Phẫu Thuật Tạo Hình (Tập 4): Chi Dưới, Thân Mình Và Bỏng – Neligan (2018)

SECTION II • Trunk Surgery
16 
Pressure sores
Robert Kwon, Juan L. Rendon, and Jeffrey E. Janis
SYNOPSIS
■ Pressure sores are a common problem associated with great morbidity
and cost.
■ They have been recognized since antiquity, though effective surgical
treatment did not evolve until the 19th century.
■ Originally thought to result from direct pressure to soft tissue
exceeding the pressure found in the blood vessels supplying the
affected area, pressure sores are now considered multifactorial entities
involving friction, shear, moisture, nutrition, and infection.
■ Successful treatment of pressure sores requires a multidisciplinary
evaluation in order to accurately stage wounds, identify/eradicate
wound/bone infection, minimize risk factors for recurrence, and
optimize wound healing potential.
■ Prevention and treatment of pressure sores should focus on correcting
these risk factors, reserving operative intervention until the patient is
optimized.
■ As with any wound, pressure sores involving infected soft tissue and/
or bone must be thoroughly debrided prior to definitive closure.
■ Locoregional fasciocutaneous and musculocutaneous flaps remain
workhorse flaps as they can provide enough viable tissue for large
defects and allow for revision in the event of recurrence.
■ Prevention remains the most effective treatment of pressure sores.
More recently, the Hospital Acquired Conditions Initiative has led to the
implementation of programs aiming to prevent complications, such as
pressure sores, through promotion of thorough risk assessment and
early identification.
Access the Historical Perspective section online at

Introduction
Terminology
Though technically and semantically inaccurate, the terms
“decubitus ulcer”, “bedsore”, and “pressure sore” are often
used interchangeably. Decubitus ulcers – derived from the
Latin decumbere, to lie down – occur over areas that have
underlying bony prominences when the subject is recumbent,
e.g., the sacrum, trochanter, heel, and occiput. Technically,
sores resulting from pressure breakdown in areas that bear
seated weight, such as the ischial tuberosities of spinal injury
patients, and ulcers due to devices, such as splints, ear probes,
or rectal tubes, are not decubitus ulcers. Nonetheless, “pres-
sure sores” is likely the best term to use when describing these
lesions, which all involve pressure as a key etiologic factor.
Pressure sores are now recognized as multifactorial condi-
tions, with pressure being only one of the many factors that
contribute to their development.
Epidemiology
Over 500 English-language articles analyzing the incidence
and prevalence of pressure sores have been published in the
last 5 years. These studies not only examine the prevalence and
incidence of pressure sores across multiple healthcare settings
– general acute care, long-term care, and home care – but also
among specific patient populations – including infants and
children, the elderly, patients with hip fractures, and terminally
ill patients. Given these disparate populations and the substan-
tial variation across individual institutions, precise determina-
tions of incidence and prevalence are challenging.
In 1999 Amlung et al.1 performed a one-day pressure ulcer
prevalence survey of 356 acute care facilities and 42 817
patients. The overall pressure ulcer prevalence rate was 14.8%;
facility-acquired ulcers accounted for 7.1%. Ten years later,
VanGilder et al.2 reviewed the results of the International Pres-
sure Ulcer Prevalence Survey (IPUPS) and found overall
prevalence and facility-acquired ulcer rates of 12.3% and 5%,
respectively. Overall prevalence rates were highest in long-
term acute care facilities (22%), while facility-acquired rates
were highest in adult intensive care units (ICUs), ranging from
8.8% in general cardiac care units to 12.1% in medical ICUs. A
total of 3.3% of ICU patients developed severe ulcers, while
10% were device-related. A broader inquiry,3 reviewing over
  Access video lecture content for this chapter online at expertconsult.com

351
Basic science
Costs
Calculating the costs associated with pressure sores is
complex. Monetary figures are subject to inflation and varia-
tion over time. While patients admitted with a primary
diagnosis of pressure sore are simple to analyze, patients are
often admitted with pressure ulcer-related problems, such as
septicemia, and carry pressure sore as a secondary diagnosis.
However, despite the uncertainty, it is clear pressure sores are
a costly problem for the healthcare system.
The National Pressure Ulcer Advisory Panel (NPUAP) has
estimated the cost to treat and heal hospital-acquired pressure
sores to be up to $100 000 per patient.18 If the additional costs,
both surgical and nonsurgical, of managing pressure sores at
nursing homes and home care facilities are considered, the
financial burden is estimated by the Agency for Healthcare
Research and Quality at approximately 11 billion dollars in
2006.19
A review from 2006 of the Healthcare Cost and Utilization
Project19 revealed 503 300 hospital stays during which pres-
sure sores were noted. Patients with pressure sores were
inpatients nearly three times longer than patients without
such a diagnosis (14.1 days versus 5.0 days). Patients with
pressure sore as a primary diagnosis cost an average of $1200
a day, while patients with pressure sore as a secondary diag-
nosis cost an average of $1600 a day, compared with an
average of $2000 a day for all other conditions. Mean cost per
hospitalization was $16 800 and $20 400 for stays with a prin-
cipal and secondary diagnosis of pressure sore, versus only
$9900 for all other conditions. Aggregate costs were calculated
to be $752 million and $10.2 billion for stays with primary and
secondary diagnosis of pressure sore, respectively.
In response to a growing body of literature demonstrating
the economic consequences of pressure sores and other
hospital-acquired conditions, the Center for Medicare &
Medicaid Services (CMS) identified eight hospital-acquired
complications as never events. In 2008, CMS implemented the
Hospital-Acquired Conditions (HACs) initiative, a policy that
denies reimbursement for several preventable conditions,
including pressure sores.20 Since then, Waters et al. utilized the
National Database of Nursing Quality Indicators (NDNQI) to
perform a quasi-experimental study of adult nursing units
(ICU and non-ICU) from 1381 US hospitals between July 2006
and December 2010 to determine the rate of stage III/IV pres-
sure sores before and after the implementation of the HACs
initiative.21 Unfortunately, nonpayment did not affect the rate
of pressure sores noted between 2006 and 2010.21 While it is
unclear whether this is due a concomitant increase in early
diagnosis, pressure sores remain prevalent and continue to be
a large economic burden.
Basic science
Multiple studies describe risks associated with the develop-
ment of pressure sores.32–34 Fisher et al. utilized a logistic
regression analysis to identify risks for pressure sores and
found that increased age, male sex, friction, shear, moisture,
malnutrition, immobility, and altered sensorium all indepen-
dently place patients at risk of developing pressure sores.33
More recently, these observations were re-demonstrated in a
prospective cohort study of 3233 patients admitted to a single
400 000 records from the survey between 1989 and 2005, found
overall and nosocomial pressure ulcer prevalence rates of
9.2% in 1989 and 15.5% in 2004. Rates were higher in long-term
acute care facilities, at 27.3%. Overall, pressure ulcer preva-
lence appears relatively stable despite significant advances in
treatment and prevention.
The prevalence of pressure ulcers in the nursing home
population has been reported to be anywhere from 2% to
28%.4,5 Data from the 2004 National Nursing Home Survey
revealed an overall 11% prevalence rate, with elderly resi-
dents, residents with recent weight loss, and short-term resi-
dents being at even higher risk.6 The reported prevalence of
pressure ulcers in long-term acute care facilities is likewise
variable, ranging from 5% to 27%,7,8 while the IPUPS reported
an overall 22% rate in this setting.
Particular populations have been identified at particularly
high risk. There is a strong association between hip fractures
and pressure sores, though incidences have been reported from
8.8% to 55%. A large European study9 revealed an overall
prevalence of 10% on arrival and 22% at discharge in this popu-
lation, with dehydration, advanced age, moist skin, higher
Braden scores, diabetes, and pulmonary disease all associated
with higher rates of ulceration. The majority were stage I, and
none was stage IV. Baumgarten et al.10 reported an 8.8% inci-
dence of hospital-acquired pressure sores in a study involving
multiple centers in the US. Another study by the same group,11
with rigorous surveillance for ulcers in a slightly older popula-
tion, revealed an incidence of 36.1%. Incidence was highest in
the acute care setting and associated with longer wait before
surgery, ICU stay, longer surgery, and general anesthetic.
Spinal cord injury (SCI) patients are at particular risk for
pressure sores due to the combination of immobility and
insensitivity. Rates have been reported to be 33–60%,12–14 and
it is the second leading cause of rehospitalization after SCI.
Gelis et al.15 reviewed pressure ulceration in the SCI popula-
tion and noted a 21–37% prevalence in the acute stage, a 2%
rate leaving a rehabilitation center, and a 15–30% rate in the
chronic stage. Identified risk factors included race, history of
previous ulceration, and tobacco use.
Anatomic distribution
In 1964, Dansereau and Conway16 published the results of
their evaluation of 649 patients from the Bronx Veterans
Administration Hospital with 1604 pressure sores among
them. The authors noted that the vast majority of pressure
sores developed in the lower part of the body, the ischial
tuberosity being the most common site, accounting for 28% of
all ulcers. In Meehan’s 199417 review of 3487 patients with
6047 pressure sores, the most common site of occurrence was
the sacrum (36%), followed by the heel (30%). More recently
VanGilder et al.2 reported that the sacrum (28.3%) and the heel
(23.6%) were the most common sites for pressure ulceration,
followed by the buttocks (17.2%).
Classically, in the early acute phase after SCI, the sacral area
tends to be the most common site of pressure sores as patients
are stabilized and treated for concomitant injuries in the
supine position. In the subacute and chronic phases after SCI,
the ischial area becomes the predominant site of pressure
sores as the patient begins to sit up in a wheelchair during
rehabilitation. However, as will be discussed later in this
chapter, this division is not absolute.

351.e1
Historical perspective
Historical perspective
Pressure sores are an ancient problem, observed at autopsy of
Egyptian mummies.22 As early as the 16th century, Ambrose
Paré recognized the importance of pressure and nutrition in
the treatment of these lesions.23 By 1873 Sir James Paget cor-
rectly surmised that pressure led to compression of the cuta-
neous vasculature, leading to necrosis.24 Though he incorrectly
attributed them to central nervous system lesions, in 1878
Charcot25 provided a detailed description of what he termed
decubitus ominosus, noting not only the clinical manifestations
of the disease but the poor prognosis they portended. Though
well over a century old, Charcot’s description could be applied
to any number of modern patients with pressure sores of
various stages:
The skin there has a rosy hue, sometimes it is dark red, and even
violet, but the dolor disappears momentarily on pressure with
the finger. […] On the morrow, or after-morrow, vesiculae or
bullae make their appearance toward the central part of the
erythematous patch; […] The subcutaneous connective tissue,
and sometimes even the subjacent muscles are themselves already
invaded by sanguine infiltration. […] The eschars, if they but
attain a certain extent, constitute, as you are aware, dangerous
foci of infection; and, in fact, putrid intoxication, denoted by a
more or less intense remittent fever.
In 1938, John Staige Davis was the first to suggest replacing
the unstable scar of a healed pressure sore with flap tissue.26
However, it was not till 1945 that Lamon described the first
closure of open pressure sores.27 Thereafter, surgical treatment
of pressure sores gained immediate attention, and by the end
of the decade most of the surgical techniques used in the
treatment of pressure sores today had been reported.
Kostrubala and Greeley recommended excision of the bony
prominence and padding of the exposed bone with local
fascia or muscled fascia flaps in 1947.28 That same year,
Conway et al. emphasized the importance of tissue laxity at
the reconstructed site to allow for joint motion and recom-
mended skin-grafting the donor sites of local rotation flaps
used for coverage.29 In 1948 Bors and Comarr used the gluteus
maximus as a muscle rotation flap,30 and the next year
Blocksma et al. rotated the biceps femoris muscle stump to
cover the exposed bone following total ischiectomy.31
In the following decades, wound care has become ever
more complex and numerous technical refinements have been
developed, but the basic concepts of patient optimization,
complete debridement, and tension-free soft-tissue coverage
remain constant.

352
SECTION II
CHAPTER 16 • Pressure sores
Pressures below this threshold were unlikely to cause tissue
necrosis, while increased pressures were correlated with
increased likelihood of ulceration. Kosiak et al.40 noted similar
findings in dog tissues, but noted that if the pressure was
released every 5 minutes, few changes occurred. Groth41
published a detailed study on the relationship between
applied pressure and the onset of tissue damage in a rabbit
model, noting an inverse relationship wherein higher pres-
sures caused damage in less time. Husain42 had similar results
in a rat model, also noting that pressure applied over a large
area was less injurious than when applied over a smaller one.
Furthermore, various tissues have different susceptibility
to pressure. Nola and Vistnes43 noted that pressure on skin
over a bone is more injurious than pressure on skin over
muscle. On the other hand, Daniel et al.44 noted that muscle
hospital where 201 were diagnosed with a hospital-acquired
pressure sore. In their analysis, Baumgarten et al. also found
that increased age, male sex, moisture caused by incontinence,
poor nutrition, and immobility limiting turning in bed all
correlated with the diagnosis of pressure sores.34 Recognition
of these factors has led to the understanding of pressure sores
as multifactorial entities and provide the basis for basic science
research to further our understanding of these processes.
Pressure
As mentioned previously, Paget described the connection
between pressure and decubitus ulcers as early as the 19th
century. Though many other factors may contribute to their
formation, pressure sores are thought to result from pressure
applied to soft tissue at a level higher than that found in the
blood vessels supplying that area for an extended time period.
In 1930 Landis performed a classic series of experiments and
found that the average capillary closing pressure is approxi-
mately 32 mmHg.35 Fronek and Zweifach reported similar
findings in their study, noting perfusion pressures between 20
and 30 mmHg (Fig. 16.1).36
Lindan et al.37 documented the human distribution of pres-
sure points by means of a “bed of springs and nails”. With the
subject supine, the points of highest pressure were the sacrum,
buttocks, heel, and occiput, all of which were subject to pres-
sures of roughly 50–60 mmHg. When sitting, pressures up to
100 mmHg were recorded over the ischial tuberosities. Sub-
jects in Lindan’s study were tested on surfaces that were
significantly softer than comparable wheelchair seats of beds,
but even on padded surfaces with wide load distributions, all
major weight-bearing areas sustained pressures in excess of
end-capillary pressures (Fig. 16.2).
However, simply applying pressure in excess of these
levels does not necessarily result in tissue ischemia. Much of
the pressure applied to tissues is carried by the connective
tissues surrounding the blood vessels. Furthermore, autoregu-
lation of local blood flow will tend to increase blood pressure
in response to applied pressure within a certain range.35,38
Efforts have been made to quantify the degree of pressure
necessary to cause tissue damage. Dinsdale39 found that pres-
sure roughly double capillary closing pressure, applied for 2
hours, resulted in irreversible ischemic damage to tissue.
Fig. 16.1  Pressure in various components of the tissue microcirculation (diameter
in µm). (Data from Fronek K, Zweifach BW. Microvascular pressure distribution in
skeletal muscle and the effects of vasodilation. Am J Physiol. 1975;228:791;
reprinted with permission from Woolsey RM, McGarry JD. The cause, prevention,
and treatment of pressure sores. Neurol Clin. 1991;9:797.)
Capillaries
Venules
Anterioles
mmHg
120
0
70
50
30
10
10
30
50
70
90
110
120
120
90
110
20
40
60
80
100
Fig. 16.2  Distribution of pressure in a healthy adult male while (A) supine,
(B) prone, (C) sitting with feet hanging freely, and (D) sitting with feet supported.
Values expressed in mmHg. (Adapted with permission from Lindan O, Greenway
RM, Piazza JM. Pressure distribution on the surface of the human body I. Evaluation
in lying and sitting positions using a “bed of springs and nails”. Arch Phys Med
Rehabil. 1965;46:378.)
C
D
A
B
10
20
30
40
45
50
60
80
100
30
10
10
10
10
20
20
30
40
10
20
40
30
10
20
40
60
20
20
10
60
20
60
80
40
20
10
10
10
45
30
20
40
50
100

353
Basic science
Dinsdale39 noted that addition of shear forces greatly decreased
the amount of pressure needed to cause ulceration in a pig
model, concluding that “a shear force is more disastrous than
a vertical force”. Goossens et al.50 noted similar results in
human subjects, finding that the addition of a small shear
component drastically reduces the level of pressure needed to
cause critical ischemia over the sacrum.
Patient transfers, sliding or dragging the patient in bed,
“boosting” patients up in bed, or allowing patients to elevate
themselves in bed by pushing with elbows and heels all cause
significant shear.46 Certain positions also cause elevated levels
of shear: patients in the semi-Fowler’s position or sliding
down in a wheelchair both experience significant shear
over the lower back and buttocks.51 This can explain why
wheelchair-bound patients may still develop a sacral pressure
sore if they are not sitting upright in their chair, despite the
fact that theoretically the ischial tuberosities should be bearing
the majority of their weight.
Moisture
Excessive moisture is not only a risk factor for pressure sores
but may also result in a separate pathology inclusive of
incontinence dermatitis, perineal dermatitis, and moisture
lesions.52 Whether a separate entity resulting in skin break-
down due primarily to moisture and irritation as opposed to
pressure is a legitimate or useful distinction is a matter of
some debate.53,54 However, it is clear that moisture is an
important factor to consider when evaluating pressure sores,
and pressure relief should not be neglected even if lesions are
thought to be primarily due to moisture. Moist skin has a
higher coefficient of friction and is prone to maceration and
excoriation.49
Though excess moisture can have many causes, urinary
and fecal incontinence is of particular concern in the etiology
of pressure sores. Incontinence is common in the elderly, and
rates are even high in the institutionalized population, with
rates from 20% to 77% for urinary incontinence55,56 and from
17% to 50% for fecal incontinence.57 In addition to causing
excess moisture, urine also negates the acidic pH of skin
through the introduction of nitrogen derivatives. Fecal con-
tamination introduces a large bacterial load. Lowthian53 noted
a fivefold increase in pressure sores in patients who were
incontinent, though he did not distinguish between urinary
and fecal incontinence. While some studies have found a
relationship between urinary incontinence and pressure
sores,58 others have failed to find a correlation while noting a
significant correlation with fecal incontinence.59–61
While excess moisture is clearly deleterious, the opposite
is also true. Excessively dry skin is prone to cracking, has
decreased tensile strength and lipid content, and impaired
barrier function, and appears to be an independent risk factor
for pressure ulceration.62,63
Malnutrition
Patients who are chronically ill and debilitated frequently
have accompanying nutritional deficiencies that manifest as
low serum albumin, prealbumin, or transferrin levels. Preva-
lence rates range from 1% to 4% in elderly patients living at
home, versus 20% in hospitalized patients and 37% in institu-
tionalized patients.64 The deleterious effects of poor nutrition
was more susceptible to injury than skin, requiring less pres-
sure for a shorter duration likely due to its increased metabolic
activity.
Friction
Friction is the force resisting relative motion between two
surfaces and is the precursor to shear. It develops between the
patient’s skin and any number of contact surfaces, including
the patient’s bedding, transfer devices such as sheets, rollers,
or slide boards, various appliances and orthotics, and mobil-
ity devices such as wheelchair cushions. Excess friction may
result in superficial skin injury such as abrasions, blisters,
and even skin tears in patients with fragile skin.45,46 While
relatively minor in isolation, such injuries may potentiate
further damage. As the integrity of the skin is compromised,
transepidermal water loss increases and allows moisture
to accumulate. Moisture in turn increases the coefficient of
friction and promotes adherence to sheets and other contact
surfaces.47
Shear (Fig. 16.3)
Reichel48 was one of the first authors to describe shear as a
risk factor for developing decubitus ulcers, noting that patients
developed more sacral pressure sores when the head of their
bed was elevated. Shear develops when friction adheres skin
and superficial tissues to sheets or bedding, which are then
stretched tightly over deeper structures. The underlying blood
vessels are then stretched, angulated, and may be injured by
this stress. Subcutaneous tissue in particular lacks tensile
strength and is particularly susceptible to shear stress.49
Fig. 16.3  Pressure, shear, and friction are related but distinct forces which
contribute to pressure sore development.
Sheet
Mattress
Friction
Shear
Friction
Pressure
Shear

