highly
contoured areas adjacent to mobile structures, such as the peridigital
skin, are often difficult to obtain a seal and the skin may be pretreated
with a topic adhesive such as Compound Benzoin Tincture (3M,
St Paul, MN) or Skip-Prep (Smith & Nephew, Inc, Largo, FL) to
help maintain adherence of the occlusive drape.
Fragile skin is at risk for irritation or breakdown with repeated
dressing changes and should be watched cautiously. In some cases,
the foam sponge may be replaced and a new occlusive drape may be
directly applied over the old drape. This technique will limit skin
irritation but should only be performed at every other dressing change.
Macerated wound edges are encountered if the foam remains in
direct contact with the normal periwound skin during vacuum therapy
(Fig. 29.19).23 This can be avoided by proper negative pressure dress
ing placement or utilizing the draping technique. A stencil of the
wound may be created before cutting the foam to prepare an exact fit
and contour of the foam. The wound margins may be protected from
maceration by applying a 1 inch border of hydrocolloid dressing
(DuoDERM®; ConvaTec, Ltd) underneath the occlusive drape.54,55 Per
sistent maceration possesses a theoretical risk for wound expansion
and should be avoided.
The robust ingrowth of granulation tissue into the sponge
may result in bleeding when the sponge is removed. The bleeding is
usually controlled with direct pressure; bedside cautery may be useful
for persistent bleeding. Performing dressing changes every 48 h will
lessen the likelihood of granulation tissue ingrowth. Pain may be
experienced with vacuum therapy and usually subsides shortly after
the initial foam compression. Excessive and prolonged discomfort
may be alleviated by titrating down the pressure setting in 25 mmHg
increments until an accepted level of comfort is achieved. The
pressure is then slowly increased to reach the target pressure, which
430
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
B
C
D
A
Figure 29.18 A 47-year-old male with diabetes and non-healing plantar wound, which has progressed to an infected wound requiring surgical
debridement. (A) Plantar wound exposed to fascia and joint capsule following excision of infected ulceration. (B) Placement of GranuFoam Silver into
wound and occlusive plastic drape. (C) Use of medial bridging technique to avoid prominence of the NPWT tubing. (D) Addition of external tissue
expander (DermaClose) over the NPWT dressing to give additional closure support.
is often associated with increased patient acceptance and satisfaction.
However, this feature is not available on all negative pressure devices.
Some patients may experience pain with dressing changes, which
is typically the result of the granulation tissue adhering to the foam.
Oral or intravenous narcotics may be coordinated with dressing
changes. Lidocaine solution and/or saline may be injected into
the foam to anesthetize the wound bed and loosen the adhesions
(Fig. 29.15C).54
Ulceration of the periwound tissue from the egress tubing
may occur if the tube is directly placed on intact skin, especially
overlying osseous structures (Fig. 29.9B). This may be avoided with
proper technique and planning prior to vacuum application. A mesen
tery of occlusive drape should be created between the tube and
the underlying skin. In some situations, the bridging technique
may be used to entirely change the location of the tube insertion into
the foam.
Chapter
Negative pressure wound therapy in lower extremity reconstruction
431
| 29 |
reported complication is a single case of non-fatal toxic-shock
syndrome.56 Other wound dressings have also been associated
with allergic reactions and toxic-shock syndrome and is a very rare
occurrence.57
CONCLUSION
Negative pressure therapy is an effective and novel approach to wound
care. The controlled subatmospheric pressure across a wound surface
promotes exuberant granulation tissue formation by increasing local
vascularity, removing excess edema, and decreasing the bacterial colo
nization. It facilitates rapid wound closure by creating a favorable
environment for delayed primary closure, skin grafting, soft tissue
flaps and healing by secondary intention.
Although NPWT is used for a variety of wounds and clinical sce
narios, it is merely an adjunct to wound management. The basic
principles of wound care and evaluation must be followed to achieve
success. Surgical debridement and antibiotics remain the essential
precursors in wound care and are usually utilized. A major advantage
of negative pressure therapy is the ability to convert a wound into a
controlled closed situation that allows for better management and
treatment of wounds in precarious situations (i.e. exposed bone,
tendon or orthopedic hardware). Complex wounds that may have
previously resulted in significant morbidity or amputation may be
effectively managed with negative pressure systems. The current litera
ture corroborates the efficacy of NPWT; however, further multicenter
randomized controlled studies are still needed.
Figure 29.19 Medial first metatarsophalangeal joint wound. Macerated
wound edge due to direct foam contact with normal surrounding skin
during vacuum therapy.
Figure 29.20 Acute foot wound in a patient with diabetes and peripheral vascular disease status post-partial-foot amputation due to infection.
(A) Note the exposed lesser metatarsals and preulcerative lesion located on the dorsal hallux interphalangeal joint. (B) Vacuum therapy initiated.
Circumferential dressing on hallux resulted in ischemia to digit. (C) Granular wound bed created over previously exposed metatarsals. An ischemic
ulceration occurred on the dorsal hallux due to the occlusive drape in a predisposed, vulnerable area.
A
B
C
Circumferential dressings should be applied cautiously, as they
create the potential for distal ischemia, especially if the extremity is
continuing to swell. Distal pulses should be routinely monitored.
Patients complaining of pain or numbness may require replacement
of the dressings or discontinuation of vacuum therapy. Digits that are
circumferentially draped are also at risk for ischemia and should be
monitored frequently, especially in patients with peripheral vascular
disease (Fig. 29.20).
Sensitivity to the foam and the occlusive drape may occur; however,
both foam dressings and the drape are latex-free. The most serious
432
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
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46. Scherer, L.A., Shiver, S., Chang, M., et al.,
2002. The vacuum assisted closure device:
a method of securing skin grafts and
improving graft survival. Arch Surg 137,
930–934.
47. DeFranzo, A.J., Marks, M.W., Argenta, L.C.,
et al., 1999. Vacuum-assisted closure for
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48. Josty, I.C., Ramaswamy, R., Laing, J.H.,
2001. Vacuum assisted closure: an
alternative strategy in the management of
degloving injuries of the foot. Br J Plast
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49. Meara, J.G., Lifei, G., Smith, J.D., et al.,
1998. Vacuum-assisted closure in the
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50. Banwell, P.E., Evison, D., Whitworth, I.M.,
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51. Jeng, S.F., Wei, F.C., 1997. Technical
refinement in the management of
circumferentially avulsed skin of the leg.
Plast Reconstr Surg 100, 1434–1441.
52. Fabian, T.S., Kaufman, H.J., Lett, E.D.,
et al., 2000. The evaluation of
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53. Blitz, N.M., Rudikoff, D., 2001. Pyoderma
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54. Krasner, D.L., 2002. Managing wound pain
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55. Short, B., Claxton, M., Armstrong, D.G.,
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56. Gwan-Nulla, D.N., Casal, R.S., 2001. Toxic
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FURTHER READING
Ballard, K., McGregor, F., 2001. Use of
vacuum-assisted closure therapy following
foot amputation. Br J Nurs 10 (15 Suppl.),
S6–12.
Birchall, L., Street, L., Clift, H., 2002.
Developing a trust-wide centralized
approach to the use of TNP. J Wound Care
11 (8), 311–314.
Brown, K.M., Harper, F.V., Aston, W.J., et al.,
2001. Vacuum-assisted closure in the
treatment of a 9-year-old child with severe
and multiple dog bite injuries of the
thorax. Ann Thorac Surg 72 (4),
1409–1410.
Deva, A.K., Buckland, G.H., Fisher, E., et al.,
2000. Topical negative pressure in wound
management. Med J Aust 173 (3),
128–131.
Fisher, A., Brady, B., 2003. Vacuum assisted
wound closure therapy. Issues Emerg
Health Technol (44), 1–6.
Fleischmann, W., Lang, E., Russ, M., 1997.
Treatment of infection by vacuum sealing.
Unfallchirurg 100 (4), 301–304.
Gerry, R., Kwei, S., Bayer, L., et al., 2007.
Silver-impregnated vacuum-assisted closure
in the treatment of recalcitrant venous
stasis ulcers. Plast Reconstr Surg 59, 58–62.
Goldstein, J.A., Iorio, M.L., Brown, B., et al.,
2010. The use of negative pressure wound
therapy for random local flaps at the ankle
region. J Foot Ankle Surg 29, 513–516.
Hopf, H.W., Humphrey, L.M., Puzziferri, N.,
et al., 2001. Adjuncts to preparing wounds
for closure: hyperbaric oxygen, growth
factors, skin substitutes, negative pressure
wound therapy (vacuum-assisted closure).
Foot Ankle Clin 6 (4), 661–682.
Jacobs, S., Simhaee, D., Marsano, A., et al.,
2009. Efficacy and mechanism of vacuum-
assisted closure (VAC) therapy in
promoting wound healing: a rodent model.
Plast Reconstr Aesthet Surg 62 (10),
1331–1338.
Mendez-Eastman, S., 1999. Use of hyperbaric
oxygen and negative pressure therapy in the
multidisciplinary care of a patient with
nonhealing wounds. J Wound Ostomy
Continence Nurs 26 (2), 67–76.
Mendez-Eastman, S., 2002. New treatment for
an old problem: negative-pressure wound
therapy. Nursing 32 (5), 58–63.
Mooney 3rd, J.F., Argenta, L.C., Marks, M.W.,
et al., 2000. Treatment of soft tissue defects
in pediatric patients using the VAC system.
Clin Orthop (376), 26–31.
Morykwas, M.J., David, L.R., Schneider, A.M.,
et al., 1999. Use of subatmospheric
pressure to prevent progression of
partial-thickness burns in a swine
model. J Burn Care Rehabil 20 (1 Pt 1),
15–21.
Morykwas, M.J., Kennedy, A., Argenta, J.P.,
et al., 1999. Use of subatmospheric
pressure to prevent doxorubicin
extravasation ulcers in a swine model.