354
SECTION II
CHAPTER 16 • Pressure sores
necessary for appropriate healing of chronic wounds and may
service as markers of healing/non-healing.81 While MMP-9
and several other proteinases and their inhibitors have been
studied in various kinds of wounds, human studies within
the arena of pressure sores remain limited.
Diagnosis
Classification
Multiple classification systems exist to describe pressure
sores. The most commonly used system is the NPUAP staging
system,82 a modification of Shea’s original classification,82,83
most recently revised in 2007 (Fig. 16.4). Though used in basic
form for many years, two additional classifications, suspected
deep-tissue injury and unstageable, have been added rela-
tively recently to the NPUAP system.
“Stage” is somewhat of a misnomer, as it implies a progres-
sion that does not reflect reality. Stage IV ulcers do not neces-
sarily start as stage I ulcers, a fact emphasized by the addition
of the suspected deep-tissue injury classification. Likewise,
healing pressure sores do not progress in reverse order but
instead granulate and close by secondary intention in the
absence of surgical treatment. Though panel members were
aware of these issues, the term “stage” was retained due to its
historical use and widespread adoption.
Patient evaluation
When evaluating a new patient with a pressure sore, a wide
variety of factors must be considered. Both the wound and
the patient should be meticulously examined. A wound
history, noting the onset, duration, prior treatments and pro-
cedures, and wound care regimen, should be documented.
Wounds should be measured in three dimensions, with notes
made regarding any tunneling or undermining. The tissue at
the margins of the wound should be examined for any signs
of occult deep-tissue injury, infection, and scarring. The base
of the wound should be characterized, noting the presence of
eschar, slough, or other necrotic tissue. If necrotic material
obscures the base of the wound, it should be debrided until a
full assessment can be performed. Granulation should be
noted in terms of both character and percentage of the wound
bed covered. Exposed tissues, such as bone, tendon, or joint,
should be noted. If easily accessible the bone can be character-
ized as hard, soft, or obviously necrotic. The amount and
character of the wound exudate should be documented as
well. A measuring tape and camera can improve documenta-
tion and make tracking progression easier.84
In addition to a thorough general history and physical,
some attention should be paid to the risk factors specific to
pressure sores. An attempt should be made to identify the
etiology of the patient’s pressure sore, though it is often
multifactorial. Sources of friction, shear, and pressure should
be evaluated and recommendations for proper pressure relief
surfaces and skin care regimens made as appropriate. If
incontinence is present an effort should be made to control
this, possibly involving the assistance of other specialties if
needed. Likewise, spasticity should be evaluated and if
needed controlled medically or surgically. Nutrition should
be evaluated with serum albumin and prealbumin. If needed,
include weight loss, negative nitrogen balance, poor wound
healing, and immunosuppression.65 Several studies have
documented a clear association between protein malnutrition
and wound healing,66–68 and patients who are severely mal-
nourished are at increased risk of sepsis, infection, in-hospital
mortality, and longer hospital stays.69,70 However, the relation-
ship between malnutrition and pressure sore prevention, as
opposed to treatment, is not entirely clear. There is certainly
a strong correlation between malnutrition and pressure
sores,71–73 but a clear causal link remains elusive.
Neurological injury
Despite extensive recommendations aimed at addressing the
issue, pressure sores remain the most common complica-
tion74,75 and the second most common cause of hospital admis-
sion76 in the SCI population. Immobility, either in bed or in a
wheelchair, leads to increased pressure, friction, and shear
that is a causative factor in all pressure sores. However, SCI
eliminates the protective sensation that would normally
stimulate them to alter their position in response to prolonged
pressure, particularly during sleep. Pressure that would be
innocuous with intermittent relief leads to pressure sore
development.51
In addition to the obvious problems of immobility and
decreased sensation, incontinence, spasticity, and psychoso-
cial issues are common problems in this population. Spasticity,
a common but not inevitable sequela of SCI, is a problem
unique to the SCI population, affecting 65–78% of patients one
year postinjury.77 Spasticity is characterized by hyperreflexia,
clonus, and increased muscle tone. While it is not included in
most pressure sore risk scales, it has effects due to direct
increase in mechanical stress and altered weight distribution,
as well as complicating patient positioning, skin inspection,
and hygiene.78
Inflammatory milieu
The role of the local inflammatory milieu within the wound
bed has gained significant attention but remains to be eluci-
dated.32 In 1994 Cooper et al. measured levels of multiple
cytokines in pressure sore wound beds from 20 patients with
stage III/IV wounds and found decreased levels of platelet-
derived growth factor (PDGF), basic fibroblast growth factor
(bFGF), epidermal growth factor (EGF), and transforming
growth factor-Beta (TGF-B).79 These cytokines play major
roles in the progression of wound healing; thus a more com-
prehensive understanding of the normal temporal character-
ization of these molecules may facilitate novel therapeutic
agents. Matrix metalloproteinases (MMPs) seem to play a role
in healing of chronic pressure sores. MMPs are zinc-dependent
proteases, which are capable of degrading various extracel-
lular matrix proteins, and more recently been shown to play
a role in cell proliferation, differentiation, apoptosis, angio-
genesis and host immunity.80 Under homeostatic conditions,
a balance must be maintained between MMPs and their
counterparts, namely tissue inhibitors of metalloproteinases
(TIMPs) in order to maintain orderly formation/degradation
of extracellular matrices. In chronic wounds from 56 patients
with Stage III/IV pressure sores, Ladwig et al. found that as
chronic wounds heal, the ratio of MMP-9 : TIMP-1 decreases,
thus suggesting that higher levels of MMP-9 and TIMP-1 are

355
Diagnosis
nutrition should be supplemented and progress of therapy
monitored with weekly serum studies. Any underlying
medical problems, such as hypertension, diabetes, or history
of cardiac disease, should be investigated and optimized.
A reasonable initial set of studies would include a complete
blood count, basic metabolic panel, creatinine, and blood urea
nitrogen. Albumin and prealbumin should be obtained at the
initial consult and regularly thereafter to evaluate for malnu-
trition and follow the progression of therapy. C-reactive
protein and erythrocyte sedimentation rate (ESR) can be
obtained to evaluate for osteomyelitis, though they will almost
certainly be positive in deeper ulcers. The evaluation of the
pressure sore patient for osteomyelitis is discussed in the next
section. Wound cultures of the open pressure sore are of little
value and should not be used to direct antibiotic therapy,85 as
opposed to needle or surgical bone biopsy.
Osteomyelitis
In 1970 Waldvogel et al.86 recognized that osteomyelitis is
responsible for wound infection and breakdown after recon-
struction of stage III and IV pressure sores (Fig. 16.5). Patients
with pressure sores complicated by osteomyelitis have signifi-
cantly longer hospitalizations than those who do not.87
Establishing the diagnosis of osteomyelitis is essential before
embarking on definitive surgical treatment of pressure sores.
A
B
C
D
Fig. 16.4  The National Pressure Ulcer Advisory Panel staging system. (A, E) Stage I: Intact skin with nonblanchable redness of a localized area usually over a bony
prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. (B, F) Stage II: Partial-thickness loss of dermis
presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister. This should not be used
to describe skin tears, tape burns, perineal dermatitis, maceration, or excoriation. (C, G) Stage III: Full-thickness tissue loss. Subcutaneous fat may be visible, but bone,
tendon, or muscle is not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. (D, H) Stage IV:
Full-thickness tissue loss with exposed bone, tendon, or muscle. Exposed bone is sufficient but not necessary to define a stage IV pressure sore. Slough or eschar may be
present on some parts of the wound bed. Often includes undermining or tunneling. May extend into muscle and/or supporting structures (e.g., fascia, tendon, or joint
capsule), making osteomyelitis possible. Bone/tendon is visible or directly palpable. (I) Suspected deep-tissue injury: Purple or maroon localized area of discolored intact
skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy,
warmer, or cooler as compared to adjacent tissue. The wound may evolve and become covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue
even with optimal treatment. (J) Unstageable: Full-thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or
eschar (tan, brown, or black) in the wound bed. Until the base of the wound is exposed, the true depth, and therefore stage, cannot be determined.
Continued

356
SECTION II
CHAPTER 16 • Pressure sores
Unrecognized osteomyelitis is a major source of morbidity
and increased costs.87
In 1988 Lewis et al.88 tried to assess the value of some
common tests in diagnosing osteomyelitis by following 61
patients with pressure sores, 52 of whom eventually had
confirmed histopathologic diagnosis of osteomyelitis from
surgical specimens. This prospective trial examined white
blood cell count, ESR, plain X-ray, technetium-99m bone
scans, computed tomography (CT) scan, and Jamshidi-needle
bone biopsy. The authors felt that the most practical, reveal-
ing, and least invasive preoperative workup involved a
combination of white blood cell count, ESR, and two-view
X-ray. Only one positive test was needed to make the diagno-
sis. Sensitivity was 89% and specificity 88% using this protocol.
Bone scans and CT scans were expensive and not very sensi-
tive. Needle bone biopsy had a sensitivity of 73% and a speci-
ficity of 96%. Of note, magnetic resonance imaging (MRI) was
not included in this analysis.
MRI has taken on a larger role in the diagnosis of osteomy-
elitis. Huang and colleagues89 analyzed 59 consecutive MRIs in
44 paralyzed patients and found an overall accuracy of 97%,
sensitivity of 98%, and specificity of 89%. The authors con-
cluded that not only was MRI accurate, it helped define the
extent of infection, which may help limit the surgical resection.
Ruan et al.90 independently confirmed these findings and feel
that MRI is superior to CT for the evaluation of osteomyelitis.
Han et al.87 reviewed their series of press ulcers and noted
that their high osteomyelitis-related complication rate – largely
E
F
G
H
Fig. 16.4, cont’d

357
Patient selection
younger patients, and those who had undergone multiple
operations for their pressure sores. The authors recommend
“intensive psychological counseling” in the treatment of the
pressure sore patient. Foster et al.99 suggest that psychological
factors play a significant role in predicting pressure sore
recurrences.
Patient selection
All patients with pressure sores should be optimized with
regard to the risk factors already enumerated. It is worth
remembering that pressure sores are rarely life-threatening,
and there is no need to rush to treatment or surgery if the
patient has not been optimized. Many more superficial
wounds will heal with conservative therapies if correctable
risk factors are identified and addressed. On the other hand,
a patient who is malnourished, bedbound on an inappropri-
ate mattress, with undiagnosed osteomyelitis, is doomed to
failure regardless of the surgical technique used.
A judgment must be made regarding whether a wound is
likely to heal successfully by secondary intention or whether
a flap is required to resurface the wound and/or fill dead
space left after debridement. In general, stage I and II pressure
sores can be treated nonoperatively, while stage III and IV
ulcers require flaps. Patients with suspected deep-tissue
injury and unstageable ulcers should be debrided until they
can be clearly staged. While surgical debridement is the gold
standard, other methods can be used as appropriate.
While operative treatment is often delayed while the
patient is optimized and risk factors corrected, it is a rare
patient who does not qualify for any attempt at reconstruc-
tion. Obviously critically ill patients who cannot tolerate
surgery should be stabilized before any sort of reconstruction
is entertained. More uncommon is the patient with multiple
severe comorbidities whose risk factors cannot be easily cor-
rected, due to either medical or social factors. In such cases,
consisting of deep abscess and sinus tracts – was a result of
their inability to diagnose osteomyelitis accurately preopera-
tively. Their group moved to a two-stage procedure, perform-
ing wound debridement and Jamshidi core needle bone
biopsy at the first operation (Fig. 16.6). If the biopsy results
were positive, closure was delayed for 6 weeks while the
osteomyelitis was treated with antibiotics; otherwise the
wound was closed with a musculocutaneous flap. The authors
also noted that bone cultures alone were not as useful as bone
cultures and histopathology of the bone biopsy together, and
found that the biopsy had a positive and negative predictive
value of 93% and 100%, respectively.
These results are in keeping with several other studies
that support the utility of bone biopsy in the diagnosis of
osteomyelitis.91–94 Marriott and Rubayi95 have used the results
of bone biopsy to determine the duration of antibiotic therapy,
in some cases truncating treatment if pathology reveals only
chronic osteomyelitis.
Ultimately, MRI appears to be accurate and noninvasive,
while providing detailed anatomic information. Bone biopsy
likewise has admirable accuracy and, perhaps most impor-
tantly, is the only method that can be used to direct antibiotic
therapy. Though local factors such as the availability of equip-
ment and economic factors should be considered, used in
conjunction MRI and bone biopsy allow for comprehensive
evaluation of osteomyelitis in the pressure sore patient.
Psychological evaluation
Psychological problems are common in the pressure sore
population. Langer96 finds 22% of patients with SCI had
diagnosable depression, considerably higher than found in
the general population. Frank et al.97 report 37.5% of patients
with SCI had a diagnosis of major depression. Akbas et al.98
report 47.4% of patients with pressure sores fulfilled the
diagnostic criteria for major depression. In their prospective
study, they found the depression rates to be higher in women,
I
J
Fig. 16.4, cont’d

358
SECTION II
CHAPTER 16 • Pressure sores
A
B
C
D
Fig. 16.5  (A–D) Bone scan, computed tomography, and magnetic resonance
imaging of severe sacral osteomyelitis.

359
Treatment
chronic wound care may be preferable to attempted recon-
struction that is doomed to failure and recurrence.
Treatment
Prevention
Obviously, prevention of pressure sores is preferable to treat-
ment. As healthcare moves towards nonpayment for nosoco-
mial pressure sores, there is an ever-greater incentive to avoid
these lesions. However, despite extensive study and recom-
mendations, overall pressure sores rates have changed little
in recent years.3,100,101
Some pressure sores may not be preventable,102–104 and
using pressure sores as an indicator of quality is a contentious
issue, particularly in light of possible negligence litigation.105
However, though no strategy has been found that reduces
pressure sore rates to zero, there are several measures, many
of which now constitute standard care, that may contribute to
pressure sore prevention.63
For the surgeon who is often consulted only after a pres-
sure sore has developed, knowledge of prevention strategies
is still critical not only to advise the consultation but also
to optimize the patient before surgery, prevent additional
pressure sores from developing, and, perhaps most critically,
to prevent postoperative recurrence.
Risk assessment
The first step in pressure sore prevention is risk assessment.
Multiple assessment scales have been devised, including
those by Braden, Gosnell, Knoll, Norton, Waterlow, and
Douglas.106 Several are designed for specific subpopulations,
and each has its merits. All suffer from potential inaccuracies
as their use is dependent on the competence of its assessor
and the setting in which it is used.
Norton107 developed an assessment scale for use in geriatric
patients. The scale incorporates general physical condition,
mental status, activity, mobility, and incontinence and ranges
from 5 to 20, with lower scores associated with greater risk.
Patients with a score of 11 or less had a 48% incidence of
pressure sores, while those with a score of 18 or greater had
a 5% incidence. Gosnell108 added nutritional status as a vari-
able to his method, which is often referred to as the “modified
Norton scale”.
The most widely used pressure sore assessment tool is the
Braden scale109 (Table 16.1). The Braden scale incorporates six
subscales that assess sensory perception, skin moisture, activ-
ity, mobility, friction and shear, and nutrition. Scores range
from 6 to 23, with higher scores associated with an increased
Grade IV pressure ulcer
Effective Jamshidi needle bone
biopsy and bone culture
JNBB –
Bone cx +
JNBB +
Bone cx –
JNBB –
Bone cx –
JNBB +
Bone cx +
Continue with IV antibiotics
for 2 weeks
Perioperative antibiotics
for 48 hours
Delayed flap reconstruction
Partial ostectomy
bony prominence
Delayed flap reconstruction
Partial ostectomy
bony prominence
Elective flap reconstruction
IV antibiotics
6 weeks
IV antibiotics
6 weeks
Effective Jamshidi needle bone
biopsy and bone culture
Effective Jamshidi needle bone
biopsy and bone culture
Aggressive wound care and
nutritional optimization
Elective flap reconstruction
(E) Protocol for managing patients with grade IV pressure ulcers. JNBB, Jamshidi core needle bone biopsy; IV, intravenous. (Reprinted with permission
from Han H, Lewis VL, Weidrich VA, et al. The value of Jamshidi core needle bone biopsy in predicting postoperative osteomyelitis in grade IV pressure ulcer. Plast Reconstr
Surg. 2002;111:118.)
Fig. 16.5, cont’d

360
SECTION II
CHAPTER 16 • Pressure sores
that interventions designed to stratify risk remain poorly
utilized.115
Skin care (Box 16.1)
Ideal skin care encompasses cleaning, hydrating, protecting,
and replenishing the skin as needed. Proper skin care can be
time- and labor-intensive and is at times neglected by physi-
cians and nurses alike.116
Common recommendations for skin cleansing involve the
use of warm soap and water followed by drying by rubbing
or patting.117 Washing involves the use of soap and surfactants,
which, while effective at removing debris, have the potential
to be irritants.118 The alkaline nature of soap also negates the
protective natural acidity of the skin, which in turn alters the
balance of resident flora on the skin.119 Drying the skin by
patting may cause less trauma,120,121 though if it leaves excess
moisture on the skin, this can lead to maceration and increased
vulnerability to friction injuries.122 Many alternative cleansers
have been marketed that address the shortcomings of soap
and water, but little data exist to recommend any particular
product at this time.123
Maintaining proper skin hydration is most often achieved
through the use of emollients, which occlude the skin surface
with a hydrophobic layer, and humectants, which attract and
absorb water from their surroundings. Numerous formula-
tions exist, many with additional surfactants and emulsifying
agents, which vary somewhat in their effectiveness, greasi-
ness, and potential for skin irritation. While the theoretic
advantages of treating dry skin are well established, 60,62,124 as
with cleansers, few data exist to recommend any one hydrat-
ing product over another.125,126
Barrier products protect the skin, particularly in the setting
of incontinence or in the presence of stomas, fistulas, or
wounds. Many preparations consist of a lipid/water emul-
sion that forms a protective film over the skin. Newer barrier
products incorporate a polymer that forms a thin semiperme-
able membrane over the skin.127 Many incorporate an antisep-
tic agent such as cetrimide or benzalkonium as well. Again,
despite their widespread use and the proliferation of products,
data on their effectiveness are scant.128
While data on individual agents are not very robust, there
is evidence that a clear skin care protocol can benefit patients.
Multiple authors have found instituting such protocols results
in reduction in pressure sore incidence rates.129 Cole and
Nesbitt130 found a reduction from 17.8% to 2% over a 3-year
period, whereas Lyder et al.131 noted an 87% reduction in a
nursing home setting. Based on the available data, the
risk of developing pressure sores. The original study noted a
score of 16 to be the threshold for pressure sore develop-
ment,109 though a different cutoff score may be more appropri-
ate in different settings.110,111
Multiple studies have examined the validity, sensitivity,
specificity, and predictive value of the various scales. Gener-
ally, assessment scales are superior to nurses’ clinical judg-
ment when predicting future pressure ulceration.106 However,
there is no evidence that use of risk assessment decreases
pressure sore incidence.112–114 Whether this is because inter-
ventions are not instituted or are ineffective is unclear.113
Given the recent efforts to improve healthcare quality,
Bergman et al. analyzed one institution’s National Surgical
Quality Improvement Program (NSQIP) database to deter-
mine adherence to multiple process-based quality indictors,
including pressure ulcer risk assessment. While this study
only looked at 143 consecutive elective abdominal surgery
admissions, authors note an adherence rate of only 35% in the
risk assessment for pressure ulcers, supporting the notion
Fig. 16.6  (A) The Jamshidi bone biopsy needle, cannula, and screw-on cap (a),
tapered point (b), pointed stylet to advance cannula through soft tissues (c), and
probe to expel specimen from cannula (d). (B) With the stylet locked in place, the
cannula is advanced through the soft tissue until bone is reached. The inset is a
close-up view showing stylet against bone cortex. (C) The stylet is removed, and
the bone cortex is penetrated with the cannula. The cannula is withdrawn, and the
procedure repeated with redirection of the instrument to obtain multiple core
samples. (D) The probe is then inserted retrograde into the tip of the cannula to
expel the specimen through the base (inset). (Reprinted with permission Powers BE,
LaRue SM, Withrow SJ, et al. Jamshidi needle biopsy for diagnosis of bone lesions
in small animals. J Am Vet Med Assoc. 1988;193:206–207.)
C
D
A
B
a
b
c
d
BOX 16.1  General skin care principles
Assess the patient’s skin daily
Cleanse skin when indicated using a pH-balanced cleanser
Avoid soap and hot water
Avoid friction and scrubbing
Minimize exposure to moisture (e.g., incontinence, wound leakage)
Use skin barrier product to protect vulnerable skin
Use emollients to maintain skin hydration