J Surg Oncol 72 (1), 14–17.
Pignatti, M., Bruti, M., Rigotti, G., 2001.
Mobile-V.A.C. for the treatment of lower
limb ulcers. Plast Reconstr Surg 108 (6),
1837–1838.
Webb, L.X., 2002. New techniques in wound
management: vacuum-assisted wound
closure. J Am Acad Orthop Surg 10 (5),
303–311.
Webb, L.X., Schmidt, U., 2001. Wound
management with vacuum therapy.
Unfallchirurg 104 (10), 918–926.
Wiseman, J., Cullington, J.R., Schaeferle 3rd,
M., et al., 2001. Aesthetic aspects of
neurofibromatosis reconstruction
with the vacuum-assisted closure
system. Aesthetic Plast Surg 25 (5),
326–331.
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CHAPTER CONTENTS
Introduction
435
Bleeding complications
436
Wound dehiscence and necrosis
438
Postoperative edema
440
Postoperative infection
440
Cutaneous myiasis
443
Life-threatening complications
443
Conclusion
444
INTRODUCTION
The final surgical outcome of any operative procedure is unknown
until healing is complete and scar remodeling has taken place. It is
the goal of any surgeon to have an optimal outcome but in some cases,
complications can occur that may compromise the end result. It is
with this thought in mind that a comprehensive treatment program
for the most common complications be discussed.
Complications can be as trivial as slight increased bleeding intra
operatively, that is easily controlled with electrocautery or ligation of
a vessel, to major complications such as cardiac arrhythmia or arrest.
As the surgeon embarks on a surgical procedure, many issues must be
addressed. The overall health status of the patient must be assessed.
Some patient factors significantly impact the final outcome such as
malnutrition, particularly a lack of adequate protein. Albumin <3.5 g/
dL has been found to adversely affect healing as has dehydration,
anemia and vitamin deficiency. Certain underlying systemic medical
conditions and medications also need to be taken into consideration
by the surgeon, as they may affect the healing potential of the patient.
It is imperative that the surgeon is aware of any underlying medical
conditions or current medications, including any non-prescription
supplements, which the patient may be taking, so as to manage the
surgical wounds appropriately.
Uncontrolled diabetes mellitus may increase the patient risk of
postoperative infection due to hyperglycemia impeding leukocytic
phagocytosis and white blood cell migration. Immunosuppression
disorders and immunosuppressive drugs such as adrenal corticoster
oids predispose the patient to delayed healing by retarding the
required inflammatory reaction that wounds must go through and
thereby, increase the risk of infection. Chemotherapeutic agents have
a similar effect on wound healing and result in immunosuppression
that can interfere with the development of wound tensile strength. A
patient on current anticoagulation therapy or a patient with an under
lying coagulation disorder such as hemophilia can predispose the
patient to hematoma formation that leads to many related postopera
tive complications.
Smoking is a major risk factor in cutaneous surgery, especially pro
cedures that involve the creation of a skin flap. Skin flaps rely on small
fragile vessels to provide blood supply to the flap and the chemical
agents found in cigarette smoke significantly affect these vessels. Vaso
constriction from these products occludes the blood supply to the flap
and results in flap necrosis and flap failure. Abstaining from smoking
is a mandatory requirement for all patients undergoing plastic or
cutaneous surgery to avoid these unnecessary complications. As the
surgeon evaluates a patient for possible surgical intervention, these
factors should all be taken into consideration to better manage the
patient perioperatively.
Although many of the above factors are not within the control of
the surgeon, there are some complications that can be avoided pro
viding the surgeon follows certain precautions. Meticulous handling
of tissues, proper placement of surgical incision (preferably within
relaxed skin tension lines, RSTLs), minimal tourniquet time, avoid
ance of deep dead space, closing of wounds without tension, and evert
ing wound edges can all lead to fewer postoperative complications.
Many surgical complications are often interrelated, with bleeding
being the most expected and most common surgical complication.
Bleeding can lead to hematoma formation postoperatively, which can
result in increased swelling and increased tension on the wound.
Increased tension on the wound may lead to wound dehiscence and
necrosis that may then increase the risk of postoperative infection.
This cascade of complications can be interrupted anywhere along its
path to alter the final outcome.
©2012 Elsevier Ltd.
Surgical complications and their treatments
Mary E. Crawford
Chapter
30
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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
agent or combined together for enhanced affect, as they all differ in
their mechanism of affecting the clotting cascade. For example, some
patients are on combination therapy for high risk conditions such as
mechanical heart valves, unstable angina or myocardial infarction in
which clopidogrel and aspirin are given together. Managing a patient
on single or multi-antithrombotic agent regimens can be challenging
and controversial. In major surgery, the discontinuation of antithrom
botic agents such as warfarin or antiplatelet agents such as aspirin is
expected in the standard of care. However, in minor procedures,
including dermatological procedures, the management of these agents
remains contentious with some surgeons discontinuing the medica
tions and others continuing through the perioperative setting. These
patients may pose an even greater risk for complications of intraopera
tive and postoperative bleeding. There is lack of evidence-based medi
cine to determine the appropriate protocol of managing patients on
anticoagulation therapy. The surgeon must therefore weigh the poten
tial risks of discontinuing the medication and an acute thrombotic
event compared with the risk of continuing the medication and bleed
ing complications. Most studies, although some anecdotal, report very
low to no increased incidence of hemorrhagic complications with
continuation of anticoagulation drugs but discontinuation of the
medications has been implicated with increased incidence of throm
botic events, some with devastating outcomes.
Some of the current recommendations for management of patients
on anticoagulants that are undergoing a cutaneous surgical procedure
are based on the level of risk that each individual patient poses at the
time of surgery. All vitamin supplements and herbal medications
should be discontinued for 10–14 days prior to surgery and resumed
1 week postoperatively. Aspirin irreversibly binds to platelets and
inhibits platelet aggregation. Aspirin ingested primarily for prevention
and not for therapy of a known condition should also be stopped 10
days before surgery and resumed once the platelet plug forms several
days postoperatively and cannot affect the stability of the clot. Non-
steroidal antiinflammatory drugs (NSAIDs) bind reversibly to the
same point on the platelet as aspirin. They also inhibit platelet func
tion, but not permanently. The effect of the NSAID is usually voided
after approximately 4 half-lives of the medication, and the surgeon
can proceed with the operative procedure with diminished risk of
bleeding, and resumed 1 week later. Medically necessary warfarin,
aspirin and even clopidogrel should be continued perioperatively to
avoid the devastating consequences of a thrombotic event. It is advised
to evaluate the INR with the use of warfarin to maintain the value in
therapeutic range of 2.5–3.0 and not allow the patient to become
super anticoagulated.
Inherited clotting disorders are more difficult for the surgeon to
regulate. Some disorders are almost impossible to detect until bleed
ing complications occur perioperatively and further investigation and
advanced testing is performed after the fact to determine the cause.
Any alteration of the intrinsic or extrinsic clotting mechanism will
lead to abnormal bleeding (see Ch. 8). One of the most common
genetic disorders is von Willebrand’s factor deficiency. Unless a patient
was aware they had this disorder and reported it in their initial history,
most surgeons would be unaware of this condition until postoperative
testing was done to reveal the deficiency. The von Willebrand’s factor
deficiency is an autosomal dominant inherited disorder. This factor
serves as a plasma carrier for Factor VIII, which is vital for the clotting
cascade as well as facilitating platelet adhesion. A decrease in von
Willebrand’s factor may lead to a decrease in Factor VIII. Laboratory
evaluation of the patient will reveal a prolonged bleeding time and a
decreased quantitative value for von Willebrand’s factor. A patient may
also have a true decrease in Factor VIII, resulting in hemophilia-A
disorder. Factor VIII regulates activation of Factor X and can lead to
gross deficiency in clotting mechanism with a multitude of postopera
tive bleeding complications. Hemophilia B, also known as Christmas
BLEEDING COMPLICATIONS
As stated above, bleeding complications are the most common peri
operative difficulties and should be anticipated during surgery. Some
bleeding occurs during every surgery and usually is not a complication
unless the surgeon is unaware of an underlying bleeding disorder and
precautions were not taken or meticulous dissection is not performed
to appropriately cauterize or ligate bleeding vessels intraoperatively.
(Other methods of obtaining hemostasis are discussed in Chapter 8.)
The surgeon must fully understand the various processes that the
bleeding vessels undergo to achieve hemostasis and where certain
disorders or medications may affect that process. There are two
methods of hemostasis that work together to resolve bleeding. The
primary method is platelet driven and after vessel injury, results in
formation of a platelet plug. The secondary method is fibrin driven
that stabilizes and matures the platelet plug. Vascular injury exposes
the subendothelial connective tissue to which platelets adhere. Col
lagen then binds to the platelet cell receptor and activates the platelets
to release a chemical that causes the platelets to begin to aggregate
and adhere to each other.
Activation of the platelets modifies the surface so that fibrinogen
can link platelets and lead to clot maturation. As the platelet plug
matures, the secondary phase begins and prothrombin converts to
thrombin and the thrombin converts the fibrinogen to fibrin. Fibrin
polymerizes with the platelet plug to form an insoluble gel. Cross-
linking of the insoluble gel produces a final mature clot (Ch. 8, Fig.
8.1). Any factor that interferes with this cascade of events may result
in undesirable bleeding perioperatively. These factors include mechan
ical failure, thrombocytopenia, platelet dysfunction, pharmacological
interference and acquired or congenital defects.