Table 16.1  The Braden scale for predicting pressure sore risk
Sensory
perception
Ability to
respond
meaningfully
to pressure-
related
discomfort
1. Completely limited
Unresponsive (does not
moan, flinch, or grasp) to
painful stimuli, due to
diminished level of
consciousness or
sedation
or
Limited ability to feel pain
over most of body
2. Very limited
Responds only to painful
stimuli. Cannot communicate
discomfort except by
moaning or restlessness
or
Has a sensory impairment
which limits the ability to feel
pain or discomfort over half
of body
3. Slightly limited
Responds to verbal
commands, but cannot
always communicate
discomfort or the need
to be turned
or
Has some sensory
impairment which
limits ability to feel
pain or discomfort in
one or two extremities
4. No impairment
Responds to verbal
commands. Has
no sensory deficit
which would limit
ability to feel or
voice discomfort
Moisture
Degree to
which skin is
exposed to
moisture
1. Constantly moist
Skin is kept moist almost
constantly by perspiration
and urine. Dampness is
detected every time
patient is moved or turned
2. Very moist
Skin is often, but not always,
moist. Linen must be
changed at least once a
shift
3. Occasionally moist
Skin is occasionally
moist, requiring an
extra linen change
approximately once a
day
4. Rarely moist
Skin is usually dry;
linen only requires
changing at
routine intervals
Activity
Degree of
physical
activity
1. Bedfast
Confined to bed
2. Chairfast
Ability to walk severely limited
or nonexistent. Cannot bear
own weight and/or must be
assisted into chair or
wheelchair
3. Walks occasionally
Walks occasionally
during day, but for very
short distances with or
without assistance.
Spends majority of
shift in bed or chair
4. Walks frequently
Walks outside room
at least twice a
day and inside
room at least
once every 2
hours during
waking hours
Mobility
Ability to
change and
control body
position
1. Completely immobile
Does not make even slight
changes in body or
extremity position without
assistance
2. Very limited
Makes occasional slight
changes in body or extremity
position but unable to make
frequent or significant
changes independently
3. Slightly limited
Makes frequent though
slight changes in body
or extremity position
independently
4. No limitation
Makes major and
frequent changes
in position without
assistance
Nutrition
Usual food
intake pattern
1. Very poor
Never eats a complete meal.
Rarely eats more than half
of any food offered. Eats
two servings or less of
protein (meat or dairy
products) per day. Takes
fluids poorly. Does not
take liquid dietary
supplement
or
Is NOP and/or maintained
on clear liquids or IVs for
more than 5 days
2. Probably inadequate
Rarely eats a complete meal
and generally eats only
about half of any food
offered. Protein intake
includes only three servings
of meat or dairy products
per day. Occasionally will
take a dietary supplement
or
Receives less than optimum
amount of liquid diet or tube
feeding
3. Adequate
Eats over half of most
meals. Eats a total of
four servings of protein
(meat, dairy products)
per day. Occasionally
will refuse a meal, but
will usually take a
supplement when
offered
or
Is on a tube-feeding or
TPN regimen which
probably meets most
of nutritional needs
4. Excellent
Eats most of every
meal. Never
refuses a meal.
Usually eats a
total of four or
more servings of
meat and dairy
products.
Occasionally eats
between meals.
Does not require
supplementation
Friction and
shear
1. Problem
Requires moderate to
maximum assistance in
moving. Complete lifting
without sliding against
sheets is impossible.
Frequently slides down in
bed or chair, requiring
frequent repositioning with
maximum assistance.
Spasticity, contractures, or
agitation leads to almost
constant friction
2. Potential problem
Moves feebly or requires
minimum assistance. During
a move skin probably slides
to some extent against
sheets, chair, restraints, or
other devices. Maintains
relatively good position in
chair or bed most of the
time but occasionally slides
down
3. No apparent problem
Moves in bed or chair
independently and has
sufficient muscle
strength to lift up
completely during
move. Maintains good
position in bed or chair
Total score
NPO, nil per os; IV, intravenous; TPN, total parenteral nutrtion.
(Reproduced from )

362
SECTION II
CHAPTER 16 • Pressure sores
are temporary, long-term use of chemodenervation agents
will result in denervation atrophy.
Surgical management of spasticity is an option when
medical therapy is insufficient. Baclofen pump implantation
is the most common surgical procedure for spasticity in
individuals with SCI and has a history of success.147,152 In
select, refractory cases, orthopedic and neurosurgical tech-
niques may be of benefit, though such procedures are unlikely
to have pressure sore prevention as their primary indication.
Local tenotomy or tendon transfer has had mixed results in
the treatment of spasticity.153 Rhizotomy has been complicated
by both inadequate treatment of spasticity154 and severe
atrophy,155 depending on the technique employed. Myelotomy
and T-myelotomy involving direct sectioning of the spinal
cord have been reported to be effective in several case
series156,157 in patients who did not have hope of regaining
motor function, though the benefits did decrease over time.158
Pressure relief
As befits its primary role in pressure sore pathogenesis,
extensive efforts have been made in modulating the pressure
through the use of various surfaces and products as well as
protocols mandating patient repositioning. Though numer-
ous support surfaces exist, most can be divided into two
general categories. Constant low-pressure (CLP) devices dis-
tribute pressure over a large area and include devices such as
static air, water, gel, bead, silicone, foam, and sheepskin sup-
ports (Fig. 16.7). Alternating-pressure (AP) devices vary the
pressure under the patient, avoiding prolonged pressure over
a single anatomic point159 (see Fig. 16.7).
Two particular types of CLP device deserve special mention,
as they are commonly used in the prevention and treatment
of pressures sores. Low air loss (LAL) beds float the patient
on air-filled cells through which warm air circulates (Fig.
16.8). The circulating air both equalizes pressure exerted on
American Wound Ostomy and Continence Nurses Society has
recently updated their guidelines for skin care.132
Incontinence
As noted previously, the relationship between urinary incon-
tinence and pressure sore incidence is not clear, with limited
evidence to suggest a causal relationship. Currently, the use
of diapers or sanitary pads in conjunction with meticulous
skin care is a reasonable option when compared to the risks
associated with extended use of a urinary catheter.133
Fecal incontinence, on the other hand, has been shown to
be a risk factor for pressure sores. At times fecal incontinence
is due to factors that are not easily correctable: cognitive
impairment, history of colorectal surgery, radiation proctopa-
thy, inflammatory bowel disease, and various neurological or
myogenic disorders of sphincter function are not easily cor-
rectable. The bladder and bowel dysfunction of SCI patients
requires specific regimens and is generally managed by a
specialist.134
However, many measures can be instituted to decrease the
impact of fecal incontinence. Possibly the most common
predisposing condition to fecal incontinence is fecal impac-
tion, which is common in older adults and may lead to
overflow incontinence.135 Conservative measures include diet
modification and a wide variety of antimotility agents,
including clonidine, cholestyramine, loperamide, codeine,
diphenoxylate, and atropine.136,137 Diarrhea may be due to
infection, which should be ruled out and treated prior to
using antidiarrheal agents. If medical management is unsuc-
cessful, surgery may be considered, ranging from attempts at
sphincterplasty to elective colostomy when other options
fail.138 Though patients and families are often reluctant to
proceed with colostomy, there is evidence overall quality of
life is improved in patients with severe fecal incontinence.139
Spasticity
Control of spasticity may not only reduce the risk of pressure
sores, but may also improve patient reports of pain and ability
to perform activities of daily living (ADL).140 However, it is
worth noting that in some cases spasticity may increase stabil-
ity in positioning, facilitate some transfers and ADLs, and
prevent osteopenia.141,142 Taken as a whole, the impact of
spasticity on quality of life is not straightforward and should
be considered before instituting treatment.
Physical therapy is the first step in treating spasticity and
an important component of care in SCI patients in general.143
Pharmacologic treatment is the next step. Diazepam, baclofen,
clonidine, tizanidine, gabapentin, and dantrolene are com-
monly used agents.144–147 Each has the potential for side effects,
including sedation, nausea, diarrhea, muscle weakness, and
cognitive effects, and treatment must be tailored to the indi-
vidual patient.147,148
Patients who cannot tolerate or do not respond to oral
therapy may benefit from intrathecal administration of
baclofen.146,149 As the drug directly accesses the central nervous
system, systemic side effects are minimized at the cost of the
risks of surgery and possible mechanical complications with
the pump. Injection with chemodenervation agents, including
phenol, ethanol, and botulinum, can be effective.150,151 Reported
complications include systemic side effects, vascular compli-
cations, skin irritation, and tissue necrosis. Though the effects
Fig. 16.7  (A) Constant low-pressure surfaces seek to distribute pressure statically,
while (B) alternating-pressure surfaces vary applied pressure over time.
A
B
Fig. 16.8  Low air loss mattress concept.

363
Treatment
only low-level evidence supporting the use of LAL mattress
or AP devices.172,175,179–182 Moreover, in addition to the increased
costs associated with the use of LAL and AP devices, the lit-
erature on LAL and AP devices demonstrate no difference or
mixed results when compared to static mattresses/overlays.
Therefore the American College of Physicians now recom-
mends that all patients identified as being at increased risk for
developing a pressure sore be placed on an advanced static
mattress, but recommends against the routine use of AP
devices in these patients.101
In addition to support surfaces, patient repositioning is
often used in an attempt to prevent pressure sores, though the
data are limited. Defloor et al.183 found a significant reduction
in pressure sore incidence when turning every 4 hours com-
bined with a specialized foam mattress was compared to
every 2 hours on a regular mattress. Given the study design
it is difficult to determine the relative contributions of the
pressure relief surface and the turning regimen. The ideal
interval and posture for repositioning are not clear given the
current data.63,184 It bears mention that repositioning is not
without its costs, both in terms of nursing time and effort,
patient discomfort, and possible dislodgement of catheters
and lines, and there is no evidence that more frequent repo-
sitioning reduces rates of pressure sores.
Cushions for wheelchairs filled with gel, foam, air, or water
are available to relieve pressure. A typical wheelchair sling
seat exerts a “hammocking” effect that can produce abnormal
scoliotic posture and pelvic obliquity (Fig. 16.10). This in turn
causes asymmetric pressure on both trochanter and ischium
that requires specialized cushions for prevention.185 Hip
adduction and internal rotation of thighs, with consequent
reduction in stability, are also seen in most paraplegics, who
lack trunk or pelvic muscle innervation and tend to sit on their
the patient and keeps the skin dry. Properly utilized, LAL
surfaces exert less than 25 mmHg on any part of the body.160,161
Air-fluidized (AF) beds circulate warm air through fine
ceramic beads, creating a unique support surface, while
having a drying effect similar to LAL beds (Fig. 16.9). With
proper use these beds exert less than 20 mmHg on the patient,
but are expensive, heavy, and cumbersome.162
Within these classifications are a multitude of beds, mat-
tresses, overlays, pads, and cushions, each with slightly dif-
ferent designs by different manufacturers. There is a daunting
body of literature comparing various specific products to one
another and with standard hospital beds. Evaluating this lit-
erature is challenging given the often small sample sizes, poor
experimental design, and lack of generalizability common in
these studies. Moreover, as new products are developed and
old ones are phased out, many studies refer to products no
longer in production or use. Despite these limitations, some
general conclusions can be drawn from the literature.163
Considerable evidence exists that the use of a pressure-
relieving overlay is superior to a standard bed in preventing
pressure sores. Multiple studies have found decreased inci-
dence and severity of pressure sores in high-risk patients with
the use of constant low-pressure devices such as overlays164–166
or sheepskin167–169 when compared to a standard hospital foam
mattress. Pooled analysis reveals a relative risk of 0.32.163 Data
also support the use of AP devices when compared to stan-
dard mattresses. Both Andersen et al.166 and Sanada170 noted a
significant reduction in pressure sore incidence with the use
of active devices, with a pooled relative risk of 0.31.163 Though
several studies have compared CLP and AP devices,166,171–173
no clear advantage has been identified, despite attempts at
pooled analysis.163
LAL, like other CLP surfaces, has been shown to be effec-
tive at preventing pressure sores,174,175 with a relative risk
estimated at 0.08.163 Comparisons with other CLP devices in
regard to prevention are limited, and no clear advantage for
either has been demonstrated.176,177 Likewise, though AF beds
are perhaps the most effective pressure-relieving devices in
widespread use, virtually no data on its role in prevention
are available, perhaps because these expensive devices are
reserved for treatment. Regardless of the type of mattress
used, they lose their ability to disperse interface pressure as
the head is elevated to 45° or higher.178 As such, patients
should avoid prolonged periods of sitting while on these
mattresses.
Given the wide array, yet variable, data on the use of pro-
tective surfaces in high-risk patients, the American College of
Physicians has formalized recommendations.101 These clinical
practice guidelines were developed after critical evaluation of
the quality of evidence and strength of recommendations of
the available literature. While there is moderate-level evidence
demonstrating improved outcomes with the use of static mat-
tresses or overlays (CLPs not including LAL beds), there is
Fig. 16.10  Hammocking effect of wheelchair sling seat producing pelvic obliquity.
Paraplegics lack innervation of the lower trunk muscles and sit on their coccyx, with
exaggerated posterior pelvic tilt. (Reprinted with permission from Letts RM.
Principles of Seating the Disabled. Boca Raton, FL: CRC Press; 1991.)
Fig. 16.9  Fluidized bed.
Air
flow

364
SECTION II
CHAPTER 16 • Pressure sores
measures implemented in pressure sore prevention become
doubly important once the transition is made to treating an
established ulcer.
Pressure relief
Pressure relief continues to be critical in the treatment of pres-
sure sores. While more advanced LAL and AF surfaces would
in theory be preferred in the treatment of established pressure
sores, the literature is mixed on this point. Ferrell et al.200
found similar results when comparing LAL beds to foam
mattresses. Ochs et al.201 in turn found AF beds to be superior
to both standard overlays and LAL beds. On the other hand
Branom and Rappl176 found LAL mattresses inferior to an
advanced foam surface, while Economides et al.202 failed to
find any superiority of an AF bed over a foam overlay. None-
theless, as mentioned previously current recommendations
support the use of low cost static mattresses overlays over
high cost LAL and AP devices.101,163,203
Spasticity
Spasticity should be addressed not only to improve patient
positioning, weight distribution, and hygiene but also to
prevent tension on the healing wound, particularly if surgical
intervention is planned.204,205 Spasticity treatment may be
complicated by a reluctance to perform surgery or implant
devices in a patient with an open wound, though this has been
reported with favorable results.205 If pump implantation is not
an option, then temporary chemodenervation should be
considered, with delayed pump placement once the wound is
healed.78
Malnutrition
While the role of nutritional status on the risk of developing
pressure sores remains unclear, its role in treatment of pres-
sure sores is better described. In 2010, Keys et al. found that
albumin levels below 3.5 g/dL were associated with ulcer
recurrence within 1 year;206 thus malnutrition should be cor-
rected and nutritional markers, including albumin and preal-
bumin, followed and trended. While many small studies have
been published examining the effect on nutritional supple-
mentation of the healing of pressure sores, many suffer from
design flaws that limit their application, prohibiting the
development of specific guidelines. In 2003, Langer et al.199 felt
the quality of the existing literature was inadequate to perform
a meta-analysis and that no firm conclusions could be drawn.
More recently, both Heyman et al.207 and Frias Soriano et al.208
found improved wound healing with oral supplementation,
but did not include controls in their studies. Van Anholt
et al.209 and Lee et al.210 both found accelerated healing with
the use of oral nutritional supplement in randomized control
trials. Taken together, the American College of Physicians
now recommends protein or amino acid supplementation in
patients with pressure sores.211 From a surgeon standpoint,
optimizing nutritional status to an albumin of at least 3.5 g/
dL will minimize chances of flap failure and recurrence.
In regards to micronutrient supplementation, there is still
little evidence to support routine supplementation of micro-
nutrients such as vitamin C or zinc in the absence of a specific
deficiency state.199,211,212 Though small, a randomized control
trial of 88 patients failed to demonstrate an increase in rate of
coccyx. Rigid-base cushions provide lumbar support and
decrease ischial pressure by allowing wider weight distribu-
tion on the posterior thighs.185 A direct correlation between
buttock–cushion interface has been noted186 (Fig. 16.11).
Houle187 and Souther et al.188 studied the effects of various
wheelchair seats and found decreased pressures over the
ischium, although none was below the capillary pressure
benchmark. The authors recommend additional measures for
pressure relief to prevent ulceration. Ragan et al.189 studied
seat interface pressures on wheelchair cushions of various
thicknesses. They found the highest subcutaneous stress
concentrated within 2 cm of the ischial tuberosity. The subcu-
taneous pressures decreased with thicker cushions, with the
maximum effectiveness obtained with an 8-cm cushion.
Increasing the thickness beyond 8 cm did not give further
benefit in reducing subcutaneous stress. As with pressure
relief mattresses, no data exist to recommend a particular type
of cushion over another at this time.163,171,190,191
The development of pressure consciousness by the patient
is an essential part of pressure sore prevention.192 Pressure
release maneuvers are reinforced to patients and should be
performed at least every 15 minutes while the patient is
seated.193
Nutrition
Multiple studies have examined the effect of nutritional
supplementation on pressure sore prevention. Despite
improvement in secondary measures such as caloric intake,
body weight, and serum nutritional markers, most studies
have failed to find reduction in pressure sore rates.194–196
Bourdel-Marchasson and Rondeau197 found a modest reduc-
tion in pressure sore rates when patients were given oral
dietary supplementation. A more recent meta-analysis by
Stratton et al.198 found a modest reduction in pressure sore
rates in patients treated with enteral tube feeds, estimating
that 19.25 patients would need to be given enteral nutritional
support to prevent one pressure sore. Overall, the evidence
that pressure sores can be prevented by nutritional supple-
mentation, much less specific formulations or micronutrient
additives, is limited.199
Nonsurgical management
Limited wounds may heal spontaneously without surgical
intervention so long as the wound is cleansed meticulously,
pressure is avoided, and risk factors are corrected. The
Fig. 16.11  Compressive force exerted on tissue by bone in an individual lying or
sitting on (left) a hard surface; (center) an effective pressure-reducing device; and
(right) an ineffective pressure-reducing device that “bottoms out”. (Reprinted with
permission from Woolsey RM, McGarry JD. The cause, prevention, and treatment of
pressure sores. Neurol Clin. 1991;9:797.)
Hard surface
Compliant surface
Bottoming out