When a blood vessel is cut, it immediately constricts to reduce the
diameter of the vessel and to slow the blood flow so that platelet
aggregation can occur. A vessel that is only partially transected may
not be able to constrict or retract, thereby preventing the reduction of
blood flow and platelet aggregation required to create the platelet
plug. Vasoconstriction may be aided with the addition of epinephrine
to the local anesthetic infiltrated in the area; however, the surgeon
should exercise caution in relying on the epinephrine to decrease
bleeding. The induced vasoconstriction may mask the bleeding
site until after closure, when the effects of the epinephrine dis
sipate and bleeding begins again. This will lead to complications
of excessive swelling and hematoma formation. All bleeding areas
should be explored and identified when possible, to avoid these
complications.
The platelet plug formation is crucial to achieving hemostasis
during any operative procedure. A reduction in the number of avail
able platelets or dysfunction of the platelets present can lead to dis
astrous bleeding complications. Thrombocytopenia is a reduction in
the number of available platelets. It may be seen with either impaired
production of platelets or increased destruction of platelets. As plate
lets are produced primarily in bone marrow, a bone marrow malfunc
tion can lead to reduced numbers of platelets. An increased destruction
of platelets can be seen with idiopathic thrombocytopenia purpura,
drug reactions, disseminated intravascular coagulation (DIC), or vas
culitis. Either way, the loss of platelet plug formation prevents the
usual cascade of events from occurring and increased complications
of bleeding.
Dysfunction of the coagulation pathway is more commonly seen as
a result of pharmacological agents or supplements ingested by the
patient. As many as 51% of patients reported utilizing vitamin and
herbal supplements, many which may affect bleeding such as vitamin
E, fish oil and gingko. Prescribed medications such as warfarin, clopi
dogrel, dipyridamole and therapeutic aspirin can be given as a single
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wound to heal by secondary intention. There is increased risk of infec
tion as the accumulated blood provides an excellent culture medium
for bacterial growth. The hematoma obstructs the phagocytic cells
from entering into the area to remove the bacteria and the presence
of the excess ferric ions makes the bacteria more virulent.
With the decreased phagocytosis, along with a more virulent bacte
rial strain, the hematoma enhances the formation of a postoperative
infection. In some cases, the hematoma will not be discovered in time
and may consolidate and become fibrotic. This will lead to increased
induration with dense scarring due to the increased fibroplasia and
can be difficult to resolve.
The best treatment for hematoma formation is prevention with
meticulous dissection and attention to hemostasis, along with com
pressive dressings and closed suction drains in deep dead spaces (Fig.
30.2). In the early stages of hematoma development, evacuation of
the hematoma may be of benefit to decrease the tension on the wound
edges. A few of the overlying sutures can be removed and then gentle
pressure on the sides of the wound may express the hematoma. The
incision is then left open and allowed to heal secondarily.
The longer the hematoma has been developing, the less effective
this method, as the hematoma is too organized. Aspiration is also
possible to remove some of the clotted blood but only early on
when the hematoma is still somewhat fluctuant. In some cases, the
hematoma applies too great a pressure on the wound and interferes
with normal postoperative healing. The hematoma should be evacu
ated under sterile operating room conditions with liberal irrigation
and vessel ligation to avoid further bleeding complications. Once
a hematoma consolidates within the wound, gentle massage and
warming of the tissues may accelerate enzymatic degradation of the
hematoma. Ultrasound, hydrotherapy and range of motion exercises
may also be helpful to break up the fibrin network of the hematoma
and reduce future scarring. Occasionally, intralesional injection of
corticosteroids can be utilized, if the wound is sufficiently healed.
Seroma formation has similar effects on the wound as the hematoma
with the extravasation of serum or serosanguineous fluid into a closed
space. Usually seen early in the inflammatory process of wound
healing, seroma is a common complication of skin grafts and is fre
quently noted in areas of previous surgery (Fig. 30.3). Serum does not
clot and, therefore, is amenable to extraction with a large-bore needle
and syringe, or if under a skin graft, a small nick can be made in the
graft to remove the fluid and allow the graft to lay down on the recipi
ent bed before loss of blood supply to the graft occurs.
disease, is a deficiency of Factor IX and is inherited only in males. It
cannot be clinically distinguished from hemophilia A. Other deficient
elements, such as fibrinogen or other clotting factors, can all lead to
bleeding complications, but are rarely tested for until postoperative
difficulties develop.
Surgical bleeding complications can be seen acutely during the
surgery, immediate postoperatively, or several days later. Acute bleed
ing is usually seen with the transection of a vessel intraoperatively.
The vessel is usually clamped and cauterized or ligated to prevent
further bleeding. In patients with some form of bleeding disorder,
whether drug induced or inherited, bleeding from small, almost invis
ible vessels may result in a persistent oozing that makes it difficult to
isolate a vessel to achieve hemostasis. A surgeon may choose to utilize
a Shaw scalpel or carbon dioxide laser to perform the incision and
dissection, as these instruments cauterize and seal the bleeding vessels
as the incision is being made.
A less common bleeding complication occurs postoperatively, gen
erally within the first few hours after the procedure with sudden
spontaneous bleeding within the wound. As the wound is already
closed, direct pressure for 10–15 min may control the bleeding and
allow early clot formation, however, if not successful, the wound may
need to be reopened and the bleeding vessel identified. This may be
a complication of the vasoconstrictive property of epinephrine that
provides the surgeon with a false sense of security that the bleeding
is well controlled upon closure. When the epinephrine effect dissi
pates, there is a risk of return of bleeding from smaller vessels that
were not cauterized at the time of the surgery. Fortunately, the vaso
constriction of epinephrine is usually short-lived and most vessels are
properly identified prior to completion of surgery.
The late sequela of postoperative bleeding is the formation of a
hematoma within the closed tissue space (Fig. 30.1). A patient will
experience increasing postoperative pain with greater swelling, scar
ring and wound complications that could increase the risk of infec
tion. It is often difficult to differentiate the formation of a hematoma
from an early postoperative infection. There is usually intense local
inflammation and pain due to increasing expansion of the hematoma
within the tissues. Pain and swelling occurs customarily earlier in
hematoma formation than in infection, usually within the first 24 h,
while infection is ordinarily within the first 72 h or longer. As the
hematoma develops, the pressure on the surgical wound could result
in necrosis of the tissue or wound dehiscence that may require the
surgeon to open the wound and evacuate the hematoma, allowing the
Figure 30.1 Late sequelae of bleeding with hematoma formation. It is
important to evacuate the hematoma at this time before it totally
coagulates.
Figure 30.2 Prevention of hematoma from deep wound site by using
small vacuum drains postoperatively.
438
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
dehiscence is left to heal slowly, there may be excessive fibrous tissue
formation along the edges of the incision.
The wound may also be compromised by the sutures implanted at
the time of closing. The sutures can be tied too tightly causing ischemia
or necrosis, especially with the postoperative edema that naturally
occurs. Conversely, sutures can become untied and the wound will
open. A suture can also lead to a sterile stitch abscess after removal.
The sterile abscess is a result of an inflammatory reaction in the suture
tract. This differs from a suture reaction, in which there is ‘spitting’ of
the stitches. This can occur if a deep suture knot is tied too closely to
the surface or a portion of a superficial stitch remains within the skin
and a small erosion occurs exposing the tuft of suture.
Wound necrosis may result from similar conditions as wound
dehiscence and can actually be one of the causes of wound dehiscence.
Necrosis can be seen with formation of a large hematoma or seroma,
infection or inadequate blood supply to the wound, usually as a result
of pressure. Flap survival is dependent on circulation from the base
to the tip of the flap. This may be compromised for a variety of
reasons, the most common being poor flap design (Fig. 30.5). In most
cases of failure due to inadequate circulation, the base of the flap
is too narrow for the length of the flap or the flap was created at
the wrong intersection of the angiosomes. It used to be dogma that
the length to base ratio could not be >3 : 1. Any longer a flap and the
pedicle could not supply adequate circulation to the apex of the flap
and necrosis would occur. The knowledge of the angiosomes and the
Figure 30.4 Wound dehiscence. (A) Frequently there will be thick fibrous
tissue formation at the edges of the incision following dehiscence.
(B) Large plantar dehiscence with maceration of skin edges.
A
B
Figure 30.3 Seroma formation. (A) Adjacent to a rotation flap.
(B) Involving the third toe, which had previously undergone several
surgeries. The serosanguineous fluid was evacuated in each case with
no further complications of healing noted.
A
B
WOUND DEHISCENCE AND NECROSIS
Wound dehiscence is almost always related to some other complicat
ing event such as hematoma or seroma formation, edema, superficial
or deep infection, or premature suture removal (Fig. 30.4). In some
situations, the sutures may be prematurely removed due to infection
or the need to express an underlying hematoma. Some patients heal
more slowly than others due to underlying systemic diseases or vas
cular compromise or smoking. Wound dehiscence is usually treated
with wound care and healing by secondary intention, although some
surgeons may choose to close a wound if it is still within the first 24 h
and there is no underlying contraindication such as infection. If the
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Surgical complications and their treatments
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Figure 30.5 Flap tip necrosis due to inadequate blood flow to tip of the
flap. Very large flaps or ones that are poorly designed also are at risk for
failure.
Figure 30.6 Hypertrophic scar with thickened raised hyperpigmentation.
Figure 30.7 Application of a thin sheet of silicone gel to hypertrophic
scar.
Figure 30.8 Keloid formation well beyond the original wound margins.
opening of choke vessels has now made this belief almost obsolete,
although many surgeons still adhere to the rule. Another reason for
flap necrosis is the inadvertent cutting or cauterization of the pedicle
arterial vessel that feeds the flap.
Necrosis of a graft that relies on the vascularity of the recipient bed
below usually occurs when a seroma or hematoma lifts the graft from
the underlying bed. A graft that is cut too small to cover the defect
and then stretched to accomplish this also is at risk for necrosis. As
with a flap and other surgical procedures, smoking results in increased
hypoxemia and eventual necrosis. In contrast to wound dehiscence,
debridement for wound necrosis is performed early only if infection
is present. Otherwise, the wound is allowed to demarcate so that only
non-viable tissue is removed.
As wound dehiscence and necrosis can result from excess tension
on the wound at the time of wound closure, surgical techniques may
be necessary to alleviate tension on the wound. The first is to perform
a relaxing incision approximately 2–3 cm away from, and parallel to,
the wound edge. The initial wound is closed first and then the relaxing
incision is undermined and closed. Another option, if available, is to
utilize a commercially available tissue expander or other device to
stretch the tissues. A final option may be to only partially close the
wound up to the point of excessive tension and then allow the remain
ing portion of the wound to close by secondary intention. These
techniques may help avoid some of the wound complications that
occur with excess tension such as wound dehiscence, necrosis, scar
widening and hypertrophic scar formation.
Scar formation postoperatively can be a frustration for the surgeon
and the patient. Hypertrophic scars are usually symptomatic, thick
ened, raised, usually pigmented scars that do not extend beyond the
margins of the wound (Fig. 30.6). The hypertrophic scars have evi
dence of neural hypertrophy, which may explain the increased pain
or itching seen when compared with normal scars. One of the treat
ments available is high potency steroid injected into scar or applied
topically. The steroid will usually decrease the erythema, itching and
pain associated with the scar but will not return it to normal. Another
popular treatment for all types of scars is the use of silicone gel
sheeting topically. The application of silicone sheeting decreases the
thickness and hyperpigmented nature of scars and softens them
significantly (Fig. 30.7).
A keloid scar formation is even more of a dilemma. The scar is
extensive, hyperpigmented and forms well beyond the original wound.
The keloidal scar can be massive and often painful (Fig. 30.8). Unfor
tunately, the keloid scar is very resistant to many treatments. Excising
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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
protracted the edema. Lymphatic vessels play a key role in removing
the protein-rich fluid from the extracellular spaces and rapidly dilate
to several times their normal caliber early in the inflammatory phase.
The prevention and treatment of excessive edema are important to
avoid unnecessary complications. Utilizing proper surgical atraumatic
techniques and anatomic dissection can prevent some edema. Injec
tion of short-acting corticosteroids mixed with local anesthetic agents,
at the time of the surgery, can help limit the intensity of early inflam
mation and control edema formation, but a certain amount of inflam
mation must take place for normal postoperative healing to occur so
use is limited. Compressive dressings can be part of the collaborative
effort along with elevation to assist lymphatic drainage and ice to
provide some vascular constriction to control postoperative edema.
NSAIDS can also be utilized to reduce the amount of inflammation
and swelling. Other treatments to reduce the degree of edema include
range of motion exercises to indirectly pump lymphatic fluid and
encourage circulation, compression therapy and massage and thera
peutic ultrasound and galvanic stimulation.
Fracture blisters and postoperative blisters may occur with the insult
of surgery, especially following osteotomies, and usually present when
large amounts of swelling occur (Fig. 30.10). There are two different
types of blisters that may form, clear-fluid filled and blood filled.
Clear-filled blisters retain some epidermal cells still attached to the
dermis whereas blood-filled blisters retain none of the epidermis. The
preferred method of treatment is to aspirate or drain under sterile
conditions, but to retain the roof of the blister to prevent infection.
A blister surrounding the wound may also occur postoperatively
due to a contact dermatitis from the skin preparation agents or agents
applied to the dressings, from the Steri-Strips or other tape applied to
the skin or from the application of a topical antibiotic to the wound.
Many patients feel compelled to apply antibiotic ointments and
creams to a wound following suture removal. There is a very high risk
of a patient having contact sensitivity to an applied antibiotic, espe
cially neomycin, the most common over-the-counter antibiotic avail
able. This should be strongly discouraged due to increased risk of
complications.
POSTOPERATIVE INFECTION
There are three elements required to produce a postoperative infec
tion: (1) a receptive host; (2) contamination by microorganisms, and
(3) a wound culture medium to support bacterial growth. The United
States Center for Disease Control and Prevention report the postop
erative infection rate for a clean, uncontaminated surgery to be <3%.
Skin provides a great barrier to invading bacteria, in that once a portal
of entry is established, bacteria can penetrate into the deeper layers
where resistance is diminished. Infection in a closed wound is much
more problematic than a superficial infection in an open wound (Fig.
30.11). During the operative setting, contamination of the wound
could occur from several sources including glove punctures, contami
nation of sterile draping and instrumentation, or ineffective skin
scrub. The length of the procedure may also play a role in the con
tamination of the wound, with the infection rate almost doubling for
every hour of operating time. So there appears to be no single factor
that influences contamination of the wound. The physiologic state of
the patient and the wound before and after the surgical procedure
appears to be a more significant factor in developing a postoperative
infection than contamination of the wound by bacteria.
Besides the overall health of the patient and contamination of the
wound, the wound must provide a culture medium for the bacteria
to flourish into a full postoperative infection. Ischemic or necrotic
wounds provide an excellent medium for bacterial growth. These
the keloid will usually just lead to more keloid formation, possibly
even larger than it was prior to excision. Injected steroids may help
some. The carbon dioxide laser may show some improvement when
employed to excise a keloid. In any event, the scar is the only aspect
of the surgery that the patient can see and efforts should be taken to
minimize scarring as much as possible with an atraumatic surgical
technique, buried sutures to reduce tension on the scar, and appropri
ate postoperative wound care. (For additional information about
scars, see Ch. 28.)
POSTOPERATIVE EDEMA
Some postoperative edema can be expected as part of the increased
vascular permeability of the normal inflammatory process. Inflamma
tion is a universal response of tissue to injury, whether traumatically
or surgically induced. The early inflammatory response serves three
purposes: initiate a massive humoral and phagocytic assault on tissue
invaded by bacteria; localize and isolate the reactive area and prevent
the spread of bacteria; and provide the initial clean up by removing
bacterial debris and dead tissue.
The inflammatory process results in four cardinal signs that can
easily be confused with signs of hematoma formation or incipient
infection. Swelling (tumor), redness (rubor), heat (calor) and pain
(dolor) are seen with the above conditions, which makes for a difficult
differentiation. The amount of postoperative edema can be excessive
as a result of a patient’s response to the injury, a more significant tissue
injury or extensive procedure, or patient non-compliance (Fig. 30.9).
The increased vascular permeability allows for the extravasation of
fluid into the extracellular tissue spaces, primarily the subcutaneous
tissue. Increased permeability may be the result of histamine and
histamine-like permeability factors that are released early on as a
result of the surgical insult or increased vascular permeability may
be due to direct vascular or cellular injury. Endothelial cell destruc
tion occurs by extensive surgical dissection and may take 1 or 2 days
to repair the area. The more damage the cells sustain, the more
Figure 30.9 Severe postoperative edema.
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Surgical complications and their treatments
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A
B
Figure 30.10 Fracture blisters. (A) Following severe edema after
osteotomies. (B,C) Due to edema and reaction to Steri-Strips.
C
A
B
Figure 30.11 Infection. (A) Closed space deep infection. The area was
swollen, hot and erythematous. (B) Superficial open wound infection.
(C) Superficial wound infection with maceration.
C
tissues lack sufficient oxygen and nutrients to cope with wound
healing and the impending infection. The necrosis may be due to
desiccation of the wound, extensive electrocautery, rough handling of
the tissue, prolonged tourniquet use, excessive edema or high concen
tration of epinephrine. Foreign bodies or implants also provide a good
culture medium for bacteria. Sutures, prostheses and fixation devices
all locally decrease a host resistance to bacteria.
As severity of wound infection increases, the enhanced inflamma
tory response has a negative effect on wound healing. Proteolytic
enzymes are released from the inflammatory cells, which speeds the
442
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
infection, but based on the site of the infection and the local condi
tions, some organisms, such as Gram-negative rods, Candida, and
anaerobic bacteria are far less common in cutaneous surgery.
The best approach to postoperative infection is prevention. The
surgeon must adhere to strict aseptic sterile protocol perioperatively
as well as being on the alert for any signs and symptoms postopera
tively that may correlate with an insidious infectious process. Prophy
lactic antibiotics are universally accepted as a method to decrease the
incidence of postoperative infections. There is some controversy and
little scientific data to substantiate when prophylactic antibiotics are
best utilized and under which circumstances, but there are accepted
anecdotal guidelines that many surgeons follow when considering
antibiotic use. Prophylactic antibiotics are often instituted when a
procedure involves the implantation of a foreign material such as
a tissue graft, metallic screw or implant, or a surgical procedure
that involves extensive dissection or prolonged wound exposure of
over 2 h.
Some hospitals now have set antibiotic protocols for surgeons to
follow as part of their “Best of Practice Guidelines”. A patient compro
mised by a heart condition or valvular defect, immunosuppressive
agents or peripheral vascular disease are also at risk of a serious and
potentially life-threatening postoperative infection, and are frequently
given a prophylactic antibiotic to try and avoid these complications.
The controversy surrounding prophylactic antibiotic use continues
with regard to which antibiotic agent to select and the appropriate
duration of antibiotic coverage. Some general concepts are that the
antibiotic must be in the tissues before the wound is opened and
exposed, the antibiotic should be directed at the most likely causative
organism and the duration of use could range from a single dose given
preoperatively to a continued regimen of up to 24 h post operative.
Beyond 24 h, there does not seem to be any enhanced protection to
the patient. The most popular choice for prophylactic antibiotic agent
is cefazolin. Cefazolin is a first-generation cephalosporin that is very
effective as a prophylactic antibiotic due to relatively high serum
levels, good bone penetration, long duration, good Staphylococcus cov
erage and some Gram-negative coverage, and reasonable cost.