365
Treatment
reviews that also failed to identify a superior dressing for
arterial ulcers,229 venous stasis ulcers,230 or surgical wounds.231
Ultimately the dressing selection should be guided by the
characteristics of the wound and should balance moisture,
bacterial control, and debridement.
Negative-pressure wound therapy
Negative-pressure wound therapy (NPWT) entails applying
topical negative pressure to a wound. The most common
commercially available system, the vacuum-assisted closure
(VAC) system, consists of an open-cell polyurethane or poly-
vinyl alcohol foam sponge with a pore size ranging from 400
to 600 µm in diameter. This sponge is cut to the appropriate
dimensions to fill the entire wound. Suction is then applied
to the sponge after it is covered with an adhesive drape to
create an airtight seal. This suction can be adjusted in intensity
and frequency. The most common settings are 125 mmHg
negative pressure and either continuous or intermittent
frequency.
The NPWT dressing has been applied to a multitude of
clinical problems,232 and its mechanism of action233 has been
extensively studied. Given its success in multiple arenas,
pressure sores seem a task to which it is well suited. Evidence
for its use is somewhat limited, however. Deva et al.234 noted
positive results in treated grade III ulcers but did not utilize
any controls. Ford et al.235 reported improved healing with
VAC dressings when compared to standard wound care, but
results did not reach significance. Joseph236 noted a greater
decrease in wound depth with NPWT dressing when com-
pared to saline dressings, but had limited follow-up and
endpoints did not include wound closure. On the other hand,
Wanner et al.237 failed to find any advantage to NPWT therapy
in treating pressure sores, a finding echoed in a larger review
by Reddy et al.203 It is perhaps surprising that more evidence
does not support the use of NPWT in this clinical scenario,
healing of pressure sores.213 Similarly, a double blind study of
14 patients treated with oral zinc failed to demonstrate any
clinical benefit in the treatment of pressure sores.214 Until
larger studies are conducted to elucidate the role of micronu-
trient supplementation in the treatment of pressure sores,
routine supplementation is not necessary.
Infection
Osteomyelitis is a common complication of deep pressure
sores and, as previously mentioned, often mandates operative
therapy. Many authors rightly emphasize the importance of
adequate debridement in the treatment of osteomyelitis.215
However, biopsy-directed antibiotic therapy is still an impor-
tant adjunct to surgery.87 While traditional therapy calls for 6
weeks of intravenous antibiotic therapy, there is some evi-
dence that shorter courses many be effective.95
Wound care
Debridement, regardless of the method used, should be the
first step in the care of pressure sores. Only once the wound
is thoroughly debrided can the full extent of the wound be
examined and staged. Necrotic material impedes wound
healing and acts as a nidus for infection. Traditional wet to
dry dressing may debride effectively but may remove healthy
tissue and granulation in addition to necrotic tissue.216 They
may also aerosolize bacteria from the wound.217 Allowing the
wound to desiccate despite evidence that wound healing
proceeds best in a moist environment is also counterproduc-
tive.218 Enzymatic debridement can be effective, though
papain preparations are no longer available in the US. Biologic
debridement is enjoying something of a resurgence, using
maggots that consume necrotic material while sparing living
tissue. Currently no evidence suggests superiority of one
agent over another.219 Ultimately, though many complemen-
tary methods of debridement are available, they are no sub-
stitute for proper sharp debridement.84
Selection among the many available dressings must be
guided by the characteristics of the wound. Lionelli and
Lawrence219 review the multitude of dressings available. In
the context of pressure sores, occlusive films and hydrocol-
loids are frequently used on more shallow ulcerations while
alginates find use in deeper, heavily exudating wounds (Fig.
16.12). It is worth noting that, even within a classification,
individual products may differ widely in their capacity for
absorption, occlusion, permeability, and cohesion.219 There
exists little evidence to recommend a particular dressing in
this context. When Bradley et al.220 performed a meta-analysis
of the various dressings and topical agents used for pressure
sore treatment, no significant differences were found.
As with dressings, numerous topical agents are used in the
hopes of improving wound healing. Antiseptic solutions are
commonly used in hopes of reducing the bacterial burden of
a wound. However, while mafenide,221 acetic acid,222,223 Dakin’s
solution,224 and iodine preparations225 have broad-spectrum
antibacterial activity, they have all been shown to kill fibro-
blasts and impede wound healing.226 If they are used at all,
they should be reserved for instances of active infection. Silver
sulfadiazine and other silver agents may be less toxic to
fibroblasts.227,228 A review by Reddy et al.203 failed to find any
convincing data to support a particular dressing or topical
agent, which correlates with the results of multiple Cochrane
Fig. 16.12  Suggested guidelines for the use of wound products in the full-
thickness, noninfected, chronic wound. (Reprinted with permission from Ladin DA.
Understanding dressings. Clin Plast Surg. 1998;25:433.)
Hydrogel and
absorbent foam
Alginate and
absorbent foam
Hydrocoloid
Wound color
Yellow
(slough)
Red
(granulation)
Black
(eschar)
Moderate
Large
Small
Exudate
quantity
Hydrocoloid
Hydrogel and
transparent film

366
SECTION II
CHAPTER 16 • Pressure sores
wound base should be palpated to identify any residual areas
of woody, scarred tissues, which require excision.
Once the soft tissue has been debrided, the underlying
bone must be evaluated and, if necessary, debrided. There
should be a very low threshold to debride back to healthy,
hard, bleeding bone using an osteotome or rongeurs. A bone
biopsy can also be taken at this time if desired.
Debridement should never be compromised to facilitate
wound closure, as incomplete debridement is a common cause
of flap failure. The affected tissue must be debrided radically
and flap coverage designed as appropriate to fill the resulting
defect, even if this may require larger, or even multiple, flaps
for complete obliteration of dead space and wound closure.
Procedure selection
Once the wound has been adequately debrided, a reconstruc-
tion method must be selected. Options for surgical coverage
of pressure sores include random skin flap, myoplasty plus
skin graft, pedicled muscle, myocutaneous, fascial, or fascio-
cutaneous flap, free flaps, and tissue expansion. The choice of
flap depends on many factors, including location of the ulcer,
the patient’s level of spinal injury, history of prior ulceration
and surgery, ambulatory status and potential, daily habits,
educational status, motivational level, and associated medical
problems.
Muscle flaps
The indications for using muscle in pressure sore surgery
remain poorly defined. As previously noted, muscle is more
susceptible to ischemic necrosis than either skin or subcutane-
ous tissue,40 at times resulting in necrotic muscle under intact
overlying skin.241 On the other hand, interposing muscle
between skin and bone resulted in a decreased rate of skin
ulceration in a rat model,43 presumably because the increased
mass of muscle can help diffuse the effects of pressure on the
skin.
Compared with skin grafts and flaps, muscle flaps have
the advantages of greater bulk for filling the wound cavity
and obliterating dead space,240 the ability to cover larger
wounds, and a better local vascular supply.242,243 Despite their
but is unclear whether this is due to inadequate data or a
reflection of the altered physiology associated with pressure
sores, which at times may render them resilient to closure by
secondary intention.
Manipulating the local wound milieu
Several studies propose the use of biologic and recombinant
agents as possible modalities for the nonsurgical treatment of
pressure sores. Robson et al. performed a double blind ran-
domized control trial in which 50 patients with stage III/IV
pressure sores were treated with recombinant bFGF; notably,
samples from patients treated with recombinant bFGF dem-
onstrated significantly increased fibroblast and capillary for-
mation than other groups.238 Similarly, Rees et al. found that
application of recombinant human platelet-derived growth
factor-BB to pressure sore wounds resulted in increased
healing as compared to placebo. Despite the high cost of
recombinant proteins, Robson et al. suggest that treatment
with recombinant cytokines may actually result in a cost
reduction as compared to surgical treatment.239 While it
remains unlikely that this will become a mainstay therapy,
recombinant agents may become an option of patients unable
to undergo surgery or as a temporizing treatment until medi-
cally optimized for surgical treatment.
Surgical treatment
Surgical guidelines
The basic tenets of surgical treatment of pressure sores remain
essentially unchanged since they were enumerated in Conway
and Griffith’s report240 over half a century ago:
• Excision of the ulcer, surrounding scar, underlying bursa,
and soft-tissue calcifications, if any
• Radical removal of underlying bone and any heterotopic
ossification
• Padding of bone stumps and filling dead space
• Resurfacing with large regional pedicled flaps
• Grafting the donor site of the flap, if necessary.
The authors also stressed two points of flap design that are
still applicable today. First, the flap should be designed as
large as possible, placing the suture line away from the area
of direct pressure. Second, the flap design should not violate
adjacent flap territories so as to preserve all options for cover-
age in the event that breakdown or recurrence dictates further
reconstruction.
Debridement
Complete debridement is the crucial first step in the operative
treatment of these lesions. Chronic pressure sores will gener-
ally have a relatively well-defined bursa in continuity with
the base of the ulcer. Application of methylene blue can make
dissecting around the margins of the bursa easier. The bursa
and any surrounding scarred tissue, calcifications, or hetero-
topic ossification should be excised completely, leaving only
healthy, pliable tissues (Fig. 16.13). The bursa commonly
extends much farther than the surface wound would indicate.
Taking a small skin margin around the wound and following
the contours of the bursa as it undermines adjacent tissues
ensures it is entirely excised. After the initial excision the
Fig. 16.13  Depiction of excision of bursa and chronic scar tissue.

367
Treatment
cutaneous branches of the deep femoral vessels. A second
successful reconstruction involved an ischial pressure sore
covered with a free medial plantar fasciocutaneous flap based
on the posterior tibial vessels.
Sekiguchi et al.256 confirm the value of free sensory plantar
flaps in the treatment of paraplegic patients who have ischial
ulcers. They reason that “while the ischial region is being
subject to enormous pressure, the plantar region with its more
resilient skin pad is no longer functioning as a weight-bearing
area. Thus [transferring] a plantar flap on to the ischial region
[…] offers a long-term solution to the problem of chronic
pressure sores”.
Tissue expansion
Expanders are tolerated very well in SCI patients. According
to Esposito et al.257 the main advantage of tissue expansion
is the advancement of sensitive skin that can be used for
pressure awareness and future ulcer prevention. Tissue
expansion is also useful in the event of an unstable wound
secondary to previous skin graft or secondary healing. Mul-
tiple reports by Braddom and Leadbetter,258 Yuan,259 Esposito
et al.,257 Neves et al.,260 and Kostakoglu et al.261 attest to the
success of tissue expansion in the treatment of recalcitrant
ulcers in paraplegics.
Kostakoglu et al.261 also described pre-expansion of tensor
fasciae latae and lumbosacral fasciocutaneous flaps in 6
patients. The authors felt expansion allowed the closure of
large wounds while still allowing for primary closure of the
donor site, while speculating that “additional benefits may
include a reduction in the mechanical shear potential for these
flaps and an improvement in their vascularity”.
Critics question the wisdom of placing a foreign body (the
expander) into a contaminated wound (all pressure sores). At
this time, the primary indication for skin expansion is to cover
shallow ulcers with no dead space to fill, particularly if sensate
skin can be used to resurface a previously insensate area.
Single- versus multiple-stage reconstruction
Several reports in the literature describe single-stage surgical
management of pressure sores.262,263 Most of these reports
involved few patients, however, until a retrospective analysis
of 120 patients operated on during a 10-year period was
published in 1999.264 Although there was a large discrepancy
between the number of patients treated in a single stage
versus the number treated in multiple stages (120 versus 10),
the hospital stay was decreased by an average of 10 weeks in
the single-stage group – 9.5 weeks versus 19 weeks. This led
to a considerable cost savings per admission. The authors list
the disadvantages of single-stage surgical management as
longer operative time and higher intraoperative blood loss.
The advantages of single-stage pressure sore management
include fewer anesthetic episodes, shorter hospital stays,
earlier rehabilitation, and lower costs. The authors reserve
multistage procedures for patients who have concurrent pres-
sure sores on the anterior and posterior trunk that are difficult
to address simultaneously.
Reconstruction by anatomic site
Many of the published descriptions of musculocutaneous
flaps offer considerable flexibility in flap design to allow
subsequent re-rotation of the cutaneous component. In most
theoretic advantages, whether the improved vascularity of
muscle flaps results in clinically significant effects on infection
and wound healing when compared to other options has not
been determined.244
Anthony and associates245 reviewed their experience with
pressure sore therapy in 60 consecutive patients treated
between 1979 and 1990, during which time their practice
transitioned toward an increased use of muscle and musculo-
cutaneous flaps. During this interval the number of operations
per ulcer declined from 1.9 to 1.1 and the time to complete
healing dropped from 12.8 to 4.8 weeks. Though they recog-
nize that advances in supportive care certainly have played a
role, the authors conclude that widespread use of muscle
flaps, which allow debridement and wound closure at a single
operation, is the single most important factor contributing to
the improved outcome.
Musculocutaneous flaps
Bruck et al.246 raised random skin flaps and latissimus dorsi
musculocutaneous flaps in pigs, which were then transferred
for coverage of iatrogenically created pelvic pressure sores.
The wounds were subsequently inoculated with Staphylococ-
cus aureus and Escherichia coli, and the flaps evaluated for their
resistance to infection-induced necrosis. Only the skin flaps
showed necrosis, leading the authors to conclude that the
muscle acts as a barrier for vertical spread of infection and
strongly recommend their use in patients with a history of
osteomyelitis.
Perforator flaps
In a break from previous literature to that point, Kroll and
Rosenfield247 challenged the assumption that muscle is neces-
sary when reconstructing pressure sores. In 1988 they reported
favorable results using fasciocutaneous flaps based on
parasacral perforators to cover midline and sacral wounds.
Koshima et al.248 developed the superior gluteal artery perfo-
rator flap, which they used to cover trochanteric and ischial
pressure sores with good results.
Advocates of perforator flap techniques argue that such
flaps not only preserve muscle but also conserve future recon-
structive options and adhere to the basic tenet of placing
suture lines away from areas of direct pressure. Higgins
et al.249 state that, until further studies are performed, “muscle
sparing should always be a goal in the ambulatory and sensate
patient, as it may prevent some functional loss and potentially
reduce postoperative pain”.
Free flaps
Though not a common option, several authors have described
free tissue transfer in the reconstruction of pressure sores,
with and without preservation of sensation. Nahai et al.250,251
and Hill et al.,252,253 among others, have described transferring
the tensor fasciae latae muscle–skin unit as a free flap for
lower trunk reconstruction. Sensation is maintained by
including the lateral femoral cutaneous nerve in the neuro-
vascular pedicle.
Chen et al.254 reported coverage of multiple extensive pres-
sure sores with a single filleted lower leg musculocutaneous
free flap, with satisfactory results. Yamamoto et al.255 report
successful coverage of a sacral pressure sore with a free lateral
thigh fasciocutaneous flap based on the first and third direct

368
SECTION II
CHAPTER 16 • Pressure sores
thinner patients, it can be unreliable in obese patients with
abundant presacral subcutaneous tissue. Additional modifi-
cations include the expansive gluteus maximus flap described
by Ramirez and colleagues,281 which is advanced in a V–Y
fashion either unilaterally or bilaterally to cover sacral ulcers.
Multiple authors have reported their success with gluteal
artery perforator flaps, and variations abound.290–292 Wong
et al.293 modified the classic gluteal rotation flap to spare the
perforators down to the level of the piriformis. Xu et al.294
designed a multi-island perforator propeller flap for use in
large sacral defects. Cheong et al.295 described an innervated
variant of the superior gluteal artery perforator flap for sacral
coverage.
Moving superiorly, both Hill et al.273 and Vyas et al.284
described random flaps from the thoracolumbar area to close
sacral wounds. Hill et al.273 described the transverse lumbosa-
cral back flap, which is based on the contralateral lumbar
perforators. The donor site is most commonly skin grafted.
Vyas et al.284 described the thoracolumbar sacral flap, which is
a very large rotational flap based on thoracolumbar perfora-
tors, which may or may not require back grafting.
Kroll and Rosenfield247 and Koshima et al.248 described
perforator-based flaps from the parasacral area for coverage
of low posterior midline defects. Kato et al.277 took this concept
a step further in their anatomic study on the lumbar artery
perforator-based island flap, identifying the second lumbar
Table 16.2  Reconstructive options in sacral pressure sores
Primary closure
White and Hamm, Ann Surg 124: 1136, 1946
Gluteal fasciocutaneous rotation-advancement flap with V-Y closure
Borman and Maral, Plast Reconstr Surg 109: 23, 2002
Reverse dermal graft
Wesser and Kahn, Plast Reconstr Surg 40: 252, 1967
Bilateral gluteus advancement flap
Parry and Mathes, Ann Plast Surg 8: 443, 1982
Interiorly based random skin flap
Conway and Griffith, Am J Surg 91: 946, 1956
Gluteus plication closure
Buchanan and Agris, Plast Reconstr Surg 72: 49, 1983
Tranverse lumbosacral arterial and random flap
Hill, Brown, and Jurkiewicz, Plast Reconstr Surg 62: 177, 1978
Sensory island flaps
Snyder and Edgerton, Plast Reconstr Surg 36: 518, 1965
Dibbell, Plast Reconstr Surg 54: 220, 1974
Daniel, Terzis, and Cunningham, Plast Reconstr Surg 58: 317, 1976
Little, Fontana, and McColluch, Plast Reconstr Surg 68: 175, 1981
Thoracocolumbar-sacral arterial/random flap
Vyas, Binns, and Wilson, Plast Reconstr Surg 65:159, 1980
Gluteal thigh arterialized flap
Hurwitz, Swartz, and Mathes, Plast Reconstr Surg 68: 521, 1981
Superior gluteus myoplasty
Ger, Surgery 69:106, 1971
Ger and Levine, Plast Reconstr Surg 58: 419, 1976
Expansive gluteus maximus flap
Ramirez, Hurwitz, and Futrell, Plast Reconstr Surg 74: 757, 1984
Turnover gluteus myopathy
Stallings, Delgado, and Converse, Plast Reconstr Surg 54: 52, 1974
Parasacral perforator-based musculocutaneous flap
Kroll and Rosenfield, Plast Reconstr Surg 81: 561, 1988
Koshima et al., Plast Reconstr Surg 91: 678, 1993
Gluteus maximus musculocutaneous flap
Minami, Mills, and Pardoe, Plast Reconstr Surg 60: 242, 1977
Parasacral peforator-based fasciocutaneous flap
Kato et al., Br J Plast Surg 52: 541, 1999
Gluteus maximus musculocutaneous island flap
Maruyama et al., Br J Plast Surg 33: 150, 1980
Stevenson et al., Plast Reconstr Surg 79: 761, 1987
Dimberger, Plast Reconstr Surg 81: 567, 1988
Parasacral peforator-based fasciocutaneous flap
Kato et al., Br J Plast Surg 52: 541, 1999
Gluteus maximus fasciocutaneous flap
Yamamoto et al., Ann Plast Surg 30: 116, 1993
(Reproduced from Janis JE, Kenkel JM. Pressure sores. In: Barton FE Jr., ed. Selected Readings in Plastic Surgery, vol. 9, no. 39. Dallas, TX: Selected Readings in
Plastic Surgery; 2003:25.)
cases this involves expanding and reshaping the skin margins
towards a more rotational flap design and away from the
limitations imposed by transposition and island flaps.
A number of techniques are available for closure of sacral
pressure sores, including wide undermining and primary
closure, random skin flaps, gluteus myoplasty, advancement
flaps, pedicle island flaps, fasciocutaneous flaps, musculocu-
taneous flaps, and free flaps240,247,248,265–288 (Table 16.2). Though
dozens of variations have been described, musculocutaneous
rotation and advancement flaps based on the gluteus maximus
remain a proven option in this area.
Parry and Mathes280 reported favorable results after sacral
coverage of pressure sores with bilateral gluteus maximus
musculocutaneous advancement flaps in ambulatory patients.
Foster et al.289 had high success rates with V–Y gluteus
maximus flaps (36/37 or 97%) as well as with gluteal island
flaps (20/22 or 91%). When the patient is ambulatory, the
authors recommend closure by means of bilateral V–Y gluteus
maximus advancement flaps based on the superior half of the
gluteus muscle to preserve muscular function.
Borman and Maral265 describe a modification of the gluteal
rotation flap, incorporating a V–Y closure, allowing closure of
defects up to 12 cm with a unilateral flap. The suggested
advantages include a smaller incision compared to a class V–Y
advancement and the ability to convert to a musculocutane-
ous V–Y advancement if necessary. Though quite hardy in