If a patient has true penicillin or cephalosporin allergy, clindamycin
is a good alternative with excellent coverage against Staphylococcus,
excellent tissue and bone penetration, and it is capable of penetrating
the bacterial glycocalyx produced around foreign implants by S. epi
dermidis. Vancomycin has been very popular in the past and often
utilized in penicillin allergy patients, however, there has been some
increasing concern regarding the development of vancomycin resist
ant strains of S. aureus and S. epidermidis.
resorption of buried sutures, decreasing wound support and increas
ing wound dehiscence. From the open wound, samples of the drain
age can be collected for culture and sensitivity studies and Gram stain.
As the culture may take a few days to return, empiric antibiotics may
be started based on the Gram stain findings, the location of the infec
tion and the most likely organisms found in that area. The first line
of coverage is usually with an antibiotic that will cover Staphylococcus
aureus until the laboratory cultures are available, along with confirma
tion of the infecting organism and antibiotic sensitivity.
It can be challenging to differentiate the early pathological process
of an infection from the normal physiological response of postopera
tive inflammation. The signs and symptoms of early infection include
severe pain unresponsive to strong analgesics, peri-incisional edema,
erythema and radiating heat. This can be seen, however, with
hematoma formation, acute gout, inflammation, tight dressings and
tight casts. It is the additional signs and symptoms that develop with
continued infection that aid in the diagnosis: fever, chills, night
sweats, loss of appetite, red streaking and lymphadenopathy. These
symptoms usually present later in the infection process.
Laboratory testing can help confirm the presence of infection as well
as the responsible organism(s). Culture and sensitivity to determine
the bacteria and the appropriate antibiotic coverage is the standard of
care for infection management. A complete blood count with an
elevated neutrophil count and an elevated white blood cell count
will also point to an ongoing infection. However, it can also be
elevated in response to the surgery itself. Blood cultures are
seldom necessary in cutaneous surgery due to the rarity of bacteremia
or septicemia.
A variety of bacteria may be cultured from the postoperative infected
wound, the most common being S. aureus. This is closely followed by
S. epidermidis, which used to be thought of as a skin contaminant in
the culture, but is now becoming more virulent and is frequently the
causative organism when implants are present. Staphylococcus infec
tions are erythematous, swollen and tender with a localized abscess
consisting of creamy thick pus (Fig. 30.12). Another common invad
ing bacteria is β-hemolytic group A streptococci. Streptococcus infec
tions are intensely red with cellulitis and extreme warmth, but no
purulence is seen, only occasional serous drainage (Fig. 30.13). Strep
tococcus infections can dissolve fibrin clots and spread rapidly leading
to septicemia if diagnosis is delayed. Gram-negative bacilli may also
be isolated from an operative infection, but is rarer in cutaneous
surgery than the Gram-positive cocci above. Escherichia coli, Klebsiella,
Proteus, Pseudomonas, Enterobacter, and Serratia are the most common
Gram-negative bacteria. Any bacteria can lead to a postoperative
Figure 30.12 Staphylococcus infection with thick purulent drainage,
maceration and erythema.
Figure 30.13 Streptococcus infection with intense spreading cellulites,
increased local heat, swelling and minimal drainage.
Chapter
Surgical complications and their treatments
443
| 30 |
the antibiotic; the antibiotic is not being delivered in adequate dosage
or is not capable of penetrating the infected tissue; a resistant strain
of bacteria has emerged or persistent deep infection or abscess is
present. The surgeon must evaluate these possibilities and alter the
treatment plan to resolve the complicating infection. A patient will
require reassurance and emotional support during the management
of this turn of events.
Cutaneous myiasis
Myiasis is the infestation of living tissue by the larvae (maggots) of
flies within the arthropod order Diptera (two-winged adult flies). The
larvae feed on the host’s dead tissue, body substances, or ingested
food. In wound myiasis, the larvae are deposited in a suppurating
wound or on decomposing flesh, such as an ulcer or open incision.
They may rarely be found in postoperative wounds after flies lay eggs,
under bandages, or lower extremity casts (Fig. 30.15). Facultative
larvae tend not to invade healthy tissue. The diagnosis is obvious
when larvae are visible on the surface of the wound and more difficult
to diagnose when they have burrowed beneath the surface. In most
cases of lower extremity myiasis, the larvae may be simply irrigated
and wiped away from the wound. They tend to leave a very clean
wound behind because they have fed on the necrotic tissue while
present. Myiasis is a self-limiting infestation with minimal morbidity
in the vast majority of cases. Patients with open wounds, postoperative
incisions and infection of the lower extremities should be educated
about the preventive measures to avoid exposure to Diptera flies, espe
cially during the warm summer months.
LIFE-THREATENING COMPLICATIONS
As the surgeon and the patient enter the operating room theater, there
are remote risks that exist in every case that, fortunately, are extremely
rare. These are life-threatening events that could be irrevocable. Events
such as anaphylaxis, cardiac arrhythmias and seizures can all occur in
any patient at any time and the operating room team members,
including the surgeon, must be ready and prepared to handle these
complications. During a seizure that is usually brought on by a vas
ovagal event, the patient must be protected from harm with the use
of a bite stick and Trendelenburg position of the table, to assist in
With the diagnosis of infection emerging postoperatively, the
surgeon must exclude multiple other diagnoses that may present simi
larly, including hematoma and severe inflammatory response. The
patient with infection will usually present with constitutional signs of
infection such as fever, chills, night sweats, lymphangitis and lym
phadenopathy. Once the clinical diagnosis of infection has been
made, the surgeon must act quickly and with purpose to avoid addi
tional potentially more severe complications. Radiographs are usually
obtained for a baseline to evaluate for any bone changes or possible
gas in the tissues. If drainage is present, a Gram stain is obtained and
this is followed by a culture and sensitivity.
Empiric antibiotics are frequently initiated, even before a culture
result is available, to try and intervene early and decrease the spread
of the infection. If the patient is to be taken to the operating room,
the culture is repeated under sterile conditions and in the deeper
tissues to obtain a more accurate identification of the organism(s)
involved without skin contaminants. Once the organism is properly
identified, the empiric antibiotic can be replaced with the appropriate
therapeutic systemic antibiotic based on the sensitivities and the bac
teriocidal action of the antibiotic with the least toxicity to the patient.
This will usually be a parenteral antibiotic, but this can also be aug
mented with an oral antibiotic. In some infections, there may be a
question as to the extent of the bacterial invasion, in which case a
magnetic resonance imaging (MRI) scan will show the extent and the
exact location of abscess formation and early marrow changes that
may indicate osteomyelitis. Technetium-99 can also be utilized to
evaluate depth of infection; however, false-positive findings can be
seen in both MRI and bone scan images, if bone work was performed
intraoperatively. Almost all postoperative infections will require anti
biotic coverage, drainage of pus from the wound, and irrigation and
debridement of any necrotic tissue. This is usually performed in the
operative setting, but can also be performed at bedside.
The wound is left open and may be closed later by delayed primary
closure or allowed to heal by secondary intention. In the early stages,
it is often advisable to pack the wound open with sterile dressings
or gauze such as iodophor (Fig. 30.14). The surgeon must closely
monitor the changing status of the wound to be certain the infection
is reacting appropriately to the intervention. If the infection does not
seem to be responding, there are many possibilities: the wrong organ
ism was isolated; there are other organisms involved not covered by
Figure 30.14 Postoperative infected wound that has been packed with
iodophor gauze.
Figure 30.15 Cutaneous myiasis. Multiple fly larvae (maggots) are seen
on the incision area when the cast was removed. They may be washed
or lavaged away from the wound easily.
444
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
that the complication exists or delaying aggressive appropriate treat
ment will usually result in more extensive complications and a loss
of confidence by the patient. Being direct and forthright with the
patient will usually provide for a more satisfied and trusting patient
that will work with you to resolve the complication.
oxygenation and blood flow to the brain. The patient is at significant
risk of aspiration during the seizure, as well as anoxia and brain
damage so the airway must be maintained.
Anaphylaxis can occur with any medication given in the periopera
tive setting. This includes the preoperative prophylactic antibiotic, the
medications given by the anesthesiologist for sedation or general
anesthetic, or any local anesthetic injected during the case. Anaphy
laxis requires immediate recognition and institution of treatment to
prevent complete circulatory collapse. This initial treatment is usually
epinephrine, fluids and the discontinuation of the medication if
identified.
Although the surgeon may have a strong suspicion in some patients
that are at risk of a cardiac event, in some cases, there is no warning.
The event may be a mild arrhythmia that was not previously diag
nosed, but may also be a malignant arrhythmia that could lead to
cardiac failure or arrest. A myocardial infarction is known to be more
likely in the diabetic or obese population, but it can also occur in a
healthy patient with an arrhythmia that occurs during the procedure
or from a reaction to a medication. Members of the operating room
team must be certified in basic and advanced cardiac life support to
allow for the best possible outcome on these calamitous events.
CONCLUSION
Through all of the training and all of the education, one aspect of
surgery will remain true: complications can and do occur even to the
best of surgeons with the best of intentions (Fig. 30.16). Managing
these complications efficiently and appropriately is our job and, when
done correctly, will hopefully result in as minimal trauma to the
patient as possible and provide the best possible outcome. Denying
Figure 30.16 Even in well-planned and executed surgical procedures a
complication may occur. The surgeon must manage these complications
efficiently and appropriately.
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Blasdale, C., Lawrence, C.M., 2008.