369
Treatment
peripherally than the skin. This both accounts for some degree
of muscle retraction and provides extra soft tissue to obliterate
dead space and additional fascia for added security and ease
of wound closure. The flap should then be undermined in the
plane beneath the gluteus maximus. The pedicle can usually
be identified at this time with relative ease as it passes superior
to the piriformis. It may be easier to proceed from lateral to
medial, as scarring and inflammation near the ulcer can
impede dissection, and the separation between the hip muscles
becomes more distinct as they approach their insertion on the
trochanter.
If additional length is needed or tension is excessive, the
flap can be partially delaminated at either the fascial or sub-
cutaneous level, so long as the major perforators are identified
and protected. The flap is then closed in multiple layers over
drains using long-lasting absorbable sutures in the muscle
and superficial fascial system and either staples or nonabsorb-
able sutures in the skin.
Drains remain in place until output is less than 20–30 cc/
day, though some may opt to use drains for an extended
period.
Ischial ulcers
Multiple techniques have been described to cover these
defects, including inferior gluteal rotation flaps, island flaps,
posterior V–Y advancement flaps, gluteal thigh flaps, perfora-
tor flaps, and free flaps274,281,289,300–311 (Table 16.3).
One of the most common options in ischial pressure sore
coverage is the posterior V–Y advancement flap. This flap can
be based on the biceps femoris muscle in ambulatory patients
or on the hamstring muscle in SCI patients. This flap is able
to fill the dead space with viable muscle and can be read-
vanced quite easily in the case of recurrence.
Some authors, however, prefer fasciocutaneous flaps over
musculocutaneous flaps in this region.312–314 Homma et al.312
reported using a posteromedial thigh fasciocutaneous flap
based on the perforators from either the gracilis or the adduc-
tor magnus muscles in the treatment of ischial pressure sores.
In 11 patients with variable follow-up, they noted two flaps
with distal necrosis.
The posterior thigh skin can be transferred based on per-
forating vessels from a cutaneous branch of the inferior gluteal
artery that accompanies the posterior femoral cutaneous
nerve between the semitendinosus and biceps femoris
muscles.247,302,309 The flap can be used repeatedly in the event
of recurrences. When the descending branch of the inferior
gluteal artery is absent – a common vascular anomaly in this
region274 – the flap can be elevated as a superiorly based
random fasciocutaneous unit supplied by multiple perfora-
tors from the cruciate anastomosis of the fascial plexus.315
In addition to the gluteal rotation flap, the superior and
inferior gluteal arteries provide multiple options for recon-
struction for ischial ulcers. The pedicle of the superior gluteal
artery perforator flap is suboptimal for reaching the ischial
region and is more useful in the coverage of sacral and tro-
chanteric ulcers. The inferior gluteal artery perforator flap, on
the other hand, is well suited to ischial reconstruction, with
multiple authors reporting results comparable to existing
methods.249,316,317 It has the advantage of sparing muscle for
future use, is associated with minimal morbidity, and has a
donor site that can often be closed directly.311
perforator as the preferred vessel. Advantages of this flap
include sparing of the muscle, a large arc of rotation, and a
donor site that can be closed primarily.
Unless the skin flaps have been reinnervated at a prelimi-
nary operation or are harvested from a site that has intact
sensation,296 the reconstructed sites will not be sensible. The
advantage of using sensory flaps for pressure sore coverage
in patients with distal SCI is the hope that sensation will
prompt behavior modifications by the patient to avoid pres-
sure on ulcer-prone areas and prevent recurrent ulceration.
Dibbell269 and Daniel et al.267 describe intercostal island flaps
to bring sensation to the sacral area. Other reports by Coleman
and Jurkiewicz297 and Mackinnon et al.298 discuss various
techniques for reinnervation of the intercostal flap and the
tensor fasciae latae flap, including nerve grafts to the intercos-
tal muscles and to the territory of the lateral femoral cutaneous
nerve.
Prado et al.299 also described innervation-sparing bilateral
perforator fasciocutaneous and myocutaneous V–Y flaps for
the closure of large sacral wounds. Though they demonstrated
no recurrence at 1.5 years and sensation was preserved with
this technique, it has the drawbacks of placing scars over the
ischium as well as preventing further readvancement of the
gluteal muscles.
DeWeerd and Weum268 modified Kato’s lumbar perforator
island flap design to include two lumbar artery perforators as
well as the intermediate nerve to preserve protective sensa-
tion. The flap is drawn as a butterfly design. At 8 weeks post-
operatively, good protective sensation was documented over
most of the flap by Semmes–Weinstein monofilament testing.
Selected technique: myocutaneous gluteal rotation
flap (Fig. 16.14 and Box 16.2)
One of many options based on the gluteus maximus muscle,
the myocutaneous gluteal rotation flap is technically straight-
forward, keeps scars off pressure-bearing surfaces, and is
easily revised or re-rotated. The muscle is useful for obliterat-
ing the dead space, which is often significant after the prepa-
ratory bursectomy and ostectomy.
The vascular supply is based on the superior gluteal artery
perforator. This vessel can easily be identified in the plane
beneath the gluteus maximus immediately superior to the
piriformis muscle.
Skin incision is marked to follow the contour of the iliac
crest and descends inferiorly, staying posterior to the greater
trochanter and the footprint of the tensor fasciae latae flaps.
Dissection is carried down through the thick subcutaneous
tissues of the hip to the level of the muscle fascia.
The fascia and muscle are then divided. It can be helpful
to bevel the incision so the muscle and fascia are divided more
BOX 16.2  Myocutaneous gluteal rotation flap
As always, complete debridement is the key to any flap surgery.
This flap can survive entirely on its major vascular pedicle. The
muscle can be disinserted and the skin and fascia divided
circumferentially without compromising the vascularity of the flap.
Creating an island design without tension is preferable to leaving a
skin bridge, which results in tension.

370
SECTION II
CHAPTER 16 • Pressure sores
A
B
C
D
Fig. 16.14  (A–F) Right gluteal musculocutaneous flap.
E
F

371
Treatment
and tensor fasciae latae flap had the poorest healing rates, 58%
(7/12) and 50% (6/12), respectively. When Ahluwalia et al.331
reviewed their series of 72 ischial wounds, the authors found
an overall complication rate of 16% and a recurrence rate of
7%. After reviewing their results the authors felt their best
results were obtained with medial thigh and biceps femoris
flaps.
Selected flap: V–Y hamstring advancement (Fig. 16.15)
Flaps from the posterior thigh are common options for ischial
reconstruction. They have the advantage of leaving the lateral
hip and buttock for use in trochanteric and sacral reconstruc-
tion. The V–Y hamstring advancement is a robust flap that is
relatively easy to raise and can be readvanced if necessary.
The vascular supply to the hamstring flap is based on
perforators of the profunda femoris, with minor contributions
from the inferior gluteal, medial circumflex, and superior
geniculate arteries. These vessels are generally not specifically
identified when elevating the flap, as they are well protected
on the deep surface of the muscle.
Superiorly the flap is bounded by the gluteal crease or the
inferior border of the ulcer. Laterally the flap extends to
the posterior border of the tensor fasciae latae, while medially
the dissection extends to the adductor magnus. Inferiorly the
flap can be extended to the popliteal fossa, though a lesser
flap can be designed as needed.
The flap is incised and dissection carried down the level of
the fascia. The muscles are divided distally at the musculo-
tendinous junction and proximally by elevating the muscles
from the ischium, though this step is often partially
Table 16.3  Reconstructive options in ischial pressure sores
Primary closure
Arregui et al., Plast Reconstr Surg 36: 583, 1965
Biceps femoris musculocutaneous flap
Tobias et al., Ann Plast Surg 6: 396, 1981
Kauer and Sonsino, Scand J Plast Reconstr Surg 20: 129, 1986
Random posterior thigh flap ± biceps femoris myoplasty
Campbell and Converse, Plast Reconstr Surg, 14: 442, 1954
Conway and Griffith, Am J Surg 91: 946, 1956
Baker, Barton, and Converse, Br J Plast Surg 31: 26, 1978
Gluteal thigh flap
Hurwitz, Swartz, and Mathes, Plast Reconstr Surg 20: 129, 1986
Inferior gluteus maximus musculoplasty
Ger and Levine, Plast Reconstr Surg 58:419, 1976
Sliding gluteus maximus flap
Ramirez, Hurwitz, and Futrell, Plast Reconstr Surg 74: 757, 1984
Inferior gluteus musculocutaneous flap
Minami, Mills, and Pardoe, Plast Reconstr Surg 60: 242, 1977
Tensor fasciae latae + vastus lateralis
Krupp, Kuhn, and Zaech, Paraplegia 21: 119, 1983
Interior gluteus musculocutaneous island flap
Rajacic et al., Br J Plast Surg 47:431, 1994
Lateral thigh fasciocutaneous flap
Maruyama, Ohnishi, and Takeudhi, Br J Plast Surg 37: 103,
1984
Hallock, Ann Plast Surg 32: 367, 1994
Gracilis musculocutaneous flap
Wingate and Friedland, Plast Reconstr Surg 62:245, 1978
Lesavoy et al., Plast Reconstr Surg, 85: 390, 1990
Anterolateral thigh fasciocutaneous island flap
Yu et al., Plast Reconstr Surg 109: 610, 2002
Gracilis musculocutaneous flap (with sartorius as a double muscle unit)
Apfelberg and Finseth, Br J Plast Surg 34:41, 1981
Rectus abdominis musculocutaneous flap
Bunkis and Fudem, Ann Plast Surg 23: 447, 1989
Mixter, Wood, and Dibbell, Plast Reconstr Surg 85: 437, 1990
Hamstring musculocutaneous flap
Hurteau et al., Plast Reconstr Surg 68: 539, 1981
Inferior gluteal artery perforator flap
Higgins et al., Br J Plast Surg 55:83, 2002
(Reproduced from Janis JE, Kenkel JM. Pressure sores. In: Barton FE Jr., ed. Selected Readings in Plastic Surgery, vol. 9, no. 39. Dallas, TX: Selected Readings in
Plastic Surgery; 2003:27.)
Alternatives for coverage of ischial pressure sores include
gracilis musculocutaneous flaps,318–321 lateral thigh fasciocuta-
neous flaps,315,322 anterolateral thigh fasciocutaneous island
flaps,319,323,324 and rectus abdominis musculocutaneous flaps
transferred through the space of Retzius to the perineum.325–327
However, because the rectus initiates vertebral flexion and
aids in respiration, urination, defecation, and vomiting,
Bunkis and Fudem325 speculate the muscle is more important,
and thus less expendable, in paraplegics than in neuromus-
cularly intact patients.
Nahai et al.250,253,328 introduced the sensate tensor fasciae
latae flap for coverage of ischial and trochanteric pressure
sores. The flap provides protective sensation in paraplegic
patients to help avert recurrence of pressure sores, sharpens
sensation of rectal filling, and enhances sitting control in a
wheelchair. Dibbell et al.329 as well as Luscher et al.330 report
successful experiences with the extended sensory tensor
fasciae latae flap, which is innervated by the lateral femoral
cutaneous nerve, for pressure sores in patients with meningo-
myelocele and paraplegia, respectively. At follow-up of 1–10
years no new or recurrent sores were noted in Luscher’s
series.
Foster et al.289 reviewed their experience with ischial pres-
sure sore coverage from 1979 to 1995. During this time, 114
consecutive patients with 139 ischial pressures sores were
treated. Analysis of these cases showed significant differences
in healing rates and complications according to the flaps used.
The inferior gluteus maximus island flap and the inferior
gluteal thigh flap had the highest success rate, 94% (32/34)
and 93% (25/27), respectively, while the V–Y hamstring flap

372
SECTION II
CHAPTER 16 • Pressure sores
A
B
C
D
Fig. 16.15  (A–E) Right posterior hamstring musculocutaneous V–Y advancement
flap.
E

373
Treatment
adductor perforator flap also has the advantage of being
medially based and often outside the field of previous
operations.
Foster et al.289 noted a success rate of 93% (68/73) when
covering trochanteric ulcers. Their most frequently used flap
was the tensor fasciae latae flap, particularly in the V–Y
design. Complications occurred in 15%, the most common
being wound dehiscence.
If more radical treatment of the trochanter is required, e.g.,
a Girdlestone procedure, then the vastus lateralis becomes the
flap of choice, either as a muscle or musculocutaneous
flap350–352 (Fig. 16.16).
Selected procedure: V–Y tensor fasciae latae flap (Fig. 16.17);
tensor fasciae latae rotation flap
The many variations on the tensor fasciae latae flap are
common options for dealing with trochanteric ulcers. A fas-
ciocutaneous or musculocutaneous rotation flap is technically
straightforward, can reach a variety of defects, and may be
readvanced if necessary.
The blood supply to the tensor fasciae latae is from branches
of the lateral circumflex femoral artery, which enter the deep
surface of the muscle anteriorly. The proximal, muscular
portion of the tensor fasciae latae is relatively small. The distal
portion of the muscle consists almost entirely of fascia but still
provides perforators to the overlying skin. If necessary, the flap
can be extended just proximal to the knee and rotated to cover
ischial or even sacral defects, though such extended flaps are
not entirely reliable unless delayed. A much more limited
dissection is possible when addressing trochanteric ulcers.
Though the blood supply to this flap is robust and relatively
reliable, minor variations are common. If necessary, the flap
accomplished during bony debridement of the ischium.
Minimal blunt dissection may be performed at the lateral and
medial margins to mobilize the flap, but it is generally not
necessary to perform a complete dissection on the undersur-
face of the muscle or to identify the major pedicle of the flap.
As with the gluteal rotation flap, it is inset in layers over
drains and the donor site is closed in linear fashion.
Trochanteric ulcers
Trochanteric ulcers are generally closed with tensor fasciae
latae250,253,328–330,332–335 or vastus lateralis flaps336–339 (Table 16.4).
The tensor fasciae latae can be transferred as muscle only, as
skin and muscle, with the skin of the anterolateral mid and
lower thigh, as an island flap, or as a free flap. For details
regarding this flap’s anatomy, vascularity, design, and eleva-
tion, the reader is referred to Nahai’s publications on the
subject.250,253,329 Lewis et al.333,340 described a modification of
the standard tensor fasciae latae musculocutaneous flap, the
tensor fasciae latae V–Y retroposition; this appears to be as
durable and versatile as its predecessor.
While the tensor fasciae latae is a workhorse option in this
region, multiple alternative and secondary options exist.
Flaps based on the gluteus maximus341–343 or medius344 can be
used to reconstruct this region. Ramirez341 recounts his experi-
ence with 20 distal gluteus maximus posterior thigh flaps.
A profusion of perforator flaps have found use in trochan-
teric reconstruction as well. The anterolateral thigh flap pro-
vides an option with considerable flexibility, allowing the
option of taking chimeric flaps if necessary.345,346 Flaps based
on the gluteal,347 ascending circumflex,348 or adductor349 per-
forators all share the advantages of minimal donor morbid-
ity and sparing of muscle for further reconstruction. The
Table 16.4  Reconstructive options in trochanteric pressure ulcers
Anteriorly based random thigh flap
Vasconez, Schneider, and Jurkewicz, Curr Probl Surg 14: 1, 1977
Tensor fasciae latae musculocutaneous flap, island
Kauer and Sonsino, Scand J Plast Reconstr Surg 20: 129, 1986
Random bipedicle flap
Conway and Griffith, Am J Surg 91: 946, 1956
Vastus lateralis myoplasty
Minami, Hentz, and Vistnes, Plast Reconstr Surg 60: 364, 1977
Dowden and McCraw, Ann Plast Surg 4: 396, 1980
Tensor fasciae latae musculocutaneous flap
Nahai et al., Ann Plast Surg 1: 372, 1978
Hill, Nahai, and Vasconez, Plast Reconstr Surg 61: 517, 1978
Withers et al., Ann Plast Surg 4: 31, 1980
Vastus lateralis musculocutaneous flap
Bovet et al., Plast Reconstr Surg 69: 830, 1982
Hauben et al., Ann Plast Surg 10: 359, 1983
Drimmer and Krasna, Plast Reconstr Surg 79:560, 1987
Tensor fasciae latae musculocutaneous flap, bipedicle
Schulman, Plast Reconstr Surg 66: 740, 1980
Gluteus medius tensor fasciae latae musculocutaneous flap
Little and Lyons, Plast Reconstr Surg 71: 366, 1983
Tensor fasciae latae musculocutaneous flap, V–Y advancement
Lewis, Cunningham, and Hugo, Ann Plast Surg 6: 34, 1981
Siddiqui, Wiedrich, and Lewis, Ann Plast Surg, 31: 313, 1993
Distally based gluteus maximus flap
Becker, Plast Reconstr Surg 63: 653, 1979
Tensor fasciae latae musculocutaneous flap, innervated
Dibbell, McCraw, and Edstrom, Plast Reconstr Surg, 64: 796, 1979
Nahai, Hill, and Hester, Plast Reconstr Surg 7: 286, 1981
Nahai, Clin Plast Surg 7: 51, 1980
Cochran, Edstrom, and Dibbell, Ann Plast Surg 7: 286, 1981
Gluteal thigh flap
Hurwitz, Swartz, and Mathes, Plast Reconstr Surg 68:521, 1981
Expansive gluteus maximus flap
Ramirez, Hurwitz, and Futrell, Plast Reconstr Surg 74: 757, 1984
Ramirez, Ann Plast Surg 18:295, 1987
(Reproduced from Janis JE, Kenkel JM. Pressure sores. In: Barton FE Jr., ed. Selected Readings in Plastic Surgery, vol. 9, no. 39. Dallas, TX: Selected Readings in
Plastic Surgery; 2003:29.)