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CHAPTER CONTENTS
Introduction
447
Etiology
449
Venous ulcers
449
Arterial ulcers
449
Diabetic ulcers
450
Pressure ulcers
450
Inflammatory ulcers
450
Wound repair physiology
451
Phase 1: inflammation
451
Phase 2: proliferation and tissue formation
452
Phase 3: tissue remodeling
452
For Recognition of Adult Immobilized Life (FRAIL)
452
Preoperative preparation
452
Medical history
452
Physical examination
453
Diagnostic assessment
453
Prevention
455
Techniques
456
Compression therapy
456
Pharmacologic therapy for venous ulcers
456
Antimicrobials and the bacterial balance of
leg ulcers
457
Background
457
Diagnosis
457
Antibiotics and antiseptics
457
Dressings for leg ulcers – moist wound healing
457
Surgical techniques
458
Wound bed preparation and debridement
458
Removal of bacteria
459
Removal of senescent cells
459
Effects of stimulation of growth factors
459
Removal of non-migratory tissue
459
Types of debridement
459
Surgical/sharp debridement
459
Mechanical debridement
460
Autolytic debridement
460
Biosurgical debridement
460
Enzymatic and chemical debridement
460
Skin grafting
461
Split- and full-thickness skin grafts
461
Preoperative preparation
461
Techniques
461
Optimizing outcomes
463
Pitfalls and their management
463
Bioengineered skin equivalents
464
Graftskin as a bioengineered skin equivalent
464
Subfascial endoscopic perforator surgery (SEPS)
465
Shave therapy for venous ulcers
466
Summary
466
INTRODUCTION
Leg ulcers result from chronic lower extremity wounds that fail to heal,
causing pain and social discomfort. With an ever-increasing aging
population, it is estimated that the cost of managing venous ulcers
alone, which account for 80% of leg ulcers, is $1 billion per year in
the USA. The average cost for one patient over a lifetime exceeds
US$40 000.1 Leg ulcers may originate from a wide variety of causes
(Table 31.1).2–4 In the vast majority, leg ulcers are the result of venous
©2012 Elsevier Ltd.
Leg ulcer managementa
Carlos A. Charles, Anna F. Falabella, Adolfo C. Fernández-Obregón
Chapter
31
aThis article was published in Surgery of the Skin, Procedural Dermatology, Carlos A
Charles, Anna F Falabella, Adolfo C Fernandez-Obregon, Leg Ulcer Management,
743–766, Copyright Elsevier (2005).
448
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
Table 31.1 Causes of leg ulcers2–4
Category
Condition
Venous
Vein thrombosis, venous incompetence, varicose veins, venous stasis, lipodermatosclerosis, complication of sclerotherapy
Arterial
Arterial obstruction, atherosclerosis, thromboangiitis obliterans, cholesterol embolism, arteriovenous malformation,
hemangioma, hypertensive ulcer, complication of sclerotherapy
Microcirculation
Diabetic microangiopathy, vasculitis
Neuropathic
Diabetes mellitus, Hansen’s disease, tabes dorsalis, syringomyelia, spina bifida, paraplegia, amyotrophic lateral sclerosis,
other neuropathic disorders
Hematologic
Sickle cell disease, thalassemia, hereditary spherocytosis, polycythemia vera, leukemia, dysproteinemias, disseminated
intravascular coagulation, idiopathic thrombocytopenia, chronic graft versus host disease, acquired homocystinuria,
warfarin necrosis, heparin necrosis
Immunologic
Bullous pemphigoid, cicatricial pemphigoid, pemphigus, epidermolysis bullosa acquisita, linear IgA bullous dermatosis,
erythema multiforme, allergic contact dermatitis
Infectious
Erythema induratum/nodular vasculitis, mycotic, bacterial, leishmania, herpes
Metabolic
Diabetes mellitus, gout, pretibial myxedema, Gaucher’s disease, prolidase deficiency, porphyria cutanea tarda, necrobiosis
lipoidica, bullous diabeticorum, diabetic dermopathy, drugs
Renal
Kyrle’s disease, reactive perforating collagenosis, calciphylaxis
Nutritional
Scurvy, malnutrition
Genetic diseases
Epidermolysis bullosa, Werner’s syndrome, Klinefelter’s syndrome
Neoplastic
Basal cell carcinoma, squamous cell carcinoma, keratoacanthoma, malignant melanoma, Kaposi’s sarcoma, malignant
eccrine poroma, angiosarcoma, cutaneous metastasis, cutaneous lymphoma
Chemical/physical
Caustic agents, decubitus ulcers, thermal injury, mechanical trauma, radiation, frostbite, factitial, Charcot’s deformity,
chronic osteomyelitis, insect bites, coral and marine life-induced ulcers
Lymphatic disease
Lymphedema, lymphangioma
Other
Pyoderma gangrenosum, panniculitis, Raynaud’s disease
disease, arterial disease, neuropathy, or a combination of these three.
Venous insufficiency is by far the most common cause of leg ulcers.
This chapter will attempt to define the most commonly encountered
leg ulcers, describe the methods used to evaluate these ulcers, and
propose appropriate therapy. An understanding of the principles of
treatment of leg ulcers is essential and can help a clinician in applying
sound methods to treat the more esoteric ulcers.
Some venous ulcers become chronic wounds after a non-healing
period of 2 months. The term chronic wound is used to define not
only non-healing ulcers of long duration, but also ulcers where many
local factors impair healing, including the presence of foreign bodies,
tissue maceration, ischemia, or other hemodynamic changes in the
microcirculation. An increase in bacterial burden and colonization
that can lead to frank infection is often present. Additionally, other
factors that may play active roles in non-healing include: malnutri
tion, diabetes mellitus, renal disease, and hematological or other sys
temic illnesses. Recent developments in the understanding of wound
healing have identified certain clinical settings responsible for the
chronic wound. There may be a lack of tissue growth factors, such as
platelet-derived growth factors, and transforming growth factor-beta
(TGF-β) compared with acute wounds. An imbalance between proteo
lytic enzymes and their inhibitors can result from overexpression
of matrix metalloproteins, resulting in abnormal degradation of the
extracellular matrix. Finally, the persistence of senescent fibroblasts
that fail to respond to growth factors and other stimulating agents
may be important in leading to chronic wounds.5 Therapies aimed at
restoring the normal environment in the wound can set the scene for
proper wound healing.
Table 31.2 Types of leg ulcers6,7
Ulcer type
Percentage of
presenting ulcers
Venous
80
Arterial
5
Diabetic/neuropathic
2
Pressure
5–20a
Microcirculation
<2
Hematologic
<2
Infectious
<2
Metabolic
<2
Neoplastic
<2
Physical/chemical
<2
Immunologic
<2
Other
<2
aIncludes all anatomic locations.
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Arterial ulcers
Arterial disease results from the narrowing of the vessel lumen by the
accumulation of cholesterol plaques and other tissue debris. The
resulting obstruction leads to the development of collateral circula
tion. Risk factors for arteriosclerotic occlusion are diabetes, smoking,
hyperlipidemia, hypertension, obesity, and age.25–27 Arteriosclerotic
occlusion usually affects the entire femoropopliteal trajectory includ
ing important distal branches (anterior peroneal, anterior tibial, and
posterior tibial), and may lead to significant distal damage. It may also
affect only small-sized branches, leading to limited skin and subcuta
neous tissue infarction. Clinically, patients experience pain or aching
in the calves when walking (intermittent claudication), often relieved
by rest. Pain tends to be severe and debilitating. On physical
A list of various types of leg ulcers and their relative frequency is
given in Table 31.2,6,7 which gives specific clinical entities associated
with each major category of leg ulcers. An excellent and more com
plete discussion on the subject of diabetic ulcers can be found in Levin
and O’Neal’s The Diabetic Foot.8
ETIOLOGY
Venous ulcers
Venous ulcers account for about 80% of all lower leg wounds.9–11
Although it is known that chronic venous insufficiency is often the
cause of venous ulceration, the exact mechanism by which ulcers
result is not known, and continues to be the subject of widespread
speculation. Gay12 and Homans13 made a connection between deep
vein damage and ulceration. Under normal ambulatory conditions,
the calf muscles serve to pump the blood back up to the heart. Without
adequate use of calf muscles, blood that collects in the saphenous
venous system and its tributaries cannot make its way swiftly out of
the deep veins, and is transmitted instead to the cutaneous vascula
ture. This all leads to chronic venous hypertension.14–16 Microcircula
tory changes associated with chronic ulcers, diabetes, and repeated
bouts of previous vessel damage lead to fibrin cuffs, seen histologically
around dermal vessels, which result in impaired cutaneous nutrition,
and ultimately ulceration.17 The action of neutrophils adhering to
tissue damaged by ambulatory venous hypertension releases highly
reactive substances, which generate free radicals, and subsequently
cause tissue injury.18
The exact mechanism by which ulcers result from this long series
of events is unknown. The ‘trap’ hypothesis suggests that venous
hypertension causes fibrinogen and other macromolecules to leak into
the dermis, and trap or bind growth factors, making them unavailable
for tissue repair.19 More recently, the entrapment of activated white
cells with their release of activated inflammatory mediators has been
thought to play a major role.20 The ‘cuff’ hypothesis proposes that the
leaked fibrinogen in the dermis polymerizes to form pericapillary
fibrin cuffs, forming a barrier to the diffusion of oxygen and other
nutrients, and leading to microvascular ischemia.21 Another theory
proposes that dermal fibroblasts from venous ulcers become unre
sponsive to the action of wound healing mediators and serve to under
mine the healing process.22 It is possible that minor trauma may also
play a role in the ulceration process. Up to 50% of patients with
chronic venous insufficiency have a history of leg injury.23 Venous
ulcers exude copious drainage – a greenish-yellowish fibrinopurulent
adherent exudate may be seen at the base of the ulcer, which may be
highly irregular in shape. Superinfection, pain, and malodorous drain
age may ensue (Fig. 31.1).
Chronic lower extremity swellings, often mistaken as originating
from cardiac, hepatic, and renal disease leads to varicosities. Erythro
cytes extravasate into the dermis under pressure and leave behind
hemosiderin deposits in the skin or cayenne pepper purpura. A pru
ritic rash often appears leading to excoriations and further dermal
staining with melanophages as a post-inflammatory event. The topical
agents used to try to keep it under check often aggravate this venous
dermatitis. Further acute inflammation produces a panniculitis, which
becomes more sclerotic with time, leading to lipodermatosclerosis
(Fig. 31.2). The latter, as proposed by Browse and Burnand,17 results
from high venous pressure leading to endothelial leakage of fibrino
gen, resulting in the formation of the pericapillary fibrin cuff and
eventual venous ulceration.24 Additionally, dystrophic calcium depos
its sometimes develop.
Figure 31.1 The most common leg ulcers. A venous leg ulcer on the
medial malleolus of a patient, with characteristic scattered varicosities
and hyperpigmentation of the periwound skin.
Figure 31.2 Diffuse hyperpigmentation associated with the indurated
skin characteristic of lipodermatosclerosis.
450
Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
occur, most patients will exhibit a preponderance of one type. Patients
may display other cutaneous markings of diabetes, such as necrobiosis
lipoidica diabeticorum, diabetic dermopathy, or diabetic bullae. The
most characteristic lesion of the diabetic foot is a mal perforans ulcera
tion (Fig. 31.4).30 The neuropathic ulcer is essentially a pressure ulcer
resulting from the individual’s loss of sensation. It is indistinguishable
from the neurotrophic ulcers seen in leprosy, tabes dorsalis, and other
neurological syndromes. The ulcer is most characteristically over the
pressure points such as the first and fifth metatarsal heads, and the
great toes. It is classically well circumscribed, with a surrounding halo
of hard callus-like material. The foot involved may have a normal
color and even strong arterial pulses. Touch, pressure, and propriocep
tion are diminished or lost. Motor and autonomic nerves may also be
involved. Weakening muscles may also lead to toe and foot deformi
ties. Loss of sweating may lead to fissuring and a Charcot foot can
develop.
Pressure ulcers
Pressure ulcers have a prevalence of 5–20% in acute care hospitals,
and approximately 8% in the domiciliary setting, 15% in nursing
homes, and up to 35% in extended care facilities.31 Immobility is a
necessary condition for pressure ulcer development, and therefore, the
most significant risk factor. Impaired nutritional states, along with
hypoalbuminemia and immobility, can lead to epidermal moisture
vapor loss, which causes maceration and then a breakdown of
the stratum corneum barrier, rendering the skin more permeable to
noxious agents and trauma. Fecal incontinence, and even slight pres
sure over skin overlying bony prominences, such as the heel or the
malleoli of the ankles, can cause enough injury under these conditions
to start the process that leads eventually to a pressure ulcer (Fig. 31.5).
Naturally, other causes of pressure ulcers need to be excluded, such as
venous stasis, arterial insufficiency, diabetes, neuropathy, vasculitis,
systemic lupus erythematosus, drug allergies, neoplasm, sickle cell
disease and other hematological abnormalities, polycythemia, pyo
derma gangrenosum, bacterial and fungal infections, and trauma.32
Inflammatory ulcers
Many diseases can lead to leg ulcers. A broad category that excludes
venous, arterial, pressure, and diabetic ulcers as well as the ulcers
resulting from neoplasms, is the inflammatory ulcer. Kerdel33 and
Paquette and Falanga34 offer excellent reviews of the subject. One
major subcategory is the vasculitis ulcer resulting from small vessel
examination there may be loss of hair, atrophy, cold surrounding skin,
and thickened toenails. Peripheral pulses may be palpable, barely
palpable, or absent. Capillary refill time is usually prolonged. Typi
cally, arterial ulcers are located over pressure points, such as the toes
and ankles. The ulcer is sharply demarcated with little granulation
tissue. It tends to have a punched out appearance (Fig. 31.3). The
wound bed often has a necrotic appearing base. Large occlusions
require surgical intervention through revascularization by means of
bypasses either using the patient’s own veins or artificial vein grafts,
or by means of intravascular procedures such as balloon dilatation
(percutaneous transluminal angioplasty), sometimes combined with
thrombolysis and the placement of stents.
Diabetic ulcers
Diabetes accounts for over 50% of lower extremity amputations in
the USA. Approximately 85% of all diabetes-related lower extremity
amputations are preceded by foot ulcers.28,29 Ulcers from diabetes
occur as neuropathic or ischemic. Although a mixture of each can
Figure 31.3 Classic ‘punched out’ appearance of an arterial ulcer with
copious yellow fibrinous exudates and poor granulation tissue.
Figure 31.4 Plantar diabetic foot ulcer.
Figure 31.5 Pressure ulcer overlying the bony prominence of the heel.
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phases – inflammation, proliferation and tissue formation, and tissue
remodeling. Each phase is characterized by a number of complex
intercellular interactions. It is important to note that these phases do
not represent separate and distinct events, but are continual and
overlapping.
Over the past few years investigators have begun to understand
how cells interact between themselves and the extracellular matrix
in the wound healing process. The clinical utility of understanding
wound healing physiology is potentially far reaching. By understand
ing the normal processes, investigators and clinicians alike can apply
targeted therapeutic modalities, in an attempt to achieve wound
closure in refractory wounds. The following section briefly reviews the
normal physiology of tissue repair and serves as a framework for the
information concerning non-healing leg ulcers and therapeutic
modalities for wound management, which will subsequently be
described in detail.
Phase 1: inflammation
The first phase of normal wound healing begins immediately after an
acute injury, and can last for 24–48 h. This phase is characterized by
the disruption of blood vessels, which leads to a local release of blood
cells and blood-borne elements. The main cellular constituent of the
inflammatory phase of tissue repair is the platelet, which initiates
clotting of the acute wound by both intrinsic and extrinsic pathways.
Platelets release a number of chemoattractant factors, which recruit
other platelets, leukocytes, endothelial cells, and fibroblasts to the
wound area. The inflammatory phase progresses with the addition of
neutrophils and macrophages, which acutely debride the wound by
scavenging cellular debris and killing bacteria, leading to the second
phase of healing (Fig. 31.6).
thrombi or emboli. Lesions beginning as palpable purpura can lead
to vesicles and pustules. The process involving immune complexes,
much like an Arthus reaction, sets off the inflammatory cascade, even
tuating in the release of vasoactive amines and other mediators. These
mediators serve to amplify the process with the deposition of more
immune complexes, leading ultimately to an ischemic area, cutaneous
necrosis, and ultimately an ulcer.
A group of conditions involve dermal thrombi in the absence
of vasculitis. They include thrombotic thrombocytopenia purpura,
disseminated intravascular coagulation, cryoglobulinemia, cryofibrin
ogenemia, purpura fulminans, coumadin necrosis, and the antiphos
pholipid syndrome (also known as the lupus anticoagulant syndrome).
Individuals with this syndrome may or may not have lupus erythema
tosus. These patients possess antibodies (IgG or IgM) that interfere
with the conversion of prothrombin to thrombin. In the laboratory
they have a prolonged activated partial thromboplastin time. Some
may have a prolongation of the prothrombin time. (The Russel viper
venom time, and Exner’s test may also be helpful.) The lesions are
purpuric, leading to ischemia and ulceration. Livedo reticularis may
be seen. There is no frank vasculitis. Lesions are often painful and heal
with atrophic scars (atrophie blanche).35
WOUND REPAIR PHYSIOLOGY
The process of normal wound healing can be looked upon as an
integration of multiple dynamic, interactive processes involving
soluble mediators, formed blood elements and blood cells, an extra
cellular matrix, and parenchymal cells. In the simplest terms, this
process is generally described as occurring in three main
Figure 31.6 A diagrammatic representation of the key events during the inflammatory phase of normal wound healing. (FGF and FGF-2, fibroblast
growth factors; IGF, insulin-like growth factor; KGF, keratinocyte growth factor; PDGF, PDGF-AB and -BB, platelet-derived growth factors; TGF-α, -β1,
-β2 and -β3, transforming growth factors; VEGF, vascular endothelial growth factor.
FGF-2
FGF-2
KGF
Fibrin clot
Epidermis
Dermis
Fat
Fibroblast
Macrophage
Neutrophil
Capillary vessel
IGF
TGF-β1
PDGF-AB
PDGF-BB
PDGF
VEGF
FGF
TGF-α
TGF-α
TGF-β1
TGF-β1
TGF-β2
TGF-β3
TGF-β1
VEGF
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Lower Extremity Soft Tissue & Cutaneous Plastic Surgery
country undertook the task of defining ‘the FRAIL’ patient, and start
the process of establishing guidelines for the medical management of
these patients. The consensus expressed by the group upheld the belief
that the traditionally held endpoint of therapy, the total healing of a
wound, may not be appropriate for many of these patients. Palliative
measures to keep patients comfortable, pain free, and with wounds
that are nonodorous and simple to manage may be just as important,
and an acceptable treatment strategy.
Palliative care is a philosophy of care that focuses on providing
support for the physical, emotional, social, and spiritual needs of
patients. These concepts have value to patients long before death is
imminent, or a terminal illness has been diagnosed. Palliative care is
best used at the onset of diagnosis and throughout the disease course,
and objectives evolve as the disease and patient’s preferences change.
Palliative care focuses on managing symptoms such as pain, losses to
independence, mobility, and degradation of self-image.
The FRAIL Committee report addressed communication and
information-sharing techniques, preventive odor management in
wounds, and detection and treatment of depression, anxiety, and
delirium. As this newly recognized patient population continues to
grow, there will be a growing need for specific pharmaceutical prod
ucts, and medical devices. A plan for continuous education for the
public and health professional is needed.39
Patients sometimes display a stoic and highly resolved preference
to refuse treatment for conditions that deserve aggressive intervention.
Not surprisingly, this can include leg ulcers. If left untreated, they can
become a chronic source of infection, which can lead to sepsis with
the potential for a fatal outcome. Approaching the problem with true
concern and compassion is essential, ensuring the dignity of the
patient is protected. Understanding a person’s right to refuse treat
ment must be carefully balanced with the proper medical manage
ment of the patient. Reasons given for refusing treatment may be
based on unfounded fears and concerns, which can be dispelled or
minimized once they have been revealed. Very often this illuminating
step is all it takes to obtain the patient’s cooperation. Psychiatric evalu
ation may be necessary if the patient is adamant about refusing care.