374
SECTION II
CHAPTER 16 • Pressure sores
greater trochanters when these areas were exposed, and
subsequently expanded the resection to encompass the entire
ischium. Conway and Griffith240 noted a decrease in recur-
rence from 38% after partial ischiectomy to 3% after total
ischiectomy.
Although total ischiectomy minimizes ipsilateral recur-
rence, secondary problems are frequent. Arregui et al.353 evalu-
ated 94 patients with pressure sores treated by total ischiectomy
over a 10-year period. Despite “good” results in 81%, there
was a 16% complication rate and a 28% occurrence of contra-
lateral ischial ulcer. The authors subsequently recommended
contralateral ischial resection on a prophylactic basis.
After total bilateral ischiectomy, however, weight is trans-
ferred to the pubic rami and perineum as well as the proximal
femur. When sitting, pressure is borne directly by the mem-
branous and proximal bulbous urethra.354 Perineal ulcers,
urethrocutaneous fistulas,355 and perineourethral diverticula30
have been reported in up to 58% of patients after complete
bilateral ischiectomy. Given the high incidence of serious
complications, total ischiectomy should be reserved for deep,
extensive, recurrent ischial pressure sores.
Proximal femoral resection with muscle flap coverage may
be indicated in instances of large and/or recalcitrant trochan-
teric ulcers complicated by osteomyelitis and ulcers involving
the hip joint.351 Patients who undergo proximal femoral resec-
tion may experience a piston effect that prevents the oblitera-
tion of dead space. Klein et al.352 addressed the issue through
the use of an external fixator for 2–3 weeks, and reported all
10 of their patients’ wounds healed, despite a 50% incidence
may be based on alternate branches of the circumflex vessels.
If the perforators to the muscle are not usable, dissection of
the descending branch of the lateral circumflex allows rela-
tively simple conversion to a pedicled anterolateral thigh flap.
The ulcer will generally define the posterior margin of the
flap. A line from the anterior superior iliac spine to the knee
marks the anterior border of the flap. Flaps up to 15–20 cm
proximal to the femoral condyle are very reliable without
delay. The inferior point of the flap can be taken just short of
the condyle if preferred. Though it may be excessive for
single-stage ulcer coverage, a lengthier flap is easier to read-
vance if necessary. The pedicle is generally roughly 10 cm
inferior to the anterior superior iliac spine and 10–15 cm
lateral to the pubic tubercle.
After incising the skin down to fascia, dissection is easiest
distally, where the tensor fasciae latae is essentially entirely
fascia. Dissecting under the fascia, it is generally easy to
identify the pedicle as the tensor fasciae latae transitions to
muscle proximally. The fascia and muscle can then be com-
pletely divided and the flap rotated to fill the defect. As with
the other flaps discussed in this section, the flap is then inset
in layers over drains and the donor site closed in linear fashion.
Bone resection
Kostrubala and Greeley28 first suggested removing the under-
lying bony prominences as an adjunct to the treatment of
patients with pressure sores. The authors initially recom-
mended excision of the posterior sacral promontories and
Fig. 16.16  (A–D) Girdlestone arthroplasty.
Vastus lateralis
Lateral circumflex
femoral artery
B
A
C
D

375
Postoperative care
and Disa et al.363 The measures used to address pressure relief,
shear, friction, moisture, skin care, incontinence, spasticity,
and nutrition should be continued aggressively through the
postoperative period, in addition to standard postoperative
care. Two additional issues that need to be addressed prior to
discharge are length of immobilization and when to restart
sitting protocols and therapy.
Traditionally pressure sore patients were kept in bed for
6–8 weeks based on experimental data indicating that wounds
reached maximum tensile strength after this period.364 More
recent studies have advocated a more rapid progression to
sitting. In a prospective, randomized trial Isik et al.365 found
equivalent complication rates when comparing 2 and 3 weeks
of immobilization, though overall length of stay was similar
and long-term follow-up was deemed inadequate to draw any
firm conclusions. Likewise, Foster et al.289 began a sitting
regimen at 10–14 days and had postoperative hospital stays
averaging 20 days, with short-term success rates of 89%.
Regardless of how long patients are kept in bed, they
should begin active and passive range-of-motion exercises of
the uninvolved extremity early in the postoperative course,193
while the affected extremity can be ranged just prior to initia-
tion of a sitting protocol. A typical regimen involves having
of pin loosening. Rubayi et al.356 prefer to use an abduction
pillow and antispasmodic drugs to control femoral motion. A
total of 24 of 26 wounds healed in the hospital, and all wounds
healed eventually.
Patients with proven osteomyelitis in the bone underlying
their pressure sore should be treated with at least partial
ostectomy. Although in principle osteomyelitis should be
treated by radical excision,215,357 the endpoint of all bony
debridement should be healthy bleeding bone,84 and osteope-
nia in paraplegics may cloud this goal. In these cases, preop-
erative imaging may be helpful in determining the extent of
bony involvement. The identified areas can then be resected
down to bleeding, healthy-appearing bone and cultures taken
from the depths of the wound. Postoperative antibiotic
therapy should be guided by the results of deep bone cultures
and biopsies.358
Postoperative care
The care of patients after pressure sore surgery has been
reviewed by multiple authors, including Vasconez et al.,359
Conway and Griffith,240 Stal et al.,360 Hentz,361 Constantian,362
A
B
Fig. 16.17  (A–D) Left tensor fasciae latae flap with backgrafting.
C
D

376
SECTION II
CHAPTER 16 • Pressure sores
variation in recurrence rates, ranging from as low as
3–6%300,361,371 to as high as 33–100%.301,313,363,372
The most extensive published experiences with pressure
sore treatment are those of Conway and Griffith240 (1000 cases)
and Dansereau and Conway’s16 update of the Bronx Veterans
Administration Hospital data (2000 cases). In their follow-up
article from 1961, Griffith and Schultz373 categorized the thera-
peutic history of the earlier series as follows:
■ Sacral ulcers: Nonsurgical treatment succeeded in 29%,
split-skin grafts in 30%. Excision of bone with the ulcer
and closure by large rotation flap achieved healing in
84%.
■ Trochanteric ulcers: 41% of patients were adequately
treated without surgery; 33% needed split-thickness skin
grafts. When ulcer, bursa, and trochanter were excised
and the wound simply sutured, 83% healed but 20%
recurred. When the trochanter was more thoroughly
removed and the site reconstructed with a rotation flap,
92% healed and only 6% recurred.
■ Ischial ulcers: Conservative therapy was successful in
18% of cases, skin graft in 17%, and partial ischiectomy
with primary suture in 46% (but with 54% recurrence).
Total ischiectomy lessened the number of recurrences to
22%, and when combined with muscle flap and regional
rotation flap, it further decreased the recurrence rate to
3%.
In 1994 Evans et al.374 reviewed their experience with the
surgical treatment of pressure sores in both paraplegic and
nonparaplegic patients. Among paraplegics the recurrence
rate was 82% with an average time to recurrence of 18.2
the patient sit for 15-minute intervals once or twice a day, then
gradually increasing the length and frequency of sitting
periods until discharge.365 Pressure release maneuvers are
performed at least every 15 minutes while the patient is
seated, and the surgical site is carefully monitored for signs
of recurrence.193
Prior to discharge, patients should have their support
surfaces re-evaluated (Fig. 16.18). This assessment is particu-
larly important in patients who have had bony resections or
multiple procedures that may result in altered weight-bearing
or pelvic and truncal instability.366 An appropriate seat cushion
should be selected, ideally with the assistance of seat mapping.
Maximum recommended pressures are 35 mmHg for patients
unable to relieve pressure themselves by lifting or leaning and
60 mmHg for those who can.367
Patient education should also be emphasized postopera-
tively. Though studies have demonstrated a positive effect of
education on patient knowledge,368,369 research relating educa-
tion to recurrence rates is lacking at this time. However, given
the evidence that recurrence rates are associated with poor
patient compliance, social factors, and communication barri-
ers,193,370 attempts at addressing these issues through educa-
tion seem reasonable.
Outcomes, prognosis, and
complications
Long-term outcome studies of patients with pressure sores are
difficult to conduct, and the existing literature reports a wide
Fig. 16.18  Seat mapping. (Reproduced from the University of Washington PM&R website: )

377
Secondary procedures
inadequate.95 The patient should be re-evaluated for risk
factors and optimized, prior to return to the operating room
for complete debridement, followed by flap advancement or
alternative flap for coverage.99,289
Every chronic wound exposed to continuous trauma carries
the risk of malignant degeneration.376 Benign-appearing
ulcerations are a frequent problem in our population and are
usually treated conservatively, yet the suspicion of malignancy
in these lesions must always be entertained, especially if the
margins of the ulcer are verrucous. The term “Marjolin’s
ulcer” is used to describe malignant degeneration in burn
scars, chronic venous ulcers, pressure sores, and sinuses
from osteomyelitis. Malignant transformation is heralded by
increased pain or discharge, foul odor, and bleeding. The
latency period of carcinomas arising from pressure sores is
approximately 20 years, compared with 30 years or more for
carcinomas arising from burn scars and stasis ulcers.377 Biopsy
is indicated in all chronically draining ulcers and tracts,
especially those with recent change in appearance or drain-
age, and should include the central area of the ulcer as well
as the margins. Early recognition and proper staging offer the
best chance for cure.378
Secondary procedures
It is critical that, before embarking on revision or repeat flap
surgery, the patient be fully re-evaluated. Assuming proper
surgical technique, the same risk factors that led to the
patient’s original ulcer are likely to be at least partially respon-
sible for recurrence, and neglecting them will reliably result
in poor outcomes.
Every pressure sore surgery should allow for the possibil-
ity of future secondary procedures. Despite favorable initial
healing rates, long-term recurrence is common, even in the
most favorable series. Assuming basic principles have been
adhered to, multiple options should still exist, even in cases
of multiple recurrences.
The simplest option may involve readvancing a previously
performed flap (Fig. 16.19). Flaps can often be readvanced
multiple times, but, as always, excessive tension must be
avoided. If tension is an issue, a change of plane, such as
advancing a fasciocutaneous flap over a previous musculocu-
taneous flap, can provide additional length without violating
another anatomic region or flap design. If a particular flap has
already been readvanced or the tissue is of poor quality due
to recurrent ulceration or scarring, a new, preferably virgin,
anatomic area should be used to address the wound. For
example, while flaps from the thigh area are commonly used
to address ischial ulcers, a superiorly based gluteal flap can
afford coverage if the posterior thigh is no longer a viable
option.
Amputation or salvage flaps should be reserved for recal-
citrant pressure sores where the ulcer is extensive to the point
of precluding closure with standard flaps, or for patients who
are severely ill because of uncontrollable infection, as these
flaps are associated with high morbidity.379–381 Likewise,
hemicorporectomy is a highly morbid382 last-resort measure
reserved for potentially life-threatening and incurable condi-
tions, as in patients with multiple, large, confluent ulcers in
the setting of malignancy or extensive pelvic osteomyelitis383,384
(Fig. 16.20).
months. In contrast, the nonparaplegic group had no recur-
rence of ulceration.
Relander and Palmer372 reviewed their experience with 66
flaps for primary coverage of pressure sores and noted a 43%
recurrence rate with cutaneous flaps and a 33% recurrence
rate with musculocutaneous flaps at 2–12-year follow-up, a
nonsignificant difference.
Disa et al.363 evaluated 40 consecutive patients with 66 pres-
sure sores and, despite a cure rate of 80%, noted a 69% recur-
rent rate within 1 year. Two subgroups with higher recurrence
rates were identified. The young, post-traumatic paraplegic
subgroup demonstrated a recurrence rate of 79% at a mean of
10.9 months. The cerebrally compromised elderly subgroup
had a 69% recurrence rate at a mean of 7.7 months. The
authors conclude that surgical treatment of pressure sores
among patients in these subgroups may not be warranted
given the high recurrence rates, which they felt resulted from
poor patient compliance. The ultimate causes of noncompli-
ance were individual personalities, an unsteady social situa-
tion, and inadequate family network.
Tavakoli et al.370 studied 27 patients with 37 ulcers who
underwent musculocutaneous flap coverage of their ischial
pressure sores with a mean follow-up of 62 months. Overall
ulcer recurrence was 41.4% and overall patient recurrence rate
was 47.8%. The recurrences were attributed by the authors to
psychological and behavioral factors, such as lifestyle activi-
ties that led to neglect of skin care, drug and alcohol abuse,
cultural barriers, and neglect of appropriate seating practices.
Kierney et al.193 reported a lower recurrence rate in 268
pressure sores treated over a 12-year period. Mean postopera-
tive follow-up was 3.7 years, and overall recurrence rate was
19%. Unlike Evans et al.,374 Kierney et al. did not find an
association between pre-existing pressure sore risk factors
and recurrence. Instead, the authors emphasize the impor-
tance of collaboration between plastic surgeons and physical
medicine rehabilitation physicians as a major determinant of
outcome.
In 2002 Singh et al.375 published one of the few studies
examining the outcome of surgical reconstruction of pressure
sores in children. The records of 19 patients in 25 pressure
sores with an average follow-up of 5.3 years were reviewed.
Site-specific and patient recurrence were 5% and 20%, respec-
tively, considerably lower than generally reported in adults
with similar follow-up.
Clearly, variable patient populations, risk factors, and
follow-up periods make comparisons difficult. With such a
wide range of outcomes, assigning a single value for recur-
rence is virtually impossible. Some question the wisdom of
surgical intervention if the higher range of recurrence rates is
legitimate.374 It may be that select subpopulations are not good
surgical candidates given their poor prognosis. However, a
thorough evaluation of a patient’s risk factors and a multidis-
ciplinary approach to treatment should be routine even for
patients who initially seem like poor candidates.193
Complications
Common postoperative complications of pressure sore
surgery include hematoma, seroma, infection, and wound
dehiscence. A breakdown in the suture line should heal with
local wound care within a week. If slough persists, then
the wound debridement, particularly of bone, was likely

378
SECTION II
CHAPTER 16 • Pressure sores
A
B
C
D
Fig. 16.19  (A–E) Readvanced right gluteal flap for recurrent sacral pressure sore.
E

379
Secondary procedures
A
B
C
D
Fig. 16.20  (A–E) Hemicorporectomy with right subtotal thigh flap.
E

380
SECTION II
CHAPTER 16 • Pressure sores
4. Cuddigan J, Frantz RA. Pressure ulcer research: pressure ulcer
treatment. A monograph from the National Pressure Ulcer
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21. Waters TM, Daniels MJ, Bazzoli GJ, et al. Effect of Medicare’s
nonpayment for hospital-acquired conditions: lessons for future
policy. JAMA Intern Med. 2015;175:347–354.This article examines the
effect of Medicare’s non-payment policy for Hospital-Acquired
Conditions on the rate of never events, including hospital acquired
pressure sores. Overall, since implementation of this policy in 2008, there
has been no improvement in the rate of hospital acquired pressure sores,
highlighting the continued challenge pressure sores place on our
healthcare system and the need for further advancement in the prevention
and treatment of pressure sores.
32. Cushing CA, Phillips LG. Evidence-based medicine: pressure
sores. Plast Reconstr Surg. 2013;132:1720–1732. This article provides
an evidence-based update regarding the pathophysiology, risk factors, as
well as non-surgical and surgical treatments for all types of pressure
sores.
36. Fronek K, Zweifach BW. Microvascular pressure distribution in
skeletal muscle and the effect of vasodilation. Am J Physiol.
1975;228:791–796.
39. Dinsdale SM. Decubitus ulcers: role of pressure and friction in
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63. Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a
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comprehensive review of randomized controlled trials examining
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evidence for the use of support surfaces, repositioning, nutritional
optimization, and moisturizing sacral surfaces.
87. Han H, Lewis VL Jr, Wiedrich TA, Patel PK. The value of Jamshidi
core needle bone biopsy in predicting postoperative osteomyelitis
in grade IV pressure ulcer patients. Plast Reconstr Surg.
2002;110:118–122.
132. Wound, Ostomy and Continence Nurses Society. WOCN Policy and
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WOCN policy and procedure manual remains the authority in accurate
diagnosis and standard of care treatment for pressure sores.
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293. Wong CH, Tan BK, Song C. The perforator-sparing buttock
rotation flap for coverage of pressure sores. Plast Reconstr Surg.
2007;119:1259–1266.
294. Xu Y, Hai H, Liang Z, et al. Pedicled fasciocutaneous flap of
multi-island design for large sacral defects. Clin Orthop Relat Res.
2009;467:2135–2141.
295. Cheong EC, Wong MT, Ong WC, et al. Sensory innervated
superior gluteal artery perforator flap for reconstruction of sacral
wound defect. Plast Reconstr Surg. 2005;115:958–959.
296. Krupp S, Kuhn W, Zaech GA. The use of innervated flaps for the
closure of ischial pressure sores. Paraplegia. 1983;21:119–126.
297. Coleman JJ 3rd, Jurkiewicz MJ. Methods of providing sensation to
anesthetic areas. Ann Plast Surg. 1984;12:177–186.
298. Mackinnon SE, Dellon AL, Patterson GA, Gruss JS. Medial
antebrachial cutaneous-lateral femoral cutaneous neurotization to
provide sensation to pressure-bearing areas in the paraplegic
patient. Ann Plast Surg. 1985;14:541–544.
299. Prado A, Ocampo C, Danilla S, et al. A new technique of
“double-A” bilateral flaps based on perforators for the treatment
of sacral defects. Plast Reconstr Surg. 2007;119:1481–1490.
300. Ger R, Levine SA. The management of decubitus ulcers by muscle
transposition. An 8-year review. Plast Reconstr Surg.
1976;58:419–428.
301. Minami RT, Mills R, Pardoe R. Gluteus maximus myocutaneous
flaps for repair of pressure sores. Plast Reconstr Surg. 1977;60:
242–249.
302. Campbell RM, Converse JM. The saddle-flap for surgical repair of
ischial decubitus ulcers. Plast Reconstr Surg (1946). 1954;14:442–443.
303. Rajacic N, Gang RK, Dashti H, Behbehani A. Treatment of ischial
pressure sores with an inferior gluteus maximus
musculocutaneous island flap: an analysis of 31 flaps. Br J Plast
Surg. 1994;47:431–434.
304. Baker DC, Barton FE Jr, Converse JM. A combined biceps and
semitendinosus muscle flap in the repair of ischial sores. Br J Plast
Surg. 1978;31:26–28.
305. Hurteau JE, Bostwick J, Nahai F, et al. V-Y advancement of
hamstring musculocutaneous flap for coverage of ischial pressure
sores. Plast Reconstr Surg. 1981;68:539–542.
306. Tobin GR, Sanders BP, Man D, Weiner LJ. The biceps femoris
myocutaneous advancement flap: a useful modification for
ischial pressure ulcer reconstruction. Ann Plast Surg. 1981;6:
396–401.
307. Kauer C, Sonsino G. The need for skin and muscle saving
techniques in the repair of decubitus ulcers. A consecutive series of
72 patients and 100 ulcers over 5 years (1979/1984). A case report.
Scand J Plast Reconstr Surg. 1986;20:129–131.
308. Kroll SS, Hamilton S. Multiple and repetitive uses of the extended
hamstring V-Y myocutaneous flap. Plast Reconstr Surg.
1989;84:296–302.
309. Paletta C, Bartell T, Shehadi S. Applications of the posterior thigh
flap. Ann Plast Surg. 1993;30:41–47.
310. Yu P, Sanger JR, Matloub HS, et al. Anterolateral thigh
fasciocutaneous island flaps in perineoscrotal reconstruction. Plast
Reconstr Surg. 2002;109:610–616, discussion 617–618.
311. Windhofer C, Brenner E, Moriggl B, Papp C. Relationship between
the descending branch of the inferior gluteal artery and the
posterior femoral cutaneous nerve applicable to flap surgery. Surg
Radiol Anat. 2002;24:253–257.
312. Homma K, Murakami G, Fujioka H, et al. Treatment of ischial
pressure ulcers with a posteromedial thigh fasciocutaneous flap.
Plast Reconstr Surg. 2001;108:1990–1996, discussion 1997.
313. Yamamoto Y, Tsutsumida A, Murazumi M, Sugihara T. Long-term
outcome of pressure sores treated with flap coverage. Plast
Reconstr Surg. 1997;100:1212–1217.
314. Wang TN, Whetzel T, Mathes SJ, Vasconez LO. A fasciocutaneous
flap for vaginal and perineal reconstruction. Plast Reconstr Surg.
1987;80:95–103.
315. Hallock GG. The random upper posterior thigh fasciocutaneous
flap. Ann Plast Surg. 1994;32:367–371.
316. Kim YS, Lew DH, Roh TS, et al. Inferior gluteal artery perforator
flap: a viable alternative for ischial pressure sores. J Plast Reconstr
Aesthet Surg. 2009;62:1347–1354.
317. Scheufler O, Farhadi J, Kovach SJ, et al. Anatomical basis and
clinical application of the infragluteal perforator flap. Plast Reconstr
Surg. 2006;118:1389–1400.
318. Wingate GB, Friedland JA. Repair of ischial pressure ulcers with
gracilis myocutaneous island flaps. Plast Reconstr Surg.
1978;62:245–248.
319. Apfelberg D, Finseth F. Double-muscle gracilis and sartorius
myocutaneous flap. Br J Plast Surg. 1981;34:41–43.
320. Lesavoy MA, Dubrow TJ, Korn HN, et al. “Sensible” flap coverage
of pressure sores in patients with meningomyelocele. Plast Reconstr
Surg. 1990;85:390–394, discussion 395–396.
321. Lin H, Hou C, Chen A, Xu Z. Treatment of ischial pressure sores
using a modified gracilis myofasciocutaneous flap. J Reconstr
Microsurg. 2010;26:153–157.
322. Maruyama Y, Ohnishi K, Takeuchi S. The lateral thigh fascio-
cutaneous flap in the repair of ischial and trochanteric defects. Br J
Plast Surg. 1984;37:103–107.
323. Gravvanis AI, Tsoutsos DA, Karakitsos D, et al. Application of the
pedicled anterolateral thigh flap to defects from the pelvis to the
knee. Microsurgery. 2006;26:432–438.
324. Lee JT, Cheng LF, Lin CM, et al. A new technique of transferring
island pedicled anterolateral thigh and vastus lateralis
myocutaneous flaps for reconstruction of recurrent ischial pressure
sores. J Plast Reconstr Aesthet Surg. 2007;60:1060–1066.
325. Bunkis J. Fudem GM. Rectus abdominis flap closure of ischiosacral
pressure sore. Ann Plast Surg. 1989;23:447–449.
326. Mixter RC, Wood WA, Dibbell DGS. Retroperitoneal transposition
of rectus abdominis myocutaneous flaps to the perineum and
back. Plast Reconstr Surg. 1990;85:437–441.
327. Pena MM, Drew GS, Smith SJ, Given KS. The inferiorly based
rectus abdominis myocutaneous flap for reconstruction of
recurrent pressure sores. Plast Reconstr Surg. 1992;89:90–95.
328. Nahai F, Silverton JS, Hill HL, Vasconez LO. The tensor fascia lata
musculocutaneous flap. Ann Plast Surg. 1978;1:372–379.
329. Dibbell DG, McCraw JB, Edstrom LE. Providing useful and
protective sensibility to the sitting area in patients with
meningomyelocele. Plast Reconstr Surg. 1979;64:796–799.
330. Luscher NJ, de Roche R, Krupp S, et al. The sensory tensor fasciae
latae flap: a 9-year follow-up. Ann Plast Surg. 1991;26:306–310,
discussion 311.
331. Ahluwalia R, Martin D, Mahoney JL. The operative treatment of
pressure wounds: a 10-year experience in flap selection. Int Wound
J. 2010;7:103–106.
332. Cochran JH Jr, Edstrom LE, Dibbell DG. Usefulness of the
innervated tensor fascia lata flap in paraplegic patients. Ann Plast
Surg. 1981;7:286–288.
333. Lewis VL Jr, Cunningham BL, Hugo NE. The tensor fascia lata V-Y
retroposition flap. Ann Plast Surg. 1981;6:34–37.
334. Schulman NH. Primary closure of trochanteric decubitus ulcers:
the bipedicle tensor fascia lata musculocutaneous flap. Plast
Reconstr Surg. 1980;66:740–744.
335. Withers EH, Franklin JD, Madden JJ Jr, Lynch JB. Further
experience with the tensor fascia lata musculocutaneous flap. Ann
Plast Surg. 1980;4:31–36.
336. Bovet JL, Nassif TM, Guimberteau JC, Baudet J. The vastus
lateralis musculocutaneous flap in the repair of trochanteric
pressure sores: technique and indications. Plast Reconstr Surg.
1982;69:830–834.