If all else fails, local adult protective services may need to be sum
moned to assist in the final disposition of the case.
PREOPERATIVE PREPARATION
Medical history
Taking a careful medical history is the beginning of evaluating leg
ulcers. It is obvious that details surrounding the development of the
ulcer with an emphasis on duration, and progression should be deter
mined as well as the presence or absence of pain, and whether certain
activities such as walking or leg elevation change the character of
pain. Venous ulcer pain is often described as a burning pain. Although
pain is generally more common with arterial disease, it may occur in
venous ulceration. Ankle swelling may occur. There is often a history
of trauma, a family history of phlebitis or varicose veins, and in
general a family tendency of thrombophilia.40
Race as a factor may be important, as noted in sickle cell disease,
hereditary spherocytosis, and thalassemia. Habits such as cigarette
smoking may add to the risk of arterial impairment and venous
thrombosis. Alcohol abuse, often associated with poor nutrition, may
directly affect wound healing. A history of nutritional deficiencies,
metabolic disorders, diabetes, hypertension, antiphospholipid syn
drome, periarteritis nodosa, pyoderma gangrenosum, atherosclerotic
heart disease, and even pregnancy may all serve as aggravating factors.
Prior history of collagen vascular disease can lead to vasculitis, which
Phase 2: proliferation and tissue formation
The second phase of wound healing is characterized by proliferation
and tissue formation and begins approximately 72 h after injury. This
phase can last up to several weeks. In this phase, the keratinocyte plays
the primary role in the tissue repair process and undergoes significant
changes in morphology and function, allowing for its migration over
the wound bed to provide coverage. Additionally, the keratinocyte
releases a number of chemokines, which stimulate cellular migration
and other key cellular functions, leading to eventual reconstitution of
the epidermis and the basement membrane.
The latter segment of the second phase of wound healing is char
acterized by the formation of granulation tissue. Fibroblasts are instru
mental in the reconstitution of the dermal matrix, termed fibroplasia,
while endothelial cells play an integral role in the development of
new blood vessels, known as angiogenesis. Additionally, the extracel
lular matrix, with its collection of proteins, growth factors, and
enzymes plays an active role in influencing the keratinocytes, fibrob
lasts, and endothelial cells.
Phase 3: tissue remodeling
The final phase of wound healing, tissue remodeling, begins at the
same time as the onset of cellular proliferation and tissue formation.
This phase can last several months after the acute injury. This phase
is one of gradual physiologic evolution and is characterized by hetero
geneous stages of healing throughout the wound; hence, the macro
molecular physical composition of the wound margin can vary greatly,
both quantitatively and qualitatively with that of the central wound
bed. Over the course of this phase, granulation tissue becomes mature
scar tissue. Several enzymes are involved in breaking down matrix
components, whereas the fibroblasts produce substances such as
fibronectin, hyaluronic acid, proteoglycans, and collagen, to ulti
mately restore the functional barrier of the skin and increase the
tensile strength of the scar. Each of these components plays an impor
tant role in the wound healing process. Fibronectin acts as a matrix
for cellular migration, as scaffolding for collagen deposition, and as
a linkage for myofibroblasts to aid in wound contraction. Hyaluronic
acid stimulates wound maturation by promoting cell migration and
division.36 Proteoglycans increase tissue strength, modify collagen
deposition, and help to modulate cellular function.37 Last, collagen is
essential for providing structural support and tensile strength, while
also playing an important role in the regulation of cellular function.
In summary, the tissue-remodeling phase of wound healing is an
evolving series of cellular events characterized by extracellular matrix
formation, which should result in complete wound maturation and
scar formation.
FOR RECOGNITION OF ADULT
IMMOBILIZED LIFE (FRAIL)
The demographics of the American population are shifting dramati
cally toward a majority of persons over the age of 65 years. Currently,
there are almost 34 million Americans aged ≥65. This number will
grow to over 69 million (20% of the population) by the year 2030.
Current average life expectancy for persons living in the USA, is over
76 years of age.38 With a constantly growing aging population, the
profile of a newly recognized patient emerges. Many suffer with
chronic wounds that fail to progress through an orderly and timely
sequence of repair.
To study this population and address their needs, an interdiscipli
nary group of healthcare professionals from different parts of the
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453
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toe. Ulcer size, shape and border description should be noted. Scars
may suggest previous ulcer activity, in support of a chronic problem.
Hyperpigmentation and hyperkeratosis along with microvaricosities
at the sides of the ankles, can be seen in cases of venous dermatitis.
Cyanosis and dark colored toes can point to significant arterial defi
ciency of the distal parts of the extremity. Atrophic changes of the skin
will lead to loss of hair and sweat glands, resulting in further skin
dryness. Pressure ulcers can be seen over bony prominences, whereas
diabetics will have ulcers on the plantar surface of the foot.
Induration and fibrosis of the dermis and underlying tissue can
progress to give the lower leg an inverted champagne bottle shape,
which is characteristic of chronic venous insufficiency, with a hard
doughy to woody texture, known as lipodermatosclerosis40,45,46
(Table 31.3)
Diagnostic assessment
Although venous disease represents the most common etiology for
leg ulceration, a thorough diagnostic assessment must be performed
to ensure an accurate diagnosis before initiating treatment. Other
common causes for leg ulcers include arterial and neuropathic disease,
though the cause of leg ulcers is commonly multifactorial, and may
include infectious, inflammatory, malignant, and connective tissue
conditions. Simple diagnostic techniques can therefore be performed
to help establish a proper diagnosis (Table 31.4).
The presence of symptoms such as claudication or rest pain in more
severe cases is characteristic of arterial insufficiency. In these patients,
the ankle-to-brachial index (ABI), may help in detecting peripheral
vascular disease (Fig. 31.8). The lower extremity systolic blood pres
sure can be measured at the bedside by placing a correctly sized cuff
around the calf and inflating it to occlude the pedal arteries. When
the pulse sounds are appreciated with Doppler ultrasonography after
deflation of the blood pressure cuff, the ankle systolic pressure is
obtained. This value is then compared with the highest brachial systo
lic pressure to determine the ABI. An ABI of ≥0.97 is normal, whereas
an ABI of ≤0.5 may indicate severe arterial disease.47,48 Values less than
0.97 categorize people with peripheral artery disease with a sensitivity
of 96–97% and a specificity of 94–100%.47 False-positive results may
occur in patients who are elderly or diabetic, thus a transcutaneous
oxygen measurement may be preferred to assess arterial circulation in
these subsets of patients. These assessments are critical because com
pression therapy, the mainstay non-invasive therapeutic modality for
venous ulcers, can lead to worsening of an arterial ulcer, or even gan
grene in a patient who has a significantly compromised peripheral
arterial circulation.49
Infectious organisms may also be of etiological significance for
acute or chronic lower extremity ulcers and should be suspected when
chronic ulcers do not follow the usual course of healing observed with
more common conditions. Tissue culture, particularly to identify
fungal or atypical mycobacterial infections may help reveal the cause
for nonhealing. Patients with underlying diseases resulting in immu
nosuppression may be predisposed to ulceration;50 therefore, the clini
cian’s index of suspicion for infection must be high for these patients.
If osteomyelitis is suspected clinically, radiography, nuclear bone
scanning, and bone biopsy should be considered.3,51 Although the
incidence of osteomyelitis in chronic ulcers is unknown, a prospective
trial in diabetic foot ulcers found that probing of sinuses and deep
ulcers was a highly sensitive method for detecting bone infection.49 If
bone is palpable at the ulcer base, with no intervening soft tissue,
osteomyelitis is probable, and further diagnostic investigation is
recommended.
Independent of the suspected cause, a wound present for >6 weeks
warrants a biopsy to exclude malignancy within the wound.52 Both
basal cell and squamous cell carcinomas can occur in longstanding
can give rise to an ulcer. The ulcer of pyoderma gangrenosum (Fig.
31.7) may herald or follow inflammatory bowel disease, collagen
vascular disease, or a lymphoproliferative disorder. Living or having
lived in areas where certain endemic diseases are prevalent, such as
Hansen’s disease, can predispose the patient to the neurotrophic ulcer
on the foot, which can be a late stage manifestation of leprosy. Travel
history to the tropics or semi-arid areas can expose travelers to certain
insects, whose bite can lead to myiasis, and the sandfly, which can be
responsible for transmitting leishmaniasis. Precipitating factors, such
as trauma, are often noted as leading to the development of factitial
or neurotrophic ulcers.
Taking a careful medication history is critical for the overall evalu
ation of any patient. Topical medication can often lead to allergic or
irritant contact dermatitis, which can be the initiating event in the
formation of a leg ulcer. Antibiotics, such as neomycin, and anesthet
ics, such as benzocaine, and even parabens used as preservatives in
widely used topical preparations, can cause an acute eruption.41
Oral medication, such as corticosteroids, anticoagulants, antineo
plastic agents, cyclosporin A, colchicine, non-steroidal antiinflamma
tory drugs, penicillamine, and salicylates can impair wound healing
and contribute indirectly to leg ulcers. With the public’s growing
awareness of alternative medicines, the popular use of herbal products
necessitates physicians to inquire whether these products, regarded by
patients as innocent, are being taken orally or being applied in topical
preparations.42–44
Physical examination
Among the initial impressions, odor may impress the examiner before
the patient disrobes or reveals the pathology. The smell may emanate
from wound contamination, or may be more specific to the type of
ulcer, and severity of infection.
The general appearance should include observation of skin color,
dryness, or swelling. Pulses need to be palpated on the skin over
the femoral, popliteal, dorsalis pedis, and posterior tibial arteries.
Neuropathy should be excluded by a light touch sensation in the great
Figure 31.7 Rolled purple-colored edges of a leg ulcer secondary to
pyoderma gangrenosum.