380.e8
SECTION II
CHAPTER 16 • Pressure sores
337. Dowden RV, McCraw JB. The vastus lateralis muscle flap:
technique and applications. Ann Plast Surg. 1980;4:396–404.
338. Hauben DJ, Smith AR, Sonneveld GJ, Van der Meulen JC. The use
of the vastus lateralis musculocutaneous flap for the repair of
trochanteric pressure sores. Ann Plast Surg. 1983;10:359–363.
339. Minami RT, Hentz VR, Vistnes LM. Use of vastus lateralis muscle
flap for repair of trochanteric pressure sores. Plast Reconstr Surg.
1977;60:364–368.
340. Siddiqui A, Wiedrich T, Lewis VL Jr. Tensor fascia lata V-Y
retroposition myocutaneous flap: clinical experience. Ann Plast
Surg. 1993;31:313–317.
341. Ramirez OM. The distal gluteus maximus advancement
musculocutaneous flap for coverage of trochanteric pressure sores.
Ann Plast Surg. 1987;18:295–302.
342. Hurwitz DJ. The distal gluteus maximus advancement
musculocutaneous flap for coverage of trochanteric pressure sores.
Ann Plast Surg. 1988;20:198–200.
343. Becker H. The distally-based gluteus maximus muscle flap. Plast
Reconstr Surg. 1979;63:653–656.
344. Little JW 3rd, Lyons JR. The gluteus medius-tensor fasciae latae
flap. Plast Reconstr Surg. 1983;71:366–371.
345. Chang SH. Anterolateral thigh island pedicled flap in trochanteric
pressure sore reconstruction. J Plast Reconstr Aesthet Surg.
2007;60:1074–1075.
346. Mehrotra S. Giant trochanteric pressure sore: use of a pedicled
chimeric perforator flap for cover. Indian J Plast Surg.
2009;42:126–129.
347. Coskunfirat OK, Ozgentas HE. Gluteal perforator flaps for
coverage of pressure sores at various locations. Plast Reconstr Surg.
2004;113:2012–2017, discussion 2018–2019.
348. Ishida LH, Munhoz AM, Montag E, et al. Tensor fasciae latae
perforator flap: minimizing donor-site morbidity in the treatment
of trochanteric pressure sores. Plast Reconstr Surg.
2005;116:1346–1352.
349. Hallock GG. The propeller flap version of the adductor muscle
perforator flap for coverage of ischial or trochanteric pressure
sores. Ann Plast Surg. 2006;56:540–542.
350. Benito-Ruiz J, Baena-Montilla P, Mena-Yago A, Miguel I.
Montanana-Vizcaino J. A complicated trochanteric pressure sore:
what is the best surgical management? Case report. Paraplegia.
1993;31:119–124.
351. Evans GR, Lewis VL Jr, Manson PN, et al. Hip joint
communication with pressure sore: the refractory wound and the
role of Girdlestone arthroplasty. Plast Reconstr Surg. 1993;
91:288–294.
352. Klein NE, Luster S, Green S, et al. Closure of defects from pressure
sores requiring proximal femoral resection. Ann Plast Surg.
1988;21:246–250.
353. Arregui J, Cannon B, Murray JE, O’Leary JJ Jr. Long-term
evaluation of ischiectomy in the treatment of pressure ulcers. Plast
Reconstr Surg. 1965;36:583–590.
354. Hackler RH, Zampieri TA. Urethral complications following
ischiectomy in spinal cord injury patients: a urethral pressure
study. J Urol. 1987;137:253–255.
355. Karaca AR, Binns JH, Blumenthal FS. Complications of total
ischiectomy for the treatment of ischial pressure sores. Plast
Reconstr Surg. 1978;62:96–99.
356. Rubayi S, Pompan D, Garland D. Proximal femoral resection and
myocutaneous flap for treatment of pressure ulcers in spinal injury
patients. Ann Plast Surg. 1991;27:132–138.
357. Anthony JP, Mathes SJ. Update on chronic osteomyelitis. Clin Plast
Surg. 1991;18:515–523.
358. Schiffman J, Golinko MS, Yan A, et al. Operative debridement of
pressure ulcers. World J Surg. 2009;33:1396–1402.
359. Vasconez LO, Schneider WJ, Jurkiewicz MJ. Pressure sores. Curr
Probl Surg. 1977;14:1–62.
360. Stal S, Serure A, Donovan W, Spira M. The perioperative
management of the patient with pressure sores. Ann Plast Surg.
1983;11:347–356.
361. Hentz VR. Management of pressure sores in a specialty center. A
reappraisal. Plast Reconstr Surg. 1979;64:683–691.
362. Constantian MB, ed. Pressure Ulcers: Principles and Techniques of
Management. Boston: Little, Brown; 1980.
363. Disa JJ, Carlton JM, Goldberg NH. Efficacy of operative cure in
pressure sore patients. Plast Reconstr Surg. 1992;89:272–278.
364. Levenson SM, Geever EF, Crowley LV, et al. The healing of rat skin
wounds. Ann Surg. 1965;161:293–308.
365. Isik FF, Engrav LH, Rand RP, et al. Reducing the period of
immobilization following pressure sore surgery: a prospective,
randomized trial. Plast Reconstr Surg. 1997;100:350–354.
366. Wagner D, Fox M, Ellis E. Developing a successful
interdisciplinary seating program. Ostomy Wound Manage.
1994;40:32–34, 36–38, 40–41.
367. Dover H, Pickard W, Swain I, Grundy D. The effectiveness of a
pressure clinic in preventing pressure sores. Paraplegia.
1992;30:267–272.
368. Garber SL, Rintala DH, Holmes SA, et al. A structured educational
model to improve pressure ulcer prevention knowledge in
veterans with spinal cord dysfunction. J Rehabil Res Dev.
2002;39:575–588.
369. Brace JA, Schubart JR. A prospective evaluation of a pressure
ulcer prevention and management E-Learning Program for
adults with spinal cord injury. Ostomy Wound Manage.
2010;56:40–50.
370. Tavakoli K, Rutkowski S, Cope C, et al. Recurrence rates of ischial
sores in para- and tetraplegics treated with hamstring flaps: an
8-year study. Br J Plast Surg. 1999;52:476–479.
371. Stevenson TR, Pollock RA, Rohrich RJ, VanderKolk CA. The
gluteus maximus musculocutaneous island flap: refinements
in design and application. Plast Reconstr Surg. 1987;79:
761–768.
372. Relander M, Palmer B. Recurrence of surgically treated
pressure sores. Scand J Plast Reconstr Surg Hand Surg.
1988;22:89–92.
373. Griffith BH, Schultz RC. The prevention and surgical treatment of
recurrent decubitus ulcers in patients with paraplegia. Plast
Reconstr Surg Transplant Bull. 1961;27:248–260.
374. Evans GR, Dufresne CR, Manson PN. Surgical correction of
pressure ulcers in an urban center: is it efficacious? Adv Wound
Care (New Rochelle). 1994;7:40–46.
375. Singh DJ, Bartlett SP, Low DW, Kirschner RE. Surgical
reconstruction of pediatric pressure sores: long-term outcome. Plast
Reconstr Surg. 2002;109:265–269, quiz 270.
376. Kerr-Valentic MA, Samimi K, Rohlen BH, et al. Marjolin’s ulcer:
modern analysis of an ancient problem. Plast Reconstr Surg.
2009;123:184–191.
377. Tutela RR Jr, Granick M, Benevenia J. Marjolin’s ulcer arising in a
pressure ulcer. Adv Skin Wound Care. 2004;17:462–467.
378. Esther RJ, Lamps L, Schwartz HS. Marjolin ulcers: secondary
carcinomas in chronic wounds. J South Orthop Assoc.
1999;8:181–187.
379. Rubayi S, Ambe MK, Garland DE, Capen D. Heterotopic
ossification as a complication of the staged total thigh muscles
flap in spinal cord injury patients. Ann Plast Surg. 1992;
29:41–46.
380. Georgiade N, Pickrell K, Maguire C. Total thigh flaps for extensive
decubitus ulcers. Plast Reconstr Surg (1946). 1956;17:220–225.
381. Niazi ZB, Salzberg CA. Operative repair of pressure ulcers. Clin
Geriatr Med. 1997;13:587–597.
382. Barnett CC Jr, Ahmad J, Janis JE, et al. Hemicorporectomy: back to
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383. Janis JE, Ahmad J, Lemmon JA, et al. A 25-year experience with
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384. Peterson R, Sardi A. Hemicorporectomy for chronic pressure ulcer
carcinoma: 7 years of follow-up. Am Surg. 2004;70:507–511.

SECTION II • Trunk Surgery
17 
Perineal reconstruction
Hakim K. Said and Otway Louie
SYNOPSIS
■ The surgical site is typically hostile after resection and/or radiation for
an underlying condition.
■ Healthy tissue transfer is usually necessary to mitigate wound-healing
challenges.
■ A proactive surgical approach can help lessen impact of
complications.
Introduction
Perineal reconstruction poses the challenge of healing a
problem area despite a number of site-specific obstacles.
Although a number of benign conditions exist that can require
resurfacing perineal skin, more frequently reconstruction is
needed after treatment of underlying cancer. Modern treat-
ment of malignancies in this region has evolved to consistently
use neoadjuvant radiation therapy, which can yield a high rate
of complications at the time of surgical intervention. Local
effects of radiation therapy and close proximity (combined in
many cases with ostomies) to bowels, reproductive organs,
and bladder can all complicate reconstructive flap inset,
contaminate the surgical site, and threaten surgical outcomes.
Successful reconstruction takes into account these impedi-
ments and minimizes the consequences of complications in
this hazardous region.
Access the Historical Perspective section online at

Basic science/disease process
The processes requiring reconstruction of the perineum
can broadly be broken into superficial and deep processes
(Table 17.1). Benign conditions primarily include hidradenitis
suppurativa, infectious destructive processes such as fasciitis
or Fournier’s gangrene, and trauma, but can range to other
rarer dermatologic conditions such as pyoderma gangreno-
sum and vasculitic ulcers. Malignant superficial lesions
usually include vulvar cancers and cutaneous lesions in the
area. These entities have in common the depth of involve-
ment, which typically leaves only an external cutaneous
deficit on the perineum (see Figs. 9.13 & 9.18). Also, radiation
treatment is unusual, so the surrounding skin is typically
healthy. Once the primary process is addressed and resolving,
the defect can begin secondary healing. Negative pressure
therapy and skin grafts can often play a useful role in shorten-
ing the time to healing. Some authors advocate locoregional
flaps to hasten treatment for superficial defects, although this
has yet to gain universal use.17 Challenges to healing in this
area include a high bacterial bioburden in many of the caus-
ative etiologies, an inherently moist surgical site, and pressure,
tension, and shearing forces, which threaten to disrupt the site
as the patient begins to mobilize. Outcomes are more favor-
able in this group.
Deep defects are primarily the result of malignancy, includ-
ing colorectal cancer, urologic, and gynecologic cancers, most
of which originate from and involve pelvic structures (see
Figs. 9.11 & 9.12). Abdominoperineal resection or exenteration
has been demonstrated to provide the best cure in these cases.
Typically, this extensive resection is accompanied by periop-
erative radiation therapy. Treatment of these more complex
defects must be individualized for the missing and exposed
structures. The bony pelvis effectively splints open the pelvic
outlet, so contraction cannot occur, and seromas are common.
Further impediments to healing such as fistulas and radiation
changes in the area generally mean these defects are frequently
contaminated, prone to infection, and will not heal without
the addition of a non-radiated tissue transfer. After extensive
resection, large areas of dead space and loss of support allow
the abdominal viscera to fall into the irradiated pelvic basin.
This can lead to pelvic hernias, adhesions, obstruction, and
fistulas, all of which can be disastrous to treat secondarily.
  Access video lecture content for this chapter online at expertconsult.com

381.e1
Historical perspective
Historical perspective
The evolution of perineal reconstruction over the last century
parallels the development of the reconstructive ladder. Since
Miles described abdominoperineal resection in 1910 for carci-
noma of the rectum, numerous methods of reconstructing the
perineum have been described. In his original paper, the peri-
neal wound was simply packed with gauze, with closure by
secondary intention or delayed primary closure.1 Brunschwig’s
introduction of pelvic exenteration provided the potential for
oncologic cure but left an even larger pelvic defect with sig-
nificant associated morbidity.2 This led to significant morbid-
ity associated with an open perineal wound, and Altmeier
subsequently introduced the concept of primary closure of the
perineal wound with continuous suction drainage.3 Although
there was some degree of success with both primary and
secondary closure of the perineum, certain perineal wounds
seemed predisposed to breakdown, particularly those that
were irradiated and contaminated. Management of the drain-
ing perineal wound proved difficult; split-thickness skin
grafts were attempted with limited success.4
The advent of axial-pattern flaps ushered in the next rung
on the reconstructive ladder for perineal reconstruction.
Although first applied for coverage of exposed bone in the
lower extremity, muscle flaps were soon utilized throughout
the body, including the perineum.5 The gluteus maximus flap
was described as a potential cure for a chronic perineal sinus.6
The rectus abdominis flap subsequently emerged to be a
workhorse in perineal reconstruction.7,8 Transverse, vertical,
and oblique skin paddles have been designed and used
effectively. The gracilis muscle has also been described exten-
sively for use in the perineum.9,10
More recently, fasciocutaneous flaps have been reported
for perineal reconstruction. Wee introduced the concept of
neuro-pudendal thigh flaps for vaginal reconstruction, creat-
ing sensate lining for the vaginal wall.11 The anterolateral
thigh flap has emerged as a versatile flap that can be applied
to perineal reconstruction as well as complex pelvic wounds.12,13
Finally, advances in microsurgery have allowed free flaps
to be performed routinely with reliable results. Although the
utility of free flaps in perineal reconstruction has been some-
what limited by the ample locoregional flaps available, there
have been reports of free flaps for coverage of large defects
in the perineal area, particularly in conjunction with sacral
defects.14 Moreover, microsurgical techniques developed over
the last decade have allowed perforator flaps to be applied to
this region of the body as well, based on essentially every
regional vascular system.15,16 In summary, significant advances
have been made over the past century for perineal reconstruc-
tion. The remainder of this chapter will describe in detail
some of the flaps routinely used today for perineal coverage,
and touch on promising advances in technique that are on the
horizon.

382
SECTION II
CHAPTER 17 • Perineal reconstruction
anticipated in advance. Preoperative consultation is important
to manage patient expectations, outline the possible extent of
surgery, and prepare for postoperative adversity. Such cases
may involve more extensive external pudendal defects (Figs.
17.2 & 17.3) or deeper structures (Fig. 17.4). In the event that
vaginal resection is necessary, preferences regarding vaginal
versus simple perineal reconstruction should be discussed,
along with a thorough dialogue about sexual function. Further
details and management of vaginal reconstruction are dis-
cussed in depth in Chapter 14.
Patient selection
Patients with superficial defects are more straightforward in
management; as their underlying process resolves, the defect
begins to heal secondarily, even in response to a conventional
wet to moist dressing regimen. Typically a modest, shallow
Nearby organs such as the bladder or vagina may also be
resected in part or whole as part of the treatment course.
Finally, the surgical incision is inherently moist, and mobiliz-
ing the patient can cause pressure or shearing stresses, further
compounding the difficulty of healing a radiated closure at
that location. Surgical outcomes reflect the many challenges
posed in this group.
Diagnosis/patient presentation
Patients with superficial disease may present at various stages
in their treatment. As a rule, reconstruction should not be
initiated until the primary process is identified and resolved
with repeated surgical debridements or excisions; underlying
medical conditions or autoimmune disorders should be
treated. Typically, areas of external pudendal skin are involved
and will require resurfacing in some fashion (Fig. 17.1).
Patients with deep disease are typically treated in conjunc-
tion with a multidisciplinary oncologic team for an underlying
malignancy. Often the extent of the defect is not obvious
until after the surgical resection is performed, and must be
Table 17.1  Processes requiring reconstruction of the perineum
Process
Etiology
Complicating factors
Reconstructive options
Superficial
(simple, mostly benign)
Hidradenitis suppurativa
Necrotizing fasciitis
Fournier’s gangrene
Trauma
Autoimmune ulcers
Vulvar cancer
Bacterial bioburden
Moisture
Mobility
Secondary healing
Negative pressure therapy
Skin graft
Fasciocutaneous perforator flaps
Deep
(complex, malignant)
Colorectal cancer
Vulvar cancer
Vaginal cancer
Uterine cancer
Bladder cancer
Radiation
Ostomies
Contamination
Dead space
Pelvic hernia
Moisture
Mobility
Rectus abdominis flap
Gracilis flap
Anterolateral thigh flap
Singapore flap
Fasciocutaneous perforator flaps
Free flap
Fig. 17.1  Perineal hidradenitis.
Fig. 17.2  Post-radiation lymphangiosarcoma after treatment of vulvar cancer.

383
Patient selection
In the case of deeper malignancies, such as colorectal,
gynecologic, or urologic cancer, radiation therapy is part of
the preoperative routine in most centers. This factor alone is
the most significant indication for flap reconstruction at the
time of resection. Large prospective series suggest that
abdominal based flaps demonstrate the most favorable out-
comes and mildest complication profile in this setting, even
compared to thigh flap reconstruction.18 This must be bal-
anced with the abdominal morbidity of the harvest. Some
surgeons prefer to avoid using abdominal flaps if ostomies
are necessary on both sides, although these can be inset
through the external oblique musculature with no additional
morbidity. A vertical skin pedicle provides the most discreet
scar, but an oblique paddle can provide more tissue by
extending off the muscle, effectively also extending its reach.
Pre-existing abdominal wall defects might direct some sur-
geons to alternative flap options. Nevertheless, Butler has
shown no increased incidence of abdominal wall problems
after abdominal flap harvest.18,19 Rarely, perineal resection can
be performed without laparotomy, and this might predispose
toward use of a non-abdominal flap option.
The complication profile of the gracilis flap is also reason-
able and represents a dramatic improvement over primary
closure under these circumstances. Early studies comparing
gracilis reconstruction to primary closure demonstrate a
dramatic reduction in infectious complications from 46% to
12% with flap reconstruction.20
The anterolateral thigh flap represents an alternative option
with documented excellent reliability for many applications,
but with less support for its use in this setting at this point.
One recent study suggests it has reliability comparable to
abdominal flaps, and other studies may corroborate this in
time.
Some surgeons favor a posterior thigh flap, harvested in
similar fashion to the anterolateral thigh flap, but the axial
nature of the perfusion off the inferior gluteal artery has been
called into question. Recent series document a wound healing
complication rate of over 50% using this method,21 which does
not compare favorably to abdominal flaps.
For defects with less dead space or requiring less bulk, skin
flap reconstruction (e.g., Singapore or perforator flaps) can be
used, although outcome data are more mixed and overall less
favorable compared to abdominal flaps. Complications are
reported to range from 7% to 62%.22–24 Recent outcome studies
are not available directly comparing this method to other
options in a head-to-head fashion.
Massive defects in pelvic support may in fact require
multiple flaps. Occasionally, pelvic floor support is needed in
the form of mesh reinforcement. In a hostile, radiated, often
contaminated surgical site, prosthetic mesh is contraindicated.
Newer bioprosthetic options provide a reinforcement alterna-
tive that is more robust in the face of complications.25
Finally, if the two abdominal flaps and eight thigh-based
flaps are unavailable or insufficient for the defect, there are
several reports of distant flaps used in conjunction with
microsurgical transfer. Composite thigh tissues can be trans-
ferred en bloc, and large surface area flaps such as the latissimus
dorsi have been reported in extreme cases.
Laparoscopic or robotic techniques represent a new fron-
tier in both extirpative and reconstructive surgeries. Per-
forming the entirety of an abdominoperineal resection is
now possible through incisions that total 2 cm in length. As
perineal defect is left. A number of publications support the
use of a negative pressure therapy plan to accelerate the
healing process. Within a matter of weeks, a healthy wound
bed can be established, confirming the suitability of these
patients for skin grafting. If the wound fails to begin the
healing process despite wound healing optimization, a more
complex approach and tissue transfer might be warranted.
Especially for superficial malignancies such as vulvar cancer,
reconstruction at the time of resection is feasible, and standard
in many centers. Application of microsurgical principles for
perforator flap dissection has been proposed in that setting.
Fig. 17.3  External perineal skin and soft-tissue loss.
Fig. 17.4  Complex perineal defect involving external skin, soft tissues, vagina, and
pelvic floor.

384
SECTION II
CHAPTER 17 • Perineal reconstruction
Fig. 17.5  Extensive but subcutaneous defect of the external perineal skin.
Fig. 17.6  Multiple regional flaps for reconstruction. Right Singapore flap used in
conjunction with bilateral V–Y advancement flaps. (Courtesy of Peter C. Neligan,
MD).
techniques are developed for resection without an open lapa-
rotomy, the necessity for harvesting non-radiated tissue to
fill the radiated pelvic basin remains. Typically this entails
harvest of the rectus muscle through the posterior sheath
using either a laparoscopic or robotic approach. Laparoscopic
tools are widely available, but the robotic equipment is less
widely available, and surgeons trained in using that for
reconstruction are rarer still. This will undoubtedly change
as the growing field of minimally invasive reconstruction
matures.
Treatment/surgical technique
Skin graft reconstruction
Benign, uncomplicated wounds of the perineum that granu-
late in response to dressing changes or negative pressure
therapy can usually be treated in a staged fashion with split-
thickness skin grafts.
Regional skin flaps
Processes such as Fournier’s gangrene may leave more exten-
sive but still subcutaneous defects that can be reconstructed
with local flaps. Exposed subcutaneous structures such as
testes can be buried under nearby intact skin if available.
These adjacent areas of intact skin on the thighs or perineum
can also be advanced using a V–Y pattern, rotational or key-
stone design to provide resurfacing (Figs. 17.5, 17.6). Some
authors have described tissue expansion in conjunction with
regional flaps to augment the amount of subcutaneous cover-
age available, for example in the case of missing scrotal
coverage.26 Perforator-based flaps have been described for
superficial defects using medial circumflex femoral vessels,17,27
profunda femoris perforating branches,28 and almost any
vascular axis in the region.15
Rectus-based reconstruction
Rectus-based flaps have emerged as workhorses for more
complex perineal reconstruction. These flaps provide well-
vascularized tissue with adequate bulk to fill dead space. In
addition, lining for external or vaginal wall coverage can be
obtained if harvested as a musculocutaneous flap. They are
known for having a wide arc of rotation with a reliable pedicle.
They have been shown to decrease the risk of perineal com-
plications in irradiated APR defects.29 When compared to
thigh-based flaps, rectus-based flaps had lower major compli-
cations without increased abdominal morbidity.18
The rectus flap can be muscular or myocutaneous, depend-
ing on whether external skin or vaginal lining is needed for
reconstruction. The right rectus is typically used, saving the
left rectus for a colostomy if needed. After the resection is
complete, the deep inferior epigastric vessels are examined to
confirm they are patent, undamaged by the resection, and
preferably pulsatile before proceeding with flap design. The
skin paddle is based on the periumbilical perforators of the
deep inferior epigastric vessels,51 and can be oriented in verti-
cal, transverse, or oblique directions (Figs. 17.7 & 17.8; see
Figs. 14.6 & 14.7). The vertical design theoretically includes
more perforators as the skin paddle overlies the length of the
rectus; however, its arc of rotation is limited by the muscle
itself, and the bulk of the muscle itself can make insetting
difficult, particularly in a narrow male pelvis. The transverse
paddle has been well described for perineal reconstruction as
well, and provides excellent cosmesis for the donor site.30
Dumanian and others have had success with an oblique
design for the rectus flap, noting the long, excellent arc of
rotation and thin, reliable skin paddle obtained.31,32,53 In addi-
tion, cadaver injection studies have shown flow in a lateral
and superior oblique direction from the periumbilical perfora-
tors. After marking the periumbilical perforators with a
Doppler, a skin paddle is designed with an axis towards the
ipsilateral tip of the scapula, ending at the anterior axillary
line. Flaps up to 12 × 30 cm can be obtained with this design.
Once the skin paddle has been marked in one of these
orientations, the skin incisions are made and dissection carried

385
Treatment/surgical technique
down to the external oblique and rectus fascia. The skin
paddle is dissected circumferentially, approaching the deep
inferior epigastric perforators coming through the rectus
muscle. The fascia immediately adjacent to these perforators
is opened, and the anterior sheath elevated off the rectus
muscle. The muscle is then dissected free of the rectus sheath,
working down toward the deep inferior epigastric vessels.
These are identified lateral to the rectus beneath the arcuate
line. The superior rectus is divided, and the muscle transposed
out of the rectus sheath. The vascular pedicle can be mobilized
but does not need to be skeletonized. The insertion of the
rectus on the pubis typically does not need to be divided
completely and is left intact at least in part to help prevent
traction injury to the pedicle.
The flap is then delivered down through the pelvis and out
to the perineum (see Fig. 14.7). The requisite skin for external
lining or vaginal reconstruction is marked, and the remainder
of the skin paddle de-epithelialized and inset under the radi-
ated skin edges (Fig. 17.9). The skin paddle may be tubed if
needed for total vaginal reconstruction (Fig. 17.10). The flap
Fig. 17.7  Design of transverse rectus abdominis myocutaneous (TRAM) flap for
perineal and pelvic reconstruction.
Fig. 17.8  Design of oblique rectus abdominis myocutaneous (ORAM) flap for
perineal and pelvic reconstruction. Note skin paddle designed around periumbilical
perforators, extending toward ipsilateral scapular tip.
Fig. 17.9  Cutaneous paddle inset for external perineal skin reconstruction.
Fig. 17.10  Cutaneous paddle inset for vaginal and perineal reconstruction.

386
SECTION II
CHAPTER 17 • Perineal reconstruction
is then inset with a layered closure. The fascial donor site is
closed primarily if possible, or the remaining anterior and
posterior sheaths are sewn together and used to span the
fascial defect. Bioprosthetic mesh may be used to repair
extensive anterior sheath defects. The abdominal skin is
closed primarily over closed suction drainage.
Gracilis flap
The gracilis flap was first introduced in its myocutaneous
form by McCraw and used as a healthy tissue to augment
genital reconstruction.33 As described, it was based on the
medial circumflex femoral vessels to the gracilis muscle, and
to the overlying skin. Subsequent studies have shown that the
perforators originating from the deep femoral system only
pass reliably through the gracilis muscle proximally. To con-
sistently capture the perfusion to distal portions of a longitu-
dinal skin paddle, the fasciocutaneous vascular network
around the gracilis muscle must be widely harvested intact
from proximal to distal as described by Whetzel.34
A line is drawn from the adductor insertion on the pubis
to the semitendinosus muscle at the medial condyle of the
knee. Centered on this axis at the anterior edge of the gracilis
muscle, the skin flap is designed as a 6–10 cm wide ellipse
that can reach up to 30 cm in length (see Fig. 14.9A). This
position is slightly more anterior than the traditional design,
which failed to harvest peri-gracilis fascia and was associated
with a less reliable skin paddle. The skin pattern is incised
distally to identify the thin, round gracilis muscle near the
knee, and a bowstring technique is used to confirm its course.
If necessary, the skin design is adjusted to overlie the anterior
edge of the muscle. The paddle is then incised anteriorly, and
beveling dissection outward ensures that the gracilis is har-
vested encased within its surrounding fat, vessels, and fascia,
essentially denuding the sartorius and adductor musculature
(Fig. 17.11; see Fig. 14.9B). The perforating branches off the
superficial femoral vessels are divided very close to their
take-off, preserving the longitudinal arcade of fasciocutane-
ous vessels in communication with the primary pedicle off the
deep femoral system proximally. The greater saphenous vein
is divided proximally and distally and preserved within the
substance of the flap as an additional venous conduit. The flap
is isolated back to its pedicle off the medial circumflex femoral
vessels, usually at 7–10 cm distal from the pubis (see Fig.
14.9F). Upgoing adductor branches are divided to yield extra
length. The muscular origin is exposed and divided off the
pubis to allow rotation of the flap 180 degrees into the
perineum. To reduce the chance of flap ptosis, the flap is
suspended from high within the perineal defect, or into the
pelvis if possible. Layered closure over drains completes the
inset (Figs. 17.12 & 17.13).
Anterolateral thigh flap
The anterolateral thigh flap was first described by Song in
1984.35 Since that time it has become a valuable tool in the
armamentarium of the reconstructive surgeon, with extensive
uses in head and neck, trunk, and lower extremity reconstruc-
tion.36 Luo first described its use in perineal reconstruction
after failed gracilis flaps in 2000.37 Increasing experience
with it in perineal reconstruction has confirmed its utility in
complex pelvic defects.12,13 It provides a regional flap that can
Fig. 17.11  Cross-sectional view of gracilis myocutaneous flap harvest. The
fasciocutaneous vascular network around the gracilis muscle must be widely
harvested to preserve perfusion to the distal tip of the skin. Adductor magnus,
vastus medialis, sartorius, and semitendinosus muscles are denuded by the harvest,
as described by Whetzel.34 (Adapted from Whetzel TP, Lechtman AN. The gracilis
myofasciocutaneous flap: vascular anatomy and clinical application. Plast Reconstr
Surg. 1997;99:1642–1652; discussion 1653–1655.)
Rectus femoris
Femur
Sartorius
Gracilis
Adductor magnus
Biceps femoris
Adductor longus
Semitendinosus
Semimembranosus
Vastus lateralis
Vastus intermedius
Vastus medialis
Sciatic nerve
Great saphenous vein
Superficial femoral artery
Fig. 17.12  Gracilis myocutaneous flap elevated before inset. Pedicle is visible
7–10 cm from pubis.

387
Treatment/surgical technique
Fig. 17.13  Bilateral gracilis myocutaneous flaps for large area external perineal
defect.
provide large, reliable skin paddles and muscle in the form of
the vastus lateralis as well.
With the patient in a supine position, a line connecting the
anterior superior iliac spine with the superolateral patella is
marked (Fig. 17.14). A circle with a 3 cm radius is marked at
the center of this longitudinal axis, delineating the most
Fig. 17.14  Design of anterolateral thigh flap, centered midway along an axis
between the anterior superior iliac spine (ASIS) and the superolateral corner of the
patella.
Anterior superior
iliac spine
Lower outer quadrant
of circle with 3 cm radius
centered on midpoint of
line between lateral
patella and anterior
superior iliac spine
Patella
common location of perforators of the descending branch of
the lateral femoral circumflex vessels. Locations of perforators
are confirmed by Doppler, and the skin paddle is designed as
an ellipse centered on these perforators.
The anterior incision is made first, dissecting down to the
fascia overlying the rectus femoris muscle (Fig. 17.15). Dissec-
tion proceeds laterally, either in a subfascial or suprafascial
plane, looking for septocutaneous perforators, which are then
followed superomedially back to the descending branch of
the lateral femoral circumflex vessels. Intramuscular perfora-
tors can be harvested with a small cuff of vastus lateralis
muscle to minimize risk of injury to the perforators. The
posterolateral incision is subsequently made and the harvest
completed.
The flap can be delivered through either a perineal or
inguinal route, as elegantly described by Yu.38 If a perineal
skin defect exists, the flap is delivered under the rectus femoris
and through a subcutaneous tunnel in the medial thigh to
reach the perineum (see Fig. 17.9). If the perineal defect can
be closed primarily, the inguinal ligament can be divided and
the vastus lateralis muscle delivered intraperitoneally through
the abdominal wall to fill any dead space in the pelvis (Fig.
17.16). The flaps are then inset with layered closure and ample
drainage.
Singapore flap
First reported by Wee, Singapore flaps are fasciocutaneous
flaps harvested from the groin ideally using non-hair-bearing
skin just lateral to the labia majora.11 These flaps are based on
Fig. 17.15  Elevation of anterolateral thigh flap, including skin, soft tissue, fascia,
and occasionally a small cuff of muscle. Perforators are pursued toward the septum
between the vastus lateralis and rectus femoris, and then followed superomedially
up to the descending branch of the lateral circumflex femoral vessels.
Tensor fasciae
latae
Lateral femoral cutaneous
nerve branch
Vastus lateralis
Rectus femoris
(under fascia)
Lateral branch of
descending branch
of lateral femoral
circumflex artery

388
SECTION II
CHAPTER 17 • Perineal reconstruction
is contraindicated and the previous flaps are not available. In
such cases, using a profunda femoris perforator flap design is
recommended (see perforator flaps, below). Not all surgeons
are comfortable with this style of dissection, and the literature
shows far fewer reports of its use in this manner. These various
issues prevent it from being a first-line choice in comparison
with the better-established and supported flaps above.
Perforator flaps
As the use of perforator-based techniques becomes more
widespread, a number of fasciocutaneous perforator or free-
style flaps have been described with good success in perineal
reconstruction. Originally described for vulvar cancer, which
results in external cutaneous defects without radiation treat-
ment, a number of authors have reported their usefulness
even in settings of deeper resection and radiated tissues.
Mostly based on perforators from the internal pudendal
artery, these include the Singapore flap, pudendal thigh flap,
lotus leaf flap, and gluteal fold flap.15,16,42,43 The latter of
these are more recent designs, which are less prone to hair-
bearing, thus eliminating the most significant liability of the
Singapore flap. Also described are local perforators from the
thigh vessels, either the profunda femoris or medial circum-
flex femoral arteries (Fig. 17.18). Many of these flaps can be
designed remotely enough to yield non-radiated tissue for
transposition into the defect. For both deep and superficial
resection defects, bilateral flaps can be employed to provide
tissue with minimal morbidity. As surgeons become more
comfortable with perforator flaps, the prevailing algorithms
for perineal reconstruction may evolve, although the strong,
reliable record of the muscle flaps still leaves them as the first
line option in most cases.
Free flap
Given the number of reliable local flap options, microsurgical
tissue transfer is rarely indicated. In extenuating circum-
stances, however, large composite flaps of skin and muscle
from the thigh can be elevated and re-anastomosed using
gluteal recipient vessels.14 Alternatively, the latissimus dorsi
muscle can be harvested on the thoracodorsal vascular system
and anastomosed to the gluteal vessels.
Minimally invasive flap harvest
The rectus flap has emerged to be a workhorse in perineal
reconstruction in these settings, as it brings in well-vascularized
tissue to an often-irradiated bed with a large amount of dead
space. However, the traditional rectus flap harvest involves a
midline laparotomy. Minimally invasive abdominoperineal
resections and pelvic exenterations are increasingly being
used to limit morbidity. In these settings, some groups have
explored the possibility of harvesting the rectus flap in a simi-
larly minimally invasive manner. Early experiences focused
on endoscopic-assisted harvests. In 1996, Bass described using
a balloon dissector to create a plane between the posterior
sheath and rectus muscle, followed by CO2 insufflation and
rectus harvest.44 Subsequently, Friedlander et al. utilized a
tripod device to improve visualization during minimally
invasive rectus harvest in cadavers.45 Both of these techniques
utilized incisions through the anterior sheath. The first clinical
case of laparoscopic harvest was performed by Greensmith in
the posterior labial arteries, tracing back from the perineal
arteries, which in turn originate from the internal pudendal
vessels. A horn-shaped flap up to 15 × 6 cm is designed lateral
to the labia majora and harvested to include deep fascia and
adductor epimysium to preserve dermal blood supply. The
original description divided the dermis at the base of the
design and tunneled the flap into the defect. In order to maxi-
mize perfusion under the most adverse circumstances, Woods
subsequently described a modification to avoid dividing the
skin at the base of the flap.39 This design added an incision
made at the posterior base of the labia majora in order to
avoid dividing the dermal circulation to the flap entirely. The
released labia are allowed to shift anteriorly, and the flaps are
transposed 70 degrees through the release incision into the
defect (Fig. 17.17; see Fig. 14.4). Although this method is well
established, in some patients it may transpose hair-bearing
skin, which can be a liability, especially in vagino-perineal
reconstruction. Some populations are less hirsute, and this
issue is less important. For use in European populations,
however, some groups advocate depilatory treatments prior
to this surgery. Newer methods using fasciocutaneous flaps
based on other perforators (see perforator flaps below) elimi-
nate this issue and are becoming a preferred solution.
Posterior thigh flap
Although this flap has been described based on axial flow
from the inferior gluteal artery,52 this pattern of perfusion has
been called into question. A significant number of flaps in this
distribution are actually based on perforators from the pro-
funda femoris vessels,28 which are frequently divided using
the flap design as traditionally described.40,41 This may relate
to the high wound healing complication rate (53%) recently
reported in a series of these flaps.21 There are settings where
this flap can be useful, especially when an abdominal approach
Fig. 17.16  Anterolateral thigh flap delivered under the inguinal ligament into the
pelvis, then out through the pelvic defect to fill the pelvic dead space and
reconstruct the perineal skin defect. The flap can be tunneled subcutaneously
across the thigh if no pelvic defect is present